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JANUARY 2011Question: 1You are evaluating a 3-year-old girl in the emergency department for fever, upper respiratory tract symptoms, and left-sided earache of 2 days’ duration. She also has had constipation. Physical examination findings are consistent with left otitis media. On abdominal examination, you palpate a smooth, firm, nontender mass in the left upper quadrant that cannot be indented and does not move with respiration. You obtain a complete blood count, serum electrolytes assessment, and urinalysis.Of the following, the MOST appropriate next step in the evaluation of this abdominal mass is:puted tomography scanB.intravenous pyelographyC.magnetic resonance imagingD.radionuclide scanE.ultrasonographyCorrect answer EThe patient described in the vignette has the classic presentation of Wilms tumor. The most common considerations in the differential diagnosis for abdominal mass are hydronephrosis, constipation, bladder distention, splenomegaly, or abdominal solid tumors. Wilms tumor and neuroblastoma are the most likely malignancies for a child who has this presentation. Although Wilms tumor rarely crosses the midline, neuroblastoma does. The most important investigative screening tool is abdominal ultrasonography, which can help to differentiate between the conditions in the differential list and guide further management. In addition, it is readily available, does not expose the child to ionizing radiation, and it is noninvasive. If ultrasonography is not readily available, next-day referral to a higher-level pediatric facility is appropriate because emergent evaluation is not indicated. If ultrasonography reveals a possible malignancy, the child should be referred to an appropriate facility for either abdominal computed tomography scan or magnetic resonance imaging. Intravenous pyelography is a good means of defining the architecture of the renal system but is not helpful in evaluating other structures. Radionuclide scan is helpful in assessing the functional aspect of the kidney without defining the anatomy.Wilms tumor or nephroblastoma is the fifth most common pediatric malignancy (7%) and most common renal malignancy (95%). The annual incidence is approximately 8 cases per 1 million children younger than 15 years of age (approximately 500 cases/year). Children of 2 to 3 years are affected most commonly, with African Americans and females at higher risk. Although most of the cases are sporadic, Wilms tumor has been associated with Beckwith-Wiedemann syndrome, WAGR syndrome (Wilms tumor, aniridia, genitourinary anomalies, mental retardation), and isolated genitourinary abnormalities (undescended testis, horseshoe kidney, hypospadias, vaginal duplication, duplicating collecting system). Even rarer is the familial variety (1.5% of all reported cases). Wilms tumor is mostly unilateral, with only 5% to 7% of cases being bilateral. The pathophysiology appears to be mutation in the WT1 tumor suppressor gene on chromosome 11p13 in the nephrogenic rests of the kidney. The rests, which are precursors of kidney cells and may persist abnormally at birth (reported in 1% of neonatal kidneys), are found in almost 40% of kidneys affected by Wilms tumor and, therefore, are considered precursor cells for the condition. Other genes associated with Wilms tumor are WTX, WT2, and CTNNB1. The differential diagnosis for other renal tumors includes renal cell carcinoma, mesoblastic nephroma, sarcomas, clear cell carcinoma, intrarenal neuroblastoma, and rhabdoid tumor.Most patients who have Wilms tumor are diagnosed after an incidental abdominal mass is found on examination. A minority of patients (20% to 30%) present with gross or microscopic hematuria, abdominal pain, fever, or hypertension. Physical examination reveals a palpable abdominal mass that is firm, usually does not cross the midline, and does not move with respiration. If Wilms tumor is suspected, care should be taken during palpation to avoid a possible capsular leak of tumor cells.?Ultrasonography is used to ascertain the location and point of origin of the mass. As noted previously, the definitive diagnostic modality is computed tomography scan, which defines the mass and aids in staging (Figure).?Helpful laboratory investigations include complete blood count, serum creatinine to assess renal function, liver function tests for possible liver metastasis, serum calcium to differentiate Wilms tumor from renal rhabdoid tumors or nephroma, and coagulation studies for associated development of acquired von Willebrand disease.???Acute complications of Wilms tumor include subcapsular hemorrhage resulting in abdominal pain, anemia, hypertension, and fever. Local extension can be associated with localized lymphadenopathy and extension of tumor thrombus into renal veins or the inferior vena cava. The inferior vena cava can be displaced and obstructed by a particularly large tumor. Doppler renal and abdominal ultrasonography help to assess the patency of these vessels; further delineation of the tumor, local extension, and vascular structure assessment is accomplished by contrast abdominal computed tomography. The most common metastatic site is the lungs (approximately 80% of cases), and 12% of all patients have hematogenous metastasis at the time of presentation. Therefore, chest radiography or computed tomography scan of the chest are appropriate for initial evaluation. Other locations of metastasis are the brain and bone.Guidelines for management are outlined by the National Wilms’ Tumor Study of the International Society of Pediatric Oncology. Most centers in the United States pursue surgical resection (with or without biopsy), followed by chemotherapy with or without radiation therapy. Five-year survival rates have increased over the years, with more than 90% survival with the current management strategies. Prognostic factors include patient age, tumor weight, histology, genetics, and anatomic extension. Loss of heterozygosity at chromosome 16q and/or 1p and high telomerase expression have been associated with poor outcome. Anaplastic histologic features are associated with recurrence; the reported recurrence rate is 50% compared with 10% to 15% for more favorable histology. Late complications associated with the therapy are renal failure (documented risk of 1%) and those related to chemotherapy (congestive cardiac failure and hepatitis) and radiation therapy (radiation nephritis, portal hypertension, ovarian dysfunction, and thyroid dysfunction if lungs were radiated). Second malignancies may develop, primarily in irradiated areas.American Board of Pediatrics Content Specification(s)Know the etiology and pathophysiology of Wilms tumor.Be familiar with ancillary studies relevant to Wilms tumorRecognize the signs and symptoms and life-threatening complications of Wilms tumor.Plan initial management of acute complications of Wilms tumor.Question: 2Emergency Medical Services (EMS) brings an 18-month-old boy to the emergency department because of altered mental status. According to his mother, for the past 2 weeks, he has been sleeping more than usual, eating poorly, and easily agitated. He began acting “lethargic” and developed vomiting several days ago, and today he became unresponsive. EMS personnel state that the patient was lethargic upon their arrival; they applied face mask oxygen and monitors and transported him without any change in his clinical status. The only finding of note in the child’s past medical history is anemia and developmental delay. The mother denies any history of trauma, fever, diarrhea, rash, or respiratory symptoms, although she says that he had constipation and occasional abdominal pain over the past week. There is no family history of seizures or other neurologic disorders. The family has just been relocated to a shelter after their apartment complex was closed by the Health Department. On physical examination, the boy’s temperature is 37.0°C, heart rate is 128 beats/min, respiratory rate is 14 breaths/min, and blood pressure is 98/70 mm Hg. He is minimally responsive to stimuli, displays withdrawal to pain in all four extremities, and has sluggishly reactive 5-mm pupils bilaterally. He occasionally moans but does not open his eyes or follow commands. He has no gag or cough response to oropharyngeal examination using a tongue depressor. Cardiovascular examination reveals only mild tachycardia; the remainder of his examination findings are within normal parameters.Of the following, the MOST appropriate next step is to:A.administer activated charcoalB.administer intravenous mannitolC.obtain a head computed tomography scanD.perform a lumbar punctureE.perform rapid sequence intubationCorrect answer EThe boy described in the vignette is displaying signs and symptoms of encephalopathy. His history of anemia, developmental delay, vague abdominal complaints, and social situation suggest lead intoxication as a likely cause. His depressed mental status, with a Glasgow Coma Scale score of approximately 7, hypoventilation, and absence of protective airway reflexes, warrants urgent endotracheal intubation for airway protection before pursuing further evaluation.Although drug ingestions are potential causes of acute encephalopathy, administration of charcoal without a clear history of timing and type of ingestion is not appropriate. Further, charcoal administration is contraindicated in a patient who has altered mental status and an inability to protect the airway. Mannitol can be administered as a temporizing measure in cases of impending cerebral herniation, which should be suspected in patients who have asymmetric pupils, focal neurologic examination findings, or the combination of hypertension, bradycardia, and irregular respirations (Cushing triad). These signs are not present in the boy in the vignette. Although a head computed tomography (CT) scan is indicated for this boy, it should not precede provision of a definitive airway. Lumbar puncture (LP) may be required in the evaluation of suspected infectious, inflammatory, or some metabolic causes of encephalopathy but should be performed only after initial stabilization and in cases where increased intracranial pressure and the risk of herniation have been excluded.?Encephalopathy refers to alterations in mental status resulting from diffuse cerebral abnormalities and can present with an altered level of consciousness, abnormal cognition or personality, or seizures. Altered levels of consciousness result when any insult disrupts neuronal function of bilateral cerebral hemispheres, the ascending reticular-activating system, or both. Neuronal function can be impaired through direct cytotoxic injury, inadequate oxygen or other nutrient delivery, electrolyte disturbances causing disruption of neurotransmission, cerebral edema, or intracranial injury.? Multiple possible causes can be divided into broad categories (Table). Historical and physical examination findings can be used to narrow the diagnostic possibilities; laboratory and radiological evaluation then can be directed at the most likely causes.?Sudden onset of neurologic abnormality without preceding symptoms is most suggestive of acute intracranial hemorrhage or seizure. Preceding fever or other infectious symptoms most likely indicate infectious causes such as meningitis, encephalitis, or sepsis.? Metabolic disorders should be suspected in young children who have recurrent episodes of encephalopathy, episodes triggered by prolonged fasting or intercurrent illness, or a history of failure to thrive or developmental delay. Toxic exposures typically present with progressive neurologic abnormalities associated with other symptoms related to the specific toxin ingested. Historical or physical examination findings suggesting trauma indicate traumatic intracranial injury as the cause.?Initial evaluation should focus on evaluating and stabilizing the airway, breathing, and circulation. Any abnormality or inability to maintain a stable airway must be addressed emergently before proceeding with a diagnostic evaluation, as with the patient in the vignette. Complete vital signs, including pulse oximetry, should be obtained and monitored continuously. Abnormalities of blood pressure, heart rate, and respirations can be either the cause or the result of the encephalopathy. Examination should include funduscopic evaluation for papilledema or retinal hemorrhages, skin examination for evidence of trauma or neurocutaneous lesions, cardiovascular examination to evaluate cardiac function and tissue perfusion, and complete neurologic examination.?Rapid bedside glucose determination can exclude hypo- or hyperglycemia as the cause of encephalopathy. Throughout the evaluation, adequate oxygenation, ventilation, perfusion, and euglycemia should be maintained. Initial laboratory evaluation should include assessment of electrolytes, renal function, hepatic enzymes, coagulation profile, acid-base status, ammonia, and complete blood count as well as toxicologic screening. Patients in whom infection is suspected should have cultures of blood and urine obtained. Additional tests should be guided by the results of the history, physical examination, and initial laboratory tests.?If no potentially reversible cause (hypoglycemia, hypoxia) is identified, head CT scan should be obtained. If no clear cause is identified through these initial tests, further evaluation should include additional metabolic (organic and amino acids, thyroid function tests), infectious (cerebrospinal fluid analysis), neurologic (electroencephalography and magnetic resonance imaging), and toxicologic (lead, specific toxins) evaluation. LP for cerebrospinal fluid analysis should not be performed in unstable patients or in those who have evidence of coagulopathy or increased intracranial pressure.Treatment of encephalopathy consists of supportive measures (establishing and maintaining stable airway, breathing, and circulation as outlined previously), symptomatic management (correction of hypo- or hyperthermia, hypoxia, bradycardia, hypo- or hyperglycemia, hypo- or hypertension), and disease-specific therapy aimed at the underlying cause (eg, antibiotics for infections, antiepileptic drugs for seizures, antidote administration for specific intoxications, insulin and fluids for diabetic ketoacidosis).??????The progression and complications of encephalopathy vary according to the underlying cause. Alterations in respiration from the neurologic insult may result in hypoxic insults to various tissues, and shock and multisystem organ failure may follow if the alterations are not corrected rapidly. Progressive cerebral edema or mass effect may result in herniation, with potential irregular respirations, hypertension, bradycardia, and ultimately death. Failure to identify and appropriately treat the underlying cause rapidly may result in progressive cerebral damage and residual developmental abnormalities, seizure disorder, or death. Inadequately treated infection may lead to sepsis, multisystem organ failure, and death.American Board of Pediatrics Content Specification(s)Know the etiology and pathophysiology of encephalopathyRecognize the signs and symptoms of encephalopathyKnow the appropriate ancillary studies required to diagnose and manage encephalopathyRecognize the life-threatening complications of encephalopathyKnow the management of acute encephalopathyQuestion: 3The mother of a 2-week-old breastfed African American infant brings her child to the emergency department because she received a call from her pediatrician that the “PKU screen” was positive for galactosemia. The baby has been acting well. The only findings of note on the physical examination are a rectal temperature of 38.1°C and mild jaundice.Of the following, the MOST appropriate course of action is to:A.begin phototherapy for breast milk jaundiceB.evaluate the infant for possible sepsisC.reassure the mother that the screening test result most likely is false-positiveD.stop all protein and fat intake and administer 10% dextrose solution intravenouslyE.stop breastfeeding and switch to a cow milk-based formulaCorrect answer BAlthough newborn screening test results are frequently false-positive (including those for galactosemia), galactosemia is a potentially life-threatening condition that should be treated promptly. Children should be switched to a formula that does not contain galactose. Cow milk-based formulas do contain galactose and should be avoided. Protein and fat intake need not be restricted. Children who have galactosemia may present with jaundice from intrinsic hepatic dysfunction as well as hemolysis; the cause should not be assumed to be breast milk jaundice. Although the mechanism remains obscure, there is a well-documented susceptibility in infants who have galactosemia to Escherichia coli infections, including urinary tract infections and bacteremia. An evaluation for sepsis is required for any febrile 2-week-old infant, irrespective of metabolic screening test results.Galactose and glucose are the two components of the disaccharide lactose, the sugar in milk. To be used in the body, galactose must be metabolized to glucose via a multistep process that involves multiple enzymes. Defects in any of these enzymes can cause the clinical condition of galactosemia. Classic galactosemia, caused by a defect in galactose-1-phosphate uridyltransferase, presents in the newborn period with jaundice (from hepatic dysfunction and hemolysis), vomiting, diarrhea, hepatomegaly, and sepsis (especially with E coli). African American children who have classic galactosemia may present later with milder symptoms due to high residual enzyme activity. Other manifestations of the condition include failure to thrive, renal tubular acidosis, and cataracts.The incidence of classic galactosemia is 1 in 47,000 newborns, with 1% of the population being carriers for the genetic defect of classic galactosemia. Other forms of galactosemia are much rarer. All states in the United States now require a test for galactosemia in newborns. Testing for this disorder is one of the 29 screening tests recommended for all newborns in the national standards announced in 2006. Other than newborn screening, the diagnosis may be made by demonstration of galactose in urine (“reducing substance” in the absence of glucosuria), but this test is neither sensitive nor specific. Therefore, all infants suspected of having galactosemia should be fed a galactose-free formula (soy-based or elemental) until diagnostic testing, including genetic tests, confirm aspecific diagnosis.American Board of Pediatrics Content Specification(s)Plan the initial management of the acute signs and symptoms of galactosemiaRecognize the acute signs and symptoms of galactosemiaUnderstand the pathophysiology of galactosemiaQuestion: 4A 1-year-old boy is brought back to the emergency department (ED) by his mother because of a possible allergic rash. He had been seen and discharged from the ED yesterday following a diagnosis of a typical febrile seizure. He had a history of high fevers for 2 days before the seizure. A complete evaluation yesterday revealed an otherwise healthy child who had a possible ear infection as the source of fever. He was discharged with a prescription for amoxicillin and antipyretics. His high fever resolved yesterday, and he was doing well when his mother noticed a faint rash on his trunk that has now spread to the extremities. The rash, which appeared after the first dose of amoxicillin, is nonpruritic. His past medical history is noncontributory, his immunizations are up to date, and he has no history of recent travel or exposure to any pets. On physical examination, the playful child has a faint erythematous macular rash on his trunk and extremities that blanches with pressure.Of the following, the MOST likely diagnosis is:A.erythema multiformeB.roseolaC.rubellaD.rubeolaE.scarlet feverCorrect answer: BThe boy described in the vignette has roseola (also known as exanthem subitum, sixth disease, pseudorubella, exanthem criticum, and three day fever). High fever that resolves abruptly, followed by the appearance of a nonpruritic, diffuse, erythematous macular rash that begins on the neck and trunk is characteristic. Human herpesvirus 6 (HHV-6) is the most common cause of roseola. Other viruses such as HHV-7, enteroviruses (coxsackievirus A and B, echoviruses), adenoviruses, and parainfluenza virus type 1 are also known to cause roseola. Ninety percent of cases are seen in children younger than 2 years of age, and cases may occur throughout the year. Other clinical features of roseola include irritability, erythematous tympanic membranes, bulging fontanelle, febrile seizures, and uvulopalatoglossal junctional macules or ulcers (Nagayama spots). Approximately 4% to 6% of affected patients present with febrile seizures. Nearly 26% of infants who have roseola have bulging fontanelles, and many are evaluated to rule out meningitis. Patients often receive treatment for otitis media because of the red tympanic membranes and fever. The resolution of fever and the occurrence of a rash that, in some instances, coincides with the use of antibiotics often lead to an erroneous diagnosis of allergic rash. The diagnosis of roseola is clinical and management is supportive. The prognosis is excellent in most cases.The differential diagnosis for roseola includes measles (rubeola), rubella, allergic drug rash, and scarlet fever. Rubella (German measles) is characterized by a simultaneous onset of fever and rash along with prominent cervical lymphadenopathy. Patients who have rubeola (measles) present with a severe prodrome of fever, cough, conjunctivitis, coryza, and enanthem (Koplik spots: described as a grain of sand on an erythematous base), followed by a confluent rash that begins on the forehead and neck and rapidly progresses caudally. The rash of scarlet fever is diffusely distributed and finely papular (goose pimple). It is more prominent on the axillae, elbows, and groin. Scarlet fever is more common in the older child (3 to 15 years). Erythema multiforme, as the name suggests, is polymorphic. The classic presentation has three components: a dusky central area or blister, a dark red inflammatory zone surrounded by a pale ring of edema, and an erythematous halo on the extreme periphery of the lesion, which combine to form target lesions. Rashes due to drug allergies are morbilliform and pruritic.American Board of Pediatrics Content Specification(s)Plan the evaluation and management of acute roseolaQuestion: 5You are examining a 3-year-old boy, who was restrained in a rear-positioned car seat and involved in a high-speed front end motor vehicle collision. Emergency medical services personnel report significant passenger space intrusion and vehicular rollover at the scene. On physical examination, the child is obtunded and has a Glasgow Coma Scale score of 8. Except for tachycardia, his vital signs are within normal limits. He has an obvious closed deformity of the left thigh. He is fully immobilized on a long spine board and cervical collar.Of the following, the radiograph that MOST likely represents significant cervical spine injury for this child is:A.Figure 1?B.? Figure 2?C.? Figure 3?D.? Figure 4?E.?Figure 5?Correct answer EThe image in Figure 5 shows a significant cervical spine injury (CSI), with increased predental space of greater than 5 mm that is consistent with atlantoaxial subluxation due to transverse ligament disruption. In addition, secondary signs of injury include soft-tissue swelling in the prevertebral space and increased interspinous distance between C1 and C2. Figure 1 demonstrates pseudosubluxation at C2-C3, a normal finding in young children. Figure 2 demonstrates a normal anteroposterior (AP) view of the cervical spine in an intubated patient. Figure 3 demonstrates physiologic anterior wedging of the vertebral bodies, pseudosubluxation, and a normal predental space in a child. The loss of cervical lordosis in this case can be physiologic and partially due to positioning from a cervical collar. Figure 4 displays the offset of lateral masses of C1, which is consistent with a pseudo-Jefferson fracture, another physiologic variant in the immature cervical spine.?Due to increased mobility of the cervical spine, ligamentous laxity, shallow facet joints, and underdeveloped spinous processes, children younger than 8 years of age are less prone to osseus injuries than adults. However, they are at greater risk for cord injuries due to their large heads relative to the cervical musculature. The age of a child also correlates with the level of injury. Because the fulcrum of motion of a young child’s head is higher up on the cervical spine, most cases of significant CSI in children younger than 8 years of age occur higher than C3; injuries in older children and adults occur most frequently at C5-C6.Variations in anatomy and ligamentous laxity permit displacement of the cervical spine that actually may be normal. Hence, the radiographic appearance of the cervical spine in children differs in several ways from that of adults. Pseudosubluxation in the upper cervical spine of a child is considered a normal finding. Among children younger than 8 years, at least 3 mm of anterior displacement may be present in 40% at C2-C3 and in 14% of children at C3-C4. This condition occurs in children up to 14 years of age. Strict radiographic criteria determine the presence of pseudosubluxation. A line drawn through the posterior arches of C1 and C3 should touch, pass through, or lie within 1 mm anterior to the anterior cortex of the posterior arch of C2 (Fig. 6). If this condition is not met, then true dislocation should be suspected.Figure 6. Radiograph demonstrating true dislocation of the cervical spineA second common feature of the pediatric spine that can be misleading is the collection of synchondroses in all cervical vertebrae. The C2 vertebra, which is especially prone to injury in young children, has a total of three synchondroses between the dens, body, and arch, which usually close between the ages of 3 and 7 years. Os terminale is a secondary ossification center at the tip of the dens that forms at 3 to 6 years of age and fuses by 12 years. Of these three synchondroses, the dens arch is most pronounced and, therefore, most frequently mistaken for a fracture. A key feature that distinguishes dens arch synchondrosis from a true fracture is that the synchondrosis is visible on an oblique but not on a straight lateral film. Subaxial vertebrae in young children have synchondroses between the posterior and anterior elements, which can be mistaken for fractures.Other radiographic features that may be misread as evidence of CSI include a lack of cervical lordosis and notable angulation at individual intervertebral spaces. Pronounced vascular channels in the ossification center also can be misconstrued as fractures. Anterior wedging up to 3 mm can resemble a compression fracture, a condition that is especially common at C3. Differential growth of C1 on C2 can resemble a pseudo-Jefferson fracture. A comparison normal radiograph is shown in figure 7.Standard radiographs for assessing potential CSI should include at least two views of the cervical spine. An AP and cross-table lateral view help identify lateral mass and transverse process fractures. The usefulness of an odontoid view in very young children is questionable. Because of its extremely low yield and the difficulty in obtaining adequate transoral views, many radiographic protocols at pediatric institutions recommend that AP and lateral plain radiographs are sufficient in the setting of trauma for children 5 years of age or younger. If a patient has normal results on these views, flexion and extension views may be obtained to evaluate stability in patients who have normal mental status, no neurologic deficits, but persistent neck pain. Dynamic radiographs should be obtained only if the patient is neurologically intact. However, the value of dynamic films is disputable in the acute setting because results are often unsatisfactory due to muscle spasm.For children younger than 8 years of age, the benefit of computed tomography (CT) scans for diagnosing CSI is limited because most injuries in this age group are ligamentous, with no osseous component. Even in children older than 8 years, 20% of CSIs are ligamentous and do not involve a fracture. Therefore, normal anatomic findings on a CT scan cannot be used to exclude a cervical injury in children and should not be used exclusively for cervical spine clearance. CT scans are superior to radiographs for defining bone anatomy. They are most useful in the setting of altered mental status and inadequate or suspicious or abnormal plain radiographs. However, their use in suspected pediatric CSIs should not be considered routine. Their benefits must be weighed against the long-term risk of radiation-induced cancer. A CT scan of the neck is the equivalent of 10 to 90 plain radiographs in radiation exposure equivalents. Among children younger than 5 years of age who undergo cervical spine CT scan, the relative lifetime risk of developing thyroid cancer is estimated to be twice the rate for the general population.Magnetic resonance imaging (MRI) can be useful in the setting of pediatric cervical spine trauma. First, MRI can be used to clear the cervical spine of a child if initial plain radiographs and CT scan show normal results but the child is obtunded, intubated, or uncooperative. Also, if results on plain films or CT scans are equivocal, an MRI can be used to clear the cervical spine. Second, if a child has persistent or delayed neurologic symptoms with normal findings on radiographs and a CT scan, an MRI may reveal soft-tissue, ligamentous, or disk injury that would otherwise remain unrecognized. Finally, MRI can provide useful prognostic information about spinal cord injury. Many findings that previously were attributed to spinal cord injury without radiograph abnormalities (SCIWORA) are visible on MRI. If it does exist, SCIWORA may result from injury to the vascular supply of the cord or a nondisruptive or self-reducing intersegmental deformity of the spinal cord.American Board of Pediatrics Content Specification(s)Define radiographic evaluation of cervical and spinal cord injuriesKnow the radiologic variants of the spine and be able to differentiate from cervical spine injuriesQuestion: 6A previously healthy 6-year old boy presents to the emergency department with a 2-week history of an enlarged right-sided cervical lymph node. His pediatrician has treated him with a 10-day course of clindamycin, but there has been no change in the size of the lymph node. The 2x2-cm node is warm, tender to palpation, and mildly erythematous. He has no skin lesions, and the remainder of his physical examination findings are normal. He had low-grade fevers before his antibiotic course but has not had any since that time. He has no history of travel. The family recently took in a stray kitten, and they have a pet iguana at home.Of the following, the MOST appropriate next step at this time is to:A.consult the surgeons for incision and drainageB.perform a Bartonella henselae antigen skin testC.place a purified protein derivative testD.reassure the family that no testing or treatment is neededE.refer the boy for excisional biopsyCorrect answer: DThe boy described in the vignette has a classic presentation of regional adenopathy from cat-scratch disease, caused by the gram-negative bacillus B henselae. The differential diagnosis includes other bacterial causes of lymphadenitis, although the lack of response to clindamycin therapy argues that this is not a typical bacterial infection. Malignancy is less likely because the node is tender, and there are no associated systemic symptoms or organomegaly.?The kitten exposure strongly suggests Bartonella as a causative organism. Young cats, who frequently have bacteremia with B henselae, serve as the reservoir for this infection, which is transmitted via a bite or scratch. However, a documented bite or scratch is not necessary to make the diagnosis. Some practitioners might diagnose the illness with an immunofluorescent antibody assay for B henselae, which is relatively sensitive and specific, but others believe the diagnosis can be made clinically in mild-to-moderate cases of regional lymphadenopathy. Incision and drainage is not recommended because of the risk of prolonged drainage and sinus tract formation. The skin test, created from the pus of cat-scratch disease-infected lymph nodes, previously was used to document infection, but it is no longer performed because of risk of transmitting infectious organisms and lack of standardization.Treatment for cat-scratch disease is controversial. In most cases, it is a self-limited illness, with lymphadenopathy resolving without intervention in 1 to 4 months. Rarely, it can persist for years. Accordingly, the parents in the vignette can be reassured that no testing or treatment is needed for their child. Usual treatment is directed at symptomatic relief. Painful, suppurative nodes can be drained via needle aspiration. Incision and drainage is not recommended, and surgical excision is unnecessary.Approximately 80% to 90% of symptomatic children who have cat-scratch disease have a local infection with regional lymphadenopathy, which develops 2 to 4 weeks after a bite or scratch, usually from a young cat. The true incidence of the disease is unknown, but it is probably very common. Typical sites of adenopathy include axillary, epitrochlear, cervical, and submandibular areas. Some 10% to 15% of nodes suppurate, and fever and mild systemic symptoms occur in 20% to 30% of infections. Other potential complications include hepatic or splenic involvement, with multiple scattered defects visible if the liver or spleen is imaged with computed tomography (CT) scan. Biopsy rarely is performed because the appearance of lesions on CT scan is characteristic. Prolonged fever of unknown origin (FUO) is another potential presentation of B henselae infection. Parinaud oculoglandular syndrome is an atypical presentation of B henselae infection. It is believed to occur from conjunctival exposure to the organism and causes nonpurulent conjunctivitis and conjunctival granulomas, with adjacent preauricular adenopathy. Rare neurologic complications include encephalopathy, cranial neuropathy, and transverse myelitis.There are few data to guide antibiotic therapy. Some authors recommend treatment for all patients with a 5-day course of azithromycin, based on a single small randomized, placebo-controlled trial that demonstrated a significant reduction in lymphadenopathy at 30 days in the azithromycin-treated group. A larger retrospective study showed a reduction in number of weeks of illness for patients treated with rifampin, ciprofloxacin, trimethoprim-sulfamethoxazole, or gentamicin compared with other antibiotic options or no treatment.?For involvement of the liver or spleen or for prolonged fever, a 10- to 14-day course of rifampin with or without gentamicin or azithromycin is recommended, although the optimal duration of therapy is unknown. All immunocompromised patients should be treated because they are at risk for bacillary angiomatosis, a life-threatening complication in which the organism disseminates widely. Skin lesions in this disorder are nontender, firm, and vary in pigmentation from skin-colored to erythematous or even purplish. They may be indistinguishable from Kaposi sarcoma, pyogenic granuloma, or other types of hemangioma.American Board of Pediatrics Content Specification(s)cat scratch diseaseQuestion: 7A 10-year-old boy is brought to the emergency department after stepping on a nail. He was wearing athletic shoes at the time of the injury. Physical examination reveals a puncture wound at the metatarsal-phalangeal area of the third toe. A foot radiograph shows no evidence for a foreign body. The emergency department physician irrigates the wound with saline and dresses it with antibiotic ointment. After ascertaining that the boy’s immunizations are up to date, he administers diphtheria and tetanus toxoids. Seven days later, the boy returns to the emergency department because of persistent pain and newly developed erythema, warmth, and swelling at the wound site. He is afebrile and has normal vital signs.Of the following, the MOST appropriate next step in the management of the wound is:A.administration of oral antibiotics to treat both Staphylococcus aureusi and Pseudomonas aeruginosaB.coring of the wound and administration of antibiotics to treat both S aureus and P aeruginosaC.coring of the wound and administration of antipseudomonal antibioticsD.further imaging to evaluate for a retained foreign body and osteomyelitis and administration of antibiotics to treat both S aureus and P aeruginosaE.further imaging to exclude a retained foreign body and intravenous administration of antistaphylococcal antibioticsCorrect answer DPuncture wounds are common in children and adolescents, accounting for 3% to 5% of traumatic injuries presenting to pediatric emergency departments. They are more common in the summer months, and more than 50% involve the plantar surface of the foot. Patients who have wounds that penetrate deeper than the epidermis are at risk for infection. The most likely causative organism is determined by where and how the wound occurred.The most common organism isolated from most puncture wounds is S aureus. Symptoms of infection due to S aureus are usually evident within 2 to 3 days. Patients presenting in this time frame should be evaluated for retained foreign body. Those who have mild symptoms may be treated with a trial of oral antistaphylococcal antibiotics and close follow-up. Patients who have lymphangitic streaking or systemic signs of infection or those who fail outpatient therapy should be admitted to the hospital to receive intravenous antibiotics.Wounds in which the puncture is through the sole of an athletic shoe, such as described for the boy in the vignette, are at additional risk for infection with P aeruginosa. Pseudomonal infections tend to present 5 to 7 days after the initial injury and usually involve osteochondritis or osteomyelitis. Wounds occurring in bodies of water are at risk for infection with AeromonasThe correct approach for the boy described in the vignette, who has signs of wound infection, is to obtain imaging to exclude a retained foreign body and to investigate for the presence of osteochondritis or osteomyelitis. This should be followed by orthopedics consultation and administration of intravenous antibiotics that have both antistaphylococcal and antipseudomonal activity.Little empiric evidence guides the management of plantar puncture wounds. Weight-bearing surfaces, such as the “ball” of the foot are prevalent sites for injuries. This area is the region of the metatarsal–phalangeal joints, and in children, both articular and physeal cartilage is present, which can become infected. Osteochondritis/osteomyelitis is much more common when the wound is in the forefoot because of the location of this cartilage. No evidence supports the use of prophylactic antibiotics to prevent later infections. There is a very low incidence of vascular and neurologic injuries associated with plantar puncture wounds.The initial management of puncture wounds should involve a search for possible retained foreign bodies, cleaning of the wound, and local wound care in an attempt to reduce the risk of later infection. Puncture wounds should not be closed with either sutures or tissue adhesive. Radiographs may show radiopaque foreign bodies, but more than 80% of foreign bodies associated with plantar wounds are not radiopaque due to the nature of the foreign body. An “underpenetrated soft tissue” radiograph may be attempted to view such objects, but sensitivity is still low. Radiographs should be obtained in deep wounds caused by glass, if the patient feels there is a retained foreign body, if the wound was caused by a metallic object that could have broken off or that is retained (eg, a sewing needle), or if there is marked tenderness below the skin or signs of an infection. If there is strong concern for a retained foreign body, other imaging modalities, including ultrasonography, computed tomography scan, or magnetic resonance imaging, may be used.The surface of puncture wounds should be cleaned well, and jagged skin edges may be trimmed. There is no evidence to support either deep-wound, high-pressure irrigation or coring of puncture wounds in their initial management. Deep irrigation under high pressure is difficult to perform, requires the administration of local anesthesia, and is associated with a theoretical risk of the dissemination of contaminating bacteria. Coring of puncture wounds was recommended in the past, but this procedure requires regional anesthesia, leads to larger wounds with prolonged healing time, and has not been shown to decrease the risk of infection. Although infection is a concern, most plantar puncture wounds heal without the onset of infection.Patients should receive appropriate updating of tetanus prophylaxis. If the patient has not received primary tetanus immunization or a primary tetanus series has not been completed, tetanus immune globulin (250 units intramuscularly) should be provided. If a primary series has been completed and it has been more than 5 years since the patient’s last booster immunization, tetanus toxoid (0.5 mL intramuscularly) should be administered, preferably in combination with diphtheria toxoid and pertussis vaccine.Patients should be instructed to remain non-weight bearing, keep the foot elevated, and soak it several times a day until the wound is healed. When patients present with signs of infection, the timing of the presentation and the circumstances of the injury may help to guide antibiotic choice. Infections due to S aureus and streptococcal species tend to present in the first few days after injury. Patients who sustain puncture wounds associated with the penetration of the sole of an athletic shoe have an increased risk of infection, including osteochondritis or osteomyelitis due to P aeruginosa. It is believed that small pieces of foam from the shoe may contaminate the wound, leading to infection with this organism. Pseudomonal infections tend to present 5 to 7 days after the initial injury. Other potential pathogens include anaerobic bacteria, Klebsiella, Serratia marcescens, Bacteroides melaninogenicus, Escherichia coli, Proteus mirabilis, and Salmonella typhi.Signs of infection should prompt a more thorough inspection for foreign bodies, including additional imaging. Ultrasonography and computed tomography scan may be helpful acutely. Magnetic resonance imaging, when available, has the added advantage of providing evidence of bone and cartilage involvement. Orthopedics consultation should be obtained and intravenous antibiotics started. Antibiotic coverage should include S aureus, streptococcal species, and P aeruginosa in the case of puncture through an athletic shoe. Options include clindamycin plus ceftazidime and an aminoglycoside. Ticarcillin or other antipseudomonal agents could be used in place of the ceftazidime and aminoglycoside. Some sources recommend the use of ciprofloxacin for pseudomonal coverage either alone or in combination with an antipseudomonal beta-lactam (eg, ceftazidime or cefepime).American Board of Pediatrics Content Specification(s)Know the anatomy and pathophysiology relevant to management of plantar puncture wounds.Discuss the indications and contraindications for management of plantar puncture wounds.Describe the key steps and potential pitfalls of managing plantar puncture wounds.Discuss the complications associated with managing plantar puncture wounds.Question: 8A 7-day old-male infant is brought to the emergency department because of poor feeding, lethargy, and difficulty breathing for the past 18 hours. He was born at term via normal spontaneous vaginal delivery to a G1P1A0 woman who did not receive prenatal care. The mother states that her breastfed infant has had no fever or vomiting. On physical examination, his temperature is 36.0°C, heart rate is 190 beats/min, respiratory rate is 70 breaths/min, blood pressure is 65/40 mm Hg in the upper extremity and 50/30 mm Hg in the lower extremity, and pulse oximetry reading is 90%. The infant appears ill, listless, and grey, and he demonstrates labored respirations, weak peripheral pulses, and a capillary refill time of 5 seconds. There are no abnormal odors, dysmorphic features, or abnormal genitalia. Point-of-care arterial blood gas reveals:·????? pH of 7.1·????? Po2 of 55 mm Hg·????? Pco2 of 50 mm Hg·????? Base excess of -15 mEq/LElectrolyte measurements include:·????? Bicarbonate of 11 mEq/L (11 mmol/L)·????? Sodium of 130 mEq/L (130 mmol/L)·????? Potassium of 6.6 mEq/L (6.6 mmol/L)·????? Chloride of 100 mEq/L (100 mmol/L)Glucose measures 42 mg/dL (2.3 mmol/L). A chest radiograph is obtained (Figure).Figure??Of the following, after administration of intravenous glucose and a crystalloid bolus, the therapeutic intervention that is MOST likely to provide immediate benefit is:A.acyclovirB.alprostadilC.cefotaximeD.hydrocortisoneE.sodium benzoateCorrect answer BThe infant described in the vignette is demonstrating signs of shock, hypoperfusion, and respiratory distress. The radiograph shows cardiomegaly with pulmonary edema. The discordance in blood pressure between the upper and lower extremities suggests a critical left heart obstruction such as coarctation of the aorta with ductal-dependant systemic circulation.?The intervention most likely to be immediately beneficial is administration of alprostadil (prostaglandin [PG]E1).In general, the differential diagnosis of a “crashing” neonate is broad (Table 1). Important considerations include sepsis, congenital heart disease, and inborn errors of metabolism. Empiric administration of parenteral antimicrobials and hydrocortisone are appropriate for this critically ill neonate, but isolated sepsis or adrenal crisis are not associated with a discrepancy in upper and lower extremity blood pressures, cardiomegaly, and pulmonary edema.?? Intravenous sodium benzoate is a scavenging agent that is best reserved for patients who have confirmed hyperammonemia, seen in association with an inborn error of metabolism such as a urea cycle defect or organic acidemia. Cardiomegaly, respiratory distress, and shock, such as described for the infant in the vignette, are not the dominant symptoms of these disorders. Symptomatic hyperammonemia from a urea cycle defect presents with vomiting and encephalopathy without acidosis or shock. The initial approach in these cases is to administer dextrose-containing fluids and eliminate protein from the diet.Acute presentation of such an ill newborn or infant should raise immediate concern about potential sepsis or ductal-dependent congenital heart disease. Risk factorsfor early onset of sepsis (< 3 days of age) areinterconnected with vertical transmission of causative organisms, including that seen with premature or prolonged rupture of chorioamniotic membranes, maternal colonization with group B beta-hemolytic Streptococcus (GBS), intrapartum maternal fever, prematurity, and chorioamnionitis. Since the advent of intrapartum antibiotic prophylaxis to prevent neonatal GBS infection, gram-negative organisms have become the most common pathogens, accounting for nearly two thirds of all infections. Among these, Escherichia coliis the most common. GBSis the most common gram-positive pathogen, and infection is associated with a rapid onset of respiratory disease and shock that often is fatal.Risk factorsfor late-onset bacterial infection (>3 days of age) are closely related to horizontal transmission of causative organisms and include endotracheal intubation, indwelling urinary and vascular catheters (especially venous catheters), lack of enteric feeding, and exposure to broad-spectrum antibiotics, which may alter normal flora and permit overgrowth and dissemination of fungal species and resistant bacteria. In contrast to early-onset infections, gram-positive organisms predominate and account for approximately two thirds of cases. Coagulase-negative staphylococci(common skin flora) are the most frequent isolates, especially among very preterm infants. However, gram-negative bacteria (eg, E coli, Klebsiella pneumoniae, Pseudomonas aeruginosa) also cause a significant proportion of late-onset bacterial infections. Fungal infections (Candida) occur frequently in small preterm infants. Herpes simplex virus (HSV) infection usually presents within the first 2 weeks after birth but can present as late as 6 weeks of age. The course of late-onset infections typically is more indolent compared with the fulminant course of early-onset disease.The initial management of sepsis involves the usual assessment of the patient's airway, breathing, and circulation (ABCs); securing intravenous access; laboratory testing, including a blood culture; and empiric antibiotic therapy. Acidosis can be corrected with judicious administration of fluids or exogenous base. Initial management of low cardiac output involves a dopamine infusion at 5 to 10 mcg/kg per minute; calcium should be administered when hypocalcemia is documented.Distress in neonates and infants younger than 2 months of age due to cardiac causes most likely represents congestive heart failure related to structural heart disease. ?Systemic or pulmonary circulation may depend on the patency of the ductus arteriosus, especially in patients presenting in the first few days after birth. An alprostadil (PGE1) infusion is indicated when ductal-dependent cardiac lesions are diagnosed or when they cannot be ruled out in a timely fashion. Absent femoral pulses orthe inability to increase the systemic arterial Pao2 to more than 150 mm Hg with a fraction of inspired oxygen (Fio2) of 1 (“hyperoxia” test) suggests a ductal-dependent lesion (Table 2), and treatment with PGE1 is warranted. A simpler method of completing the hyperoxia test is to provide 100% oxygen and observe the oxygen saturation on pulse oximetry for an increase of 10% in lung disease and minimal change with cyanotic heart disease. Echocardiography should be considered early in the evaluation if a diagnosis is not immediately forthcoming.PGE1 theoretically could aggravate the condition in some children who have total anomalous pulmonary venous connection and obstruction or in children who have other sources of congestive heart failure (Table 3), such as sepsis. Whenever possible, echocardiography should be performed before PGE1 treatment is begun. On the other hand, when critical heart disease is present and echocardiography is not immediately available, prostaglandin infusion can be lifesaving.Laboratory tests and monitoring of a neonate in distress should be tailored to the suspected diagnoses. An arterial blood gas to assess acid base status, oxygenation, and ventilation is extremely helpful for evaluation. For suspected cardiac disease, chest radiography, continuous pulse oximetry and rhythm monitoring, electrocardiography, and early echocardiography are warranted. A complete evaluation of sepsis should include blood, cerebrospinal fluid (CSF), and urine cultures. For suspected viral sepsis, an extra tube of CSF may be held in the laboratory for HSV polymerase chain reaction testing.?HSV cultures should also be obtained from skin, eye, and rectum specimens. Stool may be sent for enteroviral cultures. Endotracheal tube aspirates may be sent for viral respiratory panel cultures in suspected viral lower respiratory tract infection. The laboratory evaluation for suspected metabolic disease includes plasma ammonia, amino acids, carnitine, pyruvate, and lactate along with urine for organic acids and amino acids. In salt-wasting congenital adrenal hyperplasia due to 21-hydroxylase deficiency, serum 17-hydroxyprogesterone is elevated.?It may be prudent to save an extra vial of blood before administration of empiric hydrocortisone for appropriate testing in conjunction with the endocrinology consultation.Table 2: Cardiac Causes of Congenital Heart Failure (Ductal-dependant)Cyanotic Lesions (“blue” infant who has markedly decreased pulmonary blood flow)?Transposition of great vessels?Truncus arteriosus?Tetralogy of Fallot?Tricuspid atresia?Severe pulmonic stenosis?Total anomalous pulmonary venous return?Acyanotic Lesions (“grey” infant who has low cardiac output)?Critical coarctation of aorta?Hypoplastic left heart syndrome (aortic atresia, interrupted aortic arch, mitral valve atresia, aortic atresia)?Nonstructural Cardiac Lesions?Myocarditis?Primary cardiomyopathy?Myopathic disease due to inborn errors of metabolism?Cardiac arrhythmias (eg,? sustained supraventricular tachycardia, complete heart block)?Anomalous left coronary artery from pulmonary artery (ALCAPA)Conditions to consider in young infants who have a?more protracted congestive heart failure course include those producing significant left-to-right shunts?(eg, large ventricular septal defects, endocardial cushion defects, complete atrioventricular canal, aortopulmonary shunts, and arteriovenous malformation).?American Board of Pediatrics Content Specification(s)Recognize signs and symptoms of neonatal distress.Know indications for monitoring and laboratory procedures in recognition of neonatal distress.Recognize the maternal risk factors associated with neonatal distress.FEBRUARY 2011Question: 1There have been an unusual number of children and adults in the ED complaining of the abrupt onset of watery diarrhea and abdominal pain. Upon further investigation, you discover that there have been 23 adults and 15 children seen in the last 48 hours with similar symptoms. You call to report this unusual pattern to the local health department, who confirm that other centers are reporting a similar pattern of illness. At least 90 persons have been affected to date. The health department is planning a study to help determine the origin of the outbreak. The annual county fair started 5 days ago, and there is reason to believe that it may be the source. The fair has more than 50 food vendors, a petting zoo, and multiple other displays and events involving many types of farm animals. You ask your fellows to design a study to determine the origin of the outbreak.?Of the following, the study design MOST likely to determine the origin is a:A.case-control studyB.cross-sectional survey studyC.disease registry-based studyD.double cohort studyE.single cohort studyCorrect answer: AA case-control study design is the standard initial approach to identifying the source of outbreaks of disease such as the one described in the vignette. Such outbreaks often are caused by exposures to food, water, or other environmental “point-sources” contaminated with a microbe. Case-control studies start with persons who have a particular disease (cases). An appropriate group of “control” persons who do not have the disease, but who have similar baseline characteristics (eg, live in the same area, have similar age and sociocultural background), are selected for comparison. Both groups are examined for rates of various exposures. An exposure or characteristic that occurs more commonly among cases than controls becomes an etiologic candidate. The result typically is expressed as an odds ratio with a 95% confidence interval.The advantages of case-control designs are that they can be performed quickly and relatively inexpensively and frequently are effective for outbreaks of infectious diseases. Multiple exposures can be evaluated for a single outcome. Case-control study design may be the only feasible approach to investigate rare outcomes. Disadvantages include recall bias, in which cases may be more likely to recall an exposure or incorrectly consider themselves to have been exposed than controls. Selection of appropriate control subjects is critical. Both “overmatching” and “undermatching” on important risk factors must be weighed. Control subjects should be very similar to case subjects, with the exception of the causative exposure. Because of the relative ease of conduct and lower costs, case-control studies often are among the first types of causation assessments to be conducted.?Cohort studies are observational investigations used to examine outcomes of exposures or risk factors over time. After identification of persons who have the exposure or risk factor of interest, these individuals are monitored for development of one or more outcomes. A single cohort study follows a set of exposed persons without any controls. A double cohort studyalso follows a set of unexposed persons, which allows for estimation of relative risk for a particular outcome based on the presence or absence of an exposure. Prospective data collection eliminates recall bias, but cohort studies can be very expensive when follow-up is required over a number of years.Cohort studies are useful for learning about the natural history and health impacts or health-care system burdens of a particular exposure or disease, but they are not suited for providing a quick answer for the cause of a disease outbreak. Retrospective cohort studiessometimes can be performed using health-care databases, but this requires accurate recording of the presence or absence of a particular risk factor in the database at some point in the past, with subsequent adequate follow-up data of the subjects. A randomized, controlled trial can be considered a type of cohort study in which members of a reasonably homogeneous population, defined by inclusion and exclusion criteria, are allocated randomly into a control group and one or more intervention groups.A cross-sectional survey study is essentially a “snapshot” in time. Surveys are used in case-control studies, but the presence or absence of disease in the study subjects is known, and questionnaires seek occurrences of past exposures. In cross-sectional surveys, study participants are selected from a well-defined population, often randomly, but without knowledge of the presence or absence of a particular disease. Data for various diseases and various exposures are collected at the same point in time, and the relationships between timing of exposures (risk factors) and onsets of disease generally cannot be captured in this type of study. Disease prevalence can be estimated, but incidence generally cannot be inferred. Associations can be elucidated, but causation cannot be inferred.A disease registry is designed to capture information about risk factors or clinical features of a particular disease. Data for individuals who do not have the disease generally are not captured for comparison. Registries are particularly useful for descriptive and pathophysiologic analyses of diseases that have relatively low incidences. Standardized data collection from multiple centers can facilitate more rapid accrual of data to support further investigations of disease epidemiology and cause as well as diagnostic and therapeutic interventions. A disease registry is, in essence, a more formal version of a single cohort study or case series.Surveillance systems, such as the communicable disease reporting system of the Centers for Disease Control and Prevention (CDC), also can be considered a type of registry. When capture of disease occurrence is nearly complete due to mandatory reporting, case data can be combined with population data to determine disease incidence and then relative incidences. Surveillance efforts such as the CDC FoodNet can be helpful in determining sources of national outbreaks but are less effective for local outbreaks, where answers are needed within a few days.There is a hierarchy of validity in determining causation among observational studies. Cross-sectional studies provide the lowest level of insight. Case-control studies provide more substantial evidence that a particular disease is caused by a particular agent or risk factor, but such findings generally require confirmation with cohort studies, which provide the most convincing evidence of cause and effect. Case series and disease registries/surveillance systems typically do not include control groups without disease and, therefore, do not address causation.American Board of Pediatrics Content Specification(s)Understand the design and application of different types of observational studies: survey, case-control, cohortQuestion: 2An 8-year-old boy presents to the emergency department (ED) 1 day after attempted removal of a foreign body from the right external auditory canal. In the ED yesterday, the ED resident and ear-nose-throat (ENT) resident made multiple removal attempts with alligator forceps. The boy became increasingly uncooperative, and the bead could not be removed. He was scheduled for operative removal by the ENT surgeons in 3 days. He returns today, complaining of dizziness and decreased ability to hear in his right ear. He will not let you examine his ear.Of the following, the MOST likely cause of this child’s acute hearing loss is:A.conductive hearing loss due to cholesteatomaB.conductive hearing loss due to middle ear traumaC.conductive hearing loss due to the foreign bodyD.sensorineural hearing loss due to perilymphatic fistulaE.sensorineural hearing loss due to viral labyrinthitisCorrect answer: BSound is transmitted to the tympanic membrane, which vibrates, causing movement of the ossicles in the middle ear to create fluid waves. Cochlear hair cell receptors in the inner ear convert the fluid waves into nerve impulses, which are transmitted via the cochlear nerve to the brain. Acute hearing loss falls into two categories:?conductive hearing loss, in which transmission of sound waves to the inner ear is abnormal, and sensorineural hearing loss, in which processing of sound waves in the inner ear is defective.?For the boy described in the vignette, who underwent multiple attempts at removal of a spherical foreign body lodged in his ear, the new onset of hearing loss and dizziness should prompt concern about possible tympanic membrane disruption and ossicular damage. Spherical objects that completely occlude the canal are at high risk of being pushed further in when removal is attempted with alligator forceps, especially if the child does not cooperate with removal.?Although a completely occlusive foreign body could cause a decrease in conductive hearing, without other complications it should not cause dizziness. Cholesteatoma is an epidermal inclusion cyst of the middle ear, usually caused by chronic otitis media, that can result in slowly progressive conductive hearing loss that may be accompanied by dizziness. It should not cause acute hearing loss. Viral labyrinthitis can cause acute hearing loss and dizziness, but it occurs in the setting of infection with many viruses, including mumps, parainfluenza, adenovirus, herpes simplex virus, cytomegalovirus, and rubeola. A perilymphatic fistula is an anomalous connection between the middle and inner ear that is associated with antecedent trauma, most commonly barotrauma, which can occur with scuba diving or depressurized airplane travel.The most common cause of conductive hearing loss seen in the ED, especially among young children, is middle ear effusion. Impacted cerumen and severe otitis externa are other causes of conductive hearing loss. Acute head injury can cause hearing loss via hemotympanum, rupture of the tympanic membrane, or disruption of the inner ear ossicles.Acquired acute sensorineural hearing loss has multiple causes:Infection: bacterial meningitis, viral labyrinthitis, acute otitis mediaVascular insufficiency: Sickle cell disease, diabetes mellitus, polycythemia causing decreased cochlear blood flowAnatomic defects: perilymphatic fistulaTrauma: temporal bone fracture, noise-induced injury, barotraumaTumor: acoustic neuroma, central nervous system tumor, leukemic infiltrate, neurofibromatosisAutoimmune: neurosarcoidosis, demyelinating disordersFunctional: pseudohypoacusis caused by a conversion disorder or other psychiatric disorderOtotoxic drugs: intravenous cocaine, chemotherapeutic agents, aminoglycosidesIdiopathicEvaluation of hearing loss in the ED should include a complete physical examination with attention to the otoscopic and neurologic evaluations. Common causes of acute conductive loss such as cerumen impaction and middle ear effusion can be seen on examination. Facial nerve palsy accompanied by deafness suggests an intracranial process. Nystagmus suggests vestibular involvement.?Tuning fork tests can help distinguish between conductive and sensorineural causes. In the Weber test, in which a vibrating tuning fork is placed on the forehead in the midline, the sound lateralizes to the affected side with conductive hearing loss and away from the affected side with sensorineural hearing loss. In the Rinne test, the vibrating tuning fork is placed against the mastoid, removed when the patient senses vibration has stopped, and held up to the ear. A positive result is demonstrated when the patient can still hear the tuning fork and indicates sensorineural hearing loss. A negative result, in which the patient cannot hear the tuning fork placed next to the ear, indicates a conductive loss. If a tuning fork is placed equidistant between both ears, the sound is louder in the unaffected ear, regardless of cause.?No routine laboratory evaluation or imaging is required in cases of acute hearing loss. However, if findings on the physical examination suggest intracranial pathology, especially in the setting of trauma, computed tomography scan may be helpful. When the cause of the acute hearing loss remains unclear, prompt ENT evaluation is appropriate.American Board of Pediatrics Content Specification(s)Know the etiology by age and pathophysiology of sudden hearing lossPlan diagnostic evaluation and initial intervention for patients with sudden hearing lossRecognize serious and/or life threatening causes of sudden hearing lossQuestion: 3A 4-year-old boy who was struck by a car traveling at approximately 20 miles per hour is brought to the emergency department by ambulance. On physical examination, the awake and alert boy is crying but consolable. His temperature is 37.0°C, heart rate is 134 beats/min, respiratory rate is 24 breaths/min, and blood pressure is 94/62 mm Hg. He has a small contusion and abrasion over the right upper quadrant of his abdomen. Bowel sounds are present, and his abdomen is soft and not tender to palpation. There are no other obvious injuries of the trunk, head, neck, or extremities.Of the following, the laboratory test result that is MOST useful in excluding a serious intra-abdominal injury in this boy is:A.amylase, 68 U/LB.aspartate aminotransferase, 40 U/LC.hemoglobin, 12.6 mg/dL (126 g/L)D.lactate, 1.2 mmol/LE.total bilirubin, 0.6 mg/dL (10.3 ?mol/L)Correct answer BTrauma is the leading cause of death in children older than 1 year of age, and abdominal trauma is the third leading cause of death. However, most pediatric victims of blunt torso trauma are stable on presentation to the emergency department. Ensuring that serious intra-abdominal injuries are not missed may be challenging for the clinician. Computed tomography (CT) scan with intravenous contrast has been accepted as the gold standard for excluding solid organ injury, but abdominal CT scan in children is associated with large amounts of irradiation. The emergency department physician is often faced with the dilemma of whether CT scan is indicated in children who have blunt abdominal trauma.Although ultrasonography can aid in the exclusion of intra-abdominal injuries, it is not available in all settings. Further, its accuracy in children depends on an operator who uses it frequently in this age group.Simple laboratory tests, when used in the correct setting, may assist in decreasing the use of CT scan. Multiple studies have attempted to determine what laboratory test or combination of tests are most useful. The right upper quadrant findings and mechanism of injury described for the boy in the vignette are most concerning for hepatic injury. A normal aspartate aminotransferase (AST) value has been shown to have a relatively high negative predictive value in the setting of blunt abdominal trauma. Amylase is used to exclude pancreatic injury, but elevations in the value may be delayed. When decreased, hemoglobin has a high positive predictive value for the presence of intra-abdominal injuries, but early after an injury, the hemoglobin may be normal until equilibration. Lactate is elevated in patients experiencing shock, but solid organ injuries do not cause shock unless there is significant bleeding. Total bilirubin is not useful in the evaluation of blunt abdominal trauma.Little evidence supports the use of routine “trauma panels” in the evaluation of blunt abdominal trauma, but some laboratory studies may aid in evaluation. Laboratory test results that have been associated with the presence of intra-abdominal injury in children include: AST greater than 130 to 400 U/L, alanine aminotransferase greater than 100 to 250 U/L, low hemoglobin or hematocrit, and hematuria (>5 to 50 red blood cells (RBCs)/high-power field [hpf]). A prediction rule has been derived and validated in a small population at one center but requires validation in a large population. The rule assessed the presence or absence of six items: hypotension, abdominal tenderness, femur fracture, urinalysis with more than 5 RBCs/hpf, initial hematocrit less than 30% (0.30), and increased liver enzymes. The rule had a sensitivity of 94.9% (95% confidence interval, 90.2% to 97.8%) and a specificity of 37.1% (95% confidence interval, 34.0% to 40.3%).American Board of Pediatrics Content Specification(s)Know the indications for, limitations of, and interpret findings of non-radiologic tests, including hemoglobin, base deficit (lactate), liver function studies, amylase, urinalysis and peritoneal lavage following blunt abdominal trauma.Question: 4A 7–year–old boy is brought to the emergency department by his parents after sustaining a laceration to his right arm when he pushed on a glass door. On arrival in triage, he is somnolent and pale, with a heart rate of 140 beats/min, respiratory rate of 18 breaths/min, and blood pressure of 90/38 mm Hg. There is a large, complex laceration of his right antecubital fossa and medial arm with active, pulsatile bleeding. The parents had tried to keep pressure on the wound en route but have not been able to stop the bleeding.Of the following, the MOST appropriate first step in emergency department management is to:A.apply a tourniquet and obtain vascular accessB.apply direct pressure on the wound and obtain vascular accessC.obtain vascular access and administer 20 mL/kg 0.9% salineD.obtain vascular access and transfuse with O-negative bloodE.place sutures to control bleeding and obtain vascular accessCorrect answer: BThe boy described in the vignette has an exsanguinating external hemorrhage and signs of compensated shock. The priorities that must be addressed simultaneously are control of the hemorrhage and restoration of blood volume. The first step in attempting to control the hemorrhage is to apply direct pressure, which should be undertaken while simultaneously obtaining vascular access with at least two large-bore intravenous or intraosseous catheters.If bleeding cannot be stopped with direct pressure, use of the Windlass technique may be helpful. In this technique, a dressing is applied to the wound and held in place by a broad bandage that is secured by tying a knot directly over the wound. A pen or other cylindrical object is placed under the knot and rotated several times before being secured in place. This allows for maximal and sustained pressure directly over the wound. If the bleeding still cannot be stopped, application of a tourniquet may allow for stabilization until the patient can be brought to surgery.Although the use of tourniquets have been discouraged in the past due to concerns for ischemic injury, including injury to neurovascular structures, military experience in recent conflicts has shown they can play a safe role in temporarily controlling hemorrhage, especially in the prehospital setting. It is now accepted that a tourniquet may be left in place for up to 2 hours without significant risk of permanent ischemic injury. Multiple commercial tourniquet devices are available, and some trials have compared the effectiveness of various devices, but results do not conclusively support one device over another.Tourniquets that are applied in the prehospital setting should be left in place until the patient is transported to a site where definitive care is possible. In the emergency department, use of a tourniquet may allow for stabilization until the patient can be taken to the operating room. However, if a tourniquet has been in place and bleeding seems to be controlled, a trial of releasing it may be carefully undertaken. If hemostasis has been achieved it may sometimes be maintained after release of the tourniquet. In patients who are awake, the pain produced by ischemia with tourniquet use may require analgesics, including opioids if the patient is stable.Obtaining vascular access and attempting to restore blood volume without addressing the ongoing hemorrhage for this patient would likely be ineffective. Repair of an arterial laceration, as in this case, without operating room resources would have a small chance of success. Oversewing or stapling large scalp lacerations to obtain hemostasis can be efficacious, but this approach usually is not successful in vascular injuries of the limbs.American Board of Pediatrics Content Specification(s)Know the anatomy and pathophysiology relevant to controlling exsanguinating external hemorrhage.Discuss the indications and contraindications for controlling exsanguinating external hemorrhage.Describe the key steps and potential pitfalls in controlling exsanguinating external hemorrhage.Discuss the complications associated with controlling exsanguinating external hemorrhage.Question: 5A 7–month–old boy is referred to the pediatric emergency department with a complaint of lethargy. He had been evaluated in a rural hospital and had a normal head computed tomography (CT) scan and nonspecific findings on plain films of the abdomen. He had vomiting 3 days ago and several subsequent episodes of diarrhea. His last bowel movement was yesterday. He has had good oral intake and normal urine output. After awakening today, he seemed to be fussy intermittently and vomited once. For the past 2 hours, he has become sleepier. He had been previously healthy, as are his parents. There are no medications in the household. On physical examination, the pale and lethargic child has a rectal temperature of 37.2°C, heart rate of 114 beats/min, respiratory rate of 28 breaths/min, blood pressure of 78/48 mm Hg, and Spo2 of 98% in room air. His pupils are small but reactive, and his mucous membranes are moist. His lungs are clear, his heart has a regular rate and rhythm with normal heart sounds, and his capillary refill is 2 seconds. His abdomen is flat without hepatosplenomegaly or palpable masses. No hernia is noted. He is sleepy but arouses with vigorous stimulation. His neurologic examination results are otherwise nonfocal. You establish intravenous access; obtain bedside glucose testing, which yields normal results; and administer naloxone, which prompts no response.Of the following, the MOST reliable test to establish the most likely diagnosis quickly is:A.abdominal computed tomography (CT) scanB.abdominal ultrasonographyC.chest radiographyD.repeat abdominal radiographyE.upper gastrointestinal radiographic seriesCorrect answer BThe infant described in the vignette presents with lethargy and miosis after a mild gastrointestinal illness. His glucose value is normal, and he has no response to naloxone. Intussusception is a likely source of these findings and can be diagnosed quickly and reliably with abdominal ultrasonography. The sensitivity and specificity of this imaging modality approaches 100% when performed by an experienced ultrasonographer. Although intussusception can be diagnosed with abdominal CT scan, this time-consuming test is associated with significant radiation exposure. Abdominal radiographs may show nonspecific signs of intestinal obstruction, a target sign, a crescent sign, or a filling defect in the proximal colon. However, sensitivity and specificity are much less than for ultrasonography. In one single-center retrospective study, the presence of air in the cecum on at least two of three views (supine, lateral, and prone) had a negative predictive value of 98%. However, for patients whose clinical presentation seems consistent with intussusception, normal plain radiographs do not exclude its presence.Pneumonia and intracranial injuries can be associated with lethargy in infants. However, prior head CT was read as normal and the history in this child is more consistent with intussusception. This diagnosis should be quickly excluded to minimize the duration of ischemia before other diagnostic tests are undertaken.Intussusception is the most common cause of intestinal obstruction in infants and young children 6 to 36 months of age and the most common abdominal emergency in early childhood. More than 50% of affected children present before 1 year of age, and 80% of cases occur before 2 years. Intussusception is very rare before 9 weeks of age, but the incidence increases until about 6 to 7 months of age, where it occurs in about 60 per 100,000 infants. By 1 year of age, the rate is about half of this. Rates are higher among African American and Hispanic infants than among whites. There is a 3 to 2 male predominance.Seventy-five percent of cases are idiopathic, but 25% are associated with an underlying cause that produces a lead point. Cases associated with pathologic causes producing a lead point (eg, intestinal lymphoma, Meckel diverticulum, polyps, duplication cysts, and Henoch-Sch?nlein purpura) are much more common in children younger than 3 months or older than 5 years of age. In idiopathic cases, the presumed pathogenesis is a preceding viral infection that produces lymphoid hyperplasia in Peyer patches in the terminal ileum. A strong association with preceding adenovirus infection has been reported. The lymphoid hyperplasia acts as a lead point, causing the intussusceptum to invaginate into the more distal bowel or intussuscipiens. Ileocolic intussusception is most common, but ileoileocolic, jejunoileal or colocolic intussusception may also occur.When the intussusceptum enters the intussuscipiens, the attached mesentery, blood supply, and lymphatic drainage of the intussusceptum are compromised. The invaginated portion of the intestine develops edema and ischemia, and intestinal obstruction occurs. If not recognized and treated, the obstruction eventually can cause severe ischemia, bowel necrosis, perforation, and peritonitis.Children classically present with the sudden onset of intermittent, severe, crampy abdominal pain and inconsolable crying. Vomiting often follows and may become bilious. Initially, the child may appear comfortable and act well between episodes, but if the intussusception is not reduced, lethargy develops. Especially in infants younger than 1 year of age, lethargy may predominate early in the symptom course and may be associated with miosis and pallor. Reports have noted a transient response to naloxone in some cases. A palpable mass in the right side of the abdomen may be found. Most children have gross or occult blood in the stool, although gross blood and especially “currant jelly stools” are late findings. The classic triad of pain, a palpable sausage-shaped abdominal mass, and currant jelly stool is seen in fewer than 15% of cases.Once intussusception is diagnosed, treatment should be instituted rapidly. Pneumatic (air) or hydrostatic (contrast media) enemas are the first line of therapy and successful in more than 85% of cases. Reduction of an intussusception may be monitored with either ultrasonography or fluoroscopy. Patients should be stabilized before attempting reduction. A surgical team should be notified and on standby in case of perforation, which occurs in approximately 1% of cases. Some surgical consultants advocate the use of intravenous antibiotics before reduction, but there is no evidence to support this practice. If the patient has had prolonged symptoms (more than 1 to 2 days) or signs of peritonitis or the clinician has a high suspicion that there is a pathologic lead point (eg, patients older than age 5 years or lead point seen on ultrasonography), laparotomy should be considered. This procedure allows for manual reduction, inspection of the bowel, and resection of necrotic segments or the pathologic lead point. Laparotomy is also indicated if successful reduction cannot be achieved using an enema.Once reduced, recurrence of intussusception occurs in up to 10% of cases, usually in the first 12 to 24 hours. Traditionally, patients have been admitted to the hospital for observation, but some authors have suggested that only a brief period of emergency department observation may be needed. Symptoms of recurrence should prompt repeat investigations to rule out the presence of an intussusception. Multiple recurrences should prompt an investigation into whether a pathologic lead point is present.American Board of Pediatrics Content Specification(s)Know the etiology and pathophysiology of intussusceptionRecognize the signs and symptoms of intussusceptionKnow the indications for and interpret results of ancillary studies in patients with intussusceptionPlan the management of acute intussusception and the potential complications of the conditionQuestion: 6A 13-year-old boy who has previously diagnosed moderate persistent asthma is brought to the emergency department (ED) by prehospital personnel because he is suffering from an acute asthma exacerbation that started 2 days ago. He has had a persistent nonproductive cough, nasal congestion, wheezing, and chest “tightness” but no fever. His normal medication regimen consists of an inhaled corticosteroid, a nasal steroid spray, and albuterol as needed. He has been using his rescue inhaler every 4 hours for the past 24 hours with only minimal relief.?In the ED, you immediately administer intravenous corticosteroids and multiple albuterol/ipratropium nebulizer treatments. However, after 60 minutes of therapy, he is becoming more agitated and can only speak a few words at a time. His respiratory rate is 44 breaths/min, heart rate is 125 beats/min, and oxygen saturation is 90% on room air. In addition, he has suprasternal and subcostal retractions and diffuse inspiratory and expiratory wheezing on lung evaluation. You determine that the boy requires admission to the intensive care unit, but there will be a delay before the unit is ready to receive him. You administer oxygen and continuous nebulization of albuterol, but his physical examination findings are essentially unchanged.?Of the following, the MOST appropriate adjunctive treatment is:A.inhaled corticosteroidsB.intravenous antibioticsC.intravenous magnesium sulfateD.intravenous sedationE.oral antihistaminesCorrect answer CThe boy described in the vignette is experiencing a severe asthma exacerbation that is poorly responsive to initial management. The intensive care unit is a reasonable disposition for him, but adjunctive therapies should be considered because of his poor response. Intravenous magnesium sulfate is the only medication among the choices with enough existing evidence to recommend its use as adjunctive therapy in ED patients not responding to conventional treatments.?ED management of an acute asthma exacerbation begins with a brief history and rapid physical examination to assess the severity of the exacerbation. Cardiorespiratory monitoring with determination of the patient’s oxygen saturation is essential. For moderate-to-severe exacerbations, treatment should be started without delay along with supplemental oxygen, if necessary. Intravenous access may be required, depending on the severity of the exacerbation and the patient’s inability to take corticosteroids orally, to provide a route for medication administration for adjunctive therapy and if endotracheal intubation is necessary.Bronchodilators and anti-inflammatory agents are the cornerstone for ED treatment of acute asthma exacerbations. Inhaled, short-acting beta-2 adrenergic agonists can be administered either via a nebulizer or metered-dose inhaler. Subcutaneous epinephrine or terbutaline also has been used in severe exacerbations, but a clear benefit of systemic therapy over inhalation treatments has not been demonstrated. Ipratropium bromide, an anticholinergic agent, can be mixed with albuterol in the same nebulizer treatment and has been shown to reduce hospital admissions when used in the ED, but no significant benefits have been demonstrated when it is used for inpatient therapy.?Systemic corticosteroids reduce the increased airway inflammatory response, which characterizes the pathophysiology of asthma, through several actions:??Downregulation of cytokine production and releaseModification of inflammatory cell behavior of lymphocytes, eosinophils, and mast cells?Decreased mucus secretion and vascular leakageA number of studies have shown that corticosteroids improve outcomes when administered early. Oral administration has been shown to have equivalent effects to drug provided by the intravenous route, unless the patient is unable to take medications by mouth or has concomitant vomiting. Supplemental oral corticosteroids should be given to those patients who routinely take them. The intramuscular route can be an alternative to oral administration. ED use of inhaled corticosteroids instead of systemic corticosteroids for acute asthma exacerbations is controversial and not currently recommended. Additional therapies generally not recommended for use in the ED include: methylxanthines, antibiotics, large volumes of intravenous or oral fluids, chest physical therapy, mucolytics, antihistamines, and sedation.??Adjunctive therapy may be considered in life-threatening asthma attacks or for patients who continue to experience severe acute attacks despite conventional therapy to avoid endotracheal intubation. However, intubation should not be delayed once it has been determined to be necessary.??????????Randomized clinical controlled trials in small populations suggest that intravenous magnesium sulfate may prove beneficial, although the optimal dose is not clear. Helium-oxygen mixture-driven albuterol nebulizer treatments also may be beneficial but generally cannot be used if the patient requires more than 30% oxygen.?Additional therapies that can be considered, although they are not strongly supported by current evidence, include:?Intravenous beta-2 agonistsIntravenous leukotriene receptor antagonistsNoninvasive ventilationContinued evaluation of the patient’s response to conventional therapy is important. Recognizing impending respiratory failure in those patients who are poorly responsive or failing to respond to treatment is critical. Some of the signs and symptoms of respiratory failure are:?Hypotension or bradycardiaThe “quiet/silent” chest, indicating severe airflow restrictionDecreased work of breathing or respiratory effortDecreased level of consciousness/confusionCyanosisCauses of acute deterioration in the patient who has asthma can be due to asphyxia from severe bronchospasm with mucus plugging, pulmonary edema, cardiac dysrhythmias, tension pneumothorax or pneumopericardium leading to tamponade, fatigue from severe work of breathing, and respiratory depression from sedative agents.Several adult studies have identified two particular patient phenotypes that are predisposed to fatal asthma. The more common type that usually has a more indolent course presents with moderate-to-severe airflow obstruction and a slow response to therapy. A rarer, acute asphyxic type has a faster response to treatment. The historical features of such patients tended to identify those who are “fatality-prone.” Similarly, certain historical findings in children predict those who are more likely to have near-fatal asthma attacks: previous history of endotracheal intubation, admission to the intensive care unit, or recent use of systemic corticosteroids.American Board of Pediatrics Content Specification(s)Recognize causes of acute deterioration in asthmaRecognize signs and symptoms of respiratory failure in asthmaPlan management of acute asthmaQuestion: 7Emergency medical services personnel have transported a 2-year-old victim of an accidental drowning in a home in-ground swimming pool to the emergency department. The duration of submersion is unknown; the patient was found apneic and asystolic on the scene. Advanced life support measures were initiated and continued throughout the 15-minute transport to the hospital. Upon arrival at the emergency department, the toddler is endotracheally intubated, has received two doses of epinephrine via an intraosseous line in the right leg, and is receiving active cardiopulmonary resuscitation (CPR). On physical examination, the child is flaccid, apneic, and without a pulse. The monitor confirms asystole in two leads. Pupils are nonreactive and dilated. The initial rectal temperature is 36.0°C. Point-of-care glucose measures 120 mg/dL (6.7 mmol/L). After two additional doses of epinephrine, continued CPR, and one dose of exogenous base, the child’s condition is unchanged.Of the following, the next BEST step in management is to:A.activate the in-house extracorporeal membrane oxygenation (ECMO) teamB.administer calcium gluconateC.initiate core warming with warmed fluids via gastric lavageD.initiate external cardiac pacing at a rate of 120 beats/minE.terminate resuscitative effortsCorrect answer EThe prognosis for the child described in the vignette, who is in asystolic cardiopulmonary arrest (CPA) that is refractory to prolonged (20+ minutes) advanced life support (ALS) interventions following a “warm” water submersion event, with an unknown “downtime,” is dismal. Based on the literature, the probability of meaningful survival without severe hypoxic-ischemic encephalopathy is slim. Therefore, the most prudent course of action is to cease resuscitative efforts. Factors associated with poor prognosis in asphyxial pediatric CPA include lack of return of spontaneous circulation after two or more doses of epinephrine and effective CPR and duration of pulselessness of more than 20 minutes. Among the factors associated with a good prognosis for neurologic recovery following submersion injuries are pupillary responsiveness and a Glasgow Coma Scale score greater than 5 on arrival at the emergency department or admission to the intensive care unit.The mild hypothermia noted in these cases usually is due to a prolonged “no-flow” state. All cases described in the literature of meaningful survival with intact neurologic status after an acute submersion event have occurred in the setting of true “cold” water drowning. For hypothermia to be cerebroprotective, it must occur shortly (within 5 to 7 minutes) after submersion, as may occur from drowning in icy (<5.0°C) cold waters. The initial core temperature in such submersion victims usually is less than 34.0°C. In these situations, it is reasonable to continue ALS for up to 60 minutes or until core rewarming is achieved, using external and internal techniques. ECMO may be an option until cardiac function and core temperature are restored.For “warm” water submersion, as described in the vignette, neither ECMO nor gastric lavage with warmed fluid is appropriate. External cardiac pacing and parenteral calcium have not been proven to be beneficial in asystolic asphyxial CPA.The primary focus during management of asystolic asphyxial CPA following a submersion injury should be to provide effective chest compressions, establish adequate ventilation and oxygenation, and administer an appropriate dose of intravascular epinephrine (0.01 mg/kg of 1:10,000 solution). The management of the victim’s airway and breathing is similar to that recommended for any victim of CPA. There is no need to clear the airway of aspirated water because only a modest amount of water is aspirated in most cases and is absorbed rapidly into the central circulation without causing airway obstruction. Some victims may not aspirate because of reflex laryngospasm. The routine use of abdominal thrusts or Heimlich maneuvers is not necessary and potentially dangerous.Another unique consideration in treating drowning victims is to protect the cervical spine, if trauma is suspected. Neck injuries may be observed in diving accidents or submersion events involving teenagers in association with alcohol consumption.?Removal of wet clothing, early decompression of the stomach to facilitate ventilation, and securing a definitive airway with endotracheal intubation to prevent aspiration of swallowed pool water is important. Most victims vomit when the rescuer performs chest compressions or rescue breathing. If vomiting occurs, clinicians should turn the victim’s mouth to one side and remove vomitus using a finger, cloth, or suction. If spinal cord injury is suspected, log rolling the victim is appropriate.Survivors of CPA after drowning accidents may experience one of many complications that include acute respiratory distress syndrome, aspiration pneumonia, cerebral edema, disseminated intravascular coagulation, and an “after drop” in core temperature as cold peripheral blood is redistributed into the central circulation.American Board of Pediatrics Content Specification(s)Know the key signs, timing, and prognostic factors or mortality in submersion injuryQuestion: 8A 16-year-old boy is brought to the emergency department with a 9-day history of fever, malaise, and myalgias. Yesterday he developed strong urinary urgency but was unable to void. He also experienced one episode of bowel incontinence. Weakness in his lower extremities made it difficult for him to rise from a chair and to walk, but he had no back pain. On physical examination, the boy’s temperature is 37.8°C, heart rate is 76 beats/min, respiratory rate is 18 breaths/min, and blood pressure is 122/52 mm Hg while supine. He is awake, alert, and oriented. His muscle strength is 5/5 in the upper extremities and 3/5 in the lower extremities bilaterally. He does not perceive light touch or noxious stimuli below the level of his umbilicus. Deep tendon reflexes are 1+ in the lower extremities and 2+ in the upper extremities. Plantar reflexes are downgoing bilaterally. His rectal tone is normal, but he has no voluntary contraction of his anal sphincter. He can stand only with moderate assistance.Of the following, the MOST appropriate next step in management is:A.bone scan with radiolabeled technetiumB.cerebrospinal fluid analysis, including oligoclonal puted tomography scan of the thoracic spineD.magnetic resonance imaging with gadolinium of the thoracic spineE.plain radiography with anteroposterior, lateral, and oblique views of the thoracic spineCorrect answer: DThe boy described in the vignette is demonstrating flaccid paralysis of a few days’ duration, suggesting lower motor neuron complex involvement. The sensory level and sphincter effects are strongly suggestive of spinal cord involvement, most likely due to acute transverse myelitis (ATM). All children who develop neurologic deficits attributable to the spinal cord require urgent magnetic resonance imaging (MRI) to exclude a compressive cause. Standard plain radiography, noncontrast computed tomography scan, and bone scan cannot exclude a compressive lesion such as an epidural abscess. Although cerebrospinal fluid analysis may be part of the evaluation of a patient who has noncompressive, acute onset of flaccid paralysis, it should not precede a definitive imaging study. The timing of the appearance of signs and symptoms and accompanying features, such as a preceding viral illness, can suggest one cause over another, but there is enough clinical overlap that a compressive lesion cannot be excluded reliably without neuroimaging. A delay in initiating potentially definitive therapy such as laminectomy, radiotherapy, or chemotherapy for a compressive myelopathy contributes directly to adverse neurologic outcomes.ATM is an acute inflammatory process affecting a focal area of the spinal cord, although spinal cord involvement may be diffuse. Symptoms may progress over hours to weeks, but the maximal neurologic deficit usually occurs within 10 days of symptom onset in most patients. At the time of maximal deficit, 50% of patients have lost all movement in their legs, and virtually all have some degree of bladder dysfunction. Most patients have sensory loss below the level of lesion and hyperesthesia or normal sensation above the affected level. Radicular pain or localized back pain may be noted in 30% to 50% of patients.Neurologic symptoms attributable to the spinal cord (lower extremity weakness, sensory loss, sphincter dysfunction, abnormal deep tendon reflexes) can have either compressive or noncompressive causes. Compressive lesions of the spinal cord include epidural hematomas, epidural abscesses, herniated discs, and osteophytic ridges. Among the malignant lesions compressing the spinal cord are epidural tumors, intradural tumors, and intramedullary tumors. Most malignant lesions in pediatric patients are caused by extradural tumors, which usually arise from adjacent vertebral bone. Such lesions typically are metastatic, commonly from soft-tissue sarcomas and neuroblastoma. Intradural tumors are predominantly schwannomas, neurofibromas, and meningiomas or intradural metastatic lesions. Intramedullary spinal cord tumors include astrocytomas, ependymomas, and hemangioblastomas.Among the noncompressive disorders of the spinal cord are inflammatory conditions such as ATM and noninflammatory conditions such as ischemia (as might occur with arteriovenous malformations or embolic occlusion of the spinal arteries) and radiation myelopathy.ATM can be difficult to distinguish from Guillain-Barré syndrome (GBS), which classically presents as an acute ascending flaccid paralysis following a viral infection. ATM is more likely to present as pure lower extremity paraplegia or paraparesis with a sensory loss defined by a level. In contrast, GBS more commonly causes a gradient of weakness that affects the lower extremities more severely than the upper extremities. Paresthesias and pain may be seen in GBS, but an objective sensory loss below a specific spinal cord level is not typical. Patients who have ATM typically are febrile at presentation and generally have long tract signs (brisk deep tendon reflexes and upgoing plantar reflexes) after 10 to 14 days of illness. In contrast, patients who have GBS usually exhibit areflexia. Bladder involvement is common with ATM but uncommon with GBS. Sphincter dysfunction is attributed to autonomic dysfunction frequently noted in GBS. Cranial nerve VII (facial nerve) involvement is also common with GBS (Miller Fisher variant) and not observed in ATM. MRI demonstrates spinal cord inflammation in ATM but not in GBS. Finally, lumbar puncture demonstrates a lymphocytic pleocytosis in ATM and albumin-cytologic dissociation in GBS.Most cases of ATM are idiopathic, probably postinfectious sequelae of an infection that triggers an autoimmune response against the spinal cord. Implicated infectious agents include rubella; measles; Epstein-Barr virus; influenza; enteroviruses; Mycoplasma; and hepatitis A, B, and C. Fewer cases are attributed to direct central nervous system infection by agents such as herpes simplex virus (HSV), cytomegalovirus (CMV), varicella-zoster virus, human immunodeficiency virus (HIV), Borrelia burgdorferi, and Treponema pallidum. ATM also can occur in association with autoimmune diseases such as systemic lupus erythematosus (SLE), antiphospholipid antibody syndrome, sarcoidosis, Sj?gren syndrome, and mixed connective tissue disease. Among patients presenting with ATM, 5% to 10% develop multiple sclerosis.Children presenting with neurologic symptoms attributable to the spinal cord require MRI with gadolinium to rule out spinal cord compression. Once compression is excluded, lumbar puncture should be performed and cerebrospinal fluid sent for routine studies, as well as immunoglobulin G index, oligoclonal bands, viral polymerase chain reaction studies, Lyme antibodies, Mycoplasma antibodies, and Venereal Disease Research Laboratory (VDRL) testing for syphilis, as indicated. Serologic evaluation can include HIV studies, Lyme titers, Mycoplasma titers, hepatitis serology, VDRL, and an evaluation for underlying autoimmune disease, as indicated by findings on history and physical examination. Electromyography and evoked potentials may demonstrate the extent of neural injury and provide prognostic information.Corticosteroids are of controversial benefit in shortening the duration or altering the overall course of illness. Acute treatment of ATM consists of high-dose pulse steroids (usually 1 g methylprednisolone intravenously for 5 days). Intravenous immune globulin and plasmapheresis are of anecdotal benefit and may be used if patients do not respond to steroids. If ATM occurs in association with an underlying disease, other specific therapies may be indicated (eg, acyclovir for HSV infection, ganciclovir for CMV infection, cyclophosphamide for SLE). Approximately one third of patients recover with little or no sequelae, one third suffer moderate permanent disability, and one third have virtually no recovery and experience severe disability.American Board of Pediatrics Content Specification(s)Know the diagnosis and management principles of acute transverse myelitis.Recognize the signs and symptoms of acute transverse myelitis.Know the pathophysiology of acute transverse myelitis.MARCH 2011Question: 1A 16-year-old previously healthy boy presents to the emergency department because his parents say he is “not acting like himself.” He developed a low-grade fever 3 days ago, along with vague complaints of malaise and headache.?Today he seemed confused and lethargic and vomited several times. He could not answer questions appropriately and would stare blankly for periods of time. As he became increasingly confused and agitated, his parents decided to bring him to the emergency department. The teen has no contributory past medical history, and the family denies any recent trauma, drug or alcohol use, or prior episodes of neurologic abnormality. The only medication he has taken is three doses of ibuprofen for headache over the past 2 days. Physical examination reveals a well-developed, well-nourished, restless, and agitated teenager whose temperature is 38.2°C, heart rate is 128 beats/min, respiratory rate is 24 breaths/min, blood pressure is 138/88 mm Hg, and pulse oximetry reading is 99% on room air. He does not answer questions or follow commands but appears awake and alert. He intermittently becomes agitated and moans or shouts incomprehensible words. He does not appear to have any nuchal rigidity, and results of Kernig and Brudzinski tests are negative. The only other finding of note is mild tachycardia. Results of a complete blood count, metabolic panel, hepatic enzymes, renal function tests, and head computed tomography scan are within normal limits.Of the following, the MOST likely tests to reveal the cause of this patient’s symptoms areA.blood and cerebrospinal fluid bacterial culturesB.cerebrospinal fluid protein assessment and electromyographyC.cerebrospinal fluid viral studies and electroencephalographyD.serum ammonia assessment and coagulation profileE.urine and serum toxicologic screensCorrect answer CThe patient described in the vignette is demonstrating signs and symptoms consistent with encephalitis, most likely resulting from a viral infection. The diagnosis can be confirmed through analysis of cerebrospinal fluid (CSF) cell count, chemistries, and specific viral studies for the most common viral causes. Electroencephalography (EEG) can aid in diagnosis, with findings that can include seizure activity, diffuse or focal slowing, or focal abnormalities such as paroxysmal lateral epileptiform discharges, often seen in herpes simplex virus (HSV) encephalitis. Although bacterial infections, including sepsis and meningitis, can cause altered mental status, this patient’s history of several days of low-grade fever, vague constitutional symptoms, absence of meningismus, and gradual progression to altered personality and mental status make bacterial meningitis less likely. Assessment of CSF protein concentrations and electromyography are useful in confirming the diagnosis of Guillain-Barré syndrome, which typically presents with ascending weakness and areflexia. Serum ammonia evaluation and coagulation profile may aid in the diagnosis of hepatic encephalopathy such as seen in Reye syndrome, but this patient’s normal hepatic enzyme values make this diagnosis unlikely. Toxicologic screening is indicated in cases of encephalopathy of unclear cause but is unlikely to be diagnostic in this patient, who has no history of ingestion, no evidence of a specific toxidrome, and a progressive febrile illness over several days.?Encephalitis is defined as altered cerebral function that results from inflammation of brain tissue and can present with alterations in consciousness or personality, motor or sensory deficits, speech or movement disorders, or seizures. Among the numerous potential etiologic agents are multiple viruses, bacteria, fungi, and parasites (Table). Postviral or immunization-associated encephalomyelitis (acute demyelinating encephalomyelitis) also may present as acute encephalitis days to weeks after immunization or infection. In the United States, the most frequently implicated infectious agents are herpes simplex virus (HSV) type 1, nonpolio enteroviruses, other herpesviruses (eg, HSV type 2, Epstein-Barr, varicella-zoster, cytomegalovirus, human herpesvirus 6), and La Crosse virus. A specific cause is identified in only 30% to 40% of cases, with HSV identified most commonly (20% of cases with identified causes). Viral encephalitis can result from direct invasion of brain tissue by the virus following meningitis or viremia or through retrograde spread through peripheral nerves.In addition to the neurologic changes, affected patients typically also have fever and constitutional symptoms for several days to 1 week before presentation. Nausea, vomiting, viral respiratory symptoms, myalgias, fatigue, and headache are common associated symptoms. Rash may be present with some viral pathogens, and HSV infection may be associated with the development of genital, oral, or other vesicular lesions before the onset of encephalitis.Encephalitis is most common in children, the elderly, and immunocompromised individuals. Among neonates and young infants, HSV-2, cytomegalovirus, rubella virus, and enteroviruses are the most common causative agents. Enteroviruses and HSV-1 predominate among older infants and young children. Older children and adolescents are infected most commonly with HSV-1, Epstein-Barr virus, enteroviruses, and arthropod-borne viruses (eg, West Nile virus). Travel history, arthropod exposure, prior history of immune dysfunction, and associated signs and symptoms can help narrow the diagnostic possibilities.The diagnosis of encephalitis most commonly is based on CSF findings, although a clinical diagnosis can be made based on history and physical examination results if lumbar puncture cannot be safely performed. Typical CSF findings include a pleocytosis (50 to 500 cells) with a lymphocyte predominance, mildly elevated protein values, and normal or slightly reduced glucose concentrations. Cases that involve necrosis also may be associated with elevated CSF red blood cell values (HSV, La Crosse, Eastern Equine encephalitis). Tests designed to identify the specific causative agent include CSF polymerase chain reaction (PCR) tests for HSV and enteroviruses, “encephalitis panel” of PCR tests for common viral pathogens (varies from laboratory to laboratory), and serum antibody titers or PCR tests for specific agents. A viral pathogen also can be identified from other sites, including the nasopharynx and rectum. Brain biopsy may be necessary if the previously cited tests fail to reveal the diagnosis. In 60% to 70% of cases, the specific causative agent is not identified. Neuroimaging studies, especially magnetic resonance imaging, may aid in the diagnosis and offer prognostic information. As noted previously, EEG can aid in diagnosing encephalitis and may suggest a specific cause.?Management of encephalitis begins with stabilization of airway, breathing, and circulation and maintenance of adequate oxygenation and perfusion of the brain and other tissues. Emergent endotracheal intubation may be required for depressed mental status or an inability to maintain a stable airway. Glucose concentrations should be monitored and euglycemia maintained. Seizures should be treated aggressively. Symptomatic treatment should include maintenance of normal temperature, blood pressure, brain and other tissue perfusion, and fluid status. Sedation may be required if severe agitation prevents evaluation and management of the patient. Treatment with acyclovir should be initiated pending results of initial tests and identification of a pathogen. If bacterial infection cannot be excluded based on history and physical examination findings, broad-spectrum antibiotics should be administered until results of additional tests become available. Continuous EEG monitoring should be considered to assess for subclinical seizure activity, particularly in severe cases.?The mortality rate for encephalitis varies by causative agent, illness severity, timing of presentation, and adequacy of supportive and symptomatic care and can be as high as 70% for untreated HSV encephalitis. Complications of encephalitis include seizures, cerebral herniation, viral sepsis with multisystem organ failure, respiratory compromise as a result of cerebral dysfunction, and severe cerebral necrosis resulting in long-term disability or death.American Board of Pediatrics Content Specification(s)Know the etiology of encephalitis by ageRecognize signs and symptoms of encephalitisBe familiar with ancillary studies relevant to encephalitisRecognize life-threatening complications of encephalitisPlan management of encephalitisQuestion: 2You are reviewing with medical students the radiographs of five pediatric patients who presented to the emergency department with musculoskeletal injuries recently.Of the following, the fracture that is at the HIGHEST risk of malunion without proper immobilization isA.B.C.D.E.Correct answer EProximal or middle (waist) scaphoid fractures require urgent orthopedic consultation for immobilization in a cast because of the potential complication of bone nonunion (5% to 10% of cases). This is due to the unique blood supply of the scaphoid bone that supplies the distal portion first, followed by the proximal part. A thumb spica cast is the recommended management for complete immobilization if the fracture is at the middle or proximal portion of the scaphoid bone. Splinting alone would not provide adequate immobilization. Metacarpal fractures with displacement, significant (>30 degrees) angulation, or rotational deformity require orthopedic consultation for closed or open reduction. The fifth metacarpal bone fracture presented as an option in this question is minimally angulated and can be managed with splinting alone. The other presented fractures are a distal nonangulated fibula fracture, fracture of the proximal second and third metatarsals, and buckle fracture of the distal radius, all of which can be managed by splinting and do not require urgent orthopedic referral. None of these fractures are at high risk for nonunion.Splinting an extremity for immobilization is indicated for many musculoskeletal injuries. These include sprains and fractures (eg, Salter-Harris type fractures, buckle fractures, and fractures with less than 20 degrees of angulation); lacerations crossing a joint; complex lacerations of an extremity, including tendon, soft-tissue, and joint infections; joint dislocation; and acute arthritis.?It is used for pain management, maintenance of bony alignment, prevention of additional injuries to the affected area, and allowance for swelling that can prevent development of possible compartment syndrome. Splinting can be used for definitive care or for stability until definitive care is provided.Injury to the growth plate (physis) is common in children because this is the weakest part of the complex that includes bone, ligaments, and periosteum. Even with normal findings on radiography, if there is pain near the physis after an injury, it should be considered as a possible growth plate fracture (Salter-Harris 1). Splinting is indicated as definitive orthopedic care for a Salter-Harris Type 1 fracture, for greenstick fractures, or for buckle (torus) type fractures.If there is extremity pain and swelling, normal findings on radiography, and no involvement of the growth plates, splinting may still be considered for pain management because pediatric patients are less likely to develop joint and muscle stiffness with short-term splinting than are adults. The Table outlines various types of fractures and types of splints used for immobilization. Figure1, Figure 2, Figure 3, Figure 4, and Figure 5?illustrate some examples of injuries that can be managed with splints.Splint TypeInjuryIssues to ConsiderSling and swathe; figure of eightClavicle fracture, nondisplaced humerus fractureMay need extra padding with figure of eightPosterior, long arm, or sugar tongElbow injuries, nondisplaced proximal forearm fracturesAll avoid supination and pronation of forearm; double sugar tong avoids flexion and extension at elbowVolar or volar with dorsalDistal radius buckle fracture, carpal bone fracture except scaphoid, second to fifth metacarpal fractures, carpal tunnel syndrome, lacerations crossing the wrist jointAllows supination and pronationGutter-ulnarMetacarpal fracture (fourth/fifth)Need intrinsic plus flexion at metacarpophalangeal joint to immobolize fingers in functional positionGutter-radialMetacarpal fracture (second/third)Need intrinsic plus flexion at metacarpophalangeal joint to immobolize fingers in functional positionThumb spicaSprains, distal scaphoid fractures, uncomplicated first metacarpal and phalangeal fractures, metacarpophalangeal joint sprain?Not suitable for proximal or middle scaphoid fracturesFinger, buddy tapingUncomplicated phalangeal fractures, finger sprains and contusionRecommended slight flexion at proximal interphalangeal joint to prevent stiffness (5 to 10 degrees); place a piece of guaze between digits to prevent skin injuryKnee immobolizersKnee sprain, patellar dislocationPremade and used for comfortPosterior lower leg (ankle)Nondisplaced distal tibia and fibula fractures that are noncommunicative to joint, metatarsal fracturesAvoid splint material on the fibular head to prevent compression of common peroneal nerve; prevents plantar flexion of ankle jointAnkle stirrupNondisplaced distal tibia and fibula fracturesUsed in combination with posterior leg splint; prevents inversion and eversion at ankle jointJones compression dressing or air castAnkle sprain and contusion, foot contusionFor comfort, and patient can remove it in few days when symptom-freeHard sole shoe, buddy tapingFoot sprain, toe fracturesPlace a piece of guaze between toes to prevent skin injurySplints can be made in the emergency department with elastic bandages, cotton stocking, cotton rolls for padding, fiberglass or plaster rolls for splinting, and adhesive tape. The advantage of creating them is that they are molded to the individual patient.?Removable splints can be used when strict immobilization is not indicated because these are better tolerated and can be kept clean more easily.Skin breakdown and infections (including necrotizing fasciitis and toxic shock syndrome), pressure sores, neurovascular compromise, compartment syndrome, ischemia, dermatitis, thermal burns, and skin lacerations due to exposed splint material are potential complications of splinting procedures. The incidence of such complications can increase if the splint is applied by less experienced practitioners. Swelling can be avoided by not squeezing the splint material when molding, proper limb elevation, use of slings, avoidance of weightbearing, and use of crutches, as indicated.?Pressure sores along the joint lines can be avoided by not folding or bunching up the splint material, smoothing the splint material during application, and providing proper padding at the bony prominences. Splinting material should not be placed on areas of superficial nerves to prevent neurologic compromise (eg, along the head of fibula to prevent compression of the common peroneal nerve and including padding along the elbow for ulnar nerve). Thermal burns can be avoided by using water at room temperature for splint material. Skin laceration due to exposed splint material can be prevented by rolling the splint ends or covering it with the stockinette and cotton rolls.Muscle and joint stiffness is avoided by immobilization in anatomic position and by timely follow-up. Prolonged immobilization can result in joint stiffness, muscle atrophy, and complex regional pain syndrome or reflex sympathetic dystrophy. Therefore, prolonged splinting is contraindicated, and close follow-up evaluation after application is mandatory, usually within the first 2 weeks of application. Patients must be counseled before they are discharged from the emergency department about the need for timely splint removal and re-evaluation of the injury. They should know how to evaluate for appropriate circulation by assessment of the toes or finger tips and that the splint must be replaced if it is loose or cracked.American Board of Pediatrics Content Specification(s)Discuss the indications and contraindications for splinting proceduresKnow the anatomy and pathophysiology relevant to splinting proceduresDiscuss the complications associated with splinting proceduresDescribe the key steps and potential pitfalls of splinting proceduresQuestion: 3A 9-year-old boy is brought to the emergency department (ED) after starting a fire in a closet at home. This is the third time he has started a fire in the past month. He has a history of aggressive behaviors and learning difficulties in school. Following an emergency psychiatric evaluation, the consulting psychiatrist and emergency physician both feel that hospitalization is necessary for the safety of the child and his family. The child’s mother states she will only allow hospitalization at one facility. When contacted, that facility states that no beds currently are available and none will be available for at least 1 week. The mother refuses admission to another facility.Of the following, the MOST appropriate action for the physicians in the ED is toA.admit the child involuntarily to an appropriate psychiatric facility that has available bedsB.admit the child to an inpatient pediatric service until a bed is available at the facility the mother has requestedC.attempt outpatient management by instituting treatment with sertraline hydrochlorideD.institute intensive outpatient therapy with daily counseling sessionsE.involve the police to take the child into custody and admit him to a juvenile detention facilityCorrect answer AThe child described in the vignette presents a significant risk to himself and others. In this case, the best interests of the child and others are served by involuntary admission to a psychiatric facility.Thirty-four states currently have laws or regulations permitting the involuntary commitment of individuals for psychiatric care. In all cases, the determination must be made that the patient presents an imminent danger to him/herself or others that cannot be managed safely in an outpatient setting. The actual procedure varies by jurisdiction. Because emergency departments are frequently and increasingly called upon for the care and evaluation of children and adolescents who have psychiatric emergencies, emergency physicians must be familiar with the laws and regulations in the states in which they work, and emergency departments must have procedures in place to deal with these patients.Fascination and experimentation with fire is not unusual among children and adolescents. However, persistent fire-setting behaviors that cause or have the potential to cause property damage and injuries are usually indicative of an underlying psychiatric disorder. A significant association of fire-setting with underlying learning disabilities and psychiatric pathology, including conduct disorders, is common. A large proportion of such patients require management in an inpatient psychiatric facility.Admission to an inpatient pediatric service may be necessary if no psychiatric facility is available to admit the child. However, this is a less-than-optimal arrangement because a medical service may not have the resources available for appropriate observation of the child, and he will be unlikely to begin receiving needed psychiatric treatment in this setting. Once the physicians have made the determination that safety can only be assured in an inpatient setting, outpatient management is not an appropriate alternative. Incarceration in a juvenile detention facility is not appropriate for a child of this young age who has obvious symptoms of a psychological disorder.The concept of involuntary commitment or hospitalization is rooted in the legal principles that the state has the duty to protect each citizen from injury by another and that the state will care for a disabled citizen as good parents would care for their child. All statutes that permit involuntary commitment require that patients be an imminent danger to themselves or others or that they are substantially unable to care for themselves. Usually, parents who present with their children cooperate with recommendations for admission. When the parents resist recommendations for admission of their child, many jurisdictions allow for the commitment of the children to psychiatric facilities over the objections of the parents.Indications for involuntary commitment of children include patients who are actively suicidal or homicidal, patients who participate in dangerous activities and are unable to control these behaviors, patients who have severe substance abuse problems, patients whose aggressive behaviors put themselves or others at risk, and patients who are unable to care for themselves or be cared for in a way that safeguards their well-being (eg, a child who has anorexia nervosa and continues to lose weight despite intensive outpatient therapy).The actual procedure for involuntary commitment of children varies among jurisdictions. The principle of dangerousness is involved in almost all such statutes, but the definition of what constitutes danger is ambiguous and varies from state to state. In many states, any individual, such as the parent of a child or adolescent, a police officer, or medical professional, may petition for involuntary commitment of another. Once a petition has been made, a mental health professional frequently is required to make the determination that danger exists. Emergency physicians, psychiatrists, and other physicians are often considered designees of the local mental health commissioner and can fulfill this role. In most jurisdictions, involuntary commitment requires agreement between two physicians that commitment is necessary, and both are required to complete documentation to this effect. Even after commitment, the patient or his or her parent retains the right to consent for treatment. Specific therapy, including medications, can be provided only with their consent unless a crisis occurs and the safety of the individual or others is at risk. Many states include the provision that care must be delivered in the “least restrictive setting” possible, which also makes sense from a therapeutic standpoint.Once emergency commitment occurs, there is usually a time limit of 24 to 72 hours during which the individual may be held against his or her will (or the parents’ will). At the end of that period, the individual is entitled to a court hearing. The judge or other official may either order the individual released or continue the involuntary commitment for an extended period of time. The emergency physician may be required to participate in the court process. In the case of a parent refusing what seems to be indicated care, the physician should consider contacting child protective services on the basis of medical neglect. This may allow other resources to be brought to bear for the child. Emergency physicians must be familiar with the statutes, regulations, and procedures in their jurisdictions.American Board of Pediatrics Content Specification(s)Know the appropriate procedure for initiating a psychiatric commitment of a childRecognize the conditions under which a child requires psychiatric commitmentQuestion: 4A 3-year-old girl is brought to the emergency department for evaluation of an abnormal gait. She began having an unsteady gait this morning and has fallen several times. She vomited twice after the onset of symptoms. The family denies any recent trauma, possible ingestions, or fever. The girl had a viral upper respiratory tract infection last week but has been otherwise healthy. There are no findings of note on her past medical history. Physical examination of the well-appearing child shows no acute distress and all vital signs within normal limits for age. Neurologic examination reveals intact cranial nerves and normal tone and strength, mental status, pupillary reactivity, and deep tendon reflexes. The girl’s gait is ataxic, and she exhibits mild tremor/unsteadiness when sitting unsupported. Computed tomography scan of the brain yields normal results. Findings on a toxicologic screen, basic metabolic panel, and complete blood count are normal.Of the following, the MOST appropriate next steps in the evaluation and treatment of this patient are toA.administer intravenous lorazepam and perform electroencephalographyB.administer intravenous mannitol and obtain emergent neurosurgical consultationC.obtain a neurology consultation and admit the girl for further evaluationD.perform a lumbar puncture for cerebrospinal fluid analysis and administer intravenous antibioticsE.perform electromyography and administer intravenous immunoglobulinCorrect answer CThe girl described in the vignette is displaying typical symptoms of acute postviral cerebellar ataxia and requires a neurology consultation and hospital admission. Her mental status and neurologic examination findings make seizures unlikely, obviating the need for antiepileptic therapy and electroencephalography. These findings, in addition to the normal computed tomography (CT) scan results, suggest no acute increased intracranial pressure requiring mannitol and neurosurgical evaluation. Lumbar puncture (LP) is indicated for a patient who has evidence of meningoencephalitis, but this girl’s lack of fever, meningismus, or altered mental status make central nervous system infection unlikely. LP and electromyography are used in the diagnosis of Guillain-Barré syndrome of which the Miller Fisher variant may present with ataxia. However, this patient is not displaying cranial nerve abnormalities, autonomic dysfunction, or areflexia typically seen with this diagnosis.Acute postviral cerebellar ataxia occurs most commonly in children between the ages of 2 and 5 years. Its onset usually occurs 4 to 7 days after a viral infection. Varicella accounts for nearly 25% of cases, but other pathogens have been implicated, including Epstein-Barr virus, herpes simplex virus type 1, enteroviruses, rubeola, parvovirus, and mycoplasma. Although the pathogenesis is not known, an autoimmune reaction to an infectious agent is the predominant theory. Cerebrospinal fluid analysis typically yields normal results, as do CT scans. Abnormal signal consistent with ischemia or inflammation is seen occasionally in the cerebellum on magnetic resonance imaging or single-photon emission CT scans.?The primary symptom of cerebellar ataxia is ataxic gait, which usually is maximal at the time of onset. Tremor, fine motor abnormalities, and truncal ataxia are also frequently present. Less commonly associated symptoms include slurred speech, vomiting, and headache. Fever, meningismus, seizures, weakness, and abnormal reflexes are not seen.?The diagnosis of cerebellar ataxia requires exclusion of other potential causes of acute ataxia. The differential diagnosis includes toxic (alcohol, benzodiazepines, diphenhydramine, lead, mercury), metabolic (ornithine transcarbamylase deficiency, abetalipoproteinemia), neurodegenerative (spinocerebellar ataxia, Friedreich ataxia, ataxia-telangiectasia), infectious (meningitis, encephalitis, acute disseminated encephalomyelitis, labyrinthitis), and structural (intracranial hemorrhage, tumor, neuroblastoma) causes. History, physical examination, laboratory studies, and imaging are aimed at excluding alternative causes. The acute onset of symptoms in a patient who has had a recent viral illness in the absence of fever, nuchal rigidity, abnormal mental status, focal neurological deficits, or history of ingestion suggests cerebellar ataxia.Treatment of the patient who has suspected postviral cerebellar ataxia is supportive. No specific therapy is available, although some case series have reported improvement with steroids or intravenous immunoglobulin, but data are not sufficient to support the routine use of these therapies.?Hospitalization for administration of intravenous fluids and antiemetics and exclusion of other diagnostic possibilities is often necessary.American Board of Pediatrics Content Specification(s)Know the etiology and pathophysiology of postviral cerebellar ataxiaRecognize the signs and symptoms of postviral cerebellar ataxiaKnow the management of postviral cerebellar ataxiaQuestion: 5A 3-year-old child who is awaiting an orthopedic consultation for a complicated supracondylar fracture has received one intravenous dose of morphine sulfate for pain control. The nurse informs you that she hears some wheezing and wants you to reexamine the child. The child is sleeping comfortably in the room with a pulse oximetry reading of 96% on room air. He is snoring gently and has bilateral wheezing. There is no evidence of nasal flaring or subcostal, intercostal, suprasternal, or infrasternal retractions. He wakes up easily on gentle stimulus. Apart from the mild wheezing and fracture, he does not have any other physical finding. On inquiry, his mother mentions that he snores occasionally. In addition, he has been evaluated for recurrent episodes of wheezing and has a home nebulizer. She adds that the breathing treatments have never seemed to make him better. You obtain a chest radiograph that reveals a normal cardiac silhouette, right-sided aortic arch, and no evidence of pulmonary disease.?Of the following, the MOST likely cause for this boy’s wheezing isA.central neurogenic hypoventilationB.extrathoracic airway obstructionC.intrathoracic extrapulmonary airway obstructionD.intrathoracic intrapulmonary airway obstructionE.the boy has no airway obstructionCorrect answer: CThe boy described in the vignette has a lower respiratory tract obstruction manifesting as wheezing and an insignificant upper airway obstruction manifesting as snoring. A history of recurrent wheezing, lack of response to bronchodilators in the past, and a radiograph that reveals a right-sided aortic arch suggests the possibility of a vascular ring as the cause of airway obstruction. Chronic wheezing due to an intrathoracic extrapulmonary obstruction can be one of the presenting features of vascular ring, and in some instances, patients who have vascular rings may be misdiagnosed as having asthma. Patients who have central hypoventilation have decreased respiratory effort due to obtundation and do not have wheezing. Because of hypotonia of the pharyngeal musculature and pooling of secretions, patients demonstrate snoring suggestive of upper airway obstruction instead of wheezing.The airway can be divided into three anatomic zones: the extrathoracic airway (extends from the nose to the thoracic inlet), intrathoracic extrapulmonary airway (extends from thoracic inlet to the main stem bronchi), and intrathoracic intrapulmonary airway (airway within the lungs). The pediatric airway is more compliant than the adult airway, and the diameter changes dynamically during inspiration and exhalation. During inspiration, the negative intrapleural pressure causes the extrathoracic airway to narrow. At the same time, the greater negative intrapleural pressure causes the intrathoracic airway to expand. The opposite happens during exhalation: the increased positive intrapleural pressure narrows the intrathoracic airways and expands the extrathoracic airway.These changes in diameter are not clinically important in a normal state of health, but any condition causing airway obstruction (intra- or extraluminal) exacerbates these dynamic changes, which manifests as signs and symptoms that can help the clinician localize the site of obstruction. For example, the greater negative intrapleural pressure that is required to overcome extrathoracic airway obstructions (foreign body) causes the airway to collapse distal to the point of obstruction during inspiration, resulting in an inspiratory sound called stridor. Because the extrathoracic airway expands during expiration, patients have a relatively silent expiratory phase. If the obstruction is subglottic in location, the stridor can be biphasic because the relatively fixed diameter of the airway does not allow expansion in the expiratory phase. The chest wall is compliant in very young infants. This allows the chest wall to expand during exhalation against an obstruction and retract during inspiration, giving the appearance of paradoxic respiration. Further, the abdomen bulges out during inspiration, leading to a “seesaw” respiratory pattern. In older patients, the respiratory distress may manifest as suprasternal and infrasternal retractions.When the obstruction is intrathoracic, whether extrapulmonary (vascular ring, mediastinal tumors, enlarged lymph nodes) or intrapulmonary (asthma, bronchiolitis), the greater negative intrapleural pressure during inspiration relieves the obstruction, and the greater positive intrapleural pressure during exhalation worsens the obstruction. This results in a musical expiratory sound of wheezing. Patients who have severe alveolar disease, such as pulmonary edema, hyaline membrane disease, or pneumonia, exhibit grunting, which is produced by expiration against a partially closed glottis in an attempt to maintain positive airway pressure during expiration as long as possible to improve gas exchange. Grunting is also seen in bronchiolitis or other causes of small airway obstruction in an attempt to maintain a higher positive pressure in the airway during exhalation to reduce airway collapse.Stertor is another clinical sign of upper airway obstruction. This term is used infrequently and poorly defined in the literature. It is described as a harsh snoring sound heard over extrathoracic airways.?Stertor does not have the musical quality of stridor.?Stertor is suggestive of accumulation of secretions within extrathoracic airways.American Board of Pediatrics Content Specification(s)Recognize signs and symptoms of upper and lower airway obstructionQuestion: 6A 4-month-old boy is brought to the emergency department because of a 2-day history of poor feeding, decreased frequency of bowel movements, a weak cough, and sluggishness. Previously, the baby had nursed well, gained weight appropriately, and passed two to three stools daily. He has no history of recent travel or exposures. He has achieved normal developmental milestones. On physical examination, the baby’s axillary temperature is 35.6?C, heart rate is 170 beats/min, respiratory rate is 50 breaths/min, blood pressure is 100/59 mm Hg, and pulse oximeter reading is 98% in room air. Weight, height, and head circumference are normal for age. He appears ill and has dry mucous membranes, but he is alert and makes good eye contact. His cry is weak. His capillary refill time is 3 seconds. Neurologic evaluation demonstrates a lack of extraocular movements, absence of facial grimacing and diminished gag reflex, and significant hypotonia of all extremities. Deep tendon reflexes are present.Of the following, the test that is MOST likely to suggest the diagnosis for this infant isA.cerebrospinal fluid analysisB.cranial computed tomography scanC.electroencephalographyD.electromyographyE.serum ammonia assessmentCorrect answer: DThe acute onset of weakness, hypotonia, cranial nerve paresis (lack of facial grimacing, decreased extraocular movements, diminished gag reflex, and weak cry), clear sensorium, afebrile state, and constipation described for the infant in the vignette are highly suggestive of infant botulism. The characteristic pattern on electromyography (EMG) of incremental response with brief, small, abundant motor unit action potentials (BSAPs) can help suggest the diagnosis, but this pattern is not specific for botulism toxicity.Cranial computed tomography scan in a hypotonic infant can be helpful if hypoxic-ischemic encephalopathy or brain malformation resulting from a chromosomal disorder or a component of a multiple malformation syndrome or an isolated abnormality of brain morphogenesis is suspected. The normal growth parameters and clinical description of this infant do not suggest an organic brain syndrome. Serum ammonia assessment or electroencephalography can be helpful in the setting of acute encephalopathy due to inborn errors of metabolism or recurrent seizures. However, this infant’s alertness and good eye contact argue against these diagnoses. Although a lumbar puncture may be indicated to exclude meningitis or meningoencephalitis as a cause of the acute onset of weakness and hypotonia, the clear sensorium, and absence of fever for this infant render an infectious cause less likely.The risk factors for acquiring botulism are age younger than 12 months, ingestion of honey or corn syrup, exposure to dust and dirt, and geographic factors (the disorder is common in eastern Pennsylvania, California, and Utah). It is endemic along the Delaware River. Whether breastfeeding or bottle feeding is a risk factor is controversial. Although ingestion of honey or corn syrup has been frequently associated with infant botulism, this history may not always be present.The illness is caused by germination of ingested spores of Clostridium botulinum organisms in the infant’s gastrointestinal tract and local endogenous toxin production. The toxin is absorbed and enters the circulation, where it irreversibly blocks acetylcholine release from the cholinergic fibers at the myoneural junction, causing a flaccid paralysis. Recovery occurs only when new presynaptic terminals are generated in the neuromuscular junctions, which may take 4 to 6 weeks.Infantile botulism should be considered in any baby who is younger than 6 months of age and demonstrates weakness, poor feeding, constipation, and a weak cry. Fever is typically absent unless the baby develops complications such as aspiration pneumonia. Serious respiratory paralysis may be life-threatening and require assisted ventilation with intensive supportive measures. The diagnosis of infant botulism is confirmed by documentation of botulinum toxin in a stool sample. Serum and stool samples can be sent for toxin confirmation to the state health department or Centers for Disease Control and Prevention. EMG shows typical findings of BSAPs.The differential diagnosis of hypotonia in a 4-month-old who is afebrile can be extensive and includes infant botulism, Werdnig-Hoffman syndrome, sepsis (bacterial or viral), postinfectious neuropathy, congenital myasthenia gravis, and Guillain-Barré syndrome. EMG and nerve conduction studies can localize the site of lower motor neuron dysfunction to the anterior horn cell (spinal muscular atrophy, poliomyelitis), the peripheral nerve (infectious and postinfectious neuropathy, including Guillain-Barré syndrome), or the neuromuscular junction (congenital myasthenia or botulism). Constipation, mydriasis, and lack of response to anticholinesterase distinguish infantile botulism from myasthenia gravis.Traditional treatment of infantile botulism has been supportive. Endotracheal intubation may be necessary to protect the airway if the gag reflex is lost and is required until the gag reflex returns. Mechanical ventilation also may be needed to support gas exchange. Antibiotic therapy is not useful and actually may aggravate the disease. Aminoglycosides and clindamycin should be avoided in treating secondary bacterial infections because they are known to block the neuromuscular junction. The syndrome of inappropriate antidiuretic hormone is a common complication and should be anticipated and treated appropriately.A relatively new therapeutic tool is botulism immune globulin (BIG), which is a human-derived botulinum antitoxin. A recent study demonstrated that this agent is safe and can reduce the mean hospital stay by 50% from 5.5 weeks in untreated patients to approximately 2.5 weeks. BIG should be administered to the infant as early as possible. Although BIG is expensive (~ $45,000), it is cost-effective because of the substantial reduction in hospitalization. Infantile botulism is a self-limited disease, and the overall prognosis is good. Even before the availability of BIG, children generally recovered with minimal complications. Aggressive management of the pulmonary tract to avoid the development of atelectasis and aspiration syndrome minimizes morbidity.American Board of Pediatrics Content Specification(s)Know the etiology and pathophysiology of infantile botulismKnow the management of infantile botulismQuestion: 7An 8-year-old boy comes to the emergency department with an injury to his elbow after falling from a monkey bar on his outstretched hand. On physical examination, the left elbow is swollen, tender, and extremely painful with any range of motion. The radial pulse in the affected extremity is diminished. Flexion of the distal interphalangeal (DIP) joint of the index finger and interphalangeal (IP) joint of the thumb is weaker in the left hand than the right. Extension of the thumb and adduction of the fingers is normal. His perception of light touch, two-point discrimination, and pinprick in the left hand is normal.Capillary refill time is 2 seconds. A lateral radiograph of the left elbow is shown in the Figure.Of the following, the findings for this boy are MOST suggestive of injury to the leftA.anterior interosseus nerveB.median nerveC.musculocutaneous nerveD.radial nerveE.ulnar nerveCorrect answer AThe boy described in the vignette has sustained an extension type, severely displaced supracondylar (SC) fracture. The downstream neurovascular examination reveals a motor deficit of the long flexors of the thumb and index finger, with normal sensation and a diminished left radial pulse. This is suggestive of traumatic neurapraxia of the anterior interosseus nerve (AIN) and brachial artery injury.The AIN is the most commonly injured nerve in extension type SC fractures because it becomes tethered on the medial spike of the proximal fragment. It arises from the median nerve approximately 5 cm above the medial epicondyle of the elbow and runs along the interosseus membrane between the radius and ulna. It is principally a motor nerve that supplies the flexor pollicis longus (flexion of the IP joint of the thumb) and flexor digitorum profundus (flexion of the DIP joint) of index and middle fingers. Injury to the AIN frequently is missed because it has no sensory component.Ulnar neurapraxia is noted most frequently in flexion type SC fractures. The ulnar nerve supplies sensory branches to the dorsoulnar and volar aspect of hand and ulnar 1? fingers. The motor distribution is to the hypothenar and intrinsic muscles of the hand. The median and radial nerves also can be affected in SC fractures. Radial nerve paralysis results in inability to extend the thumb and wrist and sensory loss on the dorsum of thumb (excluding the subungual region), first web space, and hand as far ulnarward as the middle of the ring finger and as far distal as the proximal interphalangeal joint. Sensation to the volar thumb and radial 2? fingers and corresponding portion of the palm is supplied by the median nerve. Median nerve injury also results in an inability to oppose or flex the thumb, weak flexion/radial deviation of wrist, and pronation. Hence, a careful distal neurovascular examination is warranted before reduction of SC fractures. It is also important to note that sensory deficits may mask early signs of compartment syndrome.The musculocutaneous nerve?is not typically?injured in extension type?SC fractures. It lies between biceps and brachialis, supplying both of these muscles, and its function is tested by assessing flexion at the elbow.?Sensory distribution is to the lateral aspect of the forearm. The nerve does not have any motor or sensory innervation in the hand.The Seddon staging system traditionally is used to describe severity of nerve injuries. Neurapraxia is the mildest form, with reversible alteration of axonal function. Focal demyelination can occur. Nerve conduction may show slowing or block. Complete recovery occurs immediately after fracture reduction or usually within 2 weeks. In general, most neurapraxias are associated with complete recovery of motor function in 3 months and sensation within 6 months of the injury. Axonotmesis involves axon and myelin sheath disruption with an intact epineurium. Wallerian degeneration is noted distally. Functional recovery may occur but is incomplete or unpredictable. Neurotmesis is the most severe form of neural injury. There is complete disruption of the nerve. Recovery of function is not expected.Another category of peripheral nervous system injuries in the upper extremity is trauma to the brachial plexus and cervical roots. It is more likely to occur in younger patients who have less well-developed neck musculature. Usually, it is a result of lateral neck flexion away from the involved area and shoulder depression to the involved side, causing traction neurapraxia of the nerve roots and brachial plexus. A ”burner” or a “stinger” is experienced in the neck on the involved side that may radiate to the shoulder down the arm to the hand. This is a common football injury. The exact mechanism is not known, but presumably this is a pinch-stretch neurapraxia at Erb point (C5-C6 root avulsion) due to a widened head-to-shoulder distance. Characteristically, there is weakness of shoulder abduction (deltoid), elbow flexion (biceps), and external humeral rotation (spinatus). Brachial plexus injuries can occur in the context of birth trauma or from high-speed mechanisms.The clinician’s first obligation is to rule out cervical cord neurapraxia, cervical spine fracture, or ligamentous injury or compression of the cervical nerve roots. Characteristic transient brachial plexopathy results from traction to the plexus, is of short duration, and resolves within minutes. The patient demonstrates full and pain-free range of cervical motion. In contrast, cervical root injuries typically occur in older athletes. They tend to result from hyperextension with lateral neck flexion and generally are associated with radiologic evidence of cervical disk disease and developmental stenosis. The Spurling test, in which the examiner reproduces the mechanism by applying pressure to the head and forcing the spine into extension and lateral flexion toward the symptomatic side, yields positive results (reproducing the pain).Initial management must be directed at evaluation of the cervical spine, shoulder girdle, the affected upper extremity, and the peripheral nervous system. A patient who has bilateral symptoms or symptoms that include the lower extremity with or without midline cervical pain should alert the physician to the possibility of cervical spine injury. In this instance, the cervical spine should be immobilized until injury is excluded.The patient who has suspected brachial plexopathy may return to full activity if the paresthesias completely abate and the patient can demonstrate full muscle strength in the intrinsic muscles of the shoulder and upper extremity as well as full, pain-free range of neck motion.American Board of Pediatrics Content Specification(s)Understand the mechanisms of direct nerve injuryRecognize the signs and symptoms of peripheral nerve injuryUnderstand the management of peripheral nerve and plexus injuryQuestion: 8A 5-year-old girl presents to the emergency department with bleeding from her gums and headache. She has not had any fevers, cough, upper respiratory tract infections, or infectious exposures, according to her mother. The child is taking no medications. She has been home from school for 1 week with decreased activity. On physical examination, the pale child is awake and responsive. Her heart rate is 120 beats/min, respiratory rate is 26 breaths/min, blood pressure is 98/65 mm Hg, and oxygen saturation is 97% on room air. She has hypertrophied gums without ulceration, pale skin with scattered bruises, a capillary refill of less than 2 seconds, and mild hepatomegaly.Of the following, the MOST likely diagnosis for this girl isA.Epstein-Barr infectionB.herpetic stomatitisC.leukemiaD.Mycoplasma pneumoniae infectionE.phenytoin overdoseCorrect answer CThe girl described in the vignette demonstrates some of the vague presenting symptoms of leukemia. Gum hyperplasia and bleeding can be seen with both acute lymphocytic and acute myeloid leukemia. The lack of cough, normal respiratory rate, and absence of hypoxia or fever make Mycoplasma pneumoniae infection unlikely. Phenytoin usage can result in gum hyperplasia, but it is not a symptom of acute overdose. She has no viral lesions that are typical for acute herpetic stomatitis. Infections due to Epstein-Barr virus can mimic a leukemic presentation, with lymphadenopathy, atypical lymphocytosis, and splenomegaly, but the lack of pharyngitis or fever coupled with the severity of this patient’s presentation suggests leukemia as the more likely diagnosis.Cancer is the second leading cause of death among children in the United States. Acute leukemia is the most frequently seen cancer and accounts for about 26% of pediatric cancers. Making the initial diagnosis can be challenging because the symptoms can mimic other common disease processes. For example, fever is a common presenting symptom of many childhood illnesses, including cancer. Other symptoms can include malaise, weight loss, vomiting, fatigue, behavioral changes, and other vague complaints. Such symptoms may mimic infectious, rheumatologic, and other autoimmune diseases.Acute leukemia is the most common hematologic malignancy. Approximately 3,500 children are diagnosed with acute leukemia each year in the United States, and 75% of these diagnoses are acute lymphoblastic leukemia (ALL). ALL is seen mostly between the ages of 2 and 5 years. Acute myeloid leukemia (AML) is the next most common leukemia in children and has a stable incidence rate through childhood. AML has an increased incidence in patients who have Fanconi anemia; neurofibromatosis; and Down, Klinefelter, and Patau syndromes. Exposures to benzene and petroleum also have been implicated with an increased risk of developing AML.The presenting signs and symptoms of leukemia result from marrow infiltration with leukemic cells (blasts), which causes anemia, neutropenia, and thrombocytopenia. Among the other signs are fever, pallor, petechiae, purpura, bleeding, limp, bone pain, enlarged lymph nodes, enlarged liver or spleen, hyperplasia of the gingiva, leukemia cutis or chloroma, weight loss, anorexia, and local paresthesias (numb chin syndrome).Laboratory evaluation can show a high, low, or normal white blood count (WBC). Patients who have “T” cell ALL (~15% of pediatric ALL cases) can demonstrate a mediastinal mass on presentation. Those who have AML present similarly to those who have ALL, although there is a greater incidence of extramedullary abnormalities, including gingival hyperplasia, leukemia cutis (colorless to blue/purple nontender plaques/nodules), and chloroma (AML blast tumors often seen in, but not limited to, the orbital and periorbital areas).When the diagnosis of leukemia is being considered, a complete blood count (CBC) with a smear and manual differential count should be obtained. High and low WBC counts are common, as are blast cells, although peripheral blasts are not always present. Leukemia should not be automatically assumed in the face of a new-onset cytopenia because other illnesses, such as autoimmune diseases (idiopathic thrombocytopenic purpura, autoimmune hemolytic anemia), infections, other tumors with metastases, and other marrow failure syndromes (aplastic anemia) also can present with cytopenias.In addition to the CBC, clinicians should obtain chemistries, including uric acid, creatinine, electrolytes, phosphorus, and calcium; a coagulation profile (prothrombin time, partial thromboplastin time, fibrinogen, type, and screen); and blood cultures if the child is currently febrile, has a recent history of fever, or appears septic. A chest radiograph should be obtained.A hematologist/oncologist should be involved early in the care of a child in whom leukemia is suspected. Early and appropriate emergency department management can help minimize acute morbidity. Intravenous hydration, unless contraindicated, should be started at approximately 125 mL/m2 per hour (about twice maintenance rate) with 5% dextrose in ? normal saline (D5 ? NS) until alkalinizing solution (D5 ? NS with 30 mEq/L of sodium bicarbonate) is available. Specific fluid preferences and rates should be determined in conjunction with the hematology/oncology consultant because use of certain medications (recombinant urate oxidase) or an elevated phosphorus value may require an amended approach. Potassium should not be administered at the time of initial presentation, even in the presence of moderate hypokalemia, because tumor lysis (spontaneous or therapy-induced release of intracellular contents of blast cells) may result in a rapid increase in serum potassium as well as disseminated intravascular coagulation (DIC). Urine output should be maintained at approximately 3 mL/kg per hour to help avoid the complications of tumor lysis syndrome. Urine output can be augmented with mannitol or furosemide under the direction of the hematology/oncology consultant. Allopurinol also should be started in all newly diagnosed leukemia patients to address the tumor lysis and hyperuricemia that results from therapy.Critical care and nephrology consultations are appropriate for patients who have elevations in creatinine, uric acid, or potassium to consider the possibility of dialysis. Other potential medical therapies for these increased concentrations should be reviewed with the consultants.Broad-spectrum antibiotics (eg, ceftazidime) can be considered if there is concern for infection because both patients who have new-onset disease as well as those undergoing chemotherapy are often functionally neutropenic and are at high risk for infection and sepsis.Patients also may present with leukocytosis to a range greater than 100,000/mm3. This can lead to increased blood viscosity and thrombotic complications such as microvasculature cell aggregation. Subsequent complications include bleeding, respiratory failure, and central nervous system hypoxic symptoms. Symptoms may include dyspnea, headache, lethargy, visual difficulty, and confusion. Such findings may be an indication for exchange transfusion or leukophoresis, especially if the possibility of myeloid leukemia is being considered.Patients may require other blood products for active bleeding (DIC, thrombocytopenia, factor deficiencies). Coagulopathy is common in AML with cell lysis. Severe anemia may require transfusion. All blood products should be irradiated and leukocyte-reduced. Transfusion should be in small aliquots (5 mL/kg per hour of packed red blood cells or even slower for patients whose presenting hemoglobin values are less than 5 g/dL [50 g/L]). Because packed red blood cell transfusions increase blood viscosity, they should be avoided in patients who have high WBC counts. Platelets, when indicated, can be transfused even in the face of hyperleukocytosis because the platelets do not significantly add to blood viscosity.Patient disposition depends on the presentation and underlying issues. Critical care admission should be considered, as needed. Of note, the 85% complete remission rate for ALL can be reassuring to families when faced with such a difficult and life-changing diagnosis.American Board of Pediatrics Content Specification(s)Know the etiology and pathophysiology of leukemiaRecognize the signs and symptoms and life-threatening complications of leukemiaKnow the initial management strategies of acute complications of leukemiaAPRIL 2011Question: 1A 17-year-old boy presents to the emergency department with malaise and fatigue. He is a cross-country runner who has been too weak to compete for the past week. Today he is feeling very dizzy. On physical examination, he is conversant, his heart rate is 28 beats/min, and his blood pressure is 120/50 mm Hg. Electrocardiography reveals complete heart block with a ventricular rate of 25 to 30 beats/min. You elect to perform transcutaneous pacing.Of the following, the MOST appropriate medication to administer before pacing isA.amiodaroneB.doxycyclineC.lidocaineD.midazolamE.naloxoneCorrect answer DCardiac pacing can be lifesaving in cases of refractory bradycardia resulting from congenital or acquired heart disease in children. Emergency transcutaneous pacing may be lifesaving if the bradycardia is due to complete heart block or sinus node dysfunction unresponsive to ventilation, oxygenation, chest compressions, and medications. Another indication is overdrive pacing in cases of refractory tachyarrhythmia. Pacing is not useful for asystole or bradycardia due to hypoxic myocardial injury.Because transcutaneous pacing is painful, sedatives such as midazolam should be administered before initiating the procedure. Amiodarone and lidocaine may be indicated in cases of ventricular tachycardia. Antibiotics should be administered if Lyme carditis is suspected, although this is unlikely to result in immediate benefit. This patient is not exhibiting symptoms of a narcotic toxidrome and, therefore, does not require naloxone.Three methods of temporary pacing are commonly available: transcutaneous, transesophageal, or transvenous. The primary difference between them is the location of the electrodes used in pacing. In transcutaneous pacing, electrode pads are placed anteriorly and posteriorly on the thorax. In transvenous pacing, electrodes are placed transvenously into the right heart. In transesophageal pacing, the electrodes are placed in the esophagus behind the heart.After positioning the appropriate electrodes, all pacing techniques involve obtaining capture, setting the rate, and setting a marginal output current. In step one, the electrodes are connected to the external pacemaker, and a current is induced and increased until capture is evident. For transcutaneous pacing, the current usually is approximately 50 mA for adult-sized patients. A QRS complex after each pacing spike indicates successful electrical capture. A palpable pulse corresponding to the QRS complex indicates mechanical capture. If the latter is not present, causes for pulseless electrical activity (eg, hypovolemia, hypoxia) should be sought.?Once capture is established, a rate is set. This is generally faster than the underlying intrinsic rate. For overdrive pacing, the rate is set higher than the underlying dysrhythmia to suppress the intrinsic pacemaker.?In step three, the output is reduced gradually until capture is lost. The final output is set at 1.5 to 2 times the threshold plications of pacing are related to the techniques used. Transvenous pacing may be associated with all the complications of central venous access, including vessel damage and pneumothorax. One additional possibility is perforation of cardiac chambers, leading to pericardial effusion or worse.American Board of Pediatrics Content Specification(s)Know the anatomy and pathophysiology relevant to cardiac pacingKnow the indications and contraindications for cardiac pacingPlan the key steps and know the potential pitfalls in performing cardiac pacingRecognize the complications associated with cardiac pacingQuestion: 2A 5-year-old boy who is visiting his cousin in rural Michigan is brought to the emergency department (ED) after he was bitten on the hand by a rat. The bite was witnessed 6 hours ago when the two cousins were playing in the barn. The parents were able to capture the rat. Although there is no history of being bitten by other animals, the parents mention that there are a few bats in the barn and rabbits, squirrels, ferrets, coyotes, raccoons, and deer in the vicinity of the barn. The boy’s past medical history has no findings of note, and his immunizations are up to date. On physical examination, the child appears well and in no acute distress. The only clinical finding is a 1-cm laceration on the dorsum of the left hand without any evidence of infection.Of the following, the MOST appropriate management for this boy isA.active immunization with tetanus toxoid (Td) or tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis (Tdap)B.administration of prophylactic antibioticsC.observation of the rat for 10 days to guide managementD.passive immunization with rabies immune globulinE.passive immunization with tetanus immune globulinCorrect answer: BEmergency department clinicians are often asked to evaluate bite wounds, address the need for prophylactic antibiotics to prevent wound infections, and make recommendations for postexposure prophylaxis against tetanus and rabies. Use of passive or active immunization against tetanus and rabies is not indicated for the boy described in the vignette. Tetanus typically occurs in wounds that are contaminated, deep, or penetrating and have devitalized tissue. Rabies from rat bites is unlikely. Because of the break in the skin, contamination of the wound by saliva of the animal is likely. Bite wounds to the hand are generally considered high risk for infection due to higher infection rates and the potential for rapid spread of the infection along tendon sheaths.?Therefore, antibiotic prophylaxis is appropriate. When rabies is suspected in domesticated animals, observing the animal for signs of illness may be indicated to guide use of immunoprophylaxis, but there is no need to observe the rat that bit this boy for signs of rabies.Rabies virus is present in the saliva of infected animals and is transmitted by bites. The potential primary sources of wild rabies in the United States include bats, raccoons, skunks, foxes, and coyotes. Nearly all cases of human rabies in the United States are due to bat variant virus. Worldwide, most rabies cases in humans result from dog bites in areas where canine rabies is enzootic. Rabies in small rodents (squirrels, hamsters, guinea pigs, gerbils, chipmunks, rats, and mice) and lagomorphs (rabbits and hares) is rare and bites, therefore, do not require prophylaxis. The decision to immunize a potentially exposed person should be made in consultation with the local health department. Postexposure prophylaxis also may be indicated in certain situations, such as unprovoked bites from domesticated pets, unknown or incomplete history of exposure (eg, a bat in a room of a sleeping person or previously unattended child), and inability to observe the animal after exposure (wild rabies). Postexposure prophylaxis should begin as soon as possible (ideally within 24 hours). However, a delay of several days does not preclude the use of active and passive prophylaxis.Three rabies vaccines are licensed commercially for active immunoprophylaxis in the United States: human diploid cell vaccine (HDCV), rabies vaccine adsorbed (RVA), and purified chicken embryo cell vaccine (PCECV), but only HDCV and PCECV are available for use in the United States. Recent recommendations by the Centers for Disease Control and Prevention reduced the number of vaccine doses for previously unvaccinated immunocompetent persons from a series of five shots to four shots. A 1.0-mL dose of the vaccine should be administered intramuscularly on days 0, 3, 7, and 14. For immunocompromised persons, an additional dose of the vaccine should be given at 28 days for a total of 5 doses. The volume of the dose is not decreased for children. Ideally, the same product is used to complete the vaccine series. Serologic testing for seroconversion is not indicated. The deltoid area is the preferred site for vaccination because antibody response in adults who have received vaccines in the gluteal area has been suboptimal. Alternatively, the anterolateral thigh can be used in infants and young children.Human rabies immunoglobulin (RIG) is available in the United States for passive postexposure prophylaxis. Human RIG is administered in a dose of 20 IU/kg, most of which should be infiltrated locally in the wound, with the remainder administered intramuscularly. Human RIG should be used concomitantly with the first dose of vaccine. If rabies vaccine is immediately unavailable, RIG should be given alone and immunization started as soon as possible. If RIG is not available immediately, vaccine should be given and RIG provided subsequently if obtained within 7 days after initiating immunization. Purified equine RIG is not available in the United States. Where available, it is administered at a dose of 40 IU/kg and may require prior desensitization. The vaccine and immunoglobulin should be administered at sites distant from each other.Tetanus is caused by C tetani, a spore-forming, anaerobic, gram-positive bacillus. Contaminated wounds, especially wounds with devitalized tissue and deep-puncture trauma, are at greatest risk. After primary immunization with tetanus toxoid, individuals are protected for at least 10 years. The recommendations for active and passive prophylaxis depend on the age of the child, the vaccination status, and the nature of the wound (clean versus contaminated) (Table). For infants younger than 6 months of age who have not received a full 3-dose primary series of tetanus toxoid-containing vaccine, decisions on the need for TIG with wound care should be based on the mother's tetanus toxoid immunization history at the time of delivery. If tetanus immunization is incomplete at the time of wound treatment, a dose of vaccine should be given, and the immunization series should be completed according to the age-appropriate primary immunization schedule. Diphtheria and tetanus toxoids and acellular pertussis (DTaP) is the recommended and preferred vaccine for children 6 weeks through 6 years of age and for catch-up immunization for children 4 months through 6 years of age. When a booster injection is indicated for wound prophylaxis in a child younger than 7 years of age, DTaP should be used unless pertussis vaccine is contraindicated, in which case immunization with diphtheria and tetanus toxoids (DT) vaccine is recommended. When tetanus toxoid is required for wound prophylaxis in a child 7 through 10 years of age, use of adult-type diphtheria and tetanus toxoids (Td) vaccine instead of tetanus toxoid alone is advisable so that diphtheria immunity also is maintained. Adolescents 10 through 18 years of age who require a tetanus toxoid-containing vaccine as part of wound management should receive a single dose of tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis (Tdap) instead of Td if they have not received Tdap previously. If Tdap is not available or was administered previously, adolescents who need a tetanus toxoid-containing vaccine should receive Td.When TIG is required for wound prophylaxis, it is administered intramuscularly in a dose of 250 U (regardless of age or weight). Immune globulin intravenous (IGIV) or equine tetanus antitoxin is recommended if TIG is unavailable, although equine antitoxin is not available in the United States. Administration of TIG, IGIV, or equine tetanus antitoxin does not preclude initiation of active immunization with adsorbed tetanus toxoid. TIG should be administered for tetanus-prone wounds in patients infected with human immunodeficiency virus, regardless of the history of tetanus immunizations.Prophylactic antimicrobial agents are recommended for animal bite wounds to high-risk areas such as hand, face, feet, and genitals and all puncture wounds.American Board of Pediatrics Content Specification(s)Know the indications for administration of tetanus, rabies, and antibacterial prophylaxisQuestion: 3A 13-year-old boy collapses after being struck in the chest by a baseball during a preseason baseball game. He is unresponsive, with agonal breathing. Cardiopulmonary resuscitation (CPR) is started on the field, while emergency medical services is called. Of note, he has mild asthma. His sports physical 1 month ago included electrocardiography (ECG) that revealed no cardiac abnormalities.Of the following, the MOST appropriate next step in management isA.defibrillationB.endotracheal intubationC.intramuscular epinephrineD.intraosseous epinephrineE.nebulized albuterolCorrect answer: AThe boy described in the vignette most likely has suffered a cardiac arrest due to ventricular fibrillation. Commotio cordis, which occurs when the chest is struck at a critical point in the cardiac cycle, is known to induce ventricular fibrillation. Because CPR is already in progress, the next step should be to attach an automated external defibrillator and defibrillate the patient if ventricular fibrillation (VF) is seen. Although establishment of vascular access to administer medications is a priority in pediatric advanced life support, it should not precede defibrillation in cases of VF or pulseless ventricular tachycardia (VT). If adequate bag-mask ventilation is being provided, placement of an advanced airway is not a priority. Endotracheal administration of medications is less preferred than intravenous or intraosseous administration and should be undertaken only when vascular access is not possible. Although the boy is known to have asthma, a sudden collapse after a blow to the chest is not typical of an asthma attack, obviating the need for nebulized albuterol. Intramuscular epinephrine is the drug and route of choice for anaphylaxis, not cardiac arrest.Cardiopulmonary arrest is uncommon in pediatric patients. When it does occur, the most common cause is asphyxial arrest, in which a primary respiratory arrest or shock state with resulting cardiorespiratory failure leads to a secondary cardiac arrest. Sudden collapse during athletic competition, however, is very suspicious for a primary cardiac cause. For a young athlete struck in the chest by a projectile, commotio cordis is the most likely cause of the arrest. Commotio cordis occurs most commonly when a dense object, such as a baseball, hockey puck, butt end of the hockey stick, or lacrosse ball, strikes the chest at a critical point in the cardiac cycle, inducing VF. It is increasingly recognized as a cause of sudden death in athletes. Prompt recognition and initiation of CPR and defibrillation can be lifesaving. Commotio cordis also can be induced by a blow to the chest by a kick or strike from a hand. It occurs most commonly in teenagers and young adults playing competitive sports, possibly because their thin chest walls provide less protection for the heart in the event of a direct blow.VF or VT is the initial rhythm in only 5% to 15% of cases of cardiac arrest in childhood. Most cardiac arrests begin as respiratory arrest, and the most common rhythms are asystole and bradycardia with a wide QRS. However, VF or VT has been reported to occur in up to 27% of pediatric cardiac arrests at some point during the resuscitation. Pulseless electrical activity is characterized by a rhythm (not VF or VT) evident on cardiac monitoring but no associated pulse. VF is more common in older adolescents who have sudden witnessed collapse. Cardiac ion channel abnormalities increasingly are recognized as a cause of ventricular arrhythmias and sudden death in older children and young adults.Signs and symptoms of cardiopulmonary failure and arrest are unresponsiveness with weak or absent pulses and poor-to-no ventilatory effort. Agonal respirations are not considered adequate ventilation, and laypersons are prompted to provide CPR when an unresponsive victim is gasping. In the 2010 guidelines for CPR, the pulse check has been removed for laypersons in the presence of an unresponsive patient because it delays initiation of chest compressions. Health-care practitioners are directed to check for a pulse for no longer than 10 seconds in an unresponsive patient before beginning chest compressions and positive-pressure ventilations.American Board of Pediatrics Content Specification(s)Recognize signs and symptoms of cardiopulmonary failure and arrestRecognize arrhythmias leading to and associated with cardiac arrestQuestion: 4A 10-year-old boy is brought to the emergency department by emergency medical services on a long board and in a cervical collar following a motor vehicle crash. He was a restrained back seat passenger on the driver’s side in a high-speed collision in which significant passenger space intrusion was noted. First responders report that the boy experienced a brief loss of consciousness. On physical examination in the emergency department, the child is lucid, has a Glasgow Coma Scale score of 15, and has normal vital signs. Breath sounds are equal bilaterally and peripheral pulses are strong. He is in obvious discomfort from a painful ankle that appears deformed. His abdomen is soft and nontender. There is no midline cervical-thoracic-lumbar spine tenderness and no focal neurologic deficits. The remainder of his examination yields normal results. You obtain a portable cross-table lateral cervical spine radiograph FigureOf the following, the MOST appropriate next step(s) in the management of this patient’s cervical spine is(are) toA.carefully disengage the collar and obtain flexion and extension radiographs to assess for instability of the cervical spineB.clear the cervical spine if the boy has no neck pain or focal neurologic deficitsC.obtain a “swimmer’s view” radiograph of the cervical spine and clear the cervical spine if the result is normalD.obtain anteroposterior and transoral radiographs of the cervical spine and clear the cervical spine if the results are normalE.obtain computed tomography scan without contrast of the cervical spine and clear the cervical spine if the result is normalCorrect answer DThe high-risk mechanism of injury and presence of a significant distracting ankle injury described for the boy in the vignette makes clinical assessment of neck tenderness an unreliable approach. Accordingly, adjunctive radiographic studies should be used to rule out significant cervical spine injury (CSI). A three-view (anteroposterior, lateral, and transoral) plain radiographic study would be adequate to rule out significant osseus injury in this older child. The child’s neck should be immobilized in a rigid collar until the physician is confident that no evidence for significant CSI is found either on clinical examination or radiographic evaluation.The benefits of computed tomography scan over plain radiographs in a patient who is otherwise alert and has no focal neurologic deficits are marginal and must be weighed against the risk of a 50- to 100-fold higher radiation exposure. Magnetic resonance imaging is not indicated for a patient who is lucid and has no clinical evidence of spinal cord injury. When indicated, a dynamic imaging study should be performed only after complete radiographic evaluation demonstrates no abnormality. Similarly, a “swimmer’s view” radiograph is not indicated because the C7-T1 junction is sufficiently visible on the cross-table lateral film.Decision instruments have been developed that permit clinicians to reduce the use of cervical spine radiography safely in adult and pediatric patients who have sustained blunt trauma. A prospective multicenter trial evaluated the NEXUS decision instrument for identifying patients who have suffered blunt trauma and in whom radiographs of the cervical spine should be obtained. Low-risk patients must meet all five NEXUS criteria, which include: 1) absence of midline cervical tenderness, 2) no evidence of intoxication, 3) normal level of alertness, 4) normal results on neurologic examination, and 5) absence of a painful or distracting injury. If a patient fulfills all five of the NEXUS criteria, plain radiographs are of marginal value.In a subgroup analysis, none of the 603 children (from the total 3,065 children) designated as low-risk had evidence of cervical spine trauma on three-view plain radiography. The overall sensitivity of NEXUS in the pediatric population was reported as 100% (95% confidence interval, 88%, 99.6%). However, the validity of results in the younger age group has been questioned because only four of the 30 significant CSIs occurred in patients who were younger than 9 years of age and none were seen in children younger than 2 years. Therefore, the Congress of Neurologic Surgeons recommends application of NEXUS criteria for children older than 9 years of age.The unique anatomy and biomechanics of the pediatric cervical spine help explain the different radiographic features, injury patterns, and management options found in children compared with those in adults. The principal difference is that the pediatric cervical spine is intrinsically more elastic compared with the adult spine, especially in the first 8 years after birth. Such elasticity is a result of several distinct features. First, the facet joints are shallower than in the adult spine and are oriented horizontally, which has the effect of increasing translational mobility and movement during flexion and extension. Second, spinal ligaments and joint capsules can withstand significant stretching without tearing, which contributes to the occurrence of pseudosubluxation. Third, several authors have argued that the anterior wedging of the vertebral bodies allows ventral slippage between motion segments, although others have noted that the wedging that appears on radiographs is due to a ring apophysis that does not ossify before the age of 12 years, making this a radiographic rather than an anatomic finding. Finally, weak nuchal muscles also lend more flexibility to the spine.Another important feature in children younger than 8 years of age is the relatively large head compared with the body. The added weight shifts the fulcrum of movement to the upper cervical spine, with the greatest movement at C2-C3 in infants and young children. By 5 to 6 years of age, the fulcrum shifts to C3-C4, and in adolescents and young adults, the level of maximal flexion is C5-C6, the same as in mature adults. This disparity in the fulcrum of movement explains why most cervical spine injuries occur between the occiput and C2 in children younger than 9 years of age, but the distribution of cervical injuries in children older than 9 years is similar to that in adults, with fractures and fracture-dislocations predominantly occurring in the lower cervical spine.A large head relative to the body has one other critical consequence, which is to force the cervical spine into kyphosis when a child is placed on a firm backboard. In the setting of trauma, this may exacerbate a traumatic kyphotic deformity and compromise neurologic function. Semirigid cervical collars are not adequate to prevent flexion and, therefore, the torso must be raised or a recess for the occiput provided. In a recent prospective cohort study of 76 Australian children, standard immobilization combined with thoracic elevation of the shoulders in children aged 10 years and younger who had suspected CSI was effective in placing the cervical spine in neutral position. All patients required torso elevation (mean elevation, 25 mm) to rest the neck in a neutral position. Children younger than 4 years may require more elevation. The goal of elevation should be to align the patient’s external auditory meatus with the shoulders, a position that eliminates flexion. Alternatively, an occipital recess can correct misalignment.Another pitfall during immobilization at the scene is the unintended consequence of straps that may be too tight on the torso. This may lead to decreased vital capacity, particularly in a young child who may have pre-existing hypoventilation from a traumatic brain injury. Similarly, a patient who has high cord injury can sustain a phrenic nerve injury with paradoxic respirations that may be exacerbated by tight chest restraints.The long hard board used by EMS is ideal for extrication and transport. However, once the patient arrives in the emergency department, every effort should be made to transfer him or her to a firm mattress stretcher. Such a stretcher not only is more comfortable for the awake patient but is important in preventing pressure sores in an insensate or obtunded patient.American Board of Pediatrics Content Specification(s)Know the anatomy and pathophysiology relevant to cervical spine immobilizationDiscuss the indications for cervical spine immobilizationDiscuss the complications associated with cervical spine immobilizationDiscuss the key steps and potential pitfalls in performing cervical spine immobilizationQuestion: 5A 6-week-old infant is brought to the emergency department (ED) because of decreased oral intake and intermittent vomiting. On physical examination, she appears to be slightly dehydrated. You order ultrasonography to rule out pyloric stenosis. The first-year resident orders a 10-mL/kg bolus of normal saline, and a nursing orientee administers a 380-mL bolus. Upon reflection, you note that the administered fluid given seems excessive,and review indicates that the patient received 100 mL/kg. After discussion among the team, you notify the family. The child exhibits slight tachypnea, has a good urine output after administered furosemide, and is admitted for a pylorotomy.Of the following, the MOST effective action to prevent this occurrence in the future is toA.notify nursing/resident leadership for corrective action regarding personnelB.notify the Joint Commission of this sentinel eventC.perform a root cause analysis of this serious eventD.put an immediate halt to the nursing training program in the EDE.take no further action because the patient is stable and the family has been notifiedCorrect answer: CFormal follow-up of this significant event is imperative, regardless of the long-term consequences to the patient. Investigation via a root cause analysis of this serious event is a good next step. Root cause analysis helps to identify causative systematic issues, which subsequently can be modified or eliminated to improve safety for future patients. Care should be taken to avoid assigning blame and causation to individuals because this may undermine attempts to identify the true underlying cause. Notifying nursing/resident leadership for correction action or the Joint Commission about a sentinel event are appropriate in certain cases, but those avenues may not immediately address system issues that allowed the error to occur.Quality in pediatric emergency care includes many important aspects of care delivery. Not only is the quality of delivered care expected to be excellent, but the logistics of care delivery, including efficiency, availability on demand, communication at all levels, and medical coordination and handoffs, are required to be optimal. Breakdowns in any aspect of the care delivery system can lead to less-than-optimal care, quality complaints, need for service recovery, and potential medical legal review.Service metrics that suggest less-than-optimal care delivery include clinical markers such as unplanned return visits to the ED in less than 48 to 72 hours, number of misdiagnoses, ED adverse events (and near-misses), requirement for rapid response team assessment in an inpatient area or transfer to the intensive care unit shortly after admission, “left without being seen” percentages, percentage of patients who require medication reconciliation, lengths of stay for admitted and discharged patients, and waiting times before care and seeing a physician. Awareness of and investigation into such metrics can suggest opportunities for improvement to clinicians and leaders. Although the metrics are ED-focused, the solutions may lie both within the ED and elsewhere. For example, “time to room for a patient” may be influenced not only by procedures in the ED, but also by physical capacity, which is related to inpatient access. If the ED is unable to move patients rapidly to an inpatient unit, the ED capacity is effectively decreased, allowing less space for newly arriving patients.The ability to influence care delivery lies not only with the facility, system, and leadership, but also with the individual clinician. Awareness of personal and personnel limitations in training, knowledge, and competency can aid in ensuring quality and consistency of delivered care. Focus on teamwork and communications can result in a better team effort and collegial care. Optimal communication with families can identify needs and opportunities and helps prevent the frustration and depersonalization that can occur at a stressful time, in an unfamiliar environment, and with clinicians who have no previous relationship with the patient or family.Enabling timely feedback from families after delivery of care also can identify opportunities for improvement. The same is true for enabling and encouraging feedback from clinicians at all levels. Awareness and support for a blame-free environment encourages employees to feel comfortable reporting mistakes, care issues, and near-misses. Although the workload to review and assess these factors is significant, the information obtained is invaluable and likely can lead to better care delivery. Other areas of quality improvement include review of triage effectiveness; case review of all critically ill patients, including those who required resuscitation; and assessment of the stability of patients referred from outside clinicians, services, and facilities. Identification of opportunities in any or all of these areas can incrementally improve the care delivered to the patients and should help improve outcomes.The Joint Commission defines a sentinel event as: “an unexpected occurrence involving death or serious physical or psychological injury, or the risk thereof.?Serious injury specifically includes loss of limb or function. The phrase "or the risk thereof" includes any process variation for which a recurrence would carry a significant chance of a serious adverse outcome.?Such events are called "sentinel" because they signal the need for immediate investigation and response.” ( Accessed January 20, 2010.) ?It is important to note that in most sentinel events reported to the Joint Commission, poor communication was an integral component of the care delivery problem. This may include poor or lack of communication at the bedside; between clinicians; or during medical handoffs prior to, during, or after transfer from the ED. Efforts at improved personal, team, and systemwide communication should pay dividends for patient quality and safety.Attention to the national safety goals and initiatives is important to optimize care in the ED. Such national safety goals are published yearly and evaluated by the Joint Commission during their reviews of facilities that deliver emergency care. Evidence of measurement and improvement in these categories is required by the Joint Commission.American Board of Pediatrics Content Specification(s)Recognize quality assurance activities relevant to pediatric emergency medicineKnow JCAHO regulations regarding the performance of quality assurance activities in emergency medicineKnow the elements that define quality assurance in the emergency care of childrenQuestion: 6A 15-year-old boy is brought to the emergency department by emergency medical services after being struck in the right eye with a bottle rocket during a Fourth of July party. He complains of pain and decreased vision in the right eye and a mild headache. He denies loss of consciousness, nausea, vomiting, or other injuries. He has no findings of note on past medical history, and his immunizations are up to date. Physical examination reveals a well-developed teenage boy whose vital signs are within normal limits. He has a superficial abrasion on the right upper eyelid, normal vision in the left eye, and vision in the right eye limited to only light perception. Gross findings on inspection of the right eye are shown in theFigure:.Of the following, the most appropriate initial steps in the treatment of this patient areA.administration of oral ibuprofen, application of an eye patch, and computed tomography scan of the orbitsB.administration of topical anesthetic drops, patching of the affected eye, and patient dischargeC.elevation of the head of the patient’s bed, application of an eye shield, and an ophthalmology consultationD.injection of local anesthetic, emergent lateral canthotomy, and hospital admissionE.procedural sedation with midazolam and ketamine, laceration repair, and patient dischargeCorrect answer CThe patient described in the vignette has a traumatic hyphema or accumulation of blood within the anterior chamber between the iris and the cornea. Initial management includes elevation of the head of the bed to promote settling of the blood and clearing of the visual axis, pain and nausea management, application of a shield to prevent further injury, and ophthalmology evaluation. Nonsteroidal anti-inflammatory drugs and aspirin products should be avoided because of their potential to worsen bleeding. Shielding rather than patching of the eye is indicated to avoid increasing intraocular pressure and to minimize the risk of further bleeding. Lateral canthotomy is indicated in cases of significant eye trauma that involve retrobulbar hemorrhage causing orbital compartment syndrome; such patients typically display significantly elevated intraocular pressure, proptosis, limited extraocular movements, diplopia, and an afferent pupillary defect. There is no evidence of this in the patient in the vignette. The boy has no visible laceration to warrant sedation and wound repair, but if procedural sedation were necessary, ketamine should be avoided because of the potential for increased intraocular pressure.Hyphema typically results from significant blunt trauma to the orbital region. The extent of bleeding can vary from microhyphema (red blood cells in the anterior chamber seen only on slitlamp examination) to complete filling of the anterior chamber with blood (100% or “eight ball” hyphema); the bleeding description is based on the percentage of the anterior chamber occupied by blood. Pain, decreased vision, nausea, and headache are typical symptoms. Associated ocular injuries are common and may include corneal abrasions, ruptured globe, iridodialysis (separation of the iris from the corneal margins), subconjunctival hemorrhage, vitreal or retinal hemorrhages, and orbital fractures. Computed tomography scan of the orbits is indicated for patients in whom there are concerns for orbital fractures, open globe, or intraocular foreign bodies. Patients who have bleeding disorders or hemoglobinopathies (including sickle cell trait) are at increased risk for ocular complications, including rebleeding, glaucoma, or permanent vision loss. Patients in high-risk ethnic groups who have unknown sickle cell status should undergo screening.Management of hyphema includes full ocular evaluation to exclude other injuries, shielding to prevent additional trauma, and ophthalmologic consultation and follow-up evaluation. Pain and nausea should be controlled aggressively to prevent increased intraocular pressure or worsening bleeding; oral or parenteral narcotic agents or combination acetaminophen and narcotic medications are appropriate choices. Topical anesthetic agents may also be helpful, especially for patients who have corneal abrasions. Elevation of the head to 30 to 45 degrees and rest should be encouraged initially. Topical cycloplegics should be administered after an open globe is excluded. Topical steroids may be indicated but should be prescribed only with the guidance of an ophthalmologist. Topical or systemic antifibrinolytic agents have been recommended by some authors, but results vary and their use is not routinely indicated.Most patients who have hyphema can be managed as outpatients with close ophthalmology follow-up evaluation. Admission should be considered if compliance with the rest, shielding, medication, and follow-up regimen is unlikely and for patients who have bleeding disorders and hemoglobinopathies.American Board of Pediatrics Content Specification(s)Recognize hyphema and institute appropriate managementQuestion: 7A 12-year-old girl presents to the emergency department with facial injuries resulting from a bicycle accident. She fell off her bike, hitting the right side of her face on the concrete. She did not lose consciousness. She denies pain anywhere other than on her face and has had no nausea; vomiting; or changes in vision, gait, or mental status. Physical examination of the well-developed, well-nourished girl shows no acute distress and vital signs within normal limits for age. She has one laceration just below the right lower eyelid, another laceration of the right upper lip that is through-and-through involving the vermilion border, and an Ellis Class III fracture of the right upper lateral incisor. The remainder of her examination findings are normal. You would like to use a single regional block to provide anesthesia to all of her wounds as you repair her injuries.?Of the following, the MOST appropriate course for providing regional anesthesia to this patient is to instill the anesthetic in or around the:A.coronoid notchB.infraorbital foramenC.mental foramenD.mucolabial foldE.supraorbital foramenCorrect answer BThe patient described in the vignette has multiple injuries within the nerve distribution of the V2 or maxillary division of the trigeminal nerve. Providing anesthesia to all three injuries with a single block requires the instillation of local anesthetic around the infraorbital foramen, where the infraorbital nerve exits the skull. The infraorbital foramen is approximately 0.5 cm below the notch in the inferior orbital rim. A line can be drawn from the supraorbital notch, through the pupil of the eye, through the infraorbital notch and foramen, across the maxillary and mandibular premolars, and through the mental foramen. In this way, all three branches of the trigeminal nerve can be easily located.For an infraorbital block, the index finger of the nondominant hand is used to palpate a depression about 0.5 cm below the infraorbital notch, which marks the site of the infraorbital foramen. The thumb or fingers of the same hand are used to retract the upper lip. The dominant hand is used to insert the needle into the mucolabial fold just anterior to the apex of the first premolar tooth. The needle should be advanced no more than 1 to 2 cm from the insertion point toward the infraorbital foramen and along the axis of the tooth. The tip of the index finger helps to guide the needle and prevent advancement of the needle to the orbital cavity. Once the tip of the needle is positioned above the infraorbital foramen, 1 to 2 mL of anesthetic is injected.An alternative approach involves injecting the anesthetic through the skin directly into the infraorbital foramen. However, caution must be exercised with this approach because the nerve may be damaged if the needle is advanced into the foramen itself.Injection of local anesthetic at a depth of 1 to 1.5 cm into the coronoid notch of the mandible along the occlusal plane produces an alveolar nerve block; the needle should be directed slightly superior to the occlusal plane in adolescents and adults and slightly inferior to the occlusal plane in younger children. The alveolar nerve is the largest branch of the mandibular division, or V3, of the trigeminal nerve and provides innervation to the mandibular teeth, lower lip, and chin on the involved side.Local anesthetic administration medial to the supraorbital notch provides a supraorbital block, with anesthesia of the ipsilateral forehead. Injection of local anesthetic into the mental foramen provides anesthesia to the lower lip and chin on the ipsilateral side.Supraperiosteal infiltration provides anesthesia to a single tooth.?A buccal approach is used to advance the needle 1.5 cm into the mucolabial fold of the corresponding tooth. One to two milliliters of anesthetic is infiltrated along the periosteum at the apex of the root. Due to the porosity of the maxilla, supraperiosteal infiltration is effective for the maxillary teeth throughout life. However, because the mandible is significantly denser and less porous in adults, this form of anesthesia useful only for maxillary teeth in older adolescents and adults. The Table outlines the anatomy, nerve distribution, and general approach to the other common orofacial nerve blocks.Orofacial anesthesia involves local or regional infiltration of an anesthetic agent to provide pain relief or to prevent pain associated with repair of facial injuries or infections. The decision to use local infiltration or a regional block is based on the location and type of injury or infection, concern regarding distortion of landmarks with local infiltration, damage to or distortion of normal block landmarks by injury or infection, and level of cooperation of the patient. An absolute contraindication to orofacial anesthesia is a documented allergy to local anesthetic agents. Injection of anesthesia into or through infected or grossly contaminated tissues is relatively contraindicated.Small, clean wounds are usually amenable to local infiltration. Regional nerve blocks generally require the use of less anesthetic, usually only 1 to 2 mL for orofacial blocks, reducing the risk of toxicity or adverse reactions. Significant wounds to cosmetically important areas, such as lacerations through the vermilion border, may be better served with regional anesthesia to avoid distortion of key landmarks. Multiple wounds in the same nerve distribution, as described for the patient in the vignette, may be repaired with fewer injections, less time, less anesthetic, and less discomfort using a single regional block.Preparatory steps can increase the likelihood of success of orofacial nerve blocks. Depending on the patient’s age, degree of anxiety, and level of cooperation, consideration should be given to the use of distraction, restraints, medical anxiolysis, or procedural sedation before beginning the procedure. For those blocks administered via the intraoral route (supraperiosteal infiltration, infraorbital, inferior alveolar), the application of topical mucosal anesthesia before performing the block can reduce or eliminate the pain of needle insertion. The area initially is dried with a gauze pad, followed by application of topical mucosal anesthetic (20% benzocaine or 5% to 10% lidocaine) to the insertion site. Local anesthesia should be achieved within 30 to 90 seconds.A 27-gauge needle generally is recommended for injection in orofacial blocks; the use of larger-bore needles increases the pain associated with the procedure. Use of warmed and buffered anesthetic solutions can further minimize the patient’s discomfort.?Following infiltration of 1 to 2 mL of anesthetic, at least 5 minutes is required to achieve regional anesthesia. Failure to achieve anesthesia can result from improper technique, anatomic variation, insufficient anesthetic volume, or inadequate time before performing the procedure. Other complications of orofacial anesthesia include intravascular injection of anesthetic, improper needle position causing injury to adjacent structures, and allergic reaction to the anesthetic.Table: Common Orofacial Nerve BlocksV1/Opthalmic DivisionSupplies: Forehead, upper eyelid, nasal bridge and tipPoint of exit from skull: Supraorbital foramenLandmarks for block (supraorbital): Inject 0.5 to 1 cm depth medial to supraorbital notchV2/Maxillary DivisionSupplies: Lower eyelid, upper lip, anterior maxillary teethPoint of exit from skull: Infraorbital foramenLandmarks for block (infraorbital): Insert needle anterior to first maxillary premolar while marking infraorbital foramen (0.5 cm below infraorbital notch) with finger; inject at depth of 1 to 2 cmV3/Mandibular DivisionSupplies: Mandible, lower lip, chin, mandibular teethPoint of exit from skull: Mandibular foramenLandmarks for block (inferior alveolar): Grasp mandible between index finger and thumb of nondominant hand, marking coronoid notch with the intraoral digit; hold syringe along occlusal plane of the mandible, aiming slightly superior in adolescents and adults and slightly inferior in younger children; inject at depth of 1 to 1.5 cmMental NerveSupplies: Lower lip and chinPoint of exit from skull: Mental foramenLandmarks for block (mental): Insert needle over mandible along a line that crosses the supraorbital and infraorbital foramen and the premolars (palpate mental foramen); inject at a depth of 0.5 cm?American Board of Pediatrics Content Specification(s)Know the anatomy and pathophysiology relevant to orofacial anesthesia techniquesDiscuss the indications and contraindications for orofacial anesthesia techniquesDescribe the key steps and potential pitfalls of orofacial anesthesia techniquesDiscuss the complications associated with orofacial anesthesia techniquesQuestion: 8You are examining a 9-year-old boy who fell off a motocross bike during a local race. He landed on his back, and his bike landed on top of him. He did not lose consciousness, and the first responder found him awake but dazed and coughing. He was carried off the track and brought by ambulance to the general emergency department. On physical examination, the semiconscious and pale boy has a blood pressure of 53/palp mm Hg and a heart rate of 176 beats/min. He is in a cervical collar and moves his arms and legs to painful stimuli. You note no external bleeding.Of the following, the boy’s MOST likely injury isA.cardiac tamponadeB.closed femur fractureC.intracranial hemorrhageD.liver contusionE.spinal shockCorrect answer AThe boy described in the vignette presents with rapid deterioration after a traumatic injury from a fall and blunt trauma to the torso. Although all of the options can result in a critically ill patient, cardiac tamponade due to a chest injury is most likely. Rapid hemodynamic deterioration would not be expected from an isolated femur fracture, and intracranial bleeding should not result in hypotension from blood loss. Spinal shock is possible but unlikely with the tachycardia response noted with this patient. A liver contusion is possible, but the injury would need to be much more severe to present with this amount of cardiovascular compromise.A crush injury to the chest can result in a variety of problems, the most common of which are pulmonary contusion, pneumothorax, hemothorax, and rib fractures. Pulmonary, esophageal, tracheal, mediastinal, and diaphragmatic injuries may also be seen. Cardiovascular injuries can include large-vessel (aorta, vena cava, pulmonary vessels, pulmonary artery, pulmonary vein) or small-vessel (chest wall, coronary) injury, direct cardiac trauma with resultant dysrhythmia, cardiac contusion, laceration, bleeding, or rupture.A high level of suspicion is required when considering cardiac injuries due to blunt trauma. Patients who fit classic criteria of the Beck triad (jugular venous distension, decreased heart sounds, and decreased cardiac output/low arterial pressure) are not difficult to identify, but early pericardial bleeding is more difficult to detect. Clinicians should suspect potential injuries after blunt trauma such as a motor vehicle crash, fall, jump, crush, or assault. Crush injuries result from compression between the sternum and the spine. Rapid deceleration can cause a shear or cardiac tear at a point of fixation. Cardiac rupture can occur during abrupt abdominal compression that results in an elevated venous pressure that is transmitted to the right side of the heart.Bleeding into the relatively nondistensible pericardial sac can lead to pericardial tamponade, as in this boy. The classic presentation of such tamponade is chest pain/discomfort, decreased blood flow to the heart (jugular venous distention if intravascular volume and tone are adequate), poor cardiac function (may have abnormal electrocardiographic results, abnormal cardiac markers), decreased heart sounds (may be difficult to appreciate in a loud resuscitation bay), and signs of decreased cardiac output (altered mental status, poor perfusion, acidosis, and end-organ compromise).Focused assessment with sonography for trauma (FAST) can be useful to identify hemodynamically significant pericardial effusion. If FAST is not available, formal bedside echocardiography and laboratory evaluation (cardiac enzymes) may be useful.Adjunctive evaluations such as chest radiography may demonstrate findings indicative of significant chest trauma:Abnormal cardiac shadowWidened mediastinum (thymus as well as the standard anteroposterior supine radiographic technique may cause the mediastinum to appear abnormally widened)Blurred or indistinct aortic knobLeft first rib or sternal fractureRight tracheal and nasogastric tube deviationDownward displacement of the left mainstem bronchus and widened paravertebral and paratracheal stripesPleural cap (blood accumulation at left apex)After initial stabilization of children who have significant chest injuries, computed tomography (CT) scan and CT angiography may be useful. However, the percentage of patients for whom a change in management results from this additional information is relatively small. CT scans should be considered for patients in whom there is a strong clinical suspicion of underlying injury, who have a need for positive-pressure ventilation, who are unstable after a penetrating injury, or in whom tracheobronchial or vascular injury is suspected.Experienced evaluator(s) should be armed with evidence-based care algorithms tailored to the individual patient. Pericardiocentesis should be attempted in the emergency department and surgical intervention undertaken as indicated for patients who have no measurable blood pressure. Others should receive 100% oxygen; airway management; positive-pressure ventilation, if indicated; placement of intravenous lines; hematology and chemistry studies; isotonic fluid (and blood, if indicated) resuscitation; radiologic evaluation; electrocardiography; assessment of cardiac enzymes, as indicated; and rapid surgical assessment. Associated hemo- and pneumothoraces should be managed.American Board of Pediatrics Content Specification(s)Recognize cardiac trauma following blunt chest traumaRecognize pericardial tamponade following blunt chest traumaPlan the management of cardiac trauma following blunt chest traumaMAY 2011Question: 1A 10-year-old girl presents with right eye pain. She was playing in a dirt lot with other children when she began crying and complaining of pain in the eye. She is having excessive tearing from the right eye, and the eye has become increasingly red. Her mother reports that the girl complains of increased pain with bright light and cannot seem to keep the eye open. The girl does not wear glasses or contacts, has no prior medical problems, and has no other complaints. On physical examination, her vital signs are normal. She has tearing and blepharospasm of the right eye with marked scleral injection. After application of topical anesthetic drops, ocular examination reveals equal and reactive pupils; no visible hyphema, foreign body, or subconjunctival hemorrhage; and bilaterally intact extraocular movements. Visual acuity is 20/20 in the left eye and 20/80 in the right eye. Fluorescein examination shows several linear vertical corneal abrasions across the mid-cornea.Of the following, the MOST appropriate next step puted tomography scan of the orbitsB.emergent ophthalmology consultationC.measurement of ocular pHD.patient discharge with topical antibiotic therapyE.upper lid eversionCorrect answer EMultiple vertical corneal abrasions, as described for the girl in the vignette, are suggestive of a foreign body under the upper eyelid. Viewing and removing such a foreign body is facilitated by eversion of the upper lid. Topical antibiotic therapy is appropriate for the management of corneal abrasions, but failure to identify and remove a retained foreign body first results in ongoing corneal injury. Ocular pH is measured in cases of ocular chemical exposure to assess adequacy of irrigation and the risk of acid or alkali injury. Urgent or emergent ophthalmology consultation should be obtained in cases of suspected ruptured globe, embedded foreign bodies, or foreign bodies that are incompletely removed or cannot be removed without sedation or anesthesia. Computed tomography (CT) scans should be obtained in cases of ocular trauma associated with high-velocity injuries, suspected intraocular foreign bodies, or suspected orbital fractures, none of which is likely in this patient.The sclera and undersurfaces of the upper and lower lids are covered with bulbar and palpebral conjunctiva, respectively. The iris is covered by the cornea, which consists of three layers: an outer nonkeratinized epithelial layer, a stromal layer, and an endothelial layer.?Foreign material can become adherent to or embedded in any of these tissues, leading to conjunctival injection, tearing, and usually pain and blepharospasm. These responses are greater with materials that elicit inflammatory responses such as organic substances and metals. Metallic foreign bodies also may result in a rust ring, which must be removed. Foreign bodies under the upper lid cause conjunctival or corneal abrasions with blinking that typically are vertical and multiple.?All ocular foreign bodies should be removed, although the timing and methods vary according to the type and location of the foreign body and the age, level of cooperation, and associated symptoms of the patient. Corneal foreign bodies should be removed as early as possible to avoid epithelialization over them that may make removal more difficult. Young or uncooperative children may benefit from sedation or anesthesia to allow removal without increasing the risk of additional trauma. Patients who have suspected ruptured globe (irregular or nonreactive pupil, associated hyphema, leakage of aqueous humor) should undergo emergent ophthalmologic evaluation and treatment. CT scan may be indicated in these cases to exclude intraocular foreign body or associated orbital injuries. Lid eversion and attempts at foreign body removal should not be performed until an open globe has been excluded.?Ocular foreign bodies can be removed through multiple methods.?Topical anesthesia should be administered before proceeding with attempts at removal; oral or intravenous pain medications also may be indicated. Irrigation with sterile saline, sterile water, or commercially prepared eye solutions allows removal of many superficial ocular foreign bodies. A moistened cotton swab can be used for foreign bodies that appear superficial but persist after irrigation. Foreign bodies on the undersurface of the upper lid can be seen and removed best after the lid is everted. A cotton-tipped swab is placed at the upper margin of the tarsal plate externally, the upper lashes are grasped, and the lid is flipped over the swab.?Embedded foreign bodies in children often warrant ophthalmologic evaluation for removal. In a cooperative older child or adolescent, a 25- or 27-gauge needle or an eye spud can be used to scoop the foreign body gently off of the cornea or conjunctiva. Such removal can be facilitated by using a slitlamp, with the child’s forehead held against the slitlamp frame and the examiner’s hand resting on the child’s cheek. If the foreign body is incompletely removed or cannot be removed, a shield should be placed and ophthalmology consulted for evaluation and treatment.?Complications of ocular foreign body removal include failure to remove the foreign body completely; further blunt or penetrating trauma to the globe; failure to recognize a ruptured globe, resulting in extrusion of ocular contents; allergic reactions to topical anesthetics or antibiotics; and infection. Rust stains may persist after metallic foreign bodies have been removed and may gradually resolve with topical antibiotic ointment, but those that persist for 3 or more days require removal.American Board of Pediatrics Content Specification(s)Discuss the indications and contraindications for ocular foreign body removalDescribe the key steps and potential pitfalls in performing ocular foreign body removalDiscuss the complications with ocular foreign body removalKnow the anatomy and pathophysiology relevant to ocular foreign body removalQuestion: 2A 4-year-old boy who was playing outside after dinner felt a sudden sharp pain, began to bleed under his T-shirt, and developed significant distress. Examination by emergency medical service (EMS) personnel shows what appears to be a small-caliber bullet wound approximately 2 cm subxiphoid. Initial vital signs at the site are: temperature, 37.0°C; heart rate, 138 beats/min; respiratory rate, 47 breaths/min; blood pressure, 70/50 mm Hg; and oxygen saturation, 88% on room air. The EMS personnel have inserted an endotracheal tube and two large-bore intravenous catheters. His current vital signs are heart rate of 165 beats/min, respiratory rate of 40 (controlled) breaths/min, blood pressure of 50/30 mm Hg, and oxygen saturation of 61% on 100% fraction of inspired oxygen. He will arrive at the emergency department in 3 minutes.Of the following, the intervention that is MOST likely to be needed immediately for this patient isA.diagnostic peritoneal lavageB.emergency thoracotomyC.exploratory laparotomyD.insertion of a subclavian central venous catheterE.tube thoracostomyCorrect answer EThe presence of a suspected entrance wound in the abdomen with respiratory and cardiovascular signs suggests a multisystem and multicompartment injury, including a likely pneumothorax. In addition to managing the patient’s airway, tube thoracostomy is most likely to be performed immediately upon arrival in the emergency department.Emergency thoracotomy is only indicated in the patient in full cardiac arrest who has a penetrating injury. Diagnostic peritoneal lavage generally is not a useful adjunct in children; intraoperative evaluation is mandatory for this patient. Diagnostic laparoscopy may be considered in select cases that do not involve cardiovascular compromise or have evidence of significant injury. Operative intervention likely will be required for this boy but only after initial evaluation in the emergency department. The patient already has received adequate intravenous access for initial resuscitation, obviating the need for additional access.Any child who has a penetrating abdominal injury, especially from a projectile such as a bullet, should be suspected of having injuries beyond the obvious site of injury. A bullet can traverse many different areas and organ systems and be redirected by organs, bones, and vessels. Evaluation should start, as always, with the airway, breathing, and circulation, looking for any signs of compromise. This child has tachypnea, tachycardia, and hypotension, suggestive of pulmonary involvement and blood loss. Tachypnea and tachycardia can present with other causes, but in this situation, intrathoracic and intra-abdominal injuries are most likely, and administration of 100% oxygen, intravenous line placement, and fluid resuscitation are indicated. Laboratory evaluation and blood typing and cross-matching are required because the boy may need immediate transfusion if he experiences further cardiovascular deterioration. Radiologic studies, if the patient is stable, can help work through the possibilities. Portable chest and abdominal radiographs, focused assessment with sonography for trauma (FAST) examination, and bedside echocardiography can be useful adjuncts in rapid screening.Not all patients who have penetrating abdominal trauma require operative intervention. Isolated stab wounds to the abdomen can be considered for nonoperative management as long as the patient is in a center with skilled assessors who can perform serial examinations and provide rapid, on-site surgical intervention if the need arises. Even patients who have gunshot wounds to the abdomen may be considered for nonoperative management in some centers if radiographic evaluations (computed tomography [CT] scan) demonstrate no violation of the peritoneum. Of note, the track of a bullet is well seen on CT scan, but that of a stab wound is more difficult to determine. If an isolated solid viscus injury is identified, nonoperative observation may be considered at the discretion of the surgical team. There are also reports of selective nonoperative management of omental evisceration after penetrating trauma. However, if any of these injuries is associated with hemodynamic instability, evidence of hollow viscus injury (eg, peritonitis, diffuse abdominal tenderness), or associated free fluid, operative intervention is indicated. Additionally, patients who have head injuries or need for other surgical interventions may not be good candidates for nonoperative management.Errors can be made in assessment and management planning after misclassification of entry and exit wounds and missed identification of intra-abdominal retained missile fragments. Evaluations must include adjacent areas, such as the chest and pelvis, and sometimes can extend to the neck. Such evaluations are more difficult in a patient who has multiple gunshot wounds.As in this boy, extension of an intra-abdominal entry to the thorax can lead to deterioration, morbidity, and mortality. All patients who have penetrating injuries to the upper abdomen should be evaluated for thoracic trauma. Tension pneumothorax, hemothorax, pulmonary contusion, pulmonary laceration, diaphragmatic injury, tracheal or esophageal injury, cardiac tamponade, neurologic injury, and other cardiac and large/small vascular compromise can be seen in patients who have this presentation.American Board of Pediatrics Content Specification(s)Recognize and plan the management of thoracic injuries following penetrating abdominal/flank injuriesKnow the indications for operative intervention following penetrating abdominal/flank injuryQuestion: 3An 8-day-old boy is brought to the emergency department because of lethargy, cyanosis, and decreased activity. He was born at term and discharged on the second postnatal day. His mother has noticed that he has been taking longer to feed and developing perioral cyanosis with crying episodes. Today he is irritable, tired, not interested in feeding, and developing a worsening grayish-blue skin color. Physical examination shows a temperature of 36.0?C, heart rate of 165 beats/min, respiratory rate of 65 breaths/min, blood pressure of 55/32 mm Hg, and oxygen saturation of 71% on his right upper extremity. He has a sunken fontanelle, poor capillary refill, weak peripheral pulses, grade 2/6 systolic murmur, right-sided parasternal heave, and hepatomegaly.Of the following, the management strategy that is MOST likely to cause the infant’s clinical condition to deteriorate is administration ofA.10 mL/kg normal salineB.antibioticsC.dopamineD.prostaglandin E1E.supplemental oxygen to achieve 100% SpO2Correct answer: EThe infant described in the vignette has cyanotic congenital heart disease (CHD). Patients who have cyanotic CHD may present in the first few hours or days after birth with respiratory distress and develop sudden cyanosis and shock upon closure of the ductus arteriosus. Management includes immediate administration of prostaglandin E1, hydration, and limited oxygen administration. Excessive oxygenation can lead to clinical deterioration by enhancing ductal closure and decreasing pulmonary vascular resistance that, in turn, decreases the systemic vascular perfusion that depends on patency of the ductus arteriosus (blood flows from the pulmonary artery into the descending aorta via the ductus arteriosus due to elevated right-sided pressure). This right-to-left shunt is essential for patient survival until surgical correction. Dopamine and other vasopressive agents are useful in the management of children who have cardiogenic shock. Interval illness can exacerbate cardiac failure, and administration of antibiotics is not harmful for critically ill patients in whom CHD is suspected.The incidence of CHD is estimated at 5 to 10 per 1,000 live births (1% of live births). It is much higher in stillbirths (3% to 4%) and in spontaneous abortuses (10% to 25%). The most common congenital heart lesion in live births is ventricular septal defect (28% to 35%). About 50% to 60% of infants who have CHD are diagnosed by 1 month of age. With the use of ultrasonography and fetal echocardiography in high-risk pregnancies, prenatal screening has decreased the number of undiagnosed cases after birth. About one third of neonates who have CHD have critical lesions that require management within the first postnatal year. Survival has increased in infancy, and death in adults is primarily due to rhythm disturbances.Although the cause of CHD has been suggested to be multifactorial, recent studies show point mutations as the most important factor. A small percentage of cases are due to chromosomal aberrations (Table). Other cardiac conditions involving known genetic abnormalities are cardiomyopathies (hypertrophic and dilated cardiomyopathy) and arrhythmias (eg, prolonged QT syndrome).?Maternal medical conditions and teratogen exposure also have been associated with CHD (eg, maternal diabetes; systemic lupus erythematosus; viral infections such as rubella; and exposure to lithium, ethanol, warfarin, antiepileptics, and vitamin A).Fetal circulation is designed for blood to flow toward the placenta (Fig. 1). Blood from the placenta on the right side of the heart mixes with blood from the lungs on the left side of the heart at the level of foramen ovale, allowing perfusion of the head, neck, heart, and upper extremities. Mixing at the ductus arteriosus allows perfusion of the abdomen and lower extremities. This process is facilitated by elevated vascular resistance of the pulmonary system. Oxygen saturation of fetal blood is approximately26 to 38 mm Hg (returning toward and from placenta, respectively), and fetal hemoglobin aids in tissue oxygen delivery, despite the low oxygen gradient compared with that of the neonate and infant. Therefore, survival of patients who have CHD at low oxygen saturations is possible due to fetal acclimatization with low oxygen saturation in utero.At birth, pulmonary vascular resistance reduces due to opening of alveoli and dilation of pulmonary arterioles after exposure to higher ambient oxygen concentration. Systemic vascular resistance increases after removal of the placenta, aiding in diversion of right-sided blood flow toward the pulmonary system. Therefore, the returning volume of blood increases on the left side of the heart from the lungs, which helps in closure of the foramen ovale. The ductus arteriosus closes over the next few days due to the reduction in circulating prostaglandin E, increase in oxygen saturation, or other unknown mechanisms. Various forms of CHD depend on persistent fetal circulation for survival and present precipitously with the normal anatomic changes after birth, especially with ductal closure.CHD can be divided into acyanotic and cyanotic lesions (Fig. 2). The acyanotic lesions result in either volume or pressure overload on the heart, and cyanotic lesions are associated with decreased or increased pulmonary blood flow.Volume overload is due to a left-to-right shunt. Examples include ventricular septal defect, atrial septal defect, endocardial cushion defect, and patent ductus arteriosus. The age of presentation depends on the degree of pulmonary and systemic vascular resistance and size of the defect. With left-to-right shunts, patients develop symptoms of pulmonary edema, which include increased work of breathing, sweating, fatigue, irritability, and failure to thrive. Physical examination reveals hypoxia, wheezing, skin mottling, pallor, and poor capillary refill.Pressure overload lesions result from outflow tract obstruction and present earlier with severe obstructions. Dramatic symptoms of shock, circulatory collapse, and right-sided heart failure occur at closure of the ductus arteriosus. Examples include critical aortic stenosis, coarctation of the aorta, and pulmonic stenosis. Severe pulmonic stenosis in the presence of a patent foramen ovale can present with cyanosis due to a right-to-left shunt. In less severe forms, such as mild coarctation of aorta, the affected child can present later in childhood with diminished pulses in the lower extremities and upper extremity hypertension. Studies that can aid in diagnosing acyanotic CHD are chest radiography showing cardiomegaly and pulmonary edema, electrocardiography documenting ventricular hypertrophy and right or left axis deviation, and echocardiography.Reduced pulmonary blood flow in cyanotic CHD is due to obstruction at the right outflow tract, such as in tetralogy of Fallot, tricuspid and pulmonic valve atresia, and Epstein anomaly of the tricuspid valve. Systemic blood flow is maintained by a right-to-left shunt at the level of the atrial or ventricular septum, and pulmonary blood flow is maintained by the ductus arteriosus. Circulatory collapse, cyanosis, and hypoxemia ensue with closure of the ductus. The degree of cyanosis correlates with the degree of pulmonic outflow tract obstruction. Transposition of the great vessels and totally mixing lesions such as truncus arteriosus, single ventricles, and total anomalous pulmonary venous return are examples of cyanotic CHD with increased pulmonary blood flow. In these cases, pulmonary blood flow is dependent on intracardiac defects, and systemic blood flow is dependent on ductus arteriosus, facilitated by elevated pulmonary vascular resistance and reduced systemic resistance. After ductal closure, patients present with significant cyanosis and signs of shock and cardiac failure. Clinically apparent differential cyanosis (upper body blue and lower body pink) is always due to CHD.Helpful investigations in cyanotic CHD include arterial blood gases, chest radiography, electrocardiography, and echocardiography. Arterial blood gas is helpful to differentiate between cardiac and pulmonary causes of cyanosis. The hyperoxia test assesses for improvement in cyanosis after administration of 100% oxygen for 10 minutes. With cyanotic CHD lesions, arterial partial pressure of oxygen does not increase greater than 150 mm Hg, in contrast to cyanosis due to congestive cardiac failure or pulmonary pathology. Chest radiography shows evidence of decreased or increased pulmonary blood flow with diminished pulmonary vascular flow, severe acidosis, and hypoxia in patients who have persistent pulmonary hypertension. Electrocardiography exhibits the specific ventricular hypertrophy, depending on the lesion. For example, right ventricular hypertrophy is seen with tetralogy of Fallot and hypoplastic left heart syndrome and right axis deviation is seen with right atrial hypertrophy.Figure 1: Fetal circulation. A. Human circulation before birth (partly after Dawes). Red indicates more oxygenated blood, and arrows indicate the direction of flow. Highly oxygenated blood from the placenta passes through the foramen ovale from the right to the left atrium, thus bypassing the lungs. B. Percentages of combined ventricular output that return to the fetal heart, that are ejected by each ventricle, and that flow through the main vascular channels. ?American Board of Pediatrics Content Specification(s)Understand the pathophysiology and anatomy of congenital heart diseaseBe familiar with ancillary studies relevant to congenital heart diseaseQuestion: 4An obese 9-year-old boy who has poorly controlled chronic persistent asthma and obstructive sleep apnea syndrome (OSAS) has sustained an isolated Colles fracture. The orthopedic consultant has requested procedural sedation and analgesia to reduce the fracture in the emergency department. The child had received intravenous morphine on arrival. His last oral intake consisted of a few French fries 6 hours ago. On physical examination, his lungs are clear to auscultation. He has no loose teeth. Findings on his oropharyngeal examination are shown in Figure 1.Of the following, as part of the presedation assessment, this boy’s American Society of Anesthesiologists (ASA) risk level and Mallampati (MP) score are CLOSEST toA.ASA 2, MP 2B.ASA 2, MP 3C.ASA 3, MP 2D.ASA 3, MP 4E.ASA 4, MP 3Correct answer CThe decision to perform procedural sedation and analgesia (PSA) to facilitate fracture manipulation must be balanced against the risks of sedation in each patient. Careful presedation assessment begins with a focused history and physical examination. Most organizations follow the classification published by the ASA (Table 1). The MP classification system can be used to identify patients at risk for having difficult airways (Fig. 2). The adequacy of seeing the posterior oropharynx has been shown to correlate with glottic exposure during direct laryngoscopy. The patient described in the vignette, who has poorly controlled asthma, obesity, and OSAS, should be classified as ASA level 3 (ie, having moderate systemic disease that may limit his activity but is not incapacitating). His oropharyngeal examination findings suggest an MP class 2 airway.An ASA level 3 or greater and MP class 3 or greater have been shown to correlate with an increased risk of sedation-related adverse events and unexpected difficult airway, respectively. Although these data have been extrapolated from the adult anesthesiology literature, the American Academy of Pediatrics encourages practitioners to consult with appropriate subspecialists or anesthesiology about patients deemed to be at high risk for procedural sedation (Table 2). In such cases, the practitioner may defer PSA in the emergency setting and opt for complete control of the airway with general anesthesia outside the emergency department or use alternative techniques such as local or regional block anesthesia with minimal sedation.The key steps prior to performing PSA in the emergency department are:Risk stratification based on the ASA physical status classification.A focused presedation history and physical examination (Table 3).Documentation of the time of last oral intake.Preparation and set up; the acronym SOAPME may be used to review the preparatory steps (Table 4).Selection of the appropriate agents based on desired depth of sedation to best facilitate the procedure.Preoperative and elective procedure NPO guidelines have limited applicability in the emergency setting. Adverse events are more related to depth of sedation, type of procedure, and age of patients than to NPO status. Therefore, the emergency physician should weigh the risks and benefits of the procedure and sedation for each patient in deciding duration of preprocedural fasting.The indications for PSA include any procedure that is likely to invoke significant pain or distress or one that requires a relatively motionless state, such as advanced imaging studies or complex laceration repair (Table 5).The choice of agent usually involves a combination of a sedative-hypnotic (or dissociative) agent and narcotic analgesic for painful procedures. Other factors that may determine the type of medication include familiarity with a particular class of agent, institutional preference, or clinician credentialing for sedation in the emergency department. Table 6 lists the properties of the various pharmacologic agents and their major adverse effects.Airway complications are the most common adverse events during PSA. They include hypoventilation, apnea, airway obstruction, aspiration, bronchospasm, and rarely laryngospasm. Respiratory depression can be a consequence of a deeper level of sedation than anticipated or an adverse effect of the sedative-hypnotic agent used. It may be enhanced by concomitant use of narcotic analgesia. The clinician administering sedation must be proficient in early recognition of airway obstruction or hypoventilation and be prepared to intervene to secure an adequate airway. Interventions might include airway realignment, bag-mask ventilation, and intubation, if necessary.Severe laryngospasm requiring neuromuscular blockade and intubation is an infrequent complication in procedural sedation cases in the pediatric emergency department. It is precipitated by incomplete or complete closure of the true vocal cords. It is defined as absence of air exchange in the presence of chest wall movement with or without stridor, not responsive to airway repositioning and routine bag-valve-mask ventilation. Occluding the pop-off valve to generate higher pressures with bag-mask ventilation and attempting the “laryngospasm maneuver” may be temporizing measures before administering a neuromuscular blocking agent and endotracheally intubating the patient. The laryngospasm maneuver is performed by applying firm pressure in the notch located between the angle of the mandible anteriorly, the mastoid posteriorly, and the base of the skull superiorly. The purported mechanism is pressure in the notch surpassing the patient’s pain threshold that causes the vocal cords to relax. It is similar to the jaw thrust maneuver, but the pressure is directed toward the mandibular condyles rather than to the angles of the mandible.Table 1: American Society of Anesthesiologists (ASA) Risk ClassificationClass IA normal, healthy patient.Class II???A patient who has mild systemic disease (no functional limitation).Class III?A patient who has moderate or severe systemic disease that limits activity but is not incapacitating.Class IVA patient who has an incapacitating systemic disease that is a constant threat to life.Class VA moribund patient who is not expected to survive 24 hours with or without the procedure.Figure 2Table 2: High-risk Conditions for Procedural SedationSnoring, stridor, sleep apneaCraniofacial abnormalities, history of airway difficultyVomiting, bowel obstruction, gastroesophageal refluxAsthma exacerbation, pneumoniaCardiac disease, hypovolemia, sepsisAltered mental status, neurologic/neuromuscular disorderHistory of sedation failureAge <1 yearModerate or severe systemic disease that limits activity (ASA ≥ 3)Table 6: Overview of MedicationsAgentPediatric DosingOnset (min)Duration (min)CommentsSedative-hypnoticsChoral hydrate????????????PO: 25 to 100 mg/kg, after 30 min can repeat 25 to 50 mg/kg. Maximum total dose: 2 g or 100 mg/kg (whichever is less).? Single use only in neonates15 to 3060 to 120Effects unreliable if age <3 years?????DiazepamIV: initial 0.05 to 0.1 mg/kg, then titrate slowly to maximum 0.25 mg/kg4 to 560 to 120Reduce dose when used in combination with opioids?????EtomidateIV: 0.1 mg/kg; repeat if inadequate response<15 to 15Adverse effects include respiratory depression, myoclonus, nausea, emesis?????MidazolamIV (0.5 to 5 years): initial 0.05 to 0.1 mg/kg, then titrated to maximum 0.6 mg/kg?IV (6 to 12 years): initial 0.025 to 0.05 mg/kg, then titrated to maximum 0.4 mg/kg2 to 345 to 60Reduce dose when used in combination with opioids; may produce paradoxic excitementIM: 0.1 to 0.15 mg/kg10 to 2060 to 120PO: 0.5 to 0.75 mg/kg15 to 3060 to 90IN: 0.2 to 0.5 mg/kg10 to 1560PR: 0.25 to 0.5 mg/kg10 to 3060 to 90MethohexitalPR: 25 mg/kg10 to 1560Avoid if temporal lobe epilepsy or porphyriaIV: 0.5 to 1.0 mg/kg?PentobarbitalIV: 1 to 6 mg/kg, titrated in 1- to 2-mg/kg increments every 3 to 5 min to desired effect3 to 515 to 45May produce paradoxic excitement; avoid in patients who have porphyriaIM:? 2 to 6 mg/kg, maximum 100 mg10 to 1560 to 120PO/PR (<4 yrs): 3 to 6 mg/kg, maximum 100 mg?? PO/PR (>4 yrs): 1.5 to 3 mg/kg, maximum 100 mg15 to 6060 to 240?????PropofolIV: 1.0 mg/kg, followed by 0.5 mg/kg repeat doses as needed<15 to 15Frequent hypotension and respiratory depression; avoid with egg or soy allergies?????Thiopental??PR: 25 mg/kg10 to 1560 to 120Avoid in patients with porphyriaAnalgesicsFentanylIV: initial 1.0 mcg/kg up to 50 mcg/dose, may repeat every 3 min, titrate to effect3 to 530 to 60Reduce dosing when combined with benzodiazepines?????MorphineIV: initial 0.05 to 0.15 mg/kg up to 3 mg/dose, may repeat every 5 min, titrate to effect5 to 10120 to 180Reduce dosing when combined with benzodiazepinesDissociative DrugKetamineIV: 1 to 1.5 mg/kg slowly over 1 min, may repeat every 10 min as needed1Dissociation: 15?Recovery: 60Multiple contraindications. Unpleasant dreams or hallucinations rare in kids.????????????????????????IM: 4 to 5 mg/kg, may repeat (2 to 4 mg/kg) after 10 min3 to 5Dissociation: 15 to 30?Recovery: 90 to 150Often given with concurrently atropine or glycopyrrolate to counter hypersalivationInhalational DrugNitrous oxidePreset mixture with minimum 30% oxygen self-administered by demand valve mask (requires cooperative child); continuous flow nasal mask in uncooperative child with close monitoring<5<5 following discontinuationRequires specialized apparatus and gas scavenger capability; several contraindicationsReversal DrugsNaloxoneIV/IM: 0.1 mg/kg/dose up to maximum of 2 mg/dose, may repeat every 2 min as neededIV: 2IV: 20 to 40?IM: 60 to 90If shorter acting than the reversed drug, serial doses may be required?????FlumazenilIV: 0.02 mg/kg/dose, may repeat every 1 min up to 1 mg?????1–230 to 60If shorter acting than the reversed drug, serial doses may be requiredAlterations in dosing may be indicated depending on the clinical situation and the practitioner’s experience with the drugs. Individual doses may vary when used in combination with other drugs, especially when benzodiazepines are combined with opiates.Ketamine is absolutely contraindicated in patients <3 months (airway risk) or when known psychosis (may exacerbate). Relative contraindications include age <12 months, procedures involving stimulation of posterior pharynx, history of tracheal surgery or stenosis, active pulmonary infection or disease (including upper respiratory tract infection), known or suspected cardiovascular disease, suspected raised intracranial or intraocular pressure, globe injury, porphyria or thyroid dysfunction.IM=intramuscular, IN=intranasal, IV=intravenous, PO=oral, PR=rectalAmerican Board of Pediatrics Content Specification(s)Know the anatomy and pathophysiology relevant to procedural sedation and pain management techniquesDiscuss the indications and contraindications for procedural sedation and pain management techniquesDescribe the key steps and potential pitfalls in performing procedural sedation and pain management techniquesDiscuss the complications associated with procedural sedation and pain management techniquesQuestion: 5A 7-year-old girl presents to the emergency department with a 1-day history of headache and dysarthria. She has no history of trauma or signs of infection. On physical examination, she has normal vital signs but left facial and left arm weakness. A noncontrast head computed tomography scan is read as normal. You diagnose complex migraine and provide appropriate treatment, but after 2 hours, there is no improvement.?Of the following, the MOST likely cause of this girl’s condition isA.acute ischemic strokeB.brain tumorC.lupus cerebritisD.Lyme meningitisE.Todd paralysisCorrect answer ATodd paralysis after an unwitnessed seizure is a possible explanation for the symptoms described for the girl in the vignette, but it is unlikely to persist for 24 hours. It is important to rule out conditions for this child that potentially can be treated. Lyme meningitis usually has a more insidious onset. A brain tumor large enough to cause the deficits described should be visible on computed tomography scan. Lupus cerebritis usually presents with more global involvement, resulting in encephalopathy. Stroke is a difficult diagnosis to make in children, in part because it is a rare disease. In addition, the signs and symptoms of stroke in children are often nonspecific. Some conditions, such as those listed in the options, are often confused with stroke. The lack of improvement with appropriate treatment for the girl in the vignette strongly suggests the diagnosis of stroke (Table 1 and Table 2).Conditions associated with childhood stroke includecongenital heart disease, sickle cell disease, meningitis, avariety of hereditary and acquired prothrombotic states, anda number of vasculopathies (eg, moyamoya, lupus erythematosus). Cardiac disease is themost common previously recognized risk factor, and the most commonly associated conditions are complex lesions that involve right-to-left shunts.Several coagulation abnormalities have been identified in childrenwho have stroke, including antithrombin III anomalies, protein C or proteinS deficiencies, activated protein C resistance, factor V Leidenmutation, prothrombin gene mutation, and antiphospholipidantibody syndrome.A large study recently enumerated the current common causes of acute ischemic strokes?in children (Table 3).Stroke is more likely to occurin the perinatal period (within 28 days of birth) than at any other time in childhood. The causes are either maternal factors (eg, lupus erythematosus) or birth-related asphyxia. Localizing signs often are absent in neonates, which makes the onsetof stroke difficult to establish accurately. Focal seizurescan be the sole presenting symptom, rather than motor deficits. Stroke should be suspectedin neonates presenting with seizures, lethargy, or apnea.Almost 50% of strokes in children are of the hemorrhagic type compared with less than 20% in adults. Common causes include arteriovenous malformation (AVM), intracranial arterial aneurysm, coagulopathy (eg, hemophilia), thrombocytopenia, hypertension, and amphetamine/cocaine overdose.Management of stroke in children is controversial. Hemodynamic stability should be established to minimize ongoing ischemia. In cases of hemorrhagic stroke, efforts to stop the bleeding should be undertaken, including correction of thrombocytopenia and coagulopathy. Those who have sickle cell disease should receive red cell transfusion to decrease and reverse sickling. Surgical and interventional radiology options should be considered in cases such as AVM.?Several pharmacologic treatment options have been proposed for patients experiencing acute ischemic strokes, but none is supported by anything better than Class II evidence. For a comprehensive discussion, readers are referred to theAmerican Heart Association scientific statement on management of stroke in infants and children.Thrombolytic treatment, although an option, is very rarely employed in children. Delayed administrationleads to a high rate of intracerebral hemorrhagein children. If thrombolytic therapy is considered, it is important to adhereto the accepted time limits used in adults: administration ofintravenous tissue plasminogen activator (tPA) within 3 hours of stroke onset and intra-arterialtPA within 6 hours of stroke onset for anterior circulation. Unfortunately, most children present to medical attention much later, and most are not diagnosed during the specified time frame, contributing to the current lack of data on the safety and efficacy of thrombolytic therapy for stroke in children.Table 2: At-a-Glance Symptoms of Childhood Stroke SyndromesACUTE ARTERIAL ISCHEMIC STROKE OR TIAMedical descriptionLay descriptionCommentHemiparesisWeak arm or leg, facial droop, paralyzed on one sideCombination of face+arm, or face+arm+ leg strongly suspicious for strokeAphasiaStopped speaking, talking nonsense, won’t follow commandsSometimes mistaken for confusion or oppositional behaviorAtaxiaUnsteady gait, can’t walk straight, seems drunk, can’t sit steady, uncoordinated reach/graspOften associated with headache, complaint of dizziness, vomitingDysarthria (slurred speech)Speech is slurred, though word choice & comprehension are correct?Hemisensory lossNumbness on one side of bodyUsually involves one side of body & more than one body region (face+arm or face+arm+leg)New-onset focal seizures with atypical prolonged (>1 hr) postictal deficit?No previous dx of epilepsy, now has several focal seizures followed by persisting weakness in location of the seizure (usually face+arm or face+arm+leg)ACUTE CEREBRAL SINOVENOUS THROMBOSISMedical descriptionLay descriptionCommentTriad of unremitting & escalating headache, repeated vomiting and decreased mental statusLethargic, vomiting, irritable, headacheFrequently has 6th nerve palsy & papilledemaIn newborns, lethargy & seizureLethargic, poor feeding, seizures?INTRACRANIAL HEMORRHAGE (IVH, subarachnoid hemorrhage, AVM)Medical descriptionLay descriptionCommentHyperacute severe headache“Worst headache of my life”Often quickly followed by decreased mental statusSudden sustained loss of consciousness“collapsed”, hard to wake upOften preceded by c/o headache, vomiting and/or seizureOne or both of above with new focal deficitParalyzed on one side, eyes going to one side, face drooping?American Board of Pediatrics Content Specification(s)Know the causes of stroke in childrenKnow how to diagnose and manage strokes in childrenQuestion: 6A 14-year-old boy presents to the pediatric emergency department after falling off of his bicycle. Physical examination reveals a heart rate of 70 beats/min, respiratory rate of 18 breaths/min, blood pressure of 110/70 mm Hg, and oxygen saturation of 99% on room air. He has no signs of head injury, but he does have a “handlebar” mark on the right upper quadrant of his abdomen. You obtain bedside ultrasonography (Figure), which reveals free fluid in the Morrison pouch.?Figure: Abdominal ultrasonography reveals free fluid in the Morrison pouchOf the following, the MOST appropriate course of action is toA.admit the boy for serial abdominal examinationsB.perform diagnostic peritoneal lavageC.perform immediate exploratory laparotomyD.provide reassurance and arrange for outpatient follow-up evaluationE.transfuse 2 units of packed red blood cellsCorrect answer AThe boy described in the vignette has free fluid, represented in the ultrasonographic image by the black stripe between the liver and right kidney (Morrison pouch). He should be admitted to the hospital for serial abdominal examinations. Packed red blood cell transfusion is not indicated as long as the patient remains hemodynamically stable. Unlike in adult patients, positive results of a FAST (focused abdominal [or assessment] sonography for trauma) are not an indication for exploratory laparotomy. Diagnostic peritoneal lavage is rarely performed in children and is especially not indicated when it is already known that the patient has intraperitoneal free fluid (blood). Although many patients’ injuries do not progress, the risk remains and necessitates inpatient observation. Follow-up study may include serial hematocrit measurements and computed tomography (CT) scan.FAST is one of the new technologies specifically developed for the emergency department setting. The goal of FAST is rapid identification of intra-abdominal and intrathoracic trauma. The premise is that blood collects in the most dependent portions of the abdomen. In the supine patient, such locations are predictably the costophrenic angles in the thorax, pericardium, Morrison pouch (the potential space between liver and right kidney), splenorenal recess, and rectovesicular space.The FAST exam utilizes four views to detect free intraperitoneal fluid in blunt abdominal trauma:Perihepatic view (right upper quadrant) to visualize Morrison pouch, the potential space between the liver capsule and the right kidney.Perisplenic view (left upper quadrant) to view the spleen and left kidney interface.Pelvic view to detect fluid in either the rectovesicular pouch (males) or cul-de-sac (females).Pericardial view to identify pericardial fluid.Robust evidence documents that the use of FAST in adult patients who have penetrating wounds leads to more rapid definitive operative management. In blunt abdominal trauma, the evidence is less convincing. For pediatric patients, there is a desire to limit the amount of ionizing radiation from CT scan, but the evidence of benefits of FAST over CT scan in pediatric patients is limited. Part of the limitation is that the sensitivity of FAST is probably lower in pediatric patients, ranging from 60% to 80%. Many injuries in children are solid organ contusions that may be confined in the capsule and do not initially cause intraperitoneal free fluid that would be identified on ultrasonography. In contrast to adult patients, few pediatric patients undergo exploratory laparotomies, with most surgeons choosing conservative watch-and-wait strategies, even with high-grade injuries.American Board of Pediatrics Content Specification(s)Understand the role of ultrasound in the management of a major trauma victimQuestion: 7A 12-month-old boy presents to the emergency department after an unusual finding in a photograph. His mother points out that one eye has a red reflex and one eye has a white reflex. She denies any change in his usual state of health and has not noticed any visual impairment. On physical examination, you confirm the presence of white reflex in his right eye and normal red reflex in his left eye with direct ophthalmoscopy.Of the following, the MOST appropriate next step for this boy isA.follow-up evaluation tomorrow with the ophthalmologist for indirect ophthalmoscopyB.hospital admission for ocular aqueous aspiration and needle biopsyC.hospital admission for sedated ocular magnetic resonance imagingD.ocular computed tomography scan in the emergency roomE.outpatient ocular ultrasonography and follow-up evaluation by his pediatrician within the next weekCorrect answer: AThe boy described in the vignette has signs that are suspicious for retinoblastoma, and the diagnostic modality of choice is indirect ophthalmoscopy with or without sedation. Ocular ultrasonography is a useful adjunct, but it does not provide definitive findings. Although computed tomography scan can discern the associated diagnostic calcifications seen in retinoblastoma, it is contraindicated because of the occurrence of second malignancies in patients who have hereditary retinoblastoma. Magnetic resonance imaging may be indicated after the tumor is confirmed by indirect ophthalmoscopy to help in differentiating other possible causes of ocular white reflex and determining the local extent of the disease. Ocular biopsies and aqueous aspirations are contraindicated; they can lead to tumor rupture and intraocular seeding.Retinoblastoma is the most common ocular malignancy and the seventh most common pediatric cancer in the United States, with incidence of approximately 1 in 15,000 to 30,000 live births worldwide. Although no difference in sex or race incidence has been reported, lower socioeconomic status is considered to be a high risk. Retinoblastoma arises from retinal progenitor cells and has hereditary and sporadic forms. The hereditary form is autosomal dominant, although only 10% of affected patients have positive family histories. The gene responsible for retinoblastoma, the rb1 gene, is mapped on the long arm of chromosome 13, band 14.2 (13q14) and codes for production of tumor suppressor protein. Loss of its function at both the alleles is considered one of the major genetic abnormalities to occur before retinoblastoma formation. This cancer is a classic example of the “two-hit theory.” In the hereditary form, the mutation in one allele is in the germinal cells (familial or sporadic), and the second allele is affected later in life (second hit). Affected patients are at risk of primarily bilateral tumors (25% of patients), but they can have unilateral disease and if so, the tumor is multifocal (15% of patients). In the sporadic form, both alleles are affected spontaneously in the somatic cells and result in only unilateral unifocal tumors (60% of patients).?In the United States, the common age of presentation is approximately 2 years; older age (4 to 6 years) and more extensive tumor presentation are common in developing countries. The most common presentation in the United States is leukocoria or white pupillary reflex (54% to 60%), followed by strabismus (19% to 25%), painful glaucoma or signs of orbital cellulitis, and fever (5% to 10%). If a patient presents with strabismus, it is most commonly esotropia. However, if a patient has exotropia, it is almost always due to retinoblastoma. Other presenting signs include iris heterochromia due to neovascularization, vitreous hemorrhage, proptosis, hypopyon or hyphema in the anterior chamber, and anisocoria.?The presence of leukocoria (Fig. 1) indicates a large tumor. It is mostly identified by family members of the patient (close to 80%) and less commonly by physicians. Recent simulation studies have shown that leukocoria can be better identified with an oblique viewing technique combined with straight-on ophthalmoscopic examination for red reflex screening of pediatric patients (Fig. 2). When feasible, pupillary dilatation should be performed because it aids in viewing the peripheral retina (Table). The differential diagnosis of white pupillary reflex includes cataract, Coats or retinal vascular disease, toxocariasis, uveitis, vitreous hemorrhage, coloboma, and astrocytic hamartoma.The most effective method to diagnose retinoblastoma is indirect ophthalmoscopy. The tumor appears as extruding from the retina, located around the macula in younger patients (<1 year old) and around the peripheral retina in older children (1 to 2 years old). The next stage in the tumor growth is local extension either toward the preretinal space, causing retinal detachment; toward vitreous humor, causing hemorrhage; or spreading extensively toward the choroid, associated with neovascularization of iris. The tumor may spread beyond the eye, presenting as a protruding mass (as seen in developing countries) or as intracranial and hematogenous metastasis to the liver and bone marrow. Metastatic evaluation, which is only indicated if there is evidence of tumor extension beyond the globe, includes lumbar puncture, bone radionuclide scans, and bone marrow biopsy. The tumor grows fast, can be locally invasive as early as after 2 months of onset, and is likely to extend beyond the eye if not diagnosed by 6 months from onset.Treatment includes exenteration, enucleation, photocoagulation, chemotherapy, laser photoablation, transpupillary thermotherapy, cryotherapy, brachytherapy, and radiation therapy.?The survival rate approaches 95% in the United States. Poor prognostic factors include delay of 6 months in diagnosis; cataract; optic nerve, choroid, or orbital invasion; metastatic disease; and external beam radiation treatment. Leukocoria is associated with lower ocular survival. Survivors should wear protective eye goggles when playing sports and, therefore, cannot participate in sports where such protection is not allowed, such as boxing. Second malignancies are the usual cause of death in the survivors and are seen primarily in patients who have hereditary retinoblastoma (35% to 40% at 50 years postdiagnosis), especially those who received external beam radiation or ocular computed tomography scans. The second malignancies include soft-tissue sarcomas; osteogenic sarcoma; pinealoblastoma; and brain, breast, lung, and bladder cancers. Long-term follow-up is indicated for early detection.Figure 1: Leukocoria is a presenting sign of retinoblastoma. Courtesy of the media lab at Doernbecher.Figure 2: Red reflex examination. Table: Suggested Eye Drops for Dilation in InfantsFor infants younger than 9 months:A combination drop of 0.25% cyclopentolate with 2.5% phenylephrine (avoid atropine)For infants older than 9 months:One drop of 1% tropicamide or 2.5% phenylephrine either separate or in combination0.2% cyclopentolate with 1% phenylephrineAmerican Board of Pediatrics Content Specification(s)Recognize signs and symptoms of retinoblastomaPlan initial management of patients with retinoblastomaQuestion: 8A 4-week-old girl presents to the emergency department with complaints of decreased oral intake for 1 day and a temperature of 38.5?C before arrival. Her mother changed her last diaper 3 hours ago and noted scant urine output. She has been otherwise growing normally and has had no sick contacts. On physical examination, her respiratory rate is 40 breaths/min and heart rate is 160 beats/min. She has flat fontanelles and appears tired but not toxic. You decide to perform a sepsis evaluation by collecting blood, urine, and cerebrospinal fluid. Two attempts at transurethral bladder catheterization are unsuccessful due to labial adhesions. Bedside ultrasonography shows scant urine in the bladder. You administer a 20-mL/kg bolus of normal saline.Of the following, the BEST strategy to obtain a urine specimen isA.extraction of urine from the diaperB.manual lysis of the labial adhesions followed by transurethral bladder catheterizationC.placement of a urine bag for urine collectionD.suprapubic bladder aspirationE.third attempt at transurethral bladder catheterizationCorrect answer CCollection of a urine specimen is indicated for a febrile infant younger than 2 months of age as part of evaluation for possible sepsis. Suprapubic bladder aspiration (SPA) or transurethral bladder catheterization (TUC) are the two standard methods used. The simplest and most efficient of these methods is TUC, but if this is not possible due to anatomic or technical difficulties, SPA should be considered. Before undertaking this approach, it is prudent to maximize the likelihood of success by ensuring that urine is present in the bladder. Administration of an intravenous bolus of normal saline before an attempted SPA is an appropriate course of action. Antibiotics can then be administered after collection of the urine sample. Repeated attempts at TUC in the presence of labial adhesions, use of urine from the diaper, and manual lysis of the adhesions are inappropriate. A urine bag may be considered if SPA is beyond the technical abilities of the clinician.SPA has been in use since the early 1950s. If urine is obtained, the sensitivity for detection of urinary tract infection by this procedure approaches nearly 100%, making it the diagnostic gold standard. Due to the invasiveness, pain, and greater failure rate for SPA compared to TUC (successful attempts range from 23% to 90%), TUC has become the method of choice for children younger than 2 years of age. Although studies have found that TUC is less painful, the approach through a relatively nonsterile urethra does introduce a greater likelihood of bacterial contamination of the urine specimen.Beyond 2 years of age or after the child is toilet trained, the clean-catch technique is used for urine collection because of its relative ease and noninvasiveness. Specimens collected by urine bag can be used to screen for urinary tract infection in children between 2 months and 2 years of age when they are not sick enough to require immediate antibiotics. If the specimen is positive (presence of leukocyte esterase or nitrite, bacteria evident on microscopic examination of a Gram stain specimen, or detection of more than 5 white blood cells on a noncentrifuged urine specimen), then repeat urine specimen collection is indicated via TUC or SPA to confirm the infection. Antibiotics for presumed urinary tract infection should not be started on the basis of findings from specimens collected by urine bag alone.Indications for SPA are: difficulty in accessing the urethra in children younger than 2 years of age due to labial adhesions, foreskin adhesions, or any other technical problem that prevents collection of urine by TUC. ?Fecal incontinence in a child who has gastroenteritis is a relative indication. Contraindications include some genitourinary tract abnormalities, infection of the abdominal wall at the collection site, bleeding diathesis, and neutropenia. Studies have shown that pain associated with SPA can be reduced with the use of topical anesthetics and that the success of SPA is related to the patient’s hydration status. SPA success rates have increased when the procedure is used in conjunction withultrasonography (Fig. 1). Ultrasonography allows for determination of bladder volume and guidance for aspiration by showing where the bladder is closest to the abdominal wall. The minimum recommended bladder measurements for successful collection of urine are 2 cm or more in transverse and anteroposterior diameters or at least 10 mL of measured bladder urine volume.?Under sterile conditions, the patient’s abdominal wall is prepped with appropriate antiseptic and the patient is held in the frogleg position. Local anesthesia with injection or cream is recommended to reduce pain. The bladder is percussed to determine if it is full before attempting SPA. The entry point is 1 to 2 cm above the symphysis-pubis in the midline. Use of a 22-gauge 1.5-inch needle attached to a 3- to 5-mL syringe is recommended. The direction of insertion is 10 to 20 degrees from perpendicular, angled toward the umbilicus (Fig. 2). ?The plunger on the syringe is pulled back after the skin is pierced to create negative pressure until urine returns. If this is not successful, the needle can be directed more perpendicularly without removing it. If this attempt is also unsuccessful, the patient should be hydrated and the attempt may be repeated in 30 to 60 plications of SPA are rare and include intestinal penetration, infection of the abdominal wall, and transient hematuria. These can be avoided by proper identification of landmarks and use of sterile technique. Rare cases have been reported of bladder wall thickening after SPA in patients who have bleeding diatheses. Development of abdominal wall abscess has been reported in neonates who have fever and transient neutropenia. There is no evidence of bacteremia after SPA in patients who have documented urinary tract infection. When ultrasonographic guidance is used, care must be taken to avoid applying excessive pressure with the probe onto the bladder to prevent early micturition, which can be prevented by manual pressure on the urethral meatus.Figure 1: A. Position of the patient and ultrasound probe for scanning the bladder. B. Ultrasonographic image of a full urinary bladder in an infant. C. Figure 2: Needle placement for suprapubic aspiration. Reprinted with permission from Loiselle JM. Ultrasound-assisted suprapubic bladder aspiration. In: King C, Henretig FM, eds. Textbook of Pediatric Emergency Procedures. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:1223American Board of Pediatrics Content Specification(s)Discuss the indications and contraindications for suprapubic bladder aspirationKnow the anatomy and pathophysiology relevant to suprapubic bladder aspirationDiscuss complications associated with suprapubic bladder aspirationDescribe the key steps and potential pitfalls in performing suprapubic bladder aspirationJUNE 2011Question: 1A 4-year-old girl presents to the emergency department in status epilepticus of 30 minutes duration. She has a history of developmental delay, cerebral palsy, seizure disorder, and failure to thrive that required gastrostomy tube placement. Physical examination findings include perioral cyanosis, heart rate of 150 beats/min, blood pressure of 90/55 mm Hg, temperature of 40.0°C, and oxygen saturation of 85% on room air. She has coarse breath sounds bilaterally and is experiencing a generalized tonic-clonic seizure. You apply a nonrebreather mask and nasopharyngeal airway and administer 2 mg intravenous lorazepam. In 3 minutes, the girl’s respiratory rate decreases to 10 breaths/min, prompting bag-mask ventilation. After 10 minutes of bag-mask ventilation, her seizure stops and her respiratory rate improves to 35 to 40 breaths/min. However, she is taking rapid, shallow breaths and her oxygen saturation is 91% on bag-mask ventilation. She has some oral secretions, and lung auscultation documents coarse breath sounds bilaterally with decreased air entry at the bases. Her abdomen is distended, pupils are reactive to light, and extremity movements are spontaneous.Of the following, the MOST appropriate next step to relieve this girl’s respiratory distress is toA.continue bag-mask ventilationB.perform endotracheal intubationC.remove the nasopharyngeal airwayD.switch to nonrebreather oxygenation supportE.vent the gastrostomy tubeCorrect answer EThe most common complication associated with bag-mask ventilation is gastric distention, which impedes movement of the diaphragm on inspiration. Impaired diaphragmatic excursion results in respiratory distress after spontaneous breathing is restored. Gastric decompression can reverse this effect. For the girl described in the vignette, venting the gastrostomy tube can aid in gastric decompression and help relieve her respiratory distress. Other complications associated with gastric distention are emesis and aspiration. Gastric distension can be minimized by providing cricoid pressure during bag-mask ventilation.Continuation of bag-mask ventilation is not indicated because the girl now is breathing spontaneously. Although removal of the nasal airway might be appropriate, this does not address the source of her abdominal distention and respiratory distress. Providing oxygenation via a facial mask also would not alleviate gastric distention. Endotracheal intubation is not indicated at this time because the seizure has stopped and spontaneous breathing has been restored.?Respiratory compromise and resulting hypoxemia is the leading cause of cardiac arrest in children. Early identification and treatment of respiratory distress is critical to avoid hypoxemia. Oxygen can be delivered by a variety of methods, including nasal cannula, venturi masks, and nonrebreather masks for patients who have adequate spontaneous breathing.?Bag-mask ventilation is the most important and effective tool in the management of respiratory compromise when spontaneous breathing is impaired. It is especially helpful if ventilatory support is required for only a short time or to assist ventilation during insertion of an endotracheal tube or establishment of a surgical airway.?Patients who may benefit from bag-mask ventilation include those who have decreased respiratory efforts due to sedation medications, postoperative recovery, or status epilepticus. If the need for respiratory support is prolonged, this method is not optimal, in part because the airway remains unprotected. Bag-mask ventilation should be applied with caution in the presence of partial obstruction from foreign body aspiration or other upper airway obstruction, vomiting, and facial trauma.Successful bag-mask ventilation requires appropriate positioning of the airway with a jaw-thrust or chin-lift maneuver to avoid obstruction of the airway with the tongue and to align the oropharyngeal axis (Figure). The jaw-thrust maneuver is preferred over chin lift in any patient who has suspected cervical spine injury. Hyperextension of the neck can result in airway obstruction. The large occiput in neonates and infants can result in airway obstruction due to excessive neck flexion. The chin-lift technique and placement of a roll underneath the shoulders help to avoid airway obstruction, particularly in neonates and infants.The mask should enclose the mouth and the bridge of nose. Use of the E-C clamp technique to provide adequate ventilation is important. With this technique, the thumb and index finger are applied on the mask in a “C” position, and the middle, ring, and fifth finger are used to form an “E” along the mandible to provide an appropriate seal.?The other hand is used to squeeze the bag. A two-person technique (one providing the seal and the other squeezing the bag) is helpful if enough assistance is available.Two types of bags are used: self-inflating and anesthesia.?If the patient still is taking spontaneous breaths, bag squeezing should be timed with the patient’s breaths to avoid iatrogenic barotrauma. The self-inflating bags have a pressure-valve mechanism that allows for positive end-expiratory pressure, when needed, although it may provide only 60% to 90% oxygenation. Anesthesia bags require an experienced operator, a continuous flow of oxygen, and proper gas exchange to avoid carbon dioxide accumulation in the reservoir. The advantage of the anesthesia bag is that 100% oxygen can be delivered along with positive end-expiratory pressure.Before starting to use a bag-mask system, the clinician must assess the airway for any foreign bodies that may be pushed further in the airway tract. Although the most common complication is gastric distention, another possible complication is barotrauma, resulting in the development of pneumothorax.Use of oral or nasopharyngeal airways can provide adequate conduits for oxygen delivery. The oropharyngeal airway can avoid the palatal tissues and tongue blocking the posterior pharynx.?It should be used only if the patient does not have an intact gag reflex or is unconscious to avoid the complication of emesis associated with tongue contact. The nasopharyngeal airway is useful if the gag reflex is intact because there is no contact with the tongue. The patient described in the vignette is a good candidate for a nasal airway, especially because of tightening of oral and jaw muscles with a seizure that prevents adequate oxygenation from either a passive nonrebreather mask or active bag-mask ventilation.American Board of Pediatrics Content Specification(s)Discuss the indications and contraindications for bag-mask ventilationDescribe the key steps and potential pitfalls in performing bag-mask ventilationDiscuss the complications associated with bag-mask ventilationKnow the anatomy and/or pathophysiology relevant to bag-mask ventilationQuestion: 2An 8-year-old boy is brought to the emergency department for evaluation of vomiting and lethargy. He had a craniopharyngioma resected several years ago and has done well on medications, not requiring any subsequent surgeries or hospitalizations. He developed low-grade fever, vomiting, and diarrhea 3 days ago, and his symptoms have persisted. The boy has been unable to tolerate oral fluids today and has become increasingly sleepy and lethargic. His mother reports that she has not given him his regular medications for 2 days due to nausea and vomiting. On physical examination, the listless and ill-appearing boy has a temperature of 36.3°C, heart rate of 140 beats/min, respiratory rate of 22 breaths/min, and blood pressure of 82/60 mm Hg. He is somnolent but arouses with verbal stimulation. His pupils are equal and reactive to light, and the remainder of his neurologic examination findings are normal. He exhibits tachycardia, delayed capillary refill of 3 seconds, and slightly diminished peripheral pulses. All other findings are within normal parameters. Laboratory evaluation reveals:Sodium, 130 mEq/L (130 mmol/L)Potassium, 3.4 mEq/L (3.4 mmol/L)Chloride, 100 mEq/L (100 mmol/L)Bicarbonate, 14 mEq/L (14 mmol/L)Blood urea nitrogen, 26 mg/dL (9.3 mmol/L)?Creatinine, 0.7 mg/dL (61.9 μmol/L)Glucose, 42 mg/dL (2.3 mmol/L)Of the following, the MOST appropriate initial management for this boy includes administration ofA.dextrose 5% in half normal saline solution at 65 mL/hr, levothyroxine, and hydrocortisoneB.dextrose 10% in water 20 mL/kg, levothyroxine, and methylprednisolone sodiumC.dextrose 25% in water 2 mL/kg, normal saline solution 20 mL/kg, and hydrocortisoneD.normal saline solution 20 mL/kg, fludrocortisone acetate, and hydrocortisoneE.oral rehydration solution, levothyroxine, and prednisoneCorrect answer CThe boy described in the vignette is displaying signs and symptoms of hypopituitarism and secondary glucocorticoid deficiency precipitated by an acute illness and medication noncompliance. Both his hypoglycemia and hypovolemia require rapid correction, which can be facilitated through the administration of a combination of isotonic saline and dextrose. Intravenous hydrocortisone should be used in an unstable patient who has hypopituitarism for rapid correction of the cortisol deficiency and to support vascular tone. A common dosing regimen is hydrocortisone 2 mg/kg or 40 mg/m2. Because this boy’s primary deficit is pituitary, mineralocorticoid concentrations should be maintained, making fludrocortisone acetate replacement unnecessary.?In addition, hydrocortisone has both glucocorticoid and mineralocorticoid activity. Thyroid hormone replacement should not be undertaken in a patient who has hypopituitarism until cortisol concentrations have been corrected. Early correction of thyroxine concentrations may result in more rapid clearance of circulating cortisol, worsening cortisol deficiency. Hypotonic fluids, such as dextrose 10% in water, are inappropriate for volume expansion and may be particularly dangerous for a patient who has hypovolemic shock and cortisol deficiency. Oral rehydration or maintenance intravenous fluid administration is inadequate for a patient in hypovolemic shock.Hypopituitarism can result from a variety of insults, including tumors in or around the pituitary gland, therapy for such tumors such as surgery and radiation, infiltrative processes, infection, trauma, and hypothalamic dysfunction. Tumors and their treatment are the most common causes.The clinical manifestations of hypopituitarism are associated with the rate of onset, severity, and extent of pituitary injury. If the pituitary dysfunction is caused by a tumor, symptoms related to the mass may predominate, including headaches, visual disturbances, or vomiting. Deficiency of one, several, or all pituitary hormones may ensue, depending upon the location, nature, and severity of the insult.?The specific hormone(s) involved determine(s) which target glands are affected and what constellation of signs and symptoms occur. Acute onset of hormone deficiency is more likely to produce significant symptoms, while gradual loss of function may produce mild or no noticeable symptoms. The Table lists the signs, symptoms, complications, and treatment associated with specific hormone deficiencies.Treatment of hypopituitarism is based on the specific hormone deficiencies. Acute cortisol deficiency, particularly during times of physiologic stress, as with the boy in the vignette, may result in cardiovascular collapse and requires immediate replacement of cortisol as well as intravascular volume expansion. Maintenance therapy involves the use of glucocorticoid in an amount and timing designed to mimic the normal cortisol secretion pattern as closely as possible while maximizing compliance. Families should be instructed to increase dosing (“stress dose”) during times of acute illness. Management of other pituitary hormone deficiencies should be guided by clinical symptoms and hormone values and generally is the same as the treatment of hormone deficiencies associated with the involved target glands.American Board of Pediatrics Content Specification(s)Recognize signs and symptoms of hypopituitarismKnow the management of acute hypopituitarismUnderstand the complications of acute and chronic hypopituitarismQuestion: 3A 5-year-old girl presents to the emergency department with a 1-day history of fever and limp. She has complained intermittently of right leg pain over the past week, but today she began limping and then stopped bearing weight on the right leg. Her mother says that the child points to the thigh when asked where it hurts. There has been no trauma, redness, swelling, or rash. She had vomiting for 1 day last week, but that resolved. On physical examination, the well-appearing girl is alert and cooperative, and her temperature is 38.4°C, heart rate is 118 beats/min, respiratory rate is 20 breaths/min, and blood pressure is 92/60 mm Hg. The only finding of note is limited range of motion of the right hip, particularly with external rotation. She is willing to bear weight and takes a few steps, with a noticeable limp on the right leg. Laboratory evaluation reveals:?White blood cell count, 10.5x103/μL (10.5x109/L) with 48% neutrophils, no bands, and 37% lymphocytesHemoglobin, 14.8 g/dL (148 g/L)Hematocrit, 46.8% (0.468)Platelet count, 372x103/μL (372x109/L)Erythrocyte sedimentation rate (ESR), 11 mm/h (normal, <20 mm/h)C-reactive protein, 3.8 mg/dL (normal, <1 mg/dL)Ultrasonography of both hips appears normal. Anteroposterior (Fig. 1) and frog’s leg (Fig. 2) views of the hips/pelvis are obtained.Figure 1?Figure 2Of the following, the MOST appropriate next steps in management are toA.administer an analgesic and admit the girl for further evaluationB.consult orthopedics for application of a spica cast and follow-up evaluationC.discharge the girl with nonsteroidal anti-inflammatory medicationD.perform needle aspiration of the right hip under sedationE.send blood for assessment of antinuclear antibodies and consult rheumatologyCorrect answer AThe girl described in the vignette has abnormal radiographs demonstrating a “moth-eaten” appearance of the right ischium, which could represent infection (osteomyelitis) or an infiltrative process (leukemia, lymphoma, metastatic tumor). Because she has a fever, antibiotic treatment should be considered in consultation with orthopedic surgery while further evaluation is completed. In the interim, treatment with analgesic and hospital admission is the appropriate course of action. In this case, magnetic resonance imaging subsequently confirmed infiltration of the right ischium as well as the left proximal femur, and further evaluation demonstrated pre-B-cell lymphoma.If the radiographs appeared normal, this child’s presentation would be consistent with transient synovitis, and treatment with anti-inflammatory medication and outpatient follow-up would be appropriate. Although orthopedic involvement would not be inappropriate in this case, placement of a spica cast is typical for femur or hip fractures or dislocations, which is not seen on the girl’s radiographs. Needle aspiration can be performed to obtain joint fluid in cases of suspected septic arthritis, but this girl’s normal blood count and erythrocyte sedimentation rate, negative ultrasonographic findings, and ability to bear weight make this diagnosis less likely. Further, the radiographs suggest an infiltrative process of the ischium rather than a septic joint. Assessment of antinuclear antibodies can be useful in the evaluation of potential rheumatologic disorders, but this girl’s history of acute involvement of a single joint with fever, along with the radiographs, do not suggest rheumatologic disease.Limp is defined as an abnormal gait and can result from congenital, infectious, inflammatory, traumatic, or neoplastic processes involving the spine, pelvis, abdomen, or musculoskeletal and soft tissues anywhere from the hip to the toes. Table 1 lists common causes of limp according to age, and Table 2 lists causes of limp according to pathophysiology.?Evaluation of the child who has a limp begins with a thorough history and physical examination, and the information obtained is used to guide further diagnostic evaluation. Key historical data include:Fever and other infectious symptomsTraumaSystemic symptoms (pallor, fatigue, bruising/bleeding, rash, weight loss)Previous episodes of bone/joint painWith the exception of poorly fitting shoes or obvious splinter or soft-tissue injury to the sole of the foot, most cases of limp warrant radiographic evaluation. It is important to remember that pain originating from the hip may be referred to the groin, thigh, or knee due to common innervation by the obturator nerve. If infectious, inflammatory, or neoplastic causes are suspected, laboratory evaluation should include a complete blood count and differential count, peripheral smear, erythrocyte sedimentation rate, and C-reactive protein assessment. Blood culture should be obtained for febrile patients in whom osteomyelitis or septic arthritis are being considered.In a study of nearly 300 children who had acute hip pain, Kocher and associates developed a clinical evaluation tool to determine the likelihood of septic arthritis. After retrospectively reviewing all of the cases, they used univariate analysis and multiple logistic regression analyses to compare patients who had true or presumed septic arthritis with those who had other diagnoses. Four predictors were ultimately identified:FeverElevated white blood cell count (>12x103/μL [12x103/L])Elevated inflammatory marker(s) (ESR >40 mm/h)Inability to bear weightThe likelihood of septic arthritis based on number of predictors was: less than 0.2% with zero, 3% with one, 40% with two, and 99.6% with four predictors. Based on this algorithm, this girl had one predictor (fever) and a resultant 3% likelihood of having septic arthritis.If results of the initial laboratory and radiographic evaluations are normal and the child is able to bear weight, discharge with outpatient follow-up is appropriate. Children who have fever and elevated inflammatory markers or white blood cell counts should receive further evaluation for possible septic arthritis, osteomyelitis, or tumor. Such evaluation may include computed tomography scan, magnetic resonance imaging, bone scintigraphy, or ultrasonography to identify joint effusion or to guide joint aspiration. Hospitalization should be considered for patients who are unable to bear weight after administration of appropriate analgesic agents.American Board of Pediatrics Content Specification(s)Know the etiology by age and pathophysiology of limpingPlan diagnostic evaluation and initial intervention for patients who limpRecognize serious and/or life-threatening causes of limpingQuestion: 4You are evaluating an 8-week-old febrile infant in the emergency department. The previously healthy and otherwise well-appearing baby has no obvious source of fever, and a rectal temperature of 39.5°C (103.1°F) is the only abnormal vital sign. You have collected blood for culture and a complete blood cell count. You decide to use an additional 1 mL of collected blood for an additional screening test. Although the laboratory can assess both serum procalcitonin and C-reactive protein, only one test can be performed on the small volume of extra blood. You plan to choose the test based on its ability to discriminate between infants with or without serious bacterial infection.Of the following, the BEST predictor of the accuracy of serum procalcitonin over C-reactive protein for such discrimination is theA.area under receiver operating curveB.positive and negative likelihood ratioC.positive and negative predictive valueD.pretest and posttest probabilityE.sensitivity and specificityCorrect answer: ADiagnostic accuracy is the most fundamental characteristic of a test, measuring its ability to detect the presence or absence of disease. Receiver operating characteristic (ROC) plots and areas under the ROC curves (AUROCs) provide the best measures of test accuracy and can be used to compare the ability of two or more tests to discriminate over the complete spectrum of health states.The decision to choose a particular test depends on the discriminatory ability of the test, test availability and cost, cost of appropriate treatment should the test result be positive, and whether treatment is detrimental should the test result be falsely positive. A test must be both accurate and clinically useful. The clinician must use evidence-based principles and the characteristics of the test itself to decide which test is optimal for the given clinical situation. It is important to understand the difference between test characteristics before making evaluation and management decisions.The commonly used terms to define characteristics of tests are the sensitivity, specificity, positive and negative predictive values, and positive and negative likelihood ratios. Sensitivity is defined as the ability to identify correctly those who have disease (true-positives represent the proportion of people with disease who have a positive test); specificity is the ability to identify correctly those who do not have disease (true negatives represent the proportion of people without the disease who have a negative test). The primary limitation of sensitivity and specificity is that they do not provide the clinician with the probability of disease in a particular patient. Sensitivity and specificity are inherent characteristics of the test itself that do not vary with prevalence of disease.The predictive values of tests describe a patient’s probability of having disease once the results of the tests are known. Positive predictive value of a test is defined as the proportion of people who have positive test results and actually have the disease; negative predictive value is defined as the proportion of people who have negative test results and do not have disease. The major limitation of predictive values is that they are affected by the prevalence of disease in the population being tested. Published predictive values of tests should not be applied to populations whose disease prevalence differs from that of the population in the published study.The sensitivity and specificity of a test can be combined into one measure termed the likelihood ratio, which is defined as the ratio between the probability of observing the specific result in patients who have the disease in question and the probability of observing the result in patients who do not have the disease. A major advantage of likelihood ratios is that they can be used to help the clinician adapt sensitivity and specificity of tests to individual patients. The reason to perform any test is to determine posttest probability. In other words, a positive test may increase the pretest probability, and a negative test may decrease the pretest probability. Pretest and posttest probabilities are estimates of disease, not characteristics of tests.Although it is easy to understand and often convenient to categorize states of health as disease and nondisease, based on one cutoff value of the test result, this approach is not practical. For example, using a cutoff value of 15.0x103/mcL (15.0x109/L) for a white blood cell (WBC) count is convenient in a clinical setting to help discriminate between febrile infants at risk for developing serious bacterial infections. However, tests such as the WBC count are continuous variables that have a spectrum of sensitivities, specificities, predictive values, and likelihood ratios. Therefore, reporting only one value of a test’s sensitivity or specificity is misleading and a hazardous oversimplification of accuracy.In fact, when the cutoff value is increased (assuming larger values indicate a higher chance of positive outcome), the proportion of true-positives (sensitivity) and false-positives (1-specificity) decreases. ROC plots provide a graphic view of the entire spectrum of this proportion (sensitivity/1-specificity) and demonstrate the tradeoff between sensitivity and specificity. A perfect test would have sensitivity and specificity both equal to 1. Thus, the ROC curve for a perfect test would start at origin (0,0) and proceed ?vertically up the y axis to (0,1) and then horizontally to (1,1). A good test is close to this ideal. The closer the curve follows the left and top borders of the ROC space, the more accurate is the test. The closer the curve comes to the 45-degree diagonal, the less accurate is the test.The performance of a diagnostic variable can be quantified by calculating the AUROC, a measure of the accuracy of the test. The AUROC is the percentage of times the test correctly classifies two patients in a random pair (one from the disease group and one from the nondisease group). The traditionally used cutoffs for test accuracy are AUROCs of 0.9 to 1 (excellent), 0.8 to 0.9 (good), 0.7 to 0.8 (fair), 0.6 to 0.7 (poor), and 0.5 to 0.6 (fail). For example, a recent article compared test characteristics of serum procalcitonin (PCT), C-reactive protein (CRP), absolute neutrophil count (ANC), and WBC count in the emergency department evaluation of febrile children and found the following AUROC results (Figure):PCT: 0.82 (95% confidence interval [CI]: 0.78–0.86CRP: 0.85 (95% CI: 0.81–0.88)ANC?: 0.74 (95% CI: 0.70–0.78)WBC count: 0.71 (95% CI: 0.66–0.75)The difference between AUROCs for PCT or CRP and AUROCs for ANC or leukocyte count was statistically significant. There was no significant difference between AUROCs of PCT and CRP (P=0.748). The optimum statistical cutoff value for detecting serious bacterial infection was 0.8 ng/mL (sensitivity, 69.1%; specificity, 85.3%) for PCT, 32 mg/L (sensitivity, 84.0%; specificity, 75.5%) for CRP, 10.47x103/mcL (10.47x109/L) (sensitivity, 84.9%; specificity, 47.4%) for WBC count, and 6.45x103/mcL (6.45x109/L) (sensitivity, 81.8%; specificity, 62.3%) for ANC.The advantages of using ROC plots are:Graphs are easy to compare and comprehendPlots are comprehensive representations of pure accuracy (ie, discriminatory ability over the entire range of the test)They can provide an optimal cutoff for the tradeoff between sensitivity and specificity (along with confidence intervals around the cutoff) to compare between testsThe results are independent of disease prevalenceThe need for cumbersome calculations and statistical software are the obvious disadvantages of using ROC curves.American Board of Pediatrics Content Specification(s)Understand the interpretation and application of receiver-operator curves (ROC)Question: 5You are examining a 5-year-old boy who has had abdominal pain for 2 days and frequent bloody stools for 1 day. According to his mother, the boy was well until 2 days ago, when he started having a high-grade fever without any chills or rigors. He subsequently complained of crampy abdominal pain and started developing small-volume, loose stools, with six to eight episodes per day. He has no history of vomiting or change in urine output. His past medical history contains no findings of note. He has no recent history of travel or exposure to any pets. On physical examination, the tired but alert child has a temperature of 39.0°C, heart rate of 120 beats/min, respiratory rate of 22 breaths/min, blood pressure of 90/60 mm Hg, brisk capillary refill, and easily palpable peripheral pulses. He has no meningeal signs, and his mucous membranes appear to be moist. He exhibits generalized tenderness on abdominal examination but no evidence of rigidity, guarding, or any palpable mass. His rectal examination is positive for blood. His complete blood count reveals a white blood cell count of 51.0x103/μL (51.0x109/L), with a 70% neutrophilic predominance and a normal platelet count. While waiting in the emergency department, the child has a brief generalized tonic-clonic seizure.Of the following, the test that is MOST likely to establish the diagnosis isA.abdominal computed tomography scanB.barium enemaC.lumbar punctureD.stool cultureE.urinalysisCorrect answer: DThe boy described in the vignette has dysentery due to Shigella with an associated leukemoid reaction. Seizure is the most common neurologic presentation in acute shigellosis, and stool culture establishes the diagnosis.Although a lumbar puncture may part of the evaluation of a febrile child who has seizures, meningitis is unlikely in this well-appearing boy, who has no meningeal signs. Abdominal ultrasonography or a contrast enema can be used to establish the presence of intussusception, an important consideration in the differential diagnosis, but seizure is not a common manifestation of intussusception. Abdominal computed tomography scan might be helpful to assess for an inflamed appendix, which occasionally can present with bloody diarrhea due to irritation of the colon. However, the absence of localizing abdominal signs and the presence of seizures make this condition less likely. Finally, urinalysis may be helpful to evaluate for hemolytic-uremic syndrome (HUS) due to gastrointestinal infection with Escherichia coli O157H7. This bacterium produces a shiga-like toxin that can cause seizures. Although hematuria on a urinalysis can aid in the investigation of HUS, the diagnosis is established by demonstrating microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. For this combination of findings, complete blood count and serum chemistry assay are required.The World Health Organization (WHO) defines diarrhea as the passage of three or more loose or watery stools per day. Acute infectious gastroenteritis due to viruses accounts for most bouts of diarrhea in developed countries, although watery or frequent stools may be the initial manifestation of a wide spectrum of acute (Table 1) and chronic disorders (Table 2). A number of disorders causing diarrhea may be life-threatening in children, including intussusception, HUS, pseudomembranous colitis, appendicitis, toxic megacolon, and congenital secretory diarrheas.A detailed history and complete physical examination provide clues to the laboratory testing indicated for patients who have diarrhea. The first priority is to decide if the patient is clinically dehydrated. If the child is not dehydrated, and if it appears that the illness is a simple case of diarrhea due to viral gastroenteritis, no laboratory tests are required for management. If the patient does appear to be dehydrated, serum electrolytes may be useful to help guide therapy.A stool culture is indicated for assessment of bloody diarrhea. Depending on the clinical scenario, other testing for the cause of diarrhea should be considered, such as stool smear for leukocytes, ova and parasites test, and assays for Clostridium difficile toxin.A logical approach to a patient who has diarrhea is to stratify the condition by the presence or absence of fever or blood in the stool. For example, febrile patients who have nonbloody diarrhea are more likely to have viral enteritis, while febrile children who have bloody diarrhea are more likely to have infectious enteritis (Salmonella, Shigella, Campylobacter) or pseudomembranous colitis. Nonbloody diarrhea in afebrile patients could be due to viral infections, antibiotic use, overfeeding, or excessive juice intake. Afebrile children who have bloody diarrhea represent the most worrisome category because many patients who have intussusception, HUS, or pseudomembranous colitis have this symptom constellation. Milk protein allergy can also present with bloody stools in the absence of fever.American Board of Pediatrics Content Specification(s)Recognize serious and/or life?threatening causes of diarrheaPlan diagnostic evaluation and initial intervention for patients with diarrheaKnow the etiology by age and the pathophysiology of diarrheaQuestion: 6A 3-month-old boy presents to the emergency department with a rash on her diaper area, face, and neck that began 6 weeks ago and has progressed in appearance and distribution. On two earlier visits to the pediatrician, he was prescribed topical nystatin and then mupirocin with 1% hydrocortisone cream, which the mother has been applying as advised.?The infant is otherwise well, feeding normally, and gaining weight. No findings are of note in the family history. On physical examination, the infant is afebrile and appears well. His liver edge is palpable 5 cm below the costal margin. The rash, which initially was localized to the intertriginous area of the diaper area, now extends to the lower torso (Fig. 1). In addition to the scaling areas, there are some small discrete reddish-brown papules. The lesions have no unusual odors.Figure 1: Rash on the lower torso..Of the following, the MOST appropriate next step is to obtain a:plete blood countB.serum zinc measurementC.swab for bacterial cultureD.swab for potassium hydroxide preparationE.allergy skin testingCorrect answer: AIntertrigo in an infant has a wide differential diagnosis. Common causes are seborrheic dermatitis (SD), candidiasis, and atopic dermatitis. The rash described for the infant in the vignette appears to be refractory to treatment with topical steroids and antifungal agents, first-line agents that typically are used to treat SD and Candida infections, respectively. Atopic dermatitis characteristically spares the diaper area.?Allergy skin testing is neither indicated nor effective in a 3-month-old infant.Severe and recalcitrant intertriginous dermatitis may be a symptom of a more serious condition such as Langerhans cell histiocytosis (LCH), acrodermatitis enteropathica (AD), or underlying congenital or acquired immune deficiency. The rash in this infant appears to be well-demarcated, with scaly macules, papules, and plaques and some purpuric areas. In addition, discrete reddish-brown papules, petechiae, and erosions may be seen in LCH. This presentation, in conjunction with the noted hepatomegaly, is very suggestive of LCH. Infantile LCH (formerly called Letterer Siwe disease) is an aggressive form of multifocal disease that involves skin and internal organs such as the bone marrow, liver, spleen, and bones. Hepatosplenomegaly, anemia, and thrombocytopenia frequently are noted, making a complete blood count helpful for the infant in the vignette. Definitive diagnosis is established with a skin biopsy.?A serum zinc assessment would assist in the diagnosis of AD. Zinc deficiency (<50 mcg/dL [7.7 mcmol/L]) usually is associated with periorificial involvement, chronic diarrhea, alopecia, irritability, and malnutrition. Severe, intractable SD also may be seen in advanced cases of congenital HIV infection, but this infant appears well and thriving. Further, cutaneous manifestations of congenital HIV include severe erosions and ulcerations that involve the perineal area, especially the gluteal cleft.Bacterial (streptococcal) intertrigo characteristically causes well-demarcated, beefy red, macerated, moist lesions with scant bleeding and without satellite lesions. The infant usually experiences pain and discomfort during diaper changes. The rash often has a very distinct malodor. Conversely, satellite lesions are common with Candida intertrigo. These two organisms may coexist in diaper dermatitis.SD has a bimodal peak that presents between 1 and 6 months of age and during teenage years. The skin lesions typically are salmon-pink scaling patches on the face (Fig. 2), scalp (Fig. 3), external ear, and intertriginous body folds, areas that are rich in sebaceous glands. Pruritus is not a dominant feature, unlike with atopic dermatitis. The pathogenesis of SD is postulated to be the cutaneous fungus Malassezia furfur. Hence, topical agents such as 2% ketoconazole shampoo are effective. Other therapeutic agents that are helpful in severe cases include 1% to 2.5% hydrocortisone cream, 1% pimecrolimus, and 0.03% to 0.1% tacrolimus ointment. The natural course of both infantile and adolescent SD is disappearance with age.The differential diagnosis of SD includes atopic dermatitis, candidiasis, LCH, AD, streptococcal intertrigo, congenital and acquired immune deficiencies, and psoriasis vulgaris. Childhood psoriasis typically has an onset between 6 and 18 months and is characterized by well-defined, scaly plaques. There is usually a positive family history.Figure 2: Salmon-pink, scaling patches on the face of an infant who has seborrheic dermatitisFigure 3: Scaling of the scalp in an infant who has seborrheic dermatitis. American Board of Pediatrics Content Specification(s)Know the typical age(s) of onset of seborrheic dermatitisRecognize signs and symptoms of seborrheic dermatitisPlan management of acute seborrheic dermatitisDifferentiate between seborrheic dermatitis and other similar skin conditionsQuestion: 7A 5-year-old girl presents to the emergency department with primary complaints of dizziness and hearing loss in the right ear. She states that she feels as if the room is spinning around her. Her parents report that she has been uncomfortable when sitting upright for the past day or so, and she has had multiple episodes of vomiting throughout the day. They deny ingestion or trauma. She has had a mild upper respiratory tract infection for about 1 week without sore throat, pain, or headache. No one else in the family has been sick. Physical examination of the nontoxic, anxious young girl shows a temperature of 37.3°C, heart rate of 120 beats/min, blood pressure of 110/70 mm Hg, and pulse oximetry reading of 100% in room air. The girl is comfortable lying down. Otologic examination reveals no evidence of inflammation or suppuration behind the tympanic membrane. Nothing of note is apparent on her cardiovascular examination. On neurologic evaluation, you note nystagmus when she is brought to a sitting position. There are no other neurologic abnormalities.Of the following, the MOST likely diagnosis for this girl isA.acute depressive syndromeB.antifreeze ingestionC.cerebellar tumorD.labyrinthitisE.presyncopeCorrect answer DEvaluation of the child experiencing dizziness starts with determination of true vertigo or pseudovertigo. True vertigo always includes a sense of rotation of the patient relative to the environment or vice versa. It worsens with head movement, and acute events are often accompanied by nystagmus. This can be difficult to assess in a nonverbal patient. Pseudovertigo is not accompanied by the sensation of rotation. Patients who are light-headed, ataxic, weak, anxious, or hyperventilating may use the word “dizzy” to describe how they feel when, in fact, there is no true sense of rotation.Identification of the dizziness as true vertigo helps narrow the cause to a disturbance of the vestibular system, either in the central components (brainstem, cerebellum, cortex) or in the peripheral components (labyrinth). Peripheral causes are more often associated with hearing impairment; central causes usually spare the hearing. The peripheral sensory organs related to equilibrium are called the labyrinth and are composed of the semicircular canals (stimulated by rotary motion of head) and the vestibule (stimulated by gravity) (Fig. 1 and Fig. 2). The impulses from these areas are carried by the eighth cranial nerve to the vestibular nuclei in the brainstem and cerebellum. Patients who have true vertigo almost all have nystagmus, with the fast component toward the affected side and in the direction of the perceived rotation.The girl described in the vignette has true vertigo. The combination of acute-onset vertigo, vomiting, unilateral hearing loss, and nystagmus in a child who has had a recent respiratory infection strongly suggests labyrinthitis as the most likely diagnosis. There is no history or evidence of ingestion, although that should always be a consideration with acute neurologic change. Ethylene glycol (antifreeze) ingestion would not cause the symptoms described. Depression can present with a variety of symptoms, but the acute onset and persistence of nystagmus and hearing loss make an organic cause far more likely. Presyncope suggests a near-fainting, acute perfusion abnormality from a variety of causes, but presyncope is not accompanied by nystagmus. A cerebellar tumor can present with some of the reported signs and symptoms, but they are usually chronic or progressive rather than acute. In addition, cerebellar tumors often are accompanied by morning headache, ataxia, lethargy, confusion, numbness, vision impairment, speech difficulty, disorientation, and signs of increased intracranial pressure. None of these additional features are present in this child.Acute labyrinthitis is an infection of the inner ear that is seen most commonly in patients who do not (but can) have concomitant otitis media. Inflammation of the labyrinth affects both branches of the vestibulocochlear nerve (eighth cranial nerve), resulting in both hearing changes and vertigo. The condition is generally unilateral, and most children do not appear to be significantly ill. This may be the result of a systemic viral infection or a viral infection that is confined to the labyrinth. There is a strong association with a recent viral respiratory infection. Specific viruses that have been associated with labyrinthitis include herpesviruses, influenza, measles, mumps, and Epstein-Barr virus. The symptoms are usually self-limited, with typical rapid resolution of both the vertigo and hearing loss.Acute labyrinthitis can also be associated with otitis media, generally with a bacterial cause, and can be a much more serious disease. Acute labyrinthitis can be further classified as serous or suppurative. Serous labyrinthitis is caused by toxic or inflammatory mediators that invade through the oval or round windows from an adjacent infection in the middle ear. The condition can be challenging to recognize in young children and in those who have concomitant conductive hearing impairment because of fluid in the middle ear from otitis media. Suppurative labyrinthitis results from direct bacterial invasion of the labyrinth, usually from adjacent otitis media. This rare but severe infection must be treated aggressively.Suppurative or serous labyrinthitis associated with otitis media should be treated with appropriate antibiotics directed at the typical pathogens. Anatomic abnormalities or environmental exposures should be noted and managed, as needed. Specialty consultation may be indicated. Patients who have either bacterial or viral labyrinthitis may benefit from antivertiginous medications such as meclizine or dimenhydrinate for acute or severe episodes. Benzodiazepines may also be useful. Steroids may be indicated if an autoimmune cause is suspected.It is important to remember that vertigo is a symptom of an underlying disease process. Vertigo can be categorized as acute or chronic. Acute vertigo can have infectious causes, with direct or reactive inflammation due to viral, bacterial, or fungal diseases, or can be postinfectious, traumatic, toxic (ingestion), or vascular (stroke). Chronic and chronic-recurrent causes include migraine headaches, seizures, and benign paroxysmal vertigo.Among the peripheral causes of vertigo are:Suppurative?and serous (“toxic”) labyrinthitisExternal ear impactionRamsey Hunt syndrome (herpes zoster infection of ear canal and facial palsy)Cholesteatoma with a draining fistula (keratin collection on the tympanic membrane that erodes the temporal bone and labyrinth)Vestibular neuritisBenign paroxysmal vertigo (<5 years of age; characterized by short and sometimes clustered episodes associated with pain, emesis, pallor, sweating, and nystagmus)IngestionsTemporal bone fracturePosttraumatic vestibular concussionMénière disease (1- to 3-hour episodes; uncommon before 10 years of age)Central causes of vertigo include:TumorMeningitisEncephalitisIncreased intracranial pressureMultiple sclerosisTraumaSeizureMigraine (up to 19% of auras noted with presenting migraines)StrokeMotion sicknessParoxysmal torticollis of infancyAmong the medications that have ototoxic effects are anticonvulsant overdoses, aminoglycosides, furosemide, ethacrynic acid, streptomycin, minocycline, salicylates, and ethanol.Physical examination should include middle ear (canal lesion, tympanic membrane structure and integrity) and neurologic evaluations. The neurologic examination should focus on auditory, vestibular, and cerebellar systems, and the examiner should look for associated findings beyond the previously identified issues. Peripheral vertigo presents with nystagmus and auditory changes (hearing loss, tinnitus) without other associated neurologic findings.One approach to emergency department evaluation of the patient who has vertigo or pseudovertigo is outlined by Teach in the Textbook of Pediatric Emergency Medicine (6th ed). Abnormalities of the ear, including cerumen impaction or middle ear effusion, are often managed without any ancillary studies. Vertigo that occurs after acute head trauma should be evaluated further with head computed tomography (CT) scan. Patients who have abnormal findings on cold caloric testing or who have chronic or progressive symptoms with neurologic deficits other than hearing loss may have a central cause. They should be evaluated further with CT scan or magnetic resonance imaging. Laboratory evaluation is directed by the presentation. Electroencephalography may be indicated if the vertigo is associated with a decreased level of consciousness or other seizurelike activity. Audiometric evaluation may be indicated.Figure 1: Ear anatomy. From National Institute on Deafness and Other Communication Disorders.Figure 2: Inner ear anatomyAmerican Board of Pediatrics Content Specification(s)Know the etiology and pathophysiology of labyrinthitisRecognize the signs and symptoms of labyrinthitisPlan the management of labyrinthitisQuestion: 8You are talking on the phone with emergency medical services (EMS) personnel who responded to a call for a 5-year-old girl who was found having a seizure in her home. The paramedics started oxygen and intravenous fluids, measured her glucose (72 mg/dL [4.0 mmol/L]), and administered rectal diazepam, but the seizure continues. You recommend repeated diazepam administration. After two doses, the child experiences significant hypoventilation. You recommend airway management with endotracheal intubation, and the paramedics proceed as per their established airway management protocol.Of the following, this process is MOST illustrative ofA.care beyond scope of practice for EMS personnelB.evidence of EMS scope of practice limitationsC.offline medical controlD.off- and online medical controlE.online medical controlCorrect answer DThe actions described in the vignette represent an example of both offline (use of established guidelines and protocols) and online (direct contact with a medical supervisory physician) medical control. EMS personnel can function in both areas, with specific care capabilities determined by the EMS personnel classification, scope of practice, and local policies and procedures. Scope of practice is determined nationally and locally. Paramedics (EMT-P) can manage airways because of their additional education and credentialing. Emergency medical technicians (EMT), on the other hand, would be practicing outside their scope of practice if they attempted intubation. The use of offline medical control and field policies is crucial to the ability of first responders to assess and intervene rapidly in life-threatening situations. Pre-established policies enable EMS personnel (front-line provider to off-site participants) to understand options and interventions for variable presentations, which might include drowning, resuscitation, pain management, and sudden infant death, as well as logistical issues such as refusal of transport responses.When additional guidance is required, EMS personnel contact a base station and a medical command (control) physician. This contact enables standard and expected oversight and medical direction in real time (on-line medical command). The base station facility and personnel serve as a home for the oversight and additional medical expertise needed to provide effective on-site medical services. Depending on the situation, pediatric medical oversight may be especially crucial due to the provider’s limited education about, exposure to, and experience with the myriad potential presentations in this population. Pediatrics may account for only 15% to 20% of the EMS provider’s routine patient exposures, and most of those patients are not critically ill. The availability of a pediatric emergency medicine expert to help guide the care of ill children bridges the gap between clinicians who have good general skills and the pediatric-specific knowledge required to provide optimal care.Pediatricians and pediatric emergency physicians can add greatly to the development of offline field protocols and well as online medical direction. For maximum efficacy as an online medical consultant, the pediatric clinician must be literate with pediatric illness, well-versed in acute and emergency interventions, and have a strong working knowledge of the EMS environment, including provider skills, scope of practice, logistic abilities, and constraints. Clear and concise communication skills are also required.American Board of Pediatrics Content Specification(s)Distinguish between on line (direct) and off line (indirect) medical directionUnderstand the role of field policies (eg, intubation, sudden infant?death syndrome, physician on scene, treatment refusal, interfacility?transport) in managing emergency medical services for childrenUnderstand the role of the base hospitalKnow the physician's role in medical direction for pediatricsKnow the epidemiology of pediatric out of hospital careJULY 2011Question: 1You are evaluating a 4-day-old infant who was referred from an outlying emergency department for management of vomiting, decreased feeding, and lethargy. She was born at term to a 22-year-old woman who had received appropriate antenatal care. The delivery and immediate perinatal period were uneventful, and the infant and mother were discharged 2 days after the birth. The mother noticed yesterday that the baby was not breastfeeding as vigorously as before. Two episodes of emesis that she described as nonbilious and nonprojectile prompted the emergency department visit. There is no history of fever or exposure to sick contacts, and bowel and bladder movements are described as unchanged. At the referring emergency department, the infant was described as sleepy but arousable, and her vital signs were normal, except for a respiratory rate of 70 breaths/min in the presence of a normal pulse oxymetry reading in room air. Physical examination was unrevealing. Initial blood glucose measured 80 mg/dL (4.4 mmol/L), and other laboratory investigations revealed normal blood counts, serum electrolytes, serum lactate, anion gap, and urinalysis. A capillary blood gas on room air was suggestive of primary respiratory alkalosis. Chest radiography and electrocardiography before transfer were reported as normal. As you examine the baby, she continues to display tachypnea without subcostal or intercostal retractions, she is sleepy, and she does not want to feed. All other findings on physical examination are within normal parameters.Of the following, the MOST likely diagnosis isA.congenital adrenal hyperplasiaB.congenital heart diseaseC.pneumoniaD.pyloric stenosisE.urea cycle disorderCorrect answer ELethargy in the newborn is a nonspecific sign that almost always indicates severe systemic illness and warrants a comprehensive evaluation. An inborn error of metabolism should be suspected when a previously well newborn deteriorates clinically within a few days of birth. The combination of respiratory alkalosis with normal glucose, electrolytes, and anion gap described for the infant in the vignette suggests a urea cycle disorder.The presence of normal pulse oximetry values and normal chest radiography findings make pneumonia unlikely. Similarly, congenital heart disease is less likely to present with lethargy in the absence of systemic signs of congestive cardiac failure or cardiogenic shock. Pyloric stenosis generally is seen in young infants (typically 3- to 6-week-old males), who present with failure to thrive and a history of immediate postprandial nonbilious projectile emesis. Laboratory investigations reveal hypochloremic, hypokalemic metabolic alkalosis. Recent reviews on pyloric stenosis indicate that this condition is being diagnosed earlier, even before the development of the classic metabolic abnormality, but the condition is less likely to present within 3 to 4 days of birth than is a urea cycle disorder. Patients who have the salt-losing form of congenital adrenal hyperplasia, especially males, usually present by 1 to 2 weeks of age with failure to thrive, dehydration, hyponatremia, and hyperkalemia. Affected females have ambiguous genitalia.??Nitrogen, a waste product of peripheral (muscle) and enteral (dietary) protein breakdown, is converted into water-soluble urea for renal excretion by a complex metabolic pathway called the urea cycle. Hyperammonemia due to increased concentrations of nitrogen causes cerebral edema, central hyperventilation, and respiratory alkalosis, which are common early signs in newborns. Signs and symptoms of urea cycle defects are often nonspecific and can be confused with other systemic illnesses, such as sepsis, bacteremia, meningitis, metabolic abnormalities (dyselectrolytemia, hypoglycemia), and other inborn errors of metabolism. Most patients who have complete deficiency of enzymes present within 24 to 48 hours of initiation of feedings that provide the enteral protein load. As ammonia concentrations increase, patients develop poor feeding and vomiting, followed by increasing somnolence, lethargy, seizures, coma, and death. Those who have partial deficiency of the enzyme can present in late childhood or adulthood. Their presentation is characterized by episodes of hyperammonemia resulting in vomiting, mental confusion, ataxia, agitation, irritability, and combativeness, rarely progressing to seizures and coma.Hyperammonemia can also be seen in organic acidemias, fatty acid oxidation defects, and disorders of pyruvate metabolism. Patients who have organic acidemias exhibit metabolic acidosis or ketotic hypoglycemia; those who have fatty acid oxidation defects exhibit nonketotic hypoglycemia and present later in infancy. Pyruvate metabolic disorders are characterized by lactic acidemia and an elevated ammonia concentration. Other causes of hyperammonemia, including prematurity, dehydration, and liver failure, rarely result in plasma ammonia concentrations greater than 140 to 280 μg/dL (100 to 200 μmol/L).American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of urea cycle defectsQuestion: 2A 3-year-old boy who has developmental delay and tracheostomy-dependent chronic pulmonary disease presents to the emergency department with intermittent cyanotic spells over the past 3 hours. While in triage, the boy turns blue and is placed on oxygen and a monitor. A rapid assessment shows him to be awake and struggling to breathe, with significant sternal and subcostal retractions. His pulse oximetry reading is 62% with a marginal tracing. His heart rate is 134 beats/min. His eyes are open, but he is not interactive. He has no history of trauma, ingestion, foreign body aspiration, new food or environmental exposure, or previous seizure. His mother states that the entire family has been sick and this boy’s secretions have been thick and green for about 24 hours, requiring frequent suctioning.Of the following, the MOST appropriate next step in this patient’s care is to:A.administer albuterolB.administer intramuscular epinephrineC.administer lorazepam for possible seizureD.administer racemic epinephrineE.remove and replace the tracheostomy tubeCorrect answer EThe boy described in the vignette has evidence of an acute airway obstruction, and the history of thickened and colored secretions suggests a respiratory infection. The required initial management is to reestablish the patient’s patent airway. This can be accomplished by suctioning the tracheostomy, which may provide temporary relief, or changing the tracheostomy tube, which is likely plugged with thickened secretions. Most families have another tracheostomy tube with them to use. If not, replacement with a similar tube or an endotracheal tube of the same internal diameter (with care not to insert beyond the carina) can ensure a patent airway until definitive replacement. Oxygen should be delivered by face mask during tube replacement.Although there may be a reactive airway component to the patient’s illness, albuterol should not be the first intervention. There is no evidence of an acute allergic issue or anaphylaxis by history, so intramuscular epinephrine also would not be the first choice. A seizure possibly could cause respiratory obstruction and cyanosis, but this boy is awake and without seizure history, making that diagnosis and the need for lorazepam less likely. Racemic epinephrine is indicated for a patient whose respiratory distress is due to inflammation of the upper trachea (eg, croup, postextubation edema). Although this patient may have edema of the upper airway, clear evidence of obstruction should be addressed first.Knowledge of tracheal anatomy is important for the emergency care clinician. Tracheostomy tubes are placed to establish and ensure a stable airway for a variety of reasons, including upper airway obstruction, chronic ventilator needs, prolonged mechanical ventilation, obstructive sleep apnea, poor secretion control, and inadequate airway reflexes. After initial placement of a tracheostomy tube, taking it out during the healing process is associated with a high risk of losing the tract. Once the tube has been in place for more than 10 to 14 days, this is less of an issue. For a patient who has an established tracheostomy, the tract is well formed and usually amenable to straightforward tube replacement. If replacement of a recently placed tracheostomy tube is required, an otolaryngologist should be involved. The tube may need to be replaced in a controlled setting over a fiberscope, guide, or rigid bronchoscope to avoid placement into a false tract.Tracheostomy tubes are described by the internal diameter and external diameter. If the tube is too small, it may be inadequate, leading to increased airway resistance and work of breathing. More frequent suctioning is required, and there is an increased risk of obstruction from the secretions. Increased cuff pressures also are needed, potentially leading to mucosal ischemia.Typically, the tracheostomy tube has an obturator in the lumen to aid insertion. This rigid guide must be removed before ventilation. Most tubes are single-lumen, although some are double-lumen, enabling the inner tube to be removed and cleaned, as needed, while maintaining the outer tube in place. The tube may be fenestrated (holes in the tubing) or unfenestrated (open port at end only).Replacement of a tracheal cannula is well described in many textbooks and published articles. Complications of incorrect passage include airway obstruction; hypoxemia and ventilatory insufficiency; and creation of a false passage, leading to tissue damage, bleeding, and potential pneumomediastinum and pneumothorax.Ideally, the response to an obstructed tracheostomy tube should be undertaken by two clinicians. A towel or support should be placed under the patient's shoulders to extend the head and neck, functionally exposing the tracheal site, tightening the tissues around the stoma, and bringing the trachea closer to the skin surface.?Suctioning should be attempted through the current tracheostomy tube for a short period, followed by 100% oxygen administration. If this proves to be a successful temporizing measure, a more controlled tracheostomy tube change can be accomplished. If not, the tube must be immediately removed and changed. This sequence and process of tracheostomy removal and replacement also applies to a tube that has become dislodged. The tracheostomy tube strings (tape) that secure the tube to the neck should be cut and the tube removed. A new cannula should be placed through the exposed tract (Figure). The flanges of the tracheostomy tube should be fitted to the contours of the neck, and ventilation/oxygenation should commence. If placement is successful, the tube should be secured with new tracheostomy tube tape by passing the tape through the flange holes and securing it snugly at the back of the neck (preferably over an adhesive-based foam). The chest should be auscultated and the patient assessed for improvement in oxygenation and ventilation. A chest radiograph should be obtained to document appropriate placement.If the tracheal stomal tract has constricted so that a tracheal tube cannot be inserted, a different approach may be needed. Placement of a smaller tracheal tube or endotracheal tube may temporize and stabilize the situation. A small oxygen catheter (10F or 14F) also can be used in conjunction with low-flow oxygen (1 L/min up to 3 L/min) if the patient is older than 3 years of age. A tracheostomy tube then may be able to be passed over the oxygen catheter, which functions as a soft stylet or guide. If this approach is also unsuccessful, bag-mask ventilation through the mouth or stoma or intubation from the mouth may be successful interventions.American Board of Pediatrics Content Specification(s)Discuss the indications and contraindications for replacement of a tracheostomy cannulaKnow the anatomy and pathophysiology relevant to replacement of a tracheostomy cannulaDiscuss the complications associated with replacing a tracheostomy cannulaDescribe the key steps and potential pitfalls in replacing a tracheostomy cannulaQuestion: 3A mother brings her 1-year-old boy to the emergency department about 15 minutes after she found him playing with an open bottle of oil of wintergreen. The 4-ounce bottle had not been previously used, and only a small amount of fluid was missing. The child’s breath and shirt smell of wintergreen. The mother thinks he may have ingested about a teaspoon fluid.Of the following, one of the EARLIEST clinical manifestations of this patient’s acute ingestion aB.cyanosisC.hypothermiaD.seizuresE.vomitingCorrect answer EOil of wintergreen contains 98% methyl salicylate, which can be highly toxic, even in small doses, when ingested by young children such as the boy described in the vignette. One milliliter of oil of wintergreen is equivalent to approximately 1.4 g salicylate. Therefore, the maximum amount of salicylate this boy may have ingested is: 1 tsp = 5 mL x 1,400 mg = 7,000 mg. In a 10-kg child, this translates to 700 mg/kg. Toxicity is likely after a dose in excess of 150 mg/kg.Gastrointestinal symptoms, such as vomiting, are the earliest clinical manifestations of salicylate toxicity. Hyperpyrexia, not hypothermia, is associated with salicylate toxicity. Cyanosis is also not a clinical feature. Seizures and coma may occur as greater amounts of salicylate are bound to central nervous system tissues, but they are not seen early in acute poisoning.The signs and symptoms of salicylate poisoning are a result of a combination of its complex effects on the body’s acid-base status via uncoupling of oxidative phosphorylation and inhibition of certain dehydrogenase enzymatic reactions. These metabolic derangements affect a number of organ systems, resulting in a variety of signs and symptoms involving the cardiovascular, central nervous, gastrointestinal/hepatic, hematologic, renal, and respiratory systems (Table).The classic symptoms of acute salicylate poisoning are diaphoresis, hyperventilation, tinnitus or hearing loss, and gastrointestinal irritation (nausea and vomiting). However, children may not exhibit all of these symptoms, and determining if a young child has tinnitus or hearing problems can be difficult.?Ancillary studies that are helpful in the evaluation and management of salicylate poisoning include blood gases, serum salicylate measurement, urine pH, and electrolytes. Blood gas chemistry can help to differentiate the various phases in salicylate poisoning and assess the patient's metabolic stability. The initial phase consists of a pure respiratory alkalosis due to direct central stimulation on the brain's respiratory center with uncoupling of oxidative phosphorylation in the central nervous system. The renal response to respiratory alkalosis is to allow excretion of bicarbonate.?Adults often present with a mixed respiratory alkalosis and metabolic acidosis.?Young children may not respond with the same degree of sustained hyperventilation as adults. Infants usually do not present with respiratory alkalosis; their respiratory alkalosis may be transient or subtle, with metabolic acidosis manifesting earlier in their course.?In moderate-to-severe poisoning, as greater amounts of salicylate are absorbed, a widened anion gap metabolic acidosis develops through several processes:Lactate production from interruption of oxidative phosphorylationKetone formation from increased fatty acid metabolism productionRetention of phosphoric and sulfuric acids due to renal insufficiencyCompensatory hyperventilation occurs in response to the metabolic acidosis and due to stimulation of the central medullary respiratory center.???In the final stage, the metabolic acidosis worsens and compensatory metabolic mechanisms can no longer respond, with the following developments:Decrease in pH and increase in lactic acidRenal depletion of fluids and electrolytesMultiorgan dysfunction, including dysrhythmias and cardiovascular collapse, acute pulmonary edema, seizures, and coma in severe casesAssessment of serum salicylate concentrations can help confirm the diagnosis, but they do not correlate well with severity of poisoning and can be in the therapeutic range in chronic toxicity. Studies recommend measuring serum salicylate at peak concentrations, at least 4 to 6 hours after ingestion. The classic Done nomogram for salicylate toxicity does not have the same clinical utility as the Rumack-Matthew nomogram does for acetaminophen toxicity. The Done nomogram can be used to estimate poisoning severity, but it assumes the event is an acute single-salicylate ingestion. Furthermore, specimens drawn before 4 to 6 hours after a known time of ingestion are unreliable because early absorption pharmacokinetics are not at steady state. Absolute values are not a substitute for repeated clinical evaluation.???Urine alkalinization is used to enhance renal excretion of salicylic acid. Therefore, urine pH is an essential ancillary study to follow. Electrolyte derangements, specifically hypokalemia, may be present. Serial measurements, especially once urine alkalinization has started, are critical to monitoring further decreases in potassium.?Table. Signs and Symptoms of Salicylate PoisoningSystemSigns And SymptomsCardiovascularTachycardiaHypotensionDysrhythmiasElectrocardiographic changes?Central NervousCentral nervous system depression/lethargyHyperactivity/agitationDeliriumTinnitusSeizuresTremorsEncephalopathyComaCerebral edemaGastrointestinalNausea and vomitingAbdominal painGastrointestinal bleedingPancreatitisHematologicCoagulation problems:?Prolonged prothrombin timeProlonged bleeding timeDecreased platelet adhesionMetabolicHyperpyrexiaHypoglycemiaHypokalemiaHypocalcemiaAcidosisPulmonaryTachypnea/hyperventilationHyperpneaNoncardiogenic pulmonary edemaAmerican Board of Pediatrics Content Specification(s)Recognize signs and symptoms of salicylate poisoningUnderstand the usefulness of ancillary studies in salicylate poisoningQuestion: 4A 5-year-old boy is brought to the emergency department by prehospital providers after being rescued from his burning apartment building. He has partial-thickness burns on approximately 15% of his body, is currently receiving 100% oxygen via a nonrebreather face mask, and is crying in pain. He has soot on his face, singed eyelashes and nasal hairs, and developing blisters on his lips. He is coughing and starting to have difficulty breathing.Of the following, the MOST appropriate next step is to:A.administer intravenous antibioticsB.administer tetanus prophylaxisC.debride the burn woundsD.initiate hyperbaric oxygen therapyE.prepare the boy for endotracheal intubationCorrect answer EThe boy described in the vignette is displaying signs and symptoms of an inhalational burn injury, which is one type of life-threatening burn injury. Inhalational injury is a major predictor of morbidity and significant contributor to mortality after burn injury. Management priorities for life-threatening burns are maintaining an airway, adequate oxygenation and ventilation, and circulatory support. Elective intubation is vital for this boy because of the threat of increasing airway edema that could impede establishment of a definitive airway.Routine prophylactic administration of intravenous antibiotics in burn injuries is not supported by current literature. Burn wound debridement is important to minimize infection and promote wound healing, and tetanus prophylaxis is necessary for those patients at risk, but these management options should follow actions to maintain an adequate airway. Although this patient may be at risk for elevated carbon monoxide concentrations with an inhalation injury, establishing a secure airway takes priority. Hyperbaric oxygen therapy should be reserved for those individuals at risk for toxicity (eg, those who have cardiovascular disease or are pregnant) or those manifesting severe toxicity.?????Burn injuries affecting any portion of the airway/lungs have the potential to compromise a patient’s cardiovascular status and become life-threatening. Some life-threatening burn injuries and their associated signs include:?Stridor, hoarseness, carbonaceous sputum, tongue swelling, singed facial hair, and oropharyngeal blistering may indicate potential imminent airway compromise. ??Significant edema, as well as the development of a restrictive burn eschar from circumferential burns, can cause constrictive signs and symptoms, depending on the location of the burn. Burns of the chest may impair a patient’s ability to breathe, abdominal wall burns may result in abdominal compartment syndrome with impaired blood flow to intra-abdominal organs, and untreated compartment syndrome resulting from extremity burns may result in rhabdomyolysis and eventual renal failure. ??Partial- or full-thickness burns of greater than 10% total body surface area can result in hypovolemic shock unless adequate fluid resuscitation is initiated. ??High-voltage electrical burns may pose an immediate threat to life because of injury to the brain and cervical spinal cord, tetany of chest wall muscles, and cardiac arrhythmias. A wide range of presentations and signs is possible, ranging from apparently superficial minor injuries or extensive musculoskeletal injuries to unresponsiveness, pulselessness, and apnea. ??Hydrofluoric acid is a potent corrosive that causes liquefactive necrosis and bone corrosion, with the fluoride ions creating insoluble salts with calcium and magnesium. Dysrhythmias may?result from the hypocalcemia if a large surface area of skin is affected. However, surface involvement can appear to be absent or insignificant. ??Approximately 15% to 20% of children who have burn injuries are victims of nonaccidental trauma, placing them in a potentially life-threatening situation. An implausible or absent history accompanying such burns should alert the clinician that these injuries are the result of abuse. Affected patients may also have burns that have a recognizable pattern, such as a portion of an iron or immersion scald burns in a glove- or stockinglike distribution, or that occur in an unusual anatomic location, such as the axilla or in the middle of the back.American Board of Pediatrics Content Specification(s)Recognize signs of life-threatening burn injuriesQuestion: 5An 8-year-old boy presents to the emergency department (ED) accompanied by his teacher. He has a history of paroxysmal supraventricular tachycardia (SVT). He was sent to the ED by his school nurse after he complained of palpitations. You place him on a resuscitation bay stretcher for evaluation. On physical examination, the boy is alert, interactive, and in no apparent distress. Vital signs include a heart rate of 210 beats/min and blood pressure of 100/70 mm Hg. Capillary refill time at the extremities is 2 seconds. He wants to get off the stretcher and do a headstand.Of the following, the MOST appropriate next step is toA.administer oral propranololB.allow the boy to perform the headstandC.arrange for echocardiography to evaluate for intracardiac clotD.place a large-bore intravenous catheter in a proximal veinE.prepare the boy for electrocardioversionCorrect answer: BThe boy described in the vignette has stable SVT. The current Pediatric Advanced Life Support guidelines state that vagal maneuvers may be undertaken in these scenarios in an attempt to convert the SVT to a normal sinus rhythm. Such maneuvers include placing ice bags over the face, (unilateral) carotid body massage, and inducing Valsalva maneuvers. Many children who have paroxysmal SVT learn to perform these maneuvers on their own. One Valsalva-inducing maneuver is a headstand, which this child is eager to do. If such maneuvers fail to convert the SVT, the next step is to administer intravenous adenosine. Cardioversion is appropriate for refractory or unstable SVT. Echocardiography to evaluate for an intracardiac clot is not likely to be helpful unless the arrhythmia is longstanding. Propranolol may be indicated at some point in the management of SVT, but it is not the initial treatment of choice.SVT is a common arrhythmia in infants and children. The mechanism is a “short circuit” involving two branches of atrioventricular (AV) conduction fibers. One branch of the re-entrant pathway usually involves the AV node. Vagal maneuvers are used in an attempt to decrease conduction through the AV node, thereby terminating the re-entrant pathway. Less traditional vagal maneuvers include gagging and nasopharyngeal suctioning. When performed as indicated in a child who has stable SVT, few complications are associated with these attempts, although severe bradycardia or even asystole has been reported. Due to the lack of standardization of the various techniques, their effectiveness is unclear. A recent report suggests significantly increased success rates in an ED by adhering to standard procedures.American Board of Pediatrics Content Specification(s)Know the anatomy and pathophysiology relevant to converting stable supraventricular tachycardia using vagal maneuversDiscuss the indications and contraindications for converting stable supraventricular tachycardia using vagal maneuversDescribe the key steps and potential pitfalls in converting stable supraventricular tachycardia using vagal maneuversDiscuss the complications associated with converting stable supraventricular tachycardia using vagal maneuversQuestion: 6A 13-year-old boy is brought to the emergency department by emergency medical services (EMS) after a high-speed motor vehicle collision. He was found at the scene, lying next to the family vehicle. EMS personnel placed him on long board with cervical spine immobilization and provided high-flow oxygen. In the emergency department, he has a heart rate of 58 beats/min, respiratory rate of 12 breaths/min, and blood pressure of 160/80 mm Hg. Primary survey reveals a depressed mental status, with eyes only open to pain, no speech, and flexion to painful stimulus. There are significant signs of trauma to the front of his head.Of the following, the MOST important action is to:A.decrease cerebral perfusionB.prevent cerebral herniationC.prevent hypocarbiaD.prevent hypoglycemiaE.reverse neuronal damageCorrect answer BThe initial emergency department treatment priorities for children who suffer blunt trauma to the brain are to prevent secondary brain injury and stabilize the patient for further diagnosis and treatment. The goal is to preserve perfusion and oxygenation of the viable regions of the brain while preventing the mass effects that lead to ongoing injuries and herniation. For the boy described in the vignette, who has suffered a major head injury, the presence of bradycardia and systemic hypertension indicate impending cerebral herniation. To that end, one priority is to preserve cerebral blood flow by maintaining cerebral perfusion pressure (CPP = mean arterial pressure [MAP] – intracranial pressure [ICP]). This goal must be balanced against possible progression of the underlying injury. Emergency treatment that quickly lowers ICP, such as hyperventilation or administration of mannitol, usually leads to decreased CPP, compromising perfusion to viable tissues. However, such action is necessary in cases of impending herniation.Relative hypocarbia (Pco2 ~35 mm Hg) is potentially protective and, when induced by hyperventilation in the setting of acute head trauma with impending cerebral herniation, may be life-saving. Thus, hypocarbia is used to preserve cerebral perfusion, not to decrease it. Neuronal damage as a result of the primary injury is not reversible. Hypoglycemia is rare in cases of head injuries; hyperglycemia is more common and is potentially damaging.Several approaches to preventing or reducing brain trauma have been suggested. Mannitol (0.25 to 1.0 g/kg)is indicated in cases of refractory intracranial hypertension or signs and symptoms of impending herniation, although there is no empiric evidence of its efficacy in pediatric populations.??A randomized study showed that the treatment of severe traumatic brain injury with 3% saline was superior to lactated Ringer solution in children. In this study, children treated with hypertonic saline required fewer interventions, had fewer complications, and had shorter stays in the intensive care unit. Doses commonly used are between 0.1 and 1 mL/kg per hour. A recent large trial involving mostly adult patients, however, showed no benefits in neurologic recovery with early hypertonic saline treatment.Approximately 20% to 30% of children who have moderate-to-severe brain injury develop early posttraumatic seizures, occurring within 7 days of injury. Thus, prophylactic anticonvulsants, such as fosphenytoin, may reduce the incidence of seizure in the first week after injury but not thereafter.??Finally, despite promising animal models, no benefits were seen for hypothermia in children who had severe head injuries in a relatively large randomized, controlled trial.American Board of Pediatrics Content Specification(s)Understand treatment priorities in the management of children with head injuries due to blunt traumaKnow the role of pharmacology in the management of children with head injuries due to blunt traumaQuestion: 7A 2-year-old previously healthy boy from the suburbs of Memphis, Tennessee, presents with increasing lethargy over the past 24 hours and a temperature to 40.0°C. His immunizations are up to date, and he has no history of a tick bite or recent travel or exposures. On physical examination, the alert, ill-appearing boy has a diffuse blanching rash involving the trunk, arms, and legs, and his heart rate is 150 beats/min, respiratory rate is 42 breaths/min, blood pressure is 90/65 mm Hg, and capillary refill time is 2 seconds. He has no mucosal involvement, conjunctivitis, or coryza. A complete blood count reveals a total white blood cell (WBC) count of 3X103/μL (3X109/L) with a differential count of 60% segmented neutrophils, 12% bands, and 38% lymphocytes; a platelet count of 50X103/μL (50X109/L); and a hematocrit of 35% (0.35). Serum electrolyte values are normal, except for a sodium measurement of 126 mEq/L (126 mmol/L). Results of liver function tests are normal, except for an alanine aminotransferase value of 120 U/L. Coagulation profile reveals an International Normalized Ratio of 1.8. Analysis of the cerebrospinal fluid (CSF) documents a total WBC count of 75/mm3 with a predominance of mononuclear cells, 0 red blood cells, protein concentration of 70 mg/dL, and normal glucose value. The CSF Gram stain is negative.Of the following, the MOST likely diagnosis is:A.disseminated rubeolaB.disseminated staphylococcal infectionC.human monocytic ehrlichiosisD.Kawasaki diseaseE.meningococcemiaCorrect answer: CThe acute febrile illness with rash described for the boy in the vignette, coupled with laboratory findings of leukopenia, thrombocytopenia, hyponatremia, mild hepatopathy, and “aseptic” meningitis, is strongly suggestive of a tick-borne illness such as Rocky Mountain spotted fever (RMSF) or human monocytic ehrlichiosis (HME).The rash of meningococcemia is characteristically petechial or purpuric, although it can begin as a maculopapular rash. Monocytic CSF pleocytosis is not typical in patients who have meningococcemia. Clinical features of measles (rubeola) include coryza, conjunctivitis, and cough. Patients who may not be up-to-date on their measles, mumps, rubella vaccination or who are immunocompromised are at risk for developing disseminated measles. Patients who have Kawasaki disease typically present with irritability, mucositis, nonpurulent conjunctivitis, edema of the hands or feet, unilateral cervical lymphadenitis, and a morbilliform generalized rash. The peripheral leukocyte count is usually elevated. Thrombocytosis is seen in the second week of illness. Children who have Staphylococcus aureus sepsis usually have predisposing factors such as congenital heart disease, recent hospitalization, neonatal age, or an indwelling central venous catheter. Although 10% of cases can occur in children who have no identifiable risk factors, hyponatremia, leukopenia, thrombocytopenia, and a rash beginning on the ankles are not typical of staphylococcal sepsis.Fever and maculopapular rash mimicking tick fever may be noted in other conditions (Table 1). RMSF and HME are clinically indistinguishable, with the classic presentation characterized by an acute febrile illness with centripetally evolving rash and headache. They are summer illnesses transmitted by a tick bite that are more common in the Mississippi River basin than in the Rocky Mountain states. Ninety percent of cases occur in April through September; two thirds are seen in children younger than age 15 years, peaking at ages 5 to 9 years. Of note, a history of tick bite is elicited in only 50% to 60% of patients, especially in rural areas, where children often remove ticks without informing their parents.The clinical syndrome begins with sudden-onset fever and malaise after a mean 7-day incubation period. The rash appears 2 to 5 days after the fever as small, blanching macules on the ankles and wrists that spread to the palms and soles, then to the arms and legs, and finally to the trunk. Within 1 week, the rash is maculopapular, with central petechiae. As many as 15% of patients never develop a rash or it may not be recognized in dark-skinned individuals.Classic laboratory abnormalities reported in patients who have RMSF are hyponatremia and thrombocytopenia. Anemia, elevated liver function test results, elevated blood urea nitrogen, and CSF pleiocytosis may be present in 25% of patients. Children who have HME are more likely to demonstrate leukopenia with lymphopenia and mildly elevated alanine aminotransferase values. Serologic tests are used most frequently to confirm cases of RMSF (Table 2).???Because a delay in empiric antibiotics for RMSF can be fatal, clinicians must be familiar with the presentation and management. Twenty percent of untreated RMSF cases are fatal, but with administration of doxycycline, mortality drops to 5%. Appropriate antimicrobial therapy should be started immediately when the diagnosis of RMSF is suspected and should not be delayed for laboratory confirmation. The decision to treat should be based on a detailed history and the clinical presentation. The drug of choice for treating RMSF is doxycycline, regardless of the patient’s age. It is also effective against HME. Doxycycline can cause staining of the teeth in young children. However, this complication typically occurs after 5-6 courses, so concern for this complication is not a reason to delay treatment in suspected cases (Table 3).In addition to doxycycline, the initial antimicrobial management of an ill child who has a febrile illness and petechial rash might include an agent that is active against Neisseria meningitidis (eg, cefotaxime,ceftriaxone) and vancomycin to cover methicillin-resistant Staphylococcus aureus. These agents can be used in conjunction with doxycycline until the clinician is comfortable that the patient does not have meningococcal or staphylococcal sepsis.American Board of Pediatrics Content Specification(s)Recognize serious and/or life-threatening causes of maculopapular rashesInitiate appropriate diagnostic evaluation of life-threatening maculopapular rashesInitiate treatment of life-threatening maculopapular rashesQuestion: 8You are examining a 15-month-old boy who presented with altered mental status. His parents report that he had 2 days of vomiting and fever, followed by gradually decreasing alertness. There are no findings of note on his birth history. Physical examination of the lethargic child, who is breathing rapidly, shows a temperature of 37.3°C, heart rate of 160 beats/min, respiratory rate of 36 breaths/min, blood pressure of 98/45 mm Hg, and oxygen saturation of 93% in room air. His skin is warm and dry, with moderate icterus. His mother reports that blood oozed from his gums during toothbrushing last night. He has been previously healthy and was reportedly in normal good health until approximately 3 days ago. He received standard immunizations 7 days ago and is up to date on his immunization schedule.Of the following, the MOST likely cause of this child’s presentation is:A.acetaminophen toxicityB.hepatitis A immunizationC.hepatitis BD.hepatitis CE.hypothermiaCorrect answer: AThe boy described in the vignette is experiencing acute liver failure, and the most likely cause is ingestion of acetaminophen, the most common drug-related cause of acute liver failure in the United States. This healthy boy likely has not received blood transfusions, making exposure to hepatitis B and C unlikely. Immunization reactions do not result in acute liver failure. Heat stroke (not hypothermia) could cause acute liver failure, but this would not be a presenting sign, and his parents did not report any exposure to hyperthermic conditions.Fulminant hepatic failure involves acute onset of severe liver injury associated with coagulopathy and encephalopathy in patients who do not have pre-existing liver disease. The time from jaundice to encephalopathy after acute liver injury can be classified as hyperacute liver failure (0 to 1 week), acute liver failure (1 to 4 weeks), and subacute liver failure (4 to 12 weeks). Among young children, in whom encephalopathy may be absent or occur late in the process, the definition is based more on the development of coagulopathy from the liver injury. The liver failure can also be classified as fulminant or subfulminant, depending on the timing of jaundice to development of encephalopathy, if present. In general, the time to onset of encephalopathy frequently is negatively correlated with outcome. The leading causes of death are cerebral edema, sepsis, and multiorgan failure.Acute liver failure is rare but very challenging; the course is variable and mortality is high. Overall, spontaneous recovery occurs in approximately 56% of children (10% to 60%, depending the cause), with 31% requiring transplant and 13% having a fatal course. Better outcomes are seen with acetaminophen poisoning, hepatitis A, and ischemia. Drug-induced acute liver failure, hepatitis B, and indeterminate causes have higher associated mortality rates. The causes for hepatic injury that leads to failure include viral infection (most common in developing countries) and drug exposures (most common in developed countries). Hepatitis A (fecal-oral route of transmission), hepatitis B (exposure to blood or body fluids), and hepatitis E (fecal-oral route of transmission) account for most viral cases. Hepatitis A frequently is more severe in adults than children, who may be asymptomatic. Hepatitis E is the most common cause of acute liver failure in parts of Asia, including China, India, and Pakistan. Other viruses can also be involved and include herpesvirus, Epstein-Barr, cytomegalovirus, and parvovirus B19. Up to 50% of cases in children do not have a specific cause identified.Drug-related liver injury is the second leading cause of acute hepatic failure, and acetaminophen is the most commonly implicated exposure in the United States, either by intentional or nonintentional overdose. The typical time sequence can be classified as hyperacute, with rapidly progressive multiorgan failure. Drug categories related to acute liver failure include nonsteroidal anti-inflammatory medications, statins, antibiotics, antiepileptics, and antituberculosis agents as well as a variety of other medications. Among the other causes of acute liver failure are heat stroke, protracted seizures, mushroom poisoning (Amanita phalloides), metabolic disease, ischemia associated with cardiac or septic events, autoimmune disorders, pregnancy, and malignancy. Inborn errors of metabolism and other inherited disorders should be considered in newborns and young children. Recurrence has been reported after acute liver failure in children who experience repeated acetaminophen overdoses.Care revolves around management of airway, breathing, and circulation; recognition and treatment of potential multiorgan failure with organ-specific therapy; cause-specific interventions where indicated (eg, N-acetylcysteine for acetaminophen toxicity, acyclovir for herpes-related diseases, penicillin and silibinin for Amanita poisoning); and treatment of cerebral edema/increased intracranial pressure. N-acetylcysteine has also been shown to be beneficial in patients with fulminant hepatic failure even in the absence of acetaminophen toxicitiy. Other nonspecific therapies include?hypothermia, plasmapheresis, hepatic-assist devices, and liver transplant.Neurologic consequences can include encephalopathy, manifested by signs ranging from confusion to cerebral edema, intracranial hypertension, and coma. The pathogenesis is unclear but likely includes increased concentrations of circulating neurotoxins, such as ammonia. Ammonia is manufactured primarily in the small bowel and is converted to urea by a healthy liver. Reducing circulating ammonia concentrations may be helpful. Also, total body hypothermia may aid in slowing metabolism, decreasing ammonia production, and reducing cerebral uptake. Other useful general therapies aim to reduce intracranial hypertension and sepsis, avoid hypo-osmolality and seizures, and maintain cerebral perfusion. Liver transplantation is a final treatment option, with country-specific selection criteria for qualification, including age, cause of injury, presence of cerebral edema, and extent of liver dysfunction (jaundice and coagulopathy).In addition to encephalopathy and liver-related findings, the clinical impact of acute liver failure can extend to injury to the lungs, heart, kidney, pancreas, and adrenal gland. The coagulopathy abnormalities seen with fulminant liver failure (decreased procoagulant and clotting factors, impaired fibrinolytic system, and decreased number and function of platelets) have multifactorial sources. Spontaneous bleeding is unusual (<5%), even with markedly abnormal clotting studies.?Laboratory evaluation can include: complete blood count with platelet count and function as well as assessment of prothrombin time (International Normalized Ratio), antithrombin III, D-dimer, plasminogen, factors (VIII, V, VII), fibrinogen, von Willebrand factor, macroglobulin, and protein C and S. Specific laboratory analysis should be guided by gastrointestinal and hematologic consultation. If bleeding prophylaxis is desired due to coagulation profile abnormality or required due to active bleeding or preparation for invasive procedure, fresh frozen plasma, platelets, and cryoprecipitate can be considered, although potential fluid overload is a concern, as are cerebral edema, increased intracranial pressure, and potential hypersensitivity reactions. American Board of Pediatrics Content Specification(s)Recognize causes of fulminant hepatic failure, including drugs, storage diseases, and autoimmune disordersBe familiar with ancillary studies relevant to the diagnosis of fulminant hepatic failurePlan acute management of fulminant hepatic failureAUGUST 2011Question: 1A 14-year-old previously healthy boy reports that he has been experiencing chest pain for the past 2 weeks every time he plays basketball in gym class. He does not report any breathing difficulty or shortness of breath during the episodes. At first, the teacher thought he was malingering, but today she called his mother and told her that her son needed to be evaluated before he could return to class. His gym class immediately follows lunch. He had a sports physical examination over the summer that did not reveal any abnormalities. In the emergency department, he is breathing comfortably, in no distress, and denying chest pain. His lungs are clear to auscultation. He has a 2/6 systolic ejection murmur best heard at the apex and left sternal border. No physical examination maneuver reproduces the pain, and other findings on the examination are normal.Of the following, the MOST likely cause of this boy’s chest pain is:A.coronary artery abnormalityB.exercise-induced bronchospasmC.gastroesophageal reflux diseaseD.left ventricular outflow obstructionE.precordial catchCorrect answer DAlthough cardiac causes represent a minority of all diagnoses for children presenting with chest pain, chest pain with exertion should always alert the physician to the possibility of a cardiac cause. A thorough history and physical examination should be undertaken to evaluate for this possibility. Left ventricular outflow obstruction from hypertrophic cardiomyopathy is the most likely explanation for the pain experienced by the child in the vignette, based on the character of his murmur, his lack of breathing difficulty, and the absence of symptoms when he is not exerting himself. Children who have hypertrophic cardiomyopathy are at risk for ischemia with exercise as well as arrhythmias, which are the most common cause of sudden death in young athletes.Exercise-induced bronchospasm or asthma is a common cause of chest discomfort during exercise, but this child reports no breathing difficulty or wheezing and has no prior history of asthma. A previous history of asthma or wheezing in the emergency department is not necessary to diagnose exercise-induced bronchospasm. Coughing or chest tightness associated with exercise is sufficient. A trial of beta-agonist inhaler before exercise often alleviates the symptoms and confirms the diagnosis.An anomalous coronary blood vessel causing ischemia with exercise would not be expected to cause a murmur unless the boy was experiencing congestive heart failure. Gastroesophageal reflux disease, although not an uncommon cause of substernal burning chest pain, would not cause a pathologic murmur. Precordial catch or “Texidor twinge” causes sudden, sharp chest pain that lasts a few seconds and can occur at rest or with mild activity and can be exacerbated with inspiration. Its cause is unknown.?The proportion of children who have chest pain attributable to different causes varies widely, depending on the source population and case series. In studies focused on pediatric emergency department populations, cardiac causes were responsible for fewer than 5% of cases. The largest category reported in most series is idiopathic and extensive testing generally is not performed. Table 1 lists noncardiac causes of chest pain in children.If the history and physical examination findings are compatible with musculoskeletal chest pain, reassurance, rest, and analgesia with a nonsteroidal anti-inflammatory drug are sufficient treatment. Common causes of musculoskeletal chest pain and their symptoms are listed in Table 2.A thorough history and physical examination can uncover important clues to the presence of cardiac causes of chest pain. Table 3 lists some of the cardiac causes of chest pain in children, some of which can be life-threatening if not identified early. The quality of chest pain should be described, along with precipitating and alleviating factors. A specific detailed past medical history regarding asthma, sickle cell disease, Kawasaki disease, cardiac disease, and hypercholesterolemia and a family history focused on sudden cardiac death, arrhythmia, cardiomyopathy, or hypercholesterolemia should be elicited. Genetic disorders such as Marfan, Turner, and Ehlers-Danlos syndromes should be considered. Finally, a history of trauma, drug use (cocaine, methamphetamines, sympathomimetics), and psychological stressors should be sought.Some physical findings that may suggest cardiac causes include tachycardia, abnormal murmurs, friction rub, displaced point of maximal impulse, increased intensity of the murmur with a Valsalva maneuver or at the end of expiration, hepatomegaly, and edema.If a cardiac cause is suspected, electrocardiography and chest radiography are appropriate initial diagnostic interventions. Echocardiography and urgent cardiac consultation are useful in selected circumstances in which there is a high index of suspicion for pericarditis, myocarditis, cardiomyopathy, anomalous coronary artery, or left ventricular outflow obstruction. If myocardial ischemia is suspected (cocaine ingestion, pain relief with nitrates, previous history of Kawasaki disease or heart transplant), assessment of serum troponin may be helpful. If aortic dissection or rupture is a consideration (severe persistent substernal pain with hemodynamic changes, especially in a child who has Marfan or Ehlers-Danlos syndromes), computed tomography scan should be ordered and surgeons consulted emergently.?Pulmonary causes of chest pain can also be life-threatening. Pneumothorax and pulmonary embolism must be recognized and addressed promptly. Both blunt and penetrating trauma can cause severe injuries such as pulmonary contusion, hemothorax, and rarely, cardiac contusion.American Board of Pediatrics Content Specification(s)Know the etiology of by age and pathophysiology of chest painPlan the diagnostic evaluation and initial intervention for patients with chest painRecognize the serious and/or life threatening causes of chest painQuestion: 2A 3-year-old girl is brought to the emergency department with a history of blood in her stool. In the past 12 hours, she has had three large,?unformed bowel movements that her parents say contained?blood and that there was blood in the toilet. She has not vomited, and her parents state that she has had no abdominal pain. She has been afebrile and does not appear uncomfortable when passing the stool. On physical examination, the frightened, pale but active toddler is in no distress. Her heart rate is 140 beats/min, respiratory rate is 26 breaths/min, and blood pressure is 96/50 mm Hg. Her abdomen is soft, nontender, and without any masses or organomegaly. Rectal examination demonstrates dark red blood. The hematocrit is 25% (0.25), platelet count is 350x103/μL (350x109/L), white blood cell count is 9.0x103/μL (9x109/L), prothrombin time is 12.5 sec, and partial thromboplastin time is 25 sec.Of the following, the MOST appropriate next diagnostic procedure is:A.abdominal ultrasonographyB.colonoscopyC.exploratory laparotomyD.nasogastric tube placementE.99mTc-pertechnetate scanCorrect answer: EIn general, the differential diagnosis of hematochezia in a toddler can be divided into conditions causing painful or painless rectal bleeding. Large-volume, painless rectal bleeding, as described for the child in the vignette, suggests a specific, localizable lesion. The most common causes of such painless rectal bleeding in children are Meckel diverticulum and colonic juvenile polyps. Among the less common causes are hemangiomas and venous malformations.A child who has Meckel diverticulum typically presents acutely, with large-volume (>30 mL) rectal bleeding that may require transfusion, as noted in this child, who demonstrates tachycardia, pallor, and anemia. If a Meckel diverticulum is suspected, a technetium 99m pertechnetate scan identifies the lesion in approximately 80% to 90% of cases. Once confirmed, the definitive treatment is exploratory laparotomy for surgical excision of the lesion.Colonic polyps present commonly with a history of intermittent small-volume (<5 mL) rectal bleeding. A patient who has rectal bleeding and negative results on 99mTc-pertechnetate scan should undergo colonoscopy to evaluate for colitis or polyps. Ultrasonography is most useful if intussuception is suspected. Intussuception typically presents with crampy abdominal pain, emesis, currant jelly stools (representing small-volume rectal bleeding from intestinal ischemia), and an abdominal mass. Nasogastric tube placement can aid in the diagnosis and treatment of upper gastrointestinal bleeding but usually is not indicated in the management of hematochezia.Meckel diverticulum is a persistent remnant of the omphalomesenteric duct that is identified in 2% of the population. A typical Meckel diverticulum is approximately 5 cm (2 in) long and located on the antimesenteric border of the ileum, approximately 60 cm (2 ft) from the ileocecal valve in the distal ileum and, thus, usually is seen in the right lower quadrant. These findings of Meckel diverticulum are commonly referred to as the "rule of twos."Approximately 5% of affected individuals experience complications. The most common presentation in children younger than age 4 years is painless rectal bleeding due to ectopic gastric mucosa. The ectopic mucosa may secrete acid, which causes ulceration of the adjacent tissue and bleeding and may present as melena. Less common presentations include Meckel diverticulitis (which can mimic appendicitis), intestinal obstruction from intussusception or herniation, and rarely perforation from an ingested foreign body trapped in the diverticulum. Management of the Meckel diverticulum involves hemodynamic stabilization of the patient, followed by surgical resection.Nuclear medicine techniques are useful in investigating gastrointestinal bleeding, but they have limitations. Technetium 99m pertechnetate (Meckel scan) localizes within functional gastric mucus cells that usually are found within a Meckel diverticulum or intestinal duplication cyst. Such uptake can be enhanced with agents such as cimetidine, glucagon, and gastrin, which are administered before the study. False-positive results occur with ureteral obstruction, an inflammatory mass such as seen in Crohn disease, abscess, arteriovenous malformation, or intussusception. A negative scan result should not delay surgical intervention if bleeding from a Meckel diverticulum is strongly suspected clinically. Technetium 99m-labeled red cells, also called a “bleeding scan,” help to localize a lesion that bleeds intermittently or at a low rate (0.1 to 0.3 mL/min or 500 mL/day) and eludes endoscopic detection. Labeled red cells remain in circulation for up to 5 days, which allows detection of intermittent bleeding. This important feature precludes the use of other radionucleotide or angiographic tests during this period. In rare cases in which Meckel diverticulum is strongly suspected and the Meckel scan yields negative results, abdominal computed tomography scan, angiography, and exploratory laparoscopy are alternative diagnostic modalities. Treatment is surgical resection.Painful rectal bleeding suggests bowel inflammation (especially colitis) or bowel ischemia. The pain associated with colitis usually accompanies the bowel movement and is relieved by passage of stool. The most common causes of colitis are infection (eg, Salmonella, Shigella, Yersinia, Campylobacter, Escherichia coli, Clostridium difficile, and amoebae), and inflammatory bowel disease. In contrast, bowel pain associated with ischemia is crampy, severe, and independent of the bowel movement. Common causes of ischemic pain include vasculitides (eg, Henoch-Sch?nlein purpura) and intussuception. Although hemorrhoids and anal fissures can also cause painful rectal bleeding, such bleeding usually is trivial.American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of Meckel diverticulumQuestion: 3A 12-year-old boy is brought to the emergency department in extremis after he was found in the bathroom at school after lunch by other students. On physical examination, he is pale, lethargic, and minimally responsive. He is receiving oxygen, and his temperature is 36.9°C, heart rate is 43 beats/min, respiratory rate is 6 breaths/min, blood pressure is 74/20 mm Hg, and oxygen saturation is 72%.Of the following, the therapy that has the GREATEST likelihood of reversing the boy’s abnormalities isA.atropineB.calciumC.flumazenilD.naloxoneE.physostigmineCorrect answer DThe boy described in the vignette is experiencing severe bradycardia, hypotension, hypoxia, and hypoventilation. The combination of an acute, unwitnessed event and marked alteration in vital signs can have multiple causes, including seizures, cardiac arrest, foreign body aspiration, and ingestion. In this case, ingestion is a major concern. If the boy had unreactive pinpoint pupils, was a know drug abuser, had physical signs of acute drug administration (eg, needle marks), or had accompanying drug paraphernalia on his person, the diagnosis would be more straightforward, as would the treatment. Without this information, the clinician must consider multiple causes and potential interventions. As with all emergent presentations, airway, breathing, and circulation must be attended to and supported before and concurrently with specific focused interventions.Naloxone is the intervention/antidote that has the greatest chance of success in a patient who has an unknown or potential drug ingestion. It rapidly counteracts the effects of narcotic-induced respiratory insufficiency as well the subsequent physical signs and symptoms described for this boy. Naloxone may also have a positive effect if clonidine has been ingested (similar presentation to that described in the vignette), with reports of successful use in up to 50% of affected patients.Atropine may be helpful for bradycardia and the related cardiovascular abnormalities, but it does not address the hypoventilation and hypoxia. Calcium may be useful for known hypocalcemia or a known calcium channel blocker ingestion, neither of which is immediately evident or suggested by the presentation. Flumazenil is a potential option because benzodiazepine overdose can lead to respiratory insufficiency and result in severe cardiovascular aberrations. However, flumazenil is contraindicated in an unknown ingestion because it has the potential to precipitate seizures in patients who have taken tricyclic antidepressants. Physostigmine is most useful in severe anticholinergic poisoning. The classic scenario of "red as a beet, dry as a bone, blind as a bat, mad as a hatter, and hot as a hare” has some overlap with this boy’s presentation, but the admission temperature of 36.9°C does not strongly support the use of physostigmine.Subsequent history for the boy in the vignette disclosed that he had been exposed to oral narcotics while in the bathroom with several older teenagers. Administration of naloxone resulted in a rapid, although transient, improvement in vital signs and mental status. He did not need intubation but did require hospitalization in the intensive care unit for frequent monitoring and intervention. Supplemental oxygen was initially required. Multiple doses of naloxone were administered at frequent intervals over the next 14 hours. The addition of gastric decontamination with activated charcoal in such a case should be considered after consultation with local poison control experts. Patients should be observed and monitored closely for 4 hours after naloxone administration for potential deterioration as the effect of the drug abates.Opiate poisoning can be immediately reversed with the use of naloxone. The most direct route of administration is intravenous (onset of action within 2 minutes); endotracheal, intramuscular, subcutaneous, and mucosal routes of administration are also effective but might have longer onsets of action (within 2 to 5 minutes). The duration of effect is usually between 20 and 60 minutes, and repeated doses should be administered and titrated to effect (reversal of respiratory depression, airway protection, improved mental status). Care must be taken in patients who are addicted to narcotics because aggressive use of naloxone can precipitate withdrawal, characterized by agitation, diarrhea, vomiting, diaphoresis, tachycardia, hypertension, pulmonary edema, arrhythmia, and seizures.The appropriate naloxone dose for narcotic intoxication is 0.1 mg/kg to a maximum dose of 2 mg. Administration can be repeated every 2 to 3 minutes, if needed; repeat doses may be administered every 20 to 60 minutes, depending on type and severity of intoxication. Ingestions of certain agents, such as clonidine or buprenorphine, might require higher doses of naloxone. If a continuous infusion of naloxone is considered or required, the initial hourly dose should be based on the effective intermittent dose used and duration of adequate response seen. The dose should be titrated to effect and tapered gradually in an intensive care environment. Some authors suggest starting the infusion at two thirds of the effective initial dose per hour. If opiate dependency or totally reversing effects in patients receiving therapeutic narcotics is a concern, use of smaller incremental dosing, such as 0.1 to 0.2 mg/dose, may limit adverse effects.American Board of Pediatrics Content Specification(s)Know indications for use of naloxoneRecognize signs and symptoms of narcotic poisoningPlan management of acute narcotic toxicityQuestion: 4You have been asked to serve as Emergency Medical Services (EMS) medical director. In reviewing existing protocols, you recognize the need to develop a new algorithm for managing patients exposed to toxins.Of the following, the MOST appropriate role of the regional poison control center in the management of out-of-hospital toxic exposures is to provide:A.advice regarding appropriate destination facilityB.no medical advice; all patients who have toxic exposures should be immediately transportedC.on-scene evaluation of the patient and the potential toxic exposureD.recommendations regarding initial management, decontamination, and need for transportE.telephone consultation for potential hazardous material incidents onlyCorrect answer DGiven the vast number of potential toxins and the limited time devoted to poisoning in EMS training, easily accessible resources for information regarding initial assessment, management, and need for further medical care are critical for successful management of potentially poisoned patients. Regional poison control centers (PCCs) serve this role for EMS services throughout the country. They provide telephone advice and recommendations to the general public, first responders (including EMS, fire, and police personnel), and medical clinicians. Recommendations may include appropriate decontamination strategies, antidote administration, supportive care measures, and whether the exposure requires hospital evaluation and treatment of the patient(s). PCCs are not involved in local EMS and hospital protocols related to appropriate destination facilities and are not designed to provide on-scene response. Although hazardous materials incidents may benefit from PCC consultation, most calls involve individual accidental or intentional poisonings.Many EMS services include consultation with the PCC in their protocols for the management of any potential medication overdose, chemical exposure, hazardous materials incidents, or potential chemical terrorism events. Several studies have demonstrated that such consultation can result in a reduction in unnecessary hospital transports and cost savings. In more than two thirds of these cases, the PCC recommended on-scene management without hospital transport, and specific medication or antidote administration was recommended in only a small minority of cases. The PCC can also be helpful in identifying agents based on chemical/drug characteristics and patient signs and symptoms.American Board of Pediatrics Content Specification(s)Understand how the regional poison center relates to out of hospital toxicologic assessment and treatmentQuestion: 5A previously well 3-year-old boy is brought to the emergency department for the third time this month because of a persistent runny nose. His mother explains that she has taken the boy to his pediatrician, who prescribed amoxicillin for an “infection.” On physical examination, the well-appearing child has a temperature of 38.3°C. Initial examination of the nares reveals unilateral thick, greenish, foul-smelling nasal discharge.Of the following, the MOST appropriate next step is to:A.administer a nasal decongestant and undertake suctioningB.admit the boy for administration of systemic antibioticsC.obtain an urgent ear-nose-throat consultationD.prescribe a different antibiotic and schedule an outpatient follow-up visitE.probe the nares with a wire curetteCorrect answer: AThe most common cause of unilateral foul-smelling nasal discharge in children is a foreign body. In many instances, a cursory examination of the nares may not reveal a foreign body, especially in the presence of secretions. Use of nasal decongestants with suctioning aids in diagnosis and facilitates their removal. Most nasal foreign bodies can be removed successfully in the emergency department or office, and an urgent otolaryngology consultation is not required. Fever can result from complications of a chronic foreign body such as sinusitis or periorbital cellulitis and may occasionally require hospitalization for systemic antibiotics. However, the boy described in the vignette does not have any manifestations of severe systemic illness that would necessitate inpatient admission for parenteral antibiotics. Similarly, changing antibiotics without addressing the cause of persistent rhinorrhea is not appropriate. A wire curette is often used to get behind a nasal foreign body and is an important tool in management, but blind probing can lead to complications such as bleeding, impaction, or posterior displacement that can cause aspiration.Nasal foreign bodies, typically beads, buttons, toy parts, paper, cloth, erasers, food, and button batteries, are common findings in children younger than 6 years of age. Interestingly, unlike aural foreign bodies, nasal foreign bodies are twice as common in girls as in boys. The nose consists of two nasal fossae separated by a vertical septum and subdivided into three passages by the nasal turbinates. Nasal foreign bodies tend to be located on the floor of the nasal passage, just below the inferior turbinate, or in the upper nasal fossa anterior to the middle turbinate. Nasal foreign bodies can be asymptomatic or present with unilateral nasal occlusion and foul-smelling, purulent, or blood-stained nasal discharge. Because multiple foreign bodies are common, especially in small children, a complete examination should include inspection of both ears. Radiographs are of limited diagnostic value because most foreign bodies are radiolucent.Removal of nasal foreign bodies may require immobilization (papoose) of the young or uncooperative child. Before foreign body removal, 0.5% phenylephrine or oxymetazoline can be administered to reduce mucosal edema, and topical lidocaine may be applied to provide analgesia. Techniques include removal with direct viewing using forceps (alligator or Hartmann forceps), curved hooks, cerumen loops, or suction catheters (Frazier suction) and use of cyanoacrylate adhesive at the end of a blunt cotton swab. In addition, successful removal has been achieved by passing a thin, lubricated, balloon-tip catheter (5 or 6 French Foley, Fogarty, or Katz) past the foreign body, inflating the balloon, and pulling the inflated catheter balloon forward. In older and more cooperative patients, the foreign body can be expelled by asking the patient to “blow the nose” while blocking the opposite nostril. In younger children, the parent can use positive-pressure ventilation to expel the foreign body by covering the child's mouth with his or her mouth, plugging the unobstructed nostril with a finger, and delivering a rapid, soft puff of air. Positive pressure can also be delivered through the mouth using a bag mask or through the nose using oxygen tubing. Care should be taken to avoid barotrauma.An otolaryngology referral should be obtained for patients who fail initial attempts at removal, present with complications, or have a suspected mass or tumor. Immediate consultation is indicated for a corrosive foreign body (button battery). The most serious complications of nasal foreign bodies are associated with button batteries and failed removal attempts. Alkaline button batteries cause liquefaction necrosis of surrounding tissue and may lead to nasal septal perforation, burns of the nasal mucosa, or nasal meatus stenosis.American Board of Pediatrics Content Specification(s)Know the types of foreign bodies often lodged in the noseOutline the appropriate procedures for foreign body removalQuestion: 6You are evaluating a 14-year-old girl who has had fever and chills for the past 3 days. Her maximum temperature has been 39.6 ?C. She also reports nausea and abdominal discomfort, bilateral ankle redness and swelling, and a tender rash along her feet (Figure 1). Her last menstrual period was 10 days ago. On physical examination, the tired-appearing girl has a heart rate of 120 beats/min, respiratory rate of 32 breaths/min, temperature of 39.5?C, and blood pressure of 110/65 mm Hg. Her lungs are clear on auscultation, she has no cardiac murmurs, her abdomen is soft without hepatosplenomegaly, and she has bilateral lower quadrant tenderness. The white blood cell count is 21x103/μL (21x109/L) with 78% neutrophils and erythrocyte sedimentation rate is 55 mm/hr. Gram stain from the foot lesion (Figure 2) shows gram-negative intracellular diplococci.Figure 1. Maculopapular and petechial skin lesions. Figure 2. Gram stain of lesion on foot. Of the following, the MOST appropriate treatment for this girl is:A.inpatient therapy with intravenous ceftriaxoneB.inpatient therapy with intravenous ceftriaxone and oral doxycyclineC.outpatient therapy with intramuscular ceftriaxone and oral doxycyclineD.outpatient therapy with intramuscular spectinomycin and oral azithromycinE.outpatient therapy with oral levofloxacinCorrect answer: BIntracellular gram-negative diplococci are pathognomonic for Neisseria gonorrhoeae infection in the appropriate clinical scenario, such as that described for the girl in the vignette. She has disseminated gonococcal infection, for which inpatient management with intravenous ceftriaxone and oral doxycycline is the recommended treatment. Intravenous ceftriaxone monotherapy is appropriate for treatment of neonates who have gonococcal meningitis. Outpatient treatment with ceftriaxone and doxycycline is recommended for treatment of uncomplicated genital infection. Patients who have documented allergy to ceftriaxone and uncomplicated genital infection should receive spectinomycin plus oral azithromycin. Levofloxacin can be used for disseminated gonococcal infection only after culture sensitivities are proven for quinolones because N gonorrhoeae has high resistance to penicillin, tetracycline, and quinolones.?????The incubation period for gonorrhea is 2 to 7 days. Due to the presence of polymorphonuclear cells, the discharge associated with the infection is mucopurulent. In neonates, the disease can present as conjunctivitis (Figure 3), scalp abscess at the site of fetal electrode placement, arthritis, vaginitis, and meningitis. Older children may have disseminated gonococcal infection that is characterized by fever; chills; migratory arthritis of the knees, ankles, or wrists; and petechial or necrotic rash (Figure 4) along the knees or feet (patients who have lupus and complement deficiencies are at high risk). Other presentations include complicated or uncomplicated pelvic inflammatory disease (PID), perihepatitis, cervicitis (Figure 5), urethritis (Figure 6), epididymitis, proctitis, endometritis, and pharyngitis. PID due to gonorrhea usually presents during menstruation.??Gram stain can be performed on specimens from selected infection sites (cerebrospinal fluid, synovial fluid, conjunctiva, male urethra, skin lesions, vagina of pre-pubertal girls) to establish a provisional diagnosis of a gonococcal infection and is especially useful due to its low cost and rapid results. However, negative results do not rule out the infection. Gram stain is not recommended for pharyngeal, rectal, or endocervical specimens, but in urethral specimens from sympotomatic men, demonstration of polymorphonuclear leukocytes with intracellular Gram-negative diplococci can be considered diagnostic for infection with N. gonorrhea. Culture using nonselective chocolate agar is performed for specimens from sterile sites to diagnose gonococcal infections.? For nonsterile sites, culture in selective media is performed to inhibit growth of normal flora. Culture methods should always be used to evaluate for sexual abuse in pre-pubertal children because false-positive results can occur with nonculture gonococcal tests. If N gonorrhoeae is identified on culture, other microbiologic tests are performed by the laboratory to distinguish it from other Neisseria species. Among the nonculture evaluations, the nucleic acid amplification test (NAAT) is highly sensitive and specific when performed on male urethral and female endocervical or vaginal swabs and male and female urine specimens. Certain laboratories use NAAT for rectal and pharyngeal sites after meeting the standards established by Clinical Laboratory Improvement Amendments, thus avoiding the need for culture. Hence, use of various tests depends on the laboratories performing them. In summary, the recommended diagnostic tools for possible gonococcal infections are:?NAAT for genital infections: male and female urine samples, female endocervical and vaginal samples, and male urethral samplesCulture for nongenital infections: rectum, oropharynx, cerebrospinal fluid, and conjunctiva; NAAT can be used if the laboratory can perform the test for rectal and oropharyngeal samplesDNA hybridization tests: may be useful for pharyngeal and oropharyngeal samples compared with cultures (expensive, easier, but not better than cultures)Third-generation cephalosporins are the first-line treatment for gonococcal infections. Treatment recommendations, per 2010 Centers for Disease Control and Prevention guidelines, are based on the site of infection:Conjunctivitis:Neonatal: one dose of intramuscular ceftriaxone (25 to 50 mg/kg, maximum of 125 mg) and saline irrigationOlder age: one dose of intramuscular ceftriaxone (1 g maximum) and treatment for ChlamydiaDiffuse neonatal infection: ceftriaxone or cefotaxime (50 mg/kg per day) for 7 days for arthritis, bacteremia, and scalp abscess; 14 days for meningitis; and 28 days for endocarditisUncomplicated infections (cervicitis, urethritis, cervicitis, proctitis, vaginitis, pharyngitis): one dose of intramuscular ceftriaxone (250 mg) or one dose of cefixime (8 mg/kg, maximum of 400 mg).??Due to concerns?over emerging?resistance to cephalosporins, as of July 2011 the CDC recommends additional treatment with Azithromycin; dual therapy is now the standard.Epididymitis: one dose of intramuscular ceftriaxone (250 mg) and treatment for ChlamydiaDisseminated gonococcal infection: intravenous or intramuscular ceftriaxone (50 mg/kg per day, maximum of 1 g) for 7 to 10 days and treatment for ChlamydiaPelvic inflammatory disease: Table?Because Chlamydia infection often is associated with complicated and uncomplicated PID, combined treatment is indicated.?Spectinomycin (40 mg/kg intramuscularly to a maximum of 2 g) is indicated if there is allergy to cephalosporins, with one dose administered for uncomplicated infections and a 7- and 10-day course of twice-daily administration for disseminated gonococcal infection. When spectinomycin is used to treat pharyngitis, repeat throat culture is indicated because the reported efficacy is only 50% for this infection. Infants of mothers who have known gonococcal infection should receive one dose of intramuscular ceftriaxone at birth. Patients should be offered tests to rule out other sexually transmitted infections. Repeat culture for N gonorrhoeae after treatment is not required unless symptoms persist.Figure 3. Gonococcal ophthalmia in an 8-day-old neonateFigure 4. Gonococcal necrotic skin lesion.Figure 5. Colposcopic view of eroded ostium in the cervix due to gonococcal cervicitisFigure 6. Purulent penile discharge and overlying penile pyodermal lesion associated with gonococcal urethritis. Table. Treatment for Pelvic Inflammatory DiseaseaParenteral: Regimen AbCefotetan, 2 g, IV, every 12 hORCefoxitin, 2g, IV, every 6 hPLUSDoxycycline, 100 mg, orally or IV, every 12 h to complete 14 daysORParenteral: Regimen BcClindamycin, 900 mg, IV, every 8 hPLUSGentamicin: loading dose, IV or IM (2 mg/kg), followed by maintenance dose (1.5 mg/kg) every 8 h.? Single daily dosing may be substituted.NOTEParenteral therapy may be discontinued 24 hours after a patient improves clinically; continuing oral therapy should consist of doxycycline (100 mg, orally, twice a day) or clindamycin (450 mg, orally, 4 times a day) to complete a total of 14 days of therapy.Ambulatory: RegimendCeftriaxone, 250 mg, IM, onceORCefoxitin, 2g, IM, and probenecid, 1g, orally in a single doseOROther parenteral third-generation cephalosporine (eg, ceftizoxime or cefotaxime),PLUSDoxycycline, 100 mg, orally, twice a day for 14 daysWITH or WITHOUTMetronidazole, 500 mg, orally, twice a day for 14 daysAlternative Ambulatory RegimensIf parenteral cephalosporin therapy is not feasible, use of? fluoroquinolones may be considered if community prevalence and individual risk of gonorrhea is low (see std/treatment).? Tests for gonorrhea must be performed before instituting therapy and management as followed if the test is positive:GC NAA test positive: parenteral cephalosporin recommendedGC culture positive: treatment based on susceptibility resultsGC isolate: quinolone resistant or susceptibility cannot be assessed, parenteral cephalosporin recommended.American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of gonorrheaPlan management including ancillary studies of acute gonorrheaQuestion: 7A 2-year-old boy who underwent cleft palate repair 1 year ago presents with 2 days of nonbilious vomiting, occasional nonbloody diarrhea, and a low-grade tactile temperature at home. His mother has offered him juice, water, and clear soft drinks, but she says “He refuses or vomits each time we offer him anything.” He has had fewer wet diapers in the past 24 hours. On physical examination, the boy is awake but subdued and unhappy. His temperature is 38.0°C, heart rate is 132 beats/min, respiratory rate is 28 breaths/min, blood pressure is 102/65 mm Hg, and pulse oximetry reading is 99% in room air. Other than his anxiety with the examination, he exhibits no other abnormalities. His lungs are clear, his heart rate is regular, and he has no murmurs. His skin is warm and without acute rashes, and his capillary refill is less than 2 seconds on the chest. His abdomen is slightly protuberant, with active bowel sounds, mild nonspecific periumbilical tenderness, and no rebound or guarding. His genitourinary examination yields no findings of note. He attends child care 3 days a week.Of the following, the MOST reasonable initial approach to this patient is:A.administration of oral rehydration fluids containing both salt and sugarB.consultation with an otorhinolaryngologist for likely feeding intolerance due to postsurgical complicationsC.intraosseous access and administration of 20 mL/kg normal saline bolusD.placement of a peripheral intravenous line and administration of glucose-containing rehydration solution at 20 mL/hrE.reassurance of the parents, telling them to continue their current careCorrect answer AThe boy described in the vignette appears to have routine acute gastroenteritis with mild dehydration without evidence of shock or potential surgical intra-abdominal pathology. His past medical history of a repaired cleft palate should be inconsequential, unless the repair was very recent or known to be inadequate. The patient has mild tachycardia and a normal blood pressure. He is aware of his environment and acting appropriately for his age, which suggests that rapid fluid resuscitation via emergency intraosseous or vascular access is not necessary at this point. The resuscitation fluid for most patients should be nonglucose-containing crystalloid. Simple reassurance is probably not sufficient guidance for this family, especially because the fluids they are offering him are not ideal for the situation. Oral rehydration therapy (ORT), with demonstration by clinicians and education and supervision of the family members, is the most reasonable option for this boy.Several studies have noted that ORT is an effective therapy for rehydration of mild-to-moderate dehydration. Determination of the degree of dehydration has been reviewed by many authors and is summarized well in the 2010 clinical review by Colletti and associates. Prolonged capillary refill, abnormal skin turgor, and abnormal respiratory pattern were noted as the three best indicators of dehydration in the March 2009 Cochrane review of dehydration in infants and young children. The same review article notes many barriers to effective use of ORT, including unfamiliarity with published guidelines, misperception of increased time needed, misperception that ORT is contraindicated with vomiting, and patient or physician preferences. One approach to ORT is outlined in Table 1. ORT should continue for 4 to 6 hours, as tolerated by the patient or until adequate rehydration is achieved.Oral rehydration fluids typically contain sodium, potassium, chloride, carbohydrates, and a base, and they are commercially available (Table 2). Commonly used beverages (eg, sports drinks, fruit juices) are not recommended for acute rehydration because they are hyponatremic and have high carbohydrate contents.Oral rehydration has many benefits for the patient experiencing mild or moderate dehydration due to diarrhea, including lower cost than intravenous (IV) rehydration and ease of use both inside and outside the hospital environment. The quantity and timing of fluid administration can be modified, based on patient need and demand. IV rehydration and shock resuscitation is indicated for patients who have severe signs or symptoms.An antiemetic may be considered for patients such as this boy. Much has been written about ondansetron and rehydration. Although the American Academy of Pediatrics (AAP) 1996 guidelines discouraged the use of antiemetics in children younger than 5 years of age due to adverse effects of medications used at that time, many clinicians now include ondansetron as a standard part of their rehydration process. Ondansetron has a lower adverse effect profile than traditional antiemetic medications and may be an advantageous adjunct to oral rehydration. As of 2011, the AAP has neither endorsed nor encouraged the use of ondansetron in children who have vomiting due to acute gastroenteritis. The latest statement from the AAP on this subject was to endorse the 2003 recommendations published by the Centers for Disease Control and Prevention in Morbidity and Mortality Weekly Report. The authors state that “antiemetics are usually unnecessary”?and that “cost-effective analysis should be undertaken before routine pharmacologic therapy is recommended” for vomiting due to gastroenteritis.Approximately 1.5 to 3.7 million pediatric outpatient visits in the United States are due to diarrhea-related issues, with 150,000 to 200,000 children requiring hospitalization and 200 deaths per year. The cost of care for affected patients exceeds $2 billion annually. Despite the potential severity, most children present with mild or moderate dehydration, and oral rehydration is sufficient. The process, however, is time-consuming and requires a competent caregiver who can spend a significant amount of time providing incremental amounts of fluid. Oral rehydration has been shown to be efficacious in both high- and low-income populations. The 2009 Cochrane review of 17 trials compared oral and IV rehydration and involved 1,811 participants, 56% of whom were randomized to oral rehydration. Although IV rehydration was slightly favored for rehydration or maintenance of hydration, the risk difference was only 4%. The failure rate for oral rehydration therapy was 4.9% compared with 1.9% for IV therapy. Where analyzed, there were no statistical differences for weight gain at discharge, hyponatremia, hypernatremia, duration of dehydration, total fluid intake at 6 and 24 hours, or amount of sodium intake and sodium concentrations. Children who received ORT actually spent less time in the hospital than those receiving IV therapy. One complication noted in the ORT groups was paralytic ileus.American Board of Pediatrics Content Specification(s)Know the anatomy and pathophysiology relevant to oral rehydrationDiscuss the indications and contraindications for oral rehydrationDescribe the key steps and potential pitfalls in performing oral rehydrationDiscuss the complications associated with oral rehydrationQuestion: 8A 2-year old boy comes into the emergency department with a 2-cm clean laceration to his forehead, which he sustained after running into the corner of a coffee table.Of the following, the PRIMARY advantage to using tissue adhesives over simple synthetic interrupted sutures in the repair of this wound is:A.better cosmetic outcomeB.lower incidence of wound infectionC.lower rate of wound dehiscenceD.no need for local anesthesiaE.no need for routine follow-upCorrect answer: ETissue adhesives are an alternative to suturing for low-tension wounds that are linear and less than 4 cm in length, do not abut mucosal surfaces, and are not grossly contaminated. Multiple studies have shown equivalent rates of wound dehiscence and infection in wounds closed with tissue adhesive compared with suture closure if the wounds are appropriately chosen. Tissue adhesives should not be used on wounds that cross joints (because they are considered high tension) or on the hands (because frequent washing can prematurely break down the tissue adhesive). Similar cosmetic outcomes are achieved with tissue adhesive and suture closure. Because no sutures or staples need to be removed, no follow-up visit is required. As always, parents should be instructed return with the child if there are signs or symptoms of infection.Wound cleansing and debridement are the most important steps to prevent secondary infection. For the boy described in the vignette, the wound can be cleaned after administration of a topical anesthetic such as LET (lidocaine, epinephrine, and tetracaine). Irrigation into an open wound without local anesthesia is painful and likely would make the toddler uncooperative for further care, including application of the tissue adhesive. The wound needs to be dry and well approximated for appropriate application of tissue adhesive. Cyanoacrylate tissue adhesive bonds the epithelial layer of skin when the monomer chemically changes to a polymer in the presence of moisture of the skin surface. This exothermic reaction, resulting in heat generation (that may be felt by the child), is exacerbated by the presence of blood or irrigation fluid. If the wound is not well approximated, tissue adhesive enters it and keeps the edges apart. Some practitioners recommend approximating the wound with tape strips before applying tissue adhesive, rather than approximating it manually, which decreases the chance of gluing the holder to the patient.?When the wound is in the facial area, as for this boy, the clinician should take care to prevent tissue adhesive from dripping into the eyes by positioning the patient so the adhesive rolls away from the eye.?Alternately, the clinician can place a barrier of petrolatum or antibiotic ointment between the eye and the laceration. Tissue adhesive may be removed with a petrolatum-based product if it inadvertently enters the wound or adheres to an unintended surface.A systematic analysis indicated that use of tissue adhesive is less time-intensive than suturing, with a labor time of 8.6 minutes for sutures and 4.0 minutes for tissue adhesives.American Board of Pediatrics Content Specification(s)Judge the advantages, disadvantages, indications, and contraindications of tissue adhesivesSEPTEMBER 2011Question: 1A 15–year–old girl is brought to the emergency department after being found tearful and despondent at school. She is somnolent but answers questions appropriately. She says she took some pills she found at home after having a fight with her mother when she arrived home from school yesterday (about 18 hours ago). She is unsure of what the pills were. She now complains of nausea and vomited once. On physical examination, the pale and somewhat diaphoretic girl has a temperature of 36.8°C, heart rate of 84 beats/min, respiratory rate of 14 breaths/min, blood pressure of 102/67 mm Hg, and pulse oximetry of 98% in room air. Her pupils are mid-position, equal, round, and responsive to light. Extraocular movements are intact without nystagmus. The remainder of the physical examination findings are normal. A urine pregnancy test is negative; point-of-care glucose measures 93 mg/dL (5.2 mmol/L); and venous pH is 7.36, Pco2 is 45 mm Hg, and Po2 is 40 mm Hg. You obtain intravenous access and infuse 1 L of 0.9% saline. You read the electrocardiography strip as normal. Additional laboratory test results are pending.Of the following, the MOST appropriate therapy to consider and ready for administration isA.calcium ethylenediaminetetraacetic acid (EDTA)B.deferoxamineC.fomepizoleD.N-acetylcysteineE.sodium bicarbonateCorrect answer DThe adolescent girl described in the vignette has ingested an unknown medication in an apparent suicide attempt. She is somnolent and nauseous and has vomited. She has mild diaphoresis but stable vital signs, does not show signs of a classic toxidrome, does not have acidosis, and has a normal glucose value. Given her presentation and its availability, acetaminophen is the most likely substance she has ingested. N-acetylcysteine administered either orally or intravenously is a specific antidote for acetaminophen poisoning whose use may prevent hepatic injury and necrosis. The other antidotes offered are for ingested substances that?present with different and more specific clinical presentations (Table).Acetaminophen ingestion accounts for more overdoses and overdose deaths than any other medication. Acetaminophen overdose frequently results from medication errors in infants, accidental ingestion in toddlers, and intentional ingestions as part of suicide gestures or attempts in older children and adolescents. Acetaminophen is readily available to adolescents, who frequently underestimate its potential toxicity. Adolescents may not reveal what they have ingested despite direct questioning, and the emergency physician must entertain a broad differential diagnosis and obtain serum assessments of substances for which there are potential lifesaving therapies (eg, aspirin and acetaminophen).In infants and younger children, inappropriate dosing may lead to subacute or chronic overdosage and toxicity. Toddlers who sustain accidental or exploratory overdoses and adolescents who intentionally ingest acetaminophen usually have single, acute ingestions. In toddlers, these are often low dose, with a low risk of significant toxicity. In adolescents, the ingestions may be high dose, with risk for significant toxicity and even death.Toxicity may be predicted based on the amount of acetaminophen ingested if the emergency physician can be sure the estimate is accurate. The minimum toxic dose for a single ingestion is 150 mg/kg for children or 7.5 to 10 g in adults. Toxicity is highly likely in single ingestions of greater than 250 mg/kg or 12 g in a single day. In chronic ingestions, ingestions of more than 150 to 175 mg/kg over 2 to 4 days are associated with toxicity. Fever and the relative dehydration associated with routine childhood illnesses may increase the potential for toxic effects.Initial symptoms after acetaminophen ingestion are usually mild and nonspecific; many patients are asymptomatic. Nausea, vomiting, diaphoresis, pallor, and lethargy may occur over the subsequent 24 hours. Laboratory values other than those for acetaminophen are normal. Initial symptoms or lack thereof are not predictive of later manifestations of toxicity.In toxic ingestions, hepato- and nephrotoxicity become evident between 24 and 72 hours after an acute ingestion. During this time, right upper quadrant pain, hepatomegaly, and tenderness develop. Transaminases are elevated by 36 hours after ingestion, and prothrombin time is increased. Hyperamylasemia and possible clinical signs of pancreatitis as well as oliguria and azotemia develop.Elevated transaminase values peak at 72 to 96 hours. Jaundice, hepatic encephalopathy, hyperammonemia, bleeding, hypoglycemia, lactic acidosis, and renal failure may develop, depending on the degree of hepatic injury. Death from multiorgan system failure may occur at this stage.Supportive care and eventual liver transplantation may be lifesaving in cases of hepatic failure. If the patient survives and hepatic function returns, recovery occurs from 4 to 14 days after ingestion. Results of laboratory studies may remain abnormal for several weeks.Acetaminophen toxicity may also be predicted in acute, single-point ingestions that occur between 4 and 24 hours before the serum concentration is obtained by using the Matthew and Rumack nomogram (Figure). The nomogram is not useful in chronic, subacute, or prolonged ingestions, for extended-release drug formulations, or in cases of coingestions of other medications. In these cases, it is especially important to consult a poison control center (1-800-222-1222) to obtain help in guiding therapy.Activated charcoal may be used for decontamination in acute exposures, ideally within 1 hour of ingestion. N-acetylcysteine (NAC) is the antidote of choice for acetaminophen ingestion. Use is indicated when:The serum acetaminophen concentration following a single, acute ingestion exceeds the “possible hepatic toxicity” line on the nomogram (Figure)A single dose of more than 150 mg/kg or total single ingestion of more than 7.5 g has been taken when a serum acetaminophen value will not be available until more than 8 hours after ingestionPatients with suspected overdose have an unknown time of ingestion and a serum acetaminophen value greater than 10 ?g/mL (66 ?mol/L)Patients have any laboratory evidence of hepatic toxicity in the setting of possible excessive acetaminophen ingestionNAC is ideally started within 8 to 12 hours of ingestion but has been shown to be effective in most cases if started within 18 to 24 hours of ingestion. NAC may be effective even for patients who ingested acetaminophen more than 24 hours before presentation, and administration should be considered in consultation with a toxicologist or a poison control center. Although data are lacking in pediatric patients, a single randomized, controlled trial of NAC in adults who had late presentations (>24 hours after ingestion) and signs of hepatic toxicity showed that NAC administration decreased mortality by more than 50%. NAC may be given either orally or intravenously; neither route has a clear advantage in efficacy. NAC should be administered intravenously to patients who have intractable vomiting or whose medical condition is a contraindication to enteral administration. Dosing regimens vary based on route of administration:Oral AdministrationLoading dose of 140 mg/kg, then70 mg/kg orally every 4 hours for 17 dosesIntravenous administration (usually given in 5% dextrose or 0.45% sodium chloride solution)For patients <20 kg:Loading dose of 150 mg/kg in 3 mL/kg of diluent IV over 60 minutes, then50 mg/kg in 7 mL/kg of diluent over 4 hours, then100 mg/kg in 14 mL/kg of diluent over 16 hoursFor patients >20 kg to <40 kg:Loading dose of 150 mg/kg in 100 mL of diluent IV over 60 minutes, then50 mg/kg in 250 mL of diluent over 4 hours, then100 mg/kg in 500 mL of diluent over 16 hoursFor adult patients:Loading dose of 150 mg/kg in 200 mL of diluent IV over 15 minutes, then50 mg/kg in 500 mL of diluent over 4 hours, then100 mg/kg in 1,000 mL of diluent over 16 hoursFluid overload and dosing errors in young children receiving intravenous NAC have been associated with hyponatremia, seizures, and death. Intravenous NAC has also been associated with anaphylactoid reactions, especially in patients who have a history of asthma. Oxygen, epinephrine (1:1,000 for intramuscular administration), diphenhydramine, and appropriate–sized airway equipment must be immediately available for patients receiving intravenous NAC.Table: Selected Antidotes for Toxic IngestionsAntidoteIngestionSymptomsCalcium EDTALeadAbdominal pain, encephalopathy, fatigue, constipation, headacheDeferoxamineIronObtundation, abdominal pain, vomiting, hematochezia, acidosis, hypotensionFomepizoleEthylene glycolIntoxication, nausea, vomiting, stupor, coma, convulsions, acidosis, renal failureSodium bicarbonateAspirin, tricyclic antidepressantsAspirin: tachypnea, acidosis, obtundation? Tricyclic antidepressants: somnolence, seizures, electrocardiographic abnormalitiesFigure: Acetaminophen nomogramAmerican Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of acetaminophen poisoningUnderstand the usefulness of ancillary studies in acetaminophen poisoningPlan the management of acute acetaminophen toxicityQuestion: 2You are evaluating an 8-year-old boy who was struck by an automobile while crossing the street on his bicycle. Bystanders reported that he was thrown to the ground, immediately lost consciousness, and had a brief seizure. On physical examination, his estimated weight using a length-based tape is 25 kg, heart rate is 92 beats/min, respiratory rate is 22 breaths/min, and blood pressure is 75/40 mm Hg. He moans in response to a painful stimulus and forceful extends his upper and lower extremities. His right pupil is dilated and sluggishly reacting to light. You intubate him endotracheally using a rapid sequence induction technique while maintaining cervical spine immobilization and request emergent neurosurgery consultation. You obtain cranial computed tomography (CT) scan (Figure 1).Of the following, the MOST appropriate immediate treatment for this boy isA.HyperventilationFluidsAdjunctive AgentYes5% dextrose in normal saline infusion at maintenance rateFosphenytoinB.NoLactated Ringer solution bolus of 500 mLMannitolC.YesNormal saline bolus of 250 mLMannitolD.YesLactated Ringer solution bolus of 500 mLFosphenytoinE.NoLactated Ringer solution infusion at maintenance rateMannitolCorrect answer: DThe boy described in the vignette has sustained severe blunt head trauma and has clinical and radiologic signs of elevated intracranial pressure (ICP). His vital signs suggest that he is in uncompensated shock. The relative bradycardia, pupillary asymmetry, and extensor posturing suggest acute brainstem herniation. The CT scan shows a large subdural hemorrhage with midline shift and effacement of the cisterns.The immediate management priority for this boy is to institute measures to maintain cerebral perfusion pressure, decrease ICP, and prevent secondary brain injury. This can be achieved best by correction of hypotension with an intravenous isotonic fluid bolus and hyperventilation. Appropriate fluid resuscitation involves administration of 20 mL/kg of normal saline or lactated Ringer solution. Although administration of mannitol may be an appropriate intervention for patients demonstrating signs of acute brainstem herniation, such an osmotic diuretic in this case would exacerbate hypovolemia and hypotension, leading to secondary brain injury. Patients who have severe traumatic brain injury (TBI) are also at risk for posttraumatic seizures. Empiric evidence suggests that administering prophylactic anticonvulsants may prevent seizures in the first week after injury in high-risk patients.???????????????????????????????????????????????????????????????????????????????????A classification scheme for TBI is presented in Table 1. A summary of the mechanisms leading to elevated ICP following blunt head trauma are summarized in Figure 2.Children have a higher incidence of elevated ICP following TBI than adults. Diffuse TBI is the most common type of injury, resulting in a range of injury severity from concussion to diffuse axonal injury (DAI). Patients who have DAI may have normal-appearing cranial CT scans when they are obtained early after sustaining the injury. Young infants are also vulnerable to inflicted injury; most inflicted injury-related deaths involve TBI. Patients who have suffered abusive head trauma commonly present with altered mentation, coma, seizures, emesis, or irritability. A history of the mechanism of injury is often lacking or injuries may be out of proportion to the history or developmental milestones. The injury pattern includes subdural hemorrhage, subarachnoid hemorrhage, skull fractures, or DAI with or without cerebral edema. The outcome after inflicted TBI is typically poor.For epidural hematoma, the classic sequence of events after sustaining a head injury is an initial loss of consciousness, followed by a lucid interval, followed once again by an alteration in the level of consciousness. This classic presentation occurs in less than one third of the cases; in other cases there may be no history of loss of consciousness or persistent loss of consciousness from the time of the injury. The rapid increase in ICP is a result of arterial bleeding, most commonly the middle meningeal artery from injuries around the temporal region. Prompt recognition of the injury is critical to providing appropriate medical or surgical intervention. A subdural hematoma results from bleeding from bridging veins or dura and can lead to increased ICP, as seen with epidural hematomas. Deterioration generally is not as rapid as with an epidural hematoma and may occur hours to days after the initial injury. A cerebral contusion represents direct injury to the brain parenchyma and can be seen with CT scan. Subarachnoid hemorrhage is common with severe brain injury and leads to blood in the cerebrospinal fluid. A concussion is a head injury that causes at least temporary neurologic dysfunction, often with loss of consciousness of 1 minute or less. These injuries may be associated with abnormal findings on postinjury magnetic resonance imaging, although a cranial CT scan usually appears normal.A summary of the therapeutic recommendations for management of TBI are shown in Table 2. The goal is to prevent secondary insults to the brain such as hypoxia, hyperglycemia, hyperthermia, hypotension, and increasing ICP, all of which can worsen outcome.Patients who have signs of increased ICP may benefit from temporary hyperventilation. The resulting hypocarbia causes reflex cerebral vasoconstriction that, in turn, reduces the volume of the intracranial vasculature and, thus, the ICP. However, excessive or prolonged (>1 to 2 hours) hyperventilation may lead to excess vasoconstriction and decreased cerebral blood flow, so hyperventilation should be used cautiously. The target Pco2 should be approximately 35 mm Hg to achieve the optimal balance between ICP and cerebral blood flow.Mannitol at a dose of 0.25 to 1 g/kg also is used to reduce ICP, especially if there are clinical signs of impending herniation, such as dilated pupils. The high osmolarity of mannitol draws free water into the vasculature, leading to a decrease in blood viscosity and improved cerebral blood flow. The improvement in cerebral oxygenation then leads to reflex vasoconstriction and lower ICP. Mannitol also must be used with caution because its action as a diuretic may exacerbate hypovolemia and systemic hypotension. Volume expansion with 20 mL/kg normal saline is indicated if there is significant hypotension. Hypotonic fluids or glucose-containing solutions should be avoided because they can harm the injured brain. Many of these steps are taken simultaneously in the typical trauma patient.Table 2: Recommendations for Acute Management of Severe Traumatic Brain InjuryRecommendationsBlood glucoseMaintain <200 to 250 mg/dL (11.1 to 13.9 mmol/L)TemperatureAvoid hyperthermiaCool patients to 36.0 to 37.0°CConsider hypothermia (32.0 to 34.0°C) for refractory elevated ICPCBF and Paco2Consider brief periods of mild hyperventilation for impending herniationSystolic blood pressureCorrect hypovolemia rapidlyMaintain systolic blood pressure >5th percentile for age (may be beneficial to maintain systolic blood pressure >50th percentile)CPP (MAP-ICP)Elevate head of bed to 30 degrees and maintain patient head position in midlineMaintain >40 mm HgICPConsider mannitol 0.25 to 1 g/kgConsider 3% hypertonic saline 0.1 to 1 mL/kg per hourSeizuresConsider prophylactic anticonvulsantCBF=cerebral blood flow, CPP=cerebral perfusion pressure, ICP=intracranial pressure, MAP=mean arterial pressureAmerican Board of Pediatrics Content Specification(s)Define the common types of central nervous system injuries due to blunt head trauma in children, including those associated with nonaccidental trauma.Understand the mechanisms leading to increased intracranial pressure following blunt head trauma.Question: 3A 16-year-old boy presents to the emergency department after losing consciousness while walking to school this morning. He states that he has no history of headache, chest pain, or palpitations; he was “out” for few minutes; and he recovered spontaneously. He adds that he has felt dizzy for a few days. Paramedics documented a heart rate of 42 beats/min and blood pressure of 100/55 mm Hg at the scene. On physical examination in the emergency department, he has a temperature of 36.3?C, heart rate of 38 beats/min, respiratory rate of 25 breaths/min, blood pressure of 95/55 mm Hg, and capillary refill of 2 seconds. He weighs 45 kg, is 5 ft 11 in tall, and reports no orthostatic hypotension. Skin examination reveals some dry, scaly skin and yellow discoloration of his soles and palms. Twelve-lead electrocardiography shows sinus bradycardia.?Of the following, the MOST appropriate next step isA.admission to the hospital for observation?B.application of a transcutaneous pacer?C.discharge with an appointment for outpatient cardiology evaluationD.trial of intravenous normal saline bolusE.trial of one dose of intravenous epinephrineCorrect answer AOtherwise unexplained bradycardia, as described for the boy in the vignette, is an indication to rule out an eating disorder. Additional findings that should raise concern for an eating disorder are the boy’s weight (<3rd percentile) and associated skin findings. Accordingly, he should be admitted to the hospital for assessment and management of a possible eating disorder. Outpatient consultation with cardiology may be indicated if inpatient evaluation reveals an underlying cardiac abnormality. Intravenous epinephrine may be indicated in patients who have hemodynamically unstable bradycardia, and pacing may be indicated if the bradycardia is due to heart block. A normal saline bolus may be administered to patients who have syncope and orthostatic hypotension, but this therapy does not address bradycardia.??A high index of suspicion is required to diagnose eating disorders because few affected patients meet the strict criteria for bulimia nervosa and anorexia nervosa; most are classified as having “eating disorder not otherwise specified.” The latter group requires aggressive therapy to prevent progression and long-term complications. Such treatment can substantially decrease morbidity. Eating disorders affect children of both sexes and various racial backgrounds. Although most common in adolescents, eating disorders are increasingly recognized in younger children. High-risk factors include a family history of eating disorders, participation in sports or other activities that require weight limits (eg, running, gymnastics, ballet), excessive dieting, compulsive behaviors, and low self-esteem.??????Diagnosis can be aided with patient tools such as the SCOFF questionnaire, Eating Disorder Screen for Primary Care (ESP), or Eating Attitudes Test (EAT). However, negative results may not rule out the diagnosis because patients are frequently in denial and hide the symptoms.A few questions may be helpful to start a conversation about the illness and may indicate the need for detailed questioning:?Are you concerned about your weight and feel that you are fat while people around you say that you are thin?Do you skip meals to lose weight??Do you make yourself throw up after eating?Do you think you have an eating disorder?Presenting symptoms and physical examination findings seen with eating disorders are:Weight loss, cachexia, unnecessary dietingSyncope, dizzinessUnexplained vomiting, Mallory-Weiss tears, heart burn, bloating after oral intakeMenstrual irregularitiesPubertal arrestBradycardia, hypotension, hypothermia.Skin changes (lanugo hair, dry skin, carotenemia)Peripheral edema and cool extremitiesEnlargement of salivary glandsRussell sign (callous on knuckles)Flat affect, suicidal ideation, obsessive compulsive symptoms?Assessment of a patient in whom an eating disorder is suspected includes:Weight and heightVital signs and assessment for presence of bradycardia and hypotension (heart rate <50 beats/min and/or systolic blood pressure <90 mm Hg are indications for inpatient management)Temperature (<35.6?C is an indication for inpatient management)Electrocardiography (prolonged QT) and chest radiography (cardiomegaly)Complete blood count and electrolytes assessment, including calcium, magnesium, and phosphorus (potassium of 3.0 mEq/L [3.0 mmol/L] is an indication for inpatient management; other abnormalities include anemia, leucopenia, hypoglycemia, hypophosphatemia)Serum cholesterol and uric acid (elevated)Thyroid function tests (sick euthyroid)Renal function tests and urinalysisLiver function tests, total protein, and amylase and lipase measurementsAmenorrhea evaluation (serum human chorionic gonadotropin, prolactin, luteinizing hormone, and follicle-stimulating hormone)Assessment for coexisting psychiatric conditions: depression, suicidal ideation, and obsessive compulsive disorderAssessment of failure of outpatient therapy in a patient who has a known diagnosisSerious complications associated with eating disorders include:Respiratory: pneumothorax and pneumomediastinumCardiac: arrhythmias, cardiomegaly, pericardial effusion, mitral valve prolapseAbdominal: ascites, pancreatitis, Mallory-Weiss tears, renal calculi, superior mesenteric artery syndrome (with severe weight loss)Central nervous system: seizure, pubertal arrestPsychological: Suicide (patients who have bulimia nervosa at the highest risk)Refeeding syndrome: cardiac failure, fluid retention, and polyuria.??Other clinical conditions that can present similarly to eating disorders include celiac disease, inflammatory bowel disease, chronic infections, thyroid disorders, type 1 diabetes, and pituitary abnormalities.?American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of eating disordersPlan the assessment, including use of ancillary studies, in eating disordersQuestion: 4A 21-month-old boy is brought to the emergency department via helicopter after a motor vehicle collision. He was restrained in a forward-facing car seat in a mini-van that rolled over, and his car seat was dislodged from the van. He was found apneic and pulseless by emergency medical services responders. They appropriately extracted him from his car seat, began cardiopulmonary resuscitation, and accomplished endotracheal intubation at the scene. The boy’s spontaneous circulation returned rapidly without the administration of medications. En route, the helicopter paramedic reports the child’s heart rate is approximately 80 beats/min and his blood pressure was initially 130/70 mm Hg but now is 65/40 mm Hg. He has received approximately 15 mL/kg of 0.9% saline solution but no medications. Upon arrival at the emergency department, the child has an endotracheal tube in place, his eyes are open and seem to follow the activities of the medical team, his heart rate is 74 beats/min, blood pressure is 52/30 mm Hg, and oxygen saturation is 100% with an Fio2 of 1.0. He has no spontaneous respiratory effort or movement. His Glasgow Coma Scale score is 5 (eyes=3, verbal=1 (intubated), motor=1). He has no external signs of trauma except a bruise over his right forehead. Rectal tone is absent and priapism is noted. Point-of-care testing shows a hematocrit of 37% (0.37).Of the following, the BEST approach to managing this boy’s hypotension isA.0.9% sodium chloride intravenous bolus and intravenous mannitolB.0.9% sodium chloride intravenous bolus and norepinephrine infusionC.3% sodium chloride intravenous bolus and dopamine infusionD.3% sodium chloride intravenous bolus and norepinephrine infusionE.packed red cells infusion and dopamineCorrect answer: BThe boy described in the vignette has signs of neurogenic shock related to a complete spinal cord injury. Assessment and treatment of hypotension in this setting includes searching for and treating any accompanying hemorrhagic injuries, standard administration of fluid and blood products, and aggressive treatment to maintain an adequate blood pressure for spinal cord perfusion that can minimize secondary spinal cord injury. Primary α-agonists (norepinephrine or phenylephrine) have the advantage of maximizing vasoconstriction with limited effect on cardiac plete spinal cord injuries often are followed by an immediate physiologic loss of all spinal cord function caudal to the level of the injury. This state, which is associated with flaccid paralysis, complete anesthesia, absent bowel and bladder control, and loss of reflex activity that may be accompanied by priapism in males, is referred to as spinal shock. There may be an initial period of hypertension due to a surge of catecholamine release, followed by hypotension.Neurogenic shock refers to hypotension, usually associated with bradycardia believed to be due to the interruption of autonomic pathways in the spinal cord causing vasodilation and decreased vascular resistance. It is a form of distributive shock. Spinal cord ischemia is believed to be one of the major causes of neuronal injury and neurologic deficits after spinal cord injuries. Although no human clinical trials have shown benefit from aggressive treatment of hypotension in patients who have neurogenic shock, animal data show that hypotension after spinal cord injuries is associated with worse neurologic outcomes. Several case series in adult victims of spinal cord injury suggest better neurologic outcome and a lack of adverse effects with similar aggressive management.No evidence supports the superiority of a single approach to management of cardiovascular derangements in this population. Hypovolemia should be corrected and sources of blood loss sought and treated. Typical fluids for resuscitation should be administered. Hypertonic saline and mannitol are used in patients who have severe brain injuries and evidence of herniation, but there is no evidence or recommendation for their use in spinal cord injuries. Blood should be used in patients exhibiting blood loss or evidence of anemia.The choice of vasoreactive agents has not been the subject of clinical trials. Initial treatment with dopamine may be started. Agents that are primarily α-agonists, such as norepinephrine or phenylephrine, have been recommended by some experts due to their effect on vascular tone with fewer direct cardiac effects.American Board of Pediatrics Content Specification(s)Understand the pathophysiology of neurogenic shockQuestion: 5An 8-year-old boy presents to the emergency department for evaluation after being struck in the right eye with a baseball while attempting a catch in the outfield. He did not lose consciousness, has had no nausea or vomiting, and reports normal vision until the swelling obscured his right eye. He has no other injuries. On physical examination, his vital signs are within normal parameters. His left eye appears normal, with a briskly reactive pupil, and he experiences no right eye pain with extraocular movements or pupillary light examination of the left eye. His right upper and lower eyelids are markedly swollen, ecchymotic, and tender. The right globe is not visible due to swelling. Computed tomography scan of the orbits reveals only superficial soft-tissue swelling, with no evidence of fracture, foreign body, or intraorbital abnormalities.Of the following, the MOST appropriate approach to view and evaluate this boy’s globe is toA.apply direct pressure with the thumb and index finger over the soft tissues of the upper and lower lidsB.insert a lid speculum under the upper and lower lid margins, then open the speculumC.place a cotton swab at the tarsal plate margin, grasp the lashes, and invert the upper lidD.place a cotton swab on the upper and lower lids, rotate it toward the lashes, and apply pressureE.refer the patient for outpatient ophthalmology consultation within 24 hoursCorrect answer: BThe boy described in the vignette has experienced blunt trauma to the orbital area and is at risk for a ruptured globe. Normal findings on computed tomography scan do not rule out this diagnosis or other injuries such as hyphema, traumatic iritis, vitreous detachment, or retinal detachment. Any procedure that could apply direct pressure to the globe or otherwise increase intraocular pressure is contraindicated until a more thorough ophthalmologic evaluation is completed.Several potential methods can allow viewing and evaluation of the globe and periocular tissues in patients who are uncooperative or who have significant swelling. For the patient suffering traumatic injuries in whom a ruptured globe is possible, use of an ocular speculum or two lid retractors is unlikely to put pressure on the globe. Lid specula are specifically designed for this purpose: the speculum is squeezed to close the two arms, one arm of the speculum is slid under both the upper and lower lid margins, and the speculum is released. Patients may experience some discomfort from the stretching sensation, but most tolerate the procedure well. Lid retractors are designed to retract one lid, but use of two simultaneously can allow viewing of the globe. If commercial lid retractors are not available, they can be fashioned from paper clips, but care should be taken to ascertain that no particles or fragments are present at the point of bending. Uncoated, smooth clips should be used to minimize this risk. Both specula and retractors can extend any lid lacerations further and rarely can result in corneal abrasion.Pressure with the thumb and index finger can be used to counteract mild swelling or contraction of the orbicularis oculi in the uncooperative child. Pressure is placed over the superior and inferior boney orbital rims at the site of muscle insertion (not over the soft tissues of the lids), making contraction impossible. This technique can be used in the setting of trauma if care is taken to avoid pressure on the globe, but it is unlikely to facilitate viewing of the globe in a cooperative patient who has marked swelling.Cotton swabs can be used to open the lids in uncooperative patients or those who have significant swelling, but they should not be used in the setting of trauma because they apply pressure to the globe. Short swabs should be used or the sticks of standard swabs should be broken to prevent breakage during the procedure. Swabs should be placed in the midportion of both the upper and lower lids and light pressure applied to engage the relatively loose skin of the lids. Both swabs are twirled toward the lashes to begin to separate the lids, at which point posterior pressure is applied while separating the swabs toward the orbital rims. Lid eversion can result if either the direction of rotation is incorrect or pressure is inadequate, prohibiting viewing of the globe. The use of a single swab at the tarsal plate margin allows upper lid eversion, which is used to examine the upper lid fully and exclude any retained foreign bodies or facilitate complete irrigation of the eye. This procedure is not indicated for a patient who has eyelid swelling and is contraindicated in the setting of trauma.Although ophthalmology consultation may be necessary after full evaluation of the boy in the vignette, lid retraction can facilitate evaluation of visual acuity, potential corneal abrasion, hyphema, traumatic iritis, and open globe.?In addition to opening or everting the lids, pediatricians and pediatric emergency medicine physicians should be familiar with several other common general pediatric ophthalmologic procedures. Evaluation of best corrected visual acuity in both eyes should be performed in most, if not all, patients who have ocular complaints. A standard chart appropriate for the child’s age, developmental level, and reading capability should be used to assess the best corrected acuity in each eye individually. Care must be taken to shield the contralateral eye completely to prevent “cheating.” The unaffected eye should be tested first to build comfort and confidence with the process. Improvement of acuity when viewing the chart through a pinhole indicates refractive error rather than acute injury. Direct ophthalmoscopy allows assessment of the posterior retina and optic disc. Viewing can be optimized by decreasing ambient light or through the use of mydriatic drops. Having the cooperative patient concentrate on a stationary object beyond the examiner facilitates viewing of the optic disc. If examining the eye from in front of the patient, the examiner should use the ipsilateral eye to that being examined; alternatively, the examiner can examine the eyes from behind the head of a supine patient, allowing use of the examiner’s dominant eye for both of the patient’s eyes. Assessment of the presence and symmetry of the red reflex, symmetry of corneal light reflexion (Hirschberg test), and instillation of ophthalmic drops and ointments are other common pediatric ophthalmic procedures with minimal risks and complications.American Board of Pediatrics Content Specification(s)Discuss the indications and contraindications for general pediatric ophthalmic proceduresDescribe the key steps and potential pitfalls in performing general pediatric ophthalmic proceduresDiscuss the complications associated with general pediatric ophthalmic proceduresKnow the anatomy and pathophysiology relevant to general pediatric ophthalmic proceduresQuestion: 6A previously healthy adolescent girl presents with a 2-day history of lower abdominal pain and intermittent vaginal bleeding. Her last menstrual period was 8 weeks ago. On physical examination, the girl is afebrile and has a heart rate of 126 beats/min, respiratory rate of 18 breaths/min, and blood pressure of 95/60 mm Hg. She is alert but appears uncomfortable. Palpation of the lower abdomen elicits mild discomfort but no guarding. Pelvic examination reveals a closed os with blood in vault. The cervix is not friable, and there is no vaginal discharge. She demonstrates cervical motion and bilateral adnexal tenderness. A point-of-care pregnancy test is positive, and bedside transabdominal ultrasonography demonstrates an adnexal mass with freefluidin the cul de sac and Morison pouch.Of the following, the MOST appropriate next step is toA.administer anti-D immunoglobulinB.administer intravenous cefoxitin and doxycyclineC.discharge the girl with scheduled obstetric follow-up evaluation tomorrowD.obtain a quantitative β-human chorionic gonadotropin measurementE.obtain an emergent obstetric consultationCorrect answer: EThe tachycardia combined with ultrasonographic findings of free fluid in the cul-de-sac (Figure 1) and abdomen and an adnexal mass on the right (Figure 2) described for the girl in the vignette are highly suggestive of a ruptured ectopic pregnancy with hemoperitoneum. Management includes fluid resuscitation, complete blood count, typing and cross-matching of blood, and an urgent obstetric consultation for surgical intervention. Because ectopic pregnancy is a high-risk condition, patient discharge is not appropriate.A quantitative β-human chorionic gonadotropin (β-hCG) measurement would be helpful if the ultrasonographic findings were indeterminate and the patient was hemodynamically stable. A value that exceeds the discriminatory zone (2,000 mIU/mL) (see discussion below) in the absence of an intrauterine pregnancy (IUP) is suggestive of an ectopic gestation. Antibiotic administration is appropriate for suspected pelvic inflammatory disease (PID), a condition that is uncommon in pregnancy because the cervical mucus plug prevents ascending infection. Further, PID is not associated with free fluid in the abdomen. Administration of anti-D immunoglobulin is indicated for Rh-negative women who have documented first-trimester loss of established pregnancy, which may be appropriate for this girl but is not an immediate priority.Ectopic pregnancy is a high-risk condition that remains the leading cause of pregnancy-related maternal deaths in the first trimester. Fibrosis and tubal scarring from prior episodes of PID predispose to ectopic pregnancies and represent the most common identifiable cause. Other risk factors include tubal ligation or current use of an intrauterine device, treatment with infertility drugs, and peritubular adhesions from previous appendicitis or endometriosis.The classic triad of clinical signs and symptoms of ectopic gestation is a positive pregnancy test, vaginal bleeding, and abdominal pain. Vaginal bleeding is usually light. Vital signs may be normal or may indicate hemorrhagic shock, as for this girl. A relative bradycardia may be present in the patient who has tubal rupture and hemorrhage. Referred pain to the shoulder or upper abdomen may occur in the presence of hemoperitoneum causing diaphragmatic irritation. Physical examination findings are highly variable and range from normal results on pelvic examination to cervical motion tenderness and adnexal tenderness with or without mass. The abdominal examination may yield normal results or demonstrate localized or diffuse tenderness. Complications of ectopic pregnancy include rupture with hemoperitoneum, hypovolemic shock, and death. Infertility is another major morbidity that results from surgical removal of the tubal pregnancy.The most specific finding for ectopic pregnancy is the presence of a live extrauterine pregnancy, found in only 3% to 26% of ectopic gestations. More commonly, an adnexal mass may be seen that can appear as a tubal ring or a solid or complex mass. Early diagnosis is crucial to prevent major complications and sequelae. When diagnosed early, conservative management (ie, methotrexate rather than tubal ligation and removal in surgery) is a viable option that allows for a favorable outcome and can prevent loss of fallopian tubes.Studies have shown that point-of-care ultrasonography by emergency physicians is accurate and safe and decreases throughput times and overall morbidity. The typical strategy of emergency department pelvic ultrasonography protocols in patients who have first-trimester complications is to rule out an ectopic gestation by locating an intrauterine gestational sac. Studies that correlate β-hCG values with pelvic ultrasonography findings have resulted in the concept of a “discriminatory zone,” which is a value above which an IUP should be visible on ultrasonography. This value is generally between 1,000 and 2,000 mIU/mL for a transvaginal ultrasonography and between 4,000 and 6,000 mIU/mL for transabdominal ultrasonography. Typically, patients who have positive pregnancy test results, β-hCG values less than 2,000 mIU/mL, and indeterminate scan results are seen in 48 to 72 hours at an obstetrician’s office unless they have concerning clinical examination findings, ultrasonographic findings suggestive of an ectopic pregnancy (such as an adnexal mass or large peritoneal fluid collections), or comorbidities that warrant inpatient observation. IUP is likely if, in follow-up evaluation, the increase in quantitative β-hCG is greater than 66% within 48 hours, although continued close monitoring should be undertaken until an IUP is confirmed by ultrasonography.Patients whose β-hCG measures greater than 2,000 mIU/mL and who have no gestational sac identified by transvaginal ultrasonography may undergo very close outpatient follow-up evaluation or endometrial sampling. If no endometrial villi are identified, patients are given the option of surgical laparoscopy or medical methotrexate management. The algorithm in Figure 3 summarizes the approach to a patient in the emergency department who has suspected ectopic pregnancy.0000Figure 3: Treatment algorithm for suspected ectopic pregnancy in the emergency departmentAmerican Board of Pediatrics Content Specification(s)Recognized the signs and symptoms and complications of ectopic pregnancyKnow the indications for and interpret results of ancillary studies in patients with ectopic pregnancyQuestion: 7A 6-year-old girl who has a history of acute lymphocytic leukemia (ALL) is brought to the emergency department with runny nose, cough, and red eyes of 2 days’ duration. Her parents thought she felt warm yesterday, and she now has a temperature of 39.7°C, a morbilliform rash on her face (Figure 1), and a worsening cough. In triage, her respiratory rate is 44 breaths/min, heart rate is 142 beats/min, blood pressure is 94/62 mm Hg, and oxygen saturation is 91% in room air. Her chest radiograph is shown in Figure 2.Figure 1Figure 2Of the following, in addition to supportive care (oxygen, fluids, antipyretics), the MOST appropriate treatment isA.acyclovir and vancomycin intravenousB.cefotaxime and ribavirin intravenousC.immune globulin intramuscular and cefotaxime intravenousD.vancomycin and cefotaxime intravenousE.vitamin A intramuscular and vancomycin and cefotaxime intravenousCorrect answer: EThe girl described in the vignette has measles. Pneumonia is a common complication and the most common cause of death associated with this disease worldwide. In addition to treatment for her pneumonia, The World Health Organization (WHO) and the American Academy of Pediatrics (AAP) recommend treatment with vitamin A for children who have measles because such treatment in developing countries has been shown to decrease both morbidity and mortality. Even in the United States, children who have measles have been shown to have low vitamin A concentrations, which are lower in those who have more severe infections. In a Cochrane review, use of two doses on two successive days decreased mortality in children younger than 2 years of age. The WHO recommends vitamin A for all children who have acute measles, regardless of where they live. The AAP recommends that vitamin A be considered in:Patients 6 months to 2 years of age hospitalized with measles and its complications (eg, croup, pneumonia, diarrhea)Patients older than 6 months of age who have measles and any of the following risk factors and are not already receiving vitamin A: immunodeficiency, ophthalmologic evidence of vitamin A deficiency, impaired intestinal absorption, moderate-to-severe malnutrition (including eating disorders), or recent immigrants from areas in which high mortality rates from measles have been observedVitamin A for this indication is administered once daily for 2 days in the following doses:200,000 IU for children 12 months and older100,000 IU for children 6 to 11 months50,000 IU for children younger than 6 monthsThe dose may be administered parenterally or orally. A third, age-specific dose should be administered 2 to 4 weeks later to children who have clinical signs and symptoms of vitamin A deficiency.Because the girl in the vignette has presumed immunosuppression (eg, history of ALL) and severe pneumonia, broad-spectrum antibiotics also should be part of her therapy.Treatment of measles is primarily supportive. Intramuscular immune globulin may prevent or modify the infection if administered within 6 days of exposure, but it does not have a role in treatment of active infection. There is no specific antiviral therapy. Ribavirin is active against measles in vitro and has been used by both the aerosol and intravenous routes for severely affected, severely immunocompromised children, but no controlled trials have shown benefit.?Ribavirin is not licensed by the United States Food and Drug Administration for treatment of measles. Acyclovir is not indicated for treatment but could be considered if the pneumonia in the patient in the vignette was believed to be due to a coinfection with Herpes simplex virus.Measles is caused by a single-stranded RNA paramyxovirus in the genus Morbillivirus. It is transmitted by infectious droplets from the respiratory secretions of an infected person and is highly contagious, with very high secondary attack rates. Subclinical infections are very rare. Infection begins with invasion of the respiratory epithelium of the nasopharynx. Over 2 to 3 days, the virus replicates at this site and throughout the regional lymphatic system. A period of viremia follows, leading to infection of the reticuloendothelial system. With further viral replication, a second period of viremia occurs 5 to 7 days after the initial exposure, and other sites are infected. Infected persons shed virus from the nasopharynx until 3 to 4 days after they develop a rash. Shedding may be prolonged in immunosuppressed patients.The incubation period after exposure is usually 10 to 12 days, followed by a prodrome of 2 to 4 days (may be as short as 1 day or as long as 7 days). The prodrome consists of fever that increases over the period of the prodrome, cough, coryza, and conjunctivitis. White to blue-white spots on a bright red background (Koplik spots) may be found on the buccal or palatal mucosa near the end of the prodromal period until 1 to 2 days after the appearance of the rash. When found, Koplik spots (Figure?3?and Figure 4) are considered pathognomonic for measles.Rash usually develops 2 to 4 days after the onset of the prodrome and approximately 14 days after exposure. It starts at the hairline and spreads downward, initially involving the face and upper neck (Figure 5), usually reaching the hands and feet within 3 days (Figure 6). The rash is maculopapular and begins as discrete lesions but often becomes confluent, especially over the upper body and face. Initially, the rash blanches with pressure, but it often does not blanch after 3 to 4 days. A mild form of the rash develops on the palms of some individuals. Some petechiae may be seen in severely affected areas. As it begins to resolve, the rash often becomes brown, and some mild desquamation may develop in more severely affected areas. The rash may be absent in severely immunocompromised individuals.Associated symptoms of measles infection include anorexia, diarrhea, and generalized adenopathy. Photophobia, sore throat, headache, and abdominal pain may also be seen. Hemorrhagic measles, which rarely is seen in developed countries, may be related to underlying malnutrition or immunosuppression. It is characterized by very high temperatures (40.6 to 41.1°C), seizures, delirium, respiratory compromise, and hemorrhage into the skin and mucous plications occur in up to 30% of reported cases and range from mild (otitis media and diarrhea) to severe. Seizures (febrile or afebrile) are reported in 0.6% to 0.7% of cases. Pneumonia is seen in up to 6% of cases and may be viral or represent a superimposed bacterial infection. It may occur during the primary infection or as symptoms seem to be resolving. Pneumonia remains the most common cause of death in patients who have measles infections.Acute encephalitis is seen in about 0.1% of infected individuals. Typically, fever, headache, vomiting, meningismus, seizures, and coma develop about 6 days after the onset of rash (range of 1 to 15 days). Cerebrospinal fluid analysis reveals pleocytosis and high protein values.Laryngotracheobronchitis (croup) has been noted commonly in United States children hospitalized with measles. Symptoms were often severe and frequently necessitated intubation. Tracheal cultures showed bacterial superinfection in one third to one half of cases, with Staphylococcus aureus being the most frequent bacterial pathogen. Bacterial tracheitis was usually associated with a purulent exudate. Laryngotracheobronchitis was the second leading cause of death among hospitalized children in the United States.Other complications include mastoiditis, pneumothorax and pneumomediastinum, transverse myelitis, Guillain-Barré syndrome, mesenteric adenitis, appendicitis, and pancreatitis. Keratitis, iridocyclitis, and corneal ulcerations and perforations may be seen, and blindness may result. Thrombocytopenic purpura or disseminated intravascular coagulation may occur. Myocarditis and pericarditis have been reported.Figure 3: Koplik spotsFigure 4: Koplick spotsFigure 5: The rash of measlesFigure 6: The rash of measles involving the entire bodyAmerican Board of Pediatrics Content Specification(s)Recognize signs and symptoms of measlesBe familiar with the complications of measlesPlan management of acute measlesQuestion: 8The parents of a 3-year-old girl are concerned about a blistering rash on her buttock that erupted 3 days ago and seems to be spreading. The rash is only mildly pruritic and painless. The child is otherwise healthy. She attended a summer day camp 2 weeks before presentation to the emergency department. The parents are unaware of any trauma or exposure to allergens or toxic substances. On physical examination, the girl is afebrile, has normal vital signs, and has no lymphadenopathy. The only finding of note is the rash (Figure).FigureOf the following, the condition MOST characteristic of these findings isA.cellulitisB.contact dermatitisC.ecthymaD.impetigoE.second-degree burnCorrect answer: D EThe numerous superficial, rounded, nontender, red-based ulcerations on the left buttock with a varnishlike crust on the largest lesion described for the girl in the vignette are characteristic of bullous impetigo. Cellulitis involves edema, induration, warmth, erythema, and tenderness with indistinct margins. Regional lymphadenopathy, fever, chills, and malaise are also commonly noted. Second-degree or partial-thickness burns are included in the differential diagnosis of any patient who has blisters and erythema, especially if the history and physical examination raise suspicions of abuse. However, the burned area is usually very painful and well circumscribed. Acute contact dermatitis is an inflammatory response to an irritant or antigen that usually presents with clear fluid-filled bullae or vesicles on an underlying erythematous base and typically is intensely pruritic. Ecthyma is characterized by a firm, dry, dark crust with surrounding erythema and induration. Invasion well into the dermis distinguishes ecthyma from common impetigo.Bullous impetigo is a skin infection that usually occurs in children, representing approximately 10% of skin lesions seen in pediatric clinics. First described in the 1860s by Dunn and Fox, impetigo can be divided into nonbullous and bullous entities. Bullous impetigo most commonly affects children younger than 2 years. Nonbullous impetigo accounts for about 70% of cases of impetigo and typically affects traumatized skin on the face or extremities. The prevalence of nonbullous impetigo is higher in tropical climates and at lower altitudes. The infection is also associated with crowded living conditions and poor hygiene. Impetigo occurs with equal frequency in males and females.The lesions of bullous impetigo are thin-roofed bullae, often smaller than 3 cm, that rupture easily and leave honey-colored crusts. They occur on intact skin, most often the extremities, face, trunk, and buttocks. This child’s infection may have begun with a bite or a scratch on the buttock. Secondary edema or erythema and regional adenopathy are not generally seen. In approximately 80% of cases, bullous impetigo is caused by Staphylococcus aureus, phage group 2. Nonbullous impetigo is usually caused by S aureus or group A β-hemolytic streptococci (GABHS). The staphylococcal epidermolytic toxin causes intraepidermal cleavage below or within the stratum granulosum to produce the typical lesion. The vesicles enlarge into bullae, which rupture and may form the tinea-like scale that is seen in several lesions. The diagnosis is generally based on the history and physical examination findings. Laboratory studies such as antistreptolysin O titers or Gram staining and culture are not usually required.????????Most cases of bullous impetigo are self-limited and resolve with gentle wound cleansing and attention to hygiene. However, the infection can progress and the lesions are unsightly. The first line of treatment involves application of topical agents such as mupirocin or retapamulin. Mupirocin may be more effective than bacitracin or neomycin. Retapamulin is not approved for treatment of methicillin-resistant S aureus (MRSA) infections. Patients who do not benefit from use of topical agents or demonstrate disseminated lesions usually respond to administration of oral antibiotics. Prior recommendations for beta-lactam antibiotics might be outdated because of the recently reported incidence of MRSA in skin and soft-tissue infections. Suggested regimens include clindamycin or doxycycline monotherapy or trimethoprim/sulfamethoxazole (for MRSA) plus a beta-lactam (for GABHS). Some practitioners still choose to use beta-lactam antibiotics as first-line therapy and reserve antibiotics directed toward MRSA for those cases that do not respond to the initial antibiotics.Good handwashing habits and avoidance of contact with infected persons help minimize the spread of infection. Neonates and patients who have widespread disease are at greater risk for complications, which include poststreptococcal glomerulonephritis (all ages), bacteremia, sepsis, meningitis, and septic arthritis. Treatment with antibiotics does not reduce the risk of glomerulonephritis.American Board of Pediatrics Content Specification(s)Know the indications for treatment of and the therapies for impetigoOCTOBER 2011Question: 1A 3-year-old girl was playing with her older brother in the kitchen when she accidentally sprayed a household oven cleaner in her eyes. She has been screaming since it occurred and is keeping both her eyes squeezed shut. She has had no difficulty breathing and no drooling, lip or tongue swelling, or skin burns. No treatment was initiated at home.?The parents brought the container with them to the emergency department, and the label indicates that the agent is alkaline, with a pH of 9. On physical examination, the crying child is difficult to console and the only unusual vital sign is tachycardia. She has bilateral blepharospasm and mild lid edema, both sclerae are markedly injected, and she has excess tearing bilaterally.Of the following, after instilling topical anesthetic eyedrops, the MOST appropriate next step is toA.consult ophthalmologyB.instill fluorescein for Wood lamp examinationC.irrigate both eyes with normal salineD.obtain an orbital computed tomography scanE.perform visual acuity testingCorrect answer CThe girl described in the vignette has suffered ocular injury from alkali exposure. Immediate irrigation with copious volumes of normal saline or lactated Ringer solution should be initiated without delay.?Necessary steps in the evaluation, such as fluorescein examination and evaluation of visual acuity, should not be undertaken until after irrigation is completed. Ophthalmologic consultation is indicated in all significant ocular chemical exposures but should not delay initiation of irrigation. Computed tomography scan is not indicated for a patient who has chemical exposure without associated trauma.Eye irrigation should be initiated as soon as a chemical eye injury is suspected. If both eyes are involved, as with this girl, both eyes should be irrigated simultaneously. Application of tetracaine or other topical anesthetic agent, if readily available, can diminish the patient’s pain and facilitate effective irrigation.The extent and severity of damage to the eye are determined by the properties of the chemical involved, area of ocular surface affected, and duration of exposure. Alkalis are more likely to produce severe ocular injury due to their ability to penetrate deeper into the eye. Acidic chemicals produce coagulation necrosis, which forms a barrier that helps prevent deeper penetration. Hydrofluoric acid is an exception, acting more like an alkali and penetrating deeply.No specific amount of fluid or duration of time is recommended for irrigation; irrigation should continue for a minimum of 15 to 20 minutes and until ocular pH is normalized (7.4) and all particulate matter has been removed. Severe exposures may require several liters of fluid or several hours of irrigation. During irrigation, the lids should be everted to ensure decontamination of the entire ocular surface and all recesses of the lids. Any particulate matter should be removed with a cotton-tipped swab or scalpel edge. Retained particles may allow ongoing chemical exposure and injury or may cause mechanical injury, resulting in corneal abrasions.American Board of Pediatrics Content Specification(s)Know which chemicals require immediate eye decontaminationQuestion: 2A 13-year-old previously well adolescent is brought to the emergency department with complaints of weakness and occasional double vision. These symptoms started 1 month ago when she started complaining of weakness, especially in gym class. Over the past few days, the weakness has increased, and she feels tired after walking a few steps. The double vision is a particular problem at school and while doing homework. She has no history of fever, weight loss, difficulty in breathing, palpitations, change in bowel or bladder habits, or change in appetite. She has no other systemic symptoms. Menarche occurred 6 months ago. She has been bullied at school, and she attempted suicide 1 year ago by ingesting a pesticide. After that attempt, her parents decided to change her schools. The mother mentions that the family was on a camping trip 4 months ago, and on further questioning, she reports that everyone had insect bites, and this daughter needed a tick removed from her scalp. On physical examination, the adolescent is awake, oriented, and in no apparent distress. She has mild bilateral ptosis that worsens when asked to maintain a sustained upward gaze. Findings on her systemic examination, including a comprehensive neurologic evaluation, are normal.Of the following, the pathogenetic basis for this girl’s illness MOST likely involvesA.abnormal release of acetylcholine at the neuromuscular junctionB.absence of postsynaptic acetylcholine receptorsC.presence of acetylcholinesterase inhibitorsD.presence of postsynaptic acetylcholine receptor antibodiesE.presence of social stressors and behavioral issuesCorrect answer: DPtosis that worsens on prolonged upward gaze, as described for the girl in the vignette, indicates muscle fatigue and is characteristic of myasthenia gravis. The most common form of myasthenia is juvenile or late-onset myasthenia gravis, which is due to the presence of autoantibodies against the postsynaptic acetylcholine receptor at the neuromuscular junction.The neuromuscular junction consists of a presynaptic axon terminal and the postsynaptic muscle motor end plate. When an action potential reaches the presynaptic axon, a complex series of steps occurs, involving adenosine triphosphate, magnesium, calcium, and sodium, and culminating in the release of the neurotransmitter acetylcholine (Ach) in the neuromuscular junction. Ach binds to Ach receptors on the postsynaptic motor end plate to trigger depolarization. If the depolarization is of sufficient magnitude, muscle action potential is generated, leading to muscle contraction. The free Ach in the synapse is rapidly degraded by the enzyme acetylcholinesterase.Transient neonatal myasthenia gravis is seen in newborns born to women who have myasthenia following transplacental transfer of maternal anti-Ach receptor antibodies. This reversible condition can mimic congenital myasthenia and is unlikely in an adolescent. The absence of postsynaptic Ach receptors is the basis of congenital myasthenia gravis, a rare irreversible condition that manifests early in life with respiratory distress, feeding difficulties, and hypotonia.Two conditions that can mimic myasthenia gravis are tick paralysis and botulism. The acute nature of these two illnesses distinguishes them from myasthenia gravis.Tick paralysis is mediated by a toxin produced by wood or dog ticks, which causes a decrease in release of Ach at the neuromuscular junction. Patients present with weakness, loss of coordination, and ascending paralysis with sensory symptoms. Tick paralysis should be considered in the differential diagnosis of myasthenia gravis. This acute condition begins within a few hours to days after a tick bite, and the diagnosis is confirmed by locating the tick. Careful and complete removal of the tick leads to resolution of signs within hours to days.Botulism most commonly results from ingestion of foods containing botulin toxin (honey). This toxin acts by binding irreversibly to postsynaptic Ach receptors. Nausea, vomiting, and diarrhea develop within hours of ingestion, quickly followed by cranial nerve involvement (diplopia, absent gag reflex, facial muscle weakness), hypotonia, and respiratory distress. Recovery depends on regeneration of new postsynaptic receptors and is a prolonged process.Ingestion of pesticides (organophosphate chemicals) may cause a myasthenia-like syndrome due to their anticholinesterase activity, but the girl has no history of a recent ingestion. Conversion reaction should always be considered in the differential diagnosis, especially in an adolescent patient who has a history of emotional and social stressors. However, the presence of a demonstrable neurologic deficit makes this condition unlikely for this girl.Patients who have the most common form of myasthenia gravis typically present with gradually worsening ptosis and diplopia due to weakness of external ocular muscles. The symptoms worsen throughout the day and are especially prominent after repeated or sustained activity. Weakness in skeletal muscles can be demonstrated by asking the patient to hold the head up when lying in a supine position or after repeated opening and clenching of the fist. With progressive disease, patients complain of difficulty in swallowing, chewing, and facial muscle weakness, eventually leading to respiratory muscle weakness and respiratory failure. Decremental muscle response following repeated nerve stimulation on electromyography is diagnostic. Testing for serum anti-Ach receptor antibodies is not a sensitive indicator of disease.Muscle biopsy is not helpful in the diagnosis of myasthenia gravis. Transient and rapid improvement of ptosis or external opthalmoplegia in response to a short-acting anticholinesterase inhibitor (edrophonium) is confirmatory.Although some cases of mild myasthenia gravis can be managed with no medications, most patients require cholinesterase inhibitors (oral or parenteral neostigmine or pyridostigmine) administered every 4 to 6 hours. Because of the autoimmune basis of the disease, therapeutic relief can be expected in some patients with corticosteroids, plasmapheresis, immune globulin intravenous, or thymectomy. Patients who have congenital myasthenia gravis may worsen with the use of cholinesterase inhibitors; they are treated with ephedrine or diaminopyridine, both of which increase Ach release from terminal axons. Patients who have transient neonatal myasthenia gravis require cholinesterase inhibitors for a few days to weeks to allow feeding.American Board of Pediatrics Content Specification(s)Know the etiology and pathophysiology of myasthenia gravisRecognize signs and symptoms and life-threatening complications of myasthenia gravisPlan management of acute myasthenia gravisQuestion: 3You are examining an anxious 8-year-old boy who sustained a deep stellate forehead laceration after a fall onto a tree stump while running. He has not lost consciousness or vomited. His mother reports that he is afraid of needles. On physical examination, the alert boy exhibits coryza and cough, has vital signs within normal limits, and has a Glasgow Coma Scale score of 15. His lungs are clear to auscultation. The remainder of his examination findings are normal. Airway evaluation reveals a Mallampati Class 1. His last oral intake was a glass of orange juice 4 hours ago.Of the following, in conjunction with topical anesthesia, the MOST appropriate treatment option for wound management for this boy isA.inhaled nitrous oxideB.intranasal fentanylC.intranasal midazolamD.intravenous propofolE.oral chloral hydrateCorrect answer: AAlthough parenteral propofol is a viable option for wound management, the boy described in the vignette has a needle phobia, and his active upper respiratory tract infection is a relative contraindication to deep sedation. In the presence of an upper respiratory tract infection, absorption of intranasal midazolam can be erratic, and its anxiolytic effect may be unreliable in older children. Chloral hydrate has variable onset and a prolonged duration of effect and is rarely used in the emergency department setting because of the availability of more appropriate options. Intranasal fentanyl is an excellent analgesic but will provide no anxiolysis for this patient.Nitrous oxide (N2O) is the most appropriate agent for this boy because it has both analgesic and amnestic properties and does not require a needle for administration. It has a rapid onset of action (20 sec) and fast offset, rendering it ideal for use in an emergency department. Peak effect is observed in 5 minutes. N2O has low blood solubility, which permits rapid clearance with exhalation, and low lipid solubility, which limits accumulation in the mon indications for N2O use in the emergency department include fracture manipulation, abscess incision and drainage, injection of local anesthetic, removal of foreign bodies from ear or soft tissues, and other minor painful procedures. Contraindications to its use include head injury with loss of consciousness or altered mentation; current acute asthma flare; and potential for expansion of closed, gas-filled space, as with a pneumothorax, bowel obstruction, or otitis media. Adverse events associated with its use include dizziness, nausea, and emesis.Because N2O has no sedative properties, it is most effective in patients who are cooperative (ie, >4 years of age). It is available as a premixed 50:50 combination of N2O and O2 on a demand-triggered system or as a continuous flow via a mixer (maximum concentration is 70% N2O and 30% O2). Usual preprocedure fasting guidelines should be followed. Either two doctors or a nurse and doctor are required for administration: one administering the N2O and the other performing the procedure.When using the demand valve system, it is important to check the cylinder first to ensure a tight seal to the regulator pipe. An appropriate-sized mask or mouth piece is connected to the filter, and the filter is attached to the demand valve. When the cylinder is turned to the open position, the regulator records the amount of N2O left in the tank (if <500 KPa, the cylinder should be changed). The patient?should self-administer N2O with supervision for a few minutes immediately before beginning a painful procedure. A harsh sound is audible on inspiration if the gases are flowing properly. The procedure is performed with the patient continuing to breathe N2O for the duration of the painful part of the procedure and for 1 minute after the procedure is completed. The demand-triggered machine is best suited for an older child who can generate sufficient negative pressure to open the demand valve.When using the continuous flow apparatus, it is important to ensure that the oxygen and N2O tubing are connected to their respective outlets. The filter and appropriate mask are attached to the circuit, and a few drops of flavoring are added, as needed. The suction tubing must be connected to the machine and on low suction only for scavenging exhaled N2O. After turning the knob to allow the bag to inflate, 100% oxygen is administered, and the patient breathes regularly through the mask. The amount of flow is adjusted to maintain the bag as full but not overdistended. The bag should empty with the patient’s breath. The concentration of oxygen is decreased with the central knob without adjusting the flow knob; the flow of N2O and O2 are automatically adjusted. The clinician continues to decrease the O2 concentration (which increases the N2O concentration) until reaching the desired effect of 30% to 50% O2 (50% to 70% N2O). If more than 50% N2O is flowing, the patient should breathe 100% oxygen for 2 to 3 minutes after completion of the procedure. The patient may be discharged after the procedure is complete if he or she has returned to his or her preprocedure mental status.American Board of Pediatrics Content Specification(s)Know the anatomy and pathophysiology relevant to nitrous oxide administrationDescribe the key steps and potential pitfalls in nitrous oxide administrationDiscuss the complications associated with nitrous oxide administrationKnow the anatomy and pathophysiology relevant to nitrous oxide administrationQuestion: 4A 4-year-old girl who was a rear seat passenger wearing a restraint is brought to the emergency department by emergency medical services after a motor vehicle crash. Air bags were deployed, with significant front-end damage to the car. The girl did not lose consciousness. Physical examination on arrival shows a temperature of 37.2?C, heart rate of 125 beats/min, respiratory rate of 30 breaths/min, and blood pressure of 90/55 mm Hg. Her airway is intact, and she has equal breath sounds and palpable peripheral pulses. Her abdomen is not tender, she has a lap seat belt mark, her pelvis is stable, and her Glasgow Coma Scale score is 15. She has left-sided facial swelling, with lower lip buccal laceration. You initiate an intravenous normal saline fluid bolus. Repeat evaluation in 10 minutes documents a heart rate of 140 beats/min, respiratory rate of 35 breaths/min, and blood pressure of 85/50 mm Hg. You perform bedside ultrasonography (focused assessment with sonography for trauma [FAST]).Of the following, the finding on FAST that is the STRONGEST indication for urgent surgical intervention for this girl is fluid in theA.hepatorenal fossaB.pericardial sacC.perinephric areaD.pouch of DouglasE.splenorenal fossaCorrect answer BThe girl described in the vignette is developing signs of hemodynamic compromise (elevation in heart rate and slight decrease in blood pressure). The finding of fluid in the pericardial sac on FAST is the strongest indication for urgent surgical intervention to avoid the development of cardiac tamponade. Fluid in the hepatorenal or splenorenal fossa; hepatic, splenic, or renal laceration; or fluid in the pouch of Douglas may be followed clinically with continuation of intravascular resuscitation measures (fluid boluses) and abdominal computed tomography (CT) scan. If the resuscitation efforts do not correct the ongoing signs of shock, emergent laparotomy is indicated.Children are more likely to sustain blunt abdominal trauma compared with adults. Radiologic assessment of such patients includes plain radiographs, abdominal CT scans, and bedside ultrasonography. Plain abdominal radiographs have limited utility and may be helpful for detection of free air, diaphragmatic injury, excessive peritoneal fluid, and pelvic fractures. Abdominal CT scans have become the gold standard for delineating the extent of abdominal injury, although they are associated with substantial radiation exposure and may potentially delay patient care. FAST has become an important adjunct in the management of trauma, especially for immediate diagnosis of critical abdominal injury and assessment of the need for operative intervention because of the time delay associated with obtaining an abdominal CT scan. However, FAST still is used less frequently in pediatric trauma centers than CT scans due to the difference in management of abdominal trauma in pediatric compared with adult patients. There are currently no authoritative guidelines for the use of FAST in pediatric trauma.The areas evaluated with FAST are hepatorenal fossa (Fig 1), splenorenal fossa (Fig 2), pouch of Douglas (Fig. 3), and pericardial sac. Two scans performed 30 minutes apart are indicated to assess for slow buildup of peritoneal fluid. The sensitivity has been reported as 86% to 97% in various studies, although the evidence in pediatric trauma patients is limited (sensitivity of 40% to 93% and specificity of 79% to 100%). FAST has comparable sensitivity and specificity for detection of abdominal free fluid to diagnostic peritoneal lavage and abdominal CT scans in adult patients. A 5% to 10% false-negative rate has been reported for detection of fluid in the pericardial sac. The accuracy is operator-dependent, with limited value for assessment of solid organ, pancreatic, diaphragmatic, retroperitoneal, and bowel injuries. Patient characteristics that affect the accuracy of FAST include abdominal wall fat, prior scars, and abdominal wall emphysema.Based on the evidence, FAST could be used in a variety of situations involving patients who have blunt abdominal trauma. A suggested algorithm is shown in Figure 4.In hemodynamically stable patients who have significant mechanismof blunt abdominal traumaand no abdominal tenderness, FAST can be used to detect free abdominal fluid and suggest an indication for abdominal CT scan. If FAST results are negative, serial abdominal examination with repeat ultrasonography can be considered; studies have reported that the combination increases the sensitivity of identifying abdominal injury in such patients. For hemodynamically stable patients who have abdominal tenderness, a negative FAST result does not rule out the need for abdominal CT scan because there may be solid-organ injury without free abdominal fluid, especially in pediatric patients.In a hemodynamically unstable patient who has abdominal injury and is unresponsive to aggressive fluid therapy, FAST can be used instead of abdominal CT scan to avoid time delay in making management decisions. If FAST results are negative, extra-abdominal causes for hemodynamic compromise can be addressed. FAST is helpful in the unstable trauma patient who has multisystem involvement and needs operative intervention for extra-abdominal injuries to assess for an abdominal source of hemodynamic compromise.American Board of Pediatrics Content Specification(s)Know indications for and interpret findings on plain x-ray studies following blunt abdominal traumaKnow indications for and interpret findings of ultrasonography following blunt abdominal traumaQuestion: 5A 16-year-old girl presents with swelling and excruciating pain in her shoulder of 2 days’ duration. In addition, she reports fever, malaise, and diffuse body aches. She is on the school track team and has increased her training over the past 2 weeks to 3 hours each day. On further questioning, she remembers a fall 3 days ago, but she finished her run after the fall. On physical examination, the girl appears flushed and in moderate distress, with a temperature of 39.3?C, heart rate of 135 beats/min, respiratory rate of 35 breaths/min, and blood pressure of 90/55 mm Hg. She has a capillary refill of 2 to 3 seconds, clear breath sounds, no murmurs, mild abdominal discomfort, and normal findings on neurologic and joint examinations. Her shoulder is remarkably tender on palpation and appears swollen but has no bruising. She has limited ability to bear weight on the left side. You establish intravenous access, start a fluid bolus, and obtain computed tomography scan (Fig. 1).Figure 1: Computed tomography scan obtained for the patient?Of the following, the MOST critical intervention for this patient isA.blood culture from two peripheral sitesB.magnetic resonance imagingC.plain radiographyD.punch biopsyE.surgical explorationCorrect answer EThe girl described in the vignette most likely has a deep plane infection, such as necrotizing fasciitis or gangrenous myositis. Diagnosis and treatment involves emergent surgical exploration, debridement, and acquisition of deep-tissue cultures. Other investigative tools have limited diagnostic value and should not delay surgical intervention. Blood cultures are more likely to be positive if infection is caused by a single pathogen. Plain radiography or computed tomography scan is used to assess deep-tissue swelling and free air (especially for infections due to Clostridium). Magnetic resonance imaging may be helpful in differentiating between cellulitis and deep-tissue infection and the extent of spread into various compartments. Punch biopsy may yield the causative agent only if appropriate specimens are obtained from sufficient depth in the tissue.?In pediatric patients, necrotizing fasciitis is caused most commonly by a single organism, with most cases due to invasive group A Streptococcus (GAS), most commonly S pyogenes M types 1 and 3. An increasing number of cases are due to methicillin-resistant Staphylococcus aureus (MRSA). The mode of infection is either local (cuts, burns, minor blunt trauma, varicella infection, umbilical cord, circumcision) or via hematogenous spread (eg, infection of a hematoma sustained due to blunt trauma). Polymicrobial infections (aerobic infections with anaerobic bacteria such as Bacteroides, Peptostreptococcus, Prevotella, and Clostridium) occur in the setting of type 2 diabetes, postsurgery, decubitus ulcers, peripheral vascular conditions, dental infections (Ludwig angina), and animal or human bites. Another rare type is due to exposure to marine life, with Vibrio as the causative agent.The first sign of deep plane infection is pain out of proportion to the clinical findings. The infection causes destruction of soft tissue and fascial planes (Fig. 1 and Fig.?2) and thrombosis of vessels, leading to ischemia and necrosis. Over a few days, skin may show erythema (Fig. 3), dusky discoloration, bullae, or blisters. Associated symptoms of fever, myalgias, hypotension, and systemic toxicity can develop due to various toxins (exotoxins A, B, C). Leucocytosis; anemia; coagulopathy; and elevated creatine phosphokinase (CPK), creatinine, and C-reactive protein concentrations can be found.Emergent surgical intervention, including fasciotomy, debridement, and deep-tissue culture, is indicated if necrotizing fasciitis is suspected. This intervention has been shown to reduce the morbidity and mortality when combined with aggressive resuscitation and antibiotic therapy. While waiting for identification of the causative agent, first-line therapy should include broad-spectrum coverage effective against MRSA, GAS, gram-negative, and anaerobic organisms. Once the specific pathogen is identified, therapy can be narrowed. Clindamycin should be included in any regimen because it inhibits protein synthesis, thereby reducing the toxin production. If GAS is identified as the causative pathogen, therapy can be narrowed to penicillin G with clindamycin. Beta-lactam antibiotics are effective against active replicating bacteria by inhibiting the cell wall synthesis. In an established infection, many of the bacteria are in a stationary phase (ie, not actively replicating) and, thus, beta-lactam antibiotics are not effective. This phenomenon is referred to as the “Eagle” effect. Thus, clindamycin should be continued in combination with beta-lactam antibiotics because it inhibits protein synthesis at the ribosomal level and, therefore, is effective against bacteria in the stationary phase.The most common and serious associated complication is toxic shock syndrome (TSS) due to either GAS or staphylococcal infections. In severely ill patients, especially those who have TSS refractory to aggressive fluid and antibiotic therapy, immune globulin intravenous administration is suggested. Another treatment modality that has limited evidence of success is hyperbaric oxygen.Figure 2: Necrotizing fascitis due to omphalitis. Courtesy of Red Book 2009, ? American Academy of Pediatrics.Figure 3: Erythroderma rash. American Board of Pediatrics Content Specification(s)Know the etiology and pathophysiology of deep plane infections (e.g., myositis, fasciitis, and gangrene)Recognize the signs and symptoms of deep plane infectionsBe familiar with ancillary studies in deep plane infectionsPlan management of deep plane infectionsQuestion: 6You are placing a radial arterial catheter on a child who has fulminant meningococcemia, shock, and respiratory failure to obtain serial arterial blood gas measurements.Of the following, in addition to gowns and gloves, the MOST important protective measure you and your team should employ isA.face masks with eye shieldsB.foot coversC.hair netsD.N95 masksE.negative pressure roomCorrect answer ABeyond gowns and gloves, the most important additional safety equipment when performing invasive procedures is a mask with eye protection. A face mask with eye shield provides optimal protection against airway (meningococcus) and eye (blood) exposure. Foot covers and hair nets are less useful in this scenario. N95 masks are used for protection from respiratory pathogens such as tuberculosis. They offer no additional protection compared with a face mask and provide no eye protection. Similarly, a negative pressure room offers no specific eye protection.Health-care settings are fraught with potentials risks to workers. These include workplace violence, trauma from accidents, effects of sleep deprivation, and hazardous exposures. Broadly speaking, hazardous exposures can be characterized as:Drug (chemotherapy, radioactive isotopes)Needlestick (bloodborne pathogens: hepatitis B and C, human immunodeficiency virus)Exposure to body fluids and respiratory secretions (meningococcemia, tuberculosis, methicillin-resistant Staphylococcus aureus, severe acute respiratory syndrome [SARS])Hazardous materials transported to the emergency department on exposed individualsHealth-care workers must protect themselves from occupational exposures, not only to preserve their own well-being but also to avoid acting as an agent to infect or expose other patients. Due to the high acuity, high prevalence of infectious diseases, and increased number of invasive procedures, these risks are amplified in emergency departments. The Centers for Disease Control and Prevention has an extensive website outlining the strategies for prevention and procedures for postexposure prophylaxis.Key steps in protecting health-care workers from hazardous exposure include up-to-date knowledge, proper equipment, frequent training, and timely reporting and postexposure prophylaxis. Pitfalls include overreliance on passive safety equipment and delayed treatment.Methods to prevent needlestick injuries primarily encompass the use of passive safety devices such as blunt suture needles, “safety” catheters (that retract needles after being used), and needleless transfer systems. It is estimated that 75% of needlestick injuries can be prevented with the use of these technologies.Methods to prevent exposure to body secretions and respiratory secretions include the use of proper barrier equipment for each suspected disease. These include negative pressure rooms, gowns, eye protection, gloves, and various face masks.Health-care personnel must take precautions to prevent exposure when caring for patients who present after contact with hazardous materials. Personnel should have heightened suspicion for such exposures at times of mass casualty events. In addition, patients presenting with toxidromes or who are employed in high-risk occupations (eg, chemical factory workers) as well as their family members may pose a risk to the health-care team. If hazardous material exposure is suspected or confirmed, decontamination procedures should be undertaken.American Board of Pediatrics Content Specification(s)Discuss the indications for protecting health professionals against hazardous exposuresDescribe the key steps and potential pitfalls in protecting health professionals against hazardous exposuresQuestion: 7A 2-month-old infant is brought by his parents to the emergency department with left leg swelling that developed while he was in the care of a babysitter. The parents state that the babysitter told them that she did not notice any swelling of the leg while she was watching the baby. She thought he may have “felt warm” but did not measure a temperature at the time. The babysitter also denies any known injury or trauma. The infant has no known medical problems. On physical examination, the infant’s temperature is 37.4°C, heart rate is 160 beat/min, respiratory rate is 34 breaths/min, blood pressure is 89/70 mm Hg, and oxygen saturation is 99% in room air. He has obvious swelling of the left mid-thigh, with tenderness to palpation and pain with attempts to move the left hip. Plain radiographs of the left femur reveal a midshaft spiral fracture of the femoral diaphysis.Of the following, the MOST appropriate ancillary study that now should be obtained isA.bone age puted tomography scan of the ipsilateral legC.magnetic resonance imaging of the ipsilateral legD.plain radiographs of the contralateral femurE.skeletal surveyCorrect answer EPhysical injuries of any type and degree without a reason or with an implausible history or mechanism, as described for the infant in the vignette, should immediately elicit suspicion for child abuse. Vague or changing histories, multiple and major traumatic injuries with reported minor causes, and evidence of older injuries and differently-aged injuries without cause should also raise the possibility of abuse.Ancillary studies looking for additional injuries are warranted for this infant because no plausible explanation for femur fracture has been presented. The high index of suspicion for abuse supports the need to obtain a skeletal survey to look for other occult fractures. Computed tomography scan and magnetic resonance imaging of the leg might be obtained if there is a concern for infection or other abnormality. Contralateral radiographs sometimes are used to verify or exclude pathology of the affected extremity in equivocal cases. Finally, a bone age determination is used to assess the skeletal maturity when evaluating growth or pubertal disorders in children.Certain signs and symptoms are characteristic of physical abuse. Abusive skin injuries tend to occur away from bony prominences, which are the sites vulnerable to nonintentional injury, such as the forehead, anterior lower legs, and elbows. Therefore, particular attention should be paid to the head, neck, upper arms, hands, buttocks, trunk, lower back, and inner thighs. Abusive injuries also may occur in more obscure, covered, or protected body areas such as the ears (Fig. 1), angle of the jaw, axilla, groin, frenula of the lips, and tongue.Bruising is one of the earliest and most commonly recognizable signs of child physical abuse. The age and developmental abilities of the patient should be taken into consideration when evaluating bruises.?Bruising in children who are not developmentally capable of moving about always should raise suspicion for abuse. Characteristic patterned bruising can be seen when specific objects are used to inflict the trauma:Bruising from a hand slap with an open palm results in linear, parallel-spaced bruisingA punch leaves rounded bruises with linear spacing consistent with the knucklesLoop marks (Fig. 2) can be evidence a cord or rope injuryLinear parallel marks can be related to abuse from a belt or paddleBinding or ligatures leave circumferential bruises or abrasions around the wrists and anklesMultiple bites (Fig. 3) and bite marks in body locations inaccessible to the child tend to be more common in abusive injury. Human bites generally leave a distinctive elliptical or oval pattern of bruising instead of the avulsion-type injury with tissue loss or deep punctures seen in animal bites. Bites that have a measurable intercanine distance greater than 3 cm are more suggestive of an adult human bite. Further analysis and special examination techniques may be undertaken by a forensic dentist, if available.Abusive burns may result from contact with hot objects that leave patterned burn wounds mirroring the shape of the object (Fig. 4). ?Forced immersion scald burns leave a distinct, well-demarcated burn wound with little or no splash patterns and tend to be of greater severity than accidental burns. Several distinctive abusive burn patterns have been described:The glove- or stockinglike burn of the arms or legs or a well-demarcated waterline on other parts of the body?when the child is forcibly submergedThe “zebra pattern” when the body is flexed during the immersion, sparing “stripes” of unaffected skinThe “donut hole” sparing of the medial portion of the buttocks when the child is forced to sit in a bathtub of hot water and the buttocks contact the cooler bathtub surface while the surrounding skin is scalded (Fig. 5)The cigarette burn that appears as a circular, 5- to 10-mm, well-demarcated, punched-out lesion that is usually a deep partial-thickness to full-thickness burnFractures in nonambulatory children should raise suspicion for abuse. All of the extremities, skull, and thorax should be palpated carefully for tenderness or swelling. Because some fractures, especially healing ones, may not be clinically evident, a high level of suspicion is important in questionable cases. Specific fractures that are highly suggestive of child abuse include:Complex, multiple, or occipital skull fractures associated with a history of a short fallMetaphyseal fractures, also described as “corner” or “bucket-handle” fractures (Fig 6).Posterior, lateral, or multiple rib fracturesFractures of the scapula, sternum, or spinous processesInflicted traumatic brain injury in children frequently is misdiagnosed upon the child’s first encounter with clinicians because of nonspecific or absent symptoms. Such misdiagnosis is the most common cause of child abuse fatality. Presenting signs and symptoms may vary considerably from seemingly innocuous to life-threatening:Neurologic changes: irritability, limpness, lethargy, new-onset apparently unprovoked seizures, and comaGastrointestinal: vomitingRespiratory: breathing difficulties and apneaVictims of abusive head trauma have variable symptoms, depending on the severity of the injury and the timing at which the child presents. Among the more likely findings are:Subdural hemorrhages without concomitant skull fractureBilateral subdural hemorrhagesSubdural and subarachnoid hemorrhagesMultiple subdural hemorrhages of varying agesSubdural hemorrhages with multiple extensive, multilayer retinal hemorrhagesSolid and hollow viscus organs can be damaged by accidental and nonaccidental trauma. A high suspicion of abuse should be maintained when both injuries are present. Abdominal injuries are the second most common cause of child abuse fatalities. Presenting signs and symptoms can vary from irritability and lethargy to vomiting, abdominal distension, anemia, or shock. No cutaneous findings may be evident, even with significant intra-abdominal injury.Figure 1: Bruising on the inside portion of the earFigure 2: Strap and loop marks suggesting a cord or rope injuryFigure 3: Multiple bite marksFigure 4: Flat iron burn to posterior lower legFigure 5: The “donut hole” sparing of the medial portion of the buttocks associated with forced immersion in scalding hot waterFigure 6: Radiography of metaphyseal fracture, also described as “corner” or “bucket-handle” fractureAmerican Board of Pediatrics Content Specification(s)Recognize the common signs and symptoms of physical abuse in childrenQuestion: 8A 3-year-old girl who was brought to the emergency department with irritability and reported lethargy has a seizure in triage. She has no history of fever, fall, or syncope. The child stayed with her grandmother last night and has been closely supervised by her parents for the past 6 hours. Laboratory analysis demonstrates hypoglycemia and mild acidosis. You administer glucose via intravenous (IV) bolus, which results in an increase in blood glucose from 20 mg/dL (1.1 mmol/L) to 60 mg/dL (3.3 mmol/L). After 30 minutes, you reassess the glucose concentration, which is 30 mg/dL (1.7 mmol/L). Despite continued IV glucose administration, you find it difficult to maintain the girl’s blood glucose concentration over 60 mg/dL (3.3 mmol/L). The endocrinologist whom you consult requests additional laboratory studies that show increased insulin and C-peptide values.Of the following, the MOST likely diagnosis to explain these findings isA.Amanita phalloides ingestionB.exogenous insulin administrationC.glucagon ingestionD.glyburide ingestionE.octreotide ingestionCorrect answer D The persistent hypoglycemia that does not respond to standard glucose therapy described for the girl in the vignette suggests ingestion of an oral hypoglycemic agent, such as glyburide, a second-generation sulfonylurea. Other abnormalities may include hypokalemia and hypophosphatemia, which are related to increased insulin secretion caused by the hypoglycemic medication. Exogenous administration of insulin can be ruled out in this girl by the increased C-peptide value. C-peptide can be useful to distinguish between endogenous (increased by oral hypoglycemic medications) and exogenous (decreased C-peptide values) insulin and in potential factitious disorder by proxy cases, which was shown in one study to be responsible for 29% of reported pediatric sulfonylureas poisonings in the literature. Glucagon and octreotide are potential therapies for hypoglycemia and likely would result in hyperglycemia. Amanita phalloides (“death cap” mushroom) ingestion causes liver failure and is characterized by other signs and symptoms, including icterus.Oral hypoglycemic agents are prescribed for type 2 diabetes. Their primary mechanism of action is to increase circulating insulin concentrations by stimulating release of insulin from the pancreas. The sulfonylureas also inhibit insulin clearance by the liver, with some of the metabolites active in increasing insulin secretion accounting for the long duration of resultant signs and symptoms. Sulfonylurea medications are classified as first-generation (chlorpropamide, tolbutamide) and second-generation (glipizide, glyburide, glimepiride, and gliclazide). Even one pill (5 mg glipizide or 10 mg glyburide) can be potentially fatal to children who weigh 10 kg or less. The sulfonylureas are metabolized in the liver and excreted renally. The second-generation drugs have shorter elimination half-lives than the first-generation medications. The peak onset of action is within 2 to 4 hours, although the onset of hypoglycemia has been reported up to 11 to 21 hours after ingestion. The duration of action can extend up to 72 hours, far beyond the usual 12 to 24 hours seen in other overdoses. The meglitinides class of oral hypoglycemic agents (mitiglinide, repaglinide, nateglinide) can also cause hypoglycemia, but they have a faster onset and a shorter duration of action.Not all oral hypoglycemic medications cause hypoglycemia with use or overdose. For example, the mechanism of action of metformin, a biguanide agent, involves limitation of gluconeogenesis and increasing insulin receptors in muscle tissue. It does not interfere with insulin secretion. It may cause significant lactic acidosis, although this does not appear to be a common occurrence in children. Glitazones do not cause hypoglycemia, although they are associated with hepatitis and fulminant liver failure. Alpha-glucosidase inhibitors are also unlikely to cause significant hypoglycemia.More than 10,000 exposures to oral hypoglycemic medications were reported to the American Association of Poison Control Centers in 2004, with 1,400 of these occurring in children younger than 6 years of age. Of the 1,784 pediatric sulfonylurea exposures in 2005, 1,563 occurred in children younger than 6 years of age. Lung and Olsen reported 1,943 poison control center consultations for ingestion of hypoglycemic medications in children younger than 6 years of age over an 8-year period. Three hundred children developed hypoglycemia that persisted in 10% more than 12 hours after ingestion and treatment. Five children developed seizures, all before obtaining hospital care. The mean time to hypoglycemia was approximately 2 hours, with 18% who were not initially treated developing hypoglycemia more than 8 hours after ingestion, including one child in whom it occurred approximately 18 hours postingestion.Observation for 12 to 24 hours after administration of IV dextrose should be considered to monitor for late hypoglycemia. Symptoms of hypoglycemia can include altered mental status, diaphoresis, vomiting and seizures. Maintenance of euglycemia for 8 hours after ingestion is good evidence of nonsymptomatic ingestion and is considered to be the minimum time for observation after ingestion, although signs and symptoms may be delayed with free access to oral nutrition. If hypoglycemia is noted, admission and observation are indicated. Treatment options have included glucagon or diazoxide, but rebound hypoglycemia due to increased insulin release often complicates these therapies. Electrolyte abnormalities and hypotension have been associated with diazoxide, and gastrointestinal adverse effects have been noted with glucagon. Octreotide is a somatostatin receptor agonist that is the treatment of choice for children who have glucose-refractory hypoglycemia. It decreases insulin secretion and has not had significant adverse effects reported, although abdominal pain and diarrhea have been noted. Single subcutaneous as well as serial and IV infusions have been suggested in the literature. Local pharmacy experts can suggest medication doses.Children should be observed with frequent glucose monitoring for 12 hours after potential ingestion. Clinical signs and symptoms of hypoglycemia include appetite loss, weakness, behavioral changes, seizures, and coma. Administration of activated charcoal should be considered and may decrease absorption of the sulfonylurea, although the rapid gastrointestinal absorption of these drugs may make charcoal ineffective. First-generation oral hypoglycemic medications do not appear to be effectively bound by charcoal. Bolus IV dextrose (2 mL/kg dextrose 25% in water or 5 to 10 mL/kg dextrose 10% in water; 2 to 5 mL/kg dextrose 10% in water for neonates) may be effective, but it also can stimulate additional insulin release and result in increased hypoglycemia. Dextrose infusions may be required. Sublingual dextrose and intramuscular/subcutaneous glucagon (1 mg in children weighing >20 kg and 0.5 mg in children weighing <20 kg) can be considered for patients in whom IV access cannot be achieved.Other potential causes of hypoglycemia include reactive hypoglycemia (2 to 4 hours after eating), endocrine disorders, inborn errors of metabolism, insulinoma, hyperinsulinism, hereditary fructose intolerance, galactosemia, glycogen storage diseases, idiopathic ketotic hypoglycemia, fatty acid oxidation defects, and hormonal imbalances (hypopituitarism, adrenal crisis, congenital adrenal hyperplasia, Addison disease, adrenal insufficiency, glycogen storage disease, amino acid disorders, and disorders of gluconeogenesis). Among the other drugs associated with hypoglycemia are quinolones, pentamidine, quinine, beta blockers, and angiotensin-converting enzyme inhibitors.American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of oral hypoglycemic ingestionPlan management of oral hypoglycemic ingestionNOVEMBER 2011Question: 1A 10-year-old boy has been complaining of intermittent left leg pain for the past 2 months. Three weeks ago his pediatrician told him it was “growing pains.” His mother brings him to the emergency department today because the pain increased after he fell down during a soccer match. On physical examination, he has no obvious deformity of his left lower extremity, but he does complain of pain to palpation over the left tibia and there is mild swelling. You order plain radiographs (Figure) and make the child nonweight-bearing.Of the following, the MOST appropriate next step in management in the emergency department isA.bone scanB.magnetic resonance imagingC.ultrasonographyD.urgent referral to an oncologic specialistE.skeletal surveyCorrect answer DThe findings on the radiograph obtained for the boy described in the vignette are characteristic of Ewing sarcoma, an intramedullary diaphyseal lytic lesion that has poorly defined borders and intense periosteal reaction. Because these findings are classic and the boy has no associated systemic symptoms, referral to an oncologic specialist is most appropriate. Nonweight-bearing is recommended to prevent pathologic fracture until definitive treatment is undertaken.Although this boy needs a staging evaluation that typically includes magnetic resonance imaging to determine the local extent of disease, bone scan to evaluate for other bony lesions, and computed tomography scan of the chest to look for lung metastases, these studies are not needed immediately in the emergency department. The boy’s evaluation and treatment should be coordinated and managed by a team experienced in the care of children who have malignancy and by a surgeon who has expertise in malignant bone tumors. As part of the oncologic evaluation, other laboratory tests are indicated, including: complete blood count; renal and liver function panels; and assessment of inflammatory markers such as C-reactive protein, erythrocyte sedimentation rate, and lactate dehydrogenase.A skeletal survey is indicated when evaluating for occult fractures associated with abuse or for a child who has a suspected skeletal dysplasia or metabolic disorder. ?For the boy in the vignette, osteomyelitis is unlikely due to the lack of fever, the long duration of symptoms, and the appearance of the radiograph. Ultrasonography may be useful if soft-tissue infection, abscess, or acute bony injury is a consideration.This boy’s presentation is typical of bone sarcomas. Pain may be localized and present for a period of time before coming to medical attention. Incidental trauma may bring the patient to an acute care setting for evaluation. A mass may be palpated or swelling detected in a bone or joint. Systemic symptoms such as fever, malaise, and weight loss occur only in advanced disease. Ewing sarcoma can develop in any bone of the body but typically occurs in the diaphyses of long bones. In some cases, multiple layers of periosteal reaction accumulate as the tumor grows, causing the periosteum to push out and lay down new bone and creating an “onion skin” appearance.The pelvis, vertebral bodies, and chest wall are other common sites. Involvement of the vertebral bodies can lead to spinal cord impingement and associated symptoms of weakness, paresthesias, urinary retention, constipation, or fecal incontinence. Chest wall disease can lead to malignant pleural effusions and respiratory distress. Ewing sarcoma typically appears at the lateral aspect of the ribs; chondrosarcomas classically appear at the costal cartilages between the sternum and distal rib. Anaplastic sarcomas may involve the sternum.Osteogenic sarcoma is the most common malignant bone tumor, typically affecting the metaphyses of long bones. Patients also present with a history of localized dull and aching pain that may occur day and night. This may be accompanied by local swelling, a palpable mass, and decreased range of motion or joint effusion. Systemic symptoms are rare. Eighty percent of patients have localized disease at presentation; 20% have pulmonary metastases; and about 33% have elevated lactate dehydrogenase, alkaline phosphatase, or erythrocyte sedimentation rate values. The most common location for disease is around the distal femur, proximal tibia, or proximal humerus. The peak incidence is seen in teens, coincident with the growth spurt, and affected males outnumber females. Evaluation is similar to that for Ewing sarcoma, with local and staging evaluations required before planning an operative approach. Carefully planned biopsy is recommended in both types of bone malignancies to optimize the chance of a limb-sparing definitive surgical procedure.Rhabdomyosarcomas are the most common soft-tissue sarcomas. They can occur in any anatomic location, and systemic symptoms are rare. Symptoms are caused by local invasion of the nerves, leading to pain or weakness. Typically involved areas include the genitourinary tract, head and neck, and parameningeal areas. Rhabdomyosarcomas can metastasize to local lymph nodes, bone, and rarely, bone marrow. They are imaged best by magnetic resonance imaging.American Board of Pediatrics Content Specification(s)Know the appropriate ancillary studies relevant to soft tissue and bone sarcomasRecognize the signs and symptoms and life-threatening complications of bone sarcomasQuestion: 2You are examining a 15-year-old boy who fell while downhill skiing and injured his right thumb. On physical examination, you note that the thumb was hyperextended, resulting in deformity, tenderness, and swelling of the metacarpal phalangeal joint.Of the following, the additional finding that is MOST indicative of the need for operative repair rather than emergency department management isA.laceration along the palmar aspect of the metacarpal phalangeal jointB.nail bed lacerationC.oblique fracture of the metacarpal bone with less than 15 degrees of angulationD.puckering of skin on the palmar aspect of the metacarpal headE.transverse fracture of the proximal phalanxCorrect answer: DA corrugated appearance of the skin on the palmar aspect of the metacarpal phalangeal joint (MCP) indicates a volar dislocation that requires operative reduction. Although a laceration on the palmar aspect of the joint may suggest the presence of an open joint with dislocation, it is not an indication for open reduction. Such a presentation requires irrigation and debridement of the wound with simple closure. Similarly, nail bed laceration can be repaired in the emergency department in conjunction with closed reduction of the joint.Associated fracture of the metacarpal bone may make the bone unstable, but it is not an indication for open reduction. Closed reduction of an angulated metacarpal shaft fracture is indicated if there is more than 30 degrees of angulation. Open reduction may be indicated if there is an intra-articular fracture at the MCP joint, a comminuted fracture at the base of the first metacarpal (Rolando fracture), or an intra-articular fracture at the base of the first metacarpal (Bennett fracture).Transverse fracture of the proximal phalanx is not an indication for open reduction, although operative reduction may be appropriate if there is an associated Salter Harris 3 fracture of the proximal phalanx (gamekeeper thumb equivalent).Such a presentation is caused by tearing of the ulnar collateral ligament with avulsion of a piece of proximal phalanx. Severe joint laxity (ulnar laxity) or significant displacement of the fractured piece of the phalanx also is an indication for open reduction.The MCP joint is comprised of a fibrous capsule, ulnar and radial collateral ligaments, accessory collateral ligaments, superficial transverse metacarpal ligaments, and volar plate providing the anatomic stability. Appropriate examinations of the integrity of these structures include ulnar and radial stress for the collateral ligaments and passive hyperextension for volar plates.The most common mechanism of MCP dislocation is a fall on an outstretched hand with hyperextension of the joint (resulting in dorsal or volar dislocation) (Figure 1 and Figure 2), although hyperflexion also may cause joint dislocation (volar dislocation). The thumb and index fingers are affected most frequently, and dorsal dislocation is the most common type. A sprain of this joint is more frequent for the thumb and fifth digit.The metacarpal head is palpable on the palmar aspect in dorsal dislocation, and there is more obvious deformity compared to volar dislocation, with complete loss of range of motion of the joint. In volar dislocations, the joint appears less deformed, and range of motion may include some ability to flex at the joint. The volar plate is not interposed in the joint in dorsal dislocations in contrast to volar dislocations, which allows for closed reduction. An important additional radiographic finding is the presence of the sesamoid bone in the joint space, which indicates entrapment of the volar plate in the space. Another reason for lack of success with closed reduction in volar fractures is entrapment of the metacarpal head between the surrounding tendons and ligaments.Radiographs should be obtained before and after closed reduction maneuvers because the complications of reduction include fracture of the metacarpal head or proximal phalanx. A digital nerve block (flexor tendon sheath block or traditional digital nerve blocks in the web spaces on either sides of the digit) should be applied before the maneuver. A simple pull at the dislocated digit is contraindicated because it may result in volar plate entrapment in the joint space. The wrist is flexed to release stress on the flexor tendons, and with the MCP joint in hyperextension, the proximal phalanx is slid over the metacarpal head by applying sustained pressure. This maneuver allows the volar plate attached to the phalanx to slide back into its anatomic position.?Thumb dorsal dislocations have the highest success rates for closed reduction. Repeated attempts at closed reduction should be avoided to prevent joint tightening. If the first few attempts are unsuccessful, open reduction should be considered.Rare instances of successful closed reductions for volar dislocations have been reported in the literature, but most standard guidelines suggest open reduction. Dorsal or ventral approaches may be attempted intraoperatively. Treatment includes flexion of the MCP joint and extension of the phalanx back to the dorsal position. Open reduction allows release of the volar plate and repair of muscles tendons entrapping the metacarpal plications associated with treatment for MCP joint dislocations are premature osteoarthritis of the joint, osteonecrosis of the metacarpal head, and rare premature closure of the physial plate. Most of these are due to delayed or repeated attempts at reduction. The neurovascular bundle lies close to the intrinsic muscles of the hand (lumbricals) and, therefore, is at risk for injury with operative reduction from the volar approach.Figure 1: Lateral radiograph demonstrating dorsal dislocation of the metacarpophalangeal jointFigure 2: Oblique radiograph demonstrating volar dislocation of the metacarpophalangeal jointAmerican Board of Pediatrics Content Specification(s)Understand the mechanism of injury in metacarpal phalangeal dislocationRecognize and provide appropriate management for a child with metacarpal phalangeal dislocationQuestion: 3The frantic mother of a 10-month-old girl presents to the emergency department at 9:00 pm due to her daughter’s inconsolable crying and right-sided inguinal swelling of a few hours’ duration. While awaiting the doctor, the child vomits when the mother tries to feed her formula to calm her. The mother describes a similar episode 4 days ago, when she had first noticed the right-sided inguinal swelling. At that time, the swelling was diagnosed as an inguinal hernia and manually reduced in the emergency department, with elective repair scheduled in 1 week. Tonight, the mother demands the surgery immediately. On physical examination, the infant has a heart rate of 150 beats/min, respiratory rate of 40 breaths/min, temperature of 36.9?C, and blood pressure of 90/55 mm Hg. She appears to be uncomfortable, with tender inguinal swelling and a palpable soft-tissue mass on the right side. You administer appropriate analgesia.Of the following, the MOST important next step is toA.administer an intravenous fluid bolusB.attempt manual reduction in the emergency departmentC.obtain contrast computed tomography scanD.obtain urgent ultrasonography of the inguinal canalE.perform needle aspirationCorrect answer: DThe girl described in the vignette most likely has an incarcerated or strangulated inguinal hernia, with a possible ovary in the inguinal canal presenting as the palpable soft-tissue mass. In contrast to hernias in boys, urgent ultrasonography is required in girls to assess if the mass is an ovary and to ascertain its vascular supply (Figure 1 and Figure 2). The findings should guide either manual (with analgesia, sedation, and Trendelenburg position) or surgical reduction. If the mass is an ovary, prompt surgical correction is indicated to avoid recurrence with potential strangulation. A fluid bolus is of no clear benefit in this situation and does not aid in the management of the patient. Abdominal computed tomography scan is not indicated because it exposes the patient to unnecessary ionizing radiation and potentially delays care. Needle aspiration is contraindicated until the contents of the mass can be identified.Pediatric patients are more likely to have indirect inguinal hernias (95% of cases) than adults, with most found on the right side, in boys, and in preterm infants. Incarceration of the hernia is more common at a younger age, although information is conflicting about an increased risk associated with prematurity. Herniais more common in patients who have abdominal wall defects, genitourinary anomalies, connective tissue disorders, and conditions that result in abdominal distention (eg, ascites, ventriculoperitoneal shunts). In females, the hernia sac may contain ovary or fallopian tubes (reported in 10% to 20% of cases). In the case of incarceration or strangulation, the inguinal swelling can be tender, with associated clinical findings of irritability, vomiting, and abdominal distention.Although manual reduction is indicated to avoid ischemia of an incarcerated hernia, it is not appropriate if there is suspicion of bowel necrosis, which is more likely in the presence of an irreducible ovary in the hernia sac (2% to 33%).?If an incarcerated hernia is not reduced, it may result in bowel ischemia in as little as 2 hours, ovarian or testicular torsion or ischemia, and perforation and necrosis of the part of bowel in the hernia sac. Emergency surgical correction is a last resort because of the associated significant morbidity compared with elective surgery.The external inguinal ring of the inguinal canal is lateral to the pubic tubercle. The internal inguinal ring is composed of internal oblique and transverses abdominis muscles (Figure 3). The hernia sac (with intestine or peritoneal fluid) can protrude out of the external inguinal ring, resulting in a swelling lateral to the pubic tubercle, which may extend into the scrotum or labia majora. Because the size of the defect at the internal inguinal ring can predict the ease of reduction (smaller size means more difficult reduction), firm pressure at the internal inguinal ring to avoid ballooning of the inguinal sac at the ring can ease in the manual reduction. Milking of the inguinal hernia contents may be required for 5 to 15 minutes. Complications of attempted manual reduction maneuvers include bowel swelling, reduction of necrotic bowel, inappropriate reduction of hernia into the preperitoneal space, and bowel perforation. Pain after hernia reduction is a sign of possible bowel injury.Figure 3: Anatomy of the inguinal canalAmerican Board of Pediatrics Content Specification(s)Discuss the indications and contraindications for hernia reductionKnow the anatomy and pathophysiology relevant to hernia reductionDiscuss the complications associated with hernia reductionDescribe the key steps and potential pitfalls in performing hernia reductionQuestion: 4A 12-year-old boy comes into the emergency department on a Saturday afternoon 4 hours after sustaining an injury to his ear during a wrestling competition. He complains of throbbing pain to the right ear but denies other trauma, hearing loss, or dizziness. Physical examination reveals edema and erythema of the affected ear (Figure).Figure: Courtesy of the Media Lab at DoernbecherOf the following, the MOST appropriate treatment for this injury isA.application of ice 15 min/hr for 24 hoursB.fine-needle aspiration, followed by intralesional injection of cyanoacrylateC.fine-needle aspiration, followed by pressure dressingD.incision and drainage, wick placement, and pressure dressingE.pressure dressing aloneCorrect answer CThe boy described in the vignette has an auricular hematoma, an injury that results from shearing force, which separates the perichondrium from the cartilaginous structure of the outer ear. The perichondrium covers the cartilage and supplies it with nutrients and oxygen. A hematoma may compromise blood supply and lead to necrosis of the underlying cartilage and subsequent deformity, the so-called “cauliflower ear.”?Application of ice is not sufficient treatment for auricular hematomas; they must be drained promptly to prevent damage to the underlying cartilage. Either fine-needle aspiration or incision and drainage followed by compressive dressings have been recommended. Unfortunately, no well-designed, randomized, controlled trials have determined optimal treatment strategies for these lesions. Recently, a group in Japan has described excellent nonsurgical outcomes with drainage followed by intralesional injection of OK-432, a sclerosing agent used to obliterate cystic lesions such as cystic hygromas. The use of cyanoacrylate tissue adhesive has never been described for treatment of auricular hematoma. Although incision and drainage has been recommended by many specialists, wick placement is not recommended and likely would increase the rate of infection.Trauma to the head can cause damage to the auricular system. Temporal bone fracture can result from a blow to the head in the temporoparietal or frontal and occipital regions, causing longitudinal (80%) or transverse fractures (20%), respectively. Sensorineural hearing loss and vertigo may occur. Injury to the facial nerve, which runs through the temporal bone, is more common with transverse fractures. An ear canal laceration, hemotympanum, or cerebrospinal fluid otorrhea also can result. Any of those findings in the setting of head trauma should raise the index of suspicion for temporal bone fracture, and computed tomography scan with temporal cuts should be performed.A patient who complains of hearing loss or dizziness after head or barotrauma but who has normal physical examination findings and imaging may have a perilymphatic fistula, an anomalous connection between the middle and inner ear. Barotrauma may result from scuba diving or depressurized airplane travel, but it can also be caused by extreme coughing, straining, or retching. Leakage of fluid from the oval or round window of the inner ear into the middle ear leads to problems with balance and dizziness as well as hearing loss. Ear-nose-throat consultation is warranted for this presentation but is not needed for the boy described in the vignette.American Board of Pediatrics Content Specification(s)Understand urgent complications and management of ear trauma, including perichondral hematoma, hearing loss, and traumatic otorrheaQuestion: 5A 4-year-old boy presents to the emergency department with fever and headache of 5 days’ duration. In addition, he has experienced lethargy, neck stiffness, vomiting, abdominal pain, decrease in urine output, and the development of a diffuse rash over the past 24 hours. On physical examination, his heart rate is 150 beats/min, respiratory rate is 40 breaths/min, systolic blood pressure is 75/35 mm Hg, capillary refill time is 3 seconds, and oxygen saturation is 92% in room air. He appears irritable and has tachypnea, rales on the left posterior lung fields, and diffuse abdominal discomfort. He has a rash consisting of petechiae and purpuric macules over his trunk and extremities (Figure). After starting supplemental oxygen and establishing intravenous (IV) access, you obtain laboratory specimens, including blood cultures. You rapidly administer 20 mL/kg IV normal saline and begin broad-spectrum IV antibiotics. Repeat assessment of vital signs 15 minutes later shows a heart rate of 170 beats/min, systolic blood pressure of 75 mm Hg, and capillary refill time of 3 seconds.Of the following, the MOST appropriate next step is to administerA.another rapid normal saline bolusB.corticosteroidsC.IV dopamineD.IV epinephrineE.IV norepinephrineCorrect answer AThe boy described in the vignette has septic shock that has not responded to an initial bolus of IV fluid. A second fluid bolus should be started immediately to prevent further clinical deterioration while preparing for the possible use of inotropes. If three normal saline fluid boluses do not correct the shock, the shock is considered to be fluid-refractory, and inotropes are then indicated. Dopamine is generally the optimal first choice in septic shock, followed by either epinephrine (for cold shock) or norepinephrine (for warm shock). Simultaneous administration of IV antibiotics and correction of electrolyte abnormalities should be undertaken without delaying the rapid administration of up to 60 mL/kg IV fluids within the first hour of resuscitation. Although corticosteroids may be indicated for fluid- and catecholamine-resistant septic shock, such administration is not an appropriate next step for this child.Shock is divided into four types: hypovolemic, cardiogenic, distributive, and septic. The most common in the pediatric population worldwide is hypovolemic shock, usually caused by diarrheal illnesses in children younger than 5 years of age. Cardiogenic shock occurs when the pumping action of the heart is insufficient to maintain adequate blood pressure. Cardiogenic shock is most commonly seen in neonates and infants, usually due to congenital heart defects or sepsis. In other age groups, cardiogenic shock may result from myocarditis, electrolyte abnormalities, or arrhythmias. Distributive or neurogenic shock results from the maldistribution of the circulating blood volume and is rare in pediatric patients. Anaphylaxis is an example of distributive shock, and spinal cord trauma resulting in loss of sympathetic tone is an example of neurogenic shock. The fourth type of shock is septic shock, in which the systemic inflammatory response to infection causes vasodilatation and leaky capillaries, both of which lead to a decrease in blood pressure.A delay in the management of shock can lead to high morbidity and mortality, so early identification is critical. Septic shock is defined as a combination of severe sepsis with hypoperfusion or hypotension. Because hypotension is a late sign of sepsis in children, the presence of hypoperfusion with severe sepsis is also defined as septic shock. Septic shock is a combination of distributive (decreased systemic vascular resistance), cardiogenic (myocardial suppression), and hypovolemic (capillary leak) shock. Pediatric patients are more likely to show fluid-refractory and cold shock than adults because of both decreased systemic vascular resistance and decreased cardiac output relative to adults. Clinical signs include temperature irregularity, tachycardia, respiratory distress, cool or warm extremities, oliguria, altered mental status, lethargy, and coma. Among potential skin lesions are petechiae, purpura, erythroderma, and ecchymosis. Associated laboratory findings are anemia, thrombocytopenia, leukopenia or leukocytosis, lactic acidosis, electrolyte abnormalities, elevated liver enzymes, hyperbilirubinemia, and disseminated intravascular coagulation.The risk of sepsis is highest during the first 30 days after birth, and preterm neonates have the highest risk. Localized infections such as pneumonia, otitis media, and meningitis can be the primary sources of systemic sepsis in all age groups. In addition, the patient’s clinical condition can predispose to specific infectious agents. For example, hospitalization and indwelling catheters increase the risk of coagulase-negative Staphylococcus, gram-negative enteric bacterial infections, and fungal infections. Patients who have neutropenia due to chemotherapy are at high risk for infections due to Streptococcus viridans, Pseudomonas, and a-hemolytic Streptococcus. S ?pneumoniae, Pseudomonas ?aeruginosa, S aureus, and Haemophilus influenzae are common agents for sepsis in immunodeficient patients. Those who have asplenia are at high risk for sepsis due to encapsulated pathogens such as S pneumoniae and H influenzae. Complement deficiencies predispose to Neisseria meningitidis infections. Toxic shock syndromes are more likely in young individuals who do not have antibody against the toxin, such as young girls starting menstruation, or patients who have surgical wound infections, who are at the highest risk for toxic shock syndrome due to S aureus. The Table identifies various infectious causes for sepsis in pediatric patients according to age. Interestingly, these pathogens are also the likely causes of meningitis in the same age groups. Of note, group B Streptococcus and Listeria causing meningitis as well as gram-negative organisms such as Escherichia coli are almost exclusively seen in neonates.American Board of Pediatrics Content Specification(s)Define the major causes of shock by ageDifferentiate the major causes of sepsis by ageDifferentiate the major causes of meningitis by ageQuestion: 6An 8-year-old girl presents to the emergency department for evaluation of chest pain and shortness of breath. She had fevers and upper respiratory tract infection symptoms last week. Her maximal temperature was 38.4°C, but she has not had a fever in the past several days. She has had increased difficulty breathing in the past 24 hours that is exacerbated by exertion as well as chest discomfort, which is worsened when lying supine. She localizes the pain to the anterior chest but is unable to characterize it further. The family reports that she has had no complaints of nausea, vomiting, diarrhea, previous respiratory problems, or recent trauma. She has had no previous significant illnesses, hospitalizations, or surgeries. On physical examination, the girl’s temperature is 37.3°C, heart rate is 120 beats/min, respiratory rate is 28 breaths/min, blood pressure is 86/54 mm Hg, and oxygen saturation is 97% in room air. Chest examination reveals mild tachypnea without grunting, flaring, or retractions and clear lungs. Cardiovascular evaluation documents muffled heart tones without murmurs, gallops, or rubs; normal pulses; and a mildly delayed capillary refill of 2 to 3 seconds. Mild jugular venous distension is apparent with the girl in a sitting position. Abdominal examination reveals a liver edge palpable 2 cm below the right costal margin with a nontender and nondistended abdomen and no splenomegaly.Of the following, the MOST appropriate initial tests that can confirm the diagnosis areA.blood culture collection, inflammatory marker measurement, and transesophageal echocardiographyB.chest radiography, electrocardiography, and echocardiographyC.pulmonary function testing, chest radiography, and methacholine challenge testingD.troponin measurement, electrocardiography, and cardiac catheterizationE.viral panel collection, inflammatory marker measurement, and endomyocardial biopsyCorrect answer BThe girl described in the vignette is displaying signs and symptoms of pericardial effusion. Although her blood pressure is currently maintained, the presence of muffled heart tones, jugular venous distension (JVD), tachycardia, and tachypnea are all suggestive of the diagnosis. Ancillary tests that can confirm the diagnosis include electrocardiography (ECG), chest radiography (CXR), and echocardiography (Echo). Blood cultures, inflammatory markers, and transesophageal Echo are indicated in cases of suspected endocarditis, which is not likely in a previously healthy afebrile child who has muffled heart tones and JVD. Pulmonary function tests and methacholine challenge may be used to diagnose asthma and differentiate various causes of respiratory distress resulting from pulmonary disease, but this girl has clear lungs, normal pulse oximetry readings, and minimal respiratory findings. Measurement of cardiac enzymes and performance of ECG and cardiac catheterization are indicated if coronary vascular disease with ischemia or infarction is suspected, but pericarditis is far more likely in this child, given her age and the symptoms described. Although viral testing and inflammatory marker measurement may be pursued for this girl, endomyocardial biopsy is performed only in selected cases of suspected myocarditis to confirm the diagnosis and attempt to identify the specific cause.Pericardial effusion is the accumulation of an abnormal amount of fluid within the pericardial sac. Cardiac tamponade occurs when pericardial fluid accumulation or thickening/scarring of the pericardium causes impaired cardiac filling and a subsequent reduction in cardiac output. As much as 50 mL of fluid can be present in the pericardial sac of the healthy individual. As larger amounts of fluid accumulate, end-diastolic pressures increase and the pressure gradient for venous return to the heart diminishes. If the fluid accumulates slowly, symptoms may not occur until a very large effusion is present. Conversely, rapid accumulation of relatively small amounts of fluid may produce symptoms. Symptoms of pericardial effusion include shortness of breath, chest pain, abdominal pain, exercise intolerance, and fatigue. Such symptoms worsen as tamponade develops and progresses, when significant chest pain, dyspnea, and altered mental status may occur. Signs of tamponade include the classic “Beck’s triad” of hypotension, venous distension, and diminished heart tones; more chronic cases present with venous distension, ascites, and diminished heart tones. Other signs include pulsus paradoxus (Fig. 1), in which the systolic blood pressure drops more than 10 mm Hg with inspiration; tachycardia; tachypnea; and poor perfusion. If pericardial effusion produces tamponade physiology and is unrecognized or untreated, progression to severe hypotension and cardiovascular collapse is likely. In addition, as tamponade progresses, cardiac perfusion becomes impaired and myocardial ischemia may result (Fig. 2).Pericardial effusion and tamponade are usually suspected on clinical grounds. The diagnosis should be confirmed quickly, particularly in cases with evidence of tamponade. CXR usually reveals a markedly enlarged cardiac silhouette with clear lung fields and possibly a classic “water bottle” appearance of the heart shadow. The heart size may be normal or minimally enlarged when a relatively small volume of fluid accumulates rapidly. Pleural effusions may be present in some cases. ECG most often reveals generalized low voltages; ST segment flattening, inverted T waves, and depressed PR segments are also common (Fig. 3). If pericarditis is the cause for the effusion, ST segment elevation may be seen.The diagnostic test of choice for pericardial effusion is Echo. Echo not only allows identification and quantification of pericardial effusion, but it also allows assessment of cardiac function, valvular competence, wall thickness and motion, and diastolic collapse of the right ventricle suggestive of tamponade. As availability and experience with bedside ultrasonography increases in the pediatric emergency department, more rapid identification of pericardial fluid and evidence of early tamponade should be feasible. Ultrasonography can also be used to guide percutaneous drainage in those cases where emergent treatment is deemed necessary.Pericardiocentesis should be performed without delay in the presence of tamponade and hemodynamic compromise. Additional diagnostic tests should not delay performance of Echo and are guided by the suspected cause: cardiac enzymes, inflammatory markers, renal function testing, thyroid studies, blood counts and culture, viral studies, leukemia/lymphoma evaluation, and rheumatologic markers may be indicated in selected cases.Figure 2: Schematic illustration of the physiology of cardiac tamponade from an effusion. In the top left of the diagram (red letters), increased right atrial (RA) pressure results in jugular venous distension and decreased venous return in patients who develop pericardial tamponade. In the top right of the diagram (red letters), decreased cardiac output and increased systemic venous return result in a narrow pulse pressure in patients who develop cardiac tamponade..Figure 3: ECG showing teneralized low voltages, ST segment flattening, inverted T waves, and depressed PR segments associated with pericardial effusion.American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms and complications of pericardial effusion and tamponadeKnow the indications for and interpret results of ancillary studies in patients with pericardial effusion and tamponadeQuestion: 7A 6-year-old boy is brought to the emergency department because of pain and swelling in his left thumb of 2 days’ duration. He complained of pain yesterday, and his mother noticed the swelling today. He has no history of fever, but 2 weeks ago his thumb was caught in the car door. The pain from that injury lasted for 2 days, and the boy was asymptomatic after that. The boy sucks his thumb, especially at night, and occasionally bites his nails. The only significant finding on physical examination is swelling and redness on the lateral aspect of his left thumb as well as some pus collection adjacent to the nail.Of the following, the MOST appropriate next step in the treatment of this patient isA.application of cautery to drain pusB.counseling to discourage thumb suckingC.hospital admission for administration of intravenous antibioticsD.incision and drainage of the abscessE.wedge removal of the nailCorrect answer: DPain, swelling, and signs of inflammation along the lateral fingernail folds are suggestive of acute paronychia. A collection of pus indicates abscess formation that should be treated with incision and drainage. Management of paronychia is an outpatient procedure, and parenteral antibiotics are not indicated. Although counseling this patient about thumb sucking may be appropriate, this approach alone is adequate. Cautery is often used to relieve pressure from a subungual hematoma but not for acute management of a paronychia. Wedge removal of a portion of the nail is appropriate management for an ingrown toenail but is usually unnecessary in the treatment of a paronychia.Nail anatomy involves the nail root, nail bed, nail plate, eponychium (cuticle), perionychium, and hyponychium (Figure). The root, also known as the germinal matrix, produces the bulk of the nail bed. The edge of the germinal matrix is a white, crescent-shaped structure called the lunula. The nail bed is highly vascular and extends from the lunula to the hyponychium. The hyponychium is the area between the nail plate and the fingertip. It is the junction between the free edge of the nail and the skin of the fingertip and provides a waterproof barrier at the distal end of the nail bed. At the proximal end of the nail bed, the cuticle (eponychium) provides a further waterproof barrier. The cuticle is situated between the skin of the finger and the nail plate. The nail plate or the actual fingernail is made of translucent keratin and is attached laterally by folds of skin called perionychium; the edge is also known as the paronychial edge. The perionychium is the site of hangnails, ingrown nails, and an infection of the skin called paronychia.Paronychia refers to an infection of the soft tissue surrounding the nail bed and occurs when the seal between the proximal nail fold (eponychium or cuticle) and the nail plate is disrupted (Figure). Paronychia in children is often due to digital sucking, excessive nail trimming, or nail biting. Depending on the cause for disruption of the eponychium, bacterial flora can be mixed (aerobic and anaerobic) and reflect oral flora as well as common skin pathogens (staphylococci and streptococci). Infection begins as cellulitis and manifests as redness, tenderness, and swelling along the lateral nail border.In the initial stages, management is nonsurgical and includes warm soaks, elevation of the digit, and appropriate oral antibiotics. If the disease progresses, pus accumulates along the lateral nail fold, forming an abscess. Patients require incision and drainage at this stage of the disease. In most instances, use of a sterile needle or a #11 scalpel blade to lift the eponychium to relieve the accumulated pus at the nail base is sufficient. This procedure should be performed under adequate local anesthesia in the form of ethyl chloride spray or digital block with lidocaine. It is important to note that drainage involves lifting the eponychium, not incising through intact skin.In rare instances, when the pus collection involves most of the nail bed, a thin longitudinal strip of the lateral nail plate must be removed. If the infection has spread deeper to involve the proximal base of the nail, a horizontal strip of the proximal nail should be removed to drain the pus pocket. A thin strip of gauze should be left in place to ensure continued drainage. Warm soaks after removal of packing is recommended. Appropriate oral antibiotics for 5 to 7 days with or without local antibiotics can be used but are of questionable benefit. If resolution does not occur in 5 to 10 days, the patient should be evaluated for osteomyelitis. Complications of the procedure include damage to the germinal matrix of the nail bed, nail deformity, and nail scarring.Herpetic whitlow may be confused with paronychia, but closer inspection often reveals vesiculopustular lesions. Attempted drainage of herpetic whitlow is of no benefit and may complicate recovery. Management of herpetic whitlow is medical, not surgical.Figure: A. Structure of the nail. B. Course of bacterial infection).American Board of Pediatrics Content Specification(s)Discuss the indications and contraindications for incision and drainage of a paronychiaKnow the anatomy and pathophysiology relevant to incision and drainage of a paronychiaDiscuss the complications associated with incision and drainage of a paronychiaDescribe the key steps and potential pitfalls of incision and drainage of a paronychiaQuestion: 8A 9-day-old infant is brought to the emergency department because of respiratory distress and poor feeding for the past several hours. She was born at term following an uncomplicated pregnancy, labor, and delivery, weighing 3.5 kg. She was discharged with her mother at 36 hours of age. The parents report she was bottle-feeding well until about 12 hours ago, when she became fussy and did not eat as much. Overnight she has stopped eating and developed deep and rapid respirations. On physical examination, the infant appears cyanotic and exhibits tachypnea and hyperpnea. She has marked retractions and a decreased level of consciousness. Her perfusion is poor. Vital signs include a temperature of 35.8°C rectally, heart rate of 165 beats/min, respiratory rate of 58 breaths/min, blood pressure of 54/32 mm Hg in the right arm, and pulse oximetry of 82%. Breath sounds are hard to characterize, and no murmur is audible. The liver edge is palpable 2.5 cm below the right costal margin. You establish intraosseous access and rapidly infuse 20 mL/kg of 0.9% saline. Point-of-care testing (venous) shows: glucose of 118 mg/dL (6.5 mmol/L), hemoglobin of 14.5 g/dL (145 g/L), pH of 6.98, Pco2 of 24 mm Hg, Po2 of 35 mm Hg, and base excess of -26 mEq/L.Of the following, in addition to antibiotics, the most important pharmacologic treatment for this child isA.acyclovir 15 mg/kg intravenously (IV)B.digoxin 20 ?g/kg IVC.dopamine 5 ?g/kg IV per minute as a continuous infusionD.epinephrine 0.2 ?g/kg IV per minute as a continuous infusionE.prostaglandin E1 0.1 ?g IV, then 0.05 ?g/kg per minute as a continuous infusionCorrect answer ECongenital heart disease (CHD) is not uncommon, with as many as 90 children affected for every 10,000 live births. The presentation can occur at almost any age, but most cases of severe or significant disease present in the neonatal period. The presentation of the child described in the vignette is typical of a left-sided obstructive lesion and decreased systemic perfusion after closure of the ductus arteriosus. Reestablishing patency of the ductal tissue with prostaglandin E1 can be life-sparing in this situation.Neonatal herpes simplex infection can present as sepsis, but the rapid onset, decreased pulses, and cyanosis described for this infant make cardiac disease more likely. Digoxin, dopamine, and epinephrine all might be used as supportive therapies, but until systemic circulation via flow across the ductus arteriosus is established, reversal of acidosis and shock will be unlikely.The age of presentation of CHD depends on the underlying anatomy and physiology of the particular lesion (Table). In the early neonatal period, lesions that produce cyanosis or circulatory collapse predominate. Later in the first postnatal month or later infancy, lesions associated with left-to-right shunts and pulmonary fluid overload are more common. In these cases, blood flow to the lungs increases after the usual decrease in pulmonary vascular resistance that occurs over the first month after birth. Symptoms such as fast breathing and poor feeding and signs such as tachypnea, rales, tachycardia, and hepatomegaly may become evident. In some cases, for example with an atrial septal defect, the effects of longstanding increased pulmonary blood flow and resultant pulmonary hypertension are noted only in later childhood or adulthood. Lesions found later in childhood are often associated with only minimal symptoms initially but may be diagnosed due to the presence of a murmur (eg, valvular lesions) or hypertension (eg, coarctation of the aorta). Coronary artery anomalies often present later in infancy or even later in life. In these cases, circulatory collapse may occur due to cardiac ischemia that is not evident in the neonatal period. There is considerable overlap in age of presentation and how these processes present, based on the particular anatomy and physiology in the specific patient.Although left–sided obstructive lesions (eg, hypoplastic left heart syndrome, interrupted aortic arch, critical coarctation of the aorta, or critical aortic stenosis) are diagnosed in most children before discharge from the newborn nursery, for some affected children, the ductus arteriosus remains open for as long as 2 weeks. In these children, if flow across the patent ductus arteriosus is sufficient to support systemic circulation, they may be asymptomatic or have only mild symptoms. When the ductus closes, there is little or no systemic circulation. Shock ensues, and the child develops poor perfusion, cyanosis, tachypnea, and tachycardia. There is a severe metabolic acidosis.In such cases, it is imperative for the emergency physician to include CHD in the differential diagnosis. Treatment for possible sepsis should be administered and other causes of shock in neonates considered. Four-extremity blood pressures, pre- and postductal pulse oximetry, chest radiography, and electrocardiography may be helpful in establishing the diagnosis of cardiac disease. Cardiology consultation should be sought and echocardiography obtained for a definitive diagnosis. Oxygen should be administered, and depending on the severity of illness, endotracheal intubation should be considered.A fluid bolus should be administered to all neonates experiencing shock. Decreased oral intake and increased insensible losses due to tachypnea often produce some degree of hypovolemia, even in a child who has cardiogenic shock. In addition, effective filling of the left ventricle may produce increased contractility. Vasopressor support should be initiated as needed. Once effective ventilation is ensured, the metabolic acidosis may be treated with sodium bicarbonate. Ideally, this therapy should be guided by blood gas results.However, the priority for therapy is the reestablishment of flow across the ductus to the systemic circulation. Prostaglandin E1 should be administered as soon as a left–sided obstructive lesion is suspected, even before a definitive diagnosis is made. Prostaglandin E1 may cause hypotension, tachycardia, hyperthermia, and apnea. It may be delivered through central or peripheral intravenous or intraosseous access. It will cause worsening only in very rare cases (pulmonary venous obstruction or rare left atrial obstructive lesions), as seen in infradiaphragmatic total anomalous pulmonary venous return or cor triatriatum.Transport to a pediatric (cardiac) intensive care unit or pediatric cardiac center should be arranged as soon as possible. Infants who are being treated with prostaglandin E1 and are being transported to another medical facility probably should be intubated before transport because of the risk of apnea. Surgical repair is the definitive treatment for these lesions.American Board of Pediatrics Content Specification(s)Understand the pathophysiology and anatomy of congenital heart diseaseRecognize the signs and symptoms and life threatening complications of congenital cardiac lesions by ageBe familiar with ancillary studies relevant to congenital heart diseasePlan management of acutely symptomatic congenital heart diseaseDECEMBER 2011Question: 1A 12-year-old boy is caught underneath a snowmobile while riding with friends. According to the friends, the boy hit the handlebars during a high-speed crash and the vehicle landed on his chest. Upon arrival at the emergency department, you determine that his airway is intact. The only finding of note on physical examination is a contusion over the sternum and a resting tachycardia. Chest radiography shows no abnormalities.Of the following, assuming modalities are available, the MOST appropriate next test to obtain isA.aortic angiographyB.chest magnetic resonance imagingC.chest computed tomography scanD.focused assessment with sonography for trauma (FAST)E.plain films of the ribsCorrect answer DThe primary concern for the boy described in the vignette is cardiac injury due to blunt trauma, which can be challenging to evaluate. Such evaluation requires specific and efficient action because potentially devastating injuries may be subtle and progressive. Blunt chest trauma should be suspected with impact and high-force mechanisms of injury, such as described for the boy in the vignette, even without external signs of trauma. Airway, pulmonary, cardiac, gastrointestinal, vascular, musculoskeletal, and nervous system injury should be considered as well as potential associated abdominal, head, neck, and extremity involvement. Bedside ultrasonography (FAST) offers rapid and efficient assessment of cardiac function and integrity of the pericardial space, identifying fluid collection and tamponade. More thorough ultrasonography with cardiac echocardiography can help with details of flow, cardiac function, and the pericardial space. Both of these studies can be performed rapidly and provide valuable information to help direct immediate intervention and address future concerns.Chest radiography may suggest or support a diagnosis of cardiac tamponade (in conjunction with the clinical signs and symptoms), but results are not definitive, and a negative film, as with this patient, does not rule out a potentially serious abnormality. Chest computed tomography (CT) scan may be indicated, but a rapid ultrasonographic evaluation, if available, is a more appropriate and efficient initial screening tool for this patient. Plain chest radiography may provide clues to underlying injury and obviate the need for additional radiation in the form of CT scan, although one investigator reported that chest radiography missed 11% of aortic injuries in adult patients due to blunt trauma. Chest CT scan is sensitive and specific for pneumothorax, but significant air trapping should be diagnosed clinically and, if time permits, verified with chest radiography. Some researchers have suggested that bedside thoracic ultrasonography may be more sensitive that plain radiography in determining pneumothorax in the trauma patient. CT scan is the initial imaging study of choice for penetrating trauma.Plain films often identify fractured ribs, although specific rib films and a CT scan may provide a better view. Often, specific identification of fractured ribs is not necessary, although fractures of the first through third ribs can be associated with nerve and vascular injuries, and fractures of the tenth through twelfth ribs can be associated with abdominal injury. Magnetic resonance imaging (MRI) is currently not practical in the acute evaluation of a trauma patient. Angiography is helpful in specific scenarios, but echocardiography is the initial study of choice for a cardiac contusion.Chest radiographs are the initial study of choice with blunt chest trauma. Abnormalities that potentially can be identified include pneumothorax (Figure 1), hemothorax, rib and other fractures (Figure 2 and Figure 3), vascular anomalies, diaphragmatic tear (Figure 4), and cardiac silhouette abnormalities, although these may be further elucidated on additional studies such as CT scan (Figure 5, Figure 6, and Figure 7). If clinical signs or symptoms suggest cardiac or vascular abnormalities, further evaluation may be required.It is important to recognize that signs and symptoms of potentially lethal underlying chest injury can vary from an asymptomatic patient to one who exhibits profound shock. Kerr and Maconochie describe six potentially lethal chest injuries: airway obstruction, open and tension pneumothorax, hemothorax, flail chest, and cardiac tamponade. Six hidden chest injuries that they cited include cardiac contusion, aortic disruption, tracheobronchial and esophageal disruption, diaphragmatic tear, and pulmonary contusion. These authors describe radiographic findings, specific injuries, assessment modalities, and potential need for operative intervention for the “hidden injuries.” The investigative modalities suggested include chest radiography, bronchoscopy, esophagoscopy, esophagraphy, CT scan, MRI, aortography, electrocardiography, laboratory analysis, fluoroscopy, laparoscopy, and laparotomy.If the patient is in extremis, the appropriate response may need to include immediate surgical exploration and repair. If the patient is relatively stable or time permits in the less stable patient, other modalities can be considered. Noninvasive CT angiography has replaced aortography in many centers for large-vessel evaluation (irregularity, dilatation, dissection, aneurysm) and is helpful if there are concerns or suggestions of vascular abnormalities. Angiography may still have an important role in the evaluation of aortic branch vessel abnormalities. Transthoracic and transesophageal echocardiography can both provide critical information about cardiac injury and function after blunt trauma, demonstrating wall motion defects, pericardial effusion, aneurysms, and intracardiac shunts as well as important information about cardiac structure and hemodynamic profile. Intravascular ultrasonography has also been described for evaluation of potential aortic injuries.Operative treatment may be needed for significant air leaks, bleeding, and complete or partial cardiac or vascular abnormalities as well as spinal or musculoskeletal stabilization. Interventions can include evacuation of blood, closure of primary wounds, stabilization/repair of structural abnormalities, bleeding control, and insertion of vascular shunts and grafts. Operative decisions are made by thoracic and trauma experts; the emergency physician’s role is patient stabilization and assistance in suspecting/identifying potential injuries. Timing (defined as immediate or delayed) and choice of specific surgical interventions depend on the patient’s clinical status and comorbidities.Figure 1: Collapsed lungs in a patient who has tracheobronchial injury and “complete disruption of the right bronchus.” Bilateral pneumothorax (large arrows), pneumomediastinum (thin arrow), and extensive subcutaneous emphysema are visible. From Le Guen M, Beigelman C, Bouhemad B, Wenjie Y, Marmion F. Chest computed tomography with multiplanar reformatted images for diagnosing traumatic bronchial rupture: ?Figure 4: Radiograph showing the spleen in the left lower portion of the chest cavity (X and arrow) after a diaphragmatic tear.Figure 5: Left-sided pneumothorax (right side of image) on CT scan of the chest with chest tube in place. Figure 6: CT scan of a patient who has a partially cystic, partially fluid-filled structure (dark spot near spine on middle-right lower portion of image). a rib fracture (lower right portion of image), and subpleural hemorrhage representing a pulmonary contusion (lighter area near rib fracture in lower right portion of image). Figure 7: CT scan showing severe lung contusions, bilateral pneumothorax, pneumomediastinum, hematothorax, and pneumopericardium. American Board of Pediatrics Content Specification(s)Know the indications and interpret the findings of plain x?ray studies following blunt chest traumaKnow the indications and interpret the findings of angiography following blunt chest traumaKnow the indications and interpret the findings of ultrasonography following blunt chest traumaKnow the indications and interpret the findings of echocardiography following blunt chest traumaDescribe and know the indications for surgery following blunt chest trauma (ie, massive hemothorax, tamponade, great vessel injury)Question: 2A 5-year-old boy who has a longstanding seizure disorder and developmental delay arrives in the emergency department with a history of increased frequency of seizures over the past 8 hours. His parents gave him rectal diazepam at home. During triage, he develops a generalized clonic seizure. He is rushed to the resuscitation room, where intravenous access is established and he is given a dose of lorazepam and a loading dose of fosphenytoin. Overt seizure activity ceases. He has sonorous respirations with a respiratory rate of 32 breaths/min. His oxygen saturation is 85% on 50% oxygen via face mask, and he is actively drooling. After airway repositioning, his oxygen saturation transiently improves but deteriorates as soon as the jaw thrust is released. He gags with oropharyngeal suctioning, but his oxygen saturations remained unchanged.Of the following, the MOST appropriate next intervention in his airway management isA.bag-valve-mask ventilationB.endotracheal intubationC.laryngeal mask airway placementD.nasal airway placementE.oral airway placementCorrect answer: DThe boy described in the vignette appears to have a partially obstructed airway, likely from the tongue or soft palate obstructing the pharyngeal air passage. This is common in a postictal state when a child has poor neuromuscular tone. The initial steps in management are to position the airway with a jaw thrust or chin lift maneuver and to suction the oropharynx, both of which already have been attempted with limited success for this boy. Artificially stenting the airway open should be the next step. Because he has an intact gag reflex, nasal airway placement, which is less noxious and less likely to initiate vomiting, is appropriate. An oropharyngeal airway is preferred for an unresponsive patient who has no gag reflex. Bag-mask ventilation and endotracheal intubation are reserved for children who, despite all the aforementioned maneuvers, are not effectively and spontaneously ventilating. Laryngeal mask airways may be used when assisted ventilation is necessary and the patient is unable to be ventilated via bag-valve-mask and unable to be intubated with an endotracheal or nasotracheal tube.Nasal airways are sized by measuring from the nares to the tragus of the ear. Oral airways are sized by measuring from the corner of the mouth to the angle of the mandible. Improper sizing may contribute to airway obstruction. If the artificial airway is too short, it may fail to maintain an open airway by pushing the base of the tongue into the posterior pharyngeal wall. If the nasopharyngeal or oral airway is too long, it may cause a physical obstruction or initiate vomiting or laryngospasm. Small-caliber nasopharyngeal airways may obstruct with secretions easily and need to be suctioned frequently. For children who have enlarged adenoidal tissue or a bleeding diathesis, placement of a nasopharyngeal airway can precipitate bleeding.Increasing the oxygen delivery is unlikely to help this patient’s partially obstructed upper airway. Indeed, when his airway obstruction is relieved, he may not need as much or any supplemental oxygen to maintain adequate oxygenation.In the appropriate setting, oxygen delivery can be optimized by using a 100% nonrebreather face mask, which limits the entrainment of room air and can deliver oxygen concentrations of up to 100% with a tight-fighting mask and a high oxygen flow rate. A partial rebreathing mask has a reservoir for oxygen like the nonbreather face mask, and when the flow rate into the bag exceeds the patient’s minute ventilation, it can deliver up to 60% Fio2. Simple masks deliver lower concentrations of oxygen, but providing known and stable Fio2 can be unpredictable. Nasal cannula devices can deliver up to a 40% concentration of oxygen, with flow rates of up to 6 L/min delivered with humidified oxygen. They are appropriate when the child’s oxygen requirement is low. They are often used in small infants who have chronic minimal oxygen needs because they allow the child to feed spontaneously while oxygen is being delivered.American Board of Pediatrics Content Specification(s)Discuss indications and contraindications for airway adjuncts, oxygen delivery, and suctioning the upper airwayDescribe the key steps and potential pitfalls in performing airway adjuncts, oxygen delivery, and suctioning the upper airwayDiscuss the complications associated with airway adjuncts, oxygen delivery, and suctioning the upper airwayKnow the anatomy and/or pathophysiology relevant to airway adjuncts, oxygen delivery, and suctioning the upper airwayQuestion: 3A 4-year-old young boy has been brought to the emergency department by his mother because she noticed that he experiences sudden episodes during which he seems “unsteady” when standing and upset when trying to walk, complaining of a “spinning” sensation.?He has had some nasal congestion and rhinorrhea but no fever, headache, photophobia, phonophobia, neck pain, neck stiffness, or vision problems. He prefers lying down to standing and has been pulling at his ear. He has no history of trauma, loss of consciousness, syncope, or seizure activity. On physical examination, he has no focal neurologic findings or signs of external injury, but his tympanic membrane is dull with poor light reflex and decreased mobility on pneumatic otoscopy. His family history is negative for migraine headaches.Of the following, the MOST useful investigation to help determine the cause of this patient’s vertigo isA.cerebrospinal fluid puted tomography scan of the brainC.electrocardiographyD.electronystagmographyE.hearing testingCorrect answer: EVertigo can be a challenging symptom to investigate in young children because the sensation can be difficult for them to describe; they often use terms such as “spinning, sliding, turning, or feeling dizzy.” Patient history is of utmost importance in sorting through the differential diagnosis. The physical examination should focus on findings that can affect the vestibular, visual, or proprioceptive systems because proper integration of these organ systems is necessary for balance and proper spatial orientation. The boy described in the vignette appears to be experiencing acute paroxysmal episodes of vertigo, which can often be caused by middle ear disease. Determining the presence or absence of hearing loss is the most useful initial diagnostic study because it provides a means to categorize the vertigo as central or peripheral. Formal audiometric testing is not readily available in the emergency department, but the clinician can use a tuning fork to help distinguish a conductive versus sensorineural hearing loss and initially categorize potential causes of the vertigo (Table 1).Beyond middle or inner ear infection, additional causes of vertigo in young children (younger than age 14 years) include: migraine-associated dizziness or vertigo; benign paroxysmal vertigo of childhood; and labyrinthitis due to viral infections, head trauma, and medications. The causes of vertigo can be further subdivided into peripheral or central (Table 2). Peripheral causes imply a disorder with either the peripheral nerve or the labyrinth, which comprises the three semicircular canals and the two otolith organs of the vestibule: the utricle and saccule, which generate impulses based on angular acceleration, vertical acceleration, and gravitational forces on the ciliated hair cells contained within. The proprioceptive, oculovestibular, and postural sensory signals are integrated within the vestibular nuclei of the brainstem and include input from specific areas of the cortex, cerebellum, and spinal cord. Central causes of vertigo are related to problems with any of these areas and are often associated with additional neurologic symptoms (Table 3). Central causes are generally less common than peripheral, with the exception of migraine and migraine-related vertigo and dizziness.Cerebrospinal fluid studies can aid in determining whether the vertigo is due to meningitis or encephalitis, but acute vertigo without fever, neck pain, neck stiffness, or headache is an uncommon initial presentation of a central nervous system infection. Brain or other neurologic imaging investigations are useful diagnostic studies for patients who exhibit chronic, persistent, or worsening vertiginous symptoms; altered mental status; cranial nerve, sensory, or other neurologic deficits; papilledema; sensorineural hearing loss; persistent headaches; or a history of head trauma. Although less common, the more serious or life-threatening causes of vertigo are seizure disorder, vertebrobasilar disease, Arnold-Chiari malformation, multiple sclerosis, or intracranial neoplasms. Electrocardiography to evaluate a cardiac cause would be useful if this patient was an adolescent who reported dizziness (as opposed to vertigo) along with syncope or palpitations. Electronystagmography is specialized vestibular function testing that provides objective, nonspecific evaluation of a patient’s vestibular function and oculomotor systems, but it is not readily available in the emergency department.The initial management of vertigo depends on the underlying cause, although vestibulosuppressant medications (typically histamine-blocking agents such as meclizine, dimenhydrinate, and promethazine) and antiemetics can be administered temporarily while the patient is symptomatic. Particle or canalith repositioning maneuvers (Epley or Semont maneuvers) are specific therapies for those who have benign paroxysmal positional vertigo. The maneuvers consist of specific sequential head movements to move particles/debris out of the posterior or anterior semicircular canal into the vestibule. When correctly performed by an experienced practitioner, a high rate of cure can be achieved with one to two sessions.Table 1: Acute Paroxysmal VertigoHearing LossNo Hearing LossLabyrinthitisInfants—benign paroxysmal vertigo or torticollisMénière diseaseAdolescents—vestibular neuronitisPerilymphatic fistulaLabyrinthine concussionVascular occlusionParoxysmal positional vertigoTemporal bone fractureMigraine?Seizures?Subclavian stealTable 2: Categorization of Vertigo by Peripheral and Central CausesPeripheralCentralAcute labyrinthitisAcute vestibular neuronitisBenign positional paroxysmal vertigoMénière diseasePerilymphatic fistulaCerebellopontine angle tumorCerebrovascular diseaseMigraineMultiple sclerosis or other demyelinating diseaseTable 3: Clinical Presentations of VertigoPeripheralCentralOccurrenceEpisodic, sudden onsetConstantDirection of spinning/nystagmusUnidirectionalVariableNystagmus axisHorizontal, rotaryHorizontal, vertical oblique, or rotaryNystagmus typeSlow and fast phaseIrregular or equal phaseHearing loss, tinnitusPossibleNoLoss of consciousnessNoPossibleOther neurologic signs/symptomsNoCranial nerve deficits, cerebellar and pyramidal signs frequentAmerican Board of Pediatrics Content Specification(s)Know the etiology by age and the pathophysiology of vertigoPlan diagnostic evaluation and initial intervention for patients with vertigoRecognize serious and/or life?threatening causes of vertigoQuestion: 4A 5-month-old girl is brought to the emergency department because of increased fussiness and fast breathing. Her parents report that she had seemed fussy yesterday evening, and they thought that it was related to teething. They used a “teething gel” to treat her symptoms, applying it several times overnight. This morning the child was fussier, breathing fast, and refusing to eat. She had not been ill and had no history of vomiting, fever, or trauma. On physical examination, her temperature is 37.1°C, heart rate is 154 beats/min, respiratory rate is 52 breaths/min, blood pressure is 76/45 mm Hg, andoxygen saturation is 87% in room air, which does not respond to an Fio2 of 1.0 by bag-valve-mask with positive pressure. She appears alert but irritable and had moderate retractions but clear breath sounds. Her lips appear dark. Heart sounds are normal, no hepatomegaly is evident, and her capillary refill time is 3 seconds. Point-of-care testing reveals a glucose of 148 mg/dL (8.2 mmol/L), pH of 7.23, Pco2 of 21 mm Hg, Po2 of 365 mm Hg, base deficit of 19 mEq/L (19 mmol/L), and hematocrit of 35% (0.35).Of the following, the treatment that is MOST likely to address the cause of this child’s acidosis isA.ascorbic acid 200 mg orallyB.cefotaxime 75 mg/kg intravenouslyC.methylene blue 1 mg/kg intravenouslyD.prostaglandin E1 0.1 mg/kg per minute intravenouslyE.sodium bicarbonate 1 to 2 mEq/kg intravenouslyCorrect answer CThe most likely cause of the cyanosis described for the infant in the vignette is methemoglobinemia related to the use of a benzocaine-containing teething gel. The treatment for significantly symptomatic methemoglobinemia is 1 to 2 mg/kg of 1% methylene blue solution administered intravenously. Ascorbic acid is ineffective for the acute treatment of symptomatic methemoglobinemia. The infant does not have fever or other signs of sepsis that would prompt antibiotic administration. In addition, she has no symptoms of ductal-dependent obstructive cardiac lesions requiring treatment with prostaglandin E1. Sodium bicarbonate may help treat her acidosis but will not address the underlying cause.Acquired methemoglobinemia occurs when the iron molecules in hemoglobin are oxidized from the ferrous (Fe2+) to the ferric (Fe3+) state. In the ferric state, hemoglobin is unable to bind oxygen, and any other iron molecules in the same hemoglobin moiety that are still in the ferrous state have increased oxygen affinity (hemoglobin dissociation curve is shifted to the left), making them unable to release oxygen molecules and leading to impaired oxygen transport and tissue hypoxia.Methemoglobin (MHb) is produced normally in the body and usually accounts for about 1% to 1.5% of a child’s total hemoglobin. Most of this MHb is reduced back to the ferrous state by the actions of cytochrome b5 or MHb reductase. In the first few postnatal months, infants are relatively lacking in MHb reductase and, therefore, are more susceptible to oxidant stresses that may lead to the formation of increased amounts of MHb. Multiple causes of oxidant stress can precipitate an episode of methemoglobinemia in infants.Exogenous sources of oxidants are often related to the ingestion of nitrites or nitrate-containing compounds that may be converted to nitrites in the gastrointestinal tract by normal gut flora. Such conversion may be exacerbated by the relatively high pH of the infant gastrointestinal tract. Well water containing high concentrations of nitrites or nitrates (often due to agricultural runoff), certain foods, and medications can be causes of methemoglobinemia in infants. The most common medications associated with methemoglobinemia in infancy are local topical anesthetics, especially benzocaine (which is frequently used in teething gels). The United States Food and Drug Administration continues to alert health-care professionals to ongoing reports of adverse and potentially fatal effects related to the use of benzocaine-containing products in at-risk populations, including infants. Other implicated medications include EMLA, dapsone, lidocaine and other local anesthetics, metoclopramide, quinones, and sulfonamides.In very young infants, especially those of low weight for their age, methemoglobinemia may occur during diarrheal illnesses. The exact mechanism is not completely clear. Acidosis, especially hyperchloremic acidosis, may be enough of an oxidant stress to cause oxidation of hemoglobin to the ferric state. Changes in gut flora during the illness may lead to increased production of nitrites, causing increased production of MHb. Escherichia coli and Campylobacter jejuni have been implicated in some case series. Whatever the initial cause of increased MHb, the low concentrations of MHb reductase cause the child to develop high concentrations of MHb.Whenever cyanosis in a child does not respond to oxygen, methemoglobinemia should be considered. The blood may appear “chocolate brown” and does not turn red on exposure to air or oxygen. Blood co-oximetry should be obtained. Results of conventional pulse oximetry, which uses two wavelengths of red light, are inaccurate in patients who have methemoglobinemia. Newer pulse oximeters, which use multiple wavelengths of light and report concentrations of MHb and carboxyhemoglobin, can alert clinicians to the presence of methemoglobinemia.Failure to recognize this diagnosis can lead to continued hypoxia, worsening acidosis, seizures, coma, and even death. Treatment involves removal of the oxidant stress (in this case, removing any gel that might be on the infant’s gums and avoiding additional administration) and administration of methylene blue intravenously in patients who are symptomatic or who have MHb concentrations of greater than 30%.?Methylene blue should not be administered to patients who have glucose–6–phosphate dehydrogenase deficiency. Exchange transfusion or hyperbaric oxygen therapy may be useful in these patients or in those who are not responsive to methylene blue.American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of methemoglobinemiaUnderstand the usefulness of ancillary studies in methemoglobinemiaPlan the management of methemoglobinemiaQuestion: 5A previously healthy 17-year-old girl presents to the emergency department in active labor. As you prepare for the imminent delivery of her infant, you briefly review the latest guidelines on resuscitation of the newborn.Of the following, an ABSOLUTE indication of the need for resuscitation of the newly born infant isA.heart rate of 80 beats/minB.presence of any meconium staining of the amniotic fluidC.presence of thick meconiumD.pulse oximetry measurement of 70% at 1 minute of ageE.respiratory rate of 60 breaths/minCorrect answer: AThe 2010 American Heart Association guidelines for cardiopulmonary resuscitation and cardiovascular care indicate two major indicators of the need for resuscitation of the newborn: 1) respiratory abnormalities such as apnea, gasping respirations, or labored breathing; and 2) heart rate less than 100 beats/min. Normal neonatal respiratory rates range from 35 to 60 breaths/min; a respiratory rate of 60 breaths/min is not in itself an indication for resuscitation (Figure). Auscultation of the precordial pulse or palpation of the pulse at the umbilical site is recommended over palpation at other sites because studies have shown that the pulse can be more reliably detected at the umbilicus.Although pulse oximetry is helpful in ongoing neonatal resuscitation, it is not a primary tool to determine the need for initial resuscitation. It can take 1 to 2 minutes to obtain a reading and may not provide an accurate reading in low cardiac output states. In addition, research has shown that expected oxygen saturations in the first 10 minutes after birth are significantly lower then previously believed (Table 1). Resuscitation should be titrated to achieve the oxygen saturations noted. If used, the pulse oximetry probe should be placed in a preductal location, such as the right wrist or palm.No degree of meconium staining is by itself an indication for endotracheal suctioning because studies have demonstrated no improvement in outcome with this procedure in affected infants. Endotracheal suctioning should be performed only on nonvigorous babies who have meconium-stained fluid; resuscitation is not indicated in the crying or breathing infant who has good muscle tone.Routine oropharyngeal suctioning is not indicated in any infant unless there is obvious obstruction to spontaneous ventilation or the need for positive-pressure ventilation.Only 6% of term newborns require resuscitation at birth, although 80% of infants who weigh less than 1,500 g require resuscitation. Both prenatal and perinatal maternal risk factors predict the need for neonatal resuscitation (Table 2). Anticipating and planning for resuscitation in high-risk situations is warranted. Pulse oximetry monitoring is indicated when resuscitation is anticipated, positive-pressure ventilation is needed for more than a few breaths, cyanosis is persistent, or supplemental oxygen is administered.The most common signs of respiratory distress in neonates are tachypnea, grunting, nasal flaring, retractions, and cyanosis.Resuscitation with 100% Fio2 no longer is recommended routinely in neonates; beginning resuscitation with air or blended oxygen titrated to achieve saturations listed in Table 1 is preferred. Administration of 100% inspired oxygen is recommended if the heart rate is less than 60 beats/min after 90 seconds of resuscitation with lower concentrations of oxygen and should be continued until the normal heart rate recovers.Neonatal outcomes are optimized when hypo- or hyperthermia and hypoglycemia are avoided. Infant temperature should be monitored and warming measures adjusted accordingly to maintain normothermia. Selected use of intentional cooling in controlled studies has been shown to improve neurodevelopmental outcomes in infants experiencing asphyxia. In the distressed infant, point-of-care blood glucose monitoring is indicated and hypoglycemia should be promptly treated.Figure: Algorithm for newborn resuscitation. American Board of Pediatrics Content Specification(s)Recognize the signs and symptoms of neonatal distressKnow the indications for monitoring and laboratory procedures in recognition of neonatal distressRecognize the maternal risk factors associated with neonatal distressQuestion: 6You are evaluating a 4-year-old girl who has a central catheter for treatment of B-cell leukemia and was brought to the emergency department because of 2 days of fever. On physical examination, the moderately ill girl is awake and has a stable airway. Her temperature is 39.2°C, heart rate is 147 beats/min, respiratory rate is 32 breaths/min, blood pressure is 100/47 mm Hg, and oxygen saturation is 97% in room air. You note minimal erythema surrounding the insertion site of a Hickman catheter, which the parents report has been in place for 4 months. There is no evidence of tenderness, swelling, pus, or abscess at the insertion site.Of the following, the MOST appropriate next step(s) is(are) toA.administer immediate broad-spectrum antibioticsB.obtain blood cultures and administer antibioticsC.obtain a leading edge aspirate at the area of erythema and administer antibioticsD.remove and dispose of the catheter, then administer antibioticsE.swab the catheter hub and send for bacterial cultureCorrect answer BThe 2-day history of fever reported for the immunocompromised girl in the vignette raises the possibility of a catheter infection. Sepsis independent of the central line is also a possibility. Identifying the specific site of infection is critical and requires blood cultures obtained with a sterile technique before administering broad-spectrum antibiotics.Immediate removal of the central line usually is not indicated during the emergency department assessment for fever and potential central line infection. ?If the cultures eventually reveal evidence for a catheter infection, catheter removal may be indicated, depending on the specific organism causing the infection and the response to empiric therapy.?If the catheter is removed, the tip should be sent for culture. The description of the insertion site in this patient does not clearly indicate an active infection, so a leading edge aspirate would be less useful than the blood cultures. Leading edge aspirates have been recommended in the past to identify the bacterial cause in cellulitis, but their usefulness has been questioned.Central venous catheters (CVC) have been used for the past 40 years for parenteral nutrition, medication administration, and vascular access. The catheters can be classified as peripherally inserted central catheters (external catheters for short- to medium-term use), tunneled external venous catheters (Hickman and Broviac for short- to medium-term use), and totally implanted devices (port systems for medium- to long-term use). The Hickman (Figure 1) and Broviac catheters are made of silicone with a Dacron? cuff that allows tissue ingrowth to help anchor the catheter. Tunneled catheters are often preferred due to their smaller size, increased durability, and lower risk for infection compared with nontunneled catheters. Port systems (Figure 2 and Figure 3) are implanted devices consisting of a port body with a silicone membrane and a catheter. The port is accessed using a special noncoring Huber needle (Figure 4). The membrane must be punctured vertically to avoid bending the tip. Local skin anesthesia should be considered before access, and avoidance of needle rotation while inserted can help to prevent leaks.Central catheters can be placed via the internal jugular, subclavian, and femoral veins, either by Seldinger technique or direct venous exposure. Recommended catheter tip placement is at the junction of the inferior vena cava and right atrium for a CVC placed in the lower body and at the junction of the superior vena cava and right atrium for those placed through an upper body vein.Ninety percent of catheter-related bloodstream infections occur in patients who have CVCs. The rate of catheter-related infections in long-term CVCs has been reported to be between 0.6% and 27%. A 2004 report estimated that approximately 20,000 deaths occurred annually as a result of central line infections. Other authors have cited somewhat lower estimates. The average cost per infection has been estimated between $3,700 and $45,000, and infection may prolong hospitalization by an average of 7 days.Infection risk can be minimized through proper education and training of staff; adherence to strict antiseptic access techniques for line insertion, access, and dressing; and limiting the need to access the line. Prophylactic antibiotics have not been shown to be useful in preventing mortality for CVC infections.Evidence-based guidelines have been published for prevention and management of catheter-related infections. In 2008, the American College of Surgeons examined the process of using existing guidelines to generate best practice recommendations (Freel et al, 2008). The consensus group identified many areas of best practice, including recommendations for placement, maintenance, and infectious assessment. In general, appropriate and important aspects of line infection prevention, as noted in the American Academy of Pediatrics and Institute for Healthcare Improvement review of central line infection prevention publication, include: hand hygiene, maximal barrier precautions (sterile precautions), chlorhexidine skin preparation, optimal catheter site selection, and routine review of central line necessity, with prompt removal as soon as it is no longer needed.Strict aseptic precautions (sterile techniques, gloves, masks, gowns, and sterile field) must be observed when accessing any central line to minimize the risk of catheter-induced infection. The most appropriate skin disinfectant is 2% chlorhexidine, although 70% alcohol solution, an iodophor, or tincture of iodine can also be used.It is important to distinguish between catheter colonization (bacterial presence on catheter without signs of inflammation or bacteremia) and true catheter infections. True catheter infections can include signs of local infection at the catheter site, bacteremia (same organisms at catheter site and in peripheral blood culture), septic thrombophlebitis, and tunnel or pocket infections (spread of infection into the subcutaneous portion of implanted system). Infection can occur at the time of insertion, via migration of skin organisms, through contamination of materials passing through the hub, with infusate contamination, and via hematogenous spread from a distant site. The most common pathogens are coagulase-negative staphylococci, Staphylococcus aureus, and Candida.Catheter-related infection should be suspected in the presence of local inflammation or fever. Some centers advocate obtaining paired blood cultures from a peripheral vein and the central catheter in an attempt to identify the catheter as the origin of the bacteremia. Newer literature suggests that this practice does not change management, although this is a controversial issue.Swabs from the catheter hub are not recommended. If catheter removal is indicated, the actual tip should be sent for culture. Central lines may need to be removed for the following conditions: persistent bacteremia, sepsis, relapse of infection after antibiotic treatment, tunnel infections, systemic complications (osteomyelitis, abscess formation, endocarditis, thrombosis, or embolism), or if S aureus or Candida are identified by culture. Empiric antibiotic therapy is recommended for patients who have central lines and fever, directed by the underlying disease process, clinical situation, and suspected microorganisms. In practice, this generally means the use of vancomycin or another antibiotic active against methicillin-resistant staphylococci in combination with an antibiotic active against the pathogens most likely to cause sepsis in the clinical situation. Antibiotic lock use (high-concentration antibiotic solution instilled in catheter when not in use) has been reported.Thromboembolic issues can also occur with central catheters. Additional guidelines for care and potential complications are addressed in the 2009 ESPEN Guidelines on Parenteral Nutrition (Pittiruti et al) and the article on management of occlusion and thrombosis (Baskin et al).American Board of Pediatrics Content Specification(s)Know the anatomy and pathophysiology relevant to accessing indwelling central cathetersDiscuss the indications and contraindications for accessing indwelling central cathetersDescribe the key steps and potential pitfalls in accessing indwelling central cathetersDiscuss the complications associated with accessing indwelling central cathetersQuestion: 7A 12-year-old previously healthy boy is brought to the emergency department by his mother because he has been experiencing chest pain for the past 2 days. His mother states that tonight he was unable to sleep because of the pain. He describes it as a constant stabbing sensation under his ribcage. He prefers to sit up, leaning forward. Two weeks ago, he had several days of fever and upper respiratory tract symptoms that have now resolved. On physical examination, his temperature is 37.4°C, heart rate is 120 beats/min, respiratory rate is 24 breaths/min, and blood pressure is 105/65 mm Hg. Chest auscultation reveals an audible friction rub, clear breath sounds, and no murmurs. A chest radiograph shows a normal cardiothoracic silhouette. His electrocardiography (ECG) tracing is shown in the Figure.Of the following, the MOST appropriate treatment at this time isA.colchicineB.ibuprofenC.methylprednisoloneD.naproxen sodiumE.prednisoneCorrect answer: BThe boy described in the vignette has signs and symptoms suggestive of pericarditis (inflammation of the pericardium). The most likely cause in a previously healthy boy who is afebrile, nontoxic, and hemodynamically stable is viral or idiopathic. Pericarditis is primarily a self-limited illness. Goals of treatment are to control inflammation and decrease pain. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the first-line treatment, with ibuprofen being the drug of choice because of its more favorable adverse effect profile relative to the other NSAIDs (eg, naproxen). Colchicine may be added in selected cases if the patient fails to respond to ibuprofen alone or if the pericarditis is recurrent. The use of corticosteroids is controversial and generally not recommended because of the risk of reactivation of viral pathogens. Selected studies have also demonstrated an increased risk of recurrent pericarditis when corticosteroids are used.The severity of pericardial disease can range from mild pericarditis with little to no fluid apparent in the pericardial sac on echocardiography to large pericardial effusions that can lead to cardiac tamponade. Symptomatology varies with disease severity. In pediatric-specific series, the most common presenting signs are fever, chest pain, dyspnea, and tachycardia. The pain is often described as substernal, worse with inspiration, and relieved when the patient sits upright and leans forward. The pain may also radiate to the shoulder. The notable finding on physical examination is a friction rub, as described for this patient, which is usually heard best at the left lower sternal border between the second and fourth intercostal spaces and is accentuated when the patient is leaning forward. Muffled heart sounds and loss of the friction rub may be noted in the presence of a large pericardial effusion. Tachycardia is common, and narrow pulse pressure and neck vein distension may be seen in more severe disease. Pulsus paradoxus, an exaggerated decrease in systolic artery pressure during inspiration of greater than 10 mm Hg, is suggestive of cardiac tamponade. The presence of Beck triad (jugular venous distension, hypotension, and muffled heart sounds) is also indicative of tamponade. Pallor, cold extremities, agitation, decreased level of consciousness, prolonged capillary refill, and tachycardia may also be present.A standard diagnostic evaluation for pericarditis includes ECG, chest radiography, and echocardiography. Complete blood count, erythrocyte sedimentation rate, and C-reactive protein are also often ordered, but results are nondiagnostic. ECG changes are present in 90% of cases. In early pericarditis, ECG shows diffuse ST elevation and a shortened PR interval in most leads, as demonstrated in this patient. In the second stage, the ST and PR intervals normalize, but T waves flatten and subsequently invert. The third stage is characterized by a normal ECG tracing, except for T-wave inversion. When a significant pericardial effusion is present, ECG may reveal low-voltage QRS segments due to the dampening effect of pericardial fluid. The chest radiograph often appears normal in acute pericarditis; at least 250 mL of fluid in the pericardium is needed to cause visible cardiomegaly. Echocardiography is the diagnostic modality of choice, but results can appear normal if minimal fluid is present. Cardiac computed tomography scan or magnetic resonance imaging may be performed if echocardiography findings are inconclusive. Advanced imagining may be useful to differentiate pericarditis with a small effusion from constrictive pericarditis or restrictive cardiomyopathy.The most common cause of pericarditis is viral or idiopathic, which, in combination, may account for 85% of disease. Bacterial (purulent) pericarditis (5%) may occur via hematogenous spread or direct extension from adjacent structures, especially the lungs. Prompt recognition and antibiotic treatment are necessary for affected patients, who typically have a more fulminant presentation, with fever and toxicity. Common infectious pathogens are listed in Table 1. Pericardial disease also can result from immunologic, metabolic, and traumatic causes (Table 2).Patients who have suspected bacterial pericarditis require antibiotics in addition to NSAIDs. Empiric administration of broad-spectrum antibiotics that include antistaphylococcal coverage should be initiated. If tamponade is suspected, management includes a fluid bolus to increase preload, followed by pericardiocentesis. If purulent pericarditis or restrictive pericarditis is present, pericardiectomy may be necessary.Sixty percent of patients who have viral/idiopathic pericarditis recover within 1 week, and an additional 20% recover fully by 3 weeks. Worse outcome is predicted in the presence of large effusion, tamponade, or failure to improve with NSAIDs. Up to 30% of patients may have recurrent pain or friction rub.Table 1: Causes of Infectious PericarditisInfectiousPathogensFeaturesViralEnterovirus (coxsackievirus, echovirus), adenovirus, influenza, Epstein-Barr virus, human immunodeficiency virus (HIV)Typically self-limited illness following 10 to 14 days of prodromal viral symptomsBacterial (Purulent)Staphylococcus, nontypeable Haemophilus influenzae, Streptococcus, Mycoplasma, Neisseria meningitidisToxic appearance, rapid progression, hemodynamic instability, progression to tamponade if unrecognized?Mycobacterium tuberculosisSpread from mediastinal nodes or hematogenous, large effusions, ±tamponade, more common in endemic areas or HIV-positive patientsParasiticToxoplasma, EchinococcusUncommon causeFungalActinomyces, HistoplasmaUncommon cause, increased susceptibility in immunocompromised hostTable 2: Noninfectious Causes of PericarditisImmunoreactiveSystemic lupus erythematosus, juvenile idiopathic arthritis, sarcoidosis, rheumatic feverMetabolicUremiaEndocrineHypothyroidismHematologic/OncologicNeoplastic (metastatic),?bleeding diathesisTraumaticPostoperative,acute penetrating or blunt traumaAmerican Board of Pediatrics Content Specification(s)Know the etiology and pathophysiology of pericardial diseaseRecognize signs and symptoms of pericardial diseaseBe familiar with ancillary studies relevant to pericardial diseasePlan management of acute pericardial diseaseQuestion: 8A 15-year-old lacrosse player is brought to the emergency department after being pushed from behind and landing on her outstretched right hand. She had immediate pain in her wrist and arm and decreased range of motion at the wrist. She has no other complaints. On physical examination, the alert girl is in moderate discomfort, with swelling and tenderness to palpation over the middle of the radius as well as mild swelling at the ulnar aspect of the wrist. Compression of the distal radius and ulnar head with rotation produces marked pain. Radiography shows a displaced fracture at the junction of the middle third and distal third of the right radius (Figure).Figure: Reprinted with permission from Hinshelwood HL, Caro D. Galeazzi fracture--Dislocation of the wrist or isolated distal radius fractureOf the following, this injury is MOST likely to requireA.closed reduction and a long arm castB.closed reduction and a thumb spica castC.long arm cast with later physical therapyD.open reduction and fixationE.removable volar splintCorrect answer: DThe findings described for the girl in the vignette are consistent with a Galeazzi fracture (fracture of the radius associated with dislocation of the distal radioulnar joint) based on the additional clinical finding of tenderness over the radial ulnar joint. This injury has been called the “fracture of necessity” in skeletally mature individuals because surgical repair typically is needed to produce a good outcome. Usual management involves open reduction and internal fixation of the radius fracture and open or pin fixation of the distal radioulnar joint. Due to the thick periosteal capsule in younger children, closed reduction and casting with close follow-up may be appropriate for these patients.Closed reduction and a long arm or thumb spica cast might be sufficient for a simple dislocation. Thumb spica casts are also indicated for scaphoid fractures. Physical therapy may be appropriate for ligamentous injuries of the wrist without dislocation (eg, wrist sprain or carpal instability). Removable volar splints are indicated for simple buckle fractures of the radius.Wrist dislocations are relatively rare in children and may be difficult to diagnose due to the relatively unossified carpal bones in their developing skeletons. A high index of suspicion is required on the part of the emergency physician. To avoid missing this injury, it is critical to view the wrist joint adequately in children who have radial shaft fractures. Delay in diagnosis of wrist dislocations may lead to poor functional outcomes and chronic wrist pain. Early involvement of a hand specialist is warranted when such injuries are suspected. When they accompany fractures of the radial shaft, the term Galeazzi fracture is used to describe the constellation of injuries.The mechanism of injury for wrist dislocations is usually a fall on an outstretched hand, especially if it is accompanied by radial or ulnar stress. Motor vehicle collisions and contact sports (eg, football, basketball, rugby, and ice hockey) are common activities associated with these acute wrist injuries. Due to the usual mechanisms, these injuries are more common in adolescents than younger children.Dislocations of the wrist may occur between joints within the same row of carpal bones and between the proximal and distal row of carpal bones or at the distal radioulnar junction (DRUJ). The most common of the first type of dislocation is the perilunate dislocation (dislocation of the carpus). In this injury, the capitate bone is displaced dorsally on the lunate. In palmar lunate dislocation, the lunate is displaced anteriorly (toward the palm) into the carpal tunnel. The Galeazzi fracture involves a DRUJ injury in conjunction with a radial fracture.Wrist dislocations usually present, with wrist pain, swelling, and decreased range of motion. When associated with a fracture, such findings may not be appreciated, especially if the dislocation is subtle on plain radiographs. Whenever a dislocation is suspected, orthopedic consultation should be obtained, preferably with a specialist in hand surgery. If immediate consultation is not available, the wrist should be immobilized and referral made to an appropriate specialist as soon as possible. Any signs of neurovascular compromise require immediate referral to a center where an appropriate specialist is available.Isolated dislocations of the carpus may be reduced with effective regional anesthesia or procedural sedation. In these cases, if effective reduction is achieved, cast immobilization may be sufficient.American Board of Pediatrics Content Specification(s)Recognize wrist dislocationProvide appropriate management for a child with wrist dislocation ................
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