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PEM|BRS: Rheumatology & NeurologyA previously healthy 5-year-old boy presents to the pediatric emergency department with a first-time headache. His mother found him clutching his head and moaning in pain in his room. She reports no history of trauma and no relief after administration of acetaminophen. On physical examination, the afebrile boy is holding his head and whimpering, lying mostly still. His vital signs and other aspects of the examination are within normal parameters. He complains of nausea. You do not detect any signs of meningeal irritation. He resists funduscopic examination, saying that the light hurts. Computed tomography scan of the brain is read as normal.The child described in the vignette has signs and symptoms suggestive of a migraine headache. Initial management involves intravascular volume expansion and administration of nonsteroidal anti-inflammatory drugs (NSAIDs).HYPERLINK "Javascript:Emblink('236/P31587')"Although the diagnosis is often difficult to ascertain during the initial presentation in the emergency department, migraine is one of the most common causes of headaches in children, with an estimated prevalence of 3% to 10%. Up to 80% of affected children have family histories of the disorder. Children who have a history of significant motion sickness and vertigo often develop migraines.“Classic migraines,” those associated with an aura, are less common in children; “common migraines,” those not associated with an aura, predominate. In contrast to adults, unilaterality and a pulsatile nature are not common features of migraine in children. “Complicated migraines” refer to migraine headaches associated with transient neurologic deficits such as hemiplegia and ophthalmoplegia. These types of migraines often are referred to as “basilar type migraine” because of presumed involvement of the basilar arterial supply to the brain and brainstem.Other migraine variants include “Alice in Wonderland” syndrome, in which the aura involves bizarre visual perceptions, and “confusional migraine,” in which the typical affected child is male and exhibits agitation and altered levels of consciousness.The acute treatment of migraine includes an initial trial of analgesics combined with bed rest. NSAIDs appear to be more efficacious than acetaminophen. Intravenous administration of ketorolac can be used if oral intake is limited by nausea. Antiemetic medications such as metoclopramide, prochlorperazine, and promethazine may be helpful both in the treatment of nausea and the headache itself. Narcotics may be administered, although they often exacerbate the nausea.5-hydroxytryptamine agonists are not well-studied in young pediatric patients.Space-occupying lesions in the brain, such as tumors, can cause chronic intermittent headaches, and cranial computed tomography scan usually can be used for diagnosis. Intracranial rupture of an arterial venous malformation or subarachnoid hemorrhage from an arterial aneurysm can cause acute headaches. Affected children usually have neurologic deficits upon careful examination and require neurosurgical management.Tension-type headaches do occur in children. They generally are less severe than migraine headaches and are not associated with photophobia or phonophobia.?The description of the episode experienced by the boy in the vignette suggests a nonfebrile, unprovoked, generalized seizure. Current recommendations do not support routine neuroimaging in children (other than neonates) after a first unprovoked generalized seizure due to the low incidence of abnormal findings that can influence therapy or management or necessitate acute intervention. In contrast, emergent neuroimaging should be considered for any child who has had a seizure and has a history of malignancy or significant head trauma; a child who has a persistent focal neurologic deficit, prolonged postictal period, or continued alteration in mental status; or a child younger than 3 years of age who presents with a focal seizure.HYPERLINK "Javascript:Emblink('236/P31605')"Emergent neuroimaging most commonly involves noncontrast CT scan because this modality is more readily available and requires relatively less time to perform than magnetic resonance imaging (MRI). In most cases, the addition of contrast does not increase the yield significantly. However, MRI is the preferred modality if routine neuroimaging is to be obtained because of its greater sensitivity. In this patient, outpatient follow-up for electroencephalography and consultation with a neurologist is appropriate.?The unilateral facial weakness described for the boy in the vignette is due to right facial nerve (cranial nerve VII) dysfunction. Some authors call this condition Bell palsy (after Sir Charles Bell, who described similar findings following trauma to the facial nerve in 1830); others reserve that name for idiopathic presentations. Among pediatric patients, facial nerve palsy occurs more commonly in teenagers. Symptoms and signs typically evolve rapidly.Peripheral Cranial Nerve VII palsies can be clinically differentiated from a cortical lesion in the brain by the weakness or paralysis in the forehead. A brain lesion would spare the forehead. The first step in the ED evaluation of a child with a suspected peripheral cranial nerve VII palsy is to evaluate the motor function of the forehead. If the forehead musculature is weak or paralyzed, peripheral nerve palsy is confirmed. If the forehead musculature appears normal, a central process is likely and the child should be evaluated for stroke or tumor. Because the facial nerve carries parasympathetic and sensory fibers as well as lower motor neuron fibers, lacrimation, salivation, and taste over the anterior two-thirds of the tongue may be diminished.Lyme disease is a well-recognized cause of facial nerve palsy, especially during the summer in endemic areas. The tick bite may not be noticed, and patients may not manifest other, more characteristic features of Lyme disease. Initially, serum immunoglobulin M and G antibody titers may be evaluated to confirm the diagnosis, although they generally are unhelpful in early stages of the disease. Bell palsy is a manifestation of early disseminated Lyme disease, a stage at which titers usually are positive. Antibiotic therapy directed toward Borrelia burgdorferi is recommended for patients who have suspected or confirmed Lyme disease.Treatment of facial nerve palsy is controversial, except for the need for eye protection. Most patients recover fully or nearly fully, even without treatment. In a meta-analysis of adult studies published in 2001, the Quality Standards Subcommittee of the American Academy of Neurology concluded that “steroids are probably effective and acyclovir (combined with prednisone) is possibly effective in improving facial functional outcomes.” When prescribed, steroids and antivirals should be initiated within the first few days of onset. For children, however, evidence is insufficient to propose definitive recommendations regarding these therapies.The girl described in the vignette displays symptoms and examination findings consistent with increased intracranial pressure without evidence of central nervous system infection or mass lesion. The most likely diagnosis in an obese adolescent female who has these findings is idiopathic intracranial hypertension, also known as pseudotumor cerebri. Lumbar puncture (LP) is both the definitive diagnostic test and the appropriate initial therapy for pseudotumor. Elevated opening pressure (>20 cm H2O) and normal cerebrospinal fluid (CSF) cell counts and chemistries are required for the diagnosis. Pressure measurements should be made with the patient in a relaxed decubitus position (head and legs straight), and CSF should be removed until the pressure is below 20 cm H2O to provide symptomatic relief. Performance of the LP in a seated position or restrained with legs/neck flexed in the decubitus position may result in falsely elevated pressure measurements.HYPERLINK "Javascript:Emblink('236/P31642')"Although symptoms of migraine and other chronic headaches overlap significantly with those of pseudotumor, the presence of papilledema indicates increased intracranial pressure and requires further evaluation. Many patients who have pseudotumor also have chronic headache syndromes such as migraine, and administration of appropriate antimigraine medications such as prochlorperazine and sumatriptan may provide symptomatic improvement of the headaches. However, this is not first-line management for a patient suspected of having pseudotumor. This girl is not showing signs of impending herniation that requires intubation and hyperventilation or signs of a focal central nervous system lesion that necessitates emergent magnetic resonance imaging and neurosurgical evaluation.Pseudotumor is defined as elevated intracranial pressure without apparent cause; specifically, the diagnosis requires exclusion of mass lesions, hydrocephalus, or CSF abnormalities indicating inflammation or infection. Pseudotumor is more common in females, obese patients, and those in late adolescence or early adulthood. The pathogenesis is not clearly understood; several inciting factors are known, and numerous causative mechanisms have been proposed. Proposed mechanisms include overproduction of CSF by the choroid plexus, decreased absorption of CSF by the arachnoid villi, increased venous pressure due to elevated intra-abdominal pressures in obese patients, stenosis of the cerebral venous sinus outflow tracts, and endocrine or metabolic abnormalities related to obesity.?The most common symptom of pseudotumor is headache, which is present in nearly 75% of patients. The headache most commonly is diffuse, throbbing, and episodic. As with other headaches due to elevated intracranial pressure, pain frequently is exacerbated by position change and Valsalva maneuvers. Other common symptoms include nausea and vomiting, episodic vision loss, pulsatile tinnitus, and blurred or double vision. Infants may present with nonspecific symptoms such as lethargy or irritability, apathy, and poor feeding. Some patients are asymptomatic and are diagnosed after discovery of papilledema on routine ophthalmologic evaluation. Examination findings include papilledema that is usually bilateral and symmetric, cranial nerve palsies (especially the sixth cranial nerve), and occasionally diminished visual acuity and visual field deficits.Treatment of pseudotumor is aimed at symptomatic relief as well as limiting the long-term morbidity related to elevated intracranial pressure. The primary long-term complication of pseudotumor is vision loss, which typically begins with peripheral visual field deficits and preservation of central vision until very late in the course. Patients who have mild symptoms and no visual deficits can be treated with lumbar puncture for initial diagnosis and symptom relief and subsequent close follow-up. More significant or refractory symptoms may require serial lumbar punctures and the addition of medications to reduce intracranial pressure. Acetazolamide is a carbonic anhydrase inhibitor that reduces CSF production at the choroid plexus level and traditionally has been the drug of choice for treatment of pseudotumor. Topiramate has been used increasingly for chronic headache syndromes; it also acts as a partial carbonic anhydrase inhibitor and has been shown to be equally efficacious to acetazolamide for pseudotumor treatment. Topiramate also frequently is associated with weight loss, which is a desirable adverse effect, given the association of pseudotumor with obesity. Furosemide can be used for management of pseudotumor symptoms but is not considered first-line therapy.Surgical strategies are reserved for patients who have severe or rapidly progressive symptoms or who have failed therapy with serial lumbar punctures and medical management. CSF diversion by either ventriculo- or lumboperitoneal shunts can manage pseudotumor symptoms effectively. Optic nerve sheath fenestration can stabilize the visual symptoms and prevent permanent vision loss.Sydenham’s Chorea is associated with Group A Strep pharyngitis and ARF. An ASO titer is helpful; The chorea occurs 1-6 months later with an average of 2 months after the initial symptoms of pharyngitis; 80% of patients have carditis; Chorea resolves within 6 months.Acute Rhematic Fever (ARF) occurs 2-6 weeks after untreated Group A Strep infection. The diagnosis is made by a documented strep infection plus the use of the JONES criteria. Note: Most causes of reactive or infectious arthritis do NOT involve multiple joints.Patients with SLE who are on chronic steroids are at risk for spinal compression fractures.A new onset afebrile seizure in a patient may represent a bleed and they should have a CT scan.Clues to the diagnosis of infant botulism are progressive weakness, poor feeding, constipation, and the lack of irritability or fever. Peak incidence is 2-3 months of age. Admission is mandatory since these kids can develop respiratory failure.Neonatal complications of SLE include heart block, hemolytic anemia, and thrombocytopenia; the rash is erythematous arcuate macules with discrete borders and is almost psoriatic in appearance (caused by maternal SLE-associated Ab’s)Symptoms of a posterior fossa mass include “walking into walls” 3+ DTR’s and beats of clonus in the lower extremities.You can get acute dystonic reactions from metoclopramide. Tx: diphenhydramine or benztropine mesylate; Don’t be fooled into thinking it’s a seizure—get the medication history and try Benadryl first—then use benzos and get a CT if it doesn’t work.Behcet’s Disease: a chronic, relapsing vasculitis characterized by painful oral and genital aphthous ulcers, multiple skin rashes, including erythema multiforme and erythema nodosum, uveitis, arthritis, and GI and neurological manifestations. Vulvar ulcers that are recurrent and/or not responding to treatment for infectious causes should make one think of Behcet’s Disease. The patient should be referred to GYN or Surgery for a biopsy of the vulvar ulcers as well as to ophthalmology and rheumatology.A head CT, revealing a single or multiple ring-enhancing calcified lesions, sometimes with areas of focal edema, along with neurologic symptoms should make one consider Neurocystercercosis. It is caused by the larval stage of the pork tapeworm Taenia solium. It is a major cause of seizures in the immigrant population. Presents mostly in older children and adolescents due to the long incubation period as focal seizures or status epilepticus.Proteinurea, microscopic hematuria, and HTN, combined with fatigue and fever should be “red flags” for renal disease; combined with the history of rash, SLE should be highly considered. Leukopenia, normocytic normochromic anemia and thrombocytopenia may be evident on presentation.Gottron’s Sign: a scaly, red macular rash over the metacarpal-phalangeal and proximal inter-phalangeal joints and is diagnostic for juvenile dermatomyositis. Malaise, muscle aches or cramping, proximal muscle weakness, and rash are typical presenting symptoms.Reversible causes of altered mental status such as hypoglycemia and opiate ingestion should be immediately identified and treated prior to further tests or interventions. Approach: ABC’s, then check glucose, if abnormal treat; if normal, give Naloxone 0.01mg/kg, if inadequate response, give 0.1mg/kg. Then check all lytes and labs and look at pupils and neuro exam—if focal neuro exam or unreactive or unequal pupils or signs of trauma, do Head CT.Cheyne-Stokes variation is an alternation of deep and shallow breathing usually associated with metabolic encephalopathy.Decorticate posturing (flexion of the arms and extension of the legs) accompanies lesions in the cerebral hemispheres.Decerebrate posturing (extension of the arms and legs) indicates dysfunction at the level of the midbrain or cerebellum, or, alternatively, severe metabolic dysfunction.VITAMINS mneumonic for Altered Mental Status:Vascular: stroke, inflammatory cerebritis, migraineInfection: meningitis, encephalitis, brain abscess, toxin-producing bug (Shigella)ToxinsAccident/Abuse: epidural, subdural, diffuse axonal injuryMetabolic: renal, hepatic, endocrine, electrolytes, inborn error (glc, VBG, ammonia)IntussusceptionNeoplasm: tumor, hydrocephalusSeizure: post-ictal stateStatus Epilepticus Treatment:Ativan 0.1mg/kgAtivan 0.1mg/kgFosphenytoin 20mg/kg max 1g IV at max rate: 3mg/kg/minORPhenytoin 20mg/kg max 1g IV at max rate: 1mg/kg/minORPhenobarbital (2nd line after Fosphenytoin or if neonate) 20mg/kg at 1mg/kg/minFor refractory SE, use versed drip, 0.2mgkg IV load then 1mcg/kg/min dripFor refractory SE, consider giving pyridoxine (in case of an INH overdose).Should do an LP in the first febrile seizure in infants under 12 months of ageLoss of previously acquired developmental milestones is concerning for a secondary cause of pediatric headaches.Benign paroxysmal vertigo typically occurs in toddlers. This form of vertigo is characterized by abrupt attacks of ataxia and vomiting without a LOC. The spells last minutes and can occur in clusters.ACEP has recommended that a head CT be performed prior to LP only if papilledema, altered mental status, a focal finding on neurologic examination, or a clinical impression of impending herniation is present.Postinfectious Acute Cerebellar Ataxia: characterized by sudden onset of unsteady gait in an otherwise healthy child. It usually occurs in pre-school age children with a febrile illness within 3 weeks preceding the onset of ataxia and represents a post-infectious encephalitis or cerebellitis, most commonly seen after varicella infections. A CT or MRI is necessary to rule out a cerebellar mass. A workup for EBV or HSV encephalitis with an LP would be necessary for an ill-appearing child with ataxia, lethargy, and headache. Suspicion for toxic ingestion should be considered in a child with more altered sensorium in addition to ataxia; May have nystagmus, a staggering gait, dysarthria, and truncal ataxia; WBC normal; CSF shows a mild pleocytosis with normal protein; CT head normal; MRI shows abnormal signal intensity in the cerebellum, cerebral white matter, or globus pallidus. Tx: support or/ Steroids, IVIGADEM (Acute disseminated encephalomyelitis) aka parainfectious encephalitis is the most common demyelinating condition in children; seen in school aged children, presents with ataxia, abnormal motor control, altered mental status, with viral prodrome; On MRI, see large, multifocal, hyperdense areas in the brain and spinal cord on T2 weighted images; Tx: steroids, IVIGAcute dystonia is characterized by opisthotonus, lateral neck flexion, oculogyric spasm, tightening of the extremities and pain; Implicated medications are antipsychotics, dextromethorphan, cisapride, and metoclopramide. Tx: BenedrylGuillain-Barre syndrome is an acute inflammatory demyelinating polyneuropathy that appears as symmetric ascending flaccid paralysis with loss of DTR’s and variable sensory changes. CSF shows increased protein with NO pleocytosis.Myasthenia Gravis: New onset ptosis, neck muscle weakness, and difficulty swallowing are pathognomonic symptoms of myasthenia gravis. Ptosis and muscle weakness are less in the AM and worsen as the day goes on. Caused by circulating antibodies against the Ach receptor (serologic testing confirms dx)—leads to an effective deficiency in Ach. Edrophonium is a short-acting cholinesterase inhibitor (Tensilon Test) used to see if you get transient strength back—for later treatment with pyridostigmine if it works—have atropine on standby to treat a potential cholinergic crisis. Optic Neuritis: presents as an acute loss of central visual acuity, an afferent papillary defect, and a funduscopic appearance that resembles papilledema and hemorrhage. Some patient have headache and pain associated with extraocular movements. It can be bilateral. It is a risk factor for MS.Four “pearls” about Muscular Dystrophy in the ED:For those on chronic steroids, assume adrenal suppression and immunocompromiseDon’t give succinylcholine (causes malignant hyperthermia)Watch for rhabdomyolysisWatch for cardiomyopathies and heart failureJRA can cause pericarditis, cardiac tamponade, pleural effusions, and cricoarytenoiditis as well as atlanto-axial instability.Marfan Syndrome: if presents with acute onset of sharp excruciating pain in the chest, neck, jaw, scapular area, or lumbar area—think aortic dissection! If so, control HR and BP with Esmolol and sodium nitroprusside.Little League Shoulder: pain in the lateral aspect of the proximal humerus while throwing; x-rays show a widening of the proximal humeral physis; Tx—NSAID’s; rest, and PT. (SALTER I Fx of proximal humeral physis)Illiotibial Band Syndrome: positive Noble test (put thumb on lateral femoral epicondyle and actively flex/extend knee with patient supine)Sever’s Disease (Calcaneal Apophysistis)Hip disease should be considered in any child with thigh, groin, or knee painSCFE: Klein’s Line: represents a line drawn along the femoral neck on an AP view of the Hips that should bisect the lateral portion of the femoral head. In patients with mild slippage, the line will be flush with or lateral to the lateral edge of the epiphysis. Patients with unstable SCFE (can’t walk, even with crutches) require immediate Ortho consult; patients with stable SCFE (can walk with crutches) can just do an outpatient Ortho referral.LCP Disease—most can just do an outpatient ortho referral.Differentiating Transient Synovitis of the Hip from Septic Hip:A combination of several factors, including Temp > 38, WBC > 11k, ESR > 20; CRP >1; joint space difference on radiographs > 2mm, and a history of non-weight bearing is more indicative of a septic hip—needs joint aspiration!! If none of those are present, the probability of septic arthritis is < 1%If you have acute flaccid paralysis with sensory loss, bowel and bladder incontinence, and loss of rectal tone, it is suggestive of acute spinal cord pathology. The most appropriate diagnostic test is magnetic resonance imaging (MRI) of the spine. Acute transverse myelitis: This demyelinating disorder is characterized by an abrupt onset of progressive weakness in the lower extremities in conjunction with sensory loss and loss of bladder and bowel function that usually is preceded by a viral or gastrointestinal illness. Symptoms result from motor and sensory deficits attributable to involvement of one or both sides of the spinal cord. Paresthesias typically precede sensory loss and motor loss. Often there is a well-defined level of change in touch and pain sensation, and patients can experience a band of unpleasant hyperesthesia at the upper portion of the level of sensory change. The changes develop over hours or days. Tenderness to percussion of the spinal column can be elicited over the affected segment of spinal cord. Deep tendon reflexes are diminished or absent. A hyperacute presentation sometimes occurs that involves rapid onset of paraplegia, sensory abnormalities, and urinary retention and often is associated with significant back pain.????The exact cause of transverse myelitis is not known. Several organisms, including viruses such as Epstein-Barr virus, herpesvirus, influenza, rubella, mumps, and varicella and other infectious agents such as Mycoplasma and Borrelia burgdorferi, have been implicated. Although most cases are idiopathic, transverse myelitis can occur in acute disseminated encephalomyelitis, multiple sclerosis, and neuromyelitis optica (Devic disease).??MRI of the spine and brain is the investigation of choice for diagnosis and follow-up in patients who have transverse myelitis. MRI typically reveals a variable degree of swelling of the cord and diffuse or multifocal areas of abnormal bright signal on T2-weighted sequences, a finding consistent with demyelinization. In addition, imaging can rule out a cord-compressing lesion, which also can present as acute flaccid paralysis. When transverse myelitis or other demyelinating disease is suspected, brain MRI should be performed simultaneously to rule out multifocal areas of demyelinization, which may be indicative of multiple sclerosis. ??Corticosteroids in the form of high-dose methylprednisone with or without intravenous immune globulin are used to treat transverse myelitis, although efficacy remains unproven. Critical supportive therapy involves maintenance of hydration and nutrition; bladder catheterization; and anticipation and prompt treatment of urinary tract infections, pressure sores, pneumonia, and venous thrombosis. Physical therapy for the patient and psychological support for both the patient and family are of great value in facilitating recovery. Recovery can occur over weeks to months and is complete in 60% of cases. Residual deficits include bowel and bladder dysfunction and weakness in lower extremities. ??GBS is the most common cause of acute flaccid paralysis that often follows an antecedent viral or gastrointestinal illness. Nearly 50% of affected patients have autonomic dysfunction in the form of cardiac dysrhythmias, orthostatic hypotension, and bladder dysfunction. In contrast to transverse myelitis, the paralysis typically is ascending and does not involve any sensory loss in spite of paresthesias. ??Acute intermittent porphyria, an autosomal dominant disorder resulting from a partial deficiency of porphobilinogen deaminase activity, can present with a multitude of neuropsychiatric manifestations, such as proximal muscle weakness and bulbar palsy due to motor neuropathy, sensory impairment, and such psychiatric complaints as hysteria, phobias, psychosis, agitation, and delirium. In addition, gastrointestinal symptoms, primarily abdominal pain with or without nausea, vomiting, diarrhea, and abdominal distension, frequently comprise the presenting symptoms and are indicative of an acute attack. Marine poisons such as ciguatera can be detected by testing the fish on mouse bioassays, but the diagnosis is clinical, and these tests are not available easily. Ciguatera toxin is associated with consumption of large reef fish such as grouper, red snapper, amber jack, and barracuda. The fish can become contaminated during consumption of algae containing dinoflagellates, which produce the heat-stable ciguatoxin. The toxin becomes concentrated as it moves up the food chain. This disease begins with nausea, vomiting, abdominal cramping, and diarrhea, followed in 2 to 5 days by paresthesia, painful teeth, painful urination, blurred vision, nerve palsies, weakness or reversal of hot or cold sensation, and cardiovascular abnormalities (heart blocks, hypotension). ??Tick paralysis caused by Dermacentor ticks usually begins with paresthesias, followed by unsteady gait and eventual ascending paralysis. Patients do not have fever, altered sensorium, a sensory level, or bowel or bladder dysfunction. A meticulous examination almost always reveals a tick. Botulism and poliomyelitis are other conditions that should be considered in the differential diagnosis of flaccid paralysis, but they can be distinguished clinically. The paralysis in botulism typically is descending, involves bulbar musculature, and has no sensory signs or symptoms. Polio, which is rare, is associated with muscle pain that precedes asymmetric paralysis.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.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? ................
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