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JANUARY 2012Question: 1You are examining an 8-year-old girl who sustained head and neck injuries on a playground. As she was running around the monkey bars, she slipped and fell into the metal pole, sustaining injury to her anterior neck and falling backward. She cried immediately, complained of headache and throat and neck pain, and coughed up a small amount of blood. Emergency medical services personnel immobilized her and transported her to the emergency department. On physical examination, her airway is intact with no stridor, and she has equal breath sounds, no cardiac murmurs, intact peripheral pulses, and no obvious oral lacerations. She appears comfortable but wants to take off the cervical collar, stating that it is bothering her. Her respiratory rate is 28 ?breaths/min, heart rate is 108 beats/minute, blood pressure is of 110/70 mm Hg, and temperature is 37.0?C. Secondary survey reveals bruising and tenderness along the mid-tracheal line, with a 2x1-cm lateral hematoma on the right side that is unchanged from when the paramedics assessed her at the scene. She has no cervical vertebral point tenderness. Findings on the remainder of her examination are unremarkable.Of the following, the MOST important timely investigation for this patient is:A.bedside fiberoptic puted tomography (CT) scan of the cervical spineC.CT scan of the neck with angiographyD.magnetic resonance imaging of the cervical spineE.soft-tissue neck radiographyCorrect answer CThe girl described in the vignette has clinical signs of possible airway or vascular injury due to blunt trauma to her neck. She has cough with blood in sputum, and tenderness along the mid-tracheal line with a neck hematoma. Because she is clinically stable, a CT scan of the neck with angiography should be obtained to assess for possible laryngeotracheal and carotid injury. Fiberoptic laryngoscopy should be performed in the controlled setting of the operating room because the procedure can result in acute airway compromise that requires establishment of an immediate surgical airway. Further, it is not helpful in assessing for vascular injury. Cervical spine CT scan or magnetic resonance imaging may be a helpful adjunct for this patient but is not the most important immediate investigation. Soft-tissue radiography of neck is not indicated.Blunt trauma to the neck can cause substantial injury to airway cartilages, major blood vessels, and the cervical spine. The type and degree of injury depends on the mechanism and force. For example, a seat belt can cause anterior neck injury in a high-velocity motor vehicle crash or such an injury can occur in an unrestrained passenger or driver hitting the dashboard or steering wheel. A clothesline injury can occur while riding a jet ski, snowmobile, all-terrain vehicle, or bicycle, and a direct blow to the neck can be seen with inflicted trauma. The relatively large head size of pediatric patients may increase the likelihood of acceleration-deceleration neck injury in motor vehicle crashes. However, the relatively small neck size and bigger head size can prevent pediatric patients from sustaining significant neck injuries from a direct impact. Edema resulting from blunt trauma is more deleterious to the relatively small-sized pediatric airway compared to adult patients. Associated conditions may increase the likelihood of developing injury, such as an expanding hematoma resulting in airway or vascular compromise in a patient who has hemophilia.Clinical signs that should raise the suspicion for a serious injury to deep structures are:Tenderness along the mid-tracheal lineHematoma, crepitus Voice changes, stridor, hoarsenessDistortion of the airway cartilage anatomyUnequal carotid pulses, carotid bruit, Horner syndrome (due to injury to the sympathetic nerves along the carotid artery)Hematemesis, swallowing difficulty Cervical spine tendernessNeurologic findings (due to cervical or carotid/vertebral artery injuries)Associated severe torso injuryPhysical examination should include assessment for tracheal midline tenderness and carotid bruits as well as cervical spine and neurologic evaluation. Severe carotid artery injury can result in cerebral infarction or ischemia, causing motor, sensory, and speech loss on the opposite side. Nausea, visual disturbance, and vertigo can be signs of vertebral artery injury, which is rare and easily missed.CT scan is used for assessment of laryngotracheal injury (eg, cartilage fracture, vocal cord hematoma or rupture, tracheal hematoma) in a stable patient because it provides the best anatomic details of the airway cartilages. Indirect or direct fiberoptic laryngoscopy is indicated when airway injury is strongly suspected clinically in the presence of normal-appearing radiographs. Computed angiography is indicated to assess for carotid injuries (eg, tear, hematoma, thrombosis, dissections, pseudoaneurysms), but vascular angiography remains the gold standard. Doppler duplex ultrasonography can be helpful but is not indicated as the sole study to assess for vascular injuries. Magnetic resonance angiography has been reported to have high sensitivity for detecting vascular injuries in neck trauma but may be difficult to obtain in a timely fashion. Swallow studies or endoscopy may be indicated when esophageal injury is suspected.For an unstable patient, the airway should be stabilized in the operating room, when possible. Extreme caution is required during intubation (orotracheal or other routes) because a partial tracheal injury can be converted into a full tracheal rupture. Tracheal tube introducers and flexible fiberoptic laryngoscopy can be helpful in such cases. Percutaneous cricothyroidotomy with jet insufflations is a temporizing measure in children younger than 12 years of age until a more secure airway can be established in the operating room. Tracheostomy or cricothyroidotomy is used for children older than 12 years of age when endotracheal intubation cannot be accomplished. It is imperative to maintain cervical spine immobilization at all times while treating such patients. When carotid vascular injury is documented, anticoagulation should be considered for the patient who is not a surgical candidate. Chest radiography is recommended for all patients who have significant neck trauma to assess for associated pulmonary and chest wall injuries.Although multicenter studies (eg, National Emergency X-Radiography Utilization Study and Pediatric Emergency Care Applied Research Network) have been undertaken, no consensus has been reached on a clinical rule to manage cervical spine injuries in pediatric patients. The primary reason is the relatively few significant cervical spine injuries in pediatric patients, especially among those younger than 8 years of age. Hence, the recommendation is to assess patients clinically and plan their treatment individually. Factors associated with documented cervical spine injury in different studies are significant mechanism of injury, altered mental status, midline tenderness, distracting injury, focal neurologic deficit, or significant torso injury. Plain radiographs are indicated for patients who have such risk factors. Use of cervical spine CT scans or magnetic resonance imaging can be based on individual case presentations and should not be the required investigations to clear the cervical spine, thereby avoiding unnecessary radiation exposure and morbidity due to the delay in cervical spine collar removal.?Question: 2A 4-year-old girl presents to the emergency department after having three episodes of bloody emesis. She was born in China and was recently adopted and moved to the United States with her adoptive parents. She has only seen her primary physician once, who told her parents that her liver seemed enlarged. On physical examination, the anxious, pale, and diaphoretic child is afebrile and has a heart rate of 142 beats/min, respiratory rate of 24 breaths/min, and blood pressure of 81/48 mm Hg. You obtain intravenous access with two large-bore catheters and rapidly infuse 0.9% saline. Point-of-care testing documents her glucose at 128 mg/dL (7.1 mmol/L) and hematocrit at 26% (0.26). Results of other laboratory tests, including complete blood count, coagulation studies, and blood typing and cross-matching, are pending.Of the following, the MOST appropriate next step in this girl’s treatment is:A.administration of vitamin KB.consultation with a gastroenterologist for emergent endoscopyC.placement of a nasogastric tube and lavage with salineD.transfusion with O-negative bloodE.upper gastrointestinal radiographic seriesCorrect answer: CThe initial approach to a child who has gastrointestinal bleeding is to assess and stabilize the patient’s hemodynamic status, establish the level of the bleeding and whether it is ongoing, and begin to determine the underlying cause. Only after these actions should a plan for more definitive treatment be considered.The girl described in the vignette is showing signs of upper gastrointestinal (UGI) bleeding with hemodynamic instability. Intravenous access must be obtained and fluid resuscitation begun immediately. If intravenous access cannot be obtained, intraosseous access should be attempted. Blood typing and cross-matching must be obtained and blood readied for transfusion as soon as possible. A complete blood count that includes a platelet count and coagulation studies should be obtained. Patients who have underlying liver disease and varices due to portal hypertension may have both thrombocytopenia and a coagulopathy that can complicate their treatment.A nasogastric tube should be placed and lavage undertaken to establish whether bleeding is ongoing and if it is, estimate its ongoing rate. This procedure also serves to clear the stomach of blood clots and other debris and prevent aspiration. Administration of O-negative blood should be reserved for patients who do not respond to initial fluid resuscitation. Clearing the stomach of blood has not been shown to have any therapeutic effect, and ice water lavage has no role because it does not slow bleeding and can cause iatrogenic hypothermia. The girl in the vignette has emigrated from an area that has a high incidence of viral hepatitis and chronic liver disease, and her pre-existing hepatomegaly makes esophageal varices a likely cause of her UGI bleeding. This should not discourage the placement of a nasogastric tube.If a coagulopathy is present in the setting of presumed liver disease, vitamin K should be administered. However, in the presence of severe liver disease, vitamin K may be minimally effective and fresh frozen plasma or other factor replacement therapy may be needed. Pharmacologic therapy (Table 1) should be considered for patients who have varices or ongoing UGI bleeding. Acid suppression as well as reduction of portal inflow and decreasing intravariceal pressure by the use of vasoactive agents (eg, octreotide and vasopressin) are the goals of therapy. These vasoactive substances may also be useful in cases of mucosal bleeding from the UGI tract (eg, gastric or duodenal ulcers). Usually, these interventions slow the bleeding, and hemodynamic stability can be achieved.If UGI bleeding is substantial, both a pediatric gastroenterologist and pediatric surgeon should be consulted early. Usually medical therapy slows the bleeding, and hemodynamic stability can be restored, but if this cannot be achieved, emergent endoscopy may be required. The child’s airway should be protected and the endoscopy performed under general anesthesia. A UGI radiographic series is not indicated. Contrast used in this procedure can complicate endoscopy whether obtained emergently or in 1 to 2 days if hemodynamic stability is attained.UGI bleeding is defined as bleeding from the gastrointestinal tract proximal to the ligament of Treitz. UGI bleeding usually is associated with hematemesis or melena. Slower episodes of bleeding in the stomach may present with coffee ground emesis because blood that is exposed to acidic pH turns brown. In children, UGI bleeding is usually mild and self-limited. The differential diagnosis depends on the age of the child and the clinical setting (Table 2). Severe bleeding, as in the vignette, is rare. Mallory-Weiss tears associated with vomiting due to gastroenteritis and gastritis due to medications (including nonsteroidal anti-inflammatory drugs) are much more common causes. For children who are hemodynamically stable, look well, and seem to have bleeding that has resolved, close observation may be all that is needed. In cases of melena, placement of a nasogastric tube and lavage can establish if the source is from the UGI tract and whether the bleeding is ongoing.Esophageal varices related to hepatic disease, bleeding from gastric or duodenal ulcers, and bleeding from vascular malformations are all potential causes of life-threatening UGI hemorrhage. Signs of hemodynamic instability and ongoing bleeding indicate more severe disease.Table 1. Pharmacologic Therapy of Active Gastrointestinal BleedingIntravenous Inhibitors of Gastric Acid SecretionRanitidineHistamine2 antagonistContinuous infusion, 1 mg/kg followed by infusion of 2 to 4 mg/kg per dayBolus infusions, 3 to 5 mg/kg per day divided every 8 hoursPantoprazoleProton pump inhibitorChildren <40 kg: 0.5 to 1 mg/kg per day IV once dailyChildren >40 kg: 20 to 40 mg once daily (maximum, 40 mg/d)Intravenous Vasoactive AgentsOctreotideSomatostatin analog1 ?g/kg IV bolus (maximum, 50 ?g) followed by 1 ?g/kg per hour. May increase infusion rate every 8 hours to 4 ?g/kg per hour (maximum, 250 ?g per 8 hours). When bleeding is controlled, taper 50% every 12 hours May stop when at 25% of starting doseVasopressinAntidiuretic hormone0.002 to 0.005 units/kg per minute×12 hours, then taper over 24 to 48 hours (maximum, 0.2 units/min)American Board of Pediatrics Content Specification(s)Differentiate by age the etiology and the pathophysiology of upper gastrointestinal bleedingPlan diagnostic evaluation and initial intervention for patients with upper gastrointestinal bleedingRecognize serious and/or life-threatening causes of upper gastrointestinal bleedingQuestion: 3A 3-year-old boy presents to the emergency department with pain in his right ear. He has had recurrent episodes of otitis media, necessitating the placement of tympanostomy tubes bilaterally, and problems with impacted cerumen causing a mild conductive hearing loss and ear pain. The boy’s mother is concerned that he is having problems with excessive cerumen in his ear. He has had no fever or ear drainage. On physical examination, the opening of his right ear canal is completely occluded by dry and hard cerumen.Of the following, the MOST appropriate management of this patient’s impacted cerumen is:A.ear candlingB.instillation of a cerumenolyticC.irrigationD.irrigation preceded by instillation of a cerumenolyticE.manual removal?Correct answer: EThe presence of tympanostomy tubes in the boy described in the vignette is a contraindication to irrigation and the use of any cerumenolytic or cerumen-softening agents to assist with ear wax removal. Ear candling is a form of complementary medicine that involves placing the narrow end of a hollow beeswax candle into the affected ear and then lighting the broad end. No evidence supports the theory that the heat creates suction that “draws” out the cerumen. Manual removal is the only appropriate technique for treating this boy.Cerumen is a naturally occurring material found in the external auditory canal (EAC). It is composed of secretions from the ceruminous glands (modified sweat glands and sebaceous glands), primarily sloughed squamous epithelial cells, hair, glycopeptides, lipids, hyaluronic and sialic acid, lysosomal enzymes, immunoglobulins, and other foreign bodies (dirt, dust, other small particles) that are entrapped and incorporated during lateral migration to the entrance of the ear canal. Disorders that affect this natural migration and self-cleaning mechanism of the EAC can lead to increased cerumen retention and ultimately impaction. Drier cerumen, usually from age-related atrophy of the ceruminous glands, narrow or deformed EACs, and the use of cotton-tipped swabs can also contribute to impaction.?Impacted cerumen can contribute to a variety of problems, including hearing loss, ear pain or itching, aural fullness, tinnitus, dizziness, chronic cough, and otitis externa. Another indication for impacted cerumen removal is when its presence prevents needed clinical assessment of the EAC, the tympanic membrane (TM), and any other associated structures.Various techniques have been described for cerumen removal, each with advantages, disadvantages, and contraindications (Table).Complications are dependent on the removal technique and can include:PainDizzinessHearing lossTinnitusTM perforation or damageEAC injury Coughing/cardiac depression due to innervation of the EAC by a branch of the vagus nerve?Removal techniques can be divided into three major categories: 1) EAC irrigation; 2) manual removal, typically using curettes (both unlighted and lighted) as well as suction and other removal devices; and 3) cerumenolytics that are used in conjunction with irrigation or manual removal.EAC irrigation involves flushing out the cerumen with a stream of water and can be performed using a variety of devices. Ear syringes, with and without specialized irrigation tips, and oral jet irrigators have been used. Removal can be facilitated with straightening of the external ear canal by using upward and backward traction on the pinna in a teenager/adult and more back and downward traction in a child. Generally, irrigation is applied under low pressure to avoid potential damage to the TM and with body-temperature fluid to avoid inducing the caloric response and vertigo.Manual removal requires a greater level of skill than irrigation and a more cooperative patient. A monocular/binocular otoscope or operating microscope with ear speculum is needed to see the EAC properly. A headlamp can assist by enhancing illumination of the EAC. The patient is usually in a semi-reclined/reclined position, with the head facing away from the practitioner, neck flexed, and ipsilateral shoulder pulled down. A Jobson Horne curette, ring probe, or microsuction device can be used to remove the wax.Cerumenolytics/cerumen-softening agents can be used alone or in conjunction with irrigation and manual cerumen removal. Most evidence supports improved irrigation success with the use of a cerumenolytic, although the optimal timing and duration of instillation before irrigation is not clear.A number of substances used as cerumenolytics or cerumen-softening agents have been studied, including:Tap/distilled water and sterile saline solutionsWater-based preparations: acetic acid, triethanolamine polypeptide oleate condensate, docusate sodium, hydrogen peroxide, sodium bicarbonateOil-based preparations: mineral, olive, almond, and arachis oilNonwater-/nonoil-based combination preparations?Water and water-based preparations help to dissolve cerumen via hydration of the epithelial cells. Oil-based preparations are not really ceruminolytic; they help loosen the cerumen and lubricate the EAC to facilitate removal. The mechanism for nonwater/nonoil-based combination preparations is not known.A 2009 Cochrane review determined that use of any cerumenolytic agent was better than no treatment, the superiority of one type of drop over another could not be concluded, and no agent was superior to water or saline alone.American Board of Pediatrics Content Specification(s)Know the indications and contraindications for removal of impacted cerumenPlan the key steps and know the potential pitfalls in performing removal of impacted cerumenRecognize the complications associated with removal of impacted cerumenKnow the anatomy and pathophysiology relevant to removal of impacted cerumenQuestion: 4You are evaluating a 6-year-old girl for abdominal pain that began last night and has progressively worsened. The girl says the pain occasionally worsens or improves but is always present. She began vomiting this morning and has had four episodes of nonbloody, nonbilious emesis. She describes the pain as sharp and points to her left mid-abdomen when asked where the pain is maximal. She has had no fever, diarrhea, dysuria, urinary frequency or incontinence, sore throat, or respiratory symptoms. She has had no prior similar episodes, and the family history has no findings of note. On physical examination, the somewhat pale and uncomfortable girl lies in the fetal position, occasionally writhing in pain. Her temperature is 37.0°C, heart rate is 118 beats/min, respiratory rate is 18 breaths/min, and blood pressure is 100/68 mm Hg. Her head, ears, eyes, nose, and throat examination reveals only tacky mucus membranes. Findings on her abdominal examination include left flank, costovertebral angle, and lower quadrant tenderness with some voluntary guarding. There is no rebound or rigidity, bowel sounds are normal, and no masses or organomegaly are evident. Her cardiovascular examination reveals only tachycardia, her lungs are clear without any adventitial sounds or labored breathing, and the remainder of her examination findings are normal. You order intravenous fluids and pain medication.Of the following, the MOST appropriate initial test in the evaluation and treatment of this patient is:A.chest plete blood countC.pelvic ultrasonographyD.streptococcal rapid antigen testing E.urinalysis Correct answer EThe girl described in the vignette has pain and tenderness in the left flank that is suggestive of possible renal pathology. Multiple urinary tract pathologies, including urinary tract infection, urolithiasis, renal tumors, and ureteropelvic junction obstruction, can cause acute and recurrent abdominal pain in children. The pain is typically colicky and maximal in the flank region. Urinalysis is a quick, inexpensive test that can screen for urinary tract pathology as well as provide other clinically helpful information (eg, hydration status, glycosuria/ketonuria with diabetic ketoacidosis, proteinuria with nephrotic syndrome). Urinalysis for this girl revealed no white blood cells but 100 red blood cells, and abdominal computed tomography scan showed multiple left-sided renal stones, including a 6-mm obstructive stone at the left ureterovesical junction (Figure).?Although basilar pneumonia can commonly cause abdominal pain in children, the absence of fever and respiratory signs or symptoms as well as the location of the pain make this diagnosis unlikely for this girl, obviating the need for chest radiography. A complete blood count is commonly included in the evaluation for potential surgical causes of abdominal pain, but the sensitivity and specificity of this test are poor, and urinalysis is more likely to add clinically useful information for this girl. Ovarian pathology, such as cysts, torsion, tubo-ovarian abscess, and masses, commonly causes abdominal pain in adolescents and adults and occasionally in younger children. Pelvic ultrasonography may be indicated in this girl’s subsequent evaluation but would not be the initial test performed. Streptococcal pharyngitis is a known cause of abdominal pain but is typically accompanied by fever and pharyngeal inflammatory changes not present in this case.Abdominal pain can result from the stimulation of nerves within the abdominal viscera (visceral), within the parietal peritoneum or soft tissues of the abdominal wall (somatic), or in distant sites with common neural pathways (referred). Visceral pain is generally dull, aching, and poorly localized; it is often perceived as epigastric or periumbilical. Somatic pain is typically described as sharp and well localized. As inflammation of a viscus progresses, initial visceral pain is replaced by somatic pain when adjacent abdominal wall structures become inflamed.?There are multiple potential causes of both acute and chronic abdominal pain in children (Table 1), making the evaluation and management extremely challenging. Historical factors, such as the age and sex of the patient; duration, location, quality, and any migration of the pain; and presence or absence of associated symptoms (vomiting, diarrhea, fever, anorexia, weight loss, blood in stool) are critical in determining the initial diagnostic evaluation. Although the final common pathway of many of the serious causes of abdominal pain in children is peritonitis with diffuse pain and tenderness, the location of initial pain and point of maximal tenderness can help guide the initial evaluation. Appendicitis classically begins with epigastric or periumbilical pain that subsequently migrates to the right lower quadrant. Renal pathology is typically maximal in the flank region. Liver and gallbladder pathology presents with maximal pain and tenderness in the right upper quadrant. Pancreatic disease produces epigastric pain that often radiates to the back. Ovarian and other gynecologic pathologies usually produce pelvic or suprapubic pain and tenderness.The primary evaluation goals for patients who present to the emergency department with abdominal pain are first to ensure hemodynamic stability and then to attempt to exclude those conditions that demand urgent or emergent intervention (Table 2). The presence of any signs of hemodynamic compromise, evidence of trauma, or signs of peritoneal irritation (rigidity, involuntary guarding, rebound tenderness) warrant immediate surgical consultation. Intravenous fluid administration and pain control should be initiated and further evaluation and management guided by the surgical assessment. If emergent surgical evaluation is not indicated, the initial steps in evaluation are guided by findings from the history and physical examination. In addition to a thorough abdominal examination, a complete evaluation with special attention to the throat, chest, and genitourinary regions should be undertaken. Patients who have no evidence of bowel obstruction, inflammation/infection, or significant focal abdominal tenderness may not require any emergency department testing. Similarly, patients whose history and examination findings are classic or highly suggestive of acute appendicitis should undergo surgical consultation and do not require additional tests.For patients who have more equivocal historical and examination findings, multiple possible tests (Table 3?and Table 4) can be undertaken and should be individualized based on the patient’s presentation. Abdominal radiographs are helpful in excluding bowel obstruction, significant mass effect, perforation, or rarely fecaliths or radiopaque stones. Additional imaging studies may be indicated if the diagnosis remains unclear, but time, cost, and risk of radiation exposure need to be considered. Ultrasonography is the first-line imaging modality for many abdominal pathologies (eg, gallbladder disease, ovarian cysts, torsion, abscesses, intussusception) and is used initially in many centers for appendicitis as well. Computed tomography (CT) scans are often employed in cases of suspected appendicitis and are particularly helpful if there are multiple diagnostic possibilities. CT scan with contrast (intravenous with or without the addition of oral or rectal administration) is preferred for evaluation of inflammatory disorders, trauma, and tumors; noncontrast CT scan is preferred for evaluation of urolithiasis. All postmenarchal females who have significant abdominal complaints should have a pregnancy test performed and be questioned alone about sexual history and the potential for sexually transmitted infections. Patients who have significant abdominal pain and tenderness in whom the initial evaluation fails to yield a diagnosis may benefit from hospitalization for serial examinations.American Board of Pediatrics Content Specification(s)Differentiate by age the etiology and location and understand pathophysiology of abdominal painPlan diagnostic evaluation and initial intervention for patients with abdominal painRecognize serious and/or life-threatening causes of abdominal painQuestion: 5A 4-year-old boy presents to the emergency department with complaints of headache and facial swelling for 2 days.? His mother reports he also has had decreased urine output and dark urine.? On physical examination, the alert and oriented boy has a temperature of 37.0°C, heart rate of 102 beats/min, respiratory rate of 22 breaths/min, blood pressure of 138/80 mm Hg, and oxygen saturation of 99% in room air.? Results of his neurologic evaluation are normal, and there are no findings of note on the remainder of his physical examination. Urine microscopy reveals 263 red blood cells per high-power field and red cell casts.Of the following, the MOST appropriate next step in management is administration of:A.intravenous fluid bolusB.intravenous labetalolC.intravenous nicardipine infusionD.oral captoprilE.sublingual nifedipineCorrect answer: BThe edema, hematuria, and hypertension described for the boy in the vignette are classic signs of glomerulonephritis. His blood pressure of 138/80 mm Hg is well above the 99th percentile for age.? Severe, symptomatic hypertension in the setting of acute glomerulonephritis is best treated with fluid restriction and intravenous medications, beginning with bolus medications such as labetalol or hydralazine that, in some cases, may be followed by infusion medications such as nicardipine. Oral captopril (angiotensin-converting enzyme inhibitor) has a longer onset of action and is used for chronic maintenance therapy for hypertension, not in the acute setting. Sublingual nifedipine is not recommended because effects can be erratic and the medication is difficult to titrate.Glomerulonephritis results from lodging of circulating immune complexes in the glomerular basement membrane of the kidneys, which are evident on renal biopsy. ?The immune complexes are typically composed of antigens, antibodies, and complement proteins. The resulting inflammation of the glomeruli leads to both leakage of red blood cells into the urine and reduced filtering capacity of the glomerulus, causing azotemia, fluid retention, and hypertension.Several diseases associated with the acute presentation of nephritis are initially clinically indistinguishable, including lupus nephritis, immunoglobulin A nephropathy, and rapidly progressive glomerulonephritis.? The most common cause of acute glomerulonephritis in children is poststreptococcal glomerulonephritis (PSGN). Affected children typically present with edema, hypertension, and hematuria.? Urine color can range from pink to brown. The preceding infection with Streptococcus pyogenes (group A Streptococcus) can be either pharyngitis (1 to 2 weeks prior) or skin infection (2 to 4 weeks prior).Evaluation of suspected PSGN includes measurement of electrolytes, blood urea nitrogen, creatinine, and complete blood count. Complement values are low because complement is used up in the formation of immune complexes. Serum streptococcal antigen tests (antistreptolysin O or anti-DNAse B) may aid in establishing the diagnosis.? Urinalysis generally reveals hematuria and red cell casts in addition to proteinuria and pyuria. If 24-hour urine collection is obtained, most children who have glomerulonephritis exhibit modest proteinuria at most, usually less than 2 g/m2 per day.Treatment of acute PSGN focuses primarily on the recognition and management of hypertension (eg, fluid restriction, antihypertensive therapy). Determining high blood pressure requires auscultation of Korotkoff sounds; abnormal automated blood pressure readings should be confirmed with manual sphygmomanometry. For patients who have life-threatening presentations, inline measurement of blood pressure via the arterial line is recommended.Hypertensive urgency is defined as severe hypertension (>99th percentile + 5 mm Hg) without end-organ injury and may be associated with symptoms such as headache or nausea. Hypertensive emergency is defined as severe hypertension with acute end-organ injury (eg, heart, kidney, eye, brain). Cardiac injury may result in congestive heart failure or flash pulmonary edema.? Most children who have hypertensive emergency present with neurologic findings. Signs of acute hypertensive encephalopathy include seizures and altered mental status.No randomized, controlled trials have evaluated treatment of hypertensive emergency in children, but recommendations have been drawn from adult studies and several principles are widely accepted. Intravenous medications are preferred to oral medications for severe hypertension from an acute cause (such as PSGN) with or without evidence of end-organ injury. Controlled reduction of blood pressure by no more than 25% in the first 8 hours of therapy is recommended to prevent secondary ischemic end-organ damage from a sudden blood pressure reduction. Recommended parenteral medications include labetalol or hydralazine via intravenous bolus dosing and nicardipine as a titrated infusion.?American Board of Pediatrics Content Specification(s)Recognize signs and symptoms and differential diagnosis of glomerulonephritisRecognize and interpret relevant laboratory studies for glomerulonephritisPlan management of acute glomerulonephritisQuestion: 6A 10-year-old boy presents to the emergency department with a 2-week history of intermittent febrile episodes characterized by rigors, chills, sweating, and a temperature of up to 39.5?C every 48 hours. In addition, he experienced nausea, anorexia, fatigue, headache, joint pains, and cough without any vomiting and diarrhea. He recently returned from a 2-week summer safari in Africa.? Physical examination of the markedly pale and tired boy, who is complaining of a diffuse headache, shows a heart rate of 130 beats/min, respiratory rate of 35 breaths/min, blood pressure of 95/50 mm Hg, and temperature of 39.6?C.? He has clear lung sounds and no heart murmurs on auscultation; abdominal examination reveals a palpable liver and spleen. Preliminary laboratory investigations document the presence of blood parasites on the thick blood smear test.Of the following, the most appropriate laboratory investigation(s) to help plan treatment for this patient is (are):A.blood cultureB.cerebrospinal fluid white blood cell count, differential count, and cultureC.hemoglobin and hematocrit? D.random blood glucose? E.thin blood smear? Correct answer: EThe boy described in the vignette has a clinical history, symptoms, and examination findings suggestive of malaria. The causative agent of malaria is the parasite Plasmodium, with five documented species: P falciparum, P ovale, P vivax, P malariae, and P knowlesi. One of the most essential tests for determining appropriate treatment is species identification performed on thin blood smear. Not only does it aid in determining appropriate antimalarial therapy based on the regional resistance pattern, but findings contribute to the decision for adding treatment to avoid latent infection. Malaria caused by P ovale and P vivax can become latent in liver cells, resulting in malarial recurrence months later. Also, patients in endemic areas can have coinfection with more than one malaria species, which can make species identification a vitally important and challenging task. Measurement of hemoglobin and hematocrit aids in assessing the degree of anemia, which may be severe in the presence of complicated malaria infection. Random blood glucose measurement is used to assess for hypoglycemia, a common development with malaria infection and the intravenous quinine used to treat complicated malaria infection. However, neither of these tests is as essential as species identification for disease management. Blood culture or cerebrospinal fluid assessments are usually not indicated for patients who have documented malaria infection.The symptoms of fever, rigors, and chills can occur every other day (every 48 hours) for disease caused by P falciparum, P vivax, and P ovale or every third day (every 72 hours) with P malariae infection. Other clinical signs and symptoms of malaria include weakness, pallor, cough, nausea, vomiting, diarrhea, joint pains, and diffuse muscle aches. In an appropriate setting, a neonate can present with fever and sepsis due to congenital transmission of the parasite (congenital malaria). Complications of malaria are primarily associated with P falciparum infection and are due to its high parasitemia load, ability to invade all forms of red blood cells, and ability to increase red cell adherence, resulting in vascular obstruction and ischemia. Acute complications of malaria include severe hemolysis and anemia, pulmonary edema, hypoglycemia, metabolic acidosis, respiratory failure, adrenal crisis (algid malaria: hypotension and circulatory collapse), acute tubular necrosis (black water fever: black urine due to intravascular hemolysis and renal medullary necrosis), cerebral infarctions resulting in seizures, and altered mental status (cerebral malaria). Chronic complications develop following immune-mediated immunoglobulin M complex deposition that can result in nephrotic syndrome or massive splenomegaly (tropical splenomegaly syndrome).?When malaria is clinically suspected, the most important laboratory investigation is thick and thin blood smears. These should be performed every day for 72 hours to rule out malaria but should not be performed at the time of fever and rigors (at the time of fever, the parasite is released in the blood stream from the hemolyzed red blood cells). Thick smear is useful to identify Plasmodium infection; thin smear is used to identify the species and degree of parasitemia. The test is operator-dependent, with studies showing from 10 to 500 parasites/mL on blood smears. In endemic areas, rapid diagnostic tests based on detection of malarial antigens (immune chromatographic tests) can detect malaria if there are 100 to 200 parasites/mL of blood.? Inherent issues with the rapid diagnostic tests are limited ability to identify specific species that depends on the type of test, persistence of antigen after an infection is cleared, and inability to detect low parasite concentrations. Polymerase chain reaction tests can detect as few as 5 parasites/mL of blood, but the technology is expensive and not readily available.The primary issue in the treatment and prophylaxis of malaria is worldwide chloroquine resistance. To prevent further resistance to other antimalarials, the World Health Organization recommends combination therapy for treatment (eg, atovaquone with proguanil, quinine sulfate with doxycycline or tetracycline or clindamycin). Intravenous treatment (quinine or artemisinins) is recommended for complicated malaria or if parasitemia is greater than 5%. If quinine treatment is initiated, cardiac and glucose monitoring is required because of the frequent occurrence of arrhythmias and hypoglycemia. When the parasitemia is more than 10%, exchange transfusion may be helpful.If the patient does not adhere to the treatment plan, the parasite can remain in the blood at low concentrations, where it eventually multiplies, resulting in recurrent symptoms within a few weeks. Such “recrudescence” can occur with any malaria species and necessitates a repeat course of treatment with antimalarials. This phenomenon is in contrast to the previously discussed “recurrence” that occurs with P ovale and P vivax infections in which the malarial parasites remain in hepatocytes in latent phase and are released months later, causing disease recurrence. Therefore, additional treatment with primaquine or tafenoquine is required if the patient has disease caused by P ovale or P vivax. Of note, primaquine can cause hemolysis in patients who have glucose-6-phosphate deficiency, necessitating testing for this condition before initiating therapy.An important resource for the clinicians and patients is the Centers for Disease Control and Prevention malaria hotline that is available at malaria and travel.?American Board of Pediatrics Content Specification(s)Plan the evaluation and management of acute malariaRecognize the signs and symptoms of malariaQuestion: 7A 10-year-old girl arrives in the emergency department with a complaint of dysuria. She does not have a fever, and her vital signs are all within normal limits. She denies blood in urine, changes in usual bowel function, and sexual activity. Her urinalysis is clear. On physical examination, you note multiple lesions in the genital area (Figure).FigureGenital lesions in the 10-year-old girl in the vignette. Of the following, the MOST appropriate next step is to:A.arrange a follow-up appointment with pediatric dermatology in 1 weekB.contact child protective services and investigate for sexually transmitted infection(s)C.measure serum?B human chorionic gonadotropin D.prescribe podophyllin and discharge the girlE.refer the child for outpatient gynecologic evaluationCorrect answer: BThe genital lesions described for the preadolescent in the vignette appear to be genital warts, likely caused by human papillomavirus (HPV) infection. Any evidence of HPV infection in a prepubertal or sexually inactive patient, such as this girl, should raise suspicion of sexual abuse and prompt notification of child protective services, although sexual contact is not a universal cause. HPV in a potentially sexually active, postpubertal child requires further investigation into the patient’s sexual history before involving child protective services. Affected patients require dermatologic or other clinical evaluation for likely repetitive therapy, which is preferable to one-time treatment of genital warts in the emergency department. Measurement of urine rather than serum b human chorionic gonadotropin is a reasonable option if pregnancy were a concern for this girl. Initial emergency department evaluation of this preadolescent should include further investigation of sexual activity or abuse and microbiologic evaluation for other sexually transmitted infections. Although outpatient gynecologic evaluation may be considered, it is not the most appropriate next step in this case.References to anogenital warts have become more frequent in the literature over the past 20 years, but whether this represents an increasing incidence of disease is not clear. Determination of specific DNA in the lesion can help direct clinicians to a sexual or other likely cause, although such determination is not often used in practice. HPV 6, 11, 16, and 18 are more likely to be from sexual or vertical transmission; skin HPV types are more suggestive of hetero- or autoinoculation. HPV serology can also be obtained.Nonsexual transmission of HPV can occur at conception through an infected germ cell, during pregnancy via intrauterine transmission, and perinatally during the birthing process or immediately thereafter. Horizontal transmission has also been suggested from breastfeeding and other personal contacts. In addition to genital lesions, HPV infection can include skin warts and oral/laryngeal papillomas.HPV is the most common sexually transmitted infection, with a lifetime risk of 50%. Approximately 60% of those exposed to genital warts develop clinical symptoms. The lesions are often transient and, in addition to the genital warts, can lead to mucosal dysplasia and squamous cell carcinoma. Genital HPV infections are classified by their cancer-causing potential. Prevention via the HPV vaccine appears to be the most promising modality and is available for both males and females. After exposure and transmission, the infection is often not clinically evident; most patients have no symptoms or clinical findings. However, they may describe bleeding, dysuria, pain, pruritus, or irritation as well as painful intercourse, rectal pain, or urinary retention. Genital warts can be seen on the mucous membranes of the vagina, cervix, anus, and penis as well as the glans and shaft of the penis. Classic genital warts are verrucous or cauliflower-like warts but can also be flat.Genital warts are diagnosed by inspection, with magnifying aids as required. Use of acetic acid or vinegar leads to an acetowhite change on the surface of the lesion in 3 to 5 minutes, but this is a nonspecific finding. As noted previously, HPV testing is not often indicated because it does not change the course of disease or ongoing management. If the lesions are atypical (pigmented, indurated, fixed), do not respond to standard treatment, or are seen in patients who are older than 40 years of age or who are immunocompromised, biopsy may be indicated.The differential diagnosis of genital warts includes papillomatosis (male or female), Fordyce spots, skin tags (polyps), seborrheic keratosis, microglandular hyperplasia, condyloma lata (secondary syphilis), molluscum contagiosum, herpes simplex virus infection, and various premalignant and malignant conditions.Treatment is designed to alleviate symptoms and decrease viral load. Wart removal, although not curative, may help with cosmesis and psychological issues. Various treatments are available, including destructional/excisional, antiproliferative, and immune-modulating therapies. Clinicians should weigh the risks and benefits of therapeutic modalities when developing a treatment plan. The Centers for Disease Control and Prevention 2006 Sexually Transmitted Disease Treatment Guidelines recommend basing HPV treatment on patient preference because no single treatment for genital wart disease is considered superior. Clearance rates can approach 80% to 90%, depending on the treatment process, and the recurrence rate is noted to be between 5% and 50%.As with any potential sexually transmitted infection, the clinician should discuss safe sexual practices and notification of partners with the patient and investigate for related disease processes.American Board of Pediatrics Content Specification(s)Plan the management of genital wartsQuestion: 8A mother brings her 3-year-old daughter to the emergency department for evaluation of a facial wound sustained 3 days ago after she fell from a bicycle onto a concrete sidewalk. Although the girl received first aid immediately and is currently asymptomatic, her mother is worried about the cosmetic outcome and risk for scarring. Physical examination reveals a 3-cm superficial abrasion on the girl’s left cheek that is 1 cm wide, mildly erythematous, and minimally tender.Of the following, the MOST appropriate management of this wound is:A.allowing it to heal by secondary intentB.closure with sutures after debridementC.injection of growth factors locally to promote healingD.plastic surgery referral in the emergency department for skin graftingE.referral to a surgeon for delayed primary closureCorrect answer AA wound is a disruption of skin and underlying soft tissue. The principles of wound management include achieving hemostasis, reducing tissue loss, promoting wound healing, and minimizing secondary infection and scar formation. Superficial wounds, such as described for the girl in the vignette, should heal without scarring if left to heal with secondary intent (granulation tissue). Common practice recommends that primary closure should occur within 12 hours of injury. However, a recent Cochrane review suggests there is currently no systematic evidence to guide clinical decision making regarding the timing of closure of traumatic wounds. The wound described in the vignette is more superficial and not likely to require sutures. Similarly, the superficial nature of the wound precludes the need for a surgical referral for skin grafting, delayed primary closure, or use of experimental wound healing strategies such as growth factors.Whenever possible and practical, primary closure is the best method for closing an acute open wound. Primary wound closure simplifies wound care for the patient, who simply needs to keep the suture line clean and dry. Secondary wound closure requires several dressing changes per day. A wound closed primarily heals much more quickly and with less pain than a wound allowed to heal with dressings alone. Primary closure involves fewer problems with abnormal scarring and has a better cosmetic outcome.Contraindications to primary wound closure include concerns for wound infections, foreign bodies in the wound that cannot be removed, active bleeding from the wound, risk for developing too much tension, and presence of dead space under the skin closure. ?Deeper wounds should be allowed to heal by secondary intent if there is contamination with debris that cannot be adequately cleaned or if the wound has come to medical attention late. Delayed primary closure is a compromise between primary repair and allowing an acute wound to heal secondarily. This technique permits time for improved blood flow at the wound edges and the cleaning of highly contaminated wounds. Large wounds, wounds over a skin crease, and wounds with surrounding edema can be closed by delayed primary closure as long as infection is ruled out and the wound edges are not under tension.Healing of wounds is a complex physiologic process that involves interplay between different cell types (keratinocytes, fibroblasts, endothelial cells, macrophages, platelets), cytokines, and various other vasoactive substances that constitute the inflammatory response. Immediately after an injury, hemostasis is achieved by vascular vasoconstriction, formation of the platelet plug, activation of fibrin, and the coagulation pathway. Wound healing subsequently progresses through a series of well-defined stages.The inflammatory stage is characterized by recruitment of mast cells, secretion of protein called vimentin, and release of vasoactive substances. These actions increase vascular permeability while chemotaxis caused by cytokines results in migration of polymorphonuclear cells that digest bacteria and lyse foreign matter. The presence of foreign bodies, dirt, and other contaminants can lead to an arrest at this stage and predispose to chronic wound formation.The epithelization (migration) stage is characterized by basal cell proliferation and migration of epithelial cells in the wound. Migration ceases when a layer connecting the edges of the wound is formed. The physical distance between the edges of the wound influences the success of this process and is often challenged when the wound is allowed to heal by secondary intent. This stage is usually completed within 48 hours of the injury.Fibroplasia consists of proliferation of fibroblasts, collagen production, and secretion of contractile proteins from myofibroblasts, which helps to add tensile strength to the wound and brings the wound edges closer. Exuberant scarring resulting in keloid formation occurs in this stage if healing is impaired for any reason.Maturation is the final stage of wound healing and includes collagen cross-linking, remodeling, and contraction of the wound.Among the risk factors for impaired wound healing are infection, foreign bodies, decreased blood supply (eg, peripheral vascular disease, sickle cell anemia, diabetes), immobilization, malnutrition, and immunocompromised states.American Board of Pediatrics Content Specification(s)Understand the physiology of wound healingUnderstand the importance of wound explorationKnow the indications for primary, secondary, and delayed primary closure of woundsFEBRUARY 2012Question: 1A 2-year-old boy was playing on the floor at home when he began choking. After multiple unsuccessful Heimlich maneuvers, the parents called 911. Upon arrival, emergency medical services personnel noted that the boy had stridor and was lethargic. En route he became completely unresponsive with poor respiratory effort, and they initiated bag-valve-mask ventilation. Physical examination in the emergency department of the obtunded and cyanotic boy shows a heart rate of 68 beats/min, weak spontaneous respiratory effort, and poor chest rise during bag-valve-mask ventilation. Direct laryngoscopy reveals an opaque foreign body just beneath the glottis. Multiple attempts at orotracheal intubation are unsuccessful.?Of the following, the MOST appropriate next step to create a rescue airway and establish oxygenation is toA.attempt fiberoptic intubationB.begin transtracheal ventilationC.insert a combined esophageal-tracheal tubeD.intubate with a video laryngoscopeE.place a laryngeal mask airwayCorrect answer: BThe boy described in the vignette is experiencing imminent hypoxemic cardiac arrest due to airway obstruction by an aspirated foreign body. In this “can’t intubate-can’t ventilate” situation, the most expedient option is to initiate transtracheal ventilation (TTV) via a needle cricothyrotomy connected to an oxygen source. This will serve as a temporizing maneuver to reestablish oxygenation until a definitive surgical airway (tracheostomy) can be safely established by experienced personnel. The laryngeal mask airway and combined esophageal-tracheal tube are supraglottic rescue airway adjuncts that are not helpful in the face of obstruction at the level of the glottis. Fiberoptic endoscopes and video laryngoscopes are designed to enhance viewing of the glottis in the presence of abnormal anatomy or edema of the tongue or oral cavity and require time for set-up. They are not appropriate for emergency situations.?TTV is the surgical airway of choice for younger children (the exact age varies in the literature). It is simpler and faster to perform and entails less bleeding than a surgical cricothyrotomy. The classic indications are epiglottitis, angioedema, or facial trauma where abnormal supraglottic anatomy precludes access to the glottis. TTV is not helpful in the presence of infraglottic obstruction such as croup, bacterial tracheitis, or total obstruction of the airway from a foreign body below the level of the cricothyroid membrane. However, because a rescuer may not be able to predict the precise location of the obstructing foreign body, TTV should be considered if other measures have failed.?The first step in attempting TTV is to place a towel roll under the patient’s shoulders to hyperextend the neck if there are no contraindications such as suspected neck injury. This maneuver brings the larynx into an anterior position. The clinician can identify the cricothyroid membrane as an anterior, transverse indentation between the thyroid and cricoid cartilage by palpating with a fingernail. After stabilizing the larynx with the nondominant hand, the clinician punctures the membrane with a 14-gauge catheter over the needle canula, directing it in the midline, caudally, and posteriorly at a 45-degree angle. Aspiration of air signifies entry into the trachea. The cannula is connected to a high-pressure oxygen source (jet ventilation) or a manual resuscitator bag. Excessive resistance to bagging should be expected due to the turbulence generated from air flow through a 14-gauge catheter. The adaptor of a 3-0 (15-mm internal diameter) endotracheal tube fits into the intravenous catheter snugly and can provide a connection for ventilating devices. Because the size of 15-mm tracheal tube adapters can vary between manufacturers, it is always best to preassemble the cricothyrotomy equipment. The high resistance of the intravenous catheter precludes adequate ventilation by a bag-valve device. Moderate hypercarbia should be expected, and the pop-off valve must be occluded. Oxygenation may be better accomplished with specialized high-flow jet oxygen devices, but these may not be widely available. In general, jet ventilation devices should only be considered in children older than 5 years of age because of complications of excessive flow and resultant barotrauma. Even in this older age group, maintaining oxygen saturations with a bag technique is preferable. Oxygen flow rates of 1 to 5 L/min are preferred to minimize barotrauma.Gas generally is exhaled through the upper airway and out the pharynx. If upper airway obstruction is complete, pausing between insufflations may be necessary to allow for passive exhalation. An alternative approach is to use a modified Seldinger technique. Several commercial kits with dilator assemblies are available, but experience with percutaneous dilational cricothyrotomy is limited to adult patients. Such devices may be used in older children. In the semi-awake patient, lidocaine may be instilled in the tracheal lumen to suppress the cough reflex.It is important to remember that needle cricothyrotomy with TTV is best considered a temporizing means of rescue ventilation until a more definitive airway can be obtained. Complications include subcutaneous emphysema, barotrauma, catheter kinking, reflex coughing, esophageal puncture, creation of a false tract, obstruction from blood or mucus, and mucosal injury. The risk of pneumothorax, pneumomediastinum, or subcutaneous emphysema may be greater with jet ventilation devices, particularly if the catheter is not in the lumen of the trachea.American Board of Pediatrics Content Specification(s)Know the anatomy and/or pathophysiology relevant to percutaneous transtracheal ventilationKnow the indications and contraindications for percutaneous transtracheal ventilationPlan the key steps and know the potential pitfalls in performing percutaneous transtracheal ventilationRecognize the complications associated with percutaneous transtracheal ventilationQuestion: 2A 13-year-old boy is brought to the emergency department by ambulance after being injured in an all-terrain vehicle (ATV) rollover incident. He had been riding trails near his home, and when his family had not seen him for more than 1 hour, they began searching for him. He was found at the bottom of an embankment with the ATV lying on his chest. He was unconscious but breathing. They called emergency medical services, and he was flown by helicopter from the scene. Paramedics performed rapid sequence endotracheal intubation at the scene due to the boy’s altered mental status and inadequate respiratory effort. His vital signs on arrival at the emergency department are: heart rate, 140 beats/min; respiratory rate, 20 breaths/min (ventilated); blood pressure 80/60; and pulse oximetry reading of 86% on 100% oxygen. Physical examination reveals a paralyzed, sedated, and intubated patient. The end-tidal carbon dioxide colorimetric device has good color change. He is difficult to ventilate through the endotracheal tube, and there are markedly decreased breath sounds on the left side, with asymmetric chest rise.Of the following, the finding that MOST strongly suggests tension pneumothorax rather than massive hemothorax isA.asymmetric breath soundsB.distended neck veinsC.hypotensionD.muffled heard tonesE.tracheal deviationCorrect answer: BHypovolemia that results from intrathoracic accumulation of a large volume of blood in massive hemothorax typically results in flat or collapsed veins, making neck vein distension unlikely. Tension pneumothorax is typically associated with distended neck veins unless associated injuries have produced hypovolemia. Both tension pneumothorax and massive hemothorax cause diminished breath sounds on the involved side, hypotension, and tracheal/mediastinal deviation. Muffled heart tones are associated with cardiac tamponade but are not expected with either tension pneumothorax or massive hemothorax.Significant thoracic injuries are uncommon in children experiencing trauma, occurring in fewer than 10% of patients. Most thoracic injuries in children result from blunt mechanisms, and the majority are part of multisystem trauma. In critically injured patients, death is more likely to result from associated injuries, particularly brain injury. Motor vehicle crashes are the source of most pediatric thoracic injuries, followed by falls and assaults. The most common thoracic injuries seen in pediatric blunt trauma patients are pulmonary contusion, pneumothorax,hemothorax, and rib fractures (Table 1).Due to their greater chest wall compliance, children are less likely to have obvious external signs of thoracic trauma and less likely to suffer rib fractures. Examination findings that indicate possible intrathoracic injuries include tachypnea, focal chest wall tenderness, and abnormal breath sounds. During the primary survey, evidence of cardiorespiratory compromise must be identified and corrected rapidly to prevent progression to respiratory failure, shock, or death. Injuries that are immediately life-threatening, such as tension pneumothorax, massive hemothorax, open pneumothorax, and cardiac tamponade, should be identified and treated emergently during the primary survey (Table 2).Open pneumothorax, also known as a sucking chest wound, consists of a chest wall wound in communication with the pleural space. Due to the negative intrathoracic pressure with inspiration, air is entrained into the pleural space with each breath and impairs effective oxygenation and ventilation. If a completely occlusive dressing is applied and sealed on all sides, a tension pneumothorax may result.If the primary survey reveals no compromise of airway, breathing, or circulation, a thorough secondary survey should be completed. Other potentially life-threatening thoracic injuries, such as pulmonary or myocardial contusion, diaphragmatic rupture, esophageal rupture, tracheobronchial tear, or great vessel injury, should be identified during this assessment.Table 2. Life‐threatening Thoracic Injuries in ChildrenInjurySigns/SymptomsTreatmentSimple pneumothoraxChest pain, dyspnea, decreased breath sounds, hypoxiaTube thoracostomyTension pneumothoraxChest pain, dyspnea, decreased breath sounds, hypoxia, hypotension, distended neck veins, tracheal deviation to contralateral sideNeedle decompression followed by tube thoracostomyOpen pneumothoraxChest wall wound with air entrainment, decreased breath sounds and chest wall motion, dyspneaOcclusive dressing sealed on three sides, chest tube at distant siteHemothoraxChest pain, dyspnea, decreased breath soundsTube thoracostomyMassive hemothoraxDyspnea, hypoxia, hypotension, tracheal deviation to contralateral sideTube thoracostomy, transfusionCardiac tamponadeMuffled heart tones, neck vein distension, hypotensionPericardiocentesisFlail chestChest wall crepitus, paradoxic chest wall segment movementAnalgesia, oxygen, respiratory supportPulmonary contusionDyspnea, hypoxiaOxygen, respiratory support, judicious fluid managementCardiac contusionChest pain, arrhythmiaSupportive careAmerican Board of Pediatrics Content Specification(s)Know the types of intrathoracic injuries due to blunt chest traumaDifferentiate simple pneumothorax from tension pneumothoraxDifferentiate tension pneumothorax from massive hemothoraxRecognize the signs and symptoms of sucking chest wounds following blunt chest traumaQuestion: 3A 9-month-old infant is brought to the emergency department by his parents for vomiting and irritability. The family recently moved from Mexico, and his past medical history is unclear. The mother says that he breastfeeds vigorously but then vomits afterward. He cries constantly and is difficult to console. On physical examination, the infant’s skin is dry, his eyes are sunken without tears, and he has mild tachypnea and tachycardia, but other findings on his cardiac and respiratory examinations are normal. Abdominal evaluation reveals multiple small, hard masses. His capillary refill is delayed. You place an intravenous line and order laboratories tests, which show:Sodium, 155 mEq/L (155 mmol/L)Potassium, 5.3 mEq/L (5.3 mmol/L)Bicarbonate, 20 mEq/L (20 mmol/L)Blood urea nitrogen, 81 mg/dL (28.9 mmol/L)Creatinine, 0.8 mg/dL (70.7 ?mol/L)Urine specific gravity, 1.010?You provide fluid resuscitation with 0.9% normal saline, then calculate and begin replacing the free water deficit.?Of the following, the MOST appropriate next step is toA.administer desmopressin acetateB.administer hydrochlorothiazideC.admit the boy to the hospitalD.obtain abdominal ultrasonographyE.perform a water deprivation testCorrect answer: CThe infant described in the vignette likely has diabetes insipidus (DI). Immediate management steps include intravenous rehydration to restore perfusion and inpatient admission to correct free water deficit and electrolyte abnormalities slowly and investigate the cause of the DI. A water deprivation test should only be performed on an infant who is adequately hydrated and has normal electrolyte values (Table 1). Desmopressin acetate (dDAVP) may be administered after a water deprivation test to see if the polyuria responds to exogenous administration of antidiuretic hormone (an indicator of central DI), but it is not indicated in the acute setting when the diagnosis is uncertain. Hydrochlorothiazide may be used to treat nephrogenic DI but is not indicated for this acutely volume-depleted infant. Although abdominal ultrasonography may be used to identify a renal abnormality (eg, hydronephrosis) or associated abdominal findings of constipation (as in the infant in the vignette), the results would not change the initial management of DI.Patients who have DI, regardless of cause, exhibit polyuria, polydipsia, hypernatremia,and dehydration. Urine output exceeds 5 mL/kg per hour with a specific gravity of less than 1.010. Central (neurogenic) DI is the most common type of DI and is caused by insufficient production or release of antidiuretic hormone (ADH) by the hypothalamus or pituitary (Table 2). Fifty percent of neurogenic DI in children is caused by primary brain processes. A little more than 25% of all cases are idiopathic. A smaller percentage of cases are attributable to histiocytosis X. Nephrogenic DI is characterized by renal tubular resistance to ADH and is caused by lesions interfering with the renal concentrating pulsive water drinking or psychogenic polydipsia is another source of polyuria. Large volumes of water intake inhibit the secretion of vasopressin. Clinically, this form of DI can sometimes be distinguished by a decrease in the polyuria at night when intake tapers off with sleep. The response to a fluid deprivation test helps determine whether DI is caused by:Excessive intake of fluid (psychogenic DI): urinary osmolality rises modestly with deprivation and markedly (>750 mOsm/kg) with dDAVP administrationA defect in ADH production (central DI): urinary osmolality unchanged with deprivation but increases (>450 mOsm/kg) with dDAVPA defect in the renal response to ADH (nephrogenic DI): urinary osmolality unchanged with deprivation and does not increase (<200 mOsm/kg) with dDAVPClinical symptoms in infants and young children who have nephrogenic DI are nonspecific and include poor feeding, failure to thrive, and irritability. Symptoms may begin within a few weeks of birth, but diagnosis may be significantly delayed. Hypernatremia, dehydration, and fever, which can reach high temperatures and be intermittent, are frequently present. Constipation is common and is characterized by pebble like stools and hard, small masses on palpation of the abdomen, as in the infant in the vignette. Growth retardation is common because excessive fluid intake blunts the appetite and contributes to inadequate caloric intake. Intellectual disability and seizures used to be commonly associated with chronic DI, presumably due to brain injury from repeated episodes of hypernatremic dehydration. With early recognition and appropriate treatment, they no longer need to accompany the disorder.Central DI can occur at any age. It should be suspected in anyone who experiences an acute onset of polyuria, large urinary volumes, and nocturia. Such patients often express a preference for ice water.Life-threatening complications of DI include dehydration and electrolyte imbalance due toexcessive loss of free water.American Board of Pediatrics Content Specification(s)Know the etiology and understand the pathophysiology of diabetes insipidusRecognize signs and symptoms of diabetes insipidusRecognize and interpret relevant laboratory and imaging studies for diabetes insipidusRecognize life-threatening complications of diabetes insipidusPlan management of acute diabetes insipidusQuestion: 4You are evaluating a 2-year-old boy who was transferred to the emergency department from an outlying facility by ambulance. He initially presented with fever, poor perfusion, and altered mental status and was given intravenous fluids and antibiotics before transfer. The referring physician reported improvement after the fluid bolus, with the boy’s temperature at 39.0?C, heart rate at 170 beats/min, respiratory rate at 30 breaths/min, blood pressure at 80/60 mm Hg, and pulse oximetry reading at 100% in room air. The parents reported that the child had had a fever for 24 hours and developed progressive lethargy over the past 8 hours. They denied any other associated symptoms. The child was previously healthy and fully immunized. Initial vital signs upon arrival at your facility are: temperature of 39.6?C, heart rate of 200 beats/min, respiratory rate of 16 breaths/min, and blood pressure of 60/20 mm Hg. The monitor shows sinus tachycardia, with a rate between 180 and 210 beats/min. Physical examination of the pale, lethargic child shows absent peripheral pulses, delayed capillary refill, and cool and mottled skin. His pupils are 4 mm and reactive bilaterally. He is minimally responsive but has no focal findings on neurologic examination and no meningismus. During your examination, the child develops agonal respirations and bradycardia.Of the following, the MOST likely cause of this child’s collapse isA.cerebral edema with acute herniationB.decompensated shock with resultant cardiopulmonary failureC.electrolyte disturbance with secondary arrhythmiaD.hyperthermia resulting in direct end-organ injuryE.hypoxia-induced bradycardia and respiratory arrestCorrect answer BThe boy described in the vignette is suffering from septic shock with resultant cardiopulmonary failure. Failure to recognize and aggressively treat early shock results in continued end-organ hypoperfusion and progression to hypotensive or decompensated shock. Tachycardia and tachypnea are replaced by bradycardia, hypoventilation, and ultimately cardiopulmonary arrest. Although the fever and lethargy reported for the boy raise the possibility of meningitis, the absence of focal neurologic findings, asymmetric pupils, or meningismus and the presence of tachycardia and hypotension make herniation unlikely. The boy has no history of excessive fluid losses or abnormal intake to account for electrolyte disturbances and no evidence of arrhythmia other than sinus tachycardia followed by bradycardia. Although the exact temperature at which direct tissue/organ injury occurs is unclear, it is unlikely that fever itself, with temperatures less than 41.1?C, would result in cardiopulmonary failure and arrest. This boy has no history of respiratory distress or hypoxia to account for his collapse.Unlike in the adult population, sudden cardiac arrest is rare in children; most cases stem from progressive respiratory failure or shock. Failure to recognize or adequately treat the early stages of respiratory distress or shock allows progression to respiratory failure or decompensated shock and ultimately cardiopulmonary failure. Cardiopulmonary failure is characterized by inadequate oxygenation, ventilation, and perfusion caused by the combination of respiratory failure and shock. The continued and progressive lack of delivery of adequate oxygen and substrates to the various tissues leads to worsening tissue hypoxia and acidosis and eventual cardiopulmonary arrest.??Once progression to full arrest has occurred, the likelihood of survival and, particularly, a normal neurologic outcome is low. Out-of-hospital arrest has a 2% to 9% rate of survival; in-hospital arrest has better outcomes, with survival rates as high as 27%. Even with prompt initiation of high-quality cardiopulmonary resuscitation, continued tissue hypoxia and poor perfusion leads to ongoing end-organ injury. Postarrest phenomena affect all organ systems and are the result of the hypoxia, poor perfusion, and ischemia associated with the arrest. The?Table lists common recognized manifestations of postcardiac arrest syndrome.American Board of Pediatrics Content Specification(s)Understand pathophysiology of progression from cardiopulmonary failure to arrestUnderstand physiologic consequences of cardiopulmonary arrest and post arrest phenomenaQuestion: 5A 16-year-old girl presents to the emergency department with left arm swelling and pain of 1 week’s duration. She has had progressive neck swelling and lumps during the past month. Today she complains of malaise, lack of appetite, fatigue, low-grade fever, night sweats, mild cough, and breathing difficulty when lying flat. Physical examination documents a temperature of 39.0?C, ?heart rate of 120 beats/min, respiratory rate of 35 breaths/min, and blood pressure of 105/65 mm Hg. She has anterior cervical, posterior cervical, and supraclavicular lymphadenopathy of varying sizes with a few matted lymph nodes without tenderness or fluctuance. Her left upper arm is swollen with prominent veins, and she has facial plethora and associated axillary and femoral lymphadenopathy. Auscultation reveals faint rales at the lung bases and no cardiac murmurs. She has no palpable masses on breast or abdominal examination.Of the following, in addition to chest radiography, the MOST appropriate initial diagnostic investigations for directing this patient’s treatment plete blood count and Doppler ultrasonography of the left upper plete blood count, coagulation studies, and protein C and S plete blood count with peripheral smear and serum electrolytes, creatinine, and uric acid assessmentD.electrocardiography, D-dimer measurement, and computed angiography of chestE.lymph node aspirationCorrect answer CThe matted lymph nodes without tenderness, fluctuance, or erythema combined with the presence of supraclavicular lymphadenopathy and superior vena cava syndrome described for the adolescent in the vignette are most indicative of malignancy. Hence, the first line of investigation is a complete blood count with peripheral smear. In addition, assessment of renal function, electrolytes, and uric acid is required before initiating therapy to address tumor lysis syndrome. Although this girl has superior vena cava syndrome in conjunction with upper arm swelling due to thrombosis or venous stasis, she does not have clinical findings of pulmonary embolism that would require computed angiography. Evaluation for a primary hypercoagulable condition such a protein C or protein S deficiency is not indicated. Her hypercoagulopathy is likely due to her malignancy. Upper arm Doppler ultrasonography is indicated for a patient showing signs of isolated extremity swelling to rule out deep venous thrombosis, but such a study does not help to identify the primary pathology. Lymph node aspiration or excisional biopsy is reserved as part of an extensive evaluation.?Lymphadenopathy represents lymphoid tissue hyperplasia that is a response to inflammation, antigen (virus, bacteria, cutaneous conditions, insect bites), metabolic storage diseases, or accumulation of malignant lymphoid cells. It can be localized or diffuse. Examples of localized lymphadenopathy include cervical lymphadenopathy due to tonsillitis and upper respiratory tract infections, occipital lymphadenopathy due to fungal scalp infections, and axillary or femoral lymphadenopathy after injuries or infections of extremities. Chronic localized lymphadenopathy is present for more than 3 weeks. Causes may be infections (eg, mycobacteria, Bartonella henselae, Brucella, cytomegalovirus), malignancies (eg, leukemia, lymphomas, neuroblastoma, histiocytosis), or systemic illness (eg, sarcoidosis, thyroiditis). Diffuse lymphadenopathy involves two or more noncontiguous regions. Examples include conditions due to a systemic process such as systemic infections, autoimmune illness, malignancy, and medications (eg antiseizure medications).Findings on the history and physical examination usually point toward possible causes. For example, the combination of pharyngitis, tonsillitis, and reactive cervical lymphadenopathy is likely due to a viral or bacterial process. Localized lymphadenopathy of greater than 1 cm with erythema, tenderness, or overlying cellulitis can be treated presumptively with antibiotics without ancillary studies. If fluctuance is present, an abscess should be ruled out and treated accordingly.Lymphadenopathy of specific locations can suggest diagnoses:Occipital area nodes: rubella or scalp conditionsPreauricular nodes and conjunctivitis: cat scratch disease and Chlamydia (Parinaud syndrome)Isolated posterior cervical or axillary nodes: toxoplasmosisInguinal nodes: sexually transmitted infectionsLymphadenopathy in specific age groups also can suggest causes. Preauricular lymphadenopathy is seen with chlamydial conjunctivitis in neonates, and diffuse lymphadenopathy is seen with cutaneous manifestations of histiocytosis and metabolic storage diseases in infants. Acute cervical lymphadenopathy often is due to Kawasaki disease in children younger than 4 years of age and to atypical mycobacterial adenitis in those younger than 5 years. Lymphadenopathy can be due to leukemia, neuroblastoma, and non-Hodgkin lymphoma in children younger than 5 years of age, and chronic diffuse lymphadenopathy in an adolescent (Figure) may be due to lymphoma.Chronic cervical and axillary lymphadenopathy with a history of exposure to kittens suggests the need for laboratory investigations for Bartonella titers. Unilateral isolated cervical lymph node enlargement can be due to atypical mycobacterial infection, especially in the setting of fish tank exposure (M marinum). Bilateral posterior cervical lymphadenopathy with matted lymph nodes in the presence of systemic symptoms of fatigue, fever, and malaise could be due to tuberculosis (indicating a purified protein derivative test), leukemia, or lymphoma (indicating complete blood count and peripheral smear). Hodgkin lymphoma typically presents with unilateral localized lymphadenopathy that is in contrast to the bilateral lymphadenopathy seen with non-Hodgkin lymphoma.Chronic generalized lymphadenopathy in the presence of fever, malaise, and pharyngitis could be due to viral infections (eg, Epstein-Barr virus or cytomegalovirus) or malignancy. In the appropriate setting, sarcoidosis (African American child who has cervical or scalene nodes); autoimmune disorders such as systemic lupus erythematosus, rheumatoid arthritis, or hyperthyroidism; or medication exposure (most of the common antiepileptic drugs, antibiotics such as isoniazid and sulfonamides) should be considered as pathologies.Special consideration is required to plan the evaluation and management of lymphadenopathy due to malignancies, especially hematologic, the most common type of cancer in the pediatric population. Certain characteristic findings with lymphadenopathy should raise the suspicion of malignancy (Table). Associated findings of night sweats, weight loss, generalized pruritis, orthopnea, bleeding, pallor, petechiae, hepatomegaly, splenomegaly, bone pain, and superior vena cava syndrome can also be indicative of malignancyWhen a hematologic malignancy such as leukemia and lymphoma is suspected, the most important investigation is a complete blood count with peripheral smear. Further investigations include assessment of serum electrolytes, including phosphate, as well as uric acid and renal function, which can aid in initiation of emergency department management that addresses tumor lysis syndrome. Management includes administration of intravenous fluids with sodium bicarbonate and maintenance of adequate urinary output (may use diuretics). Treatment for hyperuricemia involves oral allopurinol. If the uric acid concentration is increasing rapidly or is greater than 6 mg/dL (357 ?mol/L) or if the serum creatinine value is elevated, recombinant urate oxidase is indicated (after assessing the patient for glucose-6-phosphate deficiency). If serum phosphorus values are elevated or recombinant urate oxidase is administered, alkaline fluids should be avoided. Potassium should not be added to intravenous fluids because a life-threatening elevation in serum potassium occurs with tumor lysis syndrome. Peripheral blood cultures should be obtained in patients who have fever and treatment with broad-spectrum intravenous antibiotics initiated because all such patients should be considered immunocompromised. Chest radiography is indicated to assess for mediastinal mass. If such a mass is present, airway management and protection is the priority. Other studies, including radiologic and surgical evaluation, are planned by the inpatient team and can include bone marrow aspiration, cerebrospinal fluid examination, lymph node aspiration and biopsy, and computed tomography scans.FigureFigure. Adolescent who has chronic diffuse lymphadenopathy associated with lymphomaAmerican Board of Pediatrics Content Specification(s)Differentiate by age the etiology and understand the pathophysiology of lymphadenopathyPlan diagnostic evaluation and initial intervention for patients with lymphadenopathyRecognize serious and/or life-threatening causes of lymphadenopathyQuestion: 6A 9-month-old infant is brought in by his mother after experiencing vomiting since yesterday. The emesis, which has occurred seven times, was initially milk-colored but now has a green tinge. The infant was born small for gestational age at 36 weeks’ gestation after maternal induction of labor due to oligohydramnios. She weighed 4 lb at birth and spent 4 days in the neonatal intensive care unit while transitioning from nasogastric to full oral feedings. She has gained weight well at home since discharge. She had one previous emergency department visit 3 weeks ago at another hospital for grunting and vomiting, was diagnosed with constipation, and was discharged. The vomiting did not recur until yesterday. Physical examination of the afebrile, tachypneic, and grunting infant reveals a temperature of 37.2?C, heart rate of 148 beats/min, respiratory rate of 56 breaths/min, blood pressure of 128/91 mm Hg, and oxygen saturation of 97% while breathing 2 L oxygen via nasal cannula. The alert and vigorous infant has slightly dry mucous membranes. Lung examination shows good air entry on the right and decreased breath sounds on the left, without crackles or wheezes. Cardiac evaluation documents tachycardia without appreciable murmurs. Her abdomen is soft and nondistended, but she appears to have mild diffuse tenderness with palpation. Bowel sounds are present. No hepatosplenomegaly is appreciated. You insert a nasogastric tube, obtain chest radiography (Figure) and intravenous access, and administer a fluid bolus.FigureOf the following, the action that is MOST helpful in determining management for this infant isA.bilevel positive-airway pressure ventilationB.decubitus chest radiographsC.empiric broad-spectrum antibiotic administrationD.needle decompression of the left chest followed by chest tube placementE.radiographic evaluation for bowel obstructionCorrect answer: EThe infant described in the vignette has a diaphragmatic hernia, which is demonstrated in the radiograph by the presence of intestine in the left chest. Although most infants who have congenital diaphragmatic hernia are symptomatic in the newborn period, some may present later in infancy with a complication from the hernia. This infant may be experiencing a bowel obstruction, a clue to which is the abrupt onset of emesis that is now bilious. Therefore, further evaluation with obstructive radiographic series and contrast radiography is warranted immediately to time the operative intervention appropriately. If no obstruction exists, the infant could be stabilized and nonemergent repair planned. In this case, upper gastroenterography showed a complete obstruction, and the infant was brought to the operating room emergently.Needle decompression of the left chest followed by chest tube placement should be performed only for a tension pneumothorax, which this infant does not have. Bilevel positive-pressure ventilation can cause further distension of the bowel loops within the chest and, therefore, is contraindicated. The chest radiograph does not show pneumonia and the infant is afebrile, indicating no role for empiric broad-spectrum antibiotics. Decubitus radiographs would be appropriate to help evaluate for the presence of an airway foreign body.As mentioned previously, most infants who have congenital diaphragmatic hernia present in the newborn period with respiratory distress. Decreased or absent unilateral breath sounds, displacement of heart tones, tracheal deviation, a scaphoid abdomen, or bowel sounds in the chest are all clues to diagnosis. The cause of the respiratory distress is multifactorial and related to abnormalities in development of bronchiolar branching, a hypoplastic pulmonary arterial tree with abnormal muscularization, and secondary surfactant deficiency. Pulmonary hypertension, hypoxia, acidosis, and intrapulmonary shunting complicate the hospital course of affected newborns. A chest radiograph is often all that is needed for diagnosis. The differential diagnosis includes congenital cystic adenomatoid malformation, cystic teratoma, pulmonary sequestration, a bronchogenic cyst, and neurogenic tumors. Rarely, intestinal contrast studies may be needed to confirm the presence of bowel above the diaphragm.Neonatal resuscitation for symptomatic newborns who have diaphragmatic hernia includes immediate intubation rather than bag-mask ventilation, the placement of an nasogastric tube to decompress the bowel, and sedation with or without paralysis. The goals of therapy are to avoid barotrauma, correct acidosis if present, and maintain blood pressure with vasopressive agents, if necessary. Treatment of pulmonary hypertension may be problematic. Morbidity and mortality remain high with this condition. Thirty percent of fetuses are stillborn. If alive at delivery, 30% to 50% die before transport to a neonatal center capable of managing their problems. Extracorporal membrane oxygenation may be required either before or after hernia repair to support the infant.American Board of Pediatrics Content Specification(s)Recognize signs and symptoms of diaphragmatic herniaKnow the indications for and interpret results of ancillary studies in patients with diaphragmatic herniasPlan the management of acute diaphragmatic hernia and the potential complications of this conditionQuestion: 7A 15-year-old girl presents to the emergency department with the acute onset of left lower quadrant abdominal pain, nausea, and emesis. She has urinary frequency and mild dysuria but no gross hematuria. She says she had no fever at home, but physical examination documents a temperature of 38.6?C and mild left flank tenderness. Laboratory results include a white blood cell count of 10x103/?L (10x109/L) and a creatinine of 0.8 mg/dL (70.7 ?mol/L).? Urinalysis reveals 10 to 15 red blood cells per high-power field (hpf), 5 to 10 white blood cells/hpf, and 1+ bacteria. Noncontrast computed tomography scan of the abdomen and pelvis shows moderate left hydronephrosis with perinephric stranding and hydroureter down to a 3-mm calculus in the proximal ureter as well as a 6-mm nonobstructing calculus in the left kidney. Administration of oral analgesics controls the girl’s pain in the emergency department, and her nausea resolves.Of the following, the MOST appropriate treatment for this child isA.a single dose of intravenous antibiotics, followed by outpatient therapy with an α-blocker and oral antibioticsB.admission for intravenous antibiotics and α-blocker therapyC.admission for intravenous antibiotics and urologic consultation for stent placementD.oral antibiotics, α-blocker therapy, and admission for intravenous hydrationE.oral antibiotics, oral analgesics, and outpatient urologic follow-up evaluationCorrect answer CThe girl described in the vignette has an obstructing ureteral stone and a urinary tract infection. She is at high risk for the development of frank pyelonephritis and sepsis. Accordingly, she should be admitted for initiation of intravenous antibiotics and prompt urologic intervention. Given her acute infection, the proximal location of her obstructing stone, and the presence of an even larger stone in the kidney that requires treatment, she would be best served by placement of a stent. After the infection had been adequately treated, she would most likely undergo extracorporeal shock wave lithotripsy for definitive treatment of her stones. Alternative strategies are at the urologist’s discretion and may include ureteroscopic removal.Therapy with an α-blocker (believed to act by relaxing smooth muscle in the ureteral wall) is frequently used in the outpatient management of smaller distal stones to increase their rate of passage, although no definite benefit has been documented in pediatric patients. In the absence of infection, treating the patient with oral analgesics and α-blocker therapy with outpatient urologic follow-up evaluation is reasonable. The spontaneous passage of renal calculi significantly correlates with stone size. Patients who have uncomplicated ureteral stones that are smaller than 5 mm are routinely treated as outpatients. Criteria for inpatient management include febrile urinary tract infection, intractable pain, and intractable nausea and emesis.The signs and symptoms of acute renal calculi vary by age. Adolescents typically present with the acute onset of flank pain, which may be accompanied nausea and vomiting and hematuria. Because younger children more often have nonspecific abdominal or back pain, those younger than 5 years may be evaluated for other causes of abdominal pain before renal calculi are suspected. Hematuria, gross or microscopic, is the rule, and nausea and vomiting are common in association with the pain. Voiding symptoms such as frequency and urgency are more common with distal ureteral calculi. Flank and costovertebral angle tenderness vary and are not reliable signs of the presence or absence of a stone.Diagnosis is made with imaging, sometimes obtained to evaluate other causes for the presenting complaints. A noncontrast computed tomography (CT) scan is the most sensitive and specific imaging modality for detecting renal and ureteral calculi, although it exposes the child to ionizing radiation. Most CT protocols for the detection of renal stones limit the radiation dose substantially compared with other diagnostic CT scans of the abdomen and pelvis. Renal ultrasonography, which avoids exposure to radiation, may be used to detect renal stones and to demonstrate hydronephrosis, but this modality is less sensitive at detecting ureteral calculi. An abdominal flat plate or kidney, ureter, bladder radiograph may be useful, particularly in patients who have known stone disease.Infection and sepsis represent the most serious complications of renal stone disease and require prompt treatment, as discussed previously. Acute impairment of renal function, as evidenced by an increase in creatinine, is not uncommon but is almost always transient unless high-grade obstruction remains for extended periods. For most patients, pain leads to treatment before long-term damage occurs to the kidneys.American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of renal stonesPlan the management of acute renal stones and their complicationsQuestion: 8A 4-year-old boy who was a restrained rear-seat passenger is brought in by paramedics after his family’s car was involved in a front-end collision. The paramedics placed him on a spine board and attached a cervical collar. On physical examination, the awake and alert boy complains of neck pain and says that his arms and hands “feel funny, like they are asleep.” The only finding of note on a primary and secondary survey is pain on palpation of the posterior neck. Results of his motor examination are normal, and no sensory deficits are evident. Anterior-posterior and lateral cervical spine radiographs appear normal and do not reveal any bony abnormalities or misalignment, and flexion/extension films and computed tomography scan of the cervical spine also yield normal results. After receiving a dose of ibuprofen, the boy no longer complains of neck pain, but he states that his arms still feel funny.Of the following, the MOST appropriate treatment for this child isA.discharge in a padded hard cervical collar with neurosurgical follow-up evaluationB.hospital admission and contrast myelographyC.hospital admission and magnetic resonance imaging of the cervical spineD.reexamination out of the cervical collar and if pain-free, admission for observation ?in a soft cervical collarE.reexamination out of the cervical collar and if pain-free, discharge without spinal immobilizationCorrect answer CThe boy described in this vignette may have an occult spinal cord injury. In the 1980s, the term SCIWORA (spinal cord injury without radiographic evidence) was coined to describe children who had neurologic deficits or a history of transient paresthesias, numbness, or paralysis but no evidence on plain radiography or computed tomography scan of an injury. Some of these children developed delayed onset of permanent paralysis from hours to days after their original presentations. When evaluated by magnetic resonance imaging (MRI), two thirds of cases described as SCIWORA have demonstrable injury to the spinal cord or soft tissue of the spinal column, including the ligament, capsule, muscle, or vertebral body endplate. Abnormalities found on MRI include epidural hematoma, ligamentous disruption, disc herniation, or infarction.This boy needs further evaluation with MRI and continued cervical spinal immobilization, even if he is pain-free. Immobilization cannot be achieved in a soft cervical collar; a hard cervical collar and neurosurgical consultation are indicated. Inpatient hospitalization facilitates timely evaluation and management. Myelography, in which contrast dye is injected directly into the subarachnoid space under fluoroscopy, has been supplanted by MRI, which is easier to perform and less invasive.Several physiologic factors predispose children to occult spinal cord injuries. Infants have a large ratio of head size and weight to the rest of their body, with relatively weak neck musculature. Spinal ligaments and capsules are elastic and prone to stretch without tearing. Intervertebral discs and annulus have high water content, which allows for longitudinal expansion without rupture if the spinal column is distracted. Facet joints are oriented horizontally and are shallow, which allows for motion during flexion, extension, and rotary neck movements. Children younger than 10 years of age lack an ossified uncinate process, thereby making lateral and rotary spinal column movement less restricted than in adolescents and adults. Overall, hypermobility and elasticity lead to self-reducing injuries with hyperflexion, hyperextension, or distraction. Infants and children younger than 8 years of age commonly experience upper cervical spine injuries (C1 through C3); older children and adolescents more commonly have lower cervical injuries (C4 through C8). SCIWORA can also occur after spinal cord infarction due to ischemia.Although well described, SCIWORA is a rare event in the injured child. Estimates of the percent of all pediatric spinal cord injuries categorized as SCIWORA vary widely by source but have decreased with the widespread use of MRI. Children are significantly more likely to experience these injuries than adults. The most common circumstances of injury in children younger than 8 years are motor vehicle collisions, falls, and child abuse. In older children, motor vehicle collisions and sports (gymnastics, diving, horseback riding, football, and wrestling) predominate.American Board of Pediatrics Content Specification(s)Understand the concept that cervical cord injury can occur in the absence of a radiologic abnormalityMARCH 2012Question: 1An 16-year-old girl comes into a rural emergency department because of right-sided facial swelling and pain. She has no history of trauma, difficulty swallowing, recent upper respiratory tract infection, fever, cough, or congestion. On physical examination, her right cheek appears swollen and tender but not erythematous or warm. Intraoral examination reveals gum line swelling adjacent to her upper right first molar tooth, which seems to come to a point. No drainage is evident in the area. The local dentist is on vacation out of state and will not return for 3 days. The girl is in excruciating pain despite narcotic and nonsteroidal analgesia. You consult the dentist by phone, who recommends you perform an incision and drainage.Of the following, the MOST accurate statement regarding incision and drainage of a dental abscess is thatA.antiseptic preparation of the mucosa is necessary to prevent spread of infectionB.incision and drainage must be preceded by a dose of antibioticsC.local anesthesia will be easy to obtainD.needle aspiration has been shown to be equally effectiveE.root canal or extraction is required for definitive treatmentCorrect answer: EThe adolescent described in the vignette has symptoms suggestive of a dental abscess. Abscesses begin as dental caries that, if left untreated, spread from the dentin to the pulp of the tooth. Tooth pulp is enclosed in a rigid space, and with increasing inflammation and infection, pressure builds, causing necrosis and ischemia to the pulp as well as tooth pain. Extension of infection into the surrounding tissue results in a periapical abscess. At this stage, no swelling at the gum line is visible, but the tooth is tender to percussion and biting. If dental treatment is not rendered, further inflammation ensues, with pus formation. Exudate can force its way through the alveolar bone, eventually lodging between the bone and the periosteum in the subperiosteal space. This is the point at which gum line swelling becomes evident and incision and drainage may be indicated. This stage of dental abscess is almost always accompanied by intense pain. In the early stages of subperiosteal abscess, the lesion is often indurated or hard, without an obvious fluctuant point. Incision at this stage may only yield hemorrhage because no pus has accumulated. Hot intraoral saline rinses may be used until the abscess points, at which point drainage may be accomplished.There are no clear indications for incision and drainage of intraoral abscesses in the pediatric population by nondental personnel, and it is not routinely performed in the pediatric emergency department. Antibiotics are indicated for facial cellulitis or in the presence of fever or other systemic symptoms, but if the infection is localized, as for this girl, treatment of the primary process is preferred. Incision and drainage is more common in adult practice, especially when immediate access to definitive dental care is difficult to obtain.Several criteria must be met to perform an incision and drainage. The infection must be localized, confined, and easily accessible, as in this patient. If a patient has trismus or airway compromise or is toxic, an incision and drainage procedure is not sufficient treatment. These symptoms indicate the presence of a deeper space infection that must be recognized and addressed.No antiseptic preparation of the oral mucosa is necessary. Local anesthesia may be difficult to obtain for this girl because of local pH conditions and rapid absorption into the highly inflamed area. Block anesthesia within the oral cavity, which avoids the locally inflamed and abscessed area, is ideal, but if the emergency clinician lacks experience or expertise with these procedures, it should not be attempted. Topical benzocaine gel or lidocaine/epinephrine/tetracaine may be used before injection. Local infiltration at the periphery of the swelling with 2% lidocaine or 0.5% bupivacaine with epinephrine should be performed if a regional dental block is not used. Isolating the area with 2x2-inch gauze pads before the procedure is helpful. Suction should be immediately available.A 0.5- to 1-cm incision should be made over the area of maximal fluctuance with a No. 15 or No. 11 blade scalpel. A single, quick, stabbing motion is recommended and must extend through the soft tissue down to the bone. Despite anesthesia, the patient often feels the incision, but if pus is extruded, relief quickly follows. An initial spurt of pus may be followed by a combination of blood and pus. Some practitioners recommend additional anesthesia at this point before using a hemostat to enter the incision and break up any loculations or extend the incision as necessary. The area should be “milked” to express any residual pus and irrigated with normal saline. At this point, a Penrose drain (sutured into place) or gauze may be placed in the wound to facilitate further drainage. Needle aspiration is inadequate to relieve symptoms or sufficiently drain the abscess.No evidence is available to guide the use of antibiotics after drainage, although many provide coverage if definitive treatment by a dentist will be delayed. A dentist must remove the necrotic debris from the root canal space or perform dental extraction to avoid recurrence of infection.American Board of Pediatrics Content Specification(s)Know the anatomy and pathophysiology relevant to incision and drainage of a dental abscessKnow the indications and contraindications for incision and drainage of a dental abscessPlan the key steps and know the potential pitfalls in performing incision and drainage of a dental abscessRecognize the complications associated with incision and drainage of a dental abscessQuestion: 2An 8-year-old boy is brought to the emergency department by emergency medical services after being involved in a motor vehicle crash. He was a restrained rear seat passenger in a high-speed, front-end collision. On arrival, the boy is lucid but complains of abdominal pain. Physical examination reveals a heart rate of 160 beats/min, respiratory rate of 36 breaths/min, and blood pressure of 90/60 mm Hg. The only findings of note are tenderness and some bruising of his lower abdomen (Figure). You administer two crystalloid fluid boluses of 20 mL/kg and obtain portable radiographs of the chest, cervical spine, and pelvis, which yield normal results. Findings on laboratory tests include a hematocrit of 32% (0.32) and normal alanine aminotransferase, urinalysis, and electrolytes, except for base excess of -12 mEq/L. A bedside focused assessment with sonography for trauma (FAST) examination does not reveal any free fluid in the abdomen or pelvis. Computed tomography (CT) scan of the abdomen and pelvis with intravenous contrast shows normal results. Repeat physical examination documents a heart rate of 140 beats/min and blood pressure of 78/55 mm Hg. His lower abdomen remains tender to palpation with guarding. You administer a third fluid bolus and request cross-matched blood.FigureLower abdominal bruising for the boy in the vignetteOf the following, in conjunction with surgical consultation, the MOST appropriate next step in the treatment of this patient isA.diagnostic peritoneal lavageB.exploratory laparotomyC.repeat abdominal CT scan with oral contrastD.repeat FAST examinationE.serial abdominal examinationsCorrect answer: BThe diffuse lower abdominal tenderness and guarding described for the boy in the vignette is indicative of significant intraabdominal injury (IAI) from blunt abdominal trauma (BAT). He has an abdominal wall contusion across the lower abdomen from a lap belt. The persistent tachycardia and hypotension, despite resuscitation with 40 mL/kg of fluid, is strongly suggestive of a hollow viscus injury with developing peritonitis. He meets criteria for exploratory celiotomy (Table).Although a diagnostic laparoscopy may be helpful to delineate the type of injury, definitive surgical treatment via an open laparotomy allows adequate exploration and repair of perforated bowel, an injury that can be missed on an initial CT scan. Diagnostic laparoscopy is best reserved for cases of pediatric trauma involving penetrating abdominal injury such as stab wounds to exclude peritoneal violation and delineate extent of injury, including occult diaphragmatic tears. A FAST examination is operator-dependant and lacks sufficient sensitivity to detect intraabdominal solid or hollow viscus injury. Although a repeat CT scan with oral contrast may assist in the diagnosis of bowel injury, it lacks sufficient sensitivity, involves time for oral contrast to transit the bowel, and requires transport of an unstable patient from the emergency department. Diagnostic peritoneal lavage (DPL) is a sensitive test to detect intraperitoneal blood or soilage from bowel contents, but it is invasive and associated with potential complications. Serial abdominal examinations may be appropriate in the fluid-responsive, hemodynamically stable child, unlike the child in the vignette.In accordance with Advanced Trauma Life Support guidelines, the initial resuscitation for hemodynamically unstable patients entails administration of a 20-mL/kg bolus of crystalloids such as lactated Ringer solution or normal saline. This may be repeated up to a cumulative volume of 40 to 60 mL/kg. If the patient continues to require additional fluids, serial 10-mL/kg aliquots of packed red blood cells should be administered until the patient is deemed stable. For adolescents, the initial fluid volume is typically 1 to 2 L followed by 1 to 2 units of packed red blood cells. In conjunction with volume resuscitation and surgical consultation, efforts to stop intraabdominal hemorrhage should be pursued.Insertion of two short, wide-bore catheters peripherally, above the diaphragm, as in the antecubital fossa, are best to administer large amounts of fluids rapidly. This may not always be feasible in the young child or infant, in whom any available peripheral venous site should be accessed. If intravenous access is difficult, intraosseous access is acceptable, unless contraindicated by a fractured extremity, until central venous access is established.Detection of IAI in BAT can be a challenge. Physical signs and symptoms can be unreliable, and the examination is often complicated by distracting multisystem injuries, impaired mental status, or intoxication. The diagnostic approach for pediatric patients who have BAT from high-risk mechanisms is an issue of debate. DPL is a very sensitive test for detecting intraperitoneal blood or peritoneal soilage and had been a standard procedure. However, it is invasive and is associated with complications. Further, as nonoperative management of solid organ injuries has gained acceptance among pediatric surgeons, the utility of DPL has diminished.CT scan with intravenous contrast has the advantage of being very sensitive and specific for solid organ injuries, including in the retroperitoneal area. However, it is expensive and time-consuming, exposes the child to ionizing radiation and contrast-induced nephropathy, and requires that a potentially unstable patient be transported to the radiology suite. Further, normal findings on abdominal CT scan cannot exclude hollow viscus injuries.Ultrasonography can be performed rapidly at the bedside, is inexpensive, has no known risks, and can be repeated. The FAST examination can be performed by pediatric emergency medicine physicians and is used specifically to identify free intraperitoneal blood (fluid) as a secondary marker of IAI. The diagnostic accuracy can vary, depending on the skill of the sonographer, equipment, and time since injury. Because fluid accumulates over time, results of the initial examination may be negative. Further, a minimum amount of blood or fluid is required for detection by ultrasonography. This imaging modality also does not delineate parenchymal, hollow viscus, or retroperitoneal injuries. In the hands of emergency physicians, the sensitivity of FAST in detection of hemoperitoneum varies from 56% to 75%, specificity ranges from 93% to 97%, positive likelihood ratio is 14.5, and negative likelihood ratio is 0.36. In general, the FAST examination is more accurate for ruling in than ruling out IAI. If the pretest probability of IAI is high and results of a FAST examination are negative, most blunt trauma algorithms recommend obtaining a CT scan if the child is stable. Plain radiography is useful to exclude pelvic fractures, associated thoracic trauma, and fractures of the spine that may increase the risk for IAI. Although rarely seen, the presence of free air under the diaphragm suggests the need for immediate operative intervention.A clinical prediction rule for identification of children who have IAI after BAT recently was validated at a level I trauma center. The presence of any of six high-risk variables heightened the risk for IAI:Low age-adjusted systolic blood pressureAbdominal tendernessFemur fractureAlanine aminotransferase >125 IU/L or aspartate aminotransferase >200 IU/LInitial hematocrit <30% (0.3)Urinalysis showing >5 red blood cells/high-power fieldIf such findings are refined in a multicenter cohort, the need for CT scans in the setting of BAT may be decreased.Children restrained only by lap belts or who are too small to be placed in adult seat belts are at high risk for IAI. The “lap belt” complex involves sudden deceleration, with flexion-compression type injuries of the spine (Chance fractures) in association with IAI. The latter includes duodenal perforation, mesenteric tears, transection of small bowel, and bladder rupture. The hallmark of the lap belt syndrome is abdominal wall or flank ecchymosis, as noted for the boy in the vignette.Abuse-related injuries occur from a forceful blow with a fist or blunt object to the upper abdomen. The frequent lack of external evidence of injuries warrants a high index of suspicion of injury. An inconsistent history with evidence of IAI should raise suspicion of child maltreatment. The pattern of injury can range from duodenal or jejunal hematomas or perforation to significant disruption of a solid organ, most often the liver.Table. General Indications for Operative Management of Blunt Intraabdominal Injury? Hemodynamic instability despite adequate volume resuscitation ? Decompensated shock on admission ? Packed red blood cell transfusion >40 mL/kg ? Physical examination signs of peritonitis? Radiologic evidence of pneumoperitoneum, intraperitoneal bladder rupture, or renovascular pedicle disruption? Positive findings on diagnostic peritoneal lavage performed by a trauma surgeonAmerican Board of Pediatrics Content Specification(s)Plan volume resuscitation for a child with abdominal injury due to blunt traumaUnderstand the indications for urgent laparotomy in a child with abdominal injury due to blunt traumaRecognize limits of physical examination and radiologic assessment of abdominal and retroperitoneal trauma, especially bowel, pancreatic, and mesenteric injuriesQuestion: 3A 9-year-old boy presents with a 1-week history of headache that began in the right side but now involves his entire head. He describes the pain as severe and pounding and states that it is exacerbated by movement, bright light, and loud noise. He has vomited several times since the headache began. He has been sleeping intermittently all day today. On physical examination, his temperature is 38.6°C, heart rate is 66 beats/min, respiratory rate is 18 breaths/min, blood pressure is 110/70 mm Hg, and oxygen saturation is 99% in room air. The boy appears very drowsy and does not readily answer questions. He moves all his extremities in bed but is unable to sit up or get out of bed for complete neurologic evaluation. His eye examination reveals restriction of lateral gaze in the right eye.Of the following, the MOST appropriate next step isA.dilated eye examinationB.head computed tomography scanC.magnetic resonance imaging/angiographyD.lumbar punctureE.sinus radiographCorrect answer BThe seriously ill boy described in the vignette has altered mentation, headache, and fever. The cause of the headache likely is infectious, but the severity of his presentation and signs of possible increased intracranial pressure (bradycardia, vomiting, abduscens palsy) argue for performing computed tomography scan before proceeding with lumbar puncture.Headache is a very common reason for presenting for emergency care, and serious causes are rare but potentially life-threatening. Viral infection is the predominant cause of headaches for children seen in emergency departments, but other causes of headache differ by age. Tension, migraine, and psychogenic headaches are more common in adolescents than young children. Regionalized pain due to illness or inflammation such as pharyngitis, otitis, or dental abscess is a more likely cause of headache in young children.Indications that headache is a symptom of serious illness include focal neurologic findings, altered mental status, and signs of increased intracranial pressure. Among the potentially life-threatening causes of headache in children are tumors, intracranial bleeding, venous thrombosis, cerebral abscess, and meningitis or encephalitis.Plain radiography holds little utility for emergency evaluation of headache. Sinusitis is diagnosed clinically; plain films add little diagnostic information. Head computed tomography scan is the most useful test in the emergency department but should be used judiciously to avoid unnecessary radiation exposure. Indications for emergent imaging of the noninjured patient include clinical concerns of tumor, stroke, intracranial abscess, venous thrombosis, arteriovenous malformation, or intracerebral hemorrhage. In some instances, emergent magnetic resonance imaging/angiography may preferable, but the utility of this modality is limited by both a delay in diagnosis and the need for sedation, especially for young children. Because this boy has signs of elevated intracranial pressure, results of a dilated eye examination will not be informative and may unnecessarily delay care and interfere with subsequent pupillary evaluation.Most pediatric headaches can be treated with over-the-counter analgesics (acetaminophen and ibuprofen). Severe headache requiring narcotic medications in the emergency department is unusual and should prompt further investigation. Narcotic pain medications should be used sparingly in patients who exhibit abnormal mental status or those who require careful ongoing neurologic assessment because they may mask worsening neurologic status or precipitate respiratory depression. Abortive therapy for migraine headaches can involve both medications and nonpharmacologic interventions. Sleep is purported to be the single best therapy for migraine. In addition, placing the child in a dark, quiet room removes common triggers of noise and light. Rescue medications for migraine include nonsteroidal anti-inflammatory drugs, acetaminophen, triptans, and ergotamine. Supportive care with intravenous fluids and antiemetics is widely provided, albeit with little evidence base. Intravenous steroids have little proven efficacy for most patients who have migraine, but one randomized study of adults showed nearly twice as many patients with prolonged symptoms (>72 hours) had resolution of headache after dexamethasone compared with those who received placebo.American Board of Pediatrics Content Specification(s)Differentiate by age the etiology and understand the pathophysiology of headachePlan diagnostic evaluation and initial intervention for patients with headachesRecognize serious and/or life-threatening causes of headachesQuestion: 4You are examining a 4-year-old girl who fell 20 ft from a bedroom window onto concrete. Emergency medical services personnel completed endotracheal intubation of the unconscious child at the scene because of the presence of apnea. On physical examination, you note left periocular ecchymosis and diffuse bleeding from both nares. Although her pupils are 3 mm and responsive, she has no spontaneous movement in any extremity. She is breathing on her own, but because of difficulty with ventilation and oxygenation, you administer a paralytic agent. Initial computed tomography scan of the head documents a significant fracture of the frontal bone with a large hemorrhage throughout the sagittal sinus. Shortly thereafter, the girl’s pulse rate drops precipitously, eventually disappearing, and her pupils become dilated and unresponsive to light. You initiate cardiopulmonary resuscitation and administer medications and hypertonic saline solution. In consultation with neurosurgery, you determine that she is developing a progressive intracranial hemorrhage that would not be amenable to surgical intervention. The social worker notifies you that the mother has just arrived. The woman is terrified and would like to see her child.Of the following, current evidence about family presence during resuscitation MOST strongly indicates that itA.can interfere with the chain of evidenceB.increases medicolegal exposure for physicians and the hospitalC.interferes with the ability of the team to function effectivelyD.is preferred by families of a dying childE.will be upsetting to the staffCorrect answer DFamily presence during cardiopulmonary resuscitation is increasingly common, and most parents want to be given the opportunity to be present during resuscitation of their child. Standardized psychological examinations suggest that, compared with those not present, family members present during attempted resuscitations have less anxiety and depression and more constructive grieving behavior. Studies also show that family members who are present at resuscitation would recommend it to others. Family presence during resuscitation generally is not disruptive to procedures; does not interfere with the chain of evidence; and does not create stress among staff, negatively affect their performance, or increase medicolegal exposures for physicians or the hospital.Parents or family members often fail to ask whether they can be present, but clinicians should offer the opportunity in most situations. The resuscitation team should be sensitive to the presence of family members in the room, especially when communicating with parents of chronically ill children, who are comfortable with medical equipment and emergency procedures. Designating one person to be at their side, answer their questions, and provide support is strongly advised. If the presence of family members creates undue staff stress or is considered detrimental to the resuscitation, they should be respectfully asked to leave.Parenting is an active role, and allowing the mother of this child to be at the bedside in the last few moments of her child’s life may provide comfort and help with her grieving process. Being present at the bedside allows parents to grasp the reality, realize that everything possible was done, and say goodbye their child. Such actions give the parents and the family some semblance of a closure. Preparing the parents incrementally for the child’s death allows them some time to understand what has happened. They need to know that everything reasonably possible has been done to save their child by not only the resuscitation team but also bystanders and prehospital personnel. At the same time, if the resuscitation is deemed futile, they should be told clearly and compassionately that there is no hope for survival because of oxygen deprivation to the brain and heart.Using the word “death” and avoiding medical jargon is preferred over euphemisms such as “expired” or “passed away.” After death, the family should be offered time and privacy to remain with the child. During this time, physicians and ancillary staff should refrain from saying or doing too much, quietly sitting with the family and gently touching the child, which indicates to the family that they may touch the body. The physician and staff should be available for any questions. Assistance with funeral arrangements with respect for individual cultural beliefs should be offered. Physicians should avoid comments such as “I know how you feel” or “You can have other children.” Physicians should also discuss the option of an autopsy and organ donation, when appropriate, and answer questions the family may be reluctant to ask (eg, “Will the face be disturbed?”). These discussions are mandatory in certain circumstances. Finally, the decision by the physician to attend the funeral is a personal one. It may serve the purpose of showing respect as well as helping him or her cope with his or her own sense of loss after a difficult resuscitation.A child’s reaction to the death of a loved one can vary, depending on age and maturity. Children younger than 5 years of age view death as reversible. Among children 5 to 9 years of age, death is personified as an entity that punishes and avenges. Older children tend to understand the irreversibility of this universal biologic process. Children may have a delayed grief response. They may harbor a magical hope of reappearance. Some may feel guilty, reflecting their egocentric developmental phase. Alternatively, some may exhibit extreme sorrow as the defense of denial is no longer effective. Parents faced with the sudden unexpected loss of a child may also experience a spectrum of normal responses, ranging from apparent unnatural calm to emotional decompensation to outrage. The anger is often a reflection of their sense of guilt or helplessness. Parents and caretakers can help children by recognizing that they themselves are going through a grieving period. It is not unhealthy for children to see such grief, and it is not inappropriate to permit children to attend the funeral. After the death of a family member, children should not be expected to interrupt usual social or recreational activities for many weeks or months out of respect for the individual. Children require support and reassurance from the surviving family members, but they should not be expected or forced to discuss all their feelings or put their reactions into words.American Board of Pediatrics Content Specification(s)Differentiate by age grief reactions of the family members after the sudden death of a childKnow the principles of family management that should be implemented when a child diesKnow the appropriate use of family member presence while caring for critically ill or injured children in the EDQuestion: 5A 5-year-old boy is brought by emergency medical services to the emergency department after falling from a second-floor apartment window. His mother was in the kitchen at the time and heard the child crying downstairs. She noticed that the window screen had given way and he was on the ground, crying and lying on his back. A shrub underneath the window may have broken his fall. He walked at the scene, had no documented loss of consciousness, and had abrasions on his torso and legs. After immobilizing him at the scene, paramedics transported him to the emergency department.Of the following, the Haddon matrix category that would have been MOST easy to modify to prevent this boy’s injury is theA.costB.hostC.physical environmentD.social environmentE.vehicleCorrect answer: EModifying the vehicle (window), such as having a window that opens from the top, is closed, or has a secure screen, may have prevented the injury to the boy described in the vignette.? The various components of the Haddon matrix for this injury are:Host (the person at risk for injury): childAgent: energy of fall from the windowVehicle (the object that transmits the agent to the host): windowSocial environment: child supervision, financial status of the family, laws and regulations, and policiesPhysical environment: the room with the window, the apartment building, and the surface or structures outside the windowCost is not an established category of the Haddon matrix. It is one of several factors, including equity, freedom, feasibility, and preferences, suggested in some studies to add a third dimension to the two-dimensional Haddon matrix. Such additional factors may lead to better injury prevention strategies.Unintentional injuries are the leading cause of morbidity and mortality in children older than 1 year of age. The Haddon matrix is applied to understand a problem and plan interventions and strategies for injury prevention (primary, secondary, and tertiary). Its significance has been validated over time as having a direct impact on the overall incidence of unintentional injuries. The matrix was initially conceptualized for injury prevention related to motor vehicle crashes but has been extended successfully to other public health issues. The primary Haddon matrix comprised a two-dimensional matrix that included pre-event, event, and post-event stages interacting with various epidemiologic factors, such as host, agent, vehicle, and physical and social environment. The Table?uses the matrix to describe some possible interventions to prevent injury in the vignette.Examples of successful use of the Haddon matrix for injury prevention include:Window guardsBicycle helmetsSmoke alarmsHot water heater temperature regulationGun safety locksPedestrian walkwaysCar seatsAir bagsAlcohol lawsChildproof packaging of medicationsEducation about house fires, bathtub drowning, and school violenceInjury prevention guidance at the health supervision visitSafety standards at child care, school, organized sports, and playgroundsImproved prehospital servicesAvailability of poison control centersInjury safety awareness programs for parents and caregiversInjury- and poison-proofing homes.Recent examples are cell phone laws addressing cell phone texting, hands-free cell phone systems, and free 911 cell phone calls.Of note, increased awareness and knowledge does not necessarily translate into behavioral change, which may result in failure of an intervention. For example, self-reported use of seat belts may not translate into actual use of the seat belt. Therefore, rather than an active strategy (self-application of seat belt), consideration is given to passive strategies (automatic seat belts in cars) in policy and legislation.Emergency medical services and prehospital personnel are in a uniquely important position to address injury prevention from primary to tertiary phases.? Examples include:Identification of modifiable factors related to an injury based on their field experience, such as local streets that may benefit from stop signs.Identification of gaps in existing injury prevention models and appropriate changes that can make them successful, such as a playground that has cement instead of a soft surface in the child play areas while responding to a 911 call.Availability as a resource for implementation of injury prevention strategies, such as free counseling on car seat use, appropriate smoke alarm placement in homes, and free bicycle helmet distribution.Counseling at the time of injury to prevent future injuries, such as discussing appropriate helmet use when responding to a head injury related to lack of helmet use.American Board of Pediatrics Content Specification(s)Know how the Haddon matrix is used to analyze injury eventsKnow successful injury prevention interventionsUnderstand the role of EMS/prehospital providers in injury control and preventionQuestion: 6In a town devastated by a tornado, a woman finds a teenage boy unresponsive beside a downed electrical power line. After ascertaining that the boy has no pulse and is not breathing, the woman calls 911 and initiates cardiopulmonary resuscitation (CPR). Emergency medical services personnel continue CPR upon arrival at the scene and detect ventricular fibrillation on the monitor. They restore a perfusing rhythm after two attempts at defibrillation. On arrival at the emergency department, the boy is comatose, with a heart rate of 110 beats/min (normal sinus rhythm), respiratory rate of 15 breaths/min, and blood pressure of 80/60 mm Hg. He has a small open wound with charring around the edges on his left hand and a third-degree burn of approximately 5% body surface area on his right thigh. The remainder of his physical examination findings are normal.Of the following, this patient’s injuries MOST likelyA.are associated with better survival because he was struck by a high-voltage alternating versus direct currentB.cannot be determined by his external burn woundsC.have not compromised vascular smooth muscleD.include transmural infarction causing arrhythmiasE.require minimal fluid resuscitationCorrect answer: BElectrical injuries result from the direct effect of the current on the heart, brain, cell membranes, and vascular smooth muscle. The conversion of electrical energy to heat causes additional tissue injury. High-voltage current is generally defined as greater than 600 V, which is in contrast to the 110 V found in most households in the United States.High-voltage currents (both alternating [AC] and direct [DC]), as would be expected with a downed electrical line, tend to cause the most serious and frequently fatal injuries, although fatal electrocutions have been described with household current. Contact with AC at 60 cycles per second (as in most United States households and commercial sources) may cause tetanic muscle contraction, preventing release from the source and resulting in greater exposure. It is also the repetitive frequency of AC that increases the chances of affecting the heart during the relative refractory (“vulnerable”) phase of the cardiac cycle, precipitating ventricular fibrillation. This is similar to the “R on T phenomenon” observed if cardioversion is not synchronized.Estimating the extent of tissue damage is frequently impossible from the entrance and exit wounds. The underlying tissue damage is usually far more extensive. For this same reason, the Parkland formula underestimates the degree of fluid resuscitation required. Fluid administration should be titrated to maintain diuresis to facilitate excretion of myoglobin, potassium, and other byproducts of tissue necrosis.The purported mechanism of myocardial injury and ischemia is coronary artery spasm. An electrogenic mechanism of vascular smooth muscle activation may exist in the human coronary artery. On the other hand, transmural infarction due to coronary artery occlusion following electrical shock is rare.As the current flows through the body, the greatest damage is sustained by the skin, nerves, blood vessels, and muscles. Sudden cardiac death from asystole or ventricular fibrillation or asphyxial respiratory arrest may be encountered. If the patient survives, the following conditions may be encountered: dysrhythmias, myocardial injury, cerebral edema, thrombosis of vessels, disseminated intravascular coagulation, hollow organ perforation, pulmonary contusion or pneumothorax, acute renal failure from myoglobinuria, lactic acidosis, compartment syndromes, cutaneous burns, delayed labial artery hemorrhage, tympanic membrane rupture, and fetal demise. Widespread endogenous catecholamine release can initially result in severe hypertension, tachycardia, myocardial ischemia, agitation, and seizures. Dysrhythmias occur in up to 30% of cases following high-voltage electrical shock, with sinus tachycardia and premature ventricular contractions being the most common.High-voltage AC and DC currents cause a sudden violent muscular contraction, and the victim may be thrown from the scene, incurring the risk of blunt trauma and blast type injuries. Hence, after ensuring that the scene is safe, emergency personnel should establish cervical spine precautions and follow standard Advanced Trauma Life Support protocols for blunt trauma and burn management.Clinicians should perform a thorough physical examination to evaluate apparent tissue damage and identify associated complications. Assessment of the airway, respirations, and hemodynamic status is followed by a careful search for evidence of burns and secondary trauma. A detailed neurovascular evaluation should include particular attention to mental status and evaluation of the electrically injured extremities.In general, it is important for the clinician to remember that a paucity of physical findings does not necessarily exclude potentially serious underlying involvement.American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of potentially life-threatening electrical injuriesQuestion: 7A 3-month-old boy who has trisomy 21 presents to the emergency department with persistent constipation. His parents report that he eats well, has not had vomiting, and has normal urine output. He passes stools only every 2 to 3 days and almost always needs rectal stimulation for such passage. He has mildly delayed gross motor skills due to decreased tone but no history of cardiac disease, and the parents report that his newborn screening results were normal. They are unsure when he first passed meconium in the newborn period. On physical examination, the infant has abdominal distension, but his abdomen is soft and nontender. Stool is palpable above the pubis, and his rectal vault is empty. He is circumcised, his testicles are descended bilaterally, and he has no masses or hernias. The patient does not pass stool while in the emergency department, but a sample that his parents brought from home is negative for occult blood. Abdominal radiography demonstrates mildly increased stool but no signs of obstruction or other abnormalities.Of the following, the MOST appropriate next step in this child’s care isA.immediate abdominal ultrasonographyB.immediate air-contrast enemaC.immediate computed tomography scanD.ordering of a sweat testE.referral for barium enemaCorrect answer EThe infant described in the vignette has signs and symptoms suggestive of Hirschsprung disease (HD) or congenital intestinal aganglionosis. HD is characterized by the congenital absence of ganglion cells in the myenteric and submucosal plexi of the intestine, which causes the affected intestinal segment to remain in tonic contraction. Constipation is the hallmark of the disease and usually begins at or soon after birth. Many children who have HD experience delayed passage of meconium in the perinatal period. Generally, 99% of healthy term infants and 95% of preterm infants pass meconium within 48 hours of birth.Abdominal examination of those who have HD often reveals a suprapubic mass of stool, as described for this infant. A stenotic anal segment and an empty rectal vault are usually found on rectal examination. Rectal examination frequently is followed by forceful expulsion of foul-smelling stool. Most affected children only pass stool after rectal stimulation.When HD is suspected, abdominal radiographs may be used to rule out obstruction and to ascertain that early megacolon is not present. Barium enema reveals a narrow area of colon, followed by a transition zone and subsequent dilated proximal colon. The enema should be performed without preparation and at least 1 to 2 days after any enemas or rectal examinations so as not to lead to a false-negative result. Thus, a barium enema should be delayed as long as the infant in the vignette remains stable because a rectal examination has been performed in the emergency department. Although helpful in the diagnosis and treatment of other abdominal processes such as appendicitis and intussusception, abdominal ultrasonography, air-contrast enema, and abdominal computed tomography scans contribute little to the diagnosis of HD. This patient’s presentation, along with his normal newborn screening results, makes the diagnosis of cystic fibrosis less likely, obviating the need for a sweat test.Additional supportive evidence of the presence of HD can be obtained by the use of anorectal manometry. In HD, dilation of the rectum fails to lead to the usual reflex relaxation of the internal anal sphincter. Suction or full-thickness rectal biopsy demonstrating absence of ganglion cells is diagnostic.HD occurs in approximately 1 in 5,000 live births, with a 4 to 1 male-to-female predominance. Most affected children are otherwise healthy, but HD is associated with certain disorders, such as trisomy 21 (prevalence of HD is 1 in 500 children who have trisomy 21, and about 2% of all children who have HD have trisomy 21), Waardenburg syndrome, and Smith-Lemli-Opitz syndrome.The vast majority of children are diagnosed in the first year after birth, but diagnosis may be delayed, especially if the stenotic segment is relatively short. Young children can present in extremis due to an enterocolitis characterized by megacolon with abdominal distension, fever, and explosive stools that may be bloody. Children in this condition often progress rapidly to hypovolemic shock, with ensuing sepsis and death. This remains the major cause of mortality in children who have HD. Rapid recognition of this process and aggressive fluid resuscitation, administration of broad–spectrum antibiotics, and colonic irrigations in consultation with a pediatric surgeon may be lifesaving.Distinguishing HD from functional constipation may be difficult. In addition to the characteristic historic and physical examination findings, children who have HD usually do not pass stool without rectal stimulation; those who have functional constipation usually have at least occasional large stools. Encopresis is exceedingly rare in HD. Maintaining an appropriately high index of suspicion allows the emergency physician to consider HD as a cause of constipation and make the appropriate referral for a barium enema in conjunction with a pediatric gastroenterologist or pediatric surgeon for prompt diagnosis and institution of appropriate therapy.American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of Hirschsprung diseaseKnow the indications for and interpret results of ancillary studies in suspected Hirschsprung diseaseQuestion: 8A 12-week-old infant, who was born at 36 weeks’ gestation and weighed 3.4 kg, presents with gradually increasing emesis that began at 1 week of age. The mother describes the emesis as projectile and nonbilious. She has tried multiple formula changes, frequent burping during feedings, and upright positioning after feedings, but none of these attempts have offered any relief. The parents have brought the baby to their primary care physicians three times before coming to the emergency department today. There is no history of blood in the emesis, apnea, or respiratory symptoms. Her defecation and urination patterns are normal. On physical examination, the well-appearing infant has a nondistended and soft abdomen, with no palpable masses. Her head circumference is 37 cm and weight is 3.9 kg. She can lift her head in the prone position but does not have complete head control in the sitting position. She cannot roll over. She has developed a social smile. The remainder of the physical examination findings are within normal parameters. Laboratory results include:Sodium, 142 mEq/L (142 mmol/L)Potassium, 4 mEq/L (4 mmol/L)Chloride, 94 mEq/L (94 mmol/L)Bicarbonate, 29 mEq/L (29 mmol/L)Glucose, 88 mg/dL (4.9 mmol/LBlood urea nitrogen, 10 mg/dL (3.6 mmol/L)Ultrasonography shows a normal pylorus. You request the infant’s growth charts from the primary care physician, who faxes them to the emergency department (Figure 1).lefttop00Figure 1Growth chart for the infantOf the following, the MOST appropriate next step is toA.admit the infant for additional evaluationB.discharge the infant with a recommended outpatient gastroenterology consultationC.discharge the infant with a recommended outpatient neurology consultationD.obtain urgent surgical consultationE.suggest the parents thicken the infant’s feedings and obtain a follow-up appointment with their primary care physicianCorrect answer AAll neonates regurgitate a certain amount of milk after every feeding. Such action may be a result of aerophagia, volume of feeding, or mechanical factors such as infant positioning. Emesis is more likely in preterm infants who tend to have lax gastroesophageal sphincters. However, when the emesis is frequent, organic disease must be considered. Determination of whether patients should be investigated further can be based on their weight gain and development.Although findings on physical examination of the infant described in the vignette are normal, her developmental milestones are appropriate for age, and she has demonstrated weight gain since birth, her growth velocity since the last visit to her primary care physician has slowed. The growth chart documents a decrease by 2 percentile lines. Further, her electrolyte evaluation reveals a mild hypochloremic metabolic alkalosis consistent with loss of gastric acid from persistent emesis. These findings are an indication for additional testing or consultation to exclude an organic cause of emesis, which would be best and most expediently accomplished in the inpatient setting. Hospital admission would also permit direct observation of feeding technique, type of emesis, and parent-infant interaction.In the absence of bilious emesis or signs of frank bowel obstruction (eg, abdominal distension or tenderness or constipation), emergent surgical consultation is not indicated. The infant’s normal head circumference and neurodevelopment findings argue against a neurology consultation. Although a gastroenterology consultation may be appropriate, it may be most appropriate on an inpatient basis after excluding psychosocial causes of inadequate weight gain. The growth parameters and laboratory findings suggest a problem that should be addressed immediately rather than at a later date with the primary care physician.Failure to thrive (FTT) in infancy or childhood is a sign of many disorders, including acute and chronic organic diseases as well as nonorganic causes such as abnormal parent-child interaction or neglect. It is usually defined as weight less than the 3rd percentile for age, although FTT also implies inadequate weight gain (crossing percentile lines), an inappropriately low weight for height, or both, usually in a child younger than 2 years of age.Height and weight should be plotted at each health supervision visit on a National Center for Health Statistics (NCHS) growth chart (Figure 2, Figure 3, Figure 4, Figure 5, Figure 6, Figure 7). Of note, there are specialized growth charts for specific ethnicities and children who have underlying syndromes. Head circumference should be recorded for at least the first year after birth. The NCHS graph for weight-to-height ratio can be helpful in judging whether a child is under- or overweight for height. Sequential measurements are much more useful than single determinations of weight and height in providing an overall picture of growth trends.During the first 1 to 2 years after birth, the time of greatest postnatal growth velocity, the infant “seeks his or her own curve.” Accordingly, by 2 years of age, the child’s stature reflects his or her own genetic endowment rather than the mother’s size and health. Growth during the remainder of childhood occurs at a rate of 5 to 7 cm/yr along the percentile band achieved by 24 months of age. Adolescence is characterized by an abrupt, short-lived increase in growth velocity mediated by gonadal hormones that results in an adult height that may be predicted by parental heights. Differential growth rates for various body parts can cause significant changes in body proportion during childhood. Head growth, for example, a passive phenomenon reflecting brain growth, is rapid in early infancy but largely completed by 1 year. As a result, the head comprises a decreasing fraction of total body size and weight. Another factor contributing to a child’s changing appearance with age is the relationship of height velocity to weight velocity.Development is orderly and cumulative, with one milestone regularly and predictably following another. For example, motor development proceeds according to neurologic maturation in a cephalocaudal progression. Language begins with cooing and babbling and subsequently progresses to words, “jargon,” and sentences. Cognitive development also advances in identifiable stages. The abbreviated Denver Developmental Screening Test (DDST) (Figure 8) takes 5 to 7 minutes to administer and can be used for further evaluation for possible delays in the area of fine motor, gross motor, language, and social skills. Indicators of significant language delays are shown in the Table.Table. Indicators of Significant Language DelaysAge (months)Indicators12Limited babbling; quiet child18Does not understand specific words, his or her name, or names of common objects; cannot follow simple commands24Uses few single words; does not imitate words30Does not know names of common objects or simple body parts; cannot point on command to familiar objects; no true 2-word combinations such as "No cookie," "More milk"; child is often misunderstood36No simple sentences; does not seem to understand simple explanations or discussion of events in the past or futureAmerican Board of Pediatrics Content Specification(s)Understand the significance of normal growth and developmentUnderstand growth chart trends and how to interpret themAPRIL 2012Question: 1A 6-week-old boy presents to the emergency department with lethargy, fussiness, poor oral intake, and breathing difficulty of 2 days’ duration. His oral intake today is 8 oz of formula over a 12-hour period, and he has had two scantly wet diapers. His mother states that his skin has become mottled over the past few hours. On physical examination, the fussy, mottled,? moderately distressed infant has a temperature of 36.0?C, heart rate of 240 beats/min, respiratory rate of 65 breaths/min, and blood pressure of 45/20 mm Hg. His capillary refill is 3 seconds, and he has thready peripheral pulses. He has coarse breath sounds in all lung fields, no cardiac murmurs, and hepatomegaly. You obtain electrocardiography (Figure).FigureElectrocardiographic strip for the infant in the vignetteOf the following, the MOST likely primary pathology for this patient’s shock isA.cardiac afterload elevationB.cardiac preload elevationC.intracardiac shuntingD.intravascular tone reductionE.stroke volume reductionCorrect answer EThe infant described in the vignette has primary cardiogenic shock. Electrocardiography shows narrow complex tachycardia. Cardiac output is the function of stroke volume and heart rate. The tachyarrhythmia accompanied by a reduction in ventricular filling time described for this infant suggests that reduced stroke volume is the primary pathophysiology for his shock. Intracardiac shunting is characteristic of congenital heart disease and is responsible for oxygenating the body in the presence of complex cardiac defects. This process is acutely affected by ductal-dependent lesions. Cardiac afterload elevation is due to outflow tract obstructions such as aortic stenosis and to elevated systolic blood pressure. Dilated cardiomyopathy can result in elevation of preload, which is the function of the residual ventricular volume and venous return to the heart. Both elevated preload and afterload can cause cardiogenic shock from myocardial damage over time. Reduction in the intravascular tone is helpful for cardiogenic shock (vasodilator treatment) because it decreases the work load and myocardial oxygen consumption.Cardiogenic shock is defined as tissue hypoxia primarily due to a decrease in cardiac output (eg, function of stroke volume and heart rate, with regulation by neurohormones, venous return, and systemic vascular tone). Heart rate and stroke volume can be affected by a variety of factors: myocardial contractility problem (myocardial infarction, infections, metabolic cardiomyopathies, drug toxicities), chronotropy issues (arrhythmia: high or low heart rate), structural abnormalities (congenital heart diseases, valvular defects), or afterload and preload issues (aortic stenosis, ductal-dependent lesions, mitral stenosis, atrial myxoma, constrictive pericarditis, cardiomyopathies, pulmonary hypertension). Infections, congenital structural abnormalities, cardiomyopathies, and cardiac surgery are the sources of most cases of cardiogenic shock in the pediatric population.Cardiogenic shock is also a known component in the cascade of events for other types of shock through a decrease in myocardial oxygenation (sepsis, hypovolemic, obstructive) or direct myocardial depression (sepsis). Although cardiac tamponade results in decreased cardiac output, it is primarily considered to be an obstructive cause of shock via secondary myocardial damage due to coronary blood flow compromise.Primary cardiogenic shock results in systolic or diastolic dysfunction. Systolic dysfunction is associated with a compensatory increase in systemic vascular resistance (SVR) that causes an increase in afterload with an increase in myocardial oxygen requirement. Associated tachycardia due to elevated SVR can also affect diastolic function by reducing ventricular volume. Another compensatory mechanism associated with systolic dysfunction is activation of the renin-angiotensin system, with fluid and salt retention and resultant pulmonary edema further compromising cardiac output. Diastolic dysfunction can be due to systolic dysfunction or may be a primary cause of cardiogenic shock. Examples range from ventricular hypertrophy and constrictive pericarditis to dilated cardiomyopathy with reduced ventricular filling. The end-diastolic ventricular volume and, thus, the ejection fraction can remain normal in the early stages of diastolic dysfunction.The clinical presentation of cardiogenic shock is that of congestive cardiac failure associated with signs of tissue hypoxia, including cyanosis, decrease in urine output, change in mental status, and reduced peripheral perfusion. Patient deterioration with fluid administration in the clinical setting of shock is strongly indicative of cardiogenic shock. The primary goal of therapy is to address the cardiac output, decrease systemic vascular resistance, and improve end-organ function (urine output, acidosis, mental status changes).Agents that increase the heart rate and preload (Frank-Starling principle: increase in preload results in increase in stroke volume until a threshold is achieved) and decrease the afterload are used to treat cardiogenic shock. Primary agents of therapy are dopamine, dobutamine, and epinephrine. Because marked chronotropy can cause further damage to the myocardium, use of such agents requires careful monitoring. Epinephrine should be administered cautiously because it can induce arrhythmias and exacerbate myocardial depression by increasing myocardial oxygen consumption. Dobutamine not only causes vasodilatation, but it also increases myocardial contractility. Milrinone increases cardiac output by improving systolic function, causing diastolic relaxation, and decreasing SVR without compensatory tachycardia. Other agents that result in vasodilation (nitroprusside, nitroglycerine) reduce cardiac afterload, but they also may reduce myocardial function. Agents that increase SVR (eg, norepinephrine) are not indicated in the setting of primary cardiogenic shock. Intra-aortic balloons increase coronary blood flow and cardiac output and are used if myocardial infarction is the primary pathology of shock. Ventricular assist devices or extracorporeal membrane oxygenation are indicated for refractory shock to allow myocardial recovery or as temporizing measures while the patient awaits heart transplantation.American Board of Pediatrics Content Specification(s)Understand the pathophysiology of cardiogenic shockQuestion: 2The parents of a 14-year-old girl bring her to the emergency department after a vomiting episode. They explain that she admitted to taking 10 ibuprofen and 16 multivitamins one hour ago in an attempt to “teach us a lesson.” They report that the medication amount they described was approximately what was available in the household. After she ingested the pills, she informed a friend by telephone, and the friend immediately notified the parents. On physical examination, the somewhat disheveled girl speaks softly and does not make eye contact. She becomes more agitated when her parents explain that they will not let her date a 17-year-old boy. She states, “This is why I would be better off dead.”Of the following, the MOST appropriate next step isA.administration of N-acetylcysteine while awaiting laboratory resultsB.discussion with patient and family about suicidal ideation and riskC.gastric lavage for pill fragmentsD.patient admission to the psychiatric service for suicide precautionsE.patient discharge in the parents’ care after discussion about medical riskCorrect answer: BSuicide ranks is the third most common cause of adolescent death in the United States, and more than 170 children younger than 10 years of age also commit suicide in the United States each year. Native American males have the highest risk of suicide, and African American females have the lowest risk. One study reported that 20% to 28% of homosexual and bisexual 7th- through 12th-grade girls and boys had reported attempting suicide. A risk survey in 2003 noted that 16% of students in grades 9 through 12 had planned a suicide attempt. Males outnumber females for successful suicide (commonly firearms), but females outnumber males in suicide attempts (commonly ingestions). Most successful suicidal patients meet criteria for major depressive episode or mood disorder. Suicidal ideation and attempts are common in the pediatric population, especially among adolescents, and represent the most common child and adolescent psychiatric emergency. What may seem like minor issues to adults can be major to these patients and can trigger immediate and sometime seemingly irrational actions. Nonlethal self-inflicted events, such as described for the girl in the vignette, should immediately raise awareness of future risks and should not be minimized due to the nonlethality of the actions. This discussion should be held with the patient and the family.Gastric lavage is rarely indicated after ingestion unless the material is highly toxic and recently ingested. Although an acetaminophen concentration should be measured, without a clear history of acetaminophen ingestion, administering N-acetylcysteine to this girl, at this time,?is not necessary. Although the medical issues need treatment and appropriate discussion, the mental health aspects of this case are important and must be discussed. Inpatient care might be required, but the initial action should be discussion with the patient and the family (both separately and together) to help determine the underlying medical and psychosocial issues and risk factors.Mental health problems continue to increase in the United States and are seen in all emergency departments. Underlying issues include family and personal instability, economic difficulties, cultural barriers, inadequate pediatric mental health care opportunities, and lack of adequate screening programs. Pediatric mental health conditions may be poorly recognized and require experienced and available clinicians for interventions. Any plan for pediatric patients should recognize the inherent risks in this population, the challenges of limited resources and funds, and other barriers (cultural and community) to effective assessment and care.In addition to necessary medical interventions, care of these patients in an emergency department setting requires awareness and recognition of mental illness/depression/suicidality, skilled assessments, maintenance of a safe environment, inclusion of mental health experts in the assessment and care process, and appropriate outpatient or inpatient plans for the medical and psychosocial aspects of the presentation. The emergency department visit may be precipitated by acute medical necessity (results of behavior, with specifics of delivered care based on presenting status and predisposing issues) or a perceived need for intervention for psychiatric issues. If the patient or clinician believes that care outside of the hospital has become too confusing, overwhelming, or dangerous to the patient or others, additional mental health resources should be mobilized. Suicidal/self-injurious events may be masked by medical issues (eg, lethargy, coma, trauma, intentional ingestion versus drugs of abuse) or may be suspected or evident through acute and past medical histories and physical examination findings. Acute medical, traumatic, and organic disease issues must be stabilized before or concurrent with the psychiatric investigations. Failure to recognize organic causes for apparent psychiatric presentations can place the patient at significant risk.A complete mental status examination should include evaluation of orientation, appearance, memory, cognition, behaviors, relating ability, speech, affect, thoughts, insight, judgement, strengths, and synthesis (see Baren et al, part 2, 2008). Abbreviated psychosocial screening tools such as HEADDS (home, education, activities, drug use/abuse, depression, sexual behavior, and suicidality) and SHADSS (school, home, activities, depression/self-esteem, substance abuse/abuse, sexuality, safety) can aid in the evaluation. Patients should be screened for depression and suicidal ideation/attempts. An estimated 50% of adolescents who attempt suicide have come to medical attention in the previous month.Increased lethality of suicide attempts is associated with underlying psychiatric disorder(s), one or more previous attempts, lack of mental health treatment, presence of a firearm in the home, and benzodiazepine overdose. Family history of suicide or suicide attempts, male sex, history of physical or sexual abuse, and gay/bisexual orientation are also risk factors. Poor environmental support, difficulties in school, relationship issues, other stressful life events, and impaired parental relationships also add potential risk. Use of antidepressants may increase the risk of suicidal ideation and attempts, and such drugs should not be prescribed without significant evaluation and planning. All antidepressants are required to carry a black box warning regarding this risk in patients up to 24 years of age. Although risk factors are often seen in patients who attempt suicide, they are common and do not necessarily predict, in and of themselves, that a patient will attempt suicide. Finally, it is also important to note that not all patients who attempt suicide have a previously identified risk profile.Home and safety planning for patients with depression or suicidal ideation/attempts can help decrease the risk of a successful attempt. Such planning can include removal of potentially lethal means of injury (firearms, prescription medications, alcohol, over-the-counter medications), although evidence of the impact of this action is unclear. Safety contracts are often used, but no evidence supports the benefit/risk of this approach. Establishing mutually agreeable and accessible adult supervision, emergency contacts, and appropriate follow-up is important.During assessment, direct and confidential questions (with and without a guardian present) about suicidal ideation, attempts, and plans should be asked as appropriate. Of note, if safety becomes an issue, confidentiality likely will not be maintained, and that fact should be made clear during the conversation. If responses to such questions are positive, further investigation is required to determine the nature of thoughts, events time frame, and current intent and method. Further details of this process are well outlined in Shain and The Committee on Adolescence guidelines regarding suicide and the adolescent. There is no evidence that questioning increases suicide risk in patients.Interventions can include contracting for safety, providing a safe and supportive environment, psychiatric/medical follow-up evaluation, acute psychiatric interventions, and admission for inpatient psychiatric care. The 2010 review by Newton and associates of pediatric suicidal patients noted that the use of transition interventions (education, enhanced follow-up evaluation) appeared promising for reducing suicide events and improving adherence to treatment plans after emergency department evaluation. Such interventions include postdischarge contact, intermittent follow-up evaluation and psychiatric care, and parental involvement at outpatient psychiatric sessions.American Board of Pediatrics Content Specification(s)Recognize subtle or hidden suicide attemptsPlan the management of a child who has attempted suicide, eg, hospital options, family capability, psychiatric consultationQuestion: 3A 10-year-old African American girl presents to the emergency department for evaluation of severe headache and temperatures to 39.0°C. She has had recurrent low-grade fevers and painful bilateral ankle, knee, and elbow joints for several weeks. On physical examination, her temperature is 39.0°C, heart rate is 124 beats/min, respiratory rate is 26 breaths/min, and blood pressure is 144/94 mm Hg. The triage nurse provided her with a urine specimen cup, and as you enter the room, her mother offers you the cup filled with obviously pink-tinged urine.Of the following, the laboratory test that is MOST helpful in establishing the diagnosis for this girl isA.antinuclear antibodyB.blood plete blood countD.rapid plasma reaginE.rheumatoid factorCorrect answer: AThe girl described in the vignette has fever, symmetric arthritis, hypertension, and symptoms of nephritis. This constellation of symptoms, combined with her sex and race, makes systemic lupus erythematosus (SLE) the most likely diagnosis. Emergency department care for the febrile child who has SLE should include measurement of the complete blood count and C-reactive protein, urinalysis, and cultures of blood and urine. However, an antinuclear antibody result is the only test of those listed that contributes to diagnosis with a positive result. Test results should be interpreted within the context of the clinical presentation because of the possibility of false-positive findings. Measurement of complement (C3 and CH50) and anti-DNA and antinuclear antibody titers is useful to assess disease activity. Rapid plasma reagin and rheumatoid factor values may be nonspecifically elevated in SLE. Rapid plasma reagin is most helpful in ruling out syphilis. Rheumatoid factor is more helpful in the diagnosis of rheumatoid arthritis in adult patients.SLE is an autoimmune disease that is characterized by a plethora of potential symptoms, none of which are specific to the disease. Diagnostic criteria for lupus have been established by the American College of Rheumatology and revised periodically. The current (1997) criteria are in the Table. Current recommendations require the patient to have, or have had, at least four of the 11 listed criteria.SLE presents most commonly in late adolescence or early adulthood, with only 20% of cases presenting in the first 2 decades after birth. However, SLE can present in very young children, who typically have complement deficiency that predisposes them to autoimmune disease. Among adolescents and adults, SLE is disproportionately more common in women (4:1 ratio in teens, 9:1 ratio in adults) and particularly African American women. In the first decade after birth, girls are only slightly more likely to be diagnosed (4:3 ratio). Infantile SLE (<2 years) is rare but well reported and is associated with much higher rates of organ dysfunction than prepubertal or postpubertal forms of SLE.Pediatric patients are more likely to have fever and renal, hematologic, and neurologic disease than adult patients. Common symptoms in pediatric SLE presentations include: arthritis or arthralgia, photosensitivity or malar rash, fever, nephropathy, and hematologic abnormalities (hemolytic anemia, thrombocytopenia, or leukopenia). Arthritis in SLE is typically symmetric and may involve both large and small joints. Neuropsychiatric manifestations are reported in most affected children and range from depression and cognitive problems to acute psychosis with visual hallucinations. Other neurologic manifestations include seizure, encephalopathy, and chorea. Severe headache in children who have SLE, especially those known to have positive lupus anticoagulant, should raise suspicion for cerebral venous thrombosis. Lupus nephritis is common in all age ranges, and nearly 50% of pediatric lupus nephritis patients have hypertension. Hypertension is significantly more common in African American children who have lupus nephritis. Hematologic manifestations are generally mild, with the exception of hemolytic anemia. Macrophage activation syndrome (hemophagocytic syndrome) can occur in lupus and is a potential cause of fever, cytopenias, and fulminant organ dysfunction. Corticosteroid treatment is likely to be effective in lupus-related macrophage activation syndrome, but mortality is high without treatment. The risk of thrombosis is about 28 times higher for those who have lupus anticoagulant compared with those who do not.? Parotid swelling is a common presentation of Sj?gren syndrome in children who have SLE.Pediatric patients who have acute SLE presentations are at higher risk for acute life-threatening emergencies, and childhood-onset SLE tends to be more active and cause chronic organ damage at a faster rate than does adult-onset disease. Renal disease, infections, and severe flares are the most common immediate causes of death. Febrile children who have SLE should be aggressively investigated for potential infections and may require admission for empiric intravenous antibiotic administration while awaiting culture results. Fever is also a common complaint of children experiencing acute disease flares. Renal complications include hypertensive crisis, acute renal failure, and nephrotic syndrome.Table. Diagnostic Criteria for Systemic Lupus ErythematosusCriterionDefinition1. Malar RashFixed erythema, flat or raised, over the malar eminences, tending to spare the nasolabial folds2. Discoid rashErythematous raised patches with adherent keratotic scaling and follicular plugging; atrophic3. PhotosensitivitySkin rash resulting from unusual reaction to sunlight by patient history or physician observation4. Oral ulcersOral or nasopharyngeal ulceration, usually painless, observed by physician5. Nonerosive ArthritisInvolving two or more peripheral joints, characterized by tenderness, swelling, or effusion6. SerositisPleuritis: History of pleuritic pain or rub heard by physician or pleural effusion OR Pericarditis: Documented by electrocardiography, rub, or pericardial effusion7. Renal DisorderPersistent proteinuria > 0.5 g/day or > than 3+ if quantitation not performedORCellular casts that may be red cell, hemoglobin, granular, tubular, or mixed8. Neurologic DisorderSeizures OR Psychosis in the absence of offending drugs or known metabolic derangements (uremia, ketoacidosis, or electrolyte imbalance)9. Hematologic DisorderHemolytic anemia with reticulocytosis OR Leukopenia (< 4,000/mm3 on ≥ 2 occasions) OR Lymphopenia (< 1,500/mm3 on ≥ 2 occasions) OR Thrombocytopenia (<100,000/mm3) in the absence of offending drugs10. Immunologic Disorder1. Anti‐DNA: antibody to native DNA in abnormal titerOR2. Anti‐Sm: presence of antibody to Sm nuclear antigenOR3. Positive finding of antiphospholipid antibodies on: a. An abnormal serum concentration of immunoglobulin (Ig)G or IgManticardiolipin antibodies, b. A positive test result for lupus anticoagulant using a standard method,or c. A false‐positive test result for at least 6 months confirmed byTreponema pallidum immobilization or fluorescent treponemal antibody absorption test11. Positive Antinuclear AntibodyAn abnormal titer of antinuclear antibody by immunofluorescence or an equivalent assay at any point in time and in the absence of drugsAmerican Board of Pediatrics Content Specification(s)Recognize signs and symptoms of systemic lupus erythematosus by ageRecognize life-threatening complications of systemic lupus erythematosus and its treatmentQuestion: 4A 7-year-old previously healthy boy presents to a hospital emergency department in Arizona with complaints of cramping leg pain, abdominal pain, and vomiting. He had been playing with his cousins in the barn this morning when he started complaining of pain in his left calf that has rapidly progressed to cramping of his calf muscles. He is afebrile and has not had any change in bowel or bladder habits. Although the entire extended family ate at a local restaurant last night, no one else is exhibiting any symptoms. His mother mentions that he missed his last set of immunizations. Physical examination reveals an anxious, afebrile, diaphoretic child who has a heart rate of 120 beats/min and blood pressure of 130/80 mm Hg. He has a small nonindurated, erythematous macular lesion on his left calf but no other findings of note on the rest of his systemic examination.Of the following, the MOST appropriate treatment is administration ofA.Crotalidae antiveninB.equine botulinum antitoxinC.Lactrodectus antiveninD.silibininE.tetanus immune globulinCorrect answer: CThe rapidity of symptom progression combined with local signs of inflammation described for the boy in the vignette suggests envenomation. His systemic signs suggest Lactrodectus or black widow spider envenomation, which is characterized by painful muscle spasms (local and distant from the site of spider bite), diaphoresis at the site, generalized sweating, tachycardia, hypertension, nausea, and vomiting. Thus, the boy needs to be treated with intravenous administration of Lactrodectus antivenin.Crotalidae immune antivenin is indicated for patients who have pit viper envenomation, which is characterized by immediate pain and swelling in the bitten extremity, followed by progressive edema, necrosis, bullae formation, and tissue necrosis. Systemic signs include nausea, vomiting, diaphoresis, muscle fasciculations, shock, and coagulopathy. Treatment with botulinum antitoxin is indicated when patients exhibit signs and symptoms of botulism. Tetanus immune globulin is indicated for tetanus prophylaxis in patients who are not fully immunized, or in or patients who exhibit signs and symptoms of tetanus. Patients who have food-borne botulism present with constipation, ptosis, bulbar involvement, and a flaccid paralysis; those who have tetanus present with muscle spasms (trismus, opisthotonus) that are recurrent and easily reproduced with external stimuli. Amanita poisoning due to consumption of wild mushrooms can present with the sudden onset of crampy abdominal pain, but profuse watery diarrhea is more likely and if suspected, requires treatment with a continuous intravenous infusion of silibinin, the water-soluble form of flavolignone-silymarin, which inhibits the binding and enterohepatic recirculation of phallo- and amanitotoxins.Most envenomations in the United States are caused by local fauna, although occasional introduction of non-native species through the growing trade of exotic animals such as snakes, scorpions, fish, and spiders has complicated the situation. Accordingly, emergency department physicians require access to clinical toxicologists to recognize and manage such cases. Envenomations can be broadly classified by the animal species: venomous snakes; spiders, scorpions, and insects; and marine animals (Table). Diagnosing envenomations is easy if the bite/sting is witnessed, but in many cases, the original bite may go unnoticed, especially those from spiders.Importantly, only some envenomations result in serious damage, even when a highly toxic species is involved, and not all bites require antivenin therapy. Antivenin therapy is effective when used early and only in the presence of objective criteria for its use. Antivenin poses a small but significant risk for immediate hypersensitivity reactions.Table. Features and Antivenin ManagementAnimalSigns/SymptomsSeverityAntiveninSnakesViperidae (pit vipers: cottonmouth, copperheads, rattlesnakes)Elapidae (cobras, mambas, coral snakes)Hydrophidae (sea snakes)Viperidae are cytotoxic, causing tissue necrosis and coagulopathiesElapidae and Hydrophidae elicit primarily neurotoxic and curarelike neuromuscular blocking effectsGrade 0: No envenomationGrade 1: Minimal envenomation (local swelling and pain without progression)Grade 2: Moderate (swelling and pain beyond site of injury along with some systemic or laboratory findings)Grade 3: Severe (severe local, systemic and laboratory findings)Crotalidae polyvalent immune Fab (for pit viper, rattle snake, and cottonmouth bites) antivenin indicated within 4 hours of bite for grades 2 and 3 envenomationsPatients may require doses in 5-vial increments repeated at 2-hour intervalsSpidersBlack widow (Lactrodectus)Bites result in systemic reactions related to neurotoxin, which causes release of acetylcholine and norepinephrine, leading to muscle depolarization and autonomic hyperactivityAntivenin indicated if patients have the following four or more findings:?Abdominal pain ? Hypertension ?Muscular pain ? Agitation/irritabilityUsually one vial of equine black widow antivenin is sufficientBrown recluse (Loxosceles)No antivenin requiredAmerican Board of Pediatrics Content Specification(s)Know the indications, contraindications, and methods for administration of antiveninQuestion: 5You are examining a 2-month-old boy for fussiness and not moving his right leg. His mother reports that he was well when she put him in his crib last night but has been like this since he awoke early this morning. The child was born at term and has not been ill or had to return to the hospital since birth. The mother reports that while she was changing the baby’s diaper last evening, he rolled off the changing table and she was able to catch him by the right leg. She reports that he cried briefly but then calmed easily and seemed unharmed. Physical examination reveals an alert child whose only finding of note is a swollen, tender right leg. Radiography shows a nondisplaced spiral fracture of the right femur. After providing analgesia, you splint the leg and consult orthopedics. The consultant places a hip spica cast with good alignment and stabilization. Head computed tomography (CT) scan, radiographic skeletal survey, complete blood count, hepatic function panel, amylase, lipase, and urinalysis all yield normal results. The infant is less fussy and tolerating oral feedings. After speaking with the mother, the hospital social worker reports that the woman lives with the infant and her two other children, ages 3 and 5 years. The child’s father is not involved. The mother is currently unemployed and is the only caretaker who has been with the child in the past 2 days. The mother’s parents and other extended family members live in the same city, helping with child care and providing support to the family.Of the following, in light of the mother’s report of an accidental fall and the absence of other findings of trauma, the MOST appropriate next step isA.emergent consultation with an ophthalmologistB.notification of the child’s primary physician to arrange follow-up evaluationC.notification of the local child protective services agencyD.ordering of an abdominal CT scan to rule out occult injuriesE.referral to the orthopedic consultant for further managementCorrect answer CThe findings for the infant described in the vignette are worrisome for nonaccidental injury. The mechanism of injury is suspicious because it does not match the developmental capabilities of a child of this age (ie, a 2–month-old child is not able to roll over). Whenever there is a suspicion of nonaccidental injury, it is the duty of the emergency physician to report such suspicion to the appropriate child protective agency. Although ophthalmologic consultation may provide useful information, it does not need to be obtained emergently in a stable patient.The serious nature of this injury should prompt at least the consideration of hospital admission, and the child cannot be discharged until the injury is reported to the appropriate agency and the discharge is approved by that agency. Although the child will need both primary care and specialty follow-up evaluation, the first call should be to the child protection agency with jurisdiction in this location. The chance of finding injuries on an abdominal CT scan in this patient is very low.Although laws and regulations vary, depending on jurisdiction, all 50 states have child abuse statutes that include a mandated reporting process for certain classes of professionals. In addition, federal statutes, including the Child Abuse Prevention and Treatment Act as amended by the Keeping Children and Families Safe Act of 2003, give guidelines for states to follow to be eligible for federal assistance in the development of state statutes and assistance in research and enforcement.All states require physicians to report suspected abuse. Mandated reporters also usually include nurses, mental health professionals, teachers, child care providers, and social services providers. Some states also mandate reporting by prehospital professionals (emergency medical services personnel) and clergy. The agency to which reports must be made also varies from state to state. In some states, a Child Protective Services agency exists; in others, reports are made to a Division of Children and Youth or the Department of Social Services. Almost all states require the reporting of all types of child maltreatment, including physical, sexual, and emotional abuse as well as cases of childhood neglect. Reporting usually involves both notification of the child protective agency by phone (eg, calling the “child abuse hotline”) and a follow–up written report. In cases of physical and sexual abuse, reporting to the police may also be required and is often important to aid in the investigation of allegations and the gathering and preserving of evidence. In cases of patient transfer and referral, the clinician at the receiving hospital should attempt to confirm that a report was made to appropriate authorities by the referring clinician. If new or additional findings are made, they should be reported to the child protection agency as well.Certainty is not required before making a report of suspected abuse. It is often not possible for the physician or other mandated reporter to be completely sure of the circumstances of an injury and whether the injury was accidental or nonaccidental. Physicians cite multiple factors that determine whether they file reports of suspected abuse in various cases. However, failure to report when abuse has occurred is punishable in both civil and criminal proceedings in most states, and penalties can include suspension or loss of license, fines, and even incarceration. In addition, failure to report suspected abuse may be found to constitute malpractice and put the physician at medicolegal risk. Even if a report is ultimately determined to be unfounded, all statutes provide protection for the reporter from civil or criminal liability as long as the report is made in good faith. Although not required by law, it is always good practice to communicate clearly with the family regarding all aspects of the management plan.Most importantly, failure to report may lead to continued injuries to the child or other children in the same household. Child abuse is the leading cause of traumatic death in children younger than 1 year of age, and homicide is the fifth leading overall cause of death in children ages 1 through 4 years and the fourth leading cause of death in children ages 5 through 13 years. More than 75% of childhood homicide deaths occur in children younger than 3 years of age, and most childhood homicide victims are killed by adults who they knew.The age of consent for sexual activity varies from state to state. In addition, some states modify the age of consent based on the age of the partner involved. Depending on the age of the child (adolescent) and his or her partner, physicians may be required to report to child protection agencies or the police any sexual contact, even if the patient states that it was consensual.Physicians must be familiar with the statutes where they practice. They should know what is required to be reported, how to report, and what resources are available to assist them when they have questions about reporting.American Board of Pediatrics Content Specification(s)Know the regulations concerning the reporting of child abuse, child neglect, and sexual abuseQuestion: 6You are examining a 12-year-old boy who has a history of cystic fibrosis (CF) and has been referred from an outlying facility for suspected appendicitis. He presented with a 2-day history of worsening abdominal pain that is most prominent in the right lower quadrant. He had several episodes of emesis in the past 24 hours without blood or bile. He denied any fever, diarrhea, or increase in baseline cough. His last bowel movement was 3 days ago. Laboratory testing and imaging at the referring hospital included complete blood count (white blood cell count of 12.4x103/?L [12.4x109/L] with 65% neutrophils and normal hemoglobin and platelet counts); complete metabolic panel (normal electrolyte values and renal function); and abdominal computed tomography scan, which demonstrated moderate fecal burden, particularly in the right colon, as well as multiple distended, air- and fluid-filled loops of bowel and an air-filled appendix at the upper limits of normal for size without inflammatory changes. On physical examination, the patient is small for his stated age but is alert and cooperative. His vital signs are all within normal range for age. He has diffuse abdominal tenderness that is worst in the right lower quadrant, mild distension, and hypoactive bowel sounds but no guarding or rebound. You palpate fullness in the right lower quadrant. The remainder of the findings are within normal limits.Of the following, in conjunction with the CF specialist in your institution, the MOST appropriate next steps in management includeA.intravenous antibiotic administration and emergent laparotomyB.intravenous fluid administration and air-contrast enemaC.nasogastric polyethylene glycol solution administration and hospital admissionD.oral fluid administration, education on appropriate gastroenteritis diet, and dischargeE.upper gastrointestinal radiographic series with small bowel follow-throughCorrect answer: CThe boy described in the vignette is displaying signs and symptoms of distal ileal obstruction syndrome (DIOS) as a complication of his CF. Initial management for affected patients who have no evidence of complete obstruction, peritonitis, or perforation consists of administration of a balanced intestinal lavage solution (eg, polyethylene glycol) either orally or via nasogastric tube to clear the intestinal impaction of abnormally viscous fecal material. If the patient fails to improve or has complete obstruction, treatment with either hyperosmolar contrast enema or surgery is indicated. The normal laboratory results and absence of inflammatory changes on computed tomography scan reported for this boy obviate the need for antibiotics or emergent laparotomy. Although intravenous fluids may be indicated, air-contrast enema is used in cases of suspected intussusception; enema therapy for DIOS is performed with hyperosmolar contrast media. A patient who has a history of CF, abdominal pain, and right lower quadrant mass should not receive oral rehydration or outpatient management before the retained fecal material has been cleared. An upper gastrointestinal radiographic series may be used in the evaluation of possible malrotation or gastric or proximal small bowel obstruction, but neither of these conditions is likely in this patient.CF is a common autosomal recessive genetic disorder resulting in a defective CF transmembrane conductance regulator (CFTR) protein. More than 1,500 different defects have been identified that result in the various phenotypic presentations (Table). The abnormal proteins allow abnormal chloride and fluid movement across epithelial linings in the respiratory and gastrointestinal tracts, pancreas, sweat glands, and biliary tract. CF is most common in white populations, but increasing recognition of less common genotypes and milder phenotypes coupled with improved screening has increased the rate of diagnosis in other populations. Improved screening and supportive care have greatly increased patient survival, with the current median survival in the United States now nearly 40 years.Treatment of CF patients in the emergency department requires knowledge and early recognition of the common complications by age, understanding of the basic pathophysiology of the disease, and communication with the CF center involved with the patient’s overall care. Given the abnormal fluid and electrolyte transport associated with the condition, management of the gastrointestinal and systemic complications involves appropriate hydration and correction of electrolyte abnormalities. Management of bleeding complications should include correction of coagulopathy with vitamin K or fresh frozen plasma and blood transfusion, as needed, to correct hemodynamic compromise.Pulmonary exacerbations (infection) and respiratory complications (hemoptysis, pneumothorax, chest pain) are the most common reasons for those who have CF to present to emergency departments. Patients who have respiratory presentations also require careful hydration, but avoidance of overhydration and secondary pulmonary edema is important. Evaluation should include chest radiography with comparison to prior films, sputum cultures, and assessment of oxygenation and pulmonary function. Respiratory complications often involve a combination of airway obstruction, inflammation, and infection. Combination therapy, including oxygen, bronchodilators, corticosteroids, and antibiotics, is often necessary. Noninvasive positive-pressure ventilation is a useful adjunct for those who have evidence of respiratory failure or who fail to respond to oxygen and bronchodilators alone. Intubation and mechanical ventilation may be necessary in cases of massive hemoptysis or respiratory failure not improving with noninvasive measures.American Board of Pediatrics Content Specification(s)Recognize and differentiate by age life-threatening acute complications of cystic fibrosisKnow management principles of chronic cystic fibrosisQuestion: 7An 11-year-old girl is brought to the emergency department after a high-speed rollover motor vehicle crash. She was a front seat passenger, restrained with a lap and shoulder seat belt. She was initially unconscious but did respond to emergency medical services personnel, complaining of pain in her head, neck, right shoulder and forearm, and abdomen. They did not note any movement of her lower extremities. They reported that her heart rate was 124 beats/min, respiratory rate was 12 breaths/min, blood pressure was 76/32 mm Hg, and oxygen saturation was 94% on high-flow oxygen.? On arrival at the emergency department, her Glasgow Coma Scale score is 11. Physical examination reveals that the girl is breathing spontaneously and has equal breath sounds bilaterally, she has a regular heart rate, and she has 3+ pulses in all four extremities. Her abdomen is diffusely tender and without organomegaly. She has a wide area of abrasion and petechiae over her right clavicle and lateral neck and a similar band of bruising across her abdomen, just below her umbilicus. Palpation elicits no tenderness of the posterior midline cervical spine, but tenderness is apparent at T3 through T8 vertebrae posteriorly. She has normal strength in both arms and hands but no spontaneous movement of her lower extremities. She can feel light touch to a level just below her umbilicus. Her rectal tone is diminished and her pants are soaked with urine. You suspect that the girl has sustained a spinal injury.Of the following, the MOST appropriate interpretation of her clinical presentation is thatA.her anal wink and bulbocavernous reflexes are unreliable because of her head injuryB.her hypotension is related to neurogenic shockC.her spinal injury is most likely an isolated Chance fracture due to the lap belt injuryD.the suspected level of her spinal cord injury is cervical based on motor examination findingsE.the suspected level of her spinal cord injury is low thoracic based on sensory examination findingsCorrect answer ESpinal cord injury is a rare complication of pediatric trauma, occurring in fewer than 1% of severely injured children. When present, spinal cord injury in children is often associated with head injury or multisystem trauma. Changes in vital signs may be seen in neurogenic shock. Neurogenic shock is the manifestation of unmitigated vagal stimulation after disruption of descending sympathetic pathways in the upper spinal cord, usually above the T6 level.? Relative bradycardia (unlike the tachycardia described for the girl in the vignette) in the face of hypotension and multisystem trauma should prompt the clinical suspicion of neurogenic shock.Physical examination of a child in whom spinal injury is suspected should include visual inspection and palpation of the neck and back as well as motor, sensory, and deep tendon reflex testing (Figure) of the upper and lower extremities and anogenital tone and reflexes. Motor level of spinal cord injury is defined as the lowest level with at least 3/5 strength. Determining the motor level of deficit is most useful for injuries above T1 or below L2 because there are no major muscles innervated by the T2-L1 nerve roots. ?The Table?lists the 10 muscle groups and corresponding spinal levels used by the American Spinal Injury Association (ASIA) system. Sensory level of spinal cord injury is defined as the lowest level with normal sensation. Sensory level of deficit can be used at any level, but dermatome testing is simplest in the chest and abdomen, where thoracic nerve roots supply enervation. The nipple line is at the T4 dermatome, the umbilicus at T10, and the hip girdle at T12. Because the girl can feel light touch to a level just below her umbilicus, her sensory level is at the 10th thoracic dermatome; therefore, the suspected level of her spinal cord injury is low thoracic rather than cervical. Priapism, decreased sphincter tone, incontinence, and absent anal wink reflex or bulbocavernous reflex (anal sphincter tightening when squeezing the glans or clitoris) can be tested even in an unconscious patient and if present, are ominous signs of cord injury.Spinal injury is most common in the cervical spine, followed in descending order of frequency by the thoracolumbar, lumbar, and thoracic regions. Cervical spinal injury in children is most common after axial loading injuries (eg, diving) or with high-force mechanisms, such as high-speed motor vehicle crashes. Thoracolumbar and lumbar spinal injuries are frequently associated with abdominal injury. The Chance fracture is uncommon in children but can be seen with flexion-distraction of the lumbar spine and is often associated with lap belt injury. This fracture rarely causes neurologic symptoms but when present, should raise concern for abdominal organ injury. Chance fracture typically occurs in the upper lumbar spinal region (T12-L2), but the affected region in children is usually mid-lumbar because of their lower centers of gravity. The neurologic examination findings for this girl, which are consistent with a low thoracic rather than lumbar spinal injury, make a Chance fracture unlikely.Spinal injury should be suspected in any trauma patient exhibiting neck or back pain. Focal neurologic findings (including weakness, paralysis, numbness, or tingling) represent the single most prominent red flag. However, children who have altered mental status should be presumed to be at risk until cleared by further examination. NEXUS criteria have limited sensitivity as a screen for cervical spine injury in children. A recent review of 540 children who had cervical spinal injury after blunt trauma (Leonard, 2010) found that 98% had one of the following risk factors: altered mental status; focal neurologic findings; neck pain; torticollis; substantial torso injury; and conditions predisposing to cervical spine injury, such as diving and high-risk motor vehicle crash.Table. Key Elements of Motor Examination and Corresponding Spinal Level of EnervationKey MusclesCorresponding Spinal LevelElbow flexors (biceps)C5Wrist extensors (extensor carpi radialis)C6Elbow extensors (triceps)C7Finger flexors (flexor digitorum longus)C8Fifth finger abductorsT1Hip flexors (psoas)L2Knee extensors (quadriceps)L3Ankle dorsiflexors (anterior tibialis)L4Long toe extensors (hallucis longus)L5Ankle plantar flexors (gastrocnemius)S1American Board of Pediatrics Content Specification(s)Recognize signs and symptoms of spinal injury in a child with major traumaQuestion: 8The mother of a 15-month-old child brings him to the emergency department with complaints of poor sleeping, low-grade fever, pulling at his left ear, and increased crying over the past 8 hours. He has had an upper respiratory tract infection for 2 days, with cough, runny nose, and a maximum temperature of 37.8?C, and he has slept more restlessly over the past 2 nights. He is in child care 4 days a week and recently fell when camping in the mountains. He has no rashes, vomiting, or diarrhea and has been eating normally. General physical examination demonstrates an unhappy but nontoxic, well-developed male in no distress.Of the following, the MOST likely cause for this boy’s presentation isA.mastoiditisB.otitis externaC.otitis mediaD.referred pain from a dental abscessE.temporomandibular joint syndromeCorrect answer CAlthough all of the options are potential causes of ear pain, without a history of ear drainage (otitis externa), difficulty eating (dental abscess), or abnormal ear positioning (mastoiditis), otitis media (Figure) is the most likely cause of apparent earache for the boy described in the vignette. Temporomandibular joint (TMJ) syndrome would be very unusual in a patient of this age. Earache (otalgia) as a result of otitis media can be straightforward in older children, with discrete issues and clinical findings, but the diagnosis can be more challenging in younger children who exhibit nonspecific signs and symptoms. Treatment, whether watchful waiting and reevaluation or immediate institution of antibiotic therapy, depends on the patient, symptoms, physical examination findings, and comfort of the clinician and family. The references at the end of the critique can help guide clinical approaches.The differential diagnosis for a child who presents with an earache or in whom otalgia is suspected from the history or physical examination findings is broader than an ear infection. One cause may be eustachian tube dysfunction, with a difference between internal and external pressures. Eustachian tube dysfunction can be seen with upper respiratory tract infection, allergy issues, gastroesophageal reflux, and craniofacial abnormalities and can be exacerbated by altitude changes.Otalgia can be categorized as primary (originates from ear) or secondary (pain from another site). Cutaneous and cartilaginous infections (bacterial, fungal, and viral), trauma (direct, related to piercing), allergic reaction to earrings (nickel), angioedema, and environmental issues can cause damage and pain to the external ear. As noted previously, the ear canal can become infected with bacteria or fungi (otomycosis). If such infection includes the bones of the skull, it is designated as malignant otitis externa. Acute or longer-standing foreign bodies can result in trauma and inflammatory reactions, and impacted cerumen can present with ear pain (or without pain). Tumors are rare but can occur.Otalgia related to the middle and inner ear can involve infection and inflammation. Myringitis is inflammation of the tympanic membrane (TM), with or without middle ear fluid, and can be caused by infection and trauma. Finally, otalgia can result from trauma, including perforation of the TM, ossicle injury, hemotympanum, basilar skull fracture, and barotrauma (altitude changes).Secondary causes of otalgia may be more challenging to determine. Local infection, injury, and inflammation can cause apparent ear pain. The pain may originate from crossover from spinal (C2-3) and cranial nerves (V, VII, IX, X) that innervate the ear and ear canal as well as the face and oral cavity. Secondary causes include TMJ syndrome (rare in young children), Bell palsy, mouth/throat lesions, sinusitis, parotitis, cervical spine injury, and lymphadenopathy/adenitis. Ingestions can cause tinnitus (aminoglycosides, quinidine, ethacrynic acid, nicotine, and quinine). Psychogenic issues may also result in complaints of ear pain.The history should include questions about the presence of fever, cold symptoms, drainage, and swelling; duration of abnormality; past medical history of recurrent or persistent pain despite appropriate therapy; trauma; hearing change; and exposures, including barotrauma risk. The physical examination should evaluate the entire ear (external, canal, TM), associated nodes or swelling, pain with ear motion (external otitis), canal integrity, and integrity and appearance of the TM. Secondary assessment should include an oral examination, TMJ assessment, sinus evaluation, neck examination, and facial neurologic assessment.Although the history and physical examination often uncover the cause of the otalgia, ancillary studies may have some role. Such studies can include:Head computed tomography scan (trauma, mastoiditis, malignant otitis externa, brain abscess, sinusitis)Magnetic resonance imaging (tumor)Positron emission tomography scan (tumor)Dental imaging, including panoramic radiographs (TMJ, dental abscess)Lumbar puncture (meningitis)Complete blood count and erythrocyte sedimentation rate (infection)Endoscopy (aerodigestive, nasal)Culture of ear drainageBlood cultureTympanometry and audiometry can also be useful assessment tools.Treatment is based on the cause of the otalgia.American Board of Pediatrics Content Specification(s)Differentiate by age the etiology and understand the pathophysiology of earachePlan diagnostic evaluation and initial intervention for patients with earachesMAY 2012 Question: 1A 6-month-old girl presents with a 2-day history of a high temperature and 12 hours of drooling with neck pain. Her mother reports that this illness was preceded by 1 week of coryza and cough. On physical examination, the ill-appearing girl is in no respiratory distress and has no stridor or dysphonia. She prefers to sit still in her mother’s lap. The mother states that the girl’s drooling is more than usual. The girl resists any movement of her neck. Her mouth opening and oropharyngeal examination findings are normal. She has tender, left-sided anterior cervical adenopathy without overt soft-tissue swelling. Her past medical history has no findings of note. Her temperature is 40.0°C, heart rate is 188 beats/min, respiratory rate is 30 breaths/min, blood pressure is 88/60 mm Hg, peripheral pulses are +2, and capillary refill time is less than 2 sec. The only laboratory finding of note is a total leukocyte count of 26x103/?L (26x109/L) with a left shift. A chest radiograph appears normal. Her soft-tissue neck radiograph is shown in the Figure.FigureOf the following, this girl’s clinical picture is MOST consistent withA.acute epiglottitisB.bacterial meningitisC.foreign body aspirationD.Ludwig anginaE.retropharyngeal abscessCorrect answer EThe acute febrile illness, odynophagia, leukocytosis, and enlarged retropharyngeal space on lateral radiograph of the neck described for the girl in the vignette are most consistent with a retropharyngeal abscess (RPA) or cellulitis. Although bacterial meningitis can present with high temperature, neck stiffness, and leukocytosis, affected infants are usually irritable and do not typically demonstrate odynophagia or an enlarged RP space on radiography. Acute bacterial epiglottitis, a disease that can present with similar signs and symptoms as RPA, is rare in infants immunized against Haemophilus influenzae. Moreover, this girl’s radiograph demonstrates a normal-appearing epiglottis. Ludwig angina is commonly noted in teenagers, usually from an odontogenic source, and involves infection of the floor of the mouth, with swelling, trismus, and tenderness to palpation. The RP space is not typically affected. Although a delayed presentation of a foreign body with postobstructive pneumonia can present with high temperature and odynophagia, the presence of neck pain, relatively acute onset, and an enlarged RP space with a normal chest radiograph argue against a foreign body for this girl.Normal dimensions of the prevertebral space are less than one whole width of the adjacent vertebral body in infants and less than one third the width of the adjacent body in teenagers. At the level of C6, the prevertebral space is usually less than 22 mm in teenagers and less than 14 mm in younger infants and children. The RP space can be falsely enlarged if the infant is crying or if the radiograph is obtained in neck flexion. In an appropriately obtained lateral radiograph of the soft tissue of neck, with air filling the pyriform fossa, loss of the shoulder of the air column is also suggestive of RP space enlargement. Presence of air in the RP space raises the possibility of a phlegmon or abscess. Computed tomography scan of the neck with contrast is more sensitive in making the diagnosis by distinguishing a phlegmon from cellulitis and identifying complications such as vascular thrombosis.The clinical features of commonly encountered deep neck and parapharyngeal space infections, including causes, ancillary studies, management principles, and antimicrobial coverage, are summarized in Table 1.0000It is important for the emergency physician to be aware of “red flags” among patients who have “sore throats” or pharyngitis that may suggest a deep space infection or impending airway obstruction (Table 2).Table 2. “Red Flags” Suggesting a Deep Space Infection Involving the Upper Airway?Fever >2 wks?Symptom duration >2 wks? Trismus? Drooling?Asymmetric tonsillar swelling or adenopathy?Swelling in floor of mouth or lateral neck/jaw swelling?Dysphonia (voice change)?Pain out of proportion to clinical findings?Airway obstruction, dyspnea?Inability to lay supineAmerican Board of Pediatrics Content Specification(s)Differentiate by age the etiology and understand the pathophysiology of retropharyngeal, pharyngeal, parapharyngeal, and other deep space head and neck infectionsRecognize signs and symptoms of retropharyngeal, pharyngeal, parapharyngeal, and other deep space head and neck infectionsRecognize and interpret relevant laboratory and imaging studies for retropharyngeal, parapharyngeal, and other deep space head and neck infectionsPlan management of acute retropharyngeal, pharyngeal, parapharyngeal, and other deep space head and neck infectionsQuestion: 2You receive a call from emergency medical services about a 2-year-old child who is having a seizure and being transported from a child care center. Due to a large multicar crash, no advanced life support units were available, so a basic life support crew is transporting this girl.Of the following, knowing the capabilities and equipment available to a basic life support ambulance crew, you can expect that this child MOST likely may have receivedA.airway positioning, suctioning, and placement of a peripheral intravenous catheterB.bag-valve mask ventilation, oral airway placement, and suctioningC.blood glucose measurement, airway positioning, and suctioningD.endotracheal intubation, rectal diazepam, and intravenous fluidsE.rectal acetaminophen, intranasal midazolam, and oxygenCorrect Answer: BBasic life support (BLS) ambulances carry basic airway supplies such as suction, oxygen delivery, and bag-valve mask devices; pulse oximeters and probes; and nasal and oropharyngeal airways. They do not carry advanced airway supplies such as laryngoscopes, Magill forceps, endotracheal tubes, or end-tidal carbon dioxide detectors. Further, BLS crews do not carry glucometers or medications and cannot place intravenous catheters. BLS ambulances are required to carry automated external defibrillators with both pediatric and adult pads.Before 1970, few/no standards governed what ambulances carried or how their personnel functioned. Since the early 1970s, multiple local, state, regional, and national standards were developed regarding equipment, licensing, and staffing of ambulances. Frequently, multiple different organizations publish separate guidelines for specific equipment requirements. In 2009, a collaborative document was developed and endorsed by the American College of Surgeons, American Academy of Pediatrics, National Association of Emergency Medical Services Physicians, American College of Emergency Physicians, and Emergency Medical Services for Children Stakeholder group. This document lists the equipment required on both BLS and advanced life support (ALS) ambulances, including specialized pediatric equipment. ALS ambulances are required to carry all of the equipment required on BLS units as well as the medications and advanced airway, intravenous access, and cardiac equipment required for ALS crews. The entire document can be viewed at: Board of Pediatrics Content Specification(s)Know essential basic life support and advanced life support pediatric equipment for ambulancesKnow the essential advanced life support pediatric equipment for ambulancesQuestion: 3A 5-year-old boy is referred to the emergency department by his primary care practitioner with a 1-week history of swollen joints (variable areas); a nonpruritic rash on his trunk; a 4-day history of a temperature to 103.0?C; and firm, painless nodules on his shins. Physical examination reveals no murmur or hepatosplenomegaly. The boy has never been hospitalized and has had no previous surgeries or sustained illnesses. The family has no history of arthropathies.Of the following, the MOST appropriate initial evaluation for this boy plete blood count (CBC), blood culture, and urinalysisB.CBC, electrolytes, and Treponema serologyC.electrocardiography, chest radiography, and urine cultureD.joint fluid aspiration, CBC, and blood cultureE.rapid streptococcal antigen detection test, throat culture, and erythrocyte sedimentation rateCorrect Answer: EThe boy described in the vignette has acute rheumatic fever (ARF). Major criteria for rheumatic fever include carditis (inflammation or new changing murmur), polyarthritis (migratory in limb joints), chorea (abrupt purposeless movements with or without emotional changes), erythema marginatum (nonpruritic rash that spares the face) (Figure 1), and subcutaneous nodules (painless, firm lesions on bones or tendons) (Figure 2). Minor criteria include fever; arthralgia; previous history of ARF or rheumatic heart disease; increased erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and leukocytosis; and evidence of group A streptococcal (GAS) infection (positive throat culture or rapid antigen test, elevated antistreptolysin O titer) and scarlet fever. The disease is present in the United Sates but has a much higher incidence and prevalence in developing countries.The most appropriate diagnostic tests for the child presenting with symptoms of ARF are the rapid antigen detection test, streptococcal throat culture, and ESR. Other tests that could be obtained are a CRP assessment, antistreptolysin O titer, chest radiography, and echocardiography. The migratory polyarthritis makes a bacterial joint infection unlikely (and, therefore, joint fluid aspiration unnecessary). The presentation described for this boy does not indicate a need for Treponema serology, although tertiary syphilis can present with a whole body rash and fever, often with hepatosplenomegaly. The nodules described are different from the firm, inflamed gummatous lesions with necrotic centers seen with tertiary syphilis. Although electrocardiography may be helpful to identify a prolonged PR interval (a minor manifestation of ARF), no clear indication suggests renal tract involvement, obviating the need for urinalysis.ARF is an immune-mediated multisystem inflammatory disease related to GAS infection. GAS pharyngitis is the primary precursor, but some evidence suggests that GAS skin infections (impetigo) may have a role in priming the immunologic system to respond to a future pharyngeal infection or that GAS may be transmitted from the skin to the throat, resulting in ARF.Signs and symptoms of ARF usually present 1 to 3 weeks after a streptococcal infection, which may include a mild pharyngitis for which medical evaluation was not sought. Diagnosis requires two major criteria or one major and two minor criteria and evidence of prior streptococcal infection. Only rheumatogenic strains of GAS result in ARF. ARF is a clinical diagnosis with variable presentations, including all of the criteria noted previously. Carditis occurs in 30% to 80% of patients, and approximately 60% of patients who are not treated develop chronic rheumatic fever (CRF). Chorea alone, often occurring 2 to 6 months after infection, meets the Jones criteria for diagnosis. Carditis can be characterized as murmurs on physical examination or identified by echocardiography (“silent carditis”). In the absence of ARF recurrence, approximately 65% of patients have resolution or improvement over time.Most cases of ARF can be prevented with accurate recognition of bacterial illness and antibiotic treatment within 9 days of GAS pharyngitis. GAS pharyngitis is primarily a disease of children between 5 and 15 years of age, although outbreaks have been reported in child care centers. ARF is rare in children younger than 3 years of age in the United States. Initial episodes are unusual in adults, but recurrences are common. Clinical findings include sore throat (often sudden onset), fever (temperature of 38.4 to 40.0?C), pain on swallowing, and headache; abdominal pain, nausea, and vomiting also may be reported. Tonsillar or pharyngeal edema with or without exudates can be seen in conjunction with anterior cervical lymphadenitis, palatal petechiae, a red and swollen uvula, and a scarlatiniform rash. GAS infections occur more often in the winter and early spring.Although the previously cited signs and symptoms are associated with streptococcal infection, they overlap enough with nonbacterial pathogens (viral) to require microbiologic confirmation with a throat culture or rapid antigen test. A single elevated streptococcal antigen titer does not indicate acute streptococcal pharyngitis and cannot distinguish between current infection and the carrier state. However, such titers can be useful to confirm evidence of recent streptococcal infection, which is one of the minor criteria for diagnosing ARF.Treatment is oral or intramuscular penicillin. For those allergic to penicillin, oral cephalosporins, clindamycin, macrolides, or azalide are appropriate focused therapies. Follow-up throat cultures are not recommended unless the patient remains symptomatic or has a history of rheumatic fever and high risk of recurrence. Specific treatment plans for nonresponders to initial GAS therapy can be found in multiple resources, include Gerber and associates (2009). After the onset of ARF, no prevention treatment is available for the immunologic reaction. Salicylates and antibiotics for persistent streptococcal infection are standard treatment. Specific treatment for cardiac dysfunction depends on the severity of presentation. Bed rest is recommended for routine carditis, and corticosteroids are recommended for chorea.Secondary prophylaxis for prevention of a new streptococcal infection is recommended for all patients who have ARF and includes daily oral or intermittent intramuscular penicillin (preferred) or one of the alternatives (sulfadiazine, macrolide, azalide) for penicillin-allergic individuals. The recurrence rate is approximately 10% over 5 years. Prophylaxis should be provided until the patient is at least 21 years of age or is at least 5 years removed the last ARF episode.Figure 1Erythema marginatum lesions on the posterior trunk of a 5-year-old boy who has acute rheumatic fever. These cutaneous lesions occur in approximately 10% of children who have acute rheumatic fever, may have a transient appearance, and are neither painful nor pruritic. Reprinted with permission from Red Book? Online. 2010. Courtesy of George Nankervis, MD.Figure 2The subcutaneous nodules of rheumatic fever are often attached to tendons and are sometimes noted over bony prominences of the arm, leg, or scapula. They consist of collections of Aschoff bodies.American Board of Pediatrics Content Specification(s)Know the etiology and understand the pathophysiology of rheumatic feverRecognize signs and symptoms of rheumatic feverRecognize and interpret relevant laboratory, imaging, and monitoring studies for rheumatic feverPlan management of acute rheumatic feverQuestion: 4You are evaluating a 6-year-old boy after he fell onto his outstretched right forearm. He has slight swelling to his distal forearm and appears to be in a moderate amount of pain. He has a strong radial pulse with good distal circulation and appears to have no motor or sensory deficits. You obtain radiographs of his forearm (Figure 1?and Figure 2).Figure 1Of the following, after adequate pain control, the MOST appropriate method to immobilize this boy’s fracture isA.arm sling with shoulder swatheB.figure-of-eight braceC.posterior long-arm splintD.short-arm volar splintE.thumb spica splintCorrect answer DThe boy described in the vignette has sustained a torus fracture of his distal radius. Torus fractures are a type of distal radius or ulna fracture and are often called “buckle” fractures because the periosteum “buckles” circumferentially rather than breaks. Torus fractures are inherently stable, single-cortex failures of the metaphysis due to a compression-type force. The plasticity of young children's bones and typically low-energy injuries allow this type of injury to occur without cortical separation. Torus fractures generally present with minimal deformity and require only a short-arm cast or splint for approximately 3 weeks. Recent evidence suggests better functional outcomes with removable splinting.An arm sling with shoulder swathe and a figure-of-eight brace usually are used for treatment of clavicle fractures. A posterior long-arm splint is typically used for treating distal humerus fractures, proximal forearm fractures, radial head and neck fractures, and fractures of the olecranon as well as for supporting ligamentous injuries of the elbow.? ?Thumb spica splints are used for immobilizing fractures of the first metacarpal, scaphoid and lunate fractures, and injuries of the ulnar collateral ligament.Approximately 75% of forearm fractures in children occur in the distal third of the radius and ulna. A direct force can produce these fractures, but they are most often caused by an indirect force, typically a fall on an outstretched hand with a pronated and extended wrist. The force is usually transmitted to the radius, which fractures first, followed by the ulna. Fractures at differing levels of the radius and ulna imply a significant rotational vector. If the force is insufficient to displace bone, plastic deformation or a greenstick fracture may result.One of the initial steps for management of pediatric forearm fractures is determining if the injury involves the physis or diaphysis. Salter-Harris I and II distal radial physis fractures can generally be managed with closed reduction and casting if patients present within the first 3 days of the initial injury. Fractures presenting after 3 days should not be reduced due to potential injury to the physis with reduction attempts. Salter-Harris III and IV fractures require orthopedic consultation for open reduction. Distal ulnar physis fractures are rare, and greater controversy surrounds the risk of growth arrest and need for treatment.Distal diaphyseal fractures are generally managed based on several variables:Type of fracture pattern: plastic deformation, greenstick,? complete fracture, or a combination of one type in the radius and a different type in the ulnaDegree of fracture angulation, rotation, or displacementThe amount of angulation that should remodel spontaneously tends to be greater with younger ages. Generally, up to 15 to 20 degrees of diaphyseal angulation, 45 degrees of malrotation, and complete overriding fragments may be tolerated by patients younger than 9 years of age. However, angulation only up to 10 degrees, 30 degrees of malrotation, and complete overriding fragments are tolerated in patients older than 10 years of age. Correction of the bony defect is generally indicated in plastic deformity injuries with angulation greater than 20 degrees to restore motion and correct any significant malrotation in children older than 5 years of age. Plastic deformity injuries in children younger than 5 years of age with less than 20 degrees of angulation can usually be allowed to remodel physiologically without manual reduction.Management options for greenstick fractures of the distal forearm are more controversial in terms of the necessity of fracturing the remaining intact cortex, the allowable degree of deformity, and the specifics of immobilization. Generally, clinicians agree on reduction, using rotation in the opposite direction to the deforming force. Thus, pronation is used for supination injuries with apex-volar angulation and supination for apex-dorsally angulated plete fractures of the distal radius and ulna that are nondisplaced/nonangulated are immobilized in a cast for about 4 weeks. Displaced fractures are treated with closed reduction and casting for 4 to 6 weeks. Open reduction is indicated for fractures that fail to maintain stable alignment after attempts at closed reduction, irreducible fractures, open fractures, and fractures with concomitant severe soft-tissue injury or compartment syndrome.American Board of Pediatrics Content Specification(s)Know and understand the mechanisms of injury in fractures of the distal radius and ulnaRecognize a child with fractures of the distal radius and ulnaKnow and understand the mechanisms of injury in buckle of radius fracturesRecognize a child with a buckle of radius fractureQuestion: 5The emergency communications center in your emergency department relays a call from an ambulance informing you that they are transporting a 4-year-old child who has suffered blunt head trauma. The transmission is cut off before they can provide any more information. A medical student working with you asks about the common causes of head trauma in children.Of the following, the MOST common cause for head trauma in a 4-year-old child isA.a fallB.assault, including child abuseC.being an occupant in a motor vehicle crashD.being struck by/against an object (unintentional)E.sports-relatedCorrect answer AAccording to Centers for Disease Control and Prevention (CDC) data that comprise emergency department visits, hospitalizations, and deaths, falls are the most common cause of traumatic brain injury among children 0 to 4 years of age, followed by being struck by or against an object (colliding with a moving or stationary object), motor vehicle crashes, and assault (Figure 1). Children younger than the age of 4 years have the highest rate of traumatic brain injury among all age groups (Figure 2). Motor vehicle crashes and assaults become more prevalent in the teenage population. Overall, falls are the leading cause of traumatic brain injury, with struck by/against events the second leading cause among all children ages 0 through 14 years.The major causes of nonfatal injuries due to blunt trauma are very similar to those for blunt head trauma (Table). In all age groups that include children younger than 14 years of age, falls are the most common cause of injury. The second leading cause is being unintentionally struck by or against an object. In the 15- through 19-year-old age group, being unintentionally struck by/against an object is the leading cause of blunt trauma, with falls second. The third leading cause of injury varies by age. Among infants younger than 1 year and teenagers 15 through 19 years, motor vehicle occupant injuries are third most prevalent, whereas pedal cyclists are third most prevalent in children ages 5 through 9 years and 10 through 14 years. Sports-related injuries are not common in 4-year-old children.[Data for the nonfatal injuries produced by: Office of Statistics and Programming, National Center for Injury Prevention and Control, Centers for Disease Control and Prevention. Data source: NEISS All Injury Program operated by the Consumer Product Safety Commission?(CPSC).]0000American Board of Pediatrics Content Specification(s)Differentiate the major causes of blunt trauma by ageDifferentiate the major causes of head trauma by ageQuestion: 6You are evaluating an 8-week-old girl for breathing difficulty of 3 days’ duration accompanied by progressive symptoms of lethargy, irritability, and decrease in oral intake over 3 weeks. Her regular feeding of 4 oz every 2 to 3 hours has gradually decreased to 2 oz every 4 hours. Her mother reports that the infant has been taking longer to finish her feedings and becomes sweaty and out of breath with feeding. She has decreased urine output, cough without any fever, and venous prominence along her scalp. On physical examination, the tired-appearing infant has a temperature of 36.3?C, heart rate of 165 beats/min, respiratory rate of 75 breaths/ min, and a systolic blood pressure of 55 mm Hg with capillary refill of 3 seconds. Auscultation reveals coarse breath sounds in all lung fields and a cardiac gallop without murmur, and her liver is palpable to 4 cm below the costal margin. She has a pulsating anterior fontanelle, prominent scalp veins, and significant thrill on palpation of the anterior fontanelle with extremely loud bruit on head auscultation.Of the following, the underlying cause of this infant’s apparent heart failure is BEST diagnosed definitively byA.brain computed tomography scan without contrastB.brain magnetic resonance imaging and angiographyC.coronary computed tomography angiographyD.cranial ultrasonographyE.echocardiographyCorrect answer BThe prominent scalp veins and pulsating anterior fontanelle with thrill and loud bruit on head examination described for the infant in the vignette are suggestive of cardiac failure due to a high-flow vascular lesion in the brain. The diagnostic modality of choice is brain magnetic resonance imaging and angiography (Figure). Brain computed tomography scan may reveal a possible intraparenchymal lesion but is not diagnostic. Brain computed angiography can be as helpful as magnetic resonance angiography, but it is associated with significant radiation exposure. Echocardiography is an adjunctive study to assess myocardial function in the setting of cardiac failure. Coronary computed angiography and cranial ultrasonography are not helpful in this clinical scenario.Arteriovenous malformations (AVMs) are rare high-flow vascular lesions caused by abnormal connection of arteries to veins without an intervening capillary bed (plexiform). A direct connection between an artery and vein that bypasses the capillary bed is called an arteriovenous fistula. AVMs can have either fistulous, plexiform, or mixed connections. About 50% of AVMs present in the neonatal period; the remainder present mostly in late childhood. AVMs can be inherited and are associated with various syndromes. For example, hereditary hemorrhagic telangiectasia is associated with AVMs of the brain, lungs, and liver; rare spinal AVMs with overlying skin capillary malformations are seen with Cobb syndrome; and Parkes Weber syndrome is characterized by AVMs of the extremities along with hyperplasia of underlying tissue and limb enlargement. Capillary malformation-AVM syndrome is a mixed vascular malformation syndrome associated with various cutaneous malformations and cutaneous and cerebral AVMs. A family history of AVM is an indication to rule out these syndromes.The clinical presentation of a cutaneous AVM is usually a macule or patch, with a palpable thrill or warmth, pain, and the possible auscultatory finding of bruit differentiating it from a cutaneous malformation. AVM also may present as an enlarging mass, especially in the head and neck region (with highly prominent cheek and auricle). There are four stages of clinical presentation and progression of cutaneous AVM, as per the Schobinger staging system (Table), but not all AVMs progress through all the stages in a patient’s lifetime.Because the vascular bed connecting an AVM is abnormal, the AVM may progress over years to form an aneurysm and subsequently hemorrhage. Brain AVMs are known causes of intracranial hemorrhage in the pediatric population. Children are more likely to have hemorrhage due to brain AVM than are adults. Such hemorrhage usually presents during adolescence and is characterized by the abrupt onset of severe headache, nausea, vomiting, altered mental status, and sudden death. Other associated symptoms of brain AVM are headaches, seizures, focal neurologic deficits, or ischemia due to stealing of blood from surrounding normal brain parenchyma. The first hemorrhage is associated with significant morbidity and mortality, and rebleeding can occur over years with increasing mortality rates until the AVM is completely obliterated. A rare form of deep intraparenchymal vascular malformation in the brain is vein of Galen malformation, which is an abnormal artery feeding a bed of venous malformations. The malformation may be due to arteriovenous fistula or AVM and usually presents as cardiac failure during the neonatal period or infancy. Other organs associated with AVMs are kidneys (hematuria, renal colic), lungs (hemoptysis, congestive cardiac failure, telangiectasia), and liver and gastrointestinal tract (gastrointestinal bleeding, abdominal mass, congestive cardiac failure, cutaneous hemangiomas). AVM is a rare cause of cardiac failure but should be suspected in a patient in whom no other explanations can be found for cardiac failure. Spinal cord AVM is a rare disorder that usually presents with backache and acute focal deficits due to hemorrhage. In some patients, spinal auscultation can elicit bruits.Angiography is the gold standard for diagnosing AVM. When available, ultrasonography with color duplex can be used to assess a suspected lesion. Other investigation choices are magnetic resonance imaging with angiography or computed tomography angiography. Clinical follow-up evaluation is indicated for cutaneous stage 1 lesions. With progression, a multidisciplinary approach that includes vascular, pediatric, and plastic surgery as well as interventional radiology to identify the best treatment method is indicated.FigureBrain angiography for a child who has a massive cerebral arteriovenous malformation0000American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms and complications of arteriovenous malformation and aneurysmKnow the indications for and interpret results of ancillary studies in patients with arteriovenous malformation and aneurysmQuestion: 7You are evaluating a 17-month-old girl who has a previous history of anoxic brain injury. Her mother describes putting the child to bed last night on the usual continuous feeding rate of 35 mL/hr through the gastrostomy tube. When she awakened this morning (3 hours ago), she noted that the girl’s bed was soaked with formula and the tube was lying on the mattress. She states that the child has been whimpering more this morning but has had no fever, cough, or other abnormal issues. The gastrostomy tube site has mild excoriation around the stoma, with small dried blood flecks on the skin. According to the mother, the tube was initially placed at about 8 months of age, and the last replacement was performed electively 3 weeks ago in the pediatrician’s office. On physical examination, the girl is crying, but between breaths, her abdomen appears soft and bowel sounds are present.Of the following, the MOST appropriate next step is toA.clean and reinsert the tubeB.contact the surgeon to assess the site before tube replacementC.insert a small catheter into the stomaD.insert a larger size tube for a tighter fitE.order ultrasonography to evaluate for abdominal free fluidCorrect answer CA gastrostomy is an opening created through the abdominal wall into the stomach for the purpose of feeding, administration of medications, or decompression. There are three basic types of gastrostomy tubes (Figure). A balloon tip is a tube with a balloon on the distal end, similar to an indwelling urinary catheter, and an external bumper to stabilize the tube. Initial insertion of this tube requires abdominal surgery. A percutaneous endoscopic gastrostomy (PEG) tube can be placed endoscopically and has an internal bumper secured against the abdominal mucosa and an external bumper to stabilize the tube. A low-profile gastrostomy tube is a skin-level tube that has either a balloon or mushroom tip. This tube is also known as a “button.” The advantages of this tube are the smaller chance of it being pulled out and the ease with which it can be concealed under clothing.Inadvertently dislodged gastrostomy tubes are frequently encountered in emergency department patients. They may be dislodged due to inappropriate placement, mechanical issues (balloon deflation, tube breakage), or accidental tension causing the tube to be pulled out. In addition, tubes can kink, break, leak (tube porosity), become obstructed, and migrate.Several important issues must be considered when a patient presents with a dislodged gastrostomy tube. Important historical questions include whether the tube was recently placed (<12 weeks after insertion is not sufficient time for tract formation and scarring of the stomach to the abdominal wall), how long has it been out, whether the balloon was inflated or deflated, and the child’s state (eg, fever, signs of peritonitis). Tubes that have been dislodged within about 6 weeks of initial placement should not be replaced at the bedside routinely without surgical consultation or radiologic guidance/affirmation of positioning because the gastric and abdominal walls may have separated, which can result in inappropriate tube location on replacement. If the tube was not initially placed appropriately, potential issues include perforation, fistula tract formation, and peritoneal instillation of medications or feeding materials. Such issues would likely become evident during the insertion process, not in patients who have well-established tubes.The most appropriate initial step for the girl described in the vignette is to insert a small catheter into the stoma and reassess the patient. Displaced tubes should not be reused unless tube integrity is clearly evident and other options are not available. In general, replacing the tube with a fresh tube is appropriate, but if the tube has been out for several hours, the stoma will have contracted, generally necessitating temporary stenting with a small catheter, followed by gradual dilation before definitive tube placement. However, surgical assessment typically is not necessary. Although this process can vary for each individual, mild sedation may be a reasonable adjunct. Ultrasonography can be a useful adjunct in screening for free fluid, but this child’s history and physical examination findings do not suggest the presence of peritonitis or other intraabdominal issues related to tube displacement.Among potential issues related to replacement are: inability to replace due to stoma constriction, skin lesions due to trauma of dislodgement or replacement, inaccurate replacement with formation of a false tract, placing the tube into the peritoneum or an abdominal organ, and inappropriate sizing leading to a distended stoma or gastric contents leakage onto the abdominal skin. Leakage may be due to inaccurate tube size, tube migration, recent weight loss, increased abdominal pressure, infection, granulation tissue, balloon deflation, loose or inadequate tube fixation to skin, failure of tract closure, or a stoma that is larger than the tube. Tube upsizing is an option but should be considered in conjunction with tube experts because dilation of the tract may not solve and might compound a leakage issue. Irritation may be caused by gastric leakage. A nonadhesive barrier/foam under the external stabilizer can help to absorb drainage until irritation improves. Potential topical treatments include antifungal powder, ointment, or barrier; dimethicone cream products; and pharmacologic skin barriers.The replacement tube should be assessed before insertion for correct size, balloon integrity, proper balloon inflation volume, and tube patency. After placement, the tube should be assessed for accurate location, patency, and integrity. Such assessment can be accomplished visually, via stethoscope, through aspiration of stomach contents, by instillation of contrast and radiographic assessment, and by trial of clear fluid.Other potential gastrostomy tube problems include peritonitis (usually in the peri-placement time frame), granulation tissue (treat with silver nitrate), skin irritation/excoriation (observe careful skin preparation, reduce gastric acidity, ensure proper tube size), bowel perforation, intussusception (bilious vomiting and pain, especially after meals), infection (cellulitis may be bacterial or chemical from gastric leak), proliferative gastric mucosa, intragastric mucosal ulcer, and obstruction from a distally broken segment that blocks the intestines.Skin-level tubes, which are often preferred by patients, should be evaluated routinely and potentially replaced one to four times per year. Tube clogging or occlusion can be minimized by flushing with water before and after administration of medications or feeding. Instillations of carbonated beverages and mechanical clog removal (stiff guidewire) have been used for removing blockages, but tube removal may be required.0000American Board of Pediatrics Content Specification(s)Know the indications and contraindications for gastrostomy tube replacementKnow the anatomy and pathophysiology relevant to gastrostomy tube replacementRecognize the complications associated with gastrostomy tube replacementPlan the key steps and know the potential pitfalls in performing gastrostomy tube replacementQuestion: 8A 15-year-old girl presents for evaluation of fatigue, weakness, and muscle cramps. She reports feeling tired and generally weak for several days, and she has had muscle aches and cramps for the past 24 hours. She denies any fever, respiratory symptoms, vomiting, or diarrhea. She has had nausea and decreased appetite for the past several days. She reports no change in her mental status or behavior other than a decreased activity level. She denies any numbness or tingling, changes in bowel or bladder function, or difficulty with vision or speech. Her parents state that she has been losing weight recently but she denies that she has been trying to lose weight. She has a history of depression for which she has seen a counselor and previously took escitalopram, but she stopped the medication several months ago. She is taking no other medications. On physical examination, the thin and tired-appearing girl has a flat affect but is in no acute distress. Her temperature is 37.0°C, heart rate is 98 beats/min, respiratory rate is 18 breaths/min, blood pressure is 90/60 mm Hg, height is 160 cm, and weight is 40 kg. She has tacky mucous membranes, mild tachycardia with good peripheral and central pulses, and mild diffuse abdominal tenderness. Musculoskeletal examination reveals diffuse tenderness without any edema, erythema, or abnormal bulk or tone. Neurologic examination results are normal, with the exception of 4/5 muscle strength in all extremities. She has no clonus or tremor. Laboratory evaluation documents:SerumSodium, 133 mEq/L (133 mmol/L)Potassium, 2.1 mEq/L (2.1 mmol/L)Chloride, 108 mEq/L (108 mmol/L)Bicarbonate, 16 mEq/L (16 mmol/L)Blood urea nitrogen,? 20 mg/dL (7.2 mmol/L)Creatinine, 0.8 mg/dL (70.7 ?mol/L)Glucose, 86 mg/dL (4.8 mmo/L)Magnesium, 2 mEq/L (2 mmol/L)Calcium, 9.9 mg/dL (2.5 mmol/L)Phosphate, 4.5 mg/dL (1.5 mmol/L)Serum osmolality, 290 mOsm/kg (290 mmol/kg)Urinalysis:pH, 5Specific gravity, 1.030Negative for white or red blood cells, nitrate, and leukocyte esteraseUrine:Sodium, 100 mEq/L (100 mmol/L)Potassium, 5 mEq/L (5 mmol/L)Creatinine, 100 mg/dL (8,840 ?mol/L)Osmolality, 800 mOsm/kg (800 mmol/kg)Electrocardiography reveals ST segment depression, flattened T waves, and prominent U waves.Of the following, the MOST appropriate next step in treatment for this girl is administration ofA.intravenous insulin, calcium, and sodium bicarbonateB.intravenous potassium chloride, normal saline bolusC.intravenous potassium chloride, oral amilorideD.intravenous potassium chloride, dextrose, and normal salineE.oral potassium acetate and propranololCorrect Answer: BThe girl described in the vignette has severe, symptomatic hypokalemia as a result of laxative abuse. The presence of symptoms as well as electrocardiographic changes mandate emergent treatment with intravenous potassium. Potassium chloride causes a more rapid increase in serum potassium than other potassium salts due to the slower entrance of chloride into cells, which maintains the potassium in the extracellular space. Insulin, calcium, and bicarbonate therapy are indicated in management of severe hyperkalemia but are contraindicated in a patient who has hypokalemia. The addition of amiloride therapy to intravenous potassium supplementation can be helpful if renal potassium losses are suspected. Amiloride is a potassium-sparing diuretic that works by blocking the cortical collecting tubule sodium channels. This girl’s low renal potassium concentrations do not suggest renal potassium wasting. In the absence of significant hypoglycemia, dextrose replacement should be delayed when treating hypokalemia to prevent insulin secretion, which drives potassium intracellularly and may worsen hypokalemia. Beta-blocking agents such as propranolol can be useful if potassium redistribution is suspected to be due to catecholamine excess, but this girl has no evidence of abnormal sympathetic tone or thyroid dysfunction to warrant such therapy.Hypokalemia is defined as a serum potassium concentration less than 3.5 mEq/L (3.5 mmol/L). Hypokalemia can result from excess potassium losses or redistribution of potassium into the intracellular space. The Table?summarizes the various causes of hypokalemia according to underlying pathophysiology.The patient’s history may provide information that makes the underlying cause of hypokalemia obvious. In unclear cases, analysis of urine electrolytes and osmolality can aid in differentiating renal from extrarenal losses. Calculation of the transtubular potassium gradient (TTKG) and urine potassium-to-creatinine ratio can be used to make this distinction:TTKG = (urine potassium/serum potassium) ÷ (urine osmolality/serum osmolality)TTKG <3 indicates low urinary potassium secretion and extrarenal losses.Urine potassium/creatinine ratio <13 mEq/g or 1.5 mEq/mmol indicates low urinary potassium secretion and extrarenal losses.Additional laboratory tests indicated in the evaluation of the patient who has hypokalemia include assessment of acid-base status and measurement of serum calcium, magnesium, and phosphorus; urine electrolytes; and serum and urine osmolality.Electrocardiography should be performed to assess for cardiac conduction effects associated with decreased serum potassium concentrations. Early changes include flattened T waves, prominent U waves, and ST-segment depression (Figure). At more severe degrees of hypokalemia, QRS and PR-segment prolongation are evident, and arrhythmias such as supraventricular and ventricular tachycardia can occur.Mild degrees of hypokalemia are unlikely to result in clinical symptoms; symptoms become likely once the potassium concentration decreases below 3 mEq/L (3 mmol/L). Other factors may lead to symptoms at more moderate degrees of hypokalemia, including concomitant hypomagnesemia, digoxin therapy, or significant acid-base abnormalities. Clinical effects of hypokalemia are based on the effect on cell membrane polarization throughout the body, with the primary manifestations seen in the neuromuscular and cardiovascular systems. Skeletal muscle weakness begins in the lower extremities and progresses cephalad; involvement of the respiratory muscles may result in respiratory failure in severe or prolonged cases. Smooth muscle involvement may manifest as nausea, vomiting, constipation, and urinary retention. Cardiovascular conduction abnormalities, as previously outlined, place the patient at risk for a variety of arrhythmias, including premature ventricular or atrial contractions, sinus bradycardia, supraventricular or ventricular tachycardia, and varying degrees of heart block. Hypokalemia can lead to secondary renal concentration defects, producing an acquired form of nephrogenic diabetes insipidus.Management of hypokalemia is dictated by the presence and severity of signs and symptoms, degree of hypokalemia, electrocardiographic abnormalities, and comorbid conditions. When redistribution of potassium is suspected, replacement requires extreme caution and careful monitoring of potassium concentrations and cardiovascular status because total body potassium concentrations are often normal or even elevated. Overly aggressive replacement may result in hyperkalemia and potentially fatal arrhythmias. Many cases of hypokalemia are associated with a combination of losses and redistribution, and the redistribution effect must be considered when attempting to determine the patient’s total body potassium concentrations, particularly among those who have significant acid-base abnormalities.Oral therapy should be used for patients who have no significant symptoms or electrocardiographic abnormalities unless precluded by significant vomiting. The initial oral dosing is 2 to 5 mEq/kg per day divided in three to four doses. As noted previously, potassium chloride results in more rapid and sustained increases in serum potassium concentrations; other formulations, including potassium acetate and potassium phosphate, may be considered in cases involving acidosis or associated hypophosphatemia. Patients whose potassium concentrations are less than 3 mEq/L (3 mmol/L) should be considered for intravenous therapy. Those who cannot tolerate oral therapy and those who have significant symptoms require intravenous therapy. Patients who have mild-to-moderate hypokalemia and mild or no symptoms can have potassium added to their maintenance fluids. More severe abnormalities require more rapid correction; administration of 0.5 to 1 mEq/kg over several hours with continuous electrocardiographic monitoring can increase potassium rapidly to safer concentrations. Higher concentrations and more rapid administration rates may require central access due to the irritating effect of potassium on veins. Maximal concentration and rate of potassium administration varies according to institutional policy. If the patient is having ongoing potassium losses, such losses must be factored into the rate and dose of potassium administration.Patients who have renal potassium wasting may benefit from the addition of a potassium-sparing diuretic; sodium channel blockers (amiloride, triamterene) and aldosterone antagonists (spironolactone and eplerenone) are used, depending on the suspected cause of the renal potassium losses. Correction of other metabolic abnormalities such as hypomagnesemia, alkalosis, and volume depletion are also critical to preventing ongoing redistribution of potassium and more severe symptoms.FigureIn hypokalemia, the electrocardiogram shows ST segment depression, flattening of the T waves, and the appearance of a U wave (arrow). Courtesy of A. Friedman.American Board of Pediatrics Content Specification(s)Know the etiology and understand the pathophysiology of hypokalemiaRecognize signs and symptoms of hypokalemiaRecognize and interpret relevant laboratory and monitoring studies for hypokalemiaRecognize life-threatening complications of hypokalemia and its treatmentPlan management of acute hypokalemiaJUNE 2012Question: 1A 4-week-old neonate presents to the emergency department with lethargy, pallor, vomiting, and poor oral intake of 3 weeks’ duration. The baby was born at term to a G1P1 mother without any prenatal complications. The infant has had progressively worsening vomiting after every feeding that his parents describe as nonbilious. Today he has been sleeping and has had no wet diapers for 24 hours. On physical examination, he has a temperature of 37.0°C, heart rate of 185 beats/min, respiratory rate of 18 breaths/min with slow and shallow breaths, systolic blood pressure of 55 mm Hg, oxygen saturation of 95% in room air, and capillary refill of 2 seconds. The lethargic and pale infant has sunken fontanelles, dry mucous membranes, clear breath sounds, sinus tachycardia, palpable femoral pulses, a nondistended abdomen with peristaltic waves, and normal-appearing genitalia. Bedside capillary blood analysis results are:pH, 7.59Pco2, 63 mm HgPo2, 33 mm HgBicarbonate, >50 mEq/L (50 mmol/L). Venous blood analysis results are:Sodium, 131 mEq/L (131 mmol/L)Potassium, 2.8 mEq/L (2.8 mmol/L) Chloride, 50 mEq/L (50 mmol/L)Bicarbonate, 60 mEq/L (60 mmol/L)Blood urea nitrogen, 156 mg/dL (55.7 mmol/L)Creatinine, 2.1 mg/dL (185.6 μmol/L)Glucose, 156 mg/dL (8.7 mmol/L)Anion gap, 21You begin fluid resuscitation with a 20-mL/kg bolus of normal saline and obtain bedside ultrasonography (Figure 1).Figure 1Abdominal ultrasonography showing a long, thickened pylorus consistent with pyloric stenosis. Courtesy of Siraj Amanullah MD, MPH.Of the following, the MOST appropriate next step in management for this neonate plete sepsis evaluation with antibiotic administrationB.continued fluid and electrolyte resuscitation followed by elective abdominal surgeryC.emergent exploratory laparotomyD.emergent intubation with hyperventilationE.passage of a nasogastric tube and administration of oral rehydration solutionCorrect answer BThe infant described in the vignette has pyloric stenosis (Figure 1) with severe hypokalemic hypochloremic metabolic alkalosis and compensatory respiratory acidosis. Such patients require fluid and electrolyte resuscitation, followed by surgery once the correction is achieved. Although endotracheal intubation may be considered, hyperventilation could exacerbate his alkalemia by reducing the physiologic respiratory compensation. Sepsis is always a consideration in an unstable patient, but this infant’s history and physical examination findings suggest severe dehydration. Obtaining a blood culture followed by empiric antibiotic administration may be appropriate, but a lumbar puncture (part of a “complete sepsis evaluation” at this age) should be deferred in this unstable infant. Administration of oral rehydration solution via nasogastric tube is not appropriate because of severe narrowing of the pylorus, as indicated by the lack of passage of oral contrast beyond the stomach in the abdominal series radiograph. Emergent explorative laparotomy is indicated for patients in whom mid-gut volvulus is suspected, most of whom have bilious emesis, distended abdomen, and abnormal findings on the upper gastrointestinal radiographic series. The differential diagnosis of bilious vomiting and intestinal obstruction in a neonate includes malrotation, meconium ileus, necrotizing enterocolitis, atresias, Hirschsprung disease, and intussusception (Figure 2).The exact pathophysiology of pyloric stenosis is unknown, and some evidence suggests that it is a congenital anomaly. Various congenital anomalies can present in the neonatal period with acute instability (Table). Because these anomalies can involve more than 1 organ system, a high index of suspicion is required for appropriate management in the emergency department.Figure 2Small bowel obstruction in a neonate associated with bilious emesisAmerican Board of Pediatrics Content Specification(s)Know special management techniques for congenital anomalies leading to acute neonatal instabilityQuestion: 2A 13-year-old basketball player arrives in the emergency department after colliding with an opposing player while going for a rebound and landing on his right hand. He describes immediate pain and swelling of his hand over the mid third and fourth metacarpals. On physical examination, the area is swollen and discretely tender, and his third and fourth fingers appear malaligned, with rotational abnormality. There is no evidence of an open wound. Motor and sensory examinations are limited by pain, but responses appear to be intact. While waiting for radiographs, he and his coach ask what the possible outcomes might be.Of the following, the MOST likely diagnosis and outcome areA.contusion that requires no specific treatmentB.dislocation that requires immediate closed reductionC.dislocation that requires open reductionD.fracture(s) that can be managed conservatively with castingE.fracture(s) that may require surgical repairCorrect Answer: EAlthough prognostications of injury severity and required therapy are difficult before seeing the radiographs, the injury described for the boy in the vignette most likely is a midshaft metacarpal fracture, based on the swelling and tenderness. The apparent malalignment suggests possible instability that may require surgical fixation rather than conservative casting. The presentation is not consistent with a sprain, and the midshaft location is not consistent with a dislocation of the metacarpal-phalangeal (MCP) joint as part of or the full extent of the injury. The injury may be a contusion, but the discrete tenderness and malalignment suggest a bony injury.Hand injuries are relatively common in athletes and others receiving direct trauma to the hand. Metacarpal fractures in children can occur at the base (13% to 20%), shaft (10% to 14%), neck (56% to 70%), and physial region (18%). MCP dislocations may be seen, but carpal metacarpal (CMC) dislocations are rare in children. The thumb can also have metacarpal fractures that often include avulsion injuries.Radiographic assessment of hand injuries should include three clear views: posterior-anterior, lateral, and oblique films. Orthopedic consultation or follow-up evaluation is indicated for most metacarpal fractures.Assessment of fracture stability is an important part of assessing and treating hand fractures. A stable fracture does not displace spontaneously or with motion when reduced and immobilized. The thick periosteum in a child can help with stability. Conservative closed treatment is appropriate for many metacarpal fractures, although oblique, avulsion, and comminuted fractures are often unstable.Conservative therapy may be appropriate for closed base (often transverse) fractures with no or minimal displacement. Evaluation of metacarpal fracture(s) should always include assessment and monitoring for current or developing compartment syndrome. The risk for compartment syndrome increases with multiple fractures and crush injuries. Splints or valved casts may be appropriate early in therapy to minimize the risk of compression with increased swelling. Definitive casting is preferred, when swelling allows, and strict immobilization is required. Closed reduction is frequently appropriate for displaced or dislocated metacarpal bones, but CMC dislocations and fracture/dislocations are often unstable and may require pinning and stabilization.Shaft fractures are less common in children. Most are spiral due to the torsional mechanism of injury. Rotational deformities are common in these injuries. Nondisplaced fractures can be managed with immobilization, but assurance of rotational control is important. Buddy taping of the fingers within the cast can help. Postreduction and postcasting radiographs are important to help assure proper rotational alignment. If the fracture is unstable, long, or oblique (with a tendency to shorten), stabilization with pinning may be required. Healing occurs over 4 to 6 weeks.Metacarpal neck fractures are more common, with the small finger being fractured most often. Metacarpal neck injuries occur during altercations, falls, and sporting injuries. Checking for rotational abnormality is crucial for these injuries, as is assuring that there is no open wound or foreign body (eg, tooth). Open wounds associated with fractures may require additional therapy and antibiotics. Closed reduction is appropriate for minimal displacement.Younger patients have greater remodeling potential and have been reported to remodel angulation of up to 70 degrees. In older children, initial or postreduction angulation of less than 30 to 35 degrees for the fourth or fifth finger and 10 to 20 degrees in the index and middle fingers is potentially acceptable. Others suggest a maximum acceptable angulation of 15 degrees in the fourth and fifth fingers and 10 degrees in the index and long fingers. Care for a patient presenting with angulation approaching these values should include consideration of a closed attempt at reducing the angulation. Rotational malalignment must be addressed and reduced. If unstable, pinning or open reduction may be required.Fractures through the growth plate may heal without sequelae or may have an impact on growth. Most of these injuries occur in adolescents, so the impact to the growing bone is not as significant as it would be in a younger child. MCP dislocations can be difficult to diagnose on radiography due to the cartilage present in a young child. Operative reduction is often needed because the volar plate may become entrapped and prevent closed reduction.In general, fracture immobilization should provide stability for healing, relief of pain, protection from reinjury or displacement, and restoration of normal hand function. Splinting usually requires the MCP joints to be in flexion to avoid extension contracture. The interphalangeal joints are often immobilized in full extension, with an exception made for volar plate fractures. Hardy (2004) notes several general splinting principles:Ensure reduction of fractureAvoid contractures through appropriate positioningMinimize length of immobilizationDo not immobilize uninvolved joints in stable fracturesDo not obstruct skin creases with the splintEncourage early active tendon glidingComplications of metacarpal fractures include malunion and nonunion (due to infection, poor alignment, poor immobilization) as well as rotational abnormalities resulting in digital scissoring. Joint contractures, tendon tethering, stiffening, and shortening can also be seen with healing of these injuries.American Board of Pediatrics Content Specification(s)Know and understand the mechanisms of injury in metacarpal fracturesRecognize a child with a metacarpal fractureQuestion: 3You are planning a study comparing administration of corticosteroids + antibiotics (therapy 1) with antibiotics alone (therapy 2) for community-acquired meningitis in children ages 6 weeks to 18 years of age. Your outcome of primary interest is death or poor survival compared with good survival at the time of hospital discharge. A “poor” outcome is defined as a Glasgow Outcome Score (GOS) of 1 (dead), 2 (vegetative), or 3 (severely disabled); a “good” outcome is defined as a GOS of 4 (moderate disability) or 5 (good recovery). The prior reported poor outcome rate is 20% among those treated with antibiotics alone. You hypothesize that corticosteroid use will decrease poor outcomes to 10%. You perform a power calculation with an α of 0.05 and a power of 80% and estimate that you should randomize 150 patients to each group.Of the following, a TRUE statement about your proposed study is thatA.a sample size of 300 patients will give a ? of 0.8 that the study will have sufficient sample size to detect a 50% decrease in poor outcomesB.a type II error occurs when the null hypothesis is rejected when it is trueC.statistical tests usually are two-sided, with the rejection area under the standard normal curve for the null hypothesis being 0.05 (α) for each tail of the distributionD.the null hypothesis is that poor outcomes will be lowered in the therapy 1 group by 50% compared to the therapy 2 groupE.the P value is the primary test statistic used to test hypotheses and is the probability of obtaining data as or more extreme than the observed data by chance aloneCorrect answer EA null hypothesis is a statistical hypothesis that is tested for possible rejection under the assumption that it is true. It specifies a hypothesized value for a parameter. In the vignette, the null hypothesis is that poor outcomes will occur at a rate of 20% for children who have community-acquired meningitis regardless of the treatment they receive. The alternative to the null hypothesis is that poor outcomes will not occur at a rate of 20% among those treated with corticosteroids. The “rejection” region is a set of values for a statistic for which the null hypothesis will be rejected. The purpose of statistical tests is to determine if the obtained results provide evidence to reject the null hypothesis or if the results are merely due to chance.A type I error occurs when the null hypothesis is rejected when it is, in fact, true. For the proposed study, results appearing to show that corticosteroids improved GOS when they actually did not is a type I error. A type II error occurs when the null hypothesis is not rejected when it is false. An example of this would be statistical results indicating no benefit from the addition of corticosteroids to traditional antibiotic treatment when, in actuality, they were of true benefit. The probability of a type I error is denoted by α, and the probability of a type II error by β. Thus, a type I error (α) concludes that a difference exists when it does not (false-positive); whereas a type II error (β) concludes that a difference does NOT exist, when it actually does exist (false-negative).The power is the probability of rejecting the null hypothesis when it is false. Thus,?? Power=1– probability of type II error?? =1–β?? =0.8Therefore, in this vignette, since power was selected as 0.8 (80%), the β is 0.2.The value of α usually is specified before the study, most commonly 0.05 or 5% significance. In other words, the chance of obtaining that statistic by chance alone is sufficiently low (ie, 1 out of 20). The likelihood for a study to detect a treatment effect is both a function of the specified difference from the null hypothesis assumed in the study, in this case, a decrease from 20% poor outcomes to 10%, and the number of patients enrolled in the study. In this example, the chance of making a type II error is set at 20%. Alternatively stated, the study has an 80% chance of detecting a difference at the magnitude specified if that difference truly exists. If a greater power or lower β is chosen, the required sample size will be larger.The region for rejecting the null hypothesis can have any number of rejection regions for a specified α, although usually 2 regions are used. For a 2-tailed test, the associated rejection area extends both to the right and left of a hypothesized parameter (α/2 for each side); for a 1-tailed test, the area is associated with a region to 1 side of the parameter (α). One-sided tests are used for the alternative hypothesis that μ < μo; 2-sided tests are used for alternative hypotheses that μ ≠μo.American Board of Pediatrics Content Specification(s)Define the "null hypothesis"Understand the role of power calculations in research planningKnow the factors that contribute to type I and type II errorsQuestion: 4Emergency medical services (EMS) is called to the scene of a late-night residential party by concerned friends of a 15-year-old girl whom bystanders had found “passed out” in the bathroom. On arrival, EMS personnel find the girl sitting on the floor, alert and coherent, and in no apparent distress. She appears disheveled and has suffused conjunctiva and a forehead hematoma. Despite repeated attempts, she refuses to be examined or transported to the hospital, stating that she is “fine.”? She states that she is in the 10th grade and lives nearby with her parents and two brothers, none of whom are present. The EMS personnel are unsuccessful in contacting the girl’s parents.Of the following, the MOST appropriate course of action for prehospital providers is toA.carefully document that the patient understands the risks and declined transportB.classify the case as a "do not transport" and return to service expeditiouslyC.ensure a support system is in place before leaving the patientD.obtain the girl's vital signs and if normal, do not transportE.transport her despite her wishes to decline careCorrect answer EAlthough a situation involving refusal of transport can be perceived as diverting valuable resources by tying up an ambulance unit, these encounters pose a medicolegal risk for the prehospital provider. The key issues that must be addressed in the case described in the vignette are:Is this minor competent to decline prehospital care?Under what circumstances can a minor function as an adult and decline care or make independent decisions?What are the options and appropriate steps for prehospital providers encountering patients who decline transport?Because this teenager was witnessed to have lost consciousness and she has suffused conjunctiva and evidence of head trauma, the possibility of ingestion or blunt head trauma cannot be excluded. Hence, regardless of her age, the girl is not “medically” competent to decline care. A good faith effort should be made to contact caregivers to encourage her to voluntarily submit to necessary medical care. Beyond that, any options that do not include transporting this patient for further medical evaluation are inappropriate. Law enforcement resources may be used, as appropriate, to ensure that the patient receives necessary emergency stabilization and transport.There are 3 circumstances when courts permit a minor to make independent decisions. In general, an “emancipated” minor can function as an adult, independent of his or her parents with regard to consent for medical evaluation, transport, and treatment. A “mature” minor is one who is older than a specific age (varies by state) and displays sufficient maturity and intelligence to understand risks, benefits, and alternatives of proposed treatment and make a voluntary reasonable choice on the basis of this information. Criteria for emancipation of minors and mature minor vary from state to state, and practitioners should be aware of regulations that apply in their area. Most states allow a minor to consent to evaluation and treatment without parental consent for mental health services, substance abuse, pregnancy-related care, contraceptive services, and treatment of sexually transmitted infections.Unless one of the aforementioned exceptions applies, a minor cannot make independent medical decisions. The teen in the vignette does not appear to be either an emancipated or mature minor, so she cannot decline care if it is deemed necessary, even if she is medically competent. Consultation should be sought from the medical control physician if the EMS provider is unclear about whether a limb- or life-threatening emergency exists. In most cases, patients refusing transport to the hospital clearly are not significantly injured or ill or EMS was contacted by bystanders at the scene out of fear or concern for the patient. Such actions may occur outside of the patient’s control. In these situations, EMS personnel are not necessarily obligated to transport the patient. Nevertheless, prehospital providers must remain objective in assessment of such patients and search for conditions that may affect the patients’ mental status or competency in refusing treatment. Assessment should include an evaluation of the patient complaint, mechanism and amount of injury, underlying medical conditions that may affect the level of consciousness such as diabetes, and the use of any mind-altering substances such as drugs or alcohol. All patients with whom contact is made should be evaluated on their level of competency before allowing them to decline transport to the hospital.Pertinent and thorough documentation is the key to protecting the prehospital provider from liability. Even patients who refuse to have their vital signs assessed can be evaluated without actual physical contact. For example, a patient involved in a motor vehicle crash that results in minimal damage to the vehicle who has no obvious sign of injury and refuses to have vital signs taken can be evaluated for competency through simple observation and general conversation. Patients who refuse medical care at the scene should be documented as having “declined” medical care rather than “refused” medical care. Declining care indicates that a patient has thought about the offer of care and made a conscious decision. Refusing care implies a more belligerent person who could be construed to be behaving irrationally. In addition, prehospital providers should document the patient’s activities while on scene, including the ability to have conversation with officials or making calls on a cell phone. In essence, the providers should make a special effort to document objective observations of actions that clearly demonstrate a higher level of thought processes to complete.After eliminating any contributing medical factors, providers should carefully document efforts to encourage the patient to seek medical care, including conversations with caretakers, family members, and even the patient’s physician. If the patient still declines transport and is legally able to make independent medical decisions, providers should establish that the he or she has a support system, be it a friend or relative, who will be with the patient for the next several hours to observe his or her mental status. ?A related scenario involves a “treatment standing order.” If the caregiver can produce a properly executed do-not-resuscitate (DNR) order, resuscitation can be withheld. However, patients still should be treated appropriately without initiating cardiopulmonary resuscitation if they develop cardiac or respiratory arrest. When there is doubt, the prudent approach is to begin resuscitative efforts with all skills available. If resuscitation has been initiated at the scene by bystanders, efforts should be continued until the prehospital provider has received online direction by a physician to cease resuscitation, the patient meets criteria for “definitive signs” of death, or a properly executed DNR form is produced. Providers should be aware of any state or local regulations related to out-of-hospital DNR orders.American Board of Pediatrics Content Specification(s)Know the special medicolegal problems faced by prehospital personnel caring for the minor patient, including consent, treatment refusal, and do-not-resuscitate ordersQuestion: 5A 9-year-old boy is brought to the emergency department by ambulance because of difficulty breathing. Emergency medical services personnel have been administering albuterol nebulization treatment during transport, but the boy has continued to have labored respirations with “noisy breathing.” The child’s father reports that the boy had upper respiratory tract infection symptoms more than 1 week ago. He seemed to be getting better, but he has been very fatigued for the past several days and not wanting to play. He was seen twice at an urgent care center and diagnosed first with a viral illness and subsequently walking pneumonia. He is on the second day of a 5-day azithromycin regimen. He has had no fever, diarrhea, headache, sore throat, or neck pain or stiffness. He has had some choking and vomiting associated with cough and eating. He has been unable to stand or walk for the past 2 days, and this morning he began having labored breathing. On physical examination, the lethargic and ill-appearing boy has visibly labored breathing with seesaw respirations. His temperature is 37.0°C, heart rate is 140 beats/min, respiratory rate is 36 breaths/min, blood pressure is 140/90 mm Hg, and pulse oximetry reading is 88% on a 100% nonrebreather mask. The boy follows simple commands but is unable to speak; he answers yes or no questions with head movement. He has pooling secretions, a weak cough, and no gag reflex. Neurologic examination reveals absence of lateral gaze bilaterally, generalized weakness, and absence of reflexes. He has coarse rhonchi bilaterally, extremely labored respirations with paradoxic chest/abdomen wall motion, and poor air exchange. Cardiovascular examination documents tachycardia, but there are no murmurs, gallops, or rubs, and pulses are strong throughout. The remainder of the examination findings are within normal parameters.Of the following, the MOST appropriate next step is to perform:A.arterial blood gasB.continuous albuterolC.lumbar punctureD.negative inspiratory force measurementE.rapid sequence intubationCorrect answer EThe boy described in the vignette has severe respiratory distress and respiratory failure as a result of neurologic compromise and respiratory muscle weakness. He was ultimately diagnosed with the Miller Fisher variant of Guillain-Barré syndrome. Determination of the cause of his neurologic dysfunction should not take priority over recognition and management of his compromised respiratory status, making rapid sequence intubation the immediately needed procedure. Magnetic resonance imaging and lumbar puncture may be indicated but should not precede appropriate airway management.? Although arterial blood gas measurement may be a part of this patient’s ongoing evaluation and treatment, the presence of hypoxia despite high-flow oxygen, inability to protect his airway, and significantly altered respiratory mechanics mandates emergent airway management. The presence or absence of laboratory evidence of respiratory failure, including hypercarbia, respiratory acidosis, and hypoxemia, would not alter initial management in this case. Negative inspiratory force measurement can be used to confirm or monitor respiratory muscle weakness, but it is not necessary or indicated in a child who has the obvious findings of respiratory failure. The patient has no evidence of bronchospasm to indicate the need for albuterol therapy.The primary goals of respiration are to provide adequate oxygen to meet the metabolic demands throughout the body and to eliminate carbon dioxide. This is accomplished through the complex interplay of multiple different systems. Receptors that sense chemicals, stretch, irritation, and pressure from various sites send and receive signals that lead to changes in respiratory rate and effort, vascular tone, and other actions to alter oxygen and carbon dioxide exchange. Multiple organs, tissues, and systems are involved in the control of respiration, and illness or injury to any of the components in this complex system can result in respiratory distress (Table 1?and Table 2). Disorders outside of these systems can also lead to secondary disruption of respiratory function. Injuries can result from trauma, infection, inflammation, structural abnormalities, compression, or obstruction. Systems that can directly or indirectly affect respiratory mechanics or gas exchange include:Upper airwaysLower airwaysLung parenchymaCardiovascular systemCentral nervous systemPeripheral nervous systemChest wallGastrointestinal tract/abdomenMetabolic/endocrine systemHematologic systemFailure to recognize and appropriately address respiratory distress can allow progression to respiratory failure, which can proceed to cardiopulmonary arrest if not rapidly treated. The higher metabolic demand in pediatric patients results in greater oxygen consumption and more rapid development of tissue hypoxia in the setting of respiratory distress. The pediatric patient compensates for such increased oxygen demand, leading to progressive signs and symptoms, including (from early to late):TachypneaTachycardiaNasal flaring and retractionsPallorAgitation/anxietyFatigueAltered mental statusCyanosisComaApneaBradycardiaThe initial approach to a patient who has respiratory distress includes a rapid assessment of the patency of the child’s airway, effectiveness of breathing (effort, air entry, breath sounds, respiratory rate, and pulse oximetry), pulses, and perfusion. If the child’s airway is compromised or cannot be maintained through noninvasive means, as with the boy in the vignette, endotracheal intubation should be performed immediately. If the airway is patent or can be maintained through positioning, suctioning, oropharyngeal or nasopharyngeal airway placement, or noninvasive positive pressure ventilation, oxygen should be administered and evaluation directed at identifying and treating the underlying cause of the respiratory distress.History and physical examination findings should guide the diagnostic evaluation, which may include laboratory, radiographic, microbiologic, or procedural tests (Table 3). Continued monitoring and reassessment of the patient’s vital signs and cardiorespiratory status are indicated to identify worsening of respiratory distress or progression to respiratory failure. Pulse oximetry should be included routinely with assessment of vital signs. When available, capnography can aid in the early identification of respiratory failure.Respiratory failure is defined as inadequate oxygenation or ventilation, but confirmation of the degree of hypoxemia or hypercarbia by blood gas analysis is not necessary or readily available in many cases. Clinical signs such as altered mental status, decreased respiratory effort or air exchange, bradycardia, cyanosis, or apnea are indications for emergent intervention to prevent cardiopulmonary arrest.American Board of Pediatrics Content Specification(s)Differentiate by age the etiology and understand the pathophysiology of respiratory distressPlan diagnostic evaluation and initial intervention for patients with respiratory distressRecognize serious and/or life-threatening causes of respiratory distressQuestion: 6The mother of an 11-year-old boy who has autism, asthma, and morbid obesity finds the boy unresponsive in his bedroom. She calls 911, and emergency medical services personnel bring him to the emergency department. On arrival, the boy has a diminished level of consciousness, moans to painful stimuli, and does not speak. His mother reports that he had increased thirst and bedwetting for the past 2 weeks and nausea, emesis, and “feeling warm” for the past 3 days. On physical examination, his temperature is 37.2°C, heart rate is 130 beats/min, respiratory rate is 28 breaths/min, blood pressure is 92/42 mm Hg, and oxygen saturation is 100% on supplemental oxygen. He has no signs of cranial trauma, and his pupils are 2 mm and equally reactive to light. His mucous membranes are dry. Cardiovascular examination reveals tachycardia without murmur or gallop, his lungs are clear to auscultation, and his extremities are cool with hyperpigmentation of the axillary regions. Initial laboratory results are:pH, 6.95Pco2, 25 mm HgPo2, 55 mm HgBicarbonate, 6 mEq/L (6 mmol/L)Glucose, 887 mg/dL (49.2 mmol/L)Sodium, ?130 mEq/L (130 mmol/L)Blood urea nitrogen, 50 mg/dL (17.9 mmol/L)Potassium, ?5.7 mEq/L (5.7 mmol/L)Chloride, 101 mEq/L (101 mmol/L)Urine ketones, largeUrine glucose, 4+Total leukocyte count, ?32x103/μL (32x109/L)Hemoglobin, 15 mg/dL (150 g/L)You initiate emergent management and begin formulating further treatment.Of the following, the intervention MOST likely to exacerbate this patient’s condition is administration ofA.ceftriaxoneB.insulin infusionC.naloxoneD.saline bolusE.sodium bicarbonateCorrect answer EThe findings described for the boy in the vignette most strongly suggest the diagnosis of diabetic ketoacidosis (DKA). Cerebral edema (CE) is a serious complication of DKA and may be present at the initial presentation or develop during the early course of treatment. In a population-based, 15-year multicenter study comparing patients with CE and matched controls, sodium bicarbonate administration was significantly associated with the development of CE (relative risk 4.2; 95% confidence interval, 1.5 to 12.1; P=0.008). Other risk factors for development of CE include younger age (especially <5 years), severity of acidosis, degree of hypocapnia, and elevated serum urea nitrogen. Several studies also suggest an increase in risk of CE when serum sodium fails to increase appropriately during treatment of DKA. Volume or tonicity of fluids, rate of decrease in blood glucose, or insulin infusion has not been associated with CE. Marked leukocytosis is frequently observed in severe DKA and may represent a response to metabolic stress rather than infection. Expectant parenteral ceftriaxone does not complicate the management of this patient. Similarly, empiric administration of naloxone for suspected opiate overdose does not affect the course of illness for this patient.DKA results from absolute or relative deficiency of insulin in combination with excessive stimulation of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). This causes impaired glucose use in insulin-sensitive tissues (liver, fat, and muscle), gluconeogenesis in liver and kidney, protein breakdown, lipolysis, and fatty acid breakdown to ketone bodies. This cascade of derangement progresses to ketoacidosis and dehydration.The typical signs and symptoms of uncontrolled hyperglycemia and DKA include polyuria and polydipsia. In a previously undiagnosed patient, such as the boy described in the vignette, nocturnal enuresis in a child who was previously continent at night should raise suspicion of diabetes. There may also be a history of recent weight loss. One symptom of respiratory compensation of metabolic acidosis is a pattern of deep and slow breathing (Kussmaul breathing). Affected patients may also experience chest pain or subjective dyspnea.? Some patients present with abdominal pain and vomiting. Patients in DKA demonstrate moderate-to- severe dehydration due to fluid losses from osmotic diuresis or emesis.CE is the most serious common complication of DKA in pediatrics. Warning signs of CE are recurrent or more severe headache, inappropriate slowing of heart rate not attributable to rehydration or sleep, recurrence of vomiting following initial treatment, change in neurologic status, rising blood pressure or decreased oxygen saturation, and abnormal neurogenic respiratory pattern. CE is a clinical diagnosis, and 40% of initial cranial computed tomography scans appear normal. Prompt recognition and treatment with IV mannitol, reduction in rate of IV fluid administration, elevation of the head of bed, and intubation for airway or respiratory compromise are important. If deterioration continues, 5 mL/kg of 3% saline may be administered rapidly. Other complications of DKA include hypokalemia, hypophosphatemia, hypoglycemia, cerebral venous thrombosis with or without associated CE, peripheral venous thrombosis, mucormycosis, aspiration pneumonia, rhabdomyolysis, acute pancreatitis, and acute renal failure.The following are general principles of fluid and insulin treatment in DKA:Restore perfusion, which will increase glucose uptake in the periphery, increase glomerular filtration, and reverse progressive acidosis. A rapid decline in blood glucose should follow initial hydration. Fluid replacement begins with 0.9% saline to restore circulation, followed by administration of 0.45% saline for maintenance and replacement of 5% to 10% dehydration, according to severity indicators.Arrest ketogenesis with insulin administration at 0.1 U/kg per hour after initial fluid expansion to reverse proteolysis and lipolysis while stimulating glucose uptake and utilization, thereby normalizing blood glucose concentrations. Because of the very short half-life of insulin, a bolus dose is not effective.To prevent an unduly rapid decline in blood glucose and subsequent hypoglycemia, add 5% glucose to the IV fluids when the blood glucose is approximately 300 mg/dL (16.7 mmol/L). An efficient method of glucose delivery that avoids the long delays associated with ordering fresh bags of fluids is the “two bag system.” One bag contains dextrose and appropriate sodium and potassium concentrations and the other bag contains the same sodium and potassium concentrations without dextrose.Replace electrolyte losses. Whether serum potassium concentrations are normal or elevated, a total body potassium deficit must be addressed early and sufficiently with potassium phosphate and potassium acetate or potassium chloride. Serum sodium concentrations are not reliable indicators of extracellular fluid deficit because of the osmotic effect of hyperglycemia-induced dilutional hyponatremia (pseudohyponatremia). Corrected sodium can be estimated by adding 1.6 mEq (1.6 mmol) to the measured value for every 100 mg/dL (5.6 mmol/L) blood glucose above normal.American Board of Pediatrics Content Specification(s)Recognize signs and symptoms of diabetic ketoacidosisPlan the management of acute diabetic ketoacidosisUnderstand the pathophysiology of diabetic ketoacidosisRecognize the life-threatening complications of diabetic ketoacidosisQuestion: 7A 25-month-old girl is brought to the emergency department 4 hours after ingesting an unknown number of prenatal vitamins containing ferrous sulfate. She has vomited several times and has had 1 loose stool. The alert child is holding her stomach and crying. On physical examination, her temperature is 37.3°C, respiratory rate is 30 breaths/min, heart rate is 136 beats/min, and blood pressure is 82/50 mm Hg.Of the following, the laboratory test that is MOST reliable in predicting her risk of developing severe toxicity isA.blood glucoseB.serum bicarbonateC.serum ironD.total iron-binding capacityE.white blood countCorrect answer CAccidental iron ingestion was one of the most common causes of fatal ingestions in children as recently as the 1990s. Improved safety measures and increased awareness of the potential adverse outcomes of iron toxicity have led to a dramatic decrease in associated childhood fatalities. Although a significant number of pediatric iron ingestions occur each year in the United States, fatalities and significant morbidity are rare.When assessment of serum iron concentrations was not widely available in most clinical laboratories, other ancillary tests were used in an attempt to predict which child who had ingested iron had a significant ingestion and was at risk for severe toxicity. However, serum iron is the single best laboratory test in the diagnosis and management of acute iron poisoning in children. A serum iron value greater than 500 ?g/dL (89.5 ?mol/L) obtained 4 or more hours after ingestion is predictive of an increased risk of complications.Elevated blood glucose values are neither sensitive nor specific in predicting severe poisoning. Metabolic acidosis is a major part of the presentation of children during phase III of iron toxicity, but serum bicarbonate concentrations are not as sensitive as serum iron early after the ingestion. If present, acidosis is worrisome for impending development of severe disease. Assessment of metabolic acidosis and hepatic function are helpful in the management of supportive care when children are sick.Total iron-binding capacity (TIBC) is no longer believed to be reliable in predicting iron toxicity. Its measurement is not accurate in the presence of excess serum iron or deferoxamine (the antidote for iron poisoning). Significant iron toxicity has been reported even when measured TIBC exceeds the measured serum iron concentration. White blood cell count is neither sensitive nor specific in predicting toxicity.Early iron toxicity is due to the direct irritant effect of the iron on the gastrointestinal (GI) tract. Mucosal necrosis can occur in the stomach and throughout the small intestine. Excess free iron is believed to act as a mitochondrial poison, which accounts for the effects seen several hours to days after the ingestion. The most severe of these effects are seen in the liver.As little as 20 mg/kg of ingested elemental iron has been associated with toxicity in children. Ingestions of greater than 50 mg/kg almost always produce toxic effects. Predicting the ingested dose can be difficult. Prenatal vitamins, ferrous sulfate tablets, and children’s chewable vitamins with iron are all common sources of iron ingestion in children. A typical bottle of children’s chewable multivitamins may contain as much as 1,200 mg of elemental iron.Authors divide the clinical signs and symptoms of iron ingestion into four or five phases. Phase I, as seen in the child in the vignette, is due to the mucosal injury caused by iron in the GI tract. Vomiting, diarrhea, abdominal pain, and GI blood loss are common. In very large ingestions, volume depletion and metabolic acidosis may quickly ensue, and the child may develop shock and obtundation. This phase usually lasts up to 6 hours after the ingestion.After about 6 hours, the GI symptoms frequently improve and phase II, a latent phase, may occur. During this period of 6 to 24 hours, the child may appear relatively well. If the ingestion is minor, the child may recover without other symptoms or complications. This phase is not seen in all cases. In the case of significant ingestions, recovery is temporary, and phase III ensues, which is characterized by metabolic acidosis, coma, seizures, shock, and circulatory collapse. Lactic acid accumulates and there is a large anion gap. Phase III usually begins about 12 to 24 hours after the ingestion but may have a more rapid onset when large amounts of iron are ingested.Hemodynamic instability is believed to be due to direct effects of iron on the heart, causing negative inotropy, intravascular depletion, and an inability to increase peripheral vascular resistance. Coagulopathy results from hepatic dysfunction, disseminated intravascular coagulation, and the direct effects of free iron on the coagulation cascade, including the inhibition of thrombin. In addition to inhibition of oxidative phosphorylation, lactic acid is also generated through continued poor perfusion.Within 2 days, severe hepatic toxicity may ensue. This has been termed phase IV by some authors and is usually only seen in cases involving very high serum iron concentrations (>700 ?g/dL [125.3 ?mol/L]). When this occurs, the toxicity is more severe than that seen with acetaminophen poisoning.Among patients who recover, late complications begin to appear 3 to 6 weeks later. This has usually been termed phase IV and is characterized by scar formation in the GI tract, with pyloric outlet obstruction, strictures, and fistulas due to the mucosal damage that occurred early in the course of the ingestion. The gastric outlet is the most commonly affected area. Intestinal obstruction, abdominal pain, and persistent problems may be seen.Significant iron ingestions are managed best in consultation with an expert in pediatric toxicology. Consultation can be obtained through regional poison control centers. Treatment of iron toxicity depends on the symptomatic presentation, serum iron values after 4 hours, the presence of iron pills on abdominal radiographs, and the acid–base status of the patient. Iron is radiopaque, and pills or tablets containing iron may be visible on radiographs. Although the absence of iron pills on abdominal radiographs does not exclude the possibility of toxicity, their presence is an indication to begin treatment. Abdominal radiographs can also help direct ongoing decontamination with whole bowel irrigation (WBI).Aggressive therapy must be started as soon as possible for patients who present with severe symptoms, such as lethargy, poor perfusion, hypotension, GI bleeding, or severe and/or protracted vomiting or diarrhea. Two large-bore intravenous catheters should be placed and aggressive fluid resuscitation begun. If intravenous access cannot be obtained, intraosseous lines can be placed. Abdominal radiographs, serum iron, complete blood count, coagulation profile, hepatic function tests, basic metabolic profile, and a blood gas should be obtained. In patients with significant bleeding, blood typing and cross-matching should be undertaken.Supportive measures, including fluid resuscitation and management of acidosis, should be started immediately. Specific treatment should not wait for results of laboratory tests. Intravenous deferoxamine and WBI with an osmotically neutral solution (eg, polyethylene glycol) should be started as soon as possible. No controlled trials provide information about the appropriate duration of antidotal therapy. Deferoxamine has been continued until the “vin rose” color of the urine clears or the child shows no signs or symptoms of iron toxicity for 24 hours. Some authors suggest continuing deferoxamine until the serum iron concentration has decreased to normal. Deferoxamine has been associated with hypotension, which seems to be related to the rate of infusion. Acute respiratory distress syndrome has also been reported, especially in adults. Because this seems to be associated with longer courses of treatment, suggestions have been made not to continue deferoxamine therapy for greater than 24 hours.WBI should be continued until there is a clear effluent per rectum. If significant iron load is demonstrated on abdominal radiographs, clearance also should be documented on these images. WBI usually is administered through a nasogastric tube. Protection of the airway with endotracheal intubation may be necessary in patients who have marked lethargy or present in shock.For patients who have milder GI symptoms, treatment can be based on initial laboratory and radiologic evaluation. The presence of iron pills on abdominal radiographs, acidosis on laboratory evaluation, or a serum iron concentration greater than 500 ?g/dL (89.5 ?mol/L) 4 hours or more after ingestion are indications for beginning treatment with deferoxamine and WBI. In the absence of these findings, children should be observed for at least 6 hours after ingestion. If further symptoms do not develop and the serum iron value is less than 500 ?g/dL (89.5 ?mol/L), the child can be safely discharged.American Board of Pediatrics Content Specification(s)Recognize signs and symptoms of iron poisoningRecognize and interpret relevant laboratory and monitoring studies for iron poisoningPlan the management of acute iron toxicity, including special issues in the pregnant patientQuestion: 8A 16-year-old boy presents to the emergency department with complaints of nasal pain and swelling of 48 hours’ duration. He had sustained a facial injury with epistaxis and nasal swelling when he fell from his dirt bike 2 weeks ago. Today he has purulent nasal discharge, fatigue and malaise, and temperature up to 38.6°C. Physical examination reveals nasal tenderness with overlying erythema. In addition, he has a bilaterally swollen nasal septum with overlying excoriation, redness, and purulent discharge from the left nares.Of the following, the BEST management strategy for this patient isA.nasal discharge Gram stain/culture and oral antibioticsB.nasal discharge Gram stain/culture and systemic antibioticsC.nasal septal aspiration, Gram stain/culture, and oral antibioticsD.nasal septal incision and drainage, Gram stain/culture, and oral antibioticsE.nasal septal incision and drainage, Gram stain/culture, and systemic antibioticsCorrect answer EThe patient described in the vignette has a nasal septal abscess for which the universal treatment consensus is immediate incision and drainage, systemic antibiotics, and early nasal septal reconstructive surgery. Nasal septal abscess is a frequent complication of untreated nasal septal hematoma. Seventy percent of these infections are caused by Staphylococcus aureus. This is a surgical emergency; failure to drain the abscess in a timely manner may result in nasal septal necrosis, cavernous sinus thrombosis, permanent nasal deformity, and delayed facial growth. Therefore, if a patient presents with purulent nasal discharge, it is imperative to rule out nasal septal abscess, especially with a recent history of nasal trauma.Aspiration of the nasal septum does not prevent reaccumulation of pus. Although Gram stain of the purulent discharge may help to identify the causative agent, antibiotics alone (either systemic/oral) do not prevent the complication of nasal septal necrosis. After incision and drainage, systemic antibiotics are indicated until nasal inflammation improves.Nasal discharge is generally composed of mucus glycoprotein (from epithelial cells) and plasma protein (from dilated blood vessels). Further changes in nasal discharge may be due to inflammatory cells, including lymphocytes, eosinophils, plasma cells, or neutrophils, depending on the cause of the discharge. Sneezing results from stimulation of the sensory nerves by the secretions. Various factors can increase nasal discharge:Allergens (eg, pollen, dust)Environmental factors (eg, cold, chemical, smoke exposure)Infectious agents (viruses, bacteria, fungus)Medications (eg, antihypertensives, oral contraceptives, antidepressants)Increase in parasympathetic toneHormones (pregnancy)Foreign body Systemic/local illness (eg, cystic fibrosis, Wegener granulomatosis, hypothyroidism, leukemia, ciliary dyskinesia)The Table?summarizes the varied types of nasal discharge and clinical associations. Viral rhinosinusitis remains the primary cause of nasal discharge and can be managed conservatively with saline nasal drops, humidification, and pain control. Antibiotics are indicated only if the symptoms meet the criteria for bacterial rhinosinusitis. An index of suspicion is required to identify unusual causes and plan the appropriate diagnostic evaluation. For example:Discharge in a neonate should raise the suspicion of anatomic obstructions such as choanal atresia that can be diagnosed by passing a nasal catheter to assess for patency.Purulent, foul-smelling, unilateral discharge should raise the suspicion of a foreign body.Recurrent serious bacterial infections such as pneumonia should raise the suspicion of immune deficiency and requires appropriate blood investigations.Nasal steroids or oral antihistamines are helpful and diagnostic for suspected allergic rhinitis; nasal secretion analysis and skin testing is not mandatory in such cases.Wegener granulomatosis can present with constant serosanguinous nasal discharge, cough, hemoptysis, sinusitis, ear infections, and microscopic hematuria and can be diagnosed by nasal biopsy.Nasopharyngeal cancer can present in an adolescent as recurrent new-onset epistaxis with or without facial swelling and is diagnosed via facial computed tomography scan.American Board of Pediatrics Content Specification(s)Differentiate by age the etiology and understand the pathophysiology of nasal dischargePlan diagnostic evaluation and initial intervention for patients with nasal dischargeJULY 2012Question: 1A 6-year-old girl presents to a community hospital emergency department with fever and rash. Within hours, she has deteriorated and is obtunded. After clinicians administer antibiotics, the child becomes hypotensive. Fluid resuscitation and low-dose dopamine establish a more normalized blood pressure. The community hospital has a pediatric unit (which can administer and monitor low-dose dopamine) and a general, mostly surgical, intensive care unit (ICU). A larger community hospital that has a more medically oriented ICU is 40 minutes away by ambulance, a pediatric tertiary care hospital is 1 hour away by helicopter, and a combined adult/pediatric level I trauma center is 35 minutes away by helicopter. The treating hospital has an ambulance service (basic and advanced life support), and a general helicopter service located in the community is available in 60 minutes.Of the following, the MOST appropriate disposition for this child isA.admission to the pediatric floor with a pediatric attendingB.longer flight to the pediatric centerC.shorter flight to the adult/pediatric trauma centerD.transfer to the general ICU with a surgical critical care specialist and pediatric consultationE.transfer to the larger community hospital with a pulmonary/critical care trained medical intensivistCorrect Answer: BThe child described in the vignette is clearly critically ill, and she has experienced substantial deterioration in the emergency department. Ongoing and perhaps escalating critical care is required. General pediatric capabilities are already exceeded, and the current hospital is not optimal for specialized pediatric critical care. The larger community hospital might be appropriate for temporization, but the availability of pediatric critical care medical and nursing expertise is preferred. The adult/pediatric trauma center likely has pediatric critical care capabilities, but it probably focuses on trauma. The pediatric tertiary care center is the regionalized resource for a critically ill patient and is the optimal choice for this child.Ideally, critical care or emergency medicine experts from the pediatric facility would have been consulted early in the care of this patient, as soon as the limited capabilities of the initial institution or clinicians were recognized or the available expertise was exceeded. Although extenuating circumstances may prohibit direct transfer to the pediatric tertiary care facility (eg, weather, helicopter availability), use of the regional experts to help guide care and determine an optimal temporization plan and location is in the best interest of both the patient and the clinicians.Regionalization is an important concept in the cost-effective and high-quality delivery of pediatric specialty services. It is designed to direct the correct patients to the system/institutions with appropriate resources (ideally, with significant experience and less variation) to manage their specialized needs. This can be especially critical for emergent, time-sensitive conditions such as pediatric emergency care, critical care, cardiac, trauma, toxicologic, and other specialty services. Epstein describes regionalization as the right resources (materials, personnel, and knowledge), the right patient, and the right time within a ernmental and medical organizations have recommended identification and categorization of specific capabilities of emergency departments, hospitals, and emergency care, a process that has met with variable success. Confounders to success include lack of agreed-upon (or in some cases, evidence-based) categorization, funding, managed care, local hospital issues, and clinician preferences.Ideally, such systems are cooperative, rather than competitive, to enable flow of patients to the most appropriate care without regard for financial impact to a particular facility or system. All regionalized care need not take place at a single institution; it can be within a cooperative network to ensure experienced and expert care for the particular patient issue. Regionalization can have a positive impact on specialty care availability. For example, not all communities have access to pediatric neurosurgery or cardiology, but the regional plan would have those services available to the region within a particular area. All regionalization is not based on acuity. Regionalization for general care, including specialties such as cardiology, dermatology, and obstetrics, enable patient choice as part of the process.Pediatrics has long-standing experience with acute and critical care regionalization in neonatal and trauma care. Cardiac-capable centers are often regionalized in adult medicine. Stroke regionalization opportunities are being identified for hospitals and systems, with development of stroke-capable centers. Pediatric critical care transport services have been developed, often in conjunction with pediatric regional centers, to enable critical care services to come to the patient rather than waiting for the critically ill or injured patient to present to the site of regionalization. Clear communication criteria and efficient access to experts at the regional centers can help bring the benefits of regional care to the bedside at the referral centers. Telemedicine may improve the joint care delivered in these situations as it becomes more available.American Board of Pediatrics Content Specification(s)Understand the role of regionalization of special-care receiving hospitals (eg, pediatrics, trauma, pediatric critical care)Question: 2A 5-year-old boy is brought to the emergency department for wheezing and abdominal pain. While awaiting the doctor, he experiences profuse emesis and diarrhea. On physical examination, the afebrile child is in moderate respiratory distress and has a heart rate of 72 beats/min, respiratory rate of 20 breaths/min, and blood pressure of 120/82 mm Hg. He is somnolent and has copious secretions and bibasilar rales. His pupils are 1 mm bilaterally but react minimally to light. The boy is diffusely weak, with occasional fasciculations. Deep tendon reflexes are difficult to elicit.Of the following, the MOST likely diagnosis isA.acute intermittent porphyriaB.acute lead poisoningC.botulismD.Guillain-Barré anophosphate poisoningCorrect answer EThe boy described in the vignette is in obvious distress, with copious secretions, acute bronchospasm, miosis, relative bradycardia, vomiting, and diarrhea. In the absence of fever, such findings point toward a toxin exposure with cholinergic excess. The weakness and fasciculations are manifestations of a lower motor neuron process (neuropathy). This presentation is classic for organophospate compound (OPC) toxicity, in which cholinesterase is inhibited and excess acetyl choline is produced at the preganglionic muscarinic receptors (cholinergic effector cells), at nicotinic receptors (skeletal neuromuscular junction and autonomic ganglia), and in the central nervous system (CNS).Guillain-Barré syndrome presents with ataxia, acute ascending paralysis, areflexia, and sometimes facial weakness. Botulism has an acute onset and manifests as a descending paralysis that begins with cranial neuropathies and hyporeflexia. Lead poisoning can cause vomiting, abdominal pain, and constipation, but the neuropathy is chronic. Porphyria can resemble OPC poisoning, with vomiting, abdominal pain, diarrhea or constipation, hypotonia, weakness, seizures, neuropathy, and areflexia. However, miosis, bradycardia, and bronchorrhea are not observed in any of these other conditions that produce neuropathic weakness.Signs and symptoms (Table) usually occur within 1 to 2 hours of OPC exposure, but their presentation may be delayed up to 6 to 8 hours, especially after skin exposure. The key features can be recalled with the mnemonic “SLUDGE-BM.” The cause of death in acute OPC exposure is usually respiratory failure from a combination of factors that includes increased pulmonary secretions, respiratory muscle weakness, and decreased respiratory drive from CNS depression. Diagnosis is based on history of exposure and the characteristic toxidrome. A solvent odor of OPC diluents frequently is present. The diagnosis can be confirmed with decreases in plasma pseudocholinesterase and red blood cell acetyl cholinesterase activity. However, results of these tests are usually delayed and not helpful in clinical management.Management of OPC toxicity involves careful attention to maintaining the airway and assisted ventilation, as necessary. In addition, treatment of hydrocarbon pneumonitis, seizures, and coma should be initiated as they occur. Specific antidotal therapy includes the antimuscarinic agent atropine and enzyme reactivator pralidoxime (2-PAM). Atropine in large cumulative doses may be required in severe cases. The most clinically important indication for continued administration is persistent wheezing or bronchorrhea. A common pitfall during management is delivery of inadequate doses of atropine. Adequacy of atropine dosing can be assessed by dry mouth, flushing, and dilated pupils. Atropine does not reverse the nicotinic effects, as noted in the child in the vignette. 2-PAM is a specific antidote that acts to regenerate enzyme activity at all affected sites. It is most effective if administered within 24 hours of exposure and before irreversible phosphorylation of the enzyme. A prospective study in an Egyptian hospital that specializes in poisonings showed that symptoms can occur rapidly in children. Hence, early triage is important. The initial presence of miosis or diarrhea predicts a complicated course.The threat of using chemical compounds by terrorists as weapons of mass casualties (eg, sarin gas attack in a Tokyo subway) is an increasing concern. ?Carbamates are a group of reversible acetyl cholinesterase inhibitors that could be involved in such toxic mass casualty events because they can cause fatal cholinergic crisis, similar to that of OPC poisoning. According to an algorithm (Figure) proposed in an Israeli article, treatment should consist of atropine and 2-PAM, regardless of the exact toxic compound involved. The authors speculated that the benefits in mass casualties justify the small risk (eg, respiratory cardiac arrest if administered to rapidly intravenously, laryngospasm, hypertension, and visual difficulties) of empiric administration of pralidoxime.American Board of Pediatrics Content Specification(s)Recognize signs and symptoms of organophosphate or nerve agent exposurePlan the management of acute organophosphate exposureQuestion: 3A 12-month-old girl arrives in your emergency department with her mother, who is concerned because her daughter has had a fever all day and is very tired.? The mother has been at work today and upon returning home, the teenaged cousin who was watching the infant informed the mother that the baby had slept all day. On physical examination, the infant has a temperature of 40.2°C, heart rate of 198 beats/min, respiratory rate of 38 breaths/min, blood pressure of 80/24 mm Hg, and pulse oximetry reading of 95% in room air. The child is minimally responsive to painful stimulation and barely moves when nurses place 22-gauge intravenous (IV) lines in both arms. The infant has a diffuse petechial rash over her trunk and limbs, her skin is flushed, and she has bounding pulses and a capillary refill of less than 1 second. You direct the team to begin rapid IV fluid boluses as well as IV cefotaxime. After administration of 60 mL/kg of normal saline, the child remains lethargic. Her heart rate is 196 beats/min, respiratory rate is 38 breaths/min, blood pressure is 78/22 mm Hg, and pulse oximetry reading is 96% in room air. You obtain central venous access, order a dopamine infusion, and prepare to place an arterial line.Of the following, if the perfusion does not improve, the MOST appropriate additional therapy for this patient isA.dobutamine infusionB.fresh frozen plasma transfusion 10 mL/kgC.norepinephrine infusionD.packed red blood cell transfusion 10 mL/kgE.phenylephrine infusionCorrect answer CThis infant described in the vignette is in a state of warm septic shock and has not improved after appropriate fluid boluses and the first-line vasopressor medication, dopamine. Norepinephrine is primarily a peripheral vasoconstrictor and has minimal inotropic effect. For the patient in warm shock, it redirects blood flow to the brain and viscera.?Treatment of shock in the pediatric patient begins with recognition of the shock state. Shock is defined by tachycardia with signs of decreased perfusion: altered mental status, weak pulses, prolonged capillary refill, mottled or cool extremities, or poor urine output. Most cases of shock in pediatrics are caused by depletion of or inappropriate distribution of intravascular volume. Regardless of cause, initial therapy is rapid administration of intravenous fluids. For hypovolemic shock (due to dehydration or traumatic blood loss), replacement of volume with crystalloid fluids or blood products and treatment to stop ongoing losses should suffice. Similarly, international guidelines recommend treatment of septic shock with at least three crystalloid fluid boluses (20 mL/kg) before initiating vasoactive medications.? For children who have septic shock resistant to at least three fluid boluses, American College of Critical Care Medicine guidelines recommend dopamine as the first vasopressor agent, followed by norepinephrine for warm shock (flushed, brisk capillary refill) or epinephrine for cold shock (prolonged capillary refill) (Table). In less commonly encountered shock physiology, such as anaphylaxis, cardiac failure, or neurogenic shock, vasoactive medications may be indicated earlier. Epinephrine should be used early after recognition of anaphylactic shock. Dobutamine, dopamine, or milrinone might be used to support cardiac output or reduce afterload in children who have cardiogenic shock. Phenylephrine may be used to support mean arterial pressure, thus protecting cerebral perfusion, in children who have shock and acute traumatic brain injury.?Children requiring vasoactive infusions should have intravascular blood pressure monitored, usually with an arterial line, to allow titration of the drip. The most commonly used site is the radial artery, but the dorsalis pedis, posterior tibial, femoral, and axillary arteries may also be used. The brachial artery should be avoided due to lack of collateral circulation. After cannulation of the artery, transmission of pressure along the resulting column of fluid from the blood vessel to the transducer allows immediate and continual monitoring of changes in arterial pressure, including pulse waveform, and measurement of pulsus paradoxus. Mechanical error is common, and the transducer must be appropriately zeroed to atmospheric pressure and kept at the level of the heart. Readings will be falsely high if the transducer is placed below the heart level or falsely low if the transducer is lifted above the level of the heart.? Potential complications of arterial cannulation include ischemia, bleeding, infection, nerve damage, accidental injection of hypertonic solutions, and air embolism. Central venous pressure (CVP) monitors are placed inline on central venous catheters and are commonly used in children who have shock to monitor volume status. CVP technically describes the preload to the right ventricle at the end of diastole. CVP monitors are even more sensitive to zeroing and level changes than the arterial pressure transducer and may be affected by intrathoracic or intra-abdominal pressure changes. Potential complications of CVP monitoring are those of central vein cannulation, primarily infection and thrombosis.Blood products are infrequently required in the emergency department resuscitation of children who have shock not due to acute hemorrhage. Packed red blood cells or whole blood transfusion are clearly indicated for children whose shock is caused by acute blood loss. Advanced Trauma Life Support guidelines recommend transfusion of red cell-containing products if shock is not corrected after three boluses of isotonic fluids (normal saline or lactated Ringer solution). Children who have shock and coincident anemia also may benefit from transfusion of red blood cell products. A hemoglobin value of at least 8 to 10 g/dL (80 to 100 g/L) is recommended to maximize oxygen-carrying capacity in patients who have severe sepsis or poor cardiac contractility. Point-of-care testing may be useful in guiding transfusion therapy. Those who have active bleeding or disseminated intravascular coagulation (DIC) may require replacement of clotting factors. Fresh frozen plasma can be used to correct most coagulation factors, but cryoprecipitate contains significantly more fibrinogen than whole blood or fresh frozen plasma. Cryoprecipitate infusion is more likely to provide the fibrinogen replacement needed for patients who have DIC in whom goal fibrinogen values should be greater than 100 mg/dL (2.94 μmol/L). Platelet transfusions are indicated to maintain platelet counts of at least 40 to 80x103/μL (40 to 80x109/L) for patients who have DIC or ongoing bleeding due to thrombocytopenia. For children who have active bleeding that cannot otherwise be controlled, activated factor VII infusion may be indicated as an adjunct to achieve hemostasis.American Board of Pediatrics Content Specification(s)Know the role of pharmacologic therapy for circulatory failure/shockKnow the indications for/complications of various invasive monitoring devices for shockKnow the role of blood product infusion in the management of shockQuestion: 4A 6-year-old girl presents for evaluation of persistent and worsening right neck swelling and a “mass” in her throat, which began more than 2 weeks ago. She was recently admitted to the hospital for treatment of a suspected deep neck space infection and was discharged with a prescription for clindamycin. Her mother reports that the swelling has increased significantly in the past 2 days despite the antibiotics. The child complains of a lump in her throat and difficulty swallowing. She has had no fever, pain, skin redness or changes, upper respiratory tract infection symptoms, sore throat, nausea, vomiting, or diarrhea. She has had decreased oral intake, weight loss, and fatigue. On physical examination, the girl’s vital signs are within normal range for age. She has a 4+ right tonsil pushing the uvula toward the left; the left tonsil is 1+. There is no erythema, exudate, or palatal swelling. Neck examination reveals firm, fixed, nontender swelling in the anterior and posterior cervical area on the right without overlying erythema, warmth, or fluctuance. The remainder of her examination findings are normal. Laboratory results reveal:White blood cell count, 6.9x103/?L (6.9x109/L) with 59% neutrophils, 30% lymphocytes, 8% monocytes, 2% eosinophils, and 1% basophilsHemoglobin, 11.9 g/dL (119 g/L)Hematocrit, 34% (0.34)Platelet count, 254x103/?L (254x109/L)Sodium, 135 mEq/L (135 mmol/L) Potassium, 3.6 mEq/L (3.6 mmol/L)Blood urea nitrogen, 12 mg/dL (4.3 mmol/L)Creatinine, 0.5 mg/dL (44 ?mol/L)Glucose, 81 mg/dL (4.5 mmol/L)C-reactive protein, <5 mg/L (0.5 mg/dL)You obtain computed tomography (CT) scan of her neck (Figure 1 and Figure 2).Figure 1Sagittal CT scan of the patient’s neckFigure 2Of the following, the test MOST likely to reveal the cause of the girl’s symptoms isA.biopsy of the right neck lesionB.culture of fluid aspirated from the right peritonsillar spaceC.purified protein derivative tuberculin testD.serum Bartonella henselae titersE.thyroid function testsCorrect Answer: AThe girl described in the vignette has findings concerning for a malignant process, including lack of infectious/inflammatory signs and symptoms, continued enlargement despite treatment with antibiotics, the fixed nature of the mass, and the extent/size of the lesion. Accordingly, biopsy of the lesion is the most appropriate next step and in this case revealed malignant tissue consistent with Burkitt lymphoma. Peritonsillar abscess and cellulitis, which could be diagnosed with culture of aspirated fluid, are typically seen in adolescents and are less likely in a 6-year-old child. In addition, the absence of fever, pain, erythema, or palatal swelling makes these diagnoses unlikely. The absence of any infectious signs and symptoms coupled with normal inflammatory markers decrease the possibility of cat-scratch disease and tuberculosis. This girl’s swelling in the lateral neck and tonsillar areas is not consistent with thyroid tumor or dysfunction.Neck masses in children can generally be divided according to cause (Table 1) and location (Table 2). Infectious/inflammatory masses are most common, with lymphadenopathy and lymphadenitis representing the most common causes of neck swelling in young children.The most important step in evaluating a child who has a neck mass is to exclude compromise of vital structures (airway, spinal nerves, blood vessels) and life-threatening causes of neck swelling. Potentially life-threatening causes of neck masses in children include:MalignancyLemierre syndromeInfection with mediastinal or systemic spreadExpanding hematoma due to traumaThyroid stormAirway compromise due to mass effect or inflammation of the airwayMassive subcutaneous emphysema Kawasaki disease with coronary aneurysmCompromise of vital structures by the mass should be suspected in the presence of cardiorespiratory symptoms such as unexplained tachycardia, hypotension, diffuse edema and plethora (superior vena cava syndrome), tachypnea, hoarseness, dysphagia or dysphonia, orthopnea, dyspnea, or neurologic symptoms. Although most neck masses in children (>80%) are benign, malignancy must be considered and excluded. Lymphoma, leukemia, neuroblastoma, rhabdomyosarcoma, thyroid tumors, and metastases from distant sites can present with neck swelling. Findings that may indicate a malignant cause of neck swelling include:Continued progression over more than 2 weeksFailure to regress after 4 to 6 weeksFailure to improve with appropriate therapyFixed, firm, nontender massUlceration of the overlying skinSupraclavicular or posterior cervical locationAbsence of infectious/inflammatory signs and symptomsSystemic symptoms (fatigue, weight loss, pallor, easy bruising, bone pain)Abnormal mass or lymphadenopathy in other body regionsPatient age may help narrow the differential diagnosis. Congenital lesions are more common in infants and young children, although delayed presentation even in late adulthood is possible. Infectious causes, particularly lymphadenitis and deep neck space infection, are most common in young children; traumatic lesions are more likely in older children and adolescents. Malignant causes of neck mass are more common in adolescents and adults. Malignant lesions represent only 10% to 15% of neck masses in children, and the age at presentation depends on the primary tumor type.??Evaluation of the child who has a neck mass should be guided by the history and physical examination findings. Any evidence of cardiorespiratory compromise must be addressed immediately. Patients who have uncomplicated infectious or inflammatory processes may require no testing; appropriate antibiotic therapy for lymphadenitis or reassurance and supportive care for reactive lymphadenopathy may be all that are needed. Those who have less clear causes or more severe illness should undergo further evaluation. Laboratory tests that may be helpful include complete blood count and inflammatory marker measurement. Thyroid function tests are indicated for midline masses suspicious for thyroid enlargement. If there is concern for malignancy, a complete metabolic panel and measurement of lactate dehydrogenase and uric acid are indicated. Other laboratory tests in specific clinical scenarios may include viral testing (Epstein-Barr virus, cytomegalovirus, human immunodeficiency virus), bacterial titers (Bartonella henselae), purified protein derivative tuberculin test, blood culture, and rheumatologic screening tests.CT scan is the imaging modality of choice for most neck masses because it allows full delineation of the mass as well as evaluation of the surrounding blood vessels, airways, and soft tissues. Due to increasing concerns about radiation exposure in children, magnetic resonance imaging is an alternative imaging modality, where available. Ultrasonography can be useful for cystic masses and to differentiate vascular from nonvascular lesions. Plain radiography is of limited value in the evaluation of neck masses but may be indicated in traumatic injuries or as an initial screening test in cases of suspected retropharyngeal abscess or subcutaneous emphysema.?Fine-needle aspiration, incisional or open biopsy, or excision with pathology is appropriate when malignancy is suspected or in cases that fail to follow the expected course with appropriate management. Surgical consultation is indicated for congenital lesions, suspected malignancy requiring biopsy, or abscess requiring incision and drainage. Regardless of the initial diagnosis, any neck mass that continues to progress, fails to respond to appropriate therapy, or continues to have an unclear cause requires further evaluation.American Board of Pediatrics Content Specification(s)Differentiate by age the etiology and understand the pathophysiology of neck massesPlan diagnostic evaluation and initial intervention for patients with neck massesRecognize serious and/or life-threatening causes of neck massesKnow the differential diagnosis of neck mass by locationQuestion: 5A 3-year-old boy is brought to the emergency department with a diffuse, raised rash (Figure) and swollen, painful knees and ankles. His parents state that he felt warm and the rash has spread since they first noticed it and has some purplish discoloration in a few areas of the arms and legs. The boy does not want to walk due to pain. He is drinking fluids and denies abdominal pain, vomiting, or diarrhea. He completed a 10-day course of amoxicillin for streptococcal pharyngitis last night. Physical examination findings for the alert but quiet boy include a temperature of 38.3°C, respiratory rate of 20 breaths/min, heart rate of 94 beats/min, blood pressure of 86/62 mm Hg, and pulse oximetry reading of 98% in room air. He has no scleral or conjunctival injection or discharge and no oral lesions. He has shotty adenopathy in the axillary, inguinal, and anterior and posterior cervical chains, but his neck is supple. His lungs are clear and work of breathing is normal. His heart rate and rhythm are regular without murmurs, rubs, or gallops and capillary refill is 2 seconds. His abdomen is soft and nontender without organomegaly, masses, or adenopathy. There is no swelling or rash in the genital area. The boy’s knees and ankles are mildly swollen and warm but with minimal to no erythema. He has diffuse urticarial lesions with some palpable purpura widely scattered on the arms and legs but no petechiae. Findings on neurologic examination are nonfocal and intact. Laboratory results include:Urine specific gravity, 1.015Urinalysis, negative for blood, protein, glucose, and ketonesHemoglobin, 12.2 g/dL (122 g/L) White blood cell count, 9.3x103/μL (9.3x109/L) with 1 band, 39 neutrophils, 1 basophil, 4 eosinophils, 44 lymphocytes, and 11 monocytesPlatelet count, 450x103/μL (450x109/L) C-reactive protein, 0.5 mg/L (4.76 nmol/L)Erythrocyte sedimentation rate, 18 mm/hFigureOf the following, the MOST appropriate therapy for this boy isA.azithromycin orallyB.ceftriaxone intravenouslyC.ibuprofen orallyD.ketorolac intravenouslyE.methylprednisolone intravenouslyCorrect answer CThe boy described in the vignette has a clinical course that is consistent with a serum sickness–like reaction. He is clinically stable and tolerating oral fluids. Laboratory findings are unremarkable. If his pain can be controlled with oral ibuprofen, this is the preferred therapy. Oral antihistamines may relieve itching and help the rash. Azithromycin is indicated for the treatment of streptococcal pharyngitis in penicillin-allergic patients. It is extremely unlikely that this child’s streptococcal infection has recurred in less than 24 hours, and there is no group A streptococcal resistance to β-lactam antibiotics. The boy does not have signs or symptoms of a severe infection requiring a broad-spectrum antibiotic such as ceftriaxone. Ketorolac could be used if oral nonsteroidal anti-inflammatory drugs do not provide sufficient analgesia. Corticosteroids may be helpful in patients who have serum sickness–like reactions, but they are usually reserved for those who have more severe, persistent, or recalcitrant symptoms.Serum sickness was first described in the early 20th century in patients who had received heterologous antisera. Today, antisera are rarely used as antithymocyte globulins in patients after organ transplantation and as antitoxins in the treatment of diphtheria, clostridial infections, and some envenomations. Inflixamab and rituximab are chimeric human-murine monoclonal antibodies used in the treatment of immune thrombocytopenic purpura and other autoimmune diseases. Serum sickness has been reported after the use of these agents.Classic serum sickness is a type III hypersensitivity reaction caused by the deposition of immune complexes in tissue. Immune complexes usually involve immunoglobulin (Ig)M antibodies. The complexes activate the classic pathway of complement activation. Anaphylatoxins generated in this process increase vascular permeability, stimulate histamine release, and produce bronchospasm. If mast cells are simultaneously activated by an IgE-mediated type I hypersensitivity reaction, the symptoms may be more severe. Large amounts of immune complexes are often deposited in the kidneys and vascular system, the organs that are affected most often.A serum sickness–like reaction has been described after the use of a wide variety of medications (Table). Most of these agents are low-molecular weight compounds that cannot act as antigens in their own right but bind to proteins, often after metabolism, and stimulate the production of immune complexes. Serum sickness-like reactions are usually less severe than that seen after treatment with antisera.Patients develop a fever, malaise, and rash 7 to 10 days after exposure to the inducing agent. In cases of repeat exposure, symptoms may occur in as few as 1 to 4 days. Continued exposures can produce a rapid onset of particularly severe symptoms, including severe bronchospasm and circulatory collapse.The rash is usually urticarial but may be maculopapular or have palpable purpura consistent with a vasculitis. Arthralgias, arthritis, lymphadenopathy, angioedema, and nephritis are often seen. In contrast to classic serum sickness, other manifestations are less often seen in cases of serum sickness–like reactions. Mucous membranes and usually spared, and their involvement should prompt consideration of conditions such as Stevens-Johnson syndrome. Depending on the severity of the reaction and where immune complexes are deposited, abdominal pain, neuritis, carditis, and anemia may occur. Wheezing and pericardial friction rubs may be heard. Hepatosplenomegaly may develop and, rarely, neurologic deficits may be found.In patients who have milder presentations, urinalysis to exclude renal involvement may be the only laboratory test needed. Other tests to rule out more serious causes may be helpful, depending on the clinical presentation. Leukopenia or leukocytosis may occur. The erythrocyte sedimentation rate may be elevated. Complement 3 and 4 and hemolytic complement 50 concentrations may be decreased as complement factors are consumed. Renal dysfunction may be present. Stool testing for occult blood should be performed in patients who have abdominal pain. Ultrasonography may be used to exclude intussusception. For patients who have persistent tachycardia or a friction rub, electrocardiography and echocardiography may be needed to exclude carditis. Cranial computed tomography scan should be obtained in patients who have neurologic symptoms to evaluate for hemorrhage due to vasculitis.Serum sickness and serum sickness–like reactions are self–limited, with symptoms resolving once the immune complexes are cleared (usually within a few days to up to 2 weeks). Treatment is aimed at providing symptomatic relief while monitoring for resolution and possible complications. Oral antihistamines (diphenhydramine, hydroxyzine, or nonsedating antihistamines) may be useful for treating the rash, pruritus, and angioedema. Nonsteroidal anti-inflammatory drugs may aid in relieving arthralgias and fevers. For patients who have more severe symptoms or whose symptoms fail to respond to these measures, treatment with a 7- to 10-day course of corticosteroids followed by a 2-week taper may be helpful. Most patients can be treated as outpatients, but those who have more severe manifestations and complications should be admitted to the hospital. Life–threatening complications have been treated with plasmapheresis to promote clearance of immune complexes.American Board of Pediatrics Content Specification(s)Know the etiology and understand the pathophysiology of serum sicknessRecognize signs and symptoms of serum sicknessPlan management of acute serum sicknessQuestion: 6A 4-year-old girl presents to the emergency department with a 4-week history of progressive bilateral eye pain and worsening vision loss. She was seen several months ago by an optometrist for intermittent vision problems, and he diagnosed chronic anterior uveitis. The girl did not have any pain at the time and her vision problems seemed to improve before she could be seen by her pediatrician, so her mother did not schedule a follow-up appointment. The mother explains to you that she brought her daughter to the emergency department today because the next available appointment with a pediatric ophthalmologist is in 3 weeks. The girl also has a history of intermittent limping for the past 6 months, with sporadic swelling of both her knees and ankles. She has no history of back pain, rashes, or finger or fingernail changes. On physical examination, she has swelling and overlying erythema of both knees and ankles, with decreased active and passive range of motion of those joints because of pain. She has no other apparent skin changes, and the remainder of her physical examination findings are normal.Of the following, the MOST likely diagnosis isA.inflammatory bowel diseaseB.juvenile psoriatic arthritisC.oligoarticular juvenile idiopathic arthritisD.polyarticular juvenile idiopathic arthritisE.tubulointerstitial nephritis and uveitis syndromeCorrect Answer: CAlthough a number of conditions are associated with uveitis, oligoarticular (<5 joints) juvenile idiopathic arthritis (JIA) is the most common systemic illness associated with uveitis in children. As for the girl described in the vignette, girls younger than 6 years of age who have antinuclear antibody-positive oligoarticular JIA are at greatest risk for uveitis, with an incidence of about 30%. Affected patients typically initially present with asymptomatic chronic anterior uveitis, but they can have frequent recurrences and relapses.?Polyarticular JIA involves 5 or more joints and is associated with a lower incidence of uveitis, ranging from 7% to 14%. Juvenile psoriatic arthritis is typically monoarticular and characterized either by psoriasis or dactylitis, nail dystrophy (pitting, discoloration, onycholysis), or tenosynovitis. Uveitis occurs in 10% to 20% of affected patients. Patients who have inflammatory bowel disease tend to be older than this girl and may demonstrate mild arthritis of large joints. Iridocyclitis occurs in 2% to 11% and usually coincides with the inflammatory changes in the bowel or joints. Patients who have tubulointerstitial nephritis and uveitis syndrome are more commonly adolescent females and usually have bilateral acute anterior uveitis and mild proteinuria, glycosuria, and urinary leukocytes.Up to one third of pediatric patients may have uveitis that appears asymptomatic due to the inability of younger patients to verbalize their symptoms or their ability to temporarily compensate if there is only unilateral eye involvement. When symptoms are present, complaints depend on which specific portions of the uveal tract are involved (Table 1):?0000Anterior: involving the iris and/or ciliary body (30% to 40%)Posterior: inflammation of the choroid (40% to 50%)Intermediate: involving primarily the vitreous and peripheral retina (25%)Although 29% to 50% of pediatric patients who have acute or chronic anterior uveitis have idiopathic causes for their ocular inflammation, a number of systemic illnesses and infections have been associated with the condition (Table 2).American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of uveitisBe aware of the systemic illnesses associated with uveitisQuestion: 7A 6-year-old girl presents to the emergency department because of a swollen, tender area on her right lower eyelid (Figure 1). She has been otherwise well without fever or signs of an upper respiratory tract infection. She has had similar lesions in the past but did not seek care. Her parents are concerned that these keep recurring.Figure 1Of the following, the MOST appropriate management isA.administration of dexamethasone ophthalmic solutionB.administration of gancyclovir ophthalmic gelC.administration of ketotifen ophthalmic solutionD.cleaning the eyelashes with baby shampooE.ophthalmologic consultation for incision and drainageCorrect answer DThe child described in the vignette has an external hordeolum or stye. External hordeolums are small abscesses of the glands of Zeis (sebaceous glands) or Moll (sweat glands) at the lid margin (Figure 2). They are a manifestation of staphylococcal blepharitis, an infection of the lid margins and at the bases of the eyelashes. Children who have staphylococcal blepharitis often complain of itching and burning of their eyes and tenderness around the area of inflammation. The lid margins are frequently erythematous, and scales and crusts may be present. The bulbar conjunctivae usually are not injected. Children may awaken with their eyelashes stuck together. Hordeolums usually drain spontaneously and resolve over several days or 1 to 2 weeks.Although some authors recommend treatment with ophthalmic ointments containing antistaphylococcal medications such as bacitracin or erythromycin, there is no evidence that this is required or leads to a more rapid resolution of symptoms. Recommended treatment of hordeolums includes gentle cleaning of the lid margins with baby shampoo and the use of warm compresses to encourage drainage in children who tolerate them. The safest method of cleaning the lid margins is to use a clean washcloth. The use of cotton applicators increases the risk of accidental ocular trauma, especially in young children. Culturing drainage from external hordeolums is not useful because the eyelids are typically colonized with staphylococcal species.Dexamethasone is indicated for treatment of inflammatory conditions of the eye and should only be prescribed under the direction of an ophthalmologist. Gancyclovir is indicated for the treatment of herpetic keratitis. Ketotifen is an ophthalmic antihistamine for the treatment of allergic conjunctivitis. Incision is not indicated for the treatment of external hordeolum.An internal hordeolum is an infection of the deeper Meibomian glands, a sebaceous gland with an orifice at the lid margin. Red, tender swelling of the eyelid often is present away from the lid margin. If there is no obstruction, the swelling may drain to the lid margin and look very much like a stye. If the neck of the gland is obstructed, the abscess often points to the palpebral conjunctivae. If the gland does not drain spontaneously, the eyelid should be everted to look for the pointing. Supportive treatment with cleaning of the lid margins and warm compresses is usually all that is required. Rarely, persistent redness and tenderness may be relieved by incision and drainage by an ophthalmologist. Very rarely, spreading erythema, warmth, swelling, and increasing tenderness across the lid and to the surrounding periorbital tissues may signal the development of a periorbital cellulitis requiring the use of systemic antibiotics.In contrast to hordeolums, a chalazion is a persistent, nontender bulge or nodule in the eyelid. Erythema may be present but is usually less pronounced. Chalazion is not believed to represent infection but is a sterile lipogranulomatous reaction. Chalazions usually resolve over a longer period of time than hordeolums. Local care as for hordeolums is usually all that is required. Larger chalazions and chalazions that cause significant local irritation or that become infected (increasing size, redness, warmth, and tenderness) may require ophthalmologic consultation for incision and drainage. Rarely, chalazions may drain spontaneously to the skin. Local care with good cleaning and topical antibiotics promotes healing.Figure 2Sagittal section of the upper lid showing various tear-secreting glands (top). The photograph of the eyelid margin shows droplets at the orifice of the meibomian glands (bottom). Reprinted with permission from Wright KW. Red eye/pink eye. In: McInerny TK, Adam HM, Campbell DE, Kamat DM, Kelleher KJ, eds. Textbook of Pediatric Care. Elk Grove Village, IL: American Academy of Pediatrics; 2009:1702-1716.American Board of Pediatrics Content Specification(s)Know how to evaluate and manage hordeolum and chalazionQuestion: 8A 12-year-old girl has been referred by her pediatrician to the emergency department because her last 2 menstrual cycles were 36 days long and she has not had her menstrual period in approximately 37 days. Her mother is worried that she might be pregnant. When interviewed alone, the girl denies sexual activity. Her mother is still convinced “something” must be wrong. The patient started having her menstrual periods about 5 months ago. Laboratory results previously obtained by the pediatrician included normal concentrations of thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin. She had a negative urine β-human chorionic gonadotropin (β-hCG) test result today. She denies excessive bleeding, nausea/vomiting, breast swelling or tenderness, nipple discharge or galactorrhea, headache, vision problems, excessive hair growth, weakness, fatigue, or weight loss. She is not taking any medications. Physical examination reveals Sexual Maturity Rating stage 3 breast development and pubic hair distribution and no signs of hirsutism. All other findings on her physical examination are within normal parameters.Of the following, the MOST appropriate next step is to orderA.magnetic resonance imaging of the brainB.no additional studiesC.serum free thyroxine measurementD.serum testosterone measurementE.serum von Willebrand factor measurementCorrect answer BOligomenorrhea has been defined as menses occurring at greater than 35-day intervals. However, studies have established that most normal menstrual cycles can range between 21 and 45 days in the first 3 years following menarche. The anovulatory cycles are the most likely reason for the increased cycle length, although some cycles can be ovulatory and have a prolonged follicular phase. Generally, cycles do not stabilize until the sixth postmenarchal year.?The girl described in the vignette recently experienced menarche, and her current cycle length of 36 days is within the range of normal. She has appropriate pubertal development and otherwise normal findings on physical examination. Accordingly, she can be reassured and observation continued. True oligomenorrhea requires evaluation that includes other laboratory tests (Figure 1).??The girl is not displaying any signs or symptoms of excess androgen secretion, often seen in polycystic ovary syndrome (PCOS), one of the most common causes of oligomenorrhea. Therefore, measurement of serum testosterone is not necessary. Measurement of serum free thyroxine is not indicated because the girl is not displaying any other signs or symptoms of thyroid disease. If the presenting complaint was menorrhagia or menometrorrhagia, a serum von Willebrand factor assessment might be appropriate. A substantially elevated prolactin measurement may indicate intracranial lesions, which could prompt brain magnetic resonance imaging.Generally, a more extensive evaluation of oligomenorrhea should be undertaken if the cycle length exceeds 90 days. The causes for menstrual irregularity are varied (Table), and conditions that affect any portion of the hypothalamic-pituitary-ovarian (HPO) axis can cause prolonged or missed menses. Understanding the physiology of the menstrual cycle can help to clarify the reasons for oligomenorrhea (Figure 2):Pulsatile secretion of gonadotropin-releasing hormone (GnRH) by the hypothalamus acts upon the anterior pituitary to release FSH and LHFSH increases growth of the primary ovarian follicle, which releases estrogenRising concentrations of estrogen during the first half of menses exert negative feedback on FSH release, decreasing estrogen concentrationsMid-cycle FSH exerts positive feedback on the hypothalamus and pituitary, resulting in an LH surge and ovulationAfter ovulation, the ovarian follicle, now called the corpus luteum, secretes progesterone, which stabilizes the endometriumIf fertilization does not occur, the corpus luteum involutes and progesterone concentrations decline, resulting in endometrial sheddingComplete endometrial shedding during the luteal phase does not occur due to immaturity of the hormonal feedback mechanisms.?Thus, menstrual cycles for the first 2 years after menarche are commonly anovulatory.? Cycle length has some variability until complete maturation of the HPO axis (approximately 5 to 7 years).?The initial approach to a patient presenting with oligomenorrhea or secondary amenorrhea begins with obtaining a thorough history, with particular attention to:Menstruation: age of menarche, duration and amount of menstrual flow, dysmenorrheal or premenstrual symptomsSexual and substance use history The diagnostic evaluation can proceed when oligomenorrhea or secondary amenorrhea is determined to be present (Figure 1).?Pregnancy should be ruled out and concentrations of LH and FSH measured.? If signs of hirsutism/hyperandrogenism (acne, alopecia, virilization) are present, free and total testosterone and dehydroepiandrosterone sulfate (DHEAS) should be measured. Both PCOS and congenital adrenal hyperplasia should be considered in the differential diagnosis.??If signs of hirsutism/hyperandrogenism are not present, TSH and prolactin should be measured. Elevated prolactin concentrations affect the pulsatile release of GnRH and suppress gonadotropins. Substantially higher prolactin concentrations may indicate intracranial lesions, which are better delineated with magnetic resonance imaging of the brain.???If thyroid disease is suspected or if the TSH concentration is abnormal, free thyroxine should be measured.??A progesterone challenge test is an initial intervention for patients who present with oligomenorrhea or secondary amenorrhea. An exogenous source of progesterone (10 mg of medroxyprogesterone) is administered to the patient for 7 days. Withdrawal menstrual bleeding within a few days at cessation of the test indicates adequate endogenous estrogen concentrations and suggests HPO axis immaturity or PCOS. No withdrawal bleeding implies an estrogen deficiency requiring continued testing.00000000American Board of Pediatrics Content Specification(s)Differentiate by age the etiology and understand the pathophysiology of oligomenorrheaPlan diagnostic evaluation and initial intervention for patients with oligomenorrheaAUGUST 2012Question: 1A 12-year-old girl is transferred from a hospital to a level I trauma center after being evaluated following a motor vehicle crash. She was a front seat restrained passenger in a head-on collision in which air bags were deployed and the windshield shattered. She had no documented loss of consciousness and experienced neck and chest pain with bruises and multiple facial lacerations. Her airway was intact, with no breathing difficulty or hemodynamic instability. Her lung sounds were coarse in lower lung fields, and chest radiograph showed bilateral pulmonary infiltrates consistent with pulmonary contusion. Her cervical spine radiograph and brain and abdominal computed tomography scans were reported as normal. She was placed in a cervical spine collar and immobilized for the transfer. Before transfer, she received one fluid bolus. During the 2-hour transport, the patient became sleepy and restless. When she arrives at the trauma center, she appears tired and agitated and is trying to take off her cervical collar. Physical examination reveals a temperature of 37.5°C, heart rate of 120 beats/min, respiratory rate of 35 breaths/min, blood pressure of 110/65 mm Hg, and oxygen saturation of 92% in room air. Her breath sounds are consistent with diffuse rales. Bedside capillary venous gas assessment shows a pH of 7.23, Po2 of 35 mm Hg, and Pco2 of 40 mm Hg. You endotracheally intubate the girl.?Of the following, the MOST appropriate management strategy for this patient during the course of her illness isA.extracorporeal membrane oxygenationB.high-frequency oscillatory ventilationC.pressure-support ventilationD.tracheostomyE.volume-support ventilationCorrect answer CThe girl described in the vignette has acute pulmonary injury with deteriorating airway status and possible respiratory failure. Signs of impending failure include change in mental status, agitation, and hypoxia. She is at high risk of developing acute respiratory distress syndrome (diagnosed by arterial Pao2 to Fio2 ratio of <200) and, therefore, requires a management plan to avoid this form of relatively rare pulmonary injury in pediatric patients who have lung trauma. Pressure-support ventilation has been shown to improve the outcome of patients who have acute lung injury. Volume-control ventilation has been shown to exacerbate alveolar damage in patients who have acute respiratory distress syndrome. When conventional ventilation is ineffective, high-frequency oscillatory ventilation or extracorporeal membrane oxygenation can be considered. Tracheostomy may be required in patients who experience severe lung damage and become dependent on a ventilator for chronic care.?? ??Acute respiratory failure is defined as hypoxia (Pao2 <60 mm Hg) in room air either without hypercarbia (Type 1) or with hypercarbia (Paco2 >50 mm Hg) (Type 2). Acute respiratory distress syndrome and acute lung injury are the leading causes of respiratory failure in trauma patients. Although thoracic trauma is rare in children, when present, the patient must be carefully assessed for possible airway/respiratory compromise. Common injuries that can predispose to development of respiratory failure are tension pneumothorax, flail chest, hemothorax, and pulmonary contusion.?When evaluating a trauma patient, indications for definitive airway include either protection of the airway or need for adequate oxygenation with respiratory failure. Some examples of indications in trauma patients are:Altered mental status or unconscious, especially those who have vomiting or seizures, to avoid aspirationNeck trauma associated with expanding hematomaNeck trauma with stridorBurn victims with inhalation injurySubmersion injury with aspiration and noncardiogenic pulmonary edemaDeterioration of mental status due to possible hypercarbia, hypoxia, hypovolemia, or central nervous system causeInability to maintain adequate oxygenation with noninvasive techniques (nonrebreather, bilevel positive airway pressure [BIPAP], or nasal continuous positive airway pressure [CPAP])Clinicians treating trauma patients for respiratory failure should plan for a difficult airway with adjunctive support from surgery and anesthesia teams and provide preoxygenation. Management steps include:Cervical spine precaution with jaw-thrust maneuverBag-mask ventilation with cricoid pressureSedation and paralysisConsideration of alternatives to endotracheal intubation if initial attempts are unsuccessful:?Laryngeal mask airwayLaryngeal tube airwayEmergency tracheostomyCricothyrotomyFlexible fiberoptic intubationRetrograde intubationNeedle cricothyrotomy with jet insufflationProvision of pressure-assisted mechanical ventilation with positive end-expiratory pressure (PEEP) to augment the number of alveoli for oxygenation and maintaining PEEP at the minimum value required to achieve adequate oxygenation to avoid barotraumaUse of lowest possible volume for patients who have acute respiratory distress syndrome to avoid alveolar overdistention and ventilation-related lung injury; pressure-assisted ventilation is favored over volume-assisted ventilationUse of high-frequency ventilation to allow for lowest tidal volume; frequent ventilation allows time for lungs to healConsideration of prone position when allowed (although studies have only shown oxygenation improvement), and if the patient has unilateral lung injury, having that side dependent to allow for better oxygenation and possible early healingExtracorporeal membrane oxygenation in severe casesSupportive management for acute respiratory distress syndrome includes:Restrictive fluid administrationUse of paralytic agentsEnteral nutritionConservative use of sedation, transfusionInhaled nitric oxide with mixed results (acts as a pulmonary vasodilator)Although trauma is one of the leading causes of obstructed airway, other conditions in pediatric patients can result in acute airway obstruction and respiratory failure (Table).0958215000000American Board of Pediatrics Content Specification(s)Plan the management of a child with an obstructed airway in the setting of major traumaUnderstand the management priorities in a child with respiratory failure due to traumaQuestion: 2A 16-year-old girl is brought to the emergency department from a party with altered mental status and generalized tonic-clonic seizure. Friends explain that she had been feeling a “little depressed” due to recent breakup with her boyfriend and that they took her out “to have some fun.” They also report that she may be “on some pills for depression” and “may have been drinking” at the party. On arrival, she is having generalized tonic-clonic seizures with muscle rigidity, diaphoresis, and mydriatic pupils. After administration of intravenous benzodiazepines, her temperature is 39.0°C, heart rate is 135 beats/min, respiratory rate is 35 breaths/min, and blood pressure is 145/85 mm Hg. Laboratory investigations show:Sodium, 125 mEq/L (125 mmol/L)Potassium, 5.2 mEq/L (5.2 mmol/L)Bicarbonate, 18 mEq/L (18 mmol/L)Chloride, 105 mEq/L (105 mmol/L)Glucose, 95 mg/dL (5.3 mmol/L)Serum aspirin and acetaminophen, not detectedUrinalysis:Specific gravity, >1.030pH, 7.0Ketones, negativeGlucose, negativeHemoglobin, positiveNitrites, negativeLeukocyte esterase, negativeUrine pregnancy test, negativeOf the following, the MOST likely agent causing seizures and altered mental status in this patient isA.3,4-methylenedioxymethamphetamine (MDMA)B.ethanolC.gamma-hydroxybutyric acidD.Klamath weed (St. John’s wort)E.ketamineCorrect Answer: AThe generalized tonic-clonic seizure, hyponatremia with free water retention (concentrated urine), and serotonin syndrome with possible rhabdomyolysis (muscle rigidity and urine positive for hemoglobin) described for the girl in the vignette are most suggestive of intoxication with MDMA (Ecstasy). Serotonin syndrome with MDMA is more likely with the concurrent intake of selective serotonin reuptake inhibitors (antidepressants). Seizures are seen with ethanol withdrawal or due to hypoglycemia in young children experiencing acute intoxication. Central nervous system effects due to gamma-hydroxybutyric acid (GHB) intoxication include agitation, stupor, and occasionally sudden awakening from stupor after metabolism of the drug. GHB can cause seizures but is associated with bradycardia and hypotension, and it does not cause serotonin syndrome or hyponatremia. Ketamine effects include central nervous system depression or agitation, hallucination, agitation, pupillary dilatation, horizontal nystagmus, muscle rigidity, and rarely petit mal type seizures. However, ketamine is not associated with generalized tonic-clonic seizure or free water retention. Klamath weed is an herb used for the treatment of depression and can cause photosensitivity rash when taken in large amounts. If this herb is taken with serotonin reuptake inhibitors, it can result in serotonin syndrome, but it is not associated with hyponatremia and free water retention.Amphetamines increase catecholamine release at the presynaptic terminal without having an effect on its reuptake, resulting in toxic effects similar to those associated with sympathomimetic agents:Central nervous system stimulation and euphoria, restlessness, dizzinessHypertension, strokeNausea, vomitingHyperthermiaMyocardial ischemiaMuscle rigidity and rhabdomyolysisCardiac conduction abnormalities?Modified amphetamines are used as recreational drugs and have additional selective toxic effects. MDMA and related products are called entactogens (drugs that allow “to touch within”), and their use results in loss of inhibitions and “feeling of closeness to people.” MDMA and related agents are associated with free water retention and hyponatremia (similar to syndrome of inappropriate antidiuretic hormone secretion). These actions result in altered mental status, concentrated urine, and elevated urine sodium concentrations. Chronic use of MDMA has been associated with hepatoxicity and liver failure. Ephedra and khat (plant-derived) ingestion have been associated with anxiety, arrhythmias, hypertension, myocardial ischemia, stroke, seizures, and hyperthermia (similar but less intense effects compared to amphetamines). Methamphetamine exposure has been shown to result in seizure, tachycardia, hypertension, hyperpyrexia, and reversible ischemic colitis. The modified amphetamines can be cross-contaminated with additional toxic substances, such as ketamine in MDMA tablets that can cause hallucinations and manganese toxicity that can cause extrapyramidal effects with methcathinone.?Alcohols should be considered as possible toxic substances in the patient who presents with altered mental status and high anion gap and osmolal gap. Although the osmolal gap develops acutely with ingestion, the anion gap develops once the alcohol is metabolized (Table).?Symptoms of methanol toxicity are seen after its metabolism to toxic compounds. Because this is a slow process, a latent period precedes evidence of toxicity. Severe acidosis is due to the production of formic acid, mitochondrial inhibition, and additional production of lactate and results in the early symptom of hyperventilation. Methanol causes lesser degrees of the central nervous system depression compared with other alcohols unless ingested in large amounts. Among other symptoms are nausea, emesis, chest pain, seizures, and pancreatitis. Early visual complaints include blurred vision followed by dilated pupils, optic disc hyperemia, and if left untreated, progression to irreversible blindness (whiteout or snow field perception with pale retina on funduscopic examination). Hence, a patient presenting with altered mental status, severe acidosis, osmolal gap, and negative ketones on urinalysis should be suspected of having methanol intoxication.??Symptoms due to ethylene glycol toxicity appear in three stages. Initial symptoms are euphoria due to central nervous system effects and emesis due to gastric irritation. If taken in large quantities, seizures and coma can occur within 1 hour. The second phase is associated with worsening of acidosis and resultant Kussmaul breathing, tachycardia, and rarely, hypotension. Formation of calcium oxalate crystals causes tissue damage from crystal deposition and hypocalcemia. Symptoms include hypocalcemia, cardiac conduction abnormalities, tetany, and seizures. The final phase involves renal failure, respiratory distress, and pulmonary edema developing over 24 to 72 hours. Renal damage is due to deposition of the crystals in the renal tubules, with oliguria or anuria and, in most cases, reversible renal failure. Central nervous system depression could be related to the direct effect of the metabolites or associated cerebral edema and encephalopathy. The diagnosis should be suspected in a patient who has altered mental status, severe metabolic acidosis, osmolal gap, and possibly oxalate crystals in the urine.??Isopropyl alcohol metabolizes to acetone and, therefore, results in significant ketonuria and ketonemia without anion gap. The central nervous depressant effect is more profound than that seen with ethanol. Among the other symptoms are facial flushing, headache, nausea, vomiting, and abdominal pain. When a patient presents with altered mental status without acidosis and with osmolal gap and ketonuria, isopropyl alcohol is the likely culprit.??Infants and young children can present with altered mental status, hypoglycemia, and hypothermia with or without acidosis following ethanol ingestion. Older children present with symptoms according to the blood ethanol concentrations. The symptoms range from nausea and vomiting to ataxia, disinhibition, stupor, and coma. Other documented effects include hepatitis, lactic acidosis or ketoacidosis (may occur due to abnormalities associated with ethanol metabolism or effect on hepatic gluconeogenesis), facial flushing, nystagmus, ataxia, tachycardia, hypotension, atrial fibrillation, angina in adults who have coronary artery disease, respiratory depression, and aspiration. Ethanol ingestion should be suspected in an individual who presents with altered mental status, normal anion gap with osmolal gap, and negative urinary ketones. The ingestion should be suspected in younger children who have the previously described symptom complex that includes altered mental status, hypoglycemia, and hypothermia.?0000American Board of Pediatrics Content Specification(s)Recognize signs and symptoms of ethanol ingestionRecognize signs and symptoms of isopropyl ingestionRecognize signs and symptoms of methanol ingestionRecognize signs and symptoms of ethylene glycol ingestionRecognize signs and symptoms of abuse of amphetamines, including EcstasyQuestion: 3You are reviewing a study examining the risk factors for developing renal failure in patients who present with septic shock. The study identified all patients with septic shock who were treated in the emergency department during 10 years in the institution where the authors worked. The investigators reviewed the patients' hospital records to ascertain whether they developed renal failure. The authors were interested in whether a specific antibiotic regimen started in the emergency department (regimen A) was more likely to be associated with renal failure than a different regimen (regimen B).Their results are presented below:Renal failureNo renal failureTotalRegimen A252550Regimen B104050Total3565100Of the following, the CORRECT interpretation of these results is thatA.both odds ratio and relative risk are appropriate analytical techniques in this studyB.odds of developing renal failure are 4 times higher for patients receiving regimen AC.patients receiving regimen A are 2.5 times more likely to develop renal failure than those receiving regimen BD.relative risk and odds ratio are approximately the same in this studyE.relative risk of developing renal failure is 4Correct Answer: BBoth relative risk and odds ratio are common methods for expressing the risk of developing a specific outcome. Relative risk, also known as risk ratio, is the ratio of the risk of developing a disease or condition if one is exposed to a suspected inciting factor compared to the risk in those not exposed to the factor. It is expressed in a 2 × 2 table as:Developing diseaseNo diseaseTotalExposed to factoraba+bNot exposedcdc+dTotala+cb+dAll those with the disease are a+c. All those without the disease are b+d. Those exposed to the factor are a+b, and the unexposed are c+d. Thus, the risk of developing a disease or condition if one is exposed is a/(a+b). The risk of developing a disease or condition if one is not exposed is c/(c+d). The ratio of these is:a/(a+b)?c/(c+d)The relative risk is predicated on assigning patients based on exposure and following them over time to see whether a disease or condition develops. If the condition develops at the same frequency for the exposed and unexposed groups, the relative risk is 1. If the relative risk exceeds 1, the risk of developing the condition is greater in that group. If the relative risk is less than 1, the factor being studied is protective. The relative risk can change over time; because it reflects a cumulative incidence, a longer observation period may produce different results than a shorter one.For the example, use of relative risk would be appropriate if patients were randomly assigned to 1 of the 2 regimens and observed to see whether they developed renal failure. However, the investigators began by identifying those with renal failure, so the study was not designed to determine whether renal failure developed at a different rate for those exposed or not exposed to the regimens. Thus, although one could calculate a relative risk for the study as described, (25/50)/(10/50) or 2.5, this value makes no sense in the example. In examining a study, it is critical to know whether patients are identified according to exposure (regimen A or regimen B) or by outcome (developing renal failure or not developing renal failure). Studies in which patients are assigned to groups according to outcome, called case-control studies, are particularly useful for rare diseases or for conditions that require a long time to develop (such as cancer after cigarette smoking, which may take decades to manifest).The odds ratio is used in case-control studies to describe the risk in the 2 groups because the development of disease has already been established in the study design. The odds ratio is the ratio of those exposed to the factor or treatment who have the disease compared with exposed patients who do not have the disease. In the example, the odds of developing renal failure under regimen A are 25/25 or 1/1. Note that this is different from the probability or risk, which is 25/50 or 0.5. The odds of developing renal failure under regimen B are 10/40 or 1/4. Note also that risk is always less than 1, whereas odds can be any number. For example, if 80 of 100 patients develop a disease, the risk is 80/100 or 0.8, but the odds are 80/20 or 4/1. The odds ratio in the example is (25/25)/(10/40) or 4. A shortcut of the algebra [(a/b)/(c/d)] is to express the odds ratio as (a×d)/(b×c) or (25×40)/(25×10). For this reason, some people call the odds ratio the cross product.Many people have difficulty articulating the differences between odds ratio and relative risk. In relative risk assessment, patients are followed over time for the development of disease based on their exposure status. With the odds ratio, one assesses those who have and do not have the disease to see whether they have exposure. For the unexposed population in the example, 10 develop renal failure and 40 do not, resulting in an odds ratio of 1/4.Odds ratios and relative risk approximate one another for uncommon events.? To recap the example:Renal failureNo renal failureTotalRegimen A252550Regimen B104050Total3565100Relative risk is (25/50)/(10/50) = 2.5 and odds ratio is (25×40)/(25×10) = 4.If renal failure were much less likely to develop, the results might be:Renal failureNo renal failureTotalRegimen A54550Regimen B34750Total892100In this case, relative risk is (5/50)/(3/50) = 1.67 and odds ratio is (5×47)/(3×45) = 1.7.With a case-control study, relative risk is not an appropriate measurement of risk. Because renal failure developed frequently, the relative risk and odds ratio do not approximate one another.American Board of Pediatrics Content Specification(s)Understand the use of odds ratios in the interpretation of resultsQuestion: 4A mother brings her previously healthy 2-year-old son to the emergency department because he looked pale when he woke up this morning. He has had a fever and decreased activity over past few days. He had a urinary tract infection diagnosed 3 days ago and was prescribed sulfamethoxazole-trimethoprim. On physical examination, the markedly pale boy has scleral icterus, a heart rate of 170 beats/min, respiratory rate of 40 breaths/min, and blood pressure of 90/50 mm Hg. He has no hepatosplenomegaly or lymphadenopathy. There are no findings of note on the remainder of his examination. Point-of-care laboratory study reveals a hemoglobin of 5 g/dL (50 g/L).Of the following, the MOST likely cause of this child’s anemia isA.aplastic anemia from parvoviral infectionB.glucose-6-phosphate dehydrogenase deficiencyC.hereditary spherocytosisD.sickle cell hemolytic crisisE.transient erythroblastopenia of childhoodCorrect answer BThe sudden onset of pallor and jaundice in a previously healthy toddler is suggestive of acute hemolytic anemia. The history of recent exposure to a sulfonamide-containing drug for a urinary tract infection, as described for the child in the vignette, should raise the suspicion of glucose-6-phosphate dehydrogenase (G6PD) deficiency. Trimethoprim-sulfamethoxazole, an oxidant drug, generates free oxygen radicals that are usually removed by reduced glutathione. In the presence of G6PD deficiency, available reduced glutathione is decreased, resulting in damage to the red blood cell (RBC) membrane.Aplastic anemia and transient erythroblastopenia of childhood are disorders of RBC production, so jaundice is not a typical feature. Children who have hereditary spherocytosis either present with neonatal hyperbilirubinemia or later with splenomegaly and mild-to-moderate anemia. Those who have sickle cell disease are likely to develop hemolytic crisis with illness, but symptoms of vasoocclusive crisis usually occur in the first postnatal year, making this an unusual diagnosis in a previously well child at age 2 years.Other oxidant drugs that can trigger acute hemolysis in patients who have G6PD deficiency include nitrofurantoin, aspirin, isoniazid, primaquine, and naphthalene (mothballs). Moderate-to-severe illness can also be a source of oxidant stress without medication use and may be an inciting factor in children who have G6PD deficiency. G6PD is an x-linked recessive disorder. The A (-) type seen in African American males is associated with diminishing enzyme activity as the RBC ages. Affected patients have a dramatic decrease in hemoglobin and hematocrit concentrations, with brisk reticulocytosis. The young reticulocytes produced have adequate G6PD enzyme, so resolution occurs spontaneously. The Mediterranean type of G6PD deficiency is also characterized by severe hemolysis when exposed to oxidant stress. However, the deficiency is noted in RBCs of all ages, so recovery is not spontaneous.Broadly, anemia can result from RBC destruction, as in severe hemolysis, underproduction, as in aplastic anemia or from blood loss. The reticulocyte count is helpful in distinguishing the underlying cause of anemia. An elevated reticulocyte count suggests RBC destruction or blood loss. If the count is low, the anemia is more likely due to marrow failure or RBC underproduction. A detailed list of causes of anemia, classified on the basis of the mean corpuscular volume and reticulocyte count, is shown in Table 1. The more common causes are highlighted.Pallor in childhood can have several causes (Table 2). In an acutely ill patient, it can be a sign of severe anemia or circulatory shock with peripheral vasoconstriction or hypoperfusion. The Figure?outlines a broad approach to a patient who exhibits pallor. In the acutely ill patient with pallor, the presence of jaundice or scleral icterus and tachycardia suggests rapid hemolysis. The decision to transfuse RBCs in the emergency department should be made in consultation with a hematologist and based on clinical symptoms and signs, the degree of cardiorespiratory or central nervous system compromise, the cause and course of anemia, and options for alternative therapy, noting the risks for transfusion-associated infections and reactions. Rapidly developing anemia in a jaundiced child who demonstrates tachycardia and tachypnea and has a hemoglobin reading of 5 g/dL (50 g/L), such as the boy in the vignette, has the potential to worsen, with overt congestive heart failure developing. Hence, urgent blood transfusion in consultation with hematology may be warranted. On the other hand, packed RBC (PRBC) transfusions in patients who have chronic illness or cancer are generally not recommended until the hematocrit falls below 20% to 22% or if the patient is symptomatic.PRBCs are concentrated RBCs with hematocrits of 55% to 70%. A typed and cross-matched blood product is preferred when possible. However, when transfusion cannot be delayed, as in acute blood loss or shock, O-negative (or O-positive) blood may be used. O-negative is preferred for females of childbearing age to reduce the risk for Rh sensitization. Unless rapid replacement is required for acute blood loss or shock, blood should be infused slowly (generally over 4 hours) to avoid congestive heart failure. A rule of thumb in severe compensated anemia is to give an X mL/kg aliquot, where X = patient’s hemoglobin (g/dL). For example, if the hemoglobin is 5 g/dL, as in this case, PRBCS should be transfused at 5 mL/kg over 4 hours. The volume of PRBC to achieve a desired hematocrit is calculated with the following equation:?Patient’s EBV (mL) x (Hct desired-Hct observed)?Hct of PRBC(EBV is the estimated blood volume and the hematocrit [Hct] of PRBCs is usually 55% to 70%)Leukocyte-poor PRBCs should be administered to patients undergoing intensive chemotherapy, bone marrow transplantation, or solid organ transplantation or for intrauterine transfusions, neonatal transfusions, or transfusions in those who have leukemia, lymphoma, or known or suspected immune deficiencies such as immunoglobulin A deficiency. Cytomegalovirus-negative, irradiated blood may be given to neonates or other immunocompromised patients, including those awaiting organ or marrow transplant who are cytomegalovirus-negative.American Board of Pediatrics Content Specification(s)Differentiate by age the etiology and understand the pathophysiology of pallorPlan diagnostic evaluation and initial intervention for patients with pallorRecognize serious and/or life-threatening causes of pallorQuestion: 5An 8-year-old boy is brought to the emergency department by emergency medical services after falling from the top of a 10-ft sliding board. The fall was unwitnessed, but the child was found lying on his back and crying. He denies any loss of consciousness. He complains of abdominal and “side” pain but is unable to localize the pain clearly. He denies any nausea, vomiting, numbness, tingling, or weakness. He has no findings of note on past medical history. On physical examination, the child appears uncomfortable and has intermittent grunting. His temperature is 36.7°C, heart rate is 108 beats/min, respiratory rate is 18 breaths/min, blood pressure is 108/65 mm Hg, and pulse oximetry reading is 100% in room air. Results of his head, ears, eyes, nose and throat, neck, chest, and neurologic examinations are normal. His abdomen is soft and nondistended, with vague diffuse tenderness but no guarding or rebound. He has no midline back tenderness, step-off, swelling, or bruising.?Of the following, the BEST description of findings in this patient related to a possible thoracolumbar spinal fracture is pression type fractures involving multiple levels are most expectedB.posterior spinal elements are most frequently injuredC.spinal cord injury without radiologic abnormality is rare in such a childD.the absence of spinal tenderness or neurologic findings makes the diagnosis unlikelyE.the cervical-thoracic junction and sacral regions are the most likely sites of fractureCorrect Answer: AThe boy described in the vignette experienced a fall from a significant height, which places him at high risk for significant injury, including spinal fractures. Most thoracolumbar fractures in children occur at the thoracolumbar junction, with compression-type fractures seen most frequently (Figure 1). The absence of spinal tenderness or neurologic findings does not exclude the diagnosis of a spinal fracture because most thoracolumbar fractures in children do not involve the posterior spinal elements.?Figure 1Compression-type fracture at the thoracolumbar junction. Courtesy of C. Huang, MD.Spine fractures, including thoracolumbar fractures, are less common in children than adults, with one incidence peak in those younger than 5 years (due to inappropriate lap belt use or physical abuse) and another peak in adolescents. Between 2% and 5% of all spinal injuries occur in pediatric patients. Cervical injuries are more common than thoracolumbar injuries in this population. The most common mechanisms in young children are motor vehicle crashes, falls, and child abuse; in adolescents, sports and recreational activities and motor vehicle crashes are the most common causes. The most common pediatric thoracolumbar fractures are compression fractures, with the thoracolumbar junction, lower thoracic, and upper lumbar areas most frequently involved. The cervical-thoracic junction and sacral regions are not common fracture sites. Compression fractures can result from either axial loading, as seen in falls, or hyperflexion injuries resulting in anterior compression. High-speed mechanisms, such as motor vehicle and all-terrain vehicle crashes, are more likely to cause severe injuries. Flexion-distraction type fractures resulting from hyperflexion over a lap belt, also known as “Chance” fractures, result in a horizontal fracture through the posterior elements of the vertebrae and compression fracture of the anterior vertebral body. These injuries are often associated with intra-abdominal injuries such as shearing injuries to the bowel or mesentery, vascular injuries, or solid organ injuries. In approximately 50% of cases, multiple spinal levels are involved.?Diagnosis of thoracolumbar fractures in the pediatric trauma patient requires a careful history and physical examination coupled with a high index of suspicion in high-risk mechanism injuries. Tenderness of the spine may not be present if the posterior elements are not involved, and deformity, step-offs, or overlying skin findings are rarely present. Because the injuries most commonly involve the anterior vertebral structures and multiple levels, the pain frequently is vague and poorly localized. In addition, associated multisystem injuries may mask signs and symptoms referable to the thoracolumbar spine.Neurologic findings are present in approximately 20% of all pediatric spinal fracture patients. A careful neurologic examination, including assessment of motor and sensory function, rectal tone, and reflexes, should be performed and repeated over time. Figure 2?shows the sensory and motor dermatomes corresponding to various spinal cord levels.?Spinal cord injury without radiologic abnormality (SCIWORA) is much more common in children than adults, representing 15% to 30% of spinal injuries in children compared with less than 1% of adult injuries. SCIWORA is more common in cervical injuries than thoracolumbar injuries. With the advent and increased use of magnetic resonance imaging, more spinal cord injuries can be clearly delineated. It is generally agreed that SCIWORA now includes those spinal cord injuries with no bony radiographic abnormalities. The higher incidence of SCIWORA in children is due to the greater elasticity of the vertebral column and supporting structures; the spinal canals of infants and young children can stretch up to 2 inches, but the spinal cord and neural tissues can only stretch ? inch before rupture. SCIWORA injuries are often severe or “complete” in terms of the neurologic findings distal to the level of the injury in pediatric patients. Such injuries are also considered unstable, with up to 50% showing either progression or recurrence of neurologic symptoms. Evaluation to exclude potentially treatable bony or ligamentous injuries and prolonged (up to 12 weeks) immobilization are indicated.American Board of Pediatrics Content Specification(s)Know the most common life-threatening causes of thoracolumbar spine injuries in childrenUnderstand the types and mechanisms of thoracolumbar spine injuriesUnderstand neuroanatomic clinical correlation in thoracolumbar spine injuriesQuestion: 6An 8-year-old previously healthy child presents with a 2-day history of fever with chills, headache, chest discomfort, myalgia, cough, coryza, sore throat, nausea, and abdominal pain. Physical examination of the ill-appearing child shows a temperature of 39.8°C, heart rate of 126 beats/min, respiratory rate of 30 breaths/min, blood pressure of 95/60 mm Hg, and oxygen saturation of 96% in room air. Although he is dyspneic, his lungs are clear to auscultation and he appears well hydrated. Cardiovascular examination reveals sinus tachycardia without murmur or gallop. He has no meningeal signs or rash. The remainder of his examination findings are within normal limits. The child’s mother has been investigating possible causes of these symptoms on the Internet and is concerned that he may have been exposed to a biologic agent.Of the following, the factors in this boy’s clinical presentation that are MOST suggestive of exposure to seasonal influenza rather than inhalational anthrax areA.coryza and sore throatB.dyspnea and chest discomfortC.fever and chillsD.myalgia and headachesE.nausea and abdominal painCorrect answer AInhalational anthrax is a biphasic illness that can present initially with an influenzalike syndrome characterized by fever, myalgia, headache, chills, chest pain, or abdominal pain. However, rhinorrhea and sore throat are distinctly uncommon in anthrax infection. After the prodrome, affected patients have worsening chest pain and dyspnea, progressing in 24 to 48 hours to acute respiratory distress syndrome and hypotension. A chest radiograph early in the course may appear normal, but later in the illness, it may show a widened mediastinum or pleural effusions.Recognizing sentinel bioterrorist events can be challenging. At present, the most reliable early detection system in most clinical settings is clinical acumen in diagnosing the index case sufficiently early to initiate a response cascade. This was most evident in 2001 when a community clinician rapidly recognized a case of intentional inhalational anthrax. The clinical clues to a potential bioterrorism event can include:An unexpectedly high rate of a rare or nonendemic diseaseUnusual age, occupational, geographical, or seasonal distributionUnusual mortality or morbidity ratesAgent-specific pathognomonic clues such as the classic smallpox rashPublic health clues can include:Epidemic curve showing a rapid increase in casesGeographical clustering of casesSimultaneous outbreaks of unusual diseasesAnimal casualtiesAtypical mode of transmissionUnusual antimicrobial susceptibility patternA biodrome is similar to a toxidrome. It is a constellation of signs and symptoms affecting more than one system that may appear unrelated but together provide an important clue to either a class of toxin or potentially serious biological exposure. Table 1 lists certain features of a syndrome that can used for clinical diagnosis of a bioterrorism event by identifying a geographic or temporal clustering of cases.?The Centers for Disease Control and Prevention (CDC) report in 2000 divided biologic agents into three categories based on the potential terrorist threat they may represent (Table 2). The clinical syndromes typical of potential category A conditions and diagnostic methods are listed in Table 3. The CDC provides many updated resources for clinicians and the general public, which are available at: bt.bioterrorism.0000American Board of Pediatrics Content Specification(s)Recognize key clinical features and diagnostic methods for biological exposures, including those illnesses caused by anthrax, botulinum toxin, brucellosis, encephalitides, mycotoxins, plaque, Q fever, smallpox, staphylococcal enterotoxins, tularemia, and ricinQuestion: 7A 3-day-old infant presents to the emergency department after having several episodes of vomiting. His parents state the vomiting is nonbloody and initially appeared like formula but now is bright green. The infant was born at term via an uneventful vaginal delivery. According to his mother, he had no problems drinking his formula in the first few days after birth, but he has been drinking progressively less in the past 12 hours. He has no fever, cough, respiratory distress, diarrhea, or hematochezia. He has not had a bowel movement in more than 24 hours. On physical examination, the infant appears dehydrated and his temperature is 37.6°C, heart rate is 170 beats/min, respiratory rate is 40 beats/min, and blood pressure is 85/52 mm Hg. The baby’s abdomen appears slightly distended but soft, and there are no masses on palpation. His bowel sounds are diminished. You establish intravenous access, start fluid resuscitation, and request immediate surgical consultation.?Of the following, the finding that is MOST suggestive of this infant’s diagnosis isA.bowel loops in the right hemithorax on plain chest radiographyB.coiled nasogastric catheter in the upper esophagus on plain chest radiographyC.delayed gastric emptying on nuclear imagingD.“double-bubble” sign with a paucity of distal bowel gas on plain abdominal radiographyE.“target” sign on abdominal ultrasonographyCorrect answer DMalrotation with midgut volvulus must be considered in any neonate who presents with bilious emesis, such as the child described in the vignette. Plain abdominal radiography demonstrating a “double-bubble,” with the left-sided proximal “bubble” indicating the gas-filled stomach and the second “bubble” just to the right of midline representing the proximal duodenum with a paucity of distal bowel gas, is most suggestive of duodenal obstruction (Figure 1). Such obstructions can include duodenal atresia/stenosis/webs, annular pancreas, malrotation with midgut volvulus/Ladd bands, and preduodenal position of the portal vein.??A “target” sign (Figure 2) or “pseudokidney” is an abdominal ultrasonographic finding more suggestive of intussusception, usually not seen in neonates. With intussusception, target sign can also be a finding on abdominal radiography. Delayed gastric emptying on a nuclear imaging study suggests gastroesophageal reflux, which is characterized by nonbilious emesis. The plain chest radiographic finding of bowel loops in the hemithorax (Figure 3) is indicative of a congenital diaphragmatic hernia, usually presenting with acute respiratory distress or cyanosis in the first 24 hours after birth. A coiled nasogastric tube in the proximal esophagus is consistent with esophageal atresia (Figure 4). Affected infants typically have respiratory distress, choking, drooling, and problems handling their secretions.Presenting signs and symptoms of infants who have midgut volvulus are initially consistent with a proximal intestinal obstruction; clinical progression depends on whether growing intestinal ischemia remains unrecognized. Acute symptoms include feeding intolerance with both bilious and nonbilious emesis as well as abdominal pain and distention. If vascular compromise to the intestine continues, gastrointestinal bleeding, peritonitis, and eventually shock and cardiovascular collapse can occur. Older children tend to have vaguer initial symptoms, such as recurrent intermittent abdominal pain or vomiting that may be nonbilious or bilious, failure to thrive due to malabsorption from chronic torsion of the root of the mesentery, constipation or diarrhea, hematemesis, and hematochezia. However, as intestinal ischemia continues, pain becomes the predominant symptom.??Most cases of intestinal volvulus are associated with malrotation, but this condition is not required for a volvulus to occur. A volvulus occurring in other portions of the intestinal tract, stomach, cecum, and transverse and sigmoid colon has been documented in case reports but are considered rare in infants and children.?Among the ancillary studies that could be used in the management of volvulus are stool occult blood testing, plain abdominal radiography, upper and lower gastrointestinal contrast radiography, ultrasonography, and computed tomography scan. Stool occult blood testing may yield positive results in patients who have volvulus, but this test is neither sensitive nor specific enough to be of significant utility. Other laboratory studies have no real utility and should not delay surgical consultation and operative management if a volvulus is suspected.Radiographic studies are the diagnostic mainstay for suspected volvulus. However, no ancillary studies should delay an exploratory laparotomy in a symptomatic patient who has peritonitis. Classic findings on plain abdominal radiographs demonstrate the “double-bubble,” with little distal intestinal gas. Radiographically, such findings do not distinguish malrotation with midgut volvulus from duodenal atresia. Clinical symptomatology combined with additional ancillary studies can help distinguish the conditions. Less common radiographic findings include a gasless abdomen, distal small bowel obstruction with multiple air-fluid levels, and pneumatosis intestinalis if the bowel has become gangrenous. However, plain abdominal radiographs may also appear normal in affected patients and, therefore, cannot be used to determine or exclude the diagnosis.?Upper gastrointestinal (UGI) contrast radiography using barium has traditionally been used to help determine the presence of malrotation, for which it has high specificity, thus identifying patients at greatest risk for volvulus (Figure 5). The UGI series is used to determine the position of the duodenojejunal junction (DJJ). Normally, the DJJ lies to the left of the left-sided vertical spinal pedicle at the level of the duodenal bulb on a frontal view and posteriorly on a lateral view. In malrotation with midgut volvulus, the findings include:?A displaced DJJDuodenal obstruction with proximal dilation and distal abrupt ending or “bird’s beak” appearance (Figure 6)A “corkscrew” or “spiral” pattern or configuration of the contrast in the duodenum and proximal jejunumHowever, the UGI series has only slightly better than 50% sensitivity for midgut volvulus, highlighting the importance of clinical suspicion in making the diagnosis.?Lower gastrointestinal contrast radiography can be used to locate the position of the cecum if the UGI series results are equivocal, volvulus is not suspected, and malrotation is still suspected.?Ultrasonography and computed tomography scan have lower sensitivity and specificity compared with the UGI series in diagnosing malrotation based on the relationship of the superior mesenteric vessels. Both modalities can demonstrate nonspecific, abnormal dilation of the duodenum along with findings that have been reported as highly suggestive of volvulus. The “whirl” or “whirlpool” sign (Figure 7), in which the superior mesenteric vein and mesentery are wrapped around the superior mesenteric artery, have been described as having high sensitivity for volvulus.Figure 1The “double-bubble” sign on plain abdominal radiography that suggests duodenal obstruction. Courtesy of C. Huang, MD.Figure 4Chest radiograph showing coiled nasogastric tube in the proximal esophagus, which is consistent with esophageal atresia. Courtesy of C. Huang, MD.American Board of Pediatrics Content Specification(s)Recognize signs and symptoms and complications of acute midgut volvulusKnow the indications for and interpret results of ancillary studies in patients with acute midgut volvulusQuestion: 8A 14-year-old boy is brought to the emergency department 2 hours after being crushed by a refrigerator he was helping to move. He was reportedly trapped for more than 1 hour while his brother went to get help. His brother states that the boy was answering questions after the initial injury, but when he returned with another friend to free the boy, his brother was lethargic and confused. On physical examination, the adolescent is obtunded and difficult to arouse, with a heart rate of 142 beats/min, respiratory rate of 38 breaths/min, blood pressure of 137/93 mm Hg, and pulse oximetry reading of 99% in room air. He has extensive petechiae on both lower legs and feet and bruising and swelling of both lower extremities from the groin to the ankles. You proceed with trauma management, including radiographs and laboratory testing. You place a catheter and obtain only 100 mL of rusty-colored urine. Urine dipstick results are positive for blood, but red cells are not visible on microscopy. While awaiting the remainder of laboratory results, the initial intravenous (IV) bolus of normal saline finishes and the nurse asks what fluids you want hung next. In your decision process, you try to anticipate laboratory results.Of the following, the MOST likely laboratory abnormality for this boy isA.hypercalcemiaB.hyperphosphatemiaC.hypoglycemiaD.hypokalemiaE.metabolic alkalosisCorrect Answer: BThe boy described in the vignette has suffered a severe crush injury, and the history and evidence of soft-tissue injury suggest that he is developing severe rhabdomyolysis. Potential electrolyte abnormalities in severe rhabdomyolysis include hyperkalemia, hyperphosphatemia, and hypocalcemia as well as metabolic acidosis. Hypoglycemia is not a characteristic finding.Rhabdomyolysis occurs when damage to myocytes leads to leakage of the intracellular components, including potassium, phosphorus, and myoglobin. It is more common in adolescents than young children. Any disease that leads to significant skeletal muscle injury may result in some degree of rhabdomyolysis. The most common causes of rhabdomyolysis in children are viral myositis and trauma. Other causes include aggressive exercise, prolonged seizure, hyperthermia, electrical shock, prolonged immobilization, various intoxications, and metabolic disorders of muscle enzymes. The classic presentation of rhabdomyolysis is musculoskeletal complaints of myalgia and weakness combined with pink or dark-colored urine. Among the physical examination findings are muscle tenderness and occasionally swelling. Calf tenderness in patients with a flulike syndrome has been suggested as a specific clinical sign for influenza B infection.Rhabdomyolysis is defined as a serum creatinine phosphokinase (CPK) value at least 5 times the upper limit of normal. CPK concentrations rise rapidly after the initial insult, with peaks usually occurring more than 24 hours after injury. Clearance is gradual; high concentrations persist for several days. Serum myoglobin is filtered by the kidney and passes into urine, causing it to turn pink or tea-colored. Urine test strips for hemoglobin pigments yield positive results, but no pigments or blood cells are visible on urine microscopy. The presence of such heme pigments can be considered a positive result for urine myoglobin, obviating the need for specific urine myoglobin assessment. Myoglobin measurement in the serum is a less sensitive marker because concentrations peak early after injury, and myoglobin is metabolized quickly.?In severe cases of rhabdomyolysis, acute renal failure results from a combination of insults, including tubular obstruction with myoglobin casts, prerenal insufficiency from both third spacing of fluid into injured muscle and renal vasoconstriction in the face of injury, and direct tubular cell injury from hydroxyl radicals produced by the effect of acidic urine on the myoglobin molecule. Among the clinical signs of acute kidney injury due to myoglobinuria are oliguria or anuria, hypertension, and edema. Urine appears grossly pink or tea-colored and casts are visible on microscopy. The combined effects of release of intracellular electrolytes and renal failure can lead to life-threatening electrolyte derangements, including hyperkalemia, hyperphosphatemia, and hypocalcemia. In addition, limb-threatening compartment syndrome may occur with localized rhabdomyolysis (eg, single extremity injury) in the absence of significant myoglobinuria.Management of minor rhabdomyolysis is primarily supportive, focusing on rest and pain management. For children who have uncomplicated viral myositis, home management with oral hydration may be considered. For patients who have CPK measuring more than 5,000 U/L (83.5 μkat/L) or more than 2+ heme pigments on urine dipstick test, IV fluid should be administered and titrated to maintain brisk urine output.? Adult medicine standards suggest adequate hydration to keep urine flow to at least 3 mL/kg per hour. If urine flow is inadequate when adequate IV fluids are provided, furosemide 0.5 or 1 mg/kg may be considered. Osmotic diuresis with mannitol may also be considered. Diuretic therapy with furosemide or mannitol should only be undertaken for patients who have adequate volume resuscitation, and close attention must be paid to input and output balance to avoid excessive diuresis. Forced alkalinization with IV sodium bicarbonate has been proposed, and raising urine pH theoretically might reduce the tubular toxicity of myoglobin. However, studies to date have not shown any benefit. Use of IV sodium bicarbonate should be reserved for treatment of hyperkalemia or metabolic acidosis.?Management of electrolytes in severe forms of rhabdomyolysis is complicated. Symptomatic hyperkalemia can be treated with usual therapies: potassium-binding resins, IV bicarbonate, IV calcium salts, inhaled albuterol, or IV insulin. Unfortunately, hypocalcemia may be exacerbated by alkalinization, which decreases available ionized calcium. Severe hypocalcemia with seizure or cardiac arrhythmia requires immediate therapy. Hypocalcemia is difficult to treat with IV repletion in the presence of hyperphosphatemia because the salts precipitate as calcium phosphate. If oliguric renal failure is present, and especially if severe electrolyte derangements exist, dialysis should be initiated urgently.American Board of Pediatrics Content Specification(s)Recognize signs and symptoms of rhabdomyolysis/myoglobinuriaRecognize life-threatening complications of rhabdomyolysis/myoglobinuria and its treatmentPlan management of acute rhabdomyolysis/myoglobinuriaSeptember 2012Question: 1A mother brings her 19-month-old infant to the emergency department for treatment of a cough. She explains that he has had a cold and cough for 2 days, but he has not had any labored breathing, fever, vomiting, diarrhea, or other associated symptoms of an upper respiratory tract infection. His past medical history is unremarkable, and he has never been hospitalized. His mother reports that he is “behind” on his shots; she thinks he has had one set. He is receiving no medications and is not allergic to anything. On physical examination, the infant appears small-for-age, but he is in no apparent distress. His weight is 8.8 kg, temperature is 37.0°C, heart rate is 110 beats/min, respiratory rate is 24 breaths/min, blood pressure is 88/60 mm Hg, and pulse oximetry reading is 99% in room air. Head, ear, eyes, nose, and throat examination reveals poor dentition, with multiple obvious caries and brown, decaying central incisors. His mucous membranes are moist. Cardiovascular and respiratory examinations yield normal results. His abdomen is soft, nontender, and nondistended, and he has no hepatosplenomegaly. His skin appears normal, except for dirt on his extremities and under his nails. Results of the remainder of his examination are normal. You contact his primary care provider, who reports that he was first seen at 3 months of age and has subsequently missed multiple scheduled visits. His height, weight, and head circumference were all at the 50th percentile at the 3-month visit. Results of a complete metabolic panel and urinalysis are normal. A complete blood count reveals mild anemia but is otherwise normal.Of the following, the MOST appropriate next step in management for this infant isA.chest radiographyB.child protective services reportC.emergent dental consultationD.intravenous fluid bolus administrationE.measurement of growth hormone concentrationCorrect answer BThe infant described in the vignette exhibits failure to thrive and evidence of neglect, warranting a child protective services report. He has no history of fever, respiratory distress, abnormal lung examination findings, or hypoxia to suggest the need for chest radiography. He has no clinical or laboratory evidence of dehydration or metabolic derangement that would require rehydration or metabolic testing. Although he does need dental evaluation and treatment, this is not emergent. Discharging him without addressing the clear signs of neglect is not appropriate because it fails to meet the mandated reporting requirement and puts him at risk for continued neglect and possible abuse.Neglect is the most common form of child abuse, accounting for more than 50% of reported cases and approximately 50% of identified child abuse fatalities. Although there is no clearly established definition of child neglect, it is broadly defined as the failure of the parent or guardian to provide for the needs of the child. Among the many different types or classifications of neglect are:Physical neglect: inadequate food, shelter, clothing, hygieneMedical/dental neglect: inadequate medical or dental care or failure to adhere to prescribed medical/dental treatmentsSupervisional neglect: inadequate or inappropriate supervision for the age and developmental stage of the childEmotional neglect: absence of appropriate nurturing, affection, psychological supportEducational neglect: failure to ensure adequate education through enrollment in school or appropriate home schoolingThe signs and symptoms of neglect are extremely variable and dependent upon the type(s) and severity of neglect involved. Failure to thrive without any identifiable organic cause is a common manifestation. This can be the result of a failure to provide adequate food or formula (due to either intentional withholding of food or financial issues leading to inadequate food availability), chaotic home environment with secondary feeding issues, emotional or psychological disorders resulting from the abuse and neglect, or a combination of these factors. Poor growth may be the only manifestation or may be accompanied by the consequences of malnutrition, including dehydration, immune dysfunction, vitamin deficiencies, and anemia as well as neurologic, developmental, and emotional disorders. Other manifestations of neglect include poor hygiene, poor dentition, injuries due to inadequate supervision, overdoses due to accidental or intentional ingestion of drugs or medications, heat- or cold-related injuries due to inadequate shelter or clothing, and emotional or psychological disorders.Although neglect is the most difficult form of child maltreatment to define clearly, classify, and prove, as with physical and sexual abuse, the physician seeing the child is mandated by law to report suspicion of neglect to the appropriate child protection authorities. Documentation of the signs and symptoms, all resulting injuries or illnesses, and prior episodes of other or similar episodes is critical. As in the vignette, obtaining information from the primary care provider, including growth charts, documentation of missed visits, failure to follow recommended treatments, and any prior concerns of abuse or neglect, are extremely helpful in establishing a pattern of neglect. For failure to thrive in particular, obtaining prior growth parameters is essential to identify the growth pattern and progression over time.American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of nonorganic failure to thrive as a manifestation of neglectRecognize signs of neglect other than nonorganic failure to thriveKnow the physician's role in reporting cases of child neglectQuestion: 2A 4-year-old girl is brought to the emergency department for evaluation of a “knot” in her neck. She began to complain of neck pain 2 days ago but was otherwise acting normally. Today her parents noticed a visible swelling in the right side of her neck. She has had low-grade fevers and slightly decreased oral intake. Upper respiratory tract symptoms preceded her neck pain by 1 week. She has had no change in mental status or behavior and no rash, neck stiffness, vomiting, or diarrhea. She has not complained of ear or throat pain. Her past medical history contains no findings of note, and she is up-to-date on all of her immunizations. On physical examination, the well-appearing child is active and playful. Her vital signs are normal except for a temperature of 38.0°C. Head, ears, eyes, nose, and throat evaluation reveals scant clear nasal discharge. On neck examination, she has a 3x2-cm tender, firm mass just below the right angle of the jaw with mild overlying erythema but no fluctuance. The mass is mobile. Neck range of motion is normal except for mildly decreased rotation to the right side. The remainder of her examination findings are within normal parameters.Of the following, the MOST appropriate initial management is toA.administer intravenous clindamycin and perform a neck computed tomography scanB.obtain a complete blood count and blood cultureC.place a purified protein derivative test and obtain a chest radiographD.obtain Epstein-Barr virus titers and discharge the girlE.prescribe oral clindamycin and arrange outpatient follow-upCorrect answer EThe girl described in the vignette has acute cervical lymphadenitis involving a submandibular lymph node. The most likely causative organisms are Streptococcus pyogenes and Staphylococcus aureus. Initiation of antibiotic treatment with adequate coverage of these organisms is appropriate initial therapy. Laboratory evaluations such as a complete blood count, blood culture, or viral titers are unlikely to add helpful information for management. Although tuberculosis can cause cervical lymphadenopathy, acute unilateral adenitis in the absence of other concerning symptoms or high-risk exposures is less likely to represent mycobacterial infection. Tuberculin skin testing is indicated for chronic cervical lymphadenitis; for patients with high-risk exposures or living conditions; or for associated symptoms commonly seen with tuberculosis such as cough, weight loss, or night sweats. Intravenous antibiotics and imaging studies are indicated for patients who fail to improve despite appropriate therapy and those who have evidence of complications such as retropharyngeal abscess, infected thrombus formation, or compression/invasion of adjacent vital structures.Cervical lymphadenitis is defined as enlarged, tender, inflamed lymph nodes in the neck. It is extremely common in young children, with most cases involving the submandibular or deep cervical chains that drain most of the head and neck region. Lymphadenitis results when microorganisms are transported to the involved lymph node(s) via lymphatic channels draining the respective anatomic area. The area drained by the involved node may show signs of local infection. Lymphocyte proliferation as a result of antigen or infectious agent drainage causes lymph node enlargement; pyogenic organism drainage results in acute enlargement of the node associated with warmth, erythema, and tenderness. Neutrophil proliferation within the node may cause abscess formation. The number and location of involved nodes depends upon the site, severity, and causative organism of the primary infection.The cervical lymphatic system drains the head, neck, and upper respiratory tract structures and consists of multiple lymph nodes in three different groups: Waldeyer ring, including adenoids and tonsils; occipital, pre- and postauricular, parotid, and facial nodes that surround Waldeyer ring; and submaxillary, submental, deep, and superficial jugular nodes. Any inflammation, infection, or malignant process in the structures draining to a particular lymph node group results in adenopathy in that area. Anterior cervical nodes drain the oropharynx and upper airway, posterior cervical nodes drain the scalp and nasopharynx, and supraclavicular nodes drain the lower respiratory tract and distant sites. Supraclavicular adenopathy is considered pathologic and should prompt evaluation for malignancy. Enlargement (adenopathy) or inflammation (lymphadenitis) of cervical lymph nodes is extremely common in pediatric patients and is most often the result of infection. Table 1?lists common causes of cervical lymphadenitis according to extent and duration: acute unilateral, acute bilateral, and chronic lymphadenitis.Evaluation of the child who has cervical lymphadenitis is largely based on the history and physical examination findings. In addition to examination of the head and neck, careful examination of the chest (abnormal lung sounds), abdomen (hepatosplenomegaly), skin (rash, inoculation sites), and other lymphatic areas (diffuse lymphadenopathy) should be performed. Children who have the acute onset of tender lymphadenopathy without other examination findings, such as the girl in the vignette, require no testing. Ancillary studies may be indicated (Table 2) for atypical presentations, failure to improve with appropriate therapy, systemic signs or symptoms, or chronic or bilateral lymphadenitis.One relatively common complication of cervical lymphadenitis in young children is the development of deep neck space or retropharyngeal abscess (RPA). Patients who have RPA develop limitation in neck range of motion, particularly rotation and extension. They often appear toxic and have systemic symptoms such as fever and chills.Management of uncomplicated acute cervical lymphadenitis consists of appropriate antimicrobial therapy against the most likely causative organisms. Beta-lactamase-resistant antibiotics are first line; in geographic areas with high rates of methicillin-resistant Staphylococcus aureus infection, clindamycin is often an acceptable initial antibiotic, depending on the local epidemiology and antibiotic resistance patterns. If history, physical examination, or ancillary study findings indicate specific infections such as cat-scratch disease or tuberculosis, therapy should be tailored to the specific pathogen. In addition to appropriate antimicrobial therapy, warm compresses, pain management, and appropriate oral rehydration therapy should be instituted. Follow-up evaluation with the primary care provider and instructions on the expected duration and course of the infection should be ensured.American Board of Pediatrics Content Specification(s)Know the etiology and understand the pathophysiology of cervical lymphadenitisDifferentiate by age the etiology and understand the pathophysiology of non-cervical lymphadenitisRecognize and interpret relevant laboratory and imaging studies for cervical lymphadenitisPlan management of acute cervical lymphadenitisQuestion: 3A teenager is brought to the emergency department via emergency medical services after sustaining a stab wound to the chest during a fight. On physical examination of the lethargic boy, you note that the entry wound is located on the anterior aspect of the right chest, superior and medial to the nipple line. The boy’s heart rate is 120 beats/min, respiratory rate is 30 breaths/min, and blood pressure is 80/60 mm Hg. His extremities are cool, with diminished peripheral pulses, and breath sounds are diminished on the right, with no tracheal deviation or crepitus. You place two large-bore peripheral intravenous lines and administer a 2-L normal saline fluid bolus. When you insert a right thoracostomy tube, there is immediate return of 250 mL of blood. Your initial focused assessment with sonography for trauma (FAST) examination is negative for free fluid in the abdomen or pericardial space. You endotracheally intubate and ventilate the patient. He experiences precipitous cardiopulmonary arrest while being transported to the operation theater.Of the following, the MOST likely cause for this patient’s deterioration isA.air embolismB.cardiac tamponadeC.massive endobronchial hemorrhageD.massive hemothoraxE.tension pneumothoraxCorrect Answer: AThe adolescent described in the vignette demonstrates clinical signs of shock after sustaining a “central” (transmediastinal) thoracic penetrating injury. He is at risk for pericardial tamponade as well as cardiac, pulmonary, esophageal, or great vessel injury. His precipitous circulatory collapse after initiation of positive-pressure ventilation (PPV) is most suggestive of an air embolism. A right thoracostomy tube has drained a moderate-volume right hemothorax and would also have relieved a tension pneumothorax. Significant endobronchial hemorrhage would be evident as bleeding in the endotracheal tube and difficulty ventilating the patient. Although intubation can exacerbate hypotension in the setting of pericardial tamponade by decreasing preload and right heart filling, patients usually demonstrate a transient response to volume loading and may have positive findings on FAST examination.Alveolar-venous communication due to penetrating chest trauma results in air bubbles in the pulmonary veins that, when transmitted to the coronary arteries, can cause sudden ischemia/infarction. Precipitous cardiac arrest develops immediately after intubation. A high index of clinical suspicion is warranted because the diagnosis can be overlooked. If cardiac arrest occurs, the patient should be placed in left lateral Trendelenburg (Durant) position to hold the “air” in the apex of left ventricle, immediate thoracotomy should be performed, the pulmonary hilum should be cross-clamped on the side of the injury, and air should be aspirated from the apex of the left ventricle. Therefore, use of lower tidal volumes and peak inspiratory pressures and avoidance of PPV unless absolutely necessary is prudent in the setting of penetrating chest trauma.Penetrating chest trauma can result in nonthoracic injuries. Abdominal injuries may be overlooked if careful attention is not paid to the location of the entry wound. Diaphragmatic excursion during expiration can reach the fourth intercostal space. Missed diaphragmatic injuries can result in significant delayed morbidity from bowel herniation or strangulation. In general, if the entrance wound is between the nipple line and costal margin anteriorly and the tip of the scapula to the costal margin posteriorly, the emergency physician should suspect an abdominal injury in addition to thoracic trauma.The life-threatening injuries that must be identified during the primary survey after penetrating chest trauma include tension pneumothorax, open pneumothorax (sucking chest wound), flail chest and pulmonary contusion, massive hemothorax, and cardiac tamponade.Massive hemothorax results in rapid accumulation of blood in the chest cavity. It is identified when shock is associated with absent breath sounds or dullness to percussion over one hemithorax. Rarely, mechanical effects of mediastinal shift cause distended neck veins. However, concomitant hypovolemia may cause the jugular veins to remain flat.A tension pneumothorax develops when a “one-way valve” air leak occurs from the lung or through the chest wall. The mediastinum is displaced to the opposite side, compressing the opposite lung and impairing venous return. The diagnosis is based on clinical findings of respiratory distress, shock, tracheal deviation, unilateral absent breath sounds, neck vein distension, hypoxemia, and cyanosis. The hemithorax is hyperresonant to percussion. A simple pneumothorax is also associated with decreased breath sounds but without evidence of shock, severe hypoxemia, or mediastinal shift. It can readily convert to a tension pneumothorax if unrecognized and PPV is applied. A patient who has a pneumothorax must undergo chest decompression before aeromedical transport.Cardiac trauma is commonly encountered with penetrating chest injury. The pericardial sac is a fixed fibrous structure in which a relatively small volume of blood can restrict cardiac filling slowly or rapidly. The diagnosis can be challenging. The classic Beck triad of jugular venous distension, hypotension, and muffled heart tones can be difficult to discern in a noisy emergency department or in the face of hypovolemia when the neck veins are collapsed. A FAST examination may be a valuable adjunct in rapid and accurate diagnosis of pericardial fluid. However, reports suggest that the examination has a 5% to 10% false-negative rate, depending on the skill of the operator. A false-negative FAST result may occur if the blood is clotted and appears hyperechoic on ultrasonography or in the presence of a large hole, with rapid decompression into the chest. Initial administration of fluids raises filling pressures and can improve cardiac output transiently until preparations for definitive treatment are undertaken. In cases of cardiac tamponade, intubation can result in a sudden drop in preload because of the influence of sedative agents, PPV, and application of positive end-expiratory pressure.American Board of Pediatrics Content Specification(s)Know the major causes of nonthoracic injuries associated with penetrating chest traumaRecognize the signs and symptoms of hemothorax following penetrating chest traumaDifferentiate between the signs and symptoms of simple vs. tension pneumothorax following penetrating chest traumaRecognize the signs and symptoms of cardiac trauma following penetrating chest traumaQuestion: 4A 3-year-child who has osteogenesis imperfecta presents to the emergency department with symptoms of shock after 4 days of copious diarrhea.? Physical examination reveals a temperature of 35.4°C, heart rate of 192 beats/min, respiratory rate of 48 breaths/min, blood pressure of 70/36 mm Hg, and pulse oximetry reading of 94% in room air. You determine that she is in severe shock and prepare to obtain venous access. Multiple staff members are unsuccessful at obtaining peripheral access, her parents refuse to allow you to attempt intraosseous access due to her underlying disorder, and you realize that the entire stock of pediatric central line kits was recalled last week and has not been restocked. You decide to perform a venous cutdown.Of the following, your MOST appropriate action in obtaining venous cutdown cannulation is toA.create an incision parallel to the vein directly over the anticipated locationB.dissect through the subcutaneous tissue using fine (iris) scissorsC.locate the correct incision placement using anatomic landmarksD.obtain absorbable suture to tie off the vessel distal to the cutdown siteE.use the basilic vein because it is the most easily found veinCorrect answer CFor patients not in cardiopulmonary arrest, peripheral intravenous (IV) placement should be attempted first in any child requiring vascular access. If needed, intraosseous needle placement allows rapid access for critically ill children in most cases. Venous cutdown catheterization is a procedure of last resort because even highly skilled practitioners may require several minutes to place a cannula by cutdown, but emergency medicine physicians should understand the principles of the procedure. Primary among these principles is identifying the anatomic landmarks used to determine correct placement of the incision.In addition to the unlikely scenario presented in the vignette, venous cutdown may be a viable alternative to central line placement after the initial resuscitation phase when peripheral IV placement has failed. Venous cutdown catheterization may allow a high rate of fluid resuscitation by pump or administration of continuous infusion medications that are not practical by the intraosseous route. Contraindications to venous cutdown include compartment syndrome in the chosen extremity, local trauma or infection at the site of cutdown, and traumatic disruption of vasculature proximal to the site of the cutdown. For example, disruption of the iliac vein may reduce the utility of a saphenous venous cutdown for volume infusion.Multiple locations have been described for venous cutdown access: saphenous vein on the medial ankle, saphenous vein at the groin, basilic vein medially above the elbow, and axillary vein. Each of these locations has specific risks related to nearby nerves and other vessels. The most common location for emergency use is the saphenous vein at the ankle, and the other locations should be used only by experienced clinicians. The key steps for performing the venous cutdown procedure are as follows:Position and restrain the limb. For saphenous vein access, rotate the foot laterally to expose the medial malleolus.Clean the cutdown location and surrounding skin with povidone-iodine or hexachloradine and drape to create a sterile work field.Create a 1 to 2-cm incision through the dermis perpendicular (not parallel) to the course of the vein. For saphenous vein access, this incision should be perpendicular to the long axis of the tibia and located 1 to 2 cm superior and anterior to the medial malleolus (closer for infants and further for older children).Using a curved hemostat (not iris scissors), bluntly dissect through the subcutaneous tissue and fat to expose the vein.Once the vein is identified, pass the curved hemostat under it with tips curving, spread the tips, and raise the hemostat to lift the vein. For saphenous vein access, separate the vein carefully from underlying tissues because the saphenous nerve runs just deep and anterior to the vein.Place a small silk suture (not absorbable suture) around the distal end of the vein and tie off (optional).Place a small silk suture around the proximal end of the vein but do not tie.Use a #11 scalpel blade to incise the vein, creating a flap in the wall of the vessel about halfway through the vein. Use gentle traction on the distal tie or lift gently upward on the loose ends of the proximal silk to control the vessel while making this incision.An alternative technique is to use a regular catheter over needle, as with percutaneous line placement, without incising the vein, taking advantage of seeing the vein directly. This alternative has the advantage of preserving the vein for future access.Cannulate the vessel with an appropriate size IV or central line catheter. Advancing the catheter into the vein may be easier with IV fluids running through the catheter.Tie the proximal silk suture around the cannulated vein.Close the skin incision with sutures and apply a sterile occlusive dressing.Potentials pitfalls of venous cutdown catheterization include injury to nearby nerves or arteries, complete incision that severs the vein, air embolism, and inadvertent loss of the catheter into the vein. Infection and venous thrombosis may develop later. Less serious complications include local bleeding, skin infection, or phlebitis.Identifying and successfully cannulating the saphenous vein may be more difficult than anticipated, particularly in children experiencing severe hypovolemia. In extreme shock, the saphenous vein may be collapsed and difficult to differentiate from the saphenous nerve. The saphenous vein at the groin is significantly larger and allows large-bore catheter placement, which may be necessary to provide large-volume resuscitation fluids. The saphenous vein at the groin can be isolated just lateral to where the lateral margin of the labia or scrotum joins the thigh. This location is near the femoral sheath, and the greatest risk is injury to the femoral artery, vein or nerve. The basilic vein is located superficially just proximal to the flexion of the elbow. The median cutaneous nerve runs lateral and below the basilic vein and should be identified to avoid injury. The axillary vein runs in the axillary sheath along with the axillary artery and roots of the brachial plexus. Use of this location is associated with a very high risk of complication and should be attempted only by experienced operators.American Board of Pediatrics Content Specification(s)Know the indications and contraindications for venous cutdown catheterizationPlan the key steps and know the potential pitfalls in performing venous cutdown catheterizationRecognize the complications associated with venous cutdown catheterizationKnow the anatomy and pathophysiology relevant to venous cutdown catheterizationQuestion: 5A 13-year-old boy is brought to the emergency department after collapsing while on the playground with several friends after eating lunch. He underwent intussusception reduction at age 2 and has had periodic asthma exacerbations. He has not had syncope, seizures, or trauma in the past. He is in 7th grade and is not doing well in school. On physical examination, he is groggy but responsive and appears anxious. He has a laceration on his posterior scalp and a bloody nose.Of the following, in addition to a history and physical examination, the assessment that is MOST likely to provide the definitive cause of this boy’s collapse isA.bedside glucose puted tomography scan of the headC.serum electrolyte assessmentD.serum osmolalityE.toxicologic screenCorrect Answer: EHypoglycemia immediately after lunch is unlikely for the boy described in the vignette. Computed tomography scan may be needed at some point, but it is unlikely to demonstrate intracranial hemorrhage/stroke in a child whose clinical state is improving. Although most toxicologic diagnoses can be determined with a good history and physical examination, toxicologic screening is the most likely assessment to provide definitive information for this boy. In this case, cocaine and cannabis were identified on the screen. The boy, after repeated questioning, admitted to snorting cocaine with his friends after lunch. He did not remember subsequent events until arriving at the hospital. In a previously healthy adolescent without evidence of gastrointestinal losses, electrolyte abnormalities are unlikely to account for this presentation. Serum osmolality is useful in identification of unknown alcohols or some other ingestions, but sudden collapse is not the usual presentation of alcohol intoxication.Potential substance abusers can have a variety of presentations. They can have no symptoms but a parent is concerned, they can have variable symptoms consistent with withdrawal (eg, rigors, flulike symptoms, abdominal pain, vomiting, chills), or they can be in full cardiac arrest from intentional or nonintentional overdose or unexpected reaction. As noted previously, findings on a detailed history and complete physical examination frequently can suggest the diagnosis of substance abuse, the specific cause or class of abused agents, and necessary immediate interventions.Toxicologic screens can be used for further elucidation of drug use and can help guide therapies, although a complete history and physical examination provide more timely information to determine immediate care requirements. Toxicologic screens can use urine (quick abuse screens and more inclusive longer confirmatory assessments) or serum (abuse screens and specific drug/alcohol presence and concentrations) specimens. Not all drug use is evident in urine toxicology screens. For example, ethanol may be nondetectable after 2 to 14 hours and amphetamines after about 48 hours. In contrast, chronic cocaine use may be detectable for weeks. In addition, certain drugs yield false-positive results on a toxicology screen (Table). An excellent primer on Urine Drug Testing in Clinical Practice is available at presentations of drug abuse can include altered mental status (including coma); pupillary irregularity; and changes in temperature, respiratory, heart rate, and blood pressure. Recognized toxidromes include sympathomimetic, sedative hypnotic, opiate, anticholinergic, and cholinergic syndromes.Recognizing a specific toxidrome often allows determination of a class of ingestion (or exposure) as well as specific therapies to stabilize the patient or counteract the drug effects. For example, signs of altered mental status, miosis, unresponsiveness, shallow respirations, slow respiratory rate, bradycardia, decreased bowel sounds, and hypothermia suggest an opiate toxidrome. A narcotic antagonist is appropriate therapy and a potential antidote for an opiate toxidrome. However, not all opiates are identified on a urine toxicologic screening test. For example, methadone use/misuse can present with the opiate toxidrome, but depending on the screening tool, it may not be identified on the toxicologic assessment.Substance abuse can include standard drugs of abuse and drugs that are legal but misused (eg, tobacco, alcohol, cough syrups, pain relievers). Risk factors for drug use include genetic predisposition, personal issues (eg, attention-deficit/hyperactivity syndrome, abuse, antisocial behavior, poor self-image, control issues), dysfunctional family or adult support, environmental issues (eg, drug access, acceptance in community, peer pressures, street living, concurrent mental health disorder, family history of substance abuse, sexual orientation), and poor school performance. Among nonspecific indicators of substance abuse are academic decline (eg, deterioration of short-term memory, poor judgement, truancy, school issues, poor performance) and behavioral and psychological indicators (eg, risk-taking behaviors, depression, acute psychosis, stealing, change in hygiene and appetite, drug use among peers and others). Nonspecific physical issues can encompass weight loss, red eyes, moodiness, cough, chest pain, nasal irritation, and decreased attentiveness. Additional physical signs may help with determining the causative agent. These can include increased heart rate (amphetamines, cocaine, marijuana); increased blood pressure (amphetamines, cocaine, phencyclidine); pinpoint pupils (narcotics); sluggish pupils (barbiturates); nasal irritation/ulcerations (cocaine, glue sniffing); and scars, tattoos over antecubital fossa, skin abscesses, and icterus (intravenous drug use).Newton and associates reviewed screening instruments for rapid detection of drug misuse in youth and concluded that a 2-question instrument for detecting alcohol misuse and 1-question instrument for detecting cannabis were the most useful. For alcohol, the questions were:“In the past year, have you sometimes been under the influence of alcohol in situations where you could have caused an accident or gotten hurt?”“Have there often been times when you have had a lot more to drink than you intended to have?” For cannabis use, the single question was:“In the past year, how often have you used cannabis: 0 to 1 time, more than 2 times?”American Board of Pediatrics Content Specification(s)Recognize signs and symptoms of substance abusePlan the assessment of substance abuse, including use of toxicologic screening examination Question: 6You are called to the critical care room to see a 3-year-old boy who has noisy and labored breathing.? The triage nurse has applied a mask with cool mist. The unhappy toddler is crying and clinging to his mother, and you can hear mild inspiratory stridor as the child cries.? The nurse provides you the following vital signs for the boy: temperature of 39.8°C, heart rate of 182 beats/min, respiratory rate of 48 breaths/min, unobtainable blood pressure, and pulse oximetry reading of 92% in room air/mist. On physical examination, the ill-appearing child has a stiff and arched neck while he is kicking his legs, and he is drooling. He is struggling to breathe, with suprasternal and supraclavicular retractions, subcostal retractions, and abdominal breathing. When you auscultate his chest, you hear stridor with inspiration and diminished air movement in the lung fields. The inspiratory time is longer than the expiratory time. According to the mother, the boy has had a fever for 3 days, has not eaten anything, and had little intake of liquids for the past 2 days.? She adds that his throat has been sore, causing him to drool since yesterday. He has never had stridor before. He has been previously healthy, with no hospitalizations or surgeries. He has no allergies, is taking no medications, and has received all recommended immunizations for his age.Of the following, the MOST likely cause of this child’s stridor isA.bacterial tracheitisB.croupC.epiglottitisD.laryngomalaciaE.retropharyngeal abscessCorrect answer EThis boy described in the vignette most likely has a retropharyngeal abscess. Croup may present with severe airway obstructive findings, fever, and a prodrome of illness, but drooling and meningismus are not indicative of laryngotracheitis. In addition, the child’s toxic appearance suggests a severe bacterial infectious cause for his stridor. Epiglottitis is extraordinarily rare with universal Haemophilus influenzae type b (Hib) vaccination and is more acute in onset. Bacterial tracheitis may follow a prodromal viral infection, but the findings of meningismus and drooling make retropharyngeal abscess more likely. An acute disease course and fever argue against laryngomalacia.Stridor refers to noisy air movement in the upper airway. It can be heard during inspiration, expiration, or both. Inspiratory stridor results from lesions above the level of the thoracic inlet. Expiratory stridor results from lesions inside the thoracic cavity. Expiratory stridor may be difficult to differentiate from wheezing but is usually defined by the lower pitch, greater audibility over the trachea, and lesser audibility over the lung fields. In addition, obstruction of nasal breathing at the level of the nasopharynx may create a distinctive sound known as stertor, which can be distinguished from true stridor by its snoring quality and its disappearance with crying or when the child breathes through his or her mouth.Although stridor can result from a great number of causes, the differential diagnosis can be rapidly simplified by considering the patient's age and clinical circumstances (Table 1?and Table 2).Laryngomalacia is the single most common cause of stridor in infants. It usually presents at birth and commonly resolves without intervention by the age of 18 months. Laryngomalacia describes supraglottic collapse during inspiration and may be the result of cartilaginous or neuromuscular weakness in the upper airway. It is usually diagnosed by bedside viewing with fiberoptic laryngoscopy. Crying, congestion, or supine positioning often provokes stridor in infants who have laryngomalacia.Vocal cord paralysis can be congenital or result from direct trauma after endotracheal intubation or damage to the recurrent laryngeal nerve, usually as a result of cardiac or thyroid surgery. It can be confirmed by viewing with fiberoptic or direct laryngoscopy. ?Viral laryngotracheobronchitis (croup) is the most commonly encountered cause of stridor in a previously healthy child. Croup may be caused by any of a number of viruses but is most closely associated with parainfluenza viruses (type 1 and 3), influenza virus, respiratory syncytial virus, and adenovirus. Croup often begins with fever and other symptoms of the associated viral syndrome such as cough or rhinorrhea. Stridor generally develops 1 to 3 days after the initial symptoms. Stridor in croup is frequently biphasic and usually associated with a harsh, barking cough. Drooling or difficulty swallowing is generally not associated with croup. Croup is most common in early childhood, from 1 to 6 years of age.Bacterial tracheitis occurs when bacterial superinfection follows viral airway inflammation. The most common pathogen is Staphylococcus aureus, but tracheitis can also be caused by other common respiratory pathogens such as Streptococcus pneumoniae, Moraxella catarrhalis, or non-typeable Haemophilus influenzae. The classic presentation includes fever, toxic appearance, and preceding upper respiratory tract infection symptoms with subsequent worsening.Epiglottitis is historically important but rarely encountered in the United States after widespread Hib vaccination; most cases are due to group A Streptococcus. Epiglottitis is a rapidly progressive cellulitis of the epiglottis or subglottic region. The classic presentation includes sudden onset of fever, sore throat, drooling, and tripod or leaning forward posture with neck extended. Complete airway obstruction can occur with little warning, and the child should be allowed to remain in a position of comfort. Anxiety-provoking examination or procedures should be minimized.Infection in the retropharyngeal lymph nodes may progress from adenitis to abscess in the retropharyngeal space. It is seen most commonly between 2 and 6 years of age, after which the lymph nodes atrophy. Infection is usually polymicrobial; cultures may grow S aureus, S pyogenes, S viridans, and various oral anaerobes (eg, Bacteroides, Fusobacterium, Peptostreptococcus). Retropharyngeal abscess generally presents with fever, refusal of oral intake, drooling, and meningismus or limited movement of the neck. Respiratory distress or stridor is not common but may be seen with especially large phlegmon or abscess.Airway foreign body should be suspected in any child who has the acute onset of stridor or does not have prodromal symptoms of infection. Esophageal foreign body may also present with stridor if the object is undiscovered for a prolonged period or acutely if the item is reactive, such as a disc battery.Other noninfectious causes of stridor include various airway or pharyngeal insults: inhalation burns, caustic ingestion, mediastinal masses compressing the trachea, and neck trauma such as laryngeal fracture or strangulation.The emergency department evaluation of stridor begins with assessment of airway risk. Stridor at rest indicates more restriction of the airway than stridor that occurs only with fussing or heavy breathing. Louder and higher-pitched stridor usually indicates more restriction. However, stridor becomes less obvious in the most severe cases as airflow past the obstruction declines. Severe airway obstruction can be recognized by diminished or absent air movement despite obvious work of breathing. Most children display accessory muscle use, deep retractions, and nasal flaring. Alert children may display signs of fear. As the child tires or Paco2 rises, the child’s level of alertness declines and the work of breathing may become less dramatic.For children who have severe airway obstruction, such as the child presented in the vignette, the first concern should be securing the airway. The child should be left in a position of comfort and in control of his own airway until he reaches respiratory failure or loss of consciousness or an expert team has been assembled. Airway management must involve the most expert clinicians available for pediatric airways. This may be the pediatric emergency department or critical care physician, otolaryngology, or anesthesiology. Supplemental oxygen and nebulized epinephrine can be provided while assembling the team.For a child who exhibits stridor at rest, nebulized epinephrine (either premixed 2.25% racemic epinephrine for nebulization or 5 mL of standard 1:1,000 L-epinephrine) can rapidly reduce airway swelling and improve work of breathing.Diagnosis and treatment of stridor relies heavily on clinical judgment to narrow the differential diagnosis. The most useful diagnostic tools are radiologic imaging (airway soft-tissue films or computed tomography scan of the neck) and direct laryngoscopy. For children who have suspected croup, plain radiographs of the soft tissues of the neck may show the classic “steeple sign.” The steeple sign appears as an inverted V (Figure 1) and lacks the “shoulders” or subglottic lateral convexities seen on a normal inspiratory film. The lateral neck film may also show subglottic narrowing. In the case of suspected retropharyngeal abscess, an increase in prevertebral soft tissue (Figure 2) may prompt further evaluation, but computed tomography scan of the neck with intravenous contrast is usually necessary to differentiate phlegmon from drainable abscess and allow surgical planning. In epiglottitis, lateral neck imaging shows swelling of the epiglottis, classically described as a “thumb sign” (Figure 3). Direct laryngoscopy allows viewing of upper airway foreign bodies or masses as well as functional observation of vocal cord movement and tracheal or laryngeal collapse (malacia). Laboratory testing may be useful for children who have serious bacterial infections causing stridor or to differentiate bacterial from viral causes.Figure 1Steeple sign for croup. Reprinted with permission from American Academy of Pediatrics. Parainfluenza viral infections. Figure 2Prevertebral swelling suggestive of retropharyngeal abscess. Normal soft-tissue thickness should be <50% of width of vertebral body at the upper cervical spine (C2-C4) level and no more than the width of the vertebral body in the lower neck. Prevertebral tissue measurement should be assessed on a neutral or slightly extended neck. If the child is positioned with a flexed neck, normal prevertebral tissue is compressed and appears widerFigure 3Lateral neck radiography of child who has epiglottitis. American Board of Pediatrics Content Specification(s)Differentiate by age the etiology and understand the pathophysiology of stridorPlan diagnostic evaluation and initial intervention for patients with stridorRecognize serious and/or life-threatening causes of stridorQuestion: 7A 5-year-old girl is brought to the emergency department after being struck by a truck while riding her bicycle. Bystanders estimate the truck was going about 40 miles per hour when she was hit. She was thrown several feet. When emergency medical services personnel arrived at the scene, she was crying and was unable to stand and walk. They placed her on a long spine board, placed a cervical collar, and transported her to the hospital. On arrival, her Glasgow Coma Scale score is 13, heart rate is 140 beats/min, respiratory rate is 26 breaths/min, and blood pressure is 130/89 mm Hg. Physical examination shows:Abrasions to both upper and lower armsDeformity of the right upper armA large abrasion over the right flankTender abdomen with guardingStable pelvis with anteroposterior and lateral compressions Bruising on the right hip/lateral thigh without obvious deformity or swellingAbrasion over the left medial malleolus with minimal swellingShe has normal pulses and brisk capillary refill in all extremities. You order computed tomography (CT) scan of the head and abdomen and plain films of the cervical spine, chest, right humerus, right elbow, left lower leg and ankle, and right femur.Of the following, the MOST appropriate strategy for imaging of her pelvis in the trauma assessment is toA.clear her pelvis based on clinical examination findingsB.defer imaging of the pelvis until the patient can localize the painC.include the pelvis in the abdominal CT scan of the pelvisD.obtain plain films of the pelvisE.perform a focused assessment of the pelvis using ultrasonographyCorrect answer CExtremity injury and pelvic fracture should be discovered during the secondary survey phase of trauma evaluation. Comprehensive head-to-toe examination reveals most injuries but is not reliable in the girl described in the vignette because of the presence of distracting injury pain and altered mental status.? Deferring other imaging until the patient can localize pain is not appropriate. The girl described in the vignette has severe multisystem trauma and requires CT scan of the abdomen and pelvis. Additional plain films of the pelvis are unnecessary. Ultrasonography is not a sensitive imaging modality for pelvic fracture. Focused use of plain radiographs of the right humerus, elbow, and femur and the left ankle can identify any significant extremity fractures that require immediate attention.Examination of the pelvis for fracture involves visual inspection for rotation of the iliac crests or leg-length discrepancy, palpation for bony tenderness, and exertion of pressure on the iliac bones to determine stability of the pelvic ring. The unstable pelvis should be manipulated carefully, so as not to provoke fracture-related hemorrhage.? In sexually mature young men, a rectal examination should be considered to detect a “high-riding” prostate. The vagina should be examined for frank bleeding. Blood at the urethral meatus can indicate urethral injury, possibly due to pubic symphysis injury. Such injury is vanishingly rare in children but seen routinely in adults and, thus, should be considered in the adolescent patient.Pelvic fractures are described by the Tile classification. Type A fractures do not involve the posterior pelvic arch and are stable. These include avulsions, inferior pubic ramus fracture (Figure 1), and iliac crest fracture. Types B and C fractures are unstable and involve two separate disruptions of the pelvic ring (fractures or ligament tears). Type B fractures are stable in the vertical axis but rotationally unstable. They are often associated with anterior-posterior compressive forces.? Examples include open-book fractures with separation of the pubic rami (Figure 2). Type C fractures are unstable in both horizontal and vertical axes and include both anterior and sacroiliac joint disruption (Figure 3). Type C fractures require significant vertical force and, in children, are generally seen after high-altitude falls.Unstable pelvic fractures are frequently associated with hemorrhage, and the child who has experienced major trauma and pelvic fracture often presents with hemodynamic instability, whether due to the pelvic injury or associated visceral injury.? Pelvic fractures in the child who has major trauma are strong indicators of other associated injuries. Abdominal viscera, urologic, or other orthopedic injuries predominate. Among small children, the likelihood for associated head injury is very high. All children in whom pelvic fracture is suspected should undergo emergent imaging of the abdomen and pelvis (CT scan). If a CT scan is obtained, a screening radiograph of the pelvis is unlikely to add information.Examination of the extremities begins with visual inspection for skin defects (abrasion, lacerations), soft-tissue injury (bruising, swelling), and deformities. Additional evaluation is guided by the patient's level of responsiveness. For a normally responsive patient, complete examination includes palpation of all extremities for tenderness, passive or active range of motion of all joints, and weight-bearing or ability to ambulate. For the patient who has altered mentation or whose injuries preclude ambulation, only some of these evaluative measures may be practical. For a patient who has multisystem trauma and whose injuries preclude ambulation, targeted radiographs can be used to evaluate areas of suspected injury.Figure 1Type A fracture: a left inferior ramus fracture. Courtesy of J. Anders, MD.Figure 2Type B fracture: an open-book fracture with separation of the pubic rami. Courtesy of J. Anders, MD.Figure 3Type C fracture: anterior and sacroiliac joint disruption. Courtesy of J. Anders, MD.American Board of Pediatrics Content Specification(s)Recognize signs and symptoms of extremity injury in a child with major traumaRecognize signs and symptoms of pelvic fracture in a child with major traumaQuestion: 8The mother of an 8-month-old boy brings him to the emergency department and says, “It is red and swollen down there.” You determine she is talking about his genitals. On further questioning, she explains that he has been afebrile but more irritable than usual for 2 days, and he has a red, swollen penis. She is unsure about the scrotum and testicles. He also has a diaper rash, for which she uses an antifungal cream. He was circumcised at 2 days of age.Of the following, the MOST likely cause of this infant’s presentation isA.balanitisB.Henoch-Sch?nlein purpuraC.idiopathic infantile penile swellingD.paraphimosisE.phimosisCorrect Answer: AGenitourinary (GU) issues in boys can provoke substantial anxiety for the family, patient, and clinician. The most significant GU issue is likely testicular torsion, which is not a concern for the boy described in the vignette. Balanitis (Figure 1) is the most likely diagnosis for this afebrile infant. Circumcision effectively rules out phimosis and paraphimosis (Figure 2). Infantile penile (and/or scrotal) swelling is not idiopathic. Such swelling usually has an identifiable cause such as infection, local trauma (Figure 3), or insect bite (Figure 4) or an association with more general systemic issues such as cardiac, renal, or hepatic abnormalities. Henoch-Sch?nlein purpura is characterized by scrotal involvement and often but not always includes accompanying rash. Penile trauma (intentional or nonintentional, including zipper injury in an older population [Figure 5]) is part of the differential diagnosis.Balanitis (inflammation of the glans) (Fig. 1) can occur due to poor hygiene or external irritation (contact dermatitis from soaps, bubble baths, excessive manual manipulation) and can result in scarring. Cellulitis follows a break in the skin, and colonization by Candida or bacteria may be present. A purulent discharge suggests bacterial infection. If associated with fiery red erythema, streptococcal infection should be considered. Culture or rapid antigen test can be ordered and antibiotics administered. Treatment usually consists of local hygiene, warm soaks, and topical antibiotics, although oral antibiotics (often ampicillin) might be required. In some cases, application of 0.5% hydrocortisone cream may be useful. Balanoposthitis is inflammation of the glans and foreskin; posthitis is inflammation of the foreskin alone.Phimosis and paraphimosis (Fig. 2) are issues with the foreskin in uncircumcised boys. With phimosis, the foreskin (prepuce) cannot be fully retracted over the glans of the penis. This is normal in infants due to physiologic glandular adhesions that usually break down as the child ages, enabling the foreskin to be retracted. If such eventual retraction does not occur, use of a topical corticosteroid, such as 0.1% betamethasone cream, along with gentle stretching usually is sufficient. Once resolved, daily retraction should be recommended to maintain stretched size and prevent phimosis recurrence. Association with a scarring (white ring) of the prepuce differentiates pathologic from physiologic phimosis. With paraphimosis, the foreskin remains retracted behind the coronal sulcus, which may occur due to prolonged retraction of the foreskin. The condition is important to recognize and resolve because without resolution, it can lead to ischemia of the glans. Reduction by the emergency department clinician (glans squeeze to decrease edema and forceful pushing of the glans with pulling on the foreskin) or urologic consultation is required. Sedation or a penile block may be required. On occasion, a dorsal slit is required for temporary resolution. The clinician should discuss potential elective circumcision with the patient and family.A variety of other penile issues can present to the clinician. If a child had a recent circumcision, injury may result from excessive skin removal. Topical antibiotic ointment generally is sufficient treatment, although specialty referral may be helpful for further assurance. Hypospadias (ventral location of urethral meatus) is usually noticed in the newborn period. Meatal stenosis in circumcised patients results in an upward urinary stream usually noted during toilet training. Referral to a urologist for evaluation and consideration of meatotomy is important. Smegma is desquamated epithelial cells trapped under the prepuce in a noncircumcised boy and may be characterized by ballooning of the foreskin. Reassurance that this is normal can help alleviate parental anxiety. The presentation of hair tourniquets (strangulation) may mimic paraphimosis. Prompt recognition and hair removal is important. Finally, one case report in 2003 described a benign pediatric penile pyogenic granuloma of the glans penis.Figure 1Balanoposthitis. Courtesy of PEMpix, AAP Section on Emergency Medicine.Figure 2Paraphimosis. Courtesy of PEMpix, AAP Section on Emergency Medicine.Figure 3Penile trauma from the toilet seat falling on the penis. Courtesy of PEMpix, AAP Section on Emergency Medicine.Figure 4Insect bite-associated penile angioedema. Courtesy of PEMpix, AAP Section on Emergency Medicine.Figure 5Zipper entrapment injury. Courtesy of PEMpix, AAP Section on Emergency Medicine.American Board of Pediatrics Content Specification(s)Recognize signs and symptoms of common penile problems (including penile swelling, phimosis, paraphimosis, balanoposthitis, etc)Know how to evaluate and manage penile problems (penile swelling, phimosis, paraphimosis, balanoposthitis, etc)October 2012Question: 1A 9-year-old girl is brought to the emergency department approximately 1 hour after falling about 4 feet from a fence and landing on a branch. The branch went through her shirt, which she is still wearing, and penetrated the skin of her abdomen. The girl pulled out the branch before coming to the hospital. On physical examination, you note a small area of blood on her shirt but cannot discern the extent of penetration in the abdomen. The girl is anxious and in pain, exhibits mild tachycardia, but has a normal blood pressure and capillary refill time. There is no evidence of peritonitis. Due to other emergencies, surgical consultation will be delayed for about 45 minutes; you assess the girl further and consider radiologic evaluation while waiting for a surgeon.Of the following, the MOST appropriate next step puted tomography scan to evaluate for solid organ penetrationB.fluoroscopy to evaluate for abdominal foreign bodyC.no radiographic evaluation before the patient is taken to the operating roomD.plain films to assess for free air in the abdomenE.ultrasonography to evaluate for free fluidCorrect Answer: DRadiologic evaluation should never delay appropriate operative evaluation and repair, but if clinical status allows, simultaneous radiographic and operative evaluation can yield important information. For the stable patient described in the vignette, upright or lateral abdominal films could be useful to evaluate the track of penetration and the extent of embedded foreign body as well as the presence or absence of abdominal free air. Because she is stable, immediate operative evaluation is not required (or available in this case). Fluoroscopy does not add additional information beyond that available with the plain films. Ultrasonography could be helpful to assess for fluid, but the presence of abdominal fluid does not in itself necessitate operative exploration. Computed tomography (CT) scan might add further information to the evaluation but may not be needed if physical examination or plain radiography demonstrate a need for operative evaluation.Radiologic evaluation of a penetrating abdominal injury can add valuable information in the appropriate patient. Most importantly, radiologic evaluation should not impede resuscitation or surgical evaluation when indicated (unstable, hypotensive patient; signs of peritonitis). Radiologic evaluation of the chest, abdomen, or pelvis can be a useful adjunct for the stable patient in whom the extent of penetrating injury is unclear and there is concern for debris, foreign bodies, subcutaneous air, or associated fractures in the abdomen, chest, pelvis, or adjacent compartments, and it can help direct subsequent steps. If the presence of penetration is unclear, radiographic evaluation for free air and tracking of the object, coupled with local wound exploration, might prevent unnecessary operative exploration.Of note, high-speed or fragmented foreign bodies may enter at one area and lodge or transit through other body compartments, with local or global consequences. The use of CT scan for penetrating injuries can aid in recognizing multicompartment injury and identify the trajectory of the foreign body.Ultrasonographic evaluation (focused assessment with sonography for trauma [FAST]) is a rapid approach to identifying fluid collections in the pericardium, chest, and abdomen, which can help with immediate resuscitation and planning. The FAST can be useful in specific compartment injuries or to assess significant injury to adjacent areas. It has lower sensitivity in identifying specific injuries (such as subcapsular hemorrhage, bowel perforation, diaphragm, and retroperitoneum injury) and should not be used as a sole determinant for operative versus nonoperative exploration. FAST has been shown to be a useful screening tool, when coupled with an appropriate risk assessment, in hypotensive patients to rule out an intra-abdominal injury requiring surgical intervention. A positive FAST result is often followed by a CT scan in the stable patient to elucidate injuries further.Selective management of penetrating trauma includes assessing which patients will benefit or require operative exploration and repair and which might be safely managed more conservatively. This has been a standard of practice for stab wounds, and it has been adapted for some penetrating gunshot injuries. The helical CT scan can be a useful diagnostic tool for evaluation of tangential and penetrating trauma to the abdomen and flank as well as potential extension to adjacent compartments. Although a CT scan can reliably distinguish injury to solid organs (liver, spleen), it is less reliable in determining injury to hollow viscus, diaphragm, and pancreas. CT scans for evaluation of transpelvic penetrating trauma should include intravenous, oral, and rectal contrast, if possible.Ideally, all decisions regarding evaluation and management of penetrating injuries follow guidelines developed in conjunction with pediatric trauma surgeons. The specifics of each case and indications to consider evaluation schemes should include real-time surgical consultation whenever possible.American Board of Pediatrics Content Specification(s)Know the indications for and interpret the findings on plain x-ray study following penetrating abdominal/flank injuryKnow the indications for and interpret the findings of ultrasonography following penetrating abdominal/flank injuryKnow the indications for and interpret the findings of computed tomography following penetrating abdominal/flank injuryQuestion: 2A 16-year-old girl presents with fever and abdominal pain. She has been ill for 2 to 3 days with malaise and fatigue. She denies nausea, vomiting, or diarrhea. She has had no cough, sore throat, rhinorrhea, or respiratory distress. She denies hematuria, dysuria, urgency, or frequency, but her urine output today has been less than expected. She has a history of systemic lupus erythematosus that caused renal failure and underwent kidney transplant from an unrelated living donor approximately 2 months ago. She has been recovering well postoperatively and reports compliance with all prescribed medications. On physical examination, her temperature is 38.2°C, heart rate is 92 beats/min, respiratory rate is 16 breaths/min, blood pressure is 142/92 mm Hg, and pulse oximetry reading is 99% in room air. She has a well-healed surgical wound on the lower abdomen and tenderness of the abdomen in the same region. She cannot produce urine for analysis.Of the following, the MOST likely cause of this patient's fever isA.acute viral infectionB.acute rejection of allograftC.chronic rejection of allograftD.postoperative infectionE.urinary tract infectionCorrect Answer: BOrgan rejection in the transplant patient is characterized by both specific signs and symptoms of organ failure and generalized inflammatory status. Evidence of organ dysfunction or inflammation, fever, or nonspecific findings without other explanation should prompt investigation of possible rejection. The oliguria and allograft tenderness described for the girl in the vignette, who received a kidney transplant 2 months ago, is a classic presentation of acute rejection.The three most common organ transplants in pediatrics are kidney, liver, and heart. In addition, about 100 children receive intestinal transplants and 50 receive lung transplants every year.Nonspecific signs of rejection include fever, malaise, and flulike illness and may be seen in patients with rejection of any solid organ graft. Therefore, rejection can be difficult to differentiate from infection, and in most cases, empiric antibiotic therapy is begun before biopsy to evaluate rejection. Persistent fever or elevated white blood cell count despite antibiotic therapy should raise concern for rejection. Other scenarios that should raise concern in the posttransplant patient are vague somatic complaints that cannot be otherwise explained or any evidence of dysfunction of the transplanted organ. Rejection is more likely in patients who are noncompliant with immunosuppression and, for that reason, is seen more often in adolescents than in young children. Rejection is most common in the first year after transplant but can potentially present at any point, especially if a patient has recently stopped or changed immunosuppression medications.The differential diagnosis of acute rejection is broad and varies by organ. All transplanted patients are immunosuppressed, albeit at differing levels, depending on the individual, history of rejection in the past, and time from transplant. Therefore, all patients are at risk for opportunistic infection. Infection with Epstein-Barr virus (EBV), cytomegalovirus, and adenovirus is commonly encountered and difficult to differentiate from rejection. In addition, viral infection may spur development of inflammation and acute rejection. Posttransplant lymphoproliferative disease is seen in a small percentage of transplant patients, usually associated with EBV infection. Organ-specific or surgical complications may be seen, including ascending cholangitis in liver transplant, ureteral obstruction in kidney transplant, or ischemic cardiac disease in heart transplant.About 50% of renal transplant recipients have at least one episode of acute rejection. The prevalence is slightly higher in recipients of deceased donor kidneys compared with those from living donors. Kidney transplant recipients may have pain or tenderness in their allografts, hypertension, or fluid retention/edema. Oliguria in a patient who has received a kidney transplant should raise concern for rejection but is not a reliable indicator. Patients with poor concentrating ability have normal or increased urine output. Renal allograft rejection is frequently asymptomatic, and elevation of serum creatinine may be the only positive finding.Acute rejection occurs in about 50% of all children receiving liver transplants. Few clinical signs are apparent, other than fever, which is seen in about one third of cases. Laboratory findings of elevated alkaline phosphatase and transaminases are common. Hyperbilirubinemia is uncommon in acute rejection. Acute rejection is often associated with viral infection (EBV, cytomegalovirus, adenovirus), and titers or other viral studies may be helpful. Definitive diagnosis is made by biopsy. Chronic rejection of a transplanted liver is uncommon, occurring in 5% to 10% of pediatric recipients. Chronic rejection is associated with bile duct injury and symptoms of jaundice and pruritus.Heart transplant rejection is uncommon after the initial postoperative hospitalization. Most cardiac transplant rejection is asymptomatic and found on surveillance echocardiography or biopsy. About 20% of pediatric heart recipients experience an episode of rejection with heart failure, presenting with typical symptoms: tachycardia, tachypnea, oliguria, edema, hepatomegaly, or a gallop rhythm. Chronic rejection in heart transplant is synonymous with posttransplant vascular disease. Cardiac ischemia in heart transplant patients might present with chest or abdominal pain despite lack of normal sensory enervation or might be silent, presenting only with syncope or sudden death.Intestinal transplant and lung transplant are fraught with more complications than that seen with the more commonly transplanted organs. Currently, 1-year survival after intestinal transplant is about 85%, and 5-year survival after lung transplant is 50%. Both organs have historically had higher frequencies of severe rejection and require a careful balance of immunosuppression to control rejection but avoid bacterial infection. Acute rejection should be considered in the intestinal or lung transplant patient who has fever, particularly when fever or leukocytosis persists following antibiotic therapy.? Lung transplant patients experiencing acute rejection often complain of dyspnea or hypoxia. Fever is common in these patients, and differentiation from infection requires bronchoscopy, biopsy, or bronchoalveolar lavage. About 50% of children surviving more than 5 years after lung transplant develop bronchiolitis obliterans.American Board of Pediatrics Content Specification(s)Recognize the signs of organ rejection in a pediatric transplant patientQuestion: 3A 26-month-old boy is brought to the emergency department after his mother found him with an open bottle of drain cleaner that contains sodium hydroxide. At presentation, he is drooling and has swelling of the lips and scattered burns of the oral mucosa. He is not in respiratory distress and his vital signs are within normal limits for his age.Of the following, after addressing his airway, breathing, and circulation, the MOST appropriate next step in his treatment isA.administration of a weak acid (eg, orange juice) to neutralize the alkaliB.administration of activated charcoalC.administration of intravenous corticosteroidsD.administration of water to try to dilute the alkaliE.arranging for urgent esophagoscopyCorrect answer EIngestions of caustic substances remain an important pediatric safety issue. Annually, about 8% of reported pediatric ingestions involve a household cleaning substance. In almost 50% of cases, ingestions occur when the substances have been stored outside of their original containers, often in a glass or beverage bottle. Substances that have been brought home from work places may be more dangerous because they may be more concentrated and often are not in their original packaging, making identification of the substance and its concentration more difficult. Most caustic ingestions occur in children younger than 6 years of age, with a peak incidence in toddlers between 12 and 48 months of age.Acid-containing substances usually cause surface burns and coagulation necrosis. Alkalis tend to cause deep, penetrating liquefaction necrosis and, therefore, are more often associated with deep burns and the risk for perforation, especially of the esophagus. In addition to injury caused by ingestion, both acids and alkalis can cause burns on the skin and in the eyes. Acids are found in a variety of household products, including toilet bowl and drain cleaners as well as automotive wheel cleaning products. Household bleach (5% hypochlorite) is a weak acid that, in small volumes, acts as only a mild irritant and does not require treatment. Common acids to which children are exposed include hydrochloric, sulfuric, nitric, and hydrofluoric acids. Alkalis, usually in the form of sodium hydroxide (lye), are found in oven and drain cleaners as well as powdered laundry and dishwasher detergents. Hair relaxers may be alkali and may cause oral and facial burns, but usually they do not cause significant esophageal injury due to their viscous nature and the lower likelihood of being swallowed.Ingestions as well as ocular or cutaneous exposures to acid and alkali corrosives typically cause immediate and severe burning of exposed surfaces. In the mouth, pharynx, and esophagus, they usually cause severe dysphagia and drooling. If the substance comes into contact with the glottis or upper airway, obstruction may result from edema. Significant acid ingestions usually cause gastric necrosis and may lead to perforation and the development of peritonitis. Alkali injury typically is most severe in the esophagus, where perforation causes mediastinitis.Initial management should focus on providing good supportive care, with attention to airway, breathing, and circulation. Simultaneously, attempts should be made to identify the substance involved, including a complete list of its ingredients and their concentrations. Determining whether the substance is an acid or an alkali is important because of the different clinical consequences. A regional poison control center should be consulted to help with gathering this information and making subsequent decisions about management.All children who have had alkali ingestions and show symptoms of oral burns, such as the boy described in the vignette, require emergent or urgent esophagoscopy (within 24 hours) to document the extent of injuries and plan further therapy. The role of esophagoscopy in children who have been exposed to hair relaxers is unclear. Gastric decontamination is not indicated. Charcoal does not bind acids or alkalis, may cause vomiting that can lead to worsening of existing injuries, and will make assessment of injuries during esophagoscopy more difficult.The use of corticosteroids remains controversial. First-degree burns of the esophagus usually heal without sequelae and, therefore, require no additional therapy. Corticosteroids may be associated with a decreased incidence of esophageal stricture in patients who have second-degree burns. Due to an increased incidence of infections in these patients, empiric antibiotics also are often administered if corticosteroids are used. Scarring generally occurs in patients who have third-degree burns despite treatment, so the risks associated with corticosteroid administration probably outweigh any potential benefit. For the patient in the vignette, esophagoscopy should be performed before corticosteroids are considered.Theoretically, dilution and neutralization seem appropriate, but no human trials have shown benefit. Therefore, due to the risks of complications associated with these treatments, they are not recommended. If esophageal perforation already has occurred, administering fluids may cause further extravasation into the mediastinum. In addition, administration of fluids can increase the risk of aspiration and further injury during anesthesia administration preceding esophagoscopy or the procedure itself and make the assessment of injury more difficult. Neutralization also may produce an exothermic reaction, worsening the burns that are already present.If the eyes are exposed to the corrosive agent, they should be treated with copious irrigation until ocular pH measurements show that the substance has been eliminated or neutralized. All ocular injuries involving alkalis require ophthalmologic consultation due to the propensity to produce liquefaction necrosis. Skin is decontaminated by the removal of contaminated clothing and prolonged irrigation of the skin with water. In the case of alkali exposures, the skin should be irrigated until it no longer has a “soapy” feel, indicating that all of the alkali has been removed.A special circumstance involving the skin is burns due to hydrofluoric acid (HF). HF is used in glass etching and the manufacture of plastics, electronics, and computer goods. Most exposures occur in an industrial setting, but HF may be brought home to be used as a strong cleaner. When HF contacts skin, fluoride from HF binds calcium in the skin, prompting an efflux of potassium out of the cells, which irritates nerve endings. Severe burns and vascular injuries may occur with high concentrations of HF, but even smaller concentrations cause severe pain. Treatment with calcium gluconate gel has been shown to decrease pain and minimize sequelae. In severe cases, treatment with intravenous calcium gluconate has been used. Consultation with a regional poison control center should be sought and often these patients may require transfer to a burn center.American Board of Pediatrics Content Specification(s)Know specific decontamination techniques for alkali and acid exposuresQuestion: 4You are conducting a study of a new diagnostic test that can be used to identify febrile children at high risk for having bacteremia. You have used the test with a sample of 100 bacteremic children and a sample of 100 non-bacteremic controls. You are now preparing the manuscript for publication, and you want to be sure the reader gains an appreciation of the variability of the measurements among the individuals in the 2 groups.Of the following, the BEST way to do this is to report theA.95% confidence intervalB.interquartile rangeC.mean ± standard deviationD.mean ± standard error of the meanE.modeCorrect answer CA key concept in statistics is the difference between the population and a sample of the population. The sample is used to make observations and describe them for the purposes (generally) of making inferences regarding the larger population from which the sample was drawn. Any measure has some spread or dispersion. The goal of any descriptive statistic is to describe the behavior of the data accurately and completely, including measures of central tendency (the middle of the data) and the variability or dispersion around that middle.The measures of central tendency include the mean (or average of all measurements), the median (the middle observation within a range), and the mode (the value occurring most frequently). The next task is to describe the spread or dispersion around that middle in the sample. Examining the difference between each observation and the group mean creates the standard deviation (SD). When data are normally distributed (bell-shaped curve), the SD provides some additional information. For example, approximately 95% of individuals fall within 1.96 SDs of the mean in each direction, and 99% fall within 2.58 SDs within each direction. This is the source of the ± symbol: looking 1.96 SDs to the left of the mean and another 1.96 SDs to the right, with that range including 95% of observations. The other 5% are outside that range, with 2.5% in either tail.The actual goal is determine how to draw inferences to the larger population, which requires knowledge of how representative the sample is to the population. Returning the sample to the larger population and repeating the study would provide measurements on 100 more bacteremic children and 100 more non-bacteremic controls, and another measure of the mean and SD of that sample can be obtained. The sample mean varies from sample to sample and is called the sampling distribution. One could hypothetically perform the study 1,000 times and get 1,000 means. The variation around this sampling distribution is called the standard error of the mean (SEM); it is a measure of the precision of the estimated population mean. The SEM is related to the sample SD and the sample size as follows: standard error (SE) = SD/√(sample size).The larger the sample size, the tighter the sampling distribution and the lower the SE. The expression mean ± 1.96 SEs describes an interval that contains 95% of the means if one repeatedly performed the observation with samples of the same size.Because the SE, by definition, refers to means, not individuals, a description of the desired results requires use of the SD. When measuring the parameter in the larger population, the SE estimates the interval into which that measure will fall. The probability that the true measured parameter will fall within that estimated interval is the confidence interval. Again, when repeating the study 1,000 times, the confidence interval gives the probability that those multiple iterations would yield a result falling within the interval.Ranges are another way to describe the spread of data. It is sometimes useful to present data allocated to groups of equal size. This is particularly true for nonnormal data. When the first and third quartiles are used (25th and 75th centiles), this is called the interquartile range.The mode is a measure of central tendency and does not describe the variability of measurements among individuals.American Board of Pediatrics Content Specification(s)Understand the difference between standard deviation (SD) and standard error of the mean (SEM)Question: 5A 5-year-old boy presents to the emergency department with left cheek swelling of 1 week’s duration. His mother reports that the swelling initially was minor but dramatically increased in size today (Figure 1). His oral intake has decreased, but he has no sore throat, cough, earache, or fever. He had no documented trauma to his face. He had an upper respiratory tract infection 3 weeks ago. On physical examination, the boy appears comfortable, is slightly drooling, and has no stridor. His heart rate is 95 beats/min, respiratory rate is 28 breaths/min, and temperature is 37.9°C. A 5x4-cm soft lump limited within his left cheek is compressible between the face and oral cavity when palpated. It is slightly tender but has no overlying erythema and is not fluctuant. The lump has no excoriation or erythema along the buccal mucosa. His oral examination reveals no findings of note; he has no tonsillar swelling or dental caries and he can open his mouth without difficulty. Anterior cervical lymph nodes are palpable without any other noticeable neck masses.Figure 1Of the following, while awaiting soft-tissue ultrasonography of his cheek, the MOST appropriate next step is toA.administer antibioticsB.administer oral dexamethasoneC.order serum amylase assessmentD.order serum thyroid hormone and thyroid-stimulating antibody assessmentE.plan for elective intubationCorrect answer AThe soft compressible mass in the cheek that has rapidly evolved on the day of presentation described for the boy in the vignette is consistent with a lymphangioma or a lymphatic malformation. These anomalies present most commonly in the head and neck region. The most important management issue for a rapidly expanding lymphangioma is either airway compromise or concurrent infection. Systemic antibiotics should be administered because of the potential for a concurrent infection.If the location of the lymphangioma is unlikely to cause acute airway compromise and the patient presents without any stridor or respiratory distress, careful observation is appropriate. Therefore, elective intubation is not necessary for this boy, who has only slight drooling and whose lump has not extended from the cheek into the neck.? Examples of lymphatic malformations for which elective intubation may be considered is an expanding cystic hygroma in a neonate or an expanding neck mass consistent with lymphatic malformation in an infant or toddler undergoing procedural sedation for radiologic evaluation. Dexamethasone might be considered for oral lesions with potential for airway compromise. Serum amylase assessment may be helpful if there is a suspicion of salivary gland obstruction, such as the floor of mouth for ranula or along lips or buccal mucosa for mucocele. Thyroid studies might be considered if lingual thyroid is suspected (usually at the base of tongue).The Table?summarizes various oral lesions and their clinical significance. Figure 2, Figure 3, Figure 4, Figure 5, Figure 6, Figure 7, and Figure 8?illustrate a number of oral lesions.Serious/life-threatening oral lesions are those that are associated with:Respiratory or airway compromise (eg, an expanding hemorrhagic hemangioma, oral blisters seen with Stevens-Johnson syndrome)Infections (eg, lesions associated with human immunodeficiency virus due to immune deficiency)Infectious toxin (eg, toxic shock syndrome, scarlet fever)Systemic illness (eg, Crohn disease, Kawasaki disease)Systemic malignancy (eg, gingival hyperplasia seen with monocytic leukemia, diffuse nodules seen with lymphoma)Endocrine illness (eg, buccal hyperpigmentation seen with Addison disease)Figure 2Mucosal ulcers in a patient with Stevens-Johnson syndrome. Figure 3Oral ulcers associated with Crohn disease. Figure 4Koplik spots in measles. Figure 5Oral candidiasis seen in a patient with human immunodeficiency virus. Figure 6Mucocele in the lip (minor salivary gland obstructionFigure 7Ranula along the floor of mouth (major salivary gland obstruction). These can be oral or cervical (plunging masses in neckFigure 8Eruption cyst in a neonate (bluish hue due to associated hemorrhage). American Board of Pediatrics Content Specification(s)Differentiate by age the etiology and understand the pathophysiology of oral lesionsPlan diagnostic evaluation and initial intervention for patients with oral lesionsRecognize serious and/or life-threatening causes of oral lesionsQuestion: 6A 4-year-old boy presents to the emergency department with a 1-day history of fever and neck pain with decreased range of motion. He has had a mild runny nose but denies sore throat, cough, vomiting, or other symptoms. He has no history of trauma. Physical examination of the uncomfortable but otherwise well-appearing child documents a temperature of 38.6°C, heart rate of 108 beats/min, respiratory rate of 22 breaths/min, and blood pressure of 84/52 mm Hg. He has mild torticollis, holding his neck flexed forward and chin turned to the right. There are no dental caries; gingival swelling; pharyngeal erythema; drooling; adenopathy; or cervical mass, swelling, or erythema. There is no rash. He is awake and alert and answers questions appropriately. His lungs are clear bilaterally, his heart sounds are normal, and he is warm and well perfused. You obtain a lateral neck radiograph (Figure 1). The boy experiences no improvement after you administer acetaminophen and ibuprofen. Due to continued severe pain, you order laboratory evaluation, which reveals:Hemoglobin, 12.4 g/dL (124 g/L)White blood cell count. 12x103/?L (12x109/L) with 1% bands forms and 60% segmented neutrophilsPlatelet count, 228x103/?L (228x109/L)Erythrocyte sedimentation rate, 68 mm/hC-reactive protein, 120 mg/L (normal, <10 mg/L)Figure 1Lateral neck radiographOf the following, the MOST appropriate imaging study for this patient isA.airway fluoroscopyB.barium swallow studyC.flexion-extension radiograph of the cervical spineD.magnetic resonance imaging of the neckE.panoramic radiography of the mandibleCorrect Answer: DIn young infants, stiff neck or torticollis (from the Latin for twisted neck) is usually due to congenital causes (Table). The approach to an older child who presents with acquired neck stiffness must take into account the wide range of mostly benign diagnostic possibilities as well as the potential severity of a few causative entities. Although most affected children have benign, mild, or self–limited conditions, some may be potentially life–threatening. The challenge for the emergency medicine physician is to evaluate children with minimal diagnostic testing and unnecessary interventions without delaying important testing or therapy.The presentation of the child described in the vignette is most consistent with torticollis. Torticollis is most often due to benign, self-limited irritation of the neck muscles related to minor trauma, viral infections, or mild bacterial infections of the head and neck (eg, lymphadenitis or pharyngitis due to group A β-hemolytic Streptococcus). History and physical examination are often sufficient to determine the cause in these cases. Simple laboratory evaluation (rapid strep testing or throat culture) may help to establish the diagnosis. Based on this evaluation, treatment may be provided, including topical heat therapy, analgesia with acetaminophen and nonsteroidal anti-inflammatory medications, and antibiotics if there is documentation or the presumption of a bacterial infection. Symptoms are usually relatively mild, respond to simple analgesics, and resolve within a few days.When pain associated with the symptoms of torticollis is particularly severe or symptoms do not resolve as expected, as for this boy, further investigations should be undertaken to look for more serious causes of neck pain. For a child who has severe pain and elevated inflammatory markers, entities such as osteomyelitis, diskitis, and tumors must be excluded. Axial imaging techniques (computed tomography [CT] scan or magnetic resonance imaging [MRI]) should be the next imaging study obtained. If available, MRI is preferred because of the lack of ionizing radiation. In this case, MRI (Figure 2) revealed an infiltrative process in the cervical spine. After admission, further evaluation documented neuroblastoma.Airway fluoroscopy is unlikely to reveal abnormalities in a child who has no respiratory symptoms. Barium swallow studies would provide no additional information in a child who does not have difficulty swallowing or other symptoms referable to the esophagus. Flexion-extension radiographic views may be useful in the evaluation of ligamentous injuries after trauma but are impractical in this child, who cannot voluntarily move his neck. The child does not exhibit signs and symptoms of any dental or mandibular disease that would necessitate panoramic radiographs.Bacterial meningitis is very rare in fully immunized children, although it remains an important diagnosis to exclude in children presenting with stiff neck and fever. A child who has bacterial meningitis usually has some alteration in mental status, may complain of a headache if old enough, and typically resists flexion of the neck (meningismus). In addition to being alert, the boy described in the vignette appears to have stiffness that is causing flexion and rotation of the neck, which is unusual with either bacterial or viral meningitis.The absence of drooling and the normal-appearing lateral neck radiograph make the diagnosis of retropharyngeal abscess unlikely for this patient. CT scan is often used when there is concern for a retropharyngeal abscess.Cervical spine injury must be excluded in the child who presents with a stiff neck after a history of trauma. A complete neurologic examination to exclude motor or sensory deficits should be performed. For children who have a cervical spine injury, palpation of the cervical spine often reveals tenderness. These findings may be difficult to ascertain in infants and toddlers. Cervical spine radiographs, when indicated, can exclude most bony injuries to the spine. If concern remains, MRI may be used to exclude ligamentous injuries.Minor trauma may be associated with rotatory subluxation leading to torticollis. Computed tomography scan may reveal abnormal rotation of the axis (C2 vertebrae) on the atlas (C1 vertebrae). Spinal cord involvement in these cases is extremely rare because the transverse ligament of the axis is not disrupted. For children who have torticollis due to rotatory subluxation, spasm of the sternocleidomastoid muscle (SCM) and neck pain should be on the side toward which the chin is tilted. This is due to the SCM contracting in an attempt to reduce the subluxation. If SCM spasm is due to muscle trauma or inflammation, the chin usually is turned away from the involved SCM.American Board of Pediatrics Content Specification(s)Differentiate by age the etiology and understand the pathophysiology of neck stiffnessPlan diagnostic evaluation and initial intervention for patients with neck stiffnessRecognize serious and/or life-threatening causes of neck stiffnessQuestion: 7A 12-year-old girl is brought to the emergency department after she fell off her skateboard and struck her head on the sidewalk. Bystanders reported a brief loss of consciousness. She was brought home by friends and has vomited four times. On physical examination, she appears somnolent, with a Glasgow Coma Scale (GCS) Score of 13 (eye opening: 3, best motor response: 6, best verbal response: 4). She complains of a severe headache and asks repeatedly about what has happened to her and why she is at the hospital. Her vital signs are stable, with a heart rate of 82 beats/min and a blood pressure of 112/72 mm Hg. She has a large hematoma over the right temporoparietal area and mild abrasions on her right hand, elbow, and knee. Her neck and abdomen are not tender. Neurologic examination findings, including cranial nerve examination, are symmetric and otherwise intact.Of the following, the MOST appropriate next step in management isA.abdominal ultrasonographyB.cranial computed tomography scanC.cranial magnetic resonance imagingD.observation for 4 to 6 hoursE.skull radiographyCorrect Answer: BThe girl described in the vignette exhibits several signs and symptoms associated with an increased risk of intracranial injury in the setting of blunt head trauma, which necessitates computed tomography (CT) scan to evaluate for intracranial hemorrhage. Loss of consciousness, repeated vomiting, severe headache, and GCS score less than 15 (or other signs of altered mental status) are all associated with an increased prevalence of intracranial hemorrhage (as are signs of a basilar skull fracture, which are not described in this child). In a multicenter, prospective cohort study of more than 42,000 individuals, Kuppermann and associates documented that the presence of a GCS score of less than 15 or other signs of altered mental status were associated with an approximately 5% risk of a clinically important traumatic brain injury (ciTBI). The presence of multiple risk factors probably makes an intracranial injury even more likely in this child.Abdominal ultrasonography may be useful in the evaluation of possible intra-abdominal injuries following blunt trauma. However, this girl has a normal heart rate and blood pressure and no signs or symptoms of abdominal injury. Cranial magnetic resonance imaging is often more difficult to obtain than a CT scan, takes longer, and may not be as sensitive for acute bleeding or bony fractures. Observation may be indicated for children who present with isolated vomiting, mild headache, or a history of a brief loss of consciousness who appear well in the emergency department. One study has shown that observation is associated with decreased rates of CT scanning without an increase in the finding of ciTBI. However, this girl’s risk of an intracranial hemorrhage is significant enough that obtaining a CT scan should not be delayed. Skull radiographs may show the presence of skull fractures that, in children younger than 2 years of age who look well, may help with risk stratification related to ciTBI among those who have scalp hematomas. However, they play little role in the evaluation of blunt head trauma in older children.The previously cited multicenter, prospective cohort study showed that children younger than 2 years of age who have normal mental status, are acting normally according to their parents, and do not have either scalp hematoma (except in a frontal location), a history of loss of consciousness, a palpable skull fracture, or a history of a severe mechanism of injury have less than a 0.02% risk of an intracranial injury and should not have a CT scan. Children 2 years of age and older who have normal mental status and do not have signs of a basilar skull fracture, a severe headache, or a history of loss of consciousness, vomiting, or a severe mechanism of injury have a less than 0.05% risk of intracranial injury. A prospective, multicenter study in Canadian emergency departments produced similar results and recommendations.Children who have head injuries associated with increased intracranial pressure (ICP) exhibit progressive obtundation and changes in vital signs. Increased ICP may be due to focal hemorrhage (eg, epidural or subdural hematoma) or diffuse edema. If blood pressure and, therefore, cerebral perfusion pressure falls, ischemia may result, causing worsening edema and further increases in ICP. The cranial vault is a closed and rigid container for the brain, cerebrospinal fluid (CSF), and blood. Initially, increases in brain volume due to bleeding or edema cause relatively small increases in ICP due to a buffering mechanism that allows displacement of CSF and blood. However, once the buffering mechanism and, therefore, the compliance of the intracranial space is exceeded, even small additional increases in volume cause large increases in ICP. At this point, clinical deterioration is often very rapid.Initially, patients may complain of headache and have vomiting. Frequently, they are listless or lethargic and have a decreased level of consciousness. Vital signs are commonly normal. Without treatment, intracranial hemorrhage and associated edema and increased pressure may progress to produce focal findings on neurologic examination due to herniation of a portion of the brain across the falx tentorium or downward through the foramen magnum. Focal findings on neurologic examination depend on the location of the injury and the anatomic part of the brain that is compressed. Decerebrate and decorticate posturing may be seen.“Classic” herniation syndromes are reviewed in the Table. As the brainstem is compressed, vital signs become markedly abnormal and Cushing triad (decreased heart rate, increased blood pressure, and irregular respirations) may develop. This orderly progression of signs and symptoms does not always occur, and presentation may vary, with some or all of the signs and symptoms seen at various stages.0-1143000067-1073. DOI: 10.1542/peds.2010-3373. Accessed American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of intracranial hemorrhage following blunt traumaRecognize the signs and symptoms of increased intracranial pressure and cerebral herniation following blunt head traumaQuestion: 8You are on vacation in Southern California when an earthquake occurs. You are near a building that has collapsed. The scene is loud, tense, and confusing. A few ambulances arrive. You would like to help but are not sure how to be the most effective.Of the following, the action that can provide the MOST optimal aid is toA.assume patient care because you probably have the most critical care experienceB.call 911 and request more providersC.discuss efforts with local providers and determine the best course of actionD.identify the most injured patient and stabilize that person firstE.work on evacuation of the building and look for more victimsCorrect Answer: CAlthough your skill set as a physician will be of great importance in this disaster, the most appropriate initial action to address the situation described in the vignette is to discuss and coordinate efforts with the ongoing field response plan. Emergency medicine physicians should not presume to be expert at evacuation or regional field triage plans. They should allow local experts in emergency medical services and police to provide direction and interventions, including requesting more providers and evacuating buildings. Coordinating clinical interventions with local and regional providers allows the most efficient and optimal use of resources to provide maximal benefit to the most patients.Mass casualties require field triage, and the demand for medical stabilization and intervention most likely will exceed available resources. For example, in a standard prehospital or hospital response, care is directed to the most injured with all efforts to stabilize. In a high-volume mass casualty situation, care must be directed to where the most victims can be helped, and if critical intervention for any one patient jeopardizes many others by using resources inefficiently, that care must be reconsidered. Thus, the most critically injured patient is not necessarily the first to be stabilized in a mass casualty setting.Preparation is the most important part of successful mass casualty response. Emergency physicians are likely more comfortable in their home emergency departments or regions and prepared to help most effectively in those settings. Outside of that area, clinicians need to provide services that augment the local response. The specific role of emergency physicians depends on the situation and response. Ideally, local providers (police, emergency medical services, physicians, nurses, and other professionals) have developed a process for field triage of mass casualties. Understanding the importance of this preparation and having a plan can maximize the impact of a small number of providers and optimize the care and survivability for the most victims.It is also important to recognize that local first responders may not have the same expertise and level of comfort with pediatric patients as they do with adults. A pediatric expert may be able to assist in the process specifically related to care for children.Staging is an important first component of field triage. This process effectively coordinates responses and ensures safe placement of care teams and equipment. The first step of an effective field triage system is to sort victims via primary triage into general categories, including nonaffected (potential participants in the care response team), walking wounded, injured, critically injured, and dead/nonsurvivable. Once initial sorting has occurred and depending on the number and skills of providers, a secondary, more specific triage can take place. Triage should include anatomic and physiologic assessment in the context of the mechanism of injury or illness. A dynamic process to reassess and recategorize patients is important to identify those who may require a different resource. The goal of “doing the most for the most” is the widely accepted standard. A critically trained provider delivering care exclusively to one critically ill patient in the context of multiple casualties may not represent the most appropriate effort. Ideally, the triage providers are separate from the care providers to manage the flow of the process and provide the most efficient and directed care.Field triage activities also include provider safety and scene assessment. Care includes assessment of resources, both current and expected, as well as identification of injury acuity and severity, basic stabilization, and transport to identified receiving facilities when indicated. Inclusion of medical facilities in the planning and delivery process, with recognition that the standard scope of practice/volume may be exceeded, is important. Although patients with serious traumatic injuries are ideally managed in trauma centers, such an option may not be available during a disaster. Similarly, facilities that do not routinely treat children may be required to become pediatric receiving centers, depending on the disaster severity and affected volumes.Tools available for field triage include physiologic assessments (standard vital signs) and assessment of the level of consciousness. Anatomic criteria to recognize, identify, and communicate injury patterns are useful at the time of triage and in support and transfer decision-making. For example, two long bone injuries suggest significant trauma and injury. Adding the mechanism of injury to these parameters improves the ability to predict resource needs. Also important are age and preexisting illness parameters. Elderly adults are more likely to die than children. The effect of age in the stratified pediatric population is not as clear.Various triage scores and processes are available in the literature and in practice. Awareness of these and willingness/ability to participate in the process at a predetermined or assigned role allows providers to have the greatest impact in the response. The Glasgow Coma Scale can help in triage, communication, and reassessment of victims, but it has not been demonstrated to correlate with outcome when used in a prehospital environment. JumpSTART (Figure 1) and START (Figure 2) are field triage plans that can help determine field triage needs. Decision points include age, ambulation, breathing, respiratory rate, pulse, and response to painful stimuli. Categories of patients in these plans include minor, immediate, delayed, and deceased. The National Expert Panel on Field Triage published guidelines in 2011 and describes evidence and process for field triage.Mass casualty care involving children is similar to care for all injured or ill children in that attention must be paid to the family unit whenever possible. Separation from or loss of family members can be devastating to a child. Separation of patients for their required care can add an additional layer of challenge and complexity.Figure 1Figure 2American Board of Pediatrics Content Specification(s)Know the principles of field triage for pediatric illness and injuryNovember 2012Question: 1A 14-year-old girl presented to the emergency department with 3 days of persistent headache. She has no history of fever, trauma, or ingestion. She denies upper respiratory tract infection, cough, vomiting, or diarrhea. No one else at home is ill. She reports that when the headache started, she felt sensitive to light, felt nauseated, and almost vomited. Her pain is described as constant and is currently a 10/10. Results of her physical examination are unremarkable. Her vital signs are all within normal limits except for a blood pressure of 130/70 mm Hg. Acetaminophen and ibuprofen have not resolved the headache. As part of her emergency department therapy, she is placed in a dark room and receives intravenous normal saline, prochlorperazine, and ketorolac tromethamine. About 30 minutes after therapy, you are called into the room for abnormal posturing and arm rigidity. The remainder of her evaluation is unchanged; she is afebrile with normal vital signs and is able to converse in a clear fashion.Of the following, this acute change is MOST likely due toA.evolving strokeB.extrapyramidal syndromeC.ketorolac tromethamine overdoseD.neuroleptic malignant syndromeE.prochlorperazine overdoseCorrect Answer BThis is an example of an extrapyramidal syndrome (ie, a dystonic reaction) due to the phenothiazine prochlorperazine. An early or evolving stroke is unlikely without evidence of cognitive dysfunction or weakness. Neuroleptic malignant syndrome is seen with phenothiazines but includes fever and altered mental status, which are not seen in the girl in the vignette. Nonsteroidal anti-inflammatory drugs do carry an increased risk of cardiovascular thrombotic events, including myocardial infarction and stroke, but, again, there is no evidence of either at this point. Prochlorperazine overdose is possible but would present with drowsiness, sedation, hypotension, or dysrhythmias, none of which are evident.Medications in the phenothiazine class include antipsychotics, antiemetics, and antihistamines. Classes of these drugs are aliphatic compounds (chlorpromazine, promazine, triflupromazine, methotrimeprazine, levomepromazine);? piperidines (mesoridazine, thioridazine); and piperazine (fluphenazine, perphenazine, prochlorperazine, trifluoperazine). Typical antipsychotic medications antagonize dopamine receptors in several central nervous system (CNS) areas. They can also block a variety of other central and peripheral nervous system receptors, resulting in tachycardia, dry mouth, sedation, constipation, urinary retention, closed angle glaucoma, and hypotension. Cardiac ion channels can be affected, leading to prolonged QT intervals and even torsades de pointes. Acute extrapyramidal syndromes (EPS), including dystonic reactions (as in this patient) and akathisia (restless leg syndrome) can be seen. Perchlorperazine and haloperidol are two drugs that are most likely to cause EPS. Extrapyramidal reactions may be increased with concomitant issues such as dehydration, viral illnesses (varicella, rubeola), CNS infections, and gastroenteritis. Therapy for EPS includes diphenhydramine, benztropine, and amantadine, all of which are equally effective.Symptoms of phenothiazine overdose vary depending on the individual medication and the recipient. Elderly and medication-naive patients are more likely to show effects. Symptoms of EPS can occur with an overdose or with therapeutic doses. These can occur within 1 hour or as late as 48 hours after intravenous medication is given; if given orally, the onset is slower (50% within 48 hours) and can occur up to 5 days after use. If a known overdose of less than the maximal therapeutic dose per age for a 24-hour period occurs and the patient is not affected after 4 to 6 hours of observation, the patient can often safely continue observation in a home environment.The physical examination in a patient with an antipsychotic medication overdose may not be helpful in distinguishing between various types of ingestion or overdose. Pupils can be large, small, or normal. One may see parts or all of an anticholinergic toxidrome (tachycardia, mild hyperthermia, dry skin, decreased bowel sounds), but this is not consistent. Mild hypotension may be seen. Mental status changes with overdose can range from mild sleepiness to coma. If severe hyperthermia is present, this suggests the neuroleptic malignant syndrome.There are no specific laboratory tests for phenothiazine overdoses, though the standards assessments of glucose, ? human chorionic gonadotropin, and electrocardiogram should be obtained, and screening for acetaminophen and salicylates ingestion should be considered. Drugs of abuse or comprehensive urinary toxicologic assessments may be helpful as well.Treatment is supportive and includes stopping the suspected offending medication and following a standard ABC approach. One should watch for hypotension and cardiac QRS prolongation. If severely obtunded, airway assistance may be required. Seizures, if present, can be treated with benzodiazepines. If miosis is present, a trial of naloxone is warranted. There is no evidence that activated charcoal is necessary, and, as always, this should be avoided in the patient with depressed or potentially diminishing mental status.Extrapyramidal syndromes (ie, dystonic reactions) should be treated with the medications noted above. Intravenous diphenhydramine is a recommended first choice (0.5-1.0 mg/kg in children to adult dose of 25-50 mg). Benztropine, benzodiazepines, and amantadine are alternative options as well. Management of prolonged QT intervals includes correcting abnormal and maintaining normal electrolytes and not adding medications that can prolong the QT interval (see for more information). Polymorphic ventricular tachycardia can be treated with magnesium.Neuroleptic malignant syndrome (NMS) can be seen with use of these medications. NMS is thought to be centrally mediated, perhaps with a direct effect on skeletal muscle mitochondria. NMS (ie, mental status changes, rigidity, fever and dysautonomia [eg, labile blood pressure, tachycardia, and tachypnea]) can be fatal and must be recognized and managed immediately. Mnemonics to help recognize NMS have been suggested and include FEVER (fever, encephalopathy, vitals unstable, elevated enzymes, rigidity of muscles) and FALTER (fever, autonomic instability, leukocytosis, tremor, elevated enzymes [elevated creatine phosphokinase], rigidity of muscles). Other causes of this type of presentation must be considered, including CNS infection, heat stroke, and other dysautonomias. NMS often occurs during the first 2 weeks of drug therapy but can occur after a single dose as well. Haloperidol and fluphenazine are high-potency medications where there is a higher risk of developing NMS. Associations with other medications and the exact etiology of NMS are unclear. Associated, nonspecific laboratory findings include elevated creatine phosphokinase, leukocytosis, elevation of liver function test results, and myoglobinuria. Conditions that may be related include serotonin syndrome (which also includes shivering, hyperreflexia, myoclonus, and ataxia), malignant hyperthermia (a genetic predisposition, often more severe than NMS, that occurs with halogenated inhalational anesthetics and succinylcholine), malignant catatonia (often preceded by a behavioral prodrome for weeks), drug withdrawal (eg, from baclofen), and acute intoxications (eg, with cocaine or ecstasy [MDMA]). Treatment for NMS includes stopping the medication as well as other possibly contributing psychotropic medications. Supportive care as above should be provided with fever and blood pressure control as needed. Other treatment options include dantrolene, bromocriptine, amantadine, and other medications. Most episodes resolve within 2 weeks, with mortality reported at 5% to 20%.Other neuroleptic drugs have specific adverse effect profiles that should be reviewed as needed. An example is lithium, which has documented adverse effects that include hyperparathyroidism, hypothyroidism, decreased urinary concentrating ability, and weight gain. Poison control centers should be consulted with overdose scenarios or when adverse effects are encountered or of concern.American Board of Pediatrics Content Specification(s)Recognize signs and symptoms of poisoning by phenothiazines, butyrephenone, and other neurolepticsQuestion: 2A 15-year-old boy presents to the emergency department (ED) with a 24-hour, erythematous rash that his parents say is worsening. He is on day 4 of 10 of amoxicillin for otitis media. He is currently afebrile and acting well at home. The mother called the medical advice line and was told her son needed to come to the ED immediately to rule out an allergic reaction. Evaluation in the ED reveals an alert boy with normal vital signs. His tympanic membranes are not erythematous and have minimal fluid behind them. His rash is a generalized, nontender, erythematous blanching macular rash primarily over his trunk, upper arms, upper legs, and neck (Figure). There are no blisters or lesions on his mucous membranes. The remainder of his physical examination is unremarkable.FigureOf the following, the MOST likely cause of the rash isA.anaphylaxisB.angioedemaC.Epstein-Barr virusD.penicillin allergyE.Stevens-Johnson syndromeCorrect Answer: CIn general, when rashes are associated with drug use, the potential offending drug should be stopped. The described patient does not have any evidence of anaphylaxis. Considering the association of mononucleosis and Epstein-Barr virus with amoxicillin, the patient likely has a rash related to this process. He should not carry a label of penicillin allergy at this time, but he could be advised to follow up with his primary care physician to further assess for allergic risks. Angioedema presents with rapid swelling of the subcutaneous tissue and is often accompanied by urticaria (ie, pruritic, raised, circumscribed lesions with central pallor). However, the child in the vignette has no swelling and the rash is not typical for urticaria. The lack of mucous membrane involvement makes the diagnosis of Stevens-Johnson syndrome (SJS) unlikely.Children presenting for evaluation of a rash is common in the emergency department and in general practice. When these skin eruptions occur at initiation or during drug use, the broad differential of rashes still applies but is expanded to include allergic reactions, hypersensitivity reactions, anticipated medication adverse effects, and more significant issues such as SJS and toxic epidermal necrolysis (TEN). Some rashes are predictable and expected (eg, amoxicillin use in patients who have Epstein-Barr virus [≈ 60%]; sulfonamide use in patients who have human immunodeficiency virus).Whenever investigating potential drug-related skin presentation, an accurate history of skin manifestations is important. Did the rash begin before the antibiotic or medication use? Most rashes from drug exposures occur in the first couple of weeks after therapy initiation. Were there other symptoms or signs accompanying the skin changes, and has the rash progressed? Is this an allergic (ie, unpredictable and related to an individual’s specific response) or nonallergic condition (ie, an idiosyncratic reaction, a reaction associated with a drug property, a toxic drug reaction, an exacerbation of preexisting or latent disease process, or an expected drug reaction)?Adverse drug reactions can involve many body systems, but the skin is the most frequently encountered. These can be categorized as type A (predictable, dose-dependent, and common) and type B (unpredictable, uncommon, relatively dose independent, and usually unrelated to the pharmacologic drug action). In general, type A reactions comprise about 80% of drug reactions and include issues like gastrointestinal bleeding after use of nonsteroidal anti-inflammatory drugs (NSAIDs). Type B reactions account for less than 20% of adverse drug reactions and include allergic and immune-mediated responses. Type B reactions can be further subcategorized to include drug intolerance (adverse effects at typical dosage), idiosyncratic reactions, which likely involve genetic predisposition, and allergic or hypersensitivity reactions (immune-dependent). Allergic reactions can be further subcategorized into type I (mostly immediate-type hypersensitivity reactions mediated by drug-specific IgE antibodies), type II (mediated by IgG antibodies), type III (mediated by IgM antibodies), and type IV (mediated by drug-specific T lymphocytes). These classifications are well described in the article by Hauseman, et al noted in the references.The most common manifestation of drug-related reactions is delayed skin rash. They can occur anywhere from hours to 10 days after drug use. Maculopapular exanthems are the most frequently seen drug-hypersensitivity reaction and commonly occur 8 to 11 days after medication initiation, and may even occur after a drug has been stopped for several days. These are dose-related responses that usually heal with desquamation within 2 to 10 days after stopping the drug. These responses do not progress to SJS or TEN because the involved cell types are not the same.The onset of a drug-related eruption is usually within 2 weeks of starting a new medication or sooner if there was a previous exposure. The rash can begin up to 2 weeks after the drug course is completed. Discontinuing the drug usually helps lead to symptom resolution within 1 to 2 weeks. Local therapy with antihistamines, topical steroids, and antipruritics may be helpful. On occasion, the drug may need to be continued through the rash.Urticaria and angioedema are pruritic, raised, circumscribed lesions with central pallor. Lesions change, come and go, and coalesce and are precipitated by mast cells in the skin. Angioedema involves the dermis and subcutaneous tissues and, in 50% of the cases, is seen with urticaria. It can be life-threatening if it involves the airway. These can be seen with mast cell and non–mast cell activation processes. Urticaria and angioedema can be immediate, accelerated (within hours after medication exposure), or delayed (within days after exposure). Drugs most often implicated in IgE-mediated urticaria are penicillins and cephalosporins, although reactions resulting from most antibiotics have been reported.Urticaria and pruritus caused by non–IgE-mediated mast cell degranulation are well-described drug eruptions with opiates and codeine. Dextromethorphan, an opiate derivative, can also cause pruritis and urticaria. Red man syndrome, seen with rapid vancomycin infusion, is also due to mast cell degranulation. It may have accompanying urticaria and is seen more frequently with the concomitant use of opiates.Antibiotics are frequently the cause of type I hypersensitivity reactions (IgE mediated). These are important to recognize since repeated exposure can have progressive symptoms and lead to anaphylaxis. Anaphylaxis is the most severe type I hypersensitivity reaction and affects many organ systems, including the airway, skin, gastrointestinal tract, and cardiovascular system.Medications are the most frequent cause of hypersensitivity vasculitis, but direct correlation is often challenging. Criteria for hypersensitivity vasculitis (also known as serum sickness) include age older than 16 years, possible medication cause, palpable purpura, maculopapular rash, and a biopsy result that is positive for perivascular neutrophils. Associated findings include fever, petechiae, urticaria, arthralgias, lymphadenopathy, low serum complement, and elevated erythrocyte sedimentation rate. The time frame is as described for other medication-induced lesions.Exfoliative dermatitis/erythroderma is a condition where greater than 50% of the body surface is involved with erythema and scaling. Medications account for about 10 % of these presentations.SJS involves a prodrome of fever and malaise followed by rapid onset of a mucocutaneous eruption. It is frequently precipitated by medications, often after a recurring exposure. The same is true for TEN (also known as Lyell syndrome). Painful erythematous and pruritic macules progress to vesicles, bullae, and skin sloughing. SJS typically involves a smaller portion (<10%) of the body surface area than TEN (>30%), with body surface area ranging from 10% to 30% often classified as SJS–TEN overlap. Mortality increases with increasing body surface area involvement. Medications most commonly implicated are antibiotics (sulfonamides, penicillins, and cephalosporins), antipsychotic and antiepileptic medications (carbamazepine, phenytoin, lamotrigine, and phenobarbital), analgesics, and NSAIDs. The mean onset of the disease is about 17 days, but once symptoms start, there may be rapid progression, including bullae formation within 12 to 24 hours. Symptoms seen early in an illness or drug reaction that should alert the provider to the possibility of SJS/TEN include confluent erythema (erythroderma), facial edema, skin pain, palpable purpura, skin necrosis, blisters or epidermal detachment, positive Nikolsky sign, mucous membrane erosions or crusting, and tongue swelling. Skin biopsy of a suspicious lesion can be helpful in making the diagnosis. Treatment includes immediate removal of potential triggers (drugs are identified in <75% of cases), supportive care, and specific wound care in a burn unit as needed. Intravenous immune globulin has been used successfully in adult patients. Prophylactic antibiotics and systemic steroids are usually not recommended.Pustular drug eruptions (acute generalized exanthematous pustulosis [AGEP]) can be severe and mimic SJS. Ninety percent of cases are caused by drugs, often ?-lactam antibiotics, and are usually seen within the few days after beginning drug use. These sterile pustules appear within about 3 to 5 days of drug initiation, are seen on skin folds and flexor surfaces, are not painful, and do not include the mucous membranes. The patients often have fever and leukocytosis (sometimes with eosinophilia) but do not have mucosal membrane involvement.Erythema multiforme is similar in appearance but different in histology than SJS. Lesions typically affect the skin of the distal extremities, including the palms and soles, but may be present anywhere on the body. It can be associated with medication use but is often precipitated by viral or other infections and typically has a benign course.Hypersensitivity reactions are also known as drug reactions with eosinophilia and systemic symptoms (DRESS) or drug-induced hypersensitivity syndrome (DIHS). Antiepileptics and sulfonamides are often the cause of these reactions. Hypersensitivity usually occurs 2 to 6 weeks (up to 12 weeks) after drug exposure and presents with morbilliform or erythrodermic reactions with possible bullae, purpura, or papules as well as facial edema, fever, and lymphadenopathy. It can also involve the liver, lungs, kidneys, heart, thyroid, and central nervous system. The presentation can mimic a general viral infection. If one particular anticonvulsant is implicated, others in the same class should be avoided. Cross-reactivity between phenytoin, carbamazepine, and phenobarbital has been noted. There may be a genetic predisposition to hypersensitivity as well, so family members may be at risk.Fixed drug reactions often involve distinctive reactions with erythematous and edematous plaques with a grey center and possible bullae and, when chronic, a dark postinflammatory pigmentation. Reexposure leads to lesions at the same spot. Medications noted to cause fixed drug reactions include tetracyclines, barbiturates, sulfonamides, NSAIDs, salicylates, and phenolphthalein laxatives.V-shaped erythema in the gluteal/perineal, inguinal/perigenital, or other flexor areas can occur hours to days after the first dose of certain medications. About 50% of these cases are noted to be from penicillin, amoxicillin, ceftriaxone, clindamycin, and erythromycin. This 50% is known as symmetrical drug-related intertriginous and flexural exanthema (SDRIFE).Photosensitivity is comprised of phototoxic and photoallergic reactions. Phototoxic reactions are the most common and are caused by ultraviolet absorption of light by a medication, which releases energy, damages cells, and presents similar to sunburn. These are seen with higher cumulative drug doses, and severe cases may have skin sloughing and require burn care. Phototoxic medications include amiodarone, NSAIDs, quinolones, and phenothiazines.Photoallergic reactions can occur with any amount of the drug and are lymphocyte-mediated. The offending drug absorbs light and is converted to an immunologically active compound, therefore causing a dermatitis (eczema) that is often seen in the classic photodistribution areas of the face, upper chest, and back of the hands. Medications implicated for photoallergic eruptions include topical medications, fragrances and biocides added to soaps, phenothiazines, chlorpromazine, NSAIDs, and sulfonamides (along with their phototoxic capabilities).Multiple other drug-related exanthems have been noted. These include pemphigus, bullous pemphigoid, linear IgA bullous dermatitis, acute generalized exanthematous pustulosis lichen planus, alopecia, cutaneous pseudolymphoma, acral chemotherapy reactions, and drug-induced lupus.Patients can develop multiple-drug hypersensitivity syndrome, which varies from drug intolerance to immune-mediated reactions. An example is the pseudoallergic reaction with NSAIDs. However, there can be acute and severe allergic reactions to a specific NSAID. For unclear reasons, one can see reactions with different presentations to different classes of drugs. Flare-up reactions, including a flare of an underlying issue with drug exposure, are different than multiple-drug hypersensitivities and do not represent true allergic reactions.American Board of Pediatrics Content Specification(s)Know drugs commonly associated with drug eruptionsRecognize signs and symptoms of drug reactions in the skin, including urticaria, fixed drug eruptions, and photodermatitisRecognize serious complications associated with drug reactions in the skinDifferentiate between drug reactions in the skin and common dermatoses and exanthemsQuestion: 3A 5-year-old girl is brought to the emergency department after falling from the second story loft in her home. She fell approximately 10 feet onto a hardwood floor. According to her parents, she briefly lost consciousness immediately after the fall and has remained “lethargic.” She has vomited three times since the fall. On physical examination, the child’s vital signs are within normal range for age. She opens her eyes to verbal stimuli but is otherwise oriented and obeys commands. She has bruising behind her right ear and right hemotympanum. Neurologic examination reveals a Glasgow Coma Scale score of 14, equal and briskly reactive pupils, intact extraocular movements, normal cranial nerve function, and normal motor and sensory findings. The remainder of her examination yields normal results. Computed tomography (CT) scan shows no intracranial hemorrhage but confirms your suspicion of a basilar skull fracture.Of the following, the MOST appropriate next step in the management of this girl includesA.administration of prophylactic antibioticsB.child protective services reportC.magnetic resonance imaging (MRI) of the brainD.neurosurgery and otolaryngology consultationE.oral fluid challenge and dischargeCorrect Answer DThe girl described in the vignette has a basilar skull fracture (BSF) with hemotympanum that warrants neurosurgery and otolaryngology consultation. Although the risk of meningitis is increased after BSF with cerebrospinal fluid (CSF) leak, no evidence indicates that the use of prophylactic antibiotics reduces this risk, and routine administration of prophylactic antibiotics is not recommended. This girl’s injuries are consistent with the history provided by her parents, and she has no concerning historical or examination findings to indicate the need for a child protective services report. MRI is not necessary for evaluation of uncomplicated skull fracture in a patient who has normal findings on neurologic examination. Although those who have uncomplicated skull fracture can be discharged, the presence of a BSF should prompt neurosurgical consultation before determining patient disposition.BSF occurs in 4% to 15% of pediatric head injury patients. The most common causes are motor vehicle crashes, pedestrian struck by car incidents, and falls. Fractures through the skull base can result in unique clinical findings, including:HemotympanumCSF leakage from the ear (otorrhea) or nose (rhinorrhea)Bruising around the orbit (raccoon eyes)Bruising over the mastoid process (Battle sign)Cranial nerve deficits (most commonly VI, VII, or VIII)Hearing loss (either conductive or sensorineural)As many as 80% of patients who have BSFs have one or more of these findings. In addition, 40% have some degree of hearing loss, and 11% to 15% have CSF leaks. CSF leaks resolve spontaneously in less than 1 week in most cases; CSF otorrhea is more likely (60%) than rhinorrhea (25%) to resolve spontaneously. Persistent CSF leak beyond this time may require direct operative repair or a lumbar drain to decrease intrathecal pressure. Patients in whom CSF leak persists beyond 7 days have a significantly increased risk of developing bacterial meningitis. Consideration should be given to administering pneumococcal vaccine to BSF patients who have CSF leak because Streptococcus pneumoniae is the most common causative organism.Most basilar fractures can be seen on CT scan, which also allows exclusion of any associated intracranial injuries. Intracranial injuries occur in nearly 50% of patients with BSF, with cerebral contusions and subdural and subarachnoid hematomas being most common. MRI may be indicated in cases involving focal neurologic findings or persistent CSF leak. Skull films are unlikely to show fractures through the skull base.Most patients who have BSF require no specific therapy. Hospital admission is widely practiced, although those who have nondisplaced BSF, normal findings on neurologic examination, no evidence of CSF leak, and no intracranial abnormality on CT scan may be candidates for outpatient management with follow-up evaluation. Surgical intervention may be indicated if there is significant displacement of the fracture fragments, intracranial injury requiring evacuation or decompression, cranial nerve entrapment, or disruption of the ossicles resulting in conductive hearing loss.American Board of Pediatrics Content Specification(s)Plan the evaluation and management of basilar skull fracturesQuestion: 4You are planning a study to investigate the use of ultrasonography (US) in diagnosing clavicle fractures in children. You have an ultrasound machine available in your emergency department, and you have been trained in the principles of US. You have previously used US to diagnose one clavicle fracture that was confirmed by radiograph. You plan to enroll children with suspected clavicle fractures and perform both US and radiography on all of them. You will then calculate the sensitivity and specificity of US for detection of clavicle fracture.Of the following, the BEST statement about obtaining patient or family consent for this study isA.both parents must sign the consent documentB.you do not need to obtain consent because US carries no risk of harm and all children will still be getting standard care (radiography)C.you must obtain signed and dated consent prior to conducting USD.you should obtain assent from all children enrolledE.you should obtain a waiver of consent because this is emergency care researchCorrect Answer CWhile ultrasonography poses minimal risk to the patients described, ethical principles hold that a patient (or guardian) should undergo informed consent and agree to participate prior to initiation of research measures. For minimal risk research, the signature of only one parent is expected. Assent is the child agreement to participate, albeit at a lower standard than informed consent. Children should be given the opportunity to assent (or deny assent) when developmentally appropriate.Human research subjects in the United States are covered under medical regulations known as the Common Rule. These ethical principles were developed by the World Medical Association under the Declaration of Helsinki in 1981 and codified by the United States Department of Health and Human Services in 1991. The Common Rule expects that research participants undergo informed consent prior to participation. The age of consent and ability of minors to consent to research as well as to general medical care varies by state. While all medically competent persons 18 years of age or older may consent to both medical care and research in all states, states vary in their allowances for certain minors to consent without parental involvement. In general, minors may provide sole consent for their participation in research that deals with conditions and medical care for which they can already provide consent on their own (eg, sexually transmitted infections and drug or alcohol use).For all other research, children may be able to provide assent but not informed consent to participate. Instead, permission or consent of at least one parent or legal guardian is expected prior to enrollment of the child in a prospective research study. Studies involving children that carry more than minimal risk should only be conducted if a legitimate benefit can be foreseen for the patient. This benefit cannot include financial remuneration. For example, a study of an experimental drug for seizures may be approved if it is expected to reduce the frequency of seizures in enrolled patients.? Alternatively, a study that proposes to collect blood samples from enrolled patients and use them to create a new laboratory test may be approved despite lack of benefit to the patient because there is minimal harm to the patient.US Department of Health and Human Services (HHS) regulations define minimal risk studies as those in which “the probability and magnitude of harm or discomfort anticipated in the research are not greater in and of themselves than those ordinarily encountered in daily life or during the performance of routine physical or psychological examinations or tests” ().Affirmative assent to participate in a research study should be sought from children who are capable of providing assent. It may be documented by the child’s signature or by the investigator recording verbal assent. Children with normal development are usually capable of the assent process at 7 years of age. For younger children or for older children with significant developmental delays, assent is generally not required.Waivers or exception from informed consent for emergency research can be obtained, but only in narrow circumstances. Federal regulations permit such exceptions for research that involves new or improved therapies for life-threatening conditions for which current therapy has poor outcomes. Waivers are granted only when the potential therapeutic window for initiation of the study procedure is so narrow that consent cannot be reasonably obtained prior to initiation of therapy. Obtaining such a waiver requires community consultation and notification and establishment of a data and safety monitoring board.In addition to HHS regulations covering consent, the US Food and Drug Administration Office of Good Clinical Practice promotes adherence to the intent of human subject protection guidelines in clinical trials. Concepts of good clinical practice (GCP) address the stringent application of best practices for ethical conduct of informed consent and research practices. Principles of GCP include the following:Only trained designees should obtain consent.Consent should be conducted in a language of fluency for the person providing consent.Written consent should be obtained prior to initiation of any study procedures; verbal agreement is not sufficient.American Board of Pediatrics Content Specification(s)Know the appropriate procedures for obtaining consent for the participation of a minor in researchQuestion: 5A 14-month-old child is brought to the emergency department for evaluation of blood in the diaper. The parents report that the child has had issues with constipation since changing to whole cow milk at 1 year of age. He currently has bowel movements, often large and hard, every 2 to 3 days. Today he cried during and after having a bowel movement, and the parents noticed bright red blood on the outside of the stool and on the wipe they used to clean him. He has not had other bleeding or similar episodes before. The parents deny any fever, vomiting, diarrhea, diaper or other rashes, or change in oral intake.On examination, the well-appearing and active toddler is in no distress. His vital signs are all within normal range for age. His abdomen is soft, nontender, and nondistended with normal bowel sounds; there are no palpable abdominal masses. Examination of his perineal area reveals a superficial vertical tear in the posterior (6-o’clock position) anoderm. There is no active bleeding.Of the following, the MOST appropriate next steps in the management of this patient includeA.abdominal radiograph and gastroenterology consult for sigmoidoscopyB.Child Protective Services report and sexual assault evidence plete blood cell count and serum inflammatory marker measurementD.stool softener, high-fiber diet, and sitz ical nitroglycerin, high-fiber diet, and gastroenterology follow-upCorrect Answer DThe child in the vignette has an acute anal fissure (AF) resulting from the passage of large, hard bowel movements. Initial therapy for an AF includes treatment of the underlying cause, pain management, and reduction of anal sphincter tone. In this case, use of a high-fiber diet and stool softeners should improve the size and consistency of the stool, and the use of sitz baths can aid with both pain relief and high sphincter tone. Other topical or local therapies, including topical nitrates or calcium channel blockers, can be used in cases that recur after conservative management or fail to improve but would not be first-line therapies in this toddler. An acute AF in the posterior midline of a toddler with constipation is not concerning for abuse and does not warrant evidence collection or a Child Protective Services report. Gastroenterology consultation may be indicated for chronic or complicated AF but is unnecessary in the initial evaluation and management of a patient with a simple acute AF. Blood tests, sigmoidoscopy, or colonoscopy may be performed in patients with suspected secondary AF as a result of inflammatory bowel disease or other systemic disease; there is no history or examination evidence of this in the child in the vignette.An AF is defined as a tear in the skin in the anal canal distal to the dentate line (ie, the anoderm). AFs are termed acute if they heal in less than 6 weeks and chronic if they persist beyond that time. AFs can also be classified according to etiology, with primary AF resulting from direct local trauma or irritation and secondary if they are a result of underlying disease. Causes of primary anal fissure include the following:ConstipationDiarrheaSexual AbuseAnal sexVaginal deliveryCauses of secondary anal fissures are as follows:Inflammatory bowel diseaseInfectionHuman immunodeficiency virusChlamydiaSyphilisTuberculosisSarcoidosisMalignancySquamous cell carcinomaLeukemiaPrior surgical proceduresThe vast majority of primary AFs occur in the posterior midline, with a small percentage in the anterior midline; primary AFs are rarely peripherally located. AFs are most common in infants and middle or late adulthood. In infants and toddlers, the most common causes include constipation and diarrhea. With increasing age, secondary AF and AF resulting from sexual abuse or anal sex increase in frequency.The pathogenesis of AF begins with trauma or infiltration of the anal mucosa, leading to abnormal stretching of the tissues. Once a tear occurs, a cycle of pain, muscle spasm with increased internal sphincter pressure, and further tearing begins. Because of this repeating cycle, up to 40% of AFs become chronic. The pain is often exacerbated during and immediately after passage of bowel movements and is described as a tearing or stabbing pain. Bleeding may occur and typically manifests as a small amount of bright red blood on the outside of stool or on the toilet paper or wipes used after a bowel movement. Examination of the perianal region reveals the tear in the anoderm; acute fissures resemble a new wound, while chronic fissures have raised edges and are often associated with skin tags and hypertrophied anal papillae. Other perianal diseases that can be confused with fissures or occur in conjunction with them include perianal abscesses, fistulas, and ulcers. The appearance, absence of purulence or fluctuant mass, and history should differentiate these lesions.The mainstays of treatment for AF include reduction of anal sphincter tone or pressure, pain control, and identification and treatment of the underlying cause. Because pain is exacerbated by passage of bowel movements, increasing fiber and fluid intake and use of stool softeners is a key part of the management. Sitz baths can aid with pain relief but also serve to reduce sphincter tone and decrease the risk of further tearing of the anoderm.? Manometry studies have demonstrated that resting anal pressure is elevated in patients with AF; therefore, in more severe or persistent cases, reduction of this pressure through topical or systemic medications (calcium channel blockers), dilation, surgical sphincterotomy, or local injection of botulinum toxin, has been shown to improve healing and prevent recurrence of AF. Doppler and angiography studies have demonstrated that local blood flow is lowest in the posterior midline of the anal region, and that patients with AF also have relative ischemia at the site, most likely due to muscle spasm and vascular compression. This has led to the use of nitrates and other vascular agents, either topically or systemically, in the management of AF. Topical medications generally have fewer systemic adverse effects and are preferred to systemic medications or surgery. Botulinum toxin injection, dilation, and surgical management are associated with increased rates of incontinence and are reserved for cases that fail conservative and medical management. Lesions complicated by abscess or fistula formation require drainage or excision, respectively. Identification and management of underlying diseases should be undertaken for cases of secondary AF.American Board of Pediatrics Content Specification(s)Differentiate by age the etiology of anorectal fissures/abscessesRecognize signs and symptoms of anorectal fissures/abscessesPlan the management of anorectal fissures/abscessesQuestion: 6A 3-month-old girl is brought to the emergency department for evaluation of fever. The mother is concerned because she herself was recently diagnosed with human immunodeficiency virus (HIV) infection and was told to have her daughter evaluated and tested but failed to do so. Prenatal serologies were negative, including HIV, but subsequent testing for HIV was positive. The girl has had poor weight gain but has not had any other problems. She developed a fever (up to 38.9°C) the day before evaluation. She has been feeding well and acting normally and has had no vomiting, diarrhea, rash, or respiratory symptoms.On examination, the infant appears small for age but is otherwise alert and well-appearing. Her temperature is 38.3°C, pulse rate is 160 beats/min, respiratory rate is 40 breaths/min, and blood pressure is 72/50 mm Hg. Pulse oximetry shows oxygenation is 100% on room air. The head, ears, eyes, nose, and throat examination reveals oral thrush. Cardiovascular and respiratory examinations are unremarkable. Abdominal examination reveals mild hepatosplenomegaly but is otherwise normal. The remainder of the examination is unremarkable. Laboratory evaluation reveals the following:White blood cell count, ?4,600/?L (4.6 × 109/L)Hemoglobin, 8.2 g/dL (82 g/L)Platelet count, 110 × 103/?L (110 × 109/L)Results of urinalysis show 0 white blood cells, no bacteria, and 0 red blood cells.Of the following, the BEST test(s) to establish this infant’s HIV status includeA.enzyme-linked immunosorbent antibody assay with Western blot confirmation if positiveB.HIV culture from blood, urine, and cerebrospinal fluidC.HIV DNA polymerase chain reaction with viral load confirmation if positiveD.viral load testing on the mother and enzyme-linked immunosorbent assay on the infantE.Western blot antibody assay with viral load confirmation if positiveCorrect Answer CThe infant in the vignette is being evaluated for perinatal human immunodeficiency virus (HIV) transmission. Due to the persistence of maternal antibodies, traditional antibody testing with enzyme-linked immunosorbent assay (ELISA) or Western blot technology are not recommended as first-line testing in infants under 18 months of age born to HIV-positive mothers. Polymerase chain reaction (PCR)-based testing for HIV DNA is the first-line testing for infants born to HIV-positive mothers. Positive results can then be followed up with RNA PCR, also known as a viral load test. Viral load may be falsely low or nondetectable in infants born to mothers treated with appropriate antiretroviral therapy (ART). Viral cultures for HIV are not routinely performed and require a longer time for results.? Viral load testing on the mother does not aid in establishing the status of this 3-month-old infant, since infants born to untreated HIV-positive mothers have only up to a 30% likelihood of becoming infected.With the advent of improved screening, treatment, and postexposure prophylaxis, the rate of HIV acquisition through perinatal, blood product, and occupational exposures has decreased significantly in the United States and other developed countries. The most common route of infection in developed countries is now high-risk behaviors (eg, multiple sexual partners, unprotected sex, and intravenous drug use) in adolescents and adults. Use of antiviral therapy during the third trimester and in newborns during the first 6 weeks after birth significantly reduce the rate of transmission in utero and perinatally.? Avoidance of breastfeeding further reduces the risk of maternal–infant transmission. Infants born to women known to be HIV-positive should be tested within 48 hours of birth and, if negative, retested at 2 weeks and again at 2 to 4 months of age. Some experts advocate a final test with both PCR and antibody ELISA at 18 months to prove clearance of maternal antibody and definitively establish the child’s status. Infants and young children born to untreated mothers with unknown or negative HIV status can be screened with HIV-antibody ELISA tests; positive results should be followed with viral load testing of both mother and infant.HIV is an RNA retrovirus that is transmitted through sexual contact (genital–genital, genital–anal, or genital–oral), exposure to infected body fluids (blood, semen, vaginal fluids, tissues, or breast milk), or from mother to infant in utero or peripartum. After gaining entry, the virus binds to CD4+ lymphocytes, monocytes, macrophages, dendritic cells, and intestinal endothelial cells and enters the cells. Reverse transcriptase enzyme then transcribes the RNA into DNA, allowing incorporation into the host cell’s DNA through the action of viral integrase enzymes. Messenger RNA is then produced, which leads to the synthesis of large viral polypeptides; cleavage of these large proteins by viral proteases produces new viral proteins and enzymes that couple with viral RNA to create new viral particles. The new viral particles are released from the cell, enter the serum, and then infect new cells. These steps in viral replication have been targeted in the development of HIV therapies: inhibitors of cell entry, reverse transcriptase, protease, and integrase enzymes.Most individuals infected with HIV develop symptoms of acute HIV within days to weeks of exposure. Some patients can remain asymptomatic for 6 months to a year or more after primary infection. Symptoms of acute HIV infection are generally nonspecific and resemble common viral infections.? Common symptoms include fever, lymphadenopathy, pharyngitis, mucocutaneous ulcers, rash, myalgias, arthralgias, and headache.? Hepatosplenomegaly, parotid gland enlargement, and aseptic meningitis occur in some patients. Most children with HIV present with chronic HIV due to the nonspecific symptoms of the primary acute infection. Infants and children with HIV may present with failure to thrive, chronic diarrhea, persistent thrush, lymphadenopathy, hepatosplenomegaly, prolonged fevers, and recurrent infections. Developmental delay or loss of previously attained milestones is common. Laboratory abnormalities associated with HIV infection include leukopenia, anemia, thrombocytopenia, and elevated liver transaminases.As HIV-induced loss of CD4+ lymphocytes and resultant immunodeficiency occur, opportunistic infections become likely. Although certain unusual organisms frequently occur in HIV-infected patients, it is important to consider infection with common bacterial and viral pathogens in the pediatric age group. Streptococcus pneumoniae remains the most common cause of pneumonia, bacteremia, and meningitis in HIV-positive children. The following are common opportunistic infections seen with HIV:PulmonaryPneumocystis jirovecii (previously Pneumocystis carinii, [PCP])Mycobacterium tuberculosisMycobacterium avium complexCytomegalovirusGastrointestinalCryptosporidium speciesGiardia lambliaMicrosporidiaCytomegalovirusCentral Nervous SystemCryptococcus speciesToxoplasma gondiiMycobacterium tuberculosisSkinVaricella virusMolluscum contagiosum virusFever and other infectious symptoms are common reasons for patients with HIV to present to the emergency department. Because of the underlying immune defect, careful attention to hemodynamic and respiratory status and evaluation for serious infections should be the focus. Ill-appearing patients or those with evidence of severe infection should receive empiric antibiotic therapy and be hospitalized.? Complete blood cell count should be compared to baseline for the patient, and blood cultures should be obtained.Respiratory signs and symptoms should prompt assessment of pulse oximetry and chest radiography. Children who are still in diapers or having urinary symptoms should have urinalysis and urine culture obtained. Stool studies for leukocytes and occult blood, culture, ova parasites, and Clostridium difficile should be sent in patients with significant diarrhea. Consultation with the patient’s infectious disease specialist should aid in deciding additional testing, management, and hospital admission.Treatment of children with HIV requires a multidisciplinary approach to address the general pediatric, infectious disease, nutritional, psychosocial, and developmental aspects of the disease. ART should be managed by an HIV specialist; generally, multidrug regimens aimed at the various steps of viral replication—as outlined previously—are employed to decrease viral load and reduce the risk of development of drug resistance. Specific regimen selection is based on multiple factors, including drug resistance patterns, compliance, toxicities, and availability of pediatric formulations. Initiation of treatment during acute HIV infection in older children and adults is controversial; symptomatic improvement and more rapid reduction in viral load are balanced with the risk of development of drug resistance or adverse drug effects during this period of high viral load and rapid replication. ART initiation in children older than 1 year and in adults is based upon clinical symptoms, CD4 counts, and viral load. ART is recommended in all infants under 1 year of age because of the higher mortality and risk of rapid progression in this age group. Due to the number of medications used and the need for frequent antibiotics and other therapies, drug reactions and interactions are frequent occurrences. Monitoring of blood counts, liver and pancreatic enzyme levels, renal function, and electrolytes in addition to CD4 counts and viral load is necessary over time. Poor compliance can lead to drug resistance, treatment failure, and opportunistic infections.? More information regarding antiretroviral therapy and other HIV-related guidelines can be found online ().American Board of Pediatrics Content Specification(s)Differentiate by age the etiology and understand the pathophysiology of human immunodeficiency virus infectionRecognize signs and symptoms of human immunodeficiency virus infectionRecognize and interpret relevant laboratory and imaging studies for human immunodeficiency virus infectionRecognize life-threatening complications of human immunodeficiency virus infectionPlan management of acute human immunodeficiency virus infectionQuestion: 7A 2-year-old boy is brought to the emergency department (ED) after he was found playing in a closet and sucking on mothballs at his grandmother’s house. He vomited once after his mother gagged him while removing the mothballs from his mouth. The parents have brought the moth ball box; the main ingredient is naphthalene. He smells like mothballs but is otherwise happy and alert. He has a temperature of ?37.1°C, heart rate of 116 beats/min, respiratory rate of 22 breaths/min, and blood pressure of 88/58 mm Hg. Results of his physical examination are completely unremarkable. He tolerated eating a snack in the ED.Of the following, the MOST appropriate disposition for this young boy isA.admit to hospital for 24-hour observation periodB.discharge immediately and follow up in 2 daysC.discharge immediately; there is no follow-up necessaryD.observe in the ED for 4 hours; no follow-up is necessary if he remains wellE.observe in the ED for 4 hours and follow up in 2 daysCorrect Answer: BMothballs containing naphthalene will cause few immediate symptoms but can cause intravascular hemolytic anemia in the days following ingestion. Children with glucose-6-phosphate dehydrogenase (G6PD) deficiency are at risk for severe hemolysis, but any person exposed to naphthalene may develop hemolysis. The patient may be discharged immediately because there is no specific treatment for this toxic ingestion and hemolysis will occur over a period of days. Close follow-up is important to allow recognition and timely initiation of supportive care should hemolysis result.? Naphthalene is one example of ingestion with delayed toxicity.Delayed presentations of toxic ingestions may be grouped into a few broad categories. The most concerning group is agents that lack immediate symptoms or present with mild or nonspecific symptoms but can nonetheless cause severe injury. The classic description of these agents includes 3 or 4 phases of toxicity:Phase I: Immediate symptomsPhase II: Latent periodPhase III: Delayed toxicityPhase IV: Resolution or permanent injurySome agents may have delayed toxicity when mixed with other ingestions. For example, metabolism of toxic alcohols (and development of toxicity) will be delayed by coingestion of ethanol. A second group is agents with long-acting or slow-release formulations, where symptoms may be present soon after ingestion but the scope of toxicity may not be seen for several hours. Finally, some pills may form a bezoar or concretion in the gastrointestinal (GI) tract and effectively create a slow release. Aspirin is the classic example of this phenomenon. Table 1?presents several poisonings associated with delayed toxicity that may be relevant to the pediatric emergency provider.Management of any child with a toxic ingestion begins with an attempt to identify the agent ingested, the time of ingestion, and the amount ingested. Careful consideration should be given to any drugs or toxic items to which the child may have had access. ?Physical examination and screening laboratory testing may provide other clues.? Complete blood cell count, transaminases, coagulation tests, and blood pH may be useful screening tests for the child with a suspected ingestion. Radiographs of the abdomen may reveal radiopaque ingestions or bezoar. If the child has ingested an agent known to have delayed toxicity, specific management will vary with the exact agent. Advice from a regional poison center can be reached anywhere in the United States by calling 1-800-222-1222.General principles of toxicological management should be applied and may be generally adapted to the care of a child with delayed toxicity in the following ways. The first phase of management begins with GI decontamination. Inducement of vomiting is not advised in the emergency department. Gastric lavage is indicated in extremely narrow circumstances: when the patient presents rapidly after ingestion, when the ingestion is life-threatening, when the agent is not absorbable by charcoal, and when no specific antidotes are available. If the ingested agent is absorbable by charcoal, activated charcoal should be provided at a dose of 1 g/kg of body weight. Multiple-dose activated charcoal may also be recommended in the scenario of possible life-threatening ingestion of a slow-release agent that is well bound by charcoal. Whole bowel irrigation is recommended for lead or iron ingestion. It may also be used in settings with sustained-release medications. The second phase of management is provision of specific antidotes if they exist. Table 2?describes antidotes available for specific ingestions with delayed toxicity. The third phase of management is supportive care. For children with ingestion of long-acting or slow-release medications, an observation period of 6 to 24 hours may be required. For children with ingestions where toxicity may present after a latent phase, observation or laboratory follow-up should be guided by the expected natural course.American Board of Pediatrics Content Specification(s)Know which ingestions are associated with delayed toxicity (eg, oral hypoglycemic drugs)Plan the management of ingestion of an agent associated with delayed toxicityQuestion: 8A 16-year-old girl presents to the emergency department with complaints of chest pain and nonproductive cough for the past 2 days. The chest pain is sharp in nature and worsens only when she coughs. She does mention that she occasionally feels short of breath. A review of her past records reveals 2 visits for hyperventilation and a diagnosis of psychogenic nonepileptic seizures. She denies being sexually active. Physical examination reveals a slightly anxious-appearing but otherwise comfortable adolescent with a temperature of 38.4°C, a pulse of 100 beats/min, and a respiratory rate of 26 breaths/min. She complains of pain in her left axillary region, but it is nonreproducible on examination. Air entry is equal bilaterally and her oxygen saturation is 98% on room air. While she is waiting for her chest radiography results, her fever resolves after a dose of antipyretics and she mentions that she is “feeling better.” The chest radiograph is interpreted as normal and the emergency department provider is considering discharging her with a diagnosis of musculoskeletal pain with a possible behavioral component. The radiology resident communicates that there may be a retrocardiac infiltrate with some blunting of the cardiophrenic angle.Of the following, the BEST next step in management isA.admission for parenteral puted tomography scan of the chestC.discharging home on oral antibioticsD.reassurance and outpatient counselingE.thoracentesisCorrect Answer: CThe patient described in the vignette has a parapneumonic effusion, or pleurisy, secondary to an underlying pneumonia. The patient is in no respiratory distress and can be safely managed on outpatient antibiotic therapy. Although the patient has a prior history of anxiety and psychogenic nonepileptic seizures, the present signs and symptoms are related to her pulmonary infiltrates and are not behavioral in nature. A computed tomography scan of the chest or thoracentesis would be indicated if one suspects a noninfectious cause, if the amount of accumulated fluid is large enough to cause respiratory distress, or if a specific analysis of the pleural fluid is desired. Infectious processes involving the underlying lung (eg, bacterial pneumonia, viral pneumonitis, or tuberculosis) are the most common causes of inflammation of the pleural surfaces, followed by systemic inflammatory diseases such as systemic lupus erythematosus and other rheumatologic conditions, heart failure, and metastatic intrathoracic malignancies.? Pleurisy can be seen infrequently in patients who have uremia, pancreatitis, subdiaphragmatic abscess, and aspiration pneumonia.Normally, less than 15 mL of pleural fluid exists between the visceral and parietal layer of pleurae. Pleural fluid dynamics is controlled by (a) balance between hydrostatic and osmotic pressures in the pleural space and pulmonary capillary bed, (b) permeability of the pleural membrane, and (c) lymphatic drainage.Pleurisy is categorized according to the characteristics of the pleural fluid as dry or plastic pleurisy; serofibrinous or serosanguinous pleurisy (pleural effusion); and purulent pleurisy or empyema. Both dry pleurisy and serofibrinous pleurisy are seen in patients with underlying pneumonia or rheumatologic diseases and may represent the worsening of pleural inflammation as more fluid accumulates in the pleural space. However, empyema occurs when bacteria invade the pleural space and there is an accumulation of grossly purulent fluid. Irrespective of cause, effusions go through 3 loosely defined stages: exudative, fibrinopurulent, and organizational. The exudative phase lasts for 24 to 72 hours, and the fluid is characterized by normal pH, cell count, and glucose. Radiographs demonstrate layering of fluid on lateral decubitus position. Fibrinopurulent stage is characterized by an increase in polymorphonuclear cells, bacterial invasion, fibrin deposition, and formation of loculations. The pleural fluid pH and glucose concentrations decrease while the lactate dehydrogenase levels increase. The pleural fluid in this phase does not layer on lateral decubitus position. The organizational phase is characterized by fibroblasts that form a pleural “peel” on the visceral and parietal surfaces and may restrict lung reexpansion. This phase typically develops 2 to 4 weeks in the course of the effusion.Although the signs and symptoms of the underlying disease usually overshadow those of pleural involvement, pain that is exacerbated with deep breathing, straining, or coughing is typical. As the disease progresses from dry to serofibrinous pleurisy, the leathery, rough, auscultable inspiratory pleural rub may disappear, and, depending upon the amount of fluid collection, patients show signs of pleural effusion in the form of decreased air entry, dullness on percussion, and shift of mediastinum away from the affected side. In the early stages of pleural fluid collections, chest radiography reveals opacification associated with pneumonia along with obliteration of costophrenic and cardiophrenic angles. Radiographs in supine and upright positions can also be useful to demonstrate a shift in effusion. Thoracentesis should be considered for either diagnosis (to distinguish between an exudate versus a transudate) or therapeutic purposes (in cases of large accumulations of pleural fluid). Therapy is usually directed towards the underlying disease. Tube thoracostomy may be indicated if pH of pleural fluid is less than 7.20 or if the glucose level is less than 50 mg/dL. Purulent fluid may require tube drainage with thrombolytic therapy or video-assisted thoracoscopic surgery (VATS). Most pleural effusions resolve completely and relatively rapidly.American Board of Pediatrics Content Specification(s)Know the epidemiology and etiology and understand the pathophysiology of pleuritis and costochondritisRecognize signs and symptoms of pleuritis and costochondritisRecognize and interpret relevant laboratory, imaging, and monitoring studies for pleuritis and costochondritisPlan management of acute pleuritis and costochondritisDecember 2012Question: 1A 4-year-old boy who has epilepsy is brought by emergency medical services to the emergency department in a postictal phase after suffering from a generalized tonic-clonic seizure that lasted for 5 minutes. Examination reveals a drowsy child with a heart rate of 120 beats/min, respiratory rate of 20 breaths/min, normal blood pressure, and a pulse oxymetry reading of 90% on room air. He is snoring, and there is some drooling.Of the following, the BEST next step in management is toA.administer supplemental blow-by oxygenB.perform bag-valve-mask ventilationC.place a nasopharyngeal airwayD.place an oral airwayE.suction the mouthCorrect Answer EThe patient described in the vignette is experiencing respiratory distress that is secondary to obstruction of the airway due to retained oral secretions and posterior displacement of the tongue over the hypopharynx. Before performing any rescue measures, it is important to suction secretions and clear the airway. The chin-lift or jaw-thrust maneuvers should be performed to open the airway in an unresponsive child before any more invasive airway adjuncts are utilized. These maneuvers place the airway in a neutral position and move the tongue and palatal tissues away from the posterior wall of the pharynx. Jaw-thrust, not chin-lift, maneuver along with inline immobilization of the cervical spine is essential if trauma is suspected. The placement of an airway adjunct such as a nasopharyngeal or oral airway may be necessary if the chin-lift and jaw-thrust maneuvers are unsuccessful in opening the airway. Administration of supplemental oxygen either by blow-by or with bag-valve-mask ventilation may be important but not before suctioning the mouth and repositioning the airway.Respiratory failure is defined as the inability of the respiratory system to provide sufficient amounts of oxygen to meet metabolic demands (hypoxemic failure) or excrete excessive carbon dioxide produced by the body (ventilator failure). The term respiratory distress is used to describe signs and symptoms of abnormal respiratory pattern. Although respiratory failure can present suddenly (foreign body aspiration), most patients will exhibit signs of impending respiratory failure, such as respiratory distress in the form of abnormal respiratory patterns, accessory muscle use, nasal flaring, cyanosis, and increasing lethargy, and it is incumbent on the clinician to recognize these signs, anticipate respiratory failure in certain clinical situations, and be prepared to intervene to reduce morbidity and mortality. Unlike adults, respiratory insufficiency leading to respiratory arrest typically precedes cardiac arrest for most children. It is important to recognize that the anatomic differences in the airway make pediatric patients more prone to respiratory distress. The differences include the higher, more anteriorly positioned larynx, which can get obstructed with neck hyperextension; the inherently smaller diameter of the airway that exponentially increases resistance to airflow (Poiseuille law), which is further exacerbated in presence of edema; mucus plugging or foreign bodies; relatively larger occiput, which causes passive flexion of the cervical spine and further narrows the airway by causing the posterior pharynx to buckle during resuscitation; and the relatively larger tongue, which covers the hypopharynx, especially in an unconscious child.Management of acute respiratory failure is well described in the Pediatric Advance Life Support and Advanced Pediatric Life Support guidelines and begins with a systematic evaluation of airway patency, followed by supporting breathing efforts and improving the circulation. It is essential to be prepared both in terms of availability of functioning equipment and in terms of trained personnel specific for management of pediatric respiratory failure. If noninvasive relief of obstruction fails, airway adjuncts such as oral and nasopharyngeal airways may be useful to improve ventilation. An oral airway can be used in an unconscious child to lift the tongue and pharyngeal soft tissues off of the posterior pharynx, which maintains a patent airway and is usually used when the obstruction is expected to be temporary (as described in the vignette). In contrast to an oral airway, a nasopharyngeal airway bypasses obstruction caused by the tongue and pharyngeal soft tissues with minimal contact with the tongue and is less likely to induce emesis; therefore, it is frequently used in conscious patients with upper airway obstruction (eg, adenoid hypertrophy, tonsillar hypertrophy, and macroglossia). If prolonged need for airway adjuncts is anticipated or if clinical improvement fails to occur, patients should be considered for placement of a definitive airway such as endotracheal tube or tracheostomy.American Board of Pediatrics Content Specification(s)Plan management priorities for patients in respiratory failureKnow indications for adjuncts to airway managementQuestion: 2Late Saturday evening, a trio of teenaged girlfriends present to the emergency department requesting pregnancy testing and sexually transmitted infection (STI) screening. You begin with a 16-year-old who states she is sexually active with one partner and occasionally uses condoms. Her last period was 3 weeks ago. Her last sexual activity was 24 hours ago. She reports that her partner was recently diagnosed with an STI and therefore wishes to be tested herself. She has prior history of pregnancy that ended in elective termination more than a year ago. She also has a prior history of “some kind of infection” in her genital area.Of the following, the MOST suggestive symptom(s) or sign of a diagnosis of cervicitis isA.abdominal painB.feverC.irregular vaginal bleeding (spotting)D.nausea and vomitingE.pain with urinationCorrect Answer CThe key differential diagnosis in a patient with likely sexually transmitted infection (STI) is separating uncomplicated cervicitis from pelvic inflammatory disease (PID). PID treatment includes a longer course of antibiotics, and the diagnosis requires more stringent follow-up because it carries a substantially higher risk of complications. Of the available options, the most specific symptom of cervicitis is spotting or irregular bleeding. Presence of abdominal pain, fever, or nausea and vomiting in a patient with an STI should lead to clinical diagnosis of PID with commensurate treatment. Pain with urination can be seen in patients with cervicitis but is not specific, and an alternative diagnosis of cystitis should be excluded.Urethritis and cervicitis refer to inflammation usually caused by infections of the lower reproductive tract (cervix in the female, urethra in the male). Both are most commonly caused by sexually transmitted infections—chiefly, Neisseria gonorrhoeae and Chlamydia trachomatis and, less commonly, herpes simplex virus and trichomonal infection. In addition, cervicitis may result from mechanical or chemical irritation.? Examples include irritation from intravaginal objects, latex allergy, and sensitivity to spermicide or other chemicals to which the cervix may be exposed. Urethritis, but not cervicitis, has been associated with other infectious agents, including Mycoplasma genitalium, Mycoplasma hominis, Ureaplasma urealyticum, and Ureaplasma parvum.Symptoms of cervicitis may include dysuria, urinary frequency, vaginal discharge, vaginal bleeding, and pelvic or vaginal pain, especially pain with sexual intercourse. Severe abdominal pain and fever are rarely associated with cervicitis and should raise concern for the alternative diagnosis of PID. Physical examination findings consistent with cervicitis include cervical discharge, erythema of the cervix, friability (bleeding of the cervix after minor trauma, such as insertion of a swab), and swelling or redness of the vagina. Symptoms of urethritis are generally confined to dysuria and urethral discharge. On physical examination, discharge may or may not be seen at the urethral meatus.Evaluation of cervicitis includes physical examination of the external and internal genitalia, including inspection of the cervix and bimanual examination testing for cervical motion tenderness to rule out PID. Cervicitis is a clinical diagnosis reliant on findings of discharge or friability. Laboratory testing in a woman with cervicitis should include nucleic acid amplification testing (NAAT) for Neisseria gonorrhoeae and Chlamydia trachomatis and vaginal wet prep to examine for bacterial vaginosis and trichomoniasis, which are often concurrent. The NAAT test may be performed on endocervical swab, vaginal swab, or urine specimen. The urine sample for NAAT cannot be performed on a specimen collected for urinalysis or culture. It should be obtained from the initial urine stream rather than midstream. In addition, it should be at least 30 minutes after last urination, and the patient should be instructed to not clean herself before collection. If physical examination reveals vesicles or ulcers that suggest herpes simplex virus infection, immunologic testing may be indicated.Evaluation of a male with suspected urethritis includes inspecting the external genitalia for discharge and lesions suggestive of other sexually transmitted infections, including herpes simplex virus, syphilis, and human papillomavirus. Laboratory testing should include NAAT for chlamydia and gonorrhea. NAAT can be performed on either urethral swab or urine sample. As for females, urine for NAAT should be obtained at the initiation of stream, but because of the longer male urethra, prior cleaning does not reduce test sensitivity. Trichomonas vaginalis is an unusual cause of urethritis and may be considered if there is known exposure or if urethritis persists after standard antibiotic treatment. In such cases, a urethral swab or first void urine may reveal trichomonads on microscopy.Diagnosis of both urethritis and cervicitis can be made clinically, and most patients should initiate treatment during their emergency department visit. The Table?summarizes treatment options. In addition, the United States Centers for Disease Control and Prevention maintains a Web site with current treatment guidelines for sexually transmitted infections (). For simple cervicitis or urethritis, single-dose regimens may be provided in the emergency department and directly observed therapy may be performed. Such regimens are not appropriate treatment of PID, for which 14 days of therapy is required.Discharge planning should include instructions for follow-up evaluation if symptoms persist or recur. Chronic pelvic pain, dysuria, or sexual dysfunction may be seen in both men and women following cervicitis, urethritis, or PID. Patients should be encouraged to refer any sexual partners from the last 60 days for evaluation and testing. Patients should also be instructed to abstain from sexual activity for at least 1 week and to abstain from sexual intercourse until any or all sexual partners are evaluated and treated. In addition, this may be a "teachable moment" to discuss the use of condoms in reducing the risk of future infection.American Board of Pediatrics Content Specification(s)Know the etiology of urethritis/cervicitisRecognize the signs and symptoms of urethritis/cervicitisPlan the management of urethritis/cervicitisQuestion: 3A 12-year-old boy is brought to the emergency department after falling approximately 8 feet off a railing while skateboarding. He was not wearing a helmet. His friends report that he did not move for a few minutes after the fall. He has vomited twice.He is sleepy and keeps his eyes closed but arouses and opens his eyes to voice. He asks repetitive questions about what has occurred but is otherwise oriented to person, place, and time. He follows commands. He complains of a mild headache. He has a palpable, occipital hematoma just to the right of midline. He denies neck pain and there is no cervical spine tenderness. The remainder of a neurologic examination is normal, including normal cranial nerve function. His tympanic membranes do not show hemotympanum, and there is no Battle sign on either side.Of the following, the BEST next step in management for this child isA.clinical clearance of the cervical puted tomography of the brainC.magnetic resonance imaging of the brain and cervical spineD.observation in the emergency department for 6 hoursE.radiographs of the skullCorrect Answer BThe child in the vignette shows evidence of a concussion or mild traumatic brain injury. The first step in the evaluation and management of this child in the emergency department is to exclude a significant intracranial injury that will require medical or surgical management. In many children with seemingly mild head injury, history and physical examination may be sufficient to exclude an intracranial injury.In this child, a Glasgow Coma Score (GCS) of 14 (eye opening to voice only, 3; mostly oriented speech, 5; and following commands, 6) and other signs of altered mental status (perseverating questions) suggest an increased risk of intracranial injury. A computed tomography (CT) scan to exclude an injury should be ordered.In a large, prospective cohort study authored by Kuppermann, et al, the absence of several predictive factors in children with seemingly mild head injury (GCS of 14-15), described a population that was at extremely low risk of intracranial injury and in whom the use of CT scans could be discouraged. Those predictors were slightly different according to the age of the subjects.For children younger than 2 years of age, the predictors were as follows:GCS of 14 or other signs of altered mental statusPalpable skull fractureOccipital, parietal, or temporal scalp hematomaHistory of loss of consciousness >5 secondsSevere mechanism of injuryNot acting normally according to a parent’s reportFor children 2 years of age and older, the predictors were as follows:GCS of 14 or other signs of altered mental statusSigns of a basilar skull fractureHistory of loss of consciousnessHistory of vomitingSevere mechanism of injurySevere headacheIf all of these predictors are absent, the risk of a clinically important, traumatic brain injury is less than 0.05%. In the very few injuries missed by this rule (the negative predictive value in both age groups is >99%), none required neurosurgery or resulted in death or poor outcomes. Therefore, if all of these predictors are absent, CT scans are not recommended.If the child has a GCS of 14, other signs of altered mental status, signs of a skull fracture (in children younger than 2 years old), or signs of a basilar skull fracture (in children older than 2 years), there is approximately a 4.5% risk of a clinically important finding and CT scans are recommended. For children with 1 or more of the remaining predictors (loss of consciousness, vomiting, severe mechanism of injury, nonfrontal scalp hematoma, or not acting normally according to parents in younger children or severe headache in older children) there is an intermediate risk of intracranial injury (≈ 1%). In these children, it is recommended that the child may be observed or undergo a CT scan according to physician experience, parental preference, the presence of single versus multiple predictors, and whether the child improves or worsens during the period of observation. Nigrovic and colleagues have shown that in children who are observed, use of CT is decreased without any change in outcome.The use of CT scans for the evaluation of mild head injury in children has increased over the last several years. However, greater than 90% of all brain CT scans performed in the United States for the evaluation of traumatic injury in this age group are negative. Concerns about cost and the effects of radiation should lead to efforts to minimize the use of CT scans when they are not needed to evaluate these injuries. Studies using extrapolation of radiation dose from atomic bomb blasts survivors as well as a recent cohort study have suggested that the use of cranial CT scans does lead to a small but real increase in the risk of brain tumors and leukemia in children, especially those that receive 2 to 3 scans or more.Although magnetic resonance imaging (MRI) of the brain can be used to exclude an intracranial injury in this child, MRI is often less available, more costly, and takes longer to perform. In younger children, there is more often a need to sedate the child to obtain MRI. This child has no signs or symptoms of cervical spine injury. However, his mental status is enough of a concern to preclude safe clinical clearance of his cervical spine. Radiographs of the cervical spine should be obtained unless his mental status improves to the point of allowing clinical clearance.In the absence of focal neurologic findings, it is reasonable to obtain imaging in this child before obtaining a neurosurgical consultation. In many settings, obtaining such a consult may require transfer of this child to a higher level of care. If a CT scan is performed and no intracranial lesion is found, neurosurgical consultation may not be necessary and the child may be discharged to home if his mental status improves and his vomiting ceases. The risk of intracranial injury in this child is high enough that imaging is preferred over observation alone.Although skull radiographs may be useful in children younger than 2 years of age who look well and whose only history or physical examination finding of concern is an isolated scalp hematoma, they are not useful in the evaluation of older children. In younger children who have isolated scalp hematomas, skull radiographs that show an absence of a fracture are reassuring. The child can be discharged without further imaging if looking well after 4 to 6 hours of observation.Even if the child described in the vignette has a negative CT scan, he still has the clinical findings of a concussion. Children with a concussion or mild traumatic brain injury frequently come to emergency departments for evaluation. Recognition of this injury and the provision of appropriate discharge instructions, including cognitive and physical rest until symptoms improve and how families should follow up (), is an important role of the emergency physician in the care of these children. Rest allows for more rapid recovery and can prevent a second injury, which may lead to prolonged symptoms or more serious complications.American Board of Pediatrics Content Specification(s)Know the principles of the management of minor head injuryQuestion: 4A 5-year-old boy is brought to the emergency department by his father after passing brown-colored urine for 1 day. The father recently obtained custody of his son. He mentions that the boy has had low-grade fevers without chills or rigors intermittently over the last month. The boy has been “less active” and has been complaining of vague body aches. The father denies any history of systemic complaints, trauma, or travel. The details of the past medical history are unavailable, but the father mentions that the child has had a heart condition since birth that required 2 surgeries and a “shunt placement” in his heart.The boy’s temperature is 38.2°C, resting heart rate is 128 beats/min, respiratory rate is 32 breaths/min (with mild subcostal retractions), and blood pressure is 120/76 mm Hg. He does have minimal pedal edema and bilateral basal crepitations on auscultation of his lungs. His cardiac examination is difficult to assess because of a harsh grade 3/6 systolic murmur in addition to his tachycardia. He does have a few tender, pea-sized nodules on his fingers and toes that he has noticed recently. His urine test strip examination reveals 3+ blood and is negative for nitrites.Of the following, the BEST test to establish a diagnosis isA.blood cultureB.chest radiographC.C-reactive protein levelD.renal function testsE.urine cultureCorrect Answer AThe patient described in the vignette is most likely suffering circulating immune-complex–mediated glomerulonephritis that is secondary to subacute bacterial endocarditis. The nodules on his fingers (Osler nodes) also suggest immune-complex-mediated vasculitis. Furthermore, the tachycardia, basal pulmonary crepitations, and mild respiratory distress all point towards congestive cardiac failure that can be secondary to uremia or primary myocardial failure. However, for the patient in the vignette, the history of a complex congenital heart disease along with prosthesis and low-grade fevers increases the likelihood of subacute bacterial endocarditis. The definitive diagnosis of infective endocarditis (IE) is unlikely to occur in the emergency department. This condition is associated with high morbidity; therefore, clinicians should have a high index of suspicion. Blood cultures have a 90% success rate in identifying the organisms associated with IE. Chest radiograph, C-reactive protein level, renal function tests, and urine culture may all be indicated, but a blood culture is needed for diagnosis and management of IE.In patients with IE, viridans-type streptococci (α-hemolytic streptococci) are more common in patients with underlying cardiac disease, whereas Staphylococcus aureus is more common in children without preexisting cardiac disease. Uncommon organisms include group D enterococci following lower bowel or genitourinary procedures, Pseudomonas aeruginosa or Serratia marcescens in intravenous drug users, and coagulase-negative Staphylococcus in patients with indwelling central catheters. Cases of IE with HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) group; Pasteurella multocida, Legionella species, and others have also been described. IE is more likely to occur with underlying cardiac disease (congenital [eg, valvular lesions or septal defects] or acquired [rheumatic]), especially if there is endothelial injury due to turbulent blood flow across a narrow orifice in the face of high pressure gradient or due to mechanical devices such as artificial valves. The endothelial injury leads to the formation of nonbacterial thrombotic embolus (NBTE) that subsequently serves as a nidus for circulating bacteremia to lodge. Bacteremia can occur following seemingly innocuous daily activities such as brushing teeth or following dental, genitourinary, or gastrointestinal procedures.Patients with acute IE can present abruptly with high-grade fever and chills associated with sudden deterioration of cardiac function, which is manifested as congestive cardiac failure and cardiogenic or septic shock. Manifestations of subacute IE are relatively mild with prolonged fever in the absence of any other symptoms or nonspecific myalgias, arthralgias, weight loss, or headaches. New or changing heart murmurs, especially in the presence of cardiac failure, are very suggestive of IE. Patients may also present with complications due to thromboembolic processes (eg, strokes, pulmonary emboli, or direct damage to the myocardium secondary to myocardial abscess) or rhythm abnormalities due to destruction of the conduction system. IE should always be a part of the differential diagnosis, especially in children with underlying cardiac disease, and the clinician must look for evidence of vasculitis produced by circulating antigen-antibody complexes manifested in the form of Osler nodes (tender, pea-sized intradermal nodules in the pads of the fingers and toes), Janeway lesions (painless, small, erythematous lesions on palms and soles), or splinter hemorrhages (linear lesions beneath the nails). The Duke criteria for diagnosis of IE are provided in the Table. Presence of 2 major, 1 major and 3 minor, or 5 minor criteria suggests IE.Echocardiography, either transthoracic or transesophageal, should be performed to determine the presence, extent, size, shape, and mobility of vegetations, although absence of vegetations does not rule out IE. The mortality rate of patients with IE is 20% to 25%, and serious morbidity in the form of heart failure, myocardial abscesses, toxic myocarditis, life-threatening arrhythmias, systemic emboli to the central nervous system, or pulmonary emboli via the septal defects occurs in 50% to 60% of children. Prompt initiation of broad-spectrum antibiotics is extremely important in reducing serious morbidity and should be instituted after consultation with cardiologic and infectious disease experts. In the emergency department, empiric therapy should be initiated with vancomycin plus gentamicin to cover the 3 most common organisms; namely, Streptococcus viridans, Staphylococcus aureus, and enterococci. The duration, dose, and route of antibiotics is then further determined in an inpatient setting according to the results of blood cultures and the clinical progression of the illness.Recent changes in bacterial endocarditis prophylaxis guidelines have narrowed the recommendations for antibiotic prophylaxis for dental and genitourinary procedures ().American Board of Pediatrics Content Specification(s)Know the etiology and understand the pathophysiology of infectious endocarditisRecognize signs and symptoms of infectious endocarditisPlan prophylaxis against infectious endocarditisRecognize and interpret relevant laboratory, imaging, and monitoring studies for infectious endocarditisRecognize life-threatening complications of infectious endocarditisPlan management of acute infectious endocarditisQuestion: 5A 16-year-old boy is brought to the emergency department with complaints of sudden onset bilateral complete visual loss. He was asymptomatic until a couple of hours ago, when on his way to school for his annual exams he complained of blurriness followed by complete loss of vision. He denies any history of trauma, exposure to any substances, nausea, vomiting, headache, or fever. Further inquiry reveals treatment for a forehead laceration he sustained during a fall from a bicycle a month ago. He has a strong family history of migraine in both parents and arteriovenous malformation in his great grandfather. He also mentions that he occasionally smokes marijuana and recently (1 week ago) tried some homemade beer brewed by his friend. Findings on physical examination, including his vital signs, are within normal limits except for the visual examination. He is unable to see any objects, discern any movement in front of his eyes, or count fingers, although he does blink when startled by sudden movements in front of his face. Examination of his eyes reveals normal pupillary reflexes and a normal fundus.Of the following, the BEST next step in management is puted tomography of the head with contrastB.electroencephalographyC.magnetic resonance imaging and magnetic resonance angiography of the brainD.outpatient behavioral counselingE.serum methanol levelsCorrect Answer DThe patient described in the vignette has a positive menace reflex (ie, blinking of his eyelids when the examiner’s hand is suddenly brought towards his face). This indicates that his vision is not absent. He is likely suffering from hysterical visual loss as a manifestation of a conversion disorder.There are several methods to confirm that vision is not lost in situations such as this. Patients with hysterical blindness or malingering often carefully avoid falling or bumping into objects in their path. The optokinetic reflex is manifested by nystagmic movements of the eyes when presented with a rotating object. An intact optokinetic reflex is evidence that vision is still present. Additionally, a mirror placed in front of the patient's eyes and then tilted in different directions will cause eye movement if the vision is intact.Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) may be indicated in sudden complete true visual loss but not in the patient described in the vignette. Similarly, electroencephalogram and head computed tomography would be of no value in this patient. Methanol poisoning is associated with blindness, but there is nothing to suggest that diagnosis in this patient.Trauma and infection are common causes of visual disturbances in children. Head injuries involving the visual cortex can cause complete and bilateral loss of vision. Unilateral loss of vision may occur after chemical burns (alkali), corneal abrasions or lacerations, ruptured globe, traumatic dislocation of lens, retinal detachment or tear, vitreous hemorrhage, severe hyphema, or commotio retinae. Traumatic causes of bilateral blurring or mild visual loss include ultraviolet or infrared burns; unilateral causes include corneal abrasions, traumatic cataracts, and hyphema or diplopia from a blowout fracture.Nontraumatic causes of bilateral complete visual loss include poisoning, cortical blindness, and hysteria. Nontraumatic unilateral visual loss can be further categorized as painful, which can be secondary to endophthalmitis or migraine, or painless, which can be secondary to retinal artery or vein occlusion, retinal detachment, or optic neuritis. Nontraumatic causes of mild visual loss can also be painful or painless. Painful causes include conjunctivitis, glaucoma, and uveitis, while painless causes include retinal artery occlusion, retinal vein branch occlusion, and hysterical diplopia.Visual disturbances, including symptoms of visual loss, are infrequent in children. A detailed history (Table) and a comprehensive examination will often reveal a diagnosis.A comprehensive physical examination should include inspection for any obvious trauma, infection, squint, or nystagmus. A compensatory head tilt to maintain visual capabilities may be seen in patients with diplopia. Fluorescein?staining should be used to detect corneal defects (eg, corneal abrasion or keratitis). Eversion of the eyelids should be performed if there is suspicion for an ocular foreign body or corneal abrasion. Patients with suspected globe rupture or laceration should not undergo lid retraction, fluorescein staining, or other procedures that may apply pressure to the eye. Visual acuity of each eye should be assessed in younger children who are unable to cooperate; visual behavior consistent with the patient’s age should be noted. The examiner should evaluate extraocular movements, visual fields, and pupillary appearance and response (direct and consensual light reflex). Direct ophthalmoscopy should be performed to evaluate for anterior chamber depth and presence of visible hyphema. Funduscopic examination should follow, looking for regional retinal pallor (branch retinal artery occlusion), abnormal vessels, retinal hemorrhage, and papilledema (idiopathic intracranial hypertension, intracranial mass lesions).Abnormal physical finding may include the following:Periorbital swelling (eg, eye trauma, orbital infection)Eccentric or peaked pupil or extrusion of ocular contents (ruptured globe)Obvious laceration or protruding intraocular foreign bodyProptosis (orbital cellulitis or mass)Conjunctival injection (conjunctivitis, keratitis, corneal injury)Blood (hyphema) or pus (hypopyon) in the anterior chamberPain on extraocular movement (orbital infection)A slit-lamp examination of the eye may be helpful in older, cooperative patients. Slit-lamp examination requires experience and can be used to identify hyphema, hypopyon, iritis, and lens abnormalities. The need for ancillary studies varies. Depending upon the differential diagnosis, computed tomography of the head or magnetic resonance imaging along with magnetic resonance venography may be indicated. Carotid duplex ultrasonography, magnetic resonance angiography, or computed tomography angiography should be ordered for patients with vascular risk factors (eg, diabetes, sickle cell disease, and systemic lupus erythematosus) if branch retinal artery or vein thrombosis is suspected.American Board of Pediatrics Content Specification(s)Differentiate by age the etiology and the pathophysiology of visual disturbancesPlan diagnostic evaluation and initial intervention for patients with visual disturbancesRecognize serious and/or life-threatening causes of visual disturbancesQuestion: 6A 16-year-girl with a history of bipolar disorder, depression, and attention-deficit/hyperactivity disorder is brought by emergency medical services after she was found unresponsive by her family members following an overdose of her home medications. She was very well controlled on fluvoxamine, risperidone, and valproic acid and functioning normally until the morning of admission. Upon arrival to the emergency department, she is obtunded with purposive withdrawal to painful stimuli. Her temperature is 39.8°C, heart rate is 120 beats/min, blood pressure is 126/70 mm Hg, and oxygen saturation is 100% as measured by pulse oximetry. She is noted to be diaphoretic. Her pupils are 5 to 6 mm and briskly reactive bilaterally. The remainder of her examination is notable for 4+ reflexes with sustained clonus. There was no muscle rigidity. Laboratory findings are significant for a white blood cell count of 17,400/?L (17.4 × 109/L) with no left shift. Creatine kinase level is mildly elevated. Urine pregnancy test result is negative. Electrocardiogram reveals sinus tachycardia with normal QRS and QTc intervals. Chest radiograph and cranial computed tomography are unremarkable. The results of blood electrolytes, ammonia, arterial blood gases, and cerebrospinal fluid analysis are unremarkable. Her valproic acid level is 42 mg/dL (291.2 ?mol/L).Of the following, the MOST likely diagnosis isA.malignant hyperthermiaB.neuroleptic malignant syndromeC.pontine hemorrhageD.serotonin syndromeE.valproic acid encephalopathyCorrect Answer DA patient who uses a selective serotonin reuptake inhibitor (SSRI) like fluvoxamine and presents with an acute change in mental status, hyperreflexia, hyperthermia, and autonomic dysfunction is demonstrating signs and symptoms most consistent with serotonin syndrome (SS).Two other hyperthermic syndromes can resemble SS. Neuroleptic malignant syndrome (NMS) can occur with exposure to drugs (eg, haloperidol or lithium) that affect the central dopaminergic system. It is characterized by marked spasticity of the skeletal muscle and a significantly elevated creatine kinase level (>1,000 U/L), along with fever and altered mentation. Although there is overlap in in the clinical symptoms associated with NMS and SS, NMS usually lasts longer.Malignant hyperthermia, which can also cause muscle rigidity and hyperthermia, is typically triggered by exposure to an inhalation anesthetic. Valproic acid (VPA) encephalopathy should be considered if patients are taking VPA and present with an abrupt change in behavior, seizures, or focal neurologic deficits. Unlike VPA toxicity, VPA levels and liver function tests are within normal range in VPA encephalopathy, but serum ammonia levels are markedly elevated. Pontine hemorrhage typically presents with hyperthermia, coma, apneustic respirations, and pinpoint pupils.SS is thought to be a result of excessive stimulation of 5-HT2A serotonin receptors. SS can be caused by an SSRI alone or in combination with any drug that prevents reuptake of serotonin, such as tricyclic antidepressants, dextromethorphan, meperidine, monamine oxidase inhibitors or drugs that stimulate release of serotonin (eg, cocaine and amphetamine). The new antimicrobial linezolid is a weak monoamine oxidase inhibitor and has also been implicated in cases of SS.Management entails stopping the offending agent and rapidly cooling the patient. Patients should be evaluated for possible complications, including rhabdomyolysis, metabolic acidosis, renal failure, myoglobinuria, and disseminated intravascular coagulation. Hyperthermia is responsible for death in these cases. If the patient presents within 1 hour of ingestion, gastric lavage and single-dose activated charcoal may be considered. Its use is contraindicated in patients who have depressed levels of consciousness unless their airways are protected. External cooling by packing with ice can bring the temperature down rapidly.First-line treatment of agitation, autonomic dysfunction, seizures, or hyperthermia involves sedation with benzodiazepines. Neuromuscular blockade with a non-depolarizing agent may be necessary for refractory hyperthermia. A depolarizing agent like succinyl choline should be avoided because a patient with clonus and hyperreflexia may be already breaking down muscle tissue. Severe hypertension and tachycardia should be treated with a short-acting agent such as nitroprusside or esmolol. Impaired cardiac conduction with QTc and QRS prolongation is most commonly noted with citalopram and escitalopram toxicity. It is treated with sodium bicarbonate to maintain a pH of 7.45 to 7.55. The serotonin antagonist cyproheptadine can be administered as an antidote but has limited efficacy.In a patient who presents with suspected or alleged overdose of an SSRI, the following indications warrant prolonged observation or admission:Symptomatic patients; ie, patients demonstrating mild effects like somnolence, vomiting, mydriasis, or diaphoresis may be observed for 8 hours to ensure improvementIngestion of greater than 5 times a single therapeutic dose for adults if the patient is SSRI na?ve or greater than 5 times the patient’s usual single dose of the medication (Table)Coingestants that increase susceptibility to SSAbnormal QTc or QRS intervalAmerican Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of toxicity by selective serotonin reuptake inhibitorsQuestion: 7In “Randomized Double-Blind Placebo-Controlled Trial of Two Intravenous Morphine Dosages (0.10 mg/kg and 0.15 mg/kg) in Emergency Department Patients With Moderate to Severe Acute Pain” by Birnbaum, et al, the authors state that their “study was designed to test the null hypothesis that no clinically and statistically significant difference would be found between mean changes in numeric rating scale for the 2 treatment groups. A minimum clinically significant change in patient pain severity was defined a priori as a change of 1.3 on the numeric rating scale. A sample size of 278 subjects (139 per group) was calculated to provide 95% power to detect a difference of greater than or equal to 1.3 points on numeric rating scale, assuming a 2-tailed α = 0.05 and a standard deviation of 3. The results from analysis of the primary outcome were that mean numeric rating pain score from baseline to 60 minutes decreased more (0.8 [95% CI 0.1 to 1.5], P = 0.04) in the group randomized to receive 0.15 mg/kg than in patients who received 0.10 mg/kg.”Of the following, the MOST appropriate conclusion from this study is that theA.null hypothesis was not rejected and 0.15 mg/kg is clinically equivalent to 0.1 mg/kg of morphine in its analgesic potencyB.null hypothesis was not rejected and 0.15 mg/kg is not clinically inferior to 0.1 mg/kg of morphine in its analgesic potencyC.null hypothesis was rejected and 0.1 mg/kg is clinically superior to 0.15 mg/kg of morphine in its analgesic potencyD.null hypothesis was rejected and 0.15 mg/kg is clinically superior to 0.1 mg/kg of morphine in its analgesic potencyE.null hypothesis was rejected but 0.15 mg/kg is not clinically superior to 0.1 mg/kg of morphine in its analgesic potencyCorrect Answer: EThe null hypothesis (H0) is rejected because the 95% confidence interval (CI) excludes the null value for mean difference (ie, zero) and a P = 0.04 is less than the significance level of a = 0.05. The null value for a test of difference is zero; the null value for ratios (eg, odds ratios and relative risk) is 1. However, despite achieving statistical significance, the value of this point estimate is less than the 1.3 numeric rating scale difference that represents a minimum, clinically significant difference in pain severity, as defined a priori. Hence, a 0.15 mg/kg dose of morphine is not clinically superior to 0.1 mg/kg.A hypothesis is a statement as to how the study will relate the predictors (cause) and outcomes (effect). In a traditional superiority trial, the H0 states that either no difference exists between groups or there is no association between predictor and outcome variable. The alternate hypothesis (H1) states that there is a difference between the two groups. H1 cannot be tested directly using statistical methods. The rejection of the H0 implies a vote in favor of the H1, which we accept as the default. This is the basis of formal testing of statistical significance.By convention, the level of significance is set at 5% (α = 0.05). This leads to our usual definition of statistical significance ( ie, P <0.05). The P value stands for the probability of obtaining the observed difference or effect size between groups by chance alone if, in reality, the H0 is true and there is no difference between the two groups. For the study in the vignette, a P value of 0.04 means that if H0 is true (ie, the two dosing regimens of morphine are equivalent), there is a 4% chance of seeing the observed data or more extreme data.CIs are often preferred to hypothesis tests that use P values because they emphasize the precision of the estimate by providing a range of values that are plausibly compatible with the data and allow the clinician to determine if the range is narrow enough for comfort. The 95% CI listed for the study implies that if the experiment is repeated 100 times, the true value of the point estimate of the difference in numerical pain rating will lie between 0.1 and 1.5 in 95/100 trials. CIs only reflect sampling uncertainty without capturing other forms of bias or measurement error associated with the clinical study.In general, there are 4 possible outcomes of a study as it relates to errors in hypothesis testing. A Type 1 (α) error occurs when the H0 is incorrectly rejected or when concluding that a difference exists when there isn’t one. A Type II (β) error is when the null is incorrectly accepted or when concluding that no difference exists when, in reality, there is a difference between the two groups. Power (1 - β) is the ability of a study to discern a difference when one truly exists. By convention, it should be >80% to be adequate. Type II errors can only be made in negative trials. Hence, the possibility of a Type II error must be assessed when reviewing studies that show no statistically significant difference between the groups (Figure).American Board of Pediatrics Content Specification(s)Define the "null hypothesis"Question: 8A 14-year-old presents to the emergency department for evaluation of a snake bite to his right leg. The bite occurred 1 hour before arrival. The patient was hiking with his family in a wooded area when he stepped over a log, felt a sharp pain in his right calf, and saw a snake slither away. He was unable to describe the snake but thought he heard a rattling sound. After hiking out to the trailhead, an ambulance was called and he was transported to the hospital. In addition to pain and swelling at the site of the bite, he reports perioral numbness and a metallic taste in his mouth. He is previously healthy and is up to date on his immunizations, including a tetanus booster 2 years ago.On examination, his temperature is 37.2°C, his pulse rate is 90 beats/min, his respiratory rate is 16 breaths/min, his blood pressure is 110/70 mm Hg, and pulse oximetry is 100% on room air. The child is well-appearing but in obvious discomfort. Results of his physical examination are unremarkable except for his right lower extremity. The right leg examination reveals 2 small puncture wounds with surrounding edema, ecchymosis, and tenderness in the lateral midcalf area.? There is diffuse edema of the lower leg, ankle, and foot. Distal pulses are normal, but capillary refill is delayed at 3 seconds. There is pain with both active and passive range of motion of the ankle, foot, and toes.Of the following, the MOST appropriate initial steps in the management of this patient areA.apply a tourniquet above the knee, elevate and ice the extremity, and consult orthopedics for emergent fasciotomyB.apply a constriction band above the swelling, elevate the extremity, and administer antivenomC.measure compartment pressures, perform magnetic resonance imaging, and administer prophylactic antibioticsD.perform incision and suction over the bite wounds and administer antivenom and prophylactic antibioticsE.splint the extremity in neutral position and administer pain medication and antivenomCorrect Answer: EThe patient in the vignette has suffered a venomous snake bite and is displaying significant local signs and symptoms of envenomation. The involved extremity should be splinted at or just below heart level to maximize blood flow, and the pain should be controlled with systemic analgesics and antivenom therapy should be initiated. Therapies that may worsen ischemia and tissue damage, including tourniquets, ice administration, elevation, and tight dressings, should be avoided. While the use of venous or lymphatic constriction bands proximal to the bite may be useful in the field when prolonged transport is anticipated, they are not indicated in the emergency department setting. Incision and suction has not been shown to remove significant amounts of venom, even when performed immediately after the bite, and results in additional tissue damage and risk of bleeding. Tissue ischemia and necrosis in snakebites is the result of proteolytic enzymes in venom and rarely the result of elevated compartment pressures, making both pressure measurement and fasciotomy unnecessary in most cases. Magnetic resonance imaging has no role in the initial evaluation and management of bites or stings. Although previously advocated, there is no clear evidence to support the use of prophylactic antibiotics for snakebites.Fortunately, venomous snake bites are infrequent events, with approximately 8,000 occurring annually in the United States; children are involved in a quarter of these cases. Only 10 to 15 deaths occur each year as a result of venomous snake bites. Venomous snakes indigenous to the United States are divided into 2 classes: Crotalidae (also known as pit vipers) and Elapidae. Rattlesnakes, water moccasins, and copperheads are members of the Crotalidae family, while coral snakes are the only member of the Elapidae family found naturally in the United States. Since the snake is often not captured and may not be clearly identified by the victim, providers should be familiar with the species native to their region. Even if a bite is definitely inflicted by a venomous species, up to 20% of bites may be “dry” (ie, lacking venom injection). The amount of venom injected also varies greatly and is affected by the age and size of the snake, time of last meal, circumstances of the bite, and number of strikes. Rattlesnakes (particularly the Mojave variety) and water moccasins are most likely to produce severe envenomation; copperhead and coral snakebites are less likely to cause severe or life-threatening symptoms.Snake venoms contain numerous enzymes, including proteinases and low-molecular-weight peptides. These enzymes have hemolytic, neurotoxic, nephrotoxic, necrotizing, or cardiotoxic effects. Hyaluronidase-like enzymes allow local spread of venom and produce many of the early local effects. Each venom differs in the proportion of different enzymes, leading to a different constellation of signs and symptoms. Local symptoms at the time of the bite include intense pain and the onset of erythema, edema, and, often, localized hemorrhage.? Puncture wounds produced by the fangs may not be visible because of their small size or significant local bruising, swelling, and necrosis. Early onset of perioral numbness and metallic taste is common with rattlesnake bites. With significant envenomation, systemic symptoms, including nausea, vomiting, and neurologic symptoms (diplopia, dysphagia, lethargy, weakness), begin within several hours of the bite. Hemolysis, vascular leak with hypovolemia, disseminated intravascular coagulation, and acute renal failure may occur in severe cases. Progression to shock, multisystem organ failure, and death occurs without aggressive therapy and antivenom administration.Careful observation for local and systemic signs and symptoms along with local wound care may be all that is necessary in many cases; if no significant systemic symptoms or progression of local symptoms occurs within 4 to 6 hours, antivenom is unlikely to be necessary. Cleaning and irrigation of the wounds, splinting in a neutral position below the level of the heart with loose dressings and padding, pain control, and appropriate tetanus prophylaxis should be performed immediately. Prophylactic antibiotics are no longer routinely recommended. Laboratory evaluation, including complete blood cell count, coagulation studies, renal function tests, and electrolyte panel, should be performed. Fibrinogen and fibrin split product levels and blood gas measurements may be indicated in more severe cases. Intravenous fluids should be administered to correct and maintain intravascular volume and manage hypotension; vasopressors should be used only if shock is unresponsive to fluid therapy to avoid potentially worsening ischemia and necrosis in the region of the bite. Bites characterized by only mild local signs and symptoms do not require antivenom; more extensive local symptoms or the onset of systemic symptoms or laboratory abnormalities indicate the need for antivenom therapy. Before 2000, Crotalidae antivenom was equine-derived and associated with a high rate of adverse reactions, including anaphylaxis and death; because of these risks, antivenom therapy required prior skin testing and careful dose titration and escalation, and was often reserved for moderate to severe Crotalidae envenomation. Subsequent development of a sheep-derived polyclonal antivenom that is much better tolerated has allowed more liberal use of antivenom. This antivenom was generated using the venom of several rattlesnake species and water moccasins; copperhead venom was not used, and the degree of cross-reactivity against this species is unclear. Elapidae antivenom is equine-derived. Since copperhead and coral bites are less likely to result in severe or life-threatening envenomation, the use of antivenom in these cases is less frequently indicated. The volume and number of doses is guided by the severity of symptoms. Consultation with the regional poison control center or snakebite expert can be helpful in guiding appropriate therapy.Bites and stings can result from numerous species of insects, spiders, marine and terrestrial invertebrates, marine vertebrates, rodents, and mammals. Some bites are complicated only by the local effects of the bite and risk of infection, while others, like snakebites, are associated with envenomation and the local and systemic effects of the specific venom. The specific bites and stings likely to be encountered by healthcare providers are dependent on local and regional climate and environment; providers should be familiar with the species commonly encountered in their region. Local wound care is common to the management of all bites and stings. Removal of any remaining foreign material, including stingers, spines, tentacles, or teeth of the biting organism, should be ensured. Ongoing envenomation may occur if portions of the venom apparatus remain on or in the victim, and infection or poor wound healing may result from retained foreign material. Copious irrigation of any open wounds using normal saline should be performed as early as possible; use of other irrigation solutions (eg, hydrogen peroxide and povidone-iodine) is unnecessary and may be associated with further tissue damage. Debridement of devitalized tissue aids in reducing infection risk. Specific local care may be indicated according to the species involved; for example, acetic acid aids in inactivating nematocysts of jellyfish tentacles, and soaking the involved area in hot (40°-45°C) water is recommended for stingray, scorpion, and catfish envenomation. In addition to establishing and maintaining cardiorespiratory stability, management of pain, provision of appropriate tetanus prophylaxis, and treatment of allergic symptoms (eg, with antihistamines, steroids, or epinephrine) are common to all bites and stings. Specific antivenom therapy is available for a small subset of bites and stings; consultation with local experts or the regional poison control center can aid in deciding specific therapies. The Table?reviews mechanisms of injury, wound care, and systemic therapies for the common classes of bite and sting injuries seen in the United States.American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of complications of bites and stingsPlan the management of bites/stings by type, including scorpions, spiders, ticks, and insects ................
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