Neurosurgical Emergencies

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Chapter 45 Neurosurgical Emergencies

Fred A. Fow, MD

1 What is the basic pathophysiology of increased intracranial pressure?

The theory is: The skull is a rigid compartment of fixed volume. Its three constituent parts are brain tissue, blood, and cerebrospinal fluid (CSF). Any increase in the volume of one of these constituents without a decrease in the volume of one or both of the other constituents must result in an increase in intracranial pressure (ICP) (modified Monro-Kelli hypothesis).

Greenes DS: Neurotrauma. In Fleisher GR, Ludwig S, Henretig F (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 1361–1388.

2 How does increased ICP affect cellular survival?

Cellular survival depends on cerebral blood flow delivering oxygen to meet cellular metabolic demand. Cerebral blood flow is related to cerebral perfusion pressure. Cerebral perfusion pressure (CPP) in turn is affected by changes in mean arterial pressure (MAP) or intracranial pressure ICP (CPP = MAP − ICP). Cerebrovascular autoregulation (reflex vasoconstriction/vasodilatation) allows cerebral blood flow to be maintained despite changes in cerebral perfusion pressure. Autoregulation prevents decreases in cerebral blood flow while MAP is greater than 60 mmHg and while ICP is < 40 mmHg. Outside these ranges, cerebral blood flow and oxygen delivery drop in a passively dependent fashion, resulting in cellular injury.

Greenes DS: Neurotrauma. In Fleisher GR, Ludwig S, Henretig F (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 1361–1388.

6 Describe the initial management of increased ICP.

Maintenance of airway, breathing, and circulation (ABCs) is paramount.

In the patient with suspected cervical spine trauma, immobilization is mandatory until cervical spine injury and spinal cord injury can be ruled out clinically and radiographically.

7 What are the relevant features of airway management in patients with increased ICP?

Endotracheal intubation allows for airway maintenance, protection from aspiration, maximal oxygenation, and control over ventilation. Rapid sequence induction (RSI) may help to prevent elevations in ICP and aspiration during intubation. The physician should be experienced in endotracheal intubation and have familiarity with RSI and with the specific indications and contraindications to the use of any of the agents used in RSI.

Hyperventilation causes cerebrovascular constriction, reducing cerebral blood volume and hence reducing ICP. Hyperventilation should be reserved for cases of impending herniation, as evidenced by severe alterations in mental status and vital signs changes or cases of increased ICP resistant to other modalities of treatment. Excessive or prolonged hyperventilation may result in cerebral ischemia and should be avoided.

8 Which medications are recommended in the treatment of increased ICP?

Mannitol may be used acutely to draw fluid from brain tissue in cases of impending herniation or cases of increased ICP resistant to other treatment modalities.

Hypertonic saline has been demonstrated to be an acceptable alternative to mannitol.

Dexamethasone acts more slowly, but may be employed to reduce tissue edema, such as that accompanying tumor, brain abscess, and nontraumatic hemorrhage.

Acetazolamide can be given to reduce CSF production but also has limited acute effect.

Adelson PD: Guidelines for the acute medical management of severe traumatic brain injury in infants, children and adolescents. Chapter 17. Critical pathway for the treatment of established intracranial hypertension in pediatric traumatic brain injury. Crit Care Med 4(3 Suppl):565–567, 2003.

Greenes DS: Neurotrauma. In Fleisher GR, Ludwig S, Henretig F (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 1361–1388.

Steele DW: Neurosurgical emergencies, nontraumatic. In Fleisher GR, Ludwig S, Henretig F (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 1717–1725.

9 What steps can be taken to reduce metabolic demand?

Adequate sedation helps to reduce oxygen demand and avoid any unwanted increases in ICP due to agitation.

Benzodiazepines, narcotics, and propofol should be used with caution because they may lower blood pressure and adversely affect cerebral perfusion pressure.

Barbiturate coma with pentobarbital reduces cerebral metabolic demand and ICP but requires aggressive pulmonary and hemodynamic management. As such, it is reserved for patients in whom other methods of ICP reduction have failed.

Paralysis may decrease oxygen consumption; however, this makes neurologic assessment, including recognition of seizures, problematic. Adequate sedation can obviate the need for paralysis. Avoidance of hyperthermia and of stimulation is also indicated.

Adelson PD: Guidelines for the acute medical management of severe traumatic brain injury in infants, children and adolescents. Chapter 17. Critical pathway for the treatment of established intracranial hypertension in pediatric traumatic brain injury. Crit Care Med 4(3 suppl):565–567, 2003.

Greenes DS: Neurotrauma. In Fleisher GR, Ludwig S, Henretig F (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 1361–1388.

KEY POINTS: INCREASED INTRACRANIAL PRESSURE

1 The first and most important step in the treatment of increased ICP, regardless of its cause, is maintenance of the ABCs.

2 Rapid sequence induction and endotracheal intubation allow for airway protection and help prevent elevation of ICP during intubation.

3 Hyperventilation should be reserved for cases of impending herniation.

4 Avoid excessive or prolonged hyperventilation.

5 Early recognition of signs and symptoms of increased ICP is very important if serious complications are to be avoided.

10 What are the complications of CSF shunt placement in pediatric patients?

Shunt failure occurs in 30–40% of shunt placements within the first year of placement, 15% in the second year, and 1–7% per year thereafter.

Shunt malfunction is the most common complication of shunt placement. This is often a problem of underdrainage due to distal or proximal obstruction, but overdrainage can also occur. Obstruction can result from shunt infection, catheter blockage, valve problems, catheter disconnection, or catheter migration.

Shunt infection occurs in 3–30% of shunt placements. Shunt failure as a result of malfunction or infection occurs in 30–40% of shunt placements within the first year of placement, 15% in the second year, and 1–7% per year thereafter.

Other complications include scrotal or inguinal migration, small bowel obstruction, intussusception, omental cyst torsion, persistent hiccup, abdominal pseudocyst, volvulus, colon perforation, diaphragm perforation, intra-abdominal organ perforation, and subdural hemorrhage (from overdrainage and tearing of bridging veins or from surgery).

Garton HJ: Hydrocephalus. Pediatr Clin North Am 51:305–325, 2004.

Kestle JR: Pediatric hydrocephalus: Current management. Neurol Clin 21:883–895,vii, 2003.

Madikians A: Cerebrospinal fluid shunt problems in pediatric patients. Pediatr Neurosurg 26:613–620, 1997.

11 What is the utility of “pumping a shunt” to test whether it is functioning properly?

Evacuation and refill of the shunt reservoir by pumping the reservoir is one way of assessing the respective distal and proximal patency of the shunt. Unfortunately, by itself, this test has insufficient testing characteristics upon which to base the clinical decision to operate or not operate on a patient with a suspected shunt malfunction.

Garton HJ: Hydrocephalus. Pediatr Clin North Am 51:305–325, 2004.

Piatt JH: Physical examination of patients with cerebrospinal fluid shunts: Is there useful information in pumping the shunt? Pediatrics 89:470–473, 1992.

Piatt JH: Pumping the shunt revisited. A longitudinal study. Pediatr Neurosurg 25:73–76, 1996.

12 Describe the approach to diagnosing CSF shunt malfunction.

A patient with a CSF shunt with signs or symptoms of increased ICP, increasing or new seizures, or CSF swelling along the shunt path should be evaluated with a shunt survey (plain radiography of the shunt throughout its length) and noncontrast head computed tomography (CT).

Neck pain, syringomyelia, and lower cranial nerve palsy in myelodysplastic patients, and Parinaud syndrome (paralysis of conjugate upward eye movement without paralysis of convergence) in those with a history of neoplasm, may be other cues to shunt malfunction necessitating the same workup. The shunt survey helps to delineate the location and configuration of the shunt and to identify any disconnection.

13 What is the value of head CT in evaluating for shunt malfunction?

CT shows the size of the CSF ventricles, indicating how well CSF is being drained by the shunt, and provides a more detailed look at the brain anatomy and shunt placement. Prior head CT is important for comparison of current ventricular size to baseline. Although head CT is central to the evaluation of the patient with suspected shunt malfunction, it has its own limitations. In one report, 24% of patients with surgically proven shunt malfunction had CT readings that made no mention of shunt malfunction. In another study, 16% of such patients had studies that were interpreted as unchanged from baseline. In cases where shunt malfunction is suspected, CT is not a substitute for neurosurgical consultation.

Fein JA, Cronan KM, Posner JC: Approach to the care of the technology-assisted child. In Fleisher GR, Ludwig S, Henretig F (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 1737–1758.

Garton HJ: Hydrocephalus. Pediatr Clin North Am 51:305–325, 2004.

Lee TL: Unique clinical presentation of shunt malfunction. Pediatr Neurosurg 30:122–126, 1999.

Srivastava R: Hospitalist care of the medically complex child. Pediatr Clin North Am 52:1165–1187, 2005.

14 What is the treatment of CSF shunt malfunction?

First, the ABCs. Then, measures to reduce ICP and metabolic demand (see questions 6 and 7). Specific pharmacologic interventions usually applicable here are acetazolamide and dexamethasone. More definitive therapy includes removal of CSF via shunt tap (effective with distal obstruction only) or burr hole puncture (only in the case of proximal obstruction refractory to medical management and with life-threatening symptoms), and definitive shunt revision by a neurosurgeon.

Fein JA, Cronan KM, Posner JC: Approach to the care of the technology-assisted child. In Fleisher GR, Ludwig S, Henretig F (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 1737–1758.

15 What is the slit ventricle syndrome? How is it managed?

This describes patients who have intermittent signs and symptoms of increased ICP despite small or unchanged ventricular size. Symptoms may arise from intermittent obstruction as the ventricular walls collapse around the catheter and obstruct drainage. As the ventricles fill with CSF, ICP rises. This opens the ventricles, allowing the shunt to function again. As might be expected, symptoms are worse when standing and are alleviated by lying down. Analgesia and a short course of steroids may be useful. Neurosurgical intervention is sometimes necessary.

Kestle JR: Pediatric hydrocephalus: Current management. Neurol Clinics 21:883–895, 2003.

Madikians A: Cerebrospinal fluid shunt problems in pediatric patients. Pediatr Neurosurg 26:613–620, 1997.

16 When is shunt infection most likely to occur?

Most shunt infections occur soon after shunt placement. Half occur within 2 weeks, 70–80% within 2 months, and 80–90% within 4 months.

Srivastava R: Hospitalist care of the medically complex child. Pediatr Clin North Am 52:1165–1187, 2005.

17 List the symptoms and signs of shunt infection.

Signs and symptoms of shunt infection include fever, cellulitis, headache, irritability, nausea, vomiting, lethargy, mental status change, feeding problems, bulging fontanel, seizure, diarrhea, ileus, abdominal tenderness (peritonitis), and shunt malfunction. Meningismus may be absent.

Sites of infection include the shunt lumen, the extraluminal ventricles, and the proximal and distal surgical sites. Abdominal pseudocysts can result from infection or become secondarily infected.

Srivastava R: Hospitalist care of the medically complex child. Pediatr Clin North Am 52:1165–1187, 2005.

18 What are the typical CSF findings in shunt infection?

CSF pleocytosis is often present in shunt infections, although it can be seen as a result of inflammation rather than infection in the early postoperative period, when many infections occur. In addition, the pleocytosis may be modest, as bacteria such as coagulase-negative staphylococcus, a common pathogen in shunt infections, may be protected from the body’s immune response. Some evidence suggests that the combination of fever and CSF neutrophilia (> 10% neutrophils) is highly specific (99%) and has high positive and negative predictive values (93% and 95%, respectively) for detecting or excluding shunt infection.

Lan CC: Early diagnosis of ventriculoperitoneal shunt infections and malfunctions in children with hydrocephalus. J Microbiology Immunol Infect 36:47–50, 2003.

McClinton D: Predictors of ventriculoperitoneal shunt pathology. Pediatr Infect Dis J 20:593–59, 2001.

Shah SS: Device related infections in children. Pediatr Clin North Am 52:1189–1208, 2005.

19 Can a patient have a shunt infection with normal spinal fluid collected by lumbar puncture?

Yes. If the ventricles are not communicating with the lumbar spinal fluid, ventriculitis may not be detectable by collection of lumbar spinal fluid.

Shah SS: Device related infections in children. Pediatr Clin North Am 52:1189–1208, 2005.

20 Does bacteremia commonly accompany ventriculoperitoneal shunt infection?

No. Bacteremia is unusual in cases of ventriculoperitoneal shunt infection. The shunt is not directly connected with the vascular system. Also, patients requiring shunt placement appear to have impaired CSF reabsorption into the venous system.

Shah SS: Device related infections in children. Pediatr Clin North Am 52:1189–1208, 2005.

21 Which organisms cause shunt infections, and what is the treatment for shunt infection?

Staphylococcus epidermidis and S. aureus (including methicillin-resistant strains) account for approximately 70% of infections and are the most likely pathogens in the early postoperative period, responsible for 85% of infections occurring in the first 15 days after shunt placement. Such infections are thought to result from intraoperative contamination.

Gram-negative pathogens, including Pseudomonas aeruginosa, account for about 15% of infections. Infection with gram-negative organisms is more likely to occur outside the initial postoperative period. Such infections are thought to result from ascending infection from the distal portion of the shunt.

Initial empiric treatment may include vancomycin to cover S. epidermidis and S. aureus (including methicillin-resistant strains) plus ceftazidime or a fluoroquinolone to cover gram-negative organisms, including Pseudomonas aeruginosa.

Shah SS: Device related infections in children. Pediatr Clin North Am 52:1189–1208, 2005.

22 What are some historical clues to identifying a patient with a brain tumor?

The diagnosis of brain tumor is often delayed because presenting symptoms are nonspecific and common to other childhood illnesses and conditions. Clues from the history that should prompt consideration of further evaluation, such as intracranial imaging, include vomiting (especially without fever, abdominal pain, or alteration in bowel pattern), headache, vision change (loss, diplopia, or blurriness), loss of milestones, seizures, neuroendocrine dysfunction, motor weakness, sensory change, speech problems, abnormal infantile hand preference, and neck pain or torticollis.

Less specific clues include irritability, listlessness, failure to thrive, behavioral disturbances, and appetite disturbances.

23 What clues from the physical examination may suggest a brain tumor?

Focal neurologic deficits, including cranial neuropathy, visual abnormalities (loss of visual acuity, field loss, afferent papillary defect, or nystagmus), ataxia, loss of coordination or balance, upper motor neuron signs (hyperreflexia, clonus, and paraparesis), weakness, sensory change, funduscopic evidence of increased ICP, and macrocephaly, are important to recognize and warrant investigation. A few specific syndromes of note include Parinaud syndrome (paresis of upward gaze, pupillary dilatation reactive to accommodation but not to light, nystagmus to convergence or retraction and eyelid retraction) suggestive of pineal region tumor and diencephalic syndrome (infantile failure to thrive, emaciation, increased appetite, and euphoric affect).

Dobrovoljac M, Hengartner H, Boltshauser E, et al: Delay in the diagnosis of paediatric brain tumours. Eur J Paediatr 161:663–667, 2002.

Kottesch JF, Ater J: Brain tumors in childhood. In Kliegman RM, Behrman RE, Jenson HB (eds): Nelson Textbook of Pediatrics, 17th ed, 2004. Philadelphia, Saunders, pp 1702–1709.

Ullrich NJ: Pediatric brain tumors. Neurol Clin 21:897–913, 2003.

24 Headache is a very common pediatric symptom. What are the historical features of headache that should prompt concern for brain tumor?

Recurrent morning headaches; headaches awakening the child from sleep; intense, prolonged, incapacitating headaches; and changes in headache quality, frequency, and pattern are the classic distinguishing features of “brain tumor headaches” described by Honig and Charney in 1982. Other features of headache that should raise concern are associated vomiting; exacerbation by bending, coughing, laughing, or the Valsalva maneuver; and posterior headache.

Honig P, Charney EB: Children with brain tumor headaches—distinguishing features. Am J Dis Child 136:122–124, 1982.

Piatt JH: Recognizing neurosurgical conditions in the pediatrician’s office. Pediatr Clin North Am 51:327–357, 2004.

KEY POINTS: CHARACTERISTICS OF BRAIN TUMOR HEADACHES

1 Recurrent morning headaches

2 Prolonged incapacitating headaches

3 Changes in headache quality, frequency, and pattern

25 What are the predisposing factors that may lead to brain abscess?

Hematogenous spread is the most common source of brain abscess in children. Cyanotic congenital heart disease is an important risk factor in this regard. Endocarditis (especially left-sided and acute), deep neck vein phlebitis from parapharyngeal infection (Lemierre disease), and chronic pyogenic lung disease are also potential sources. Other sources of hematogenous spread include focal suppurative infections of bone, teeth, or the abdomen. Brain abscess can follow endoscopy as a result of spinal venous plexus contamination. Contiguous spread is the second most common source of brain abscess and can occur from infections of the middle ear, sinus, orbit, face, or scalp. Most patients with bacterial meningitis do not develop brain abscess. Penetrating skull injury, open skull fracture, recent neurosurgery, intracerebral hematoma, and neoplasm are other possible sources for brain abscess.

26 What are the possible factors leading to subdural empyema and epidural abscesses?

Subdural empyema: In young children, the usual source for subdural empyema is direct spread of infection from the meninges. In older children and adolescents, the usual source is contiguous spread through linking emissary veins from extracranial sites following otitis media, sinusitis, or osteomyelitis of the skull. Other causes cited include infection related to prior craniotomy, skull trauma, ventriculoperitoneal shunt, preexisting hematoma, halo-pin traction, hematogenous spread (such as from the lung), or endoscopic procedures.

Epidural abscess: Cranial epidural abscess is rare. Its usual source is contiguous spread of infection from sinusitis, otitis media, orbital cellulitis, or osteomyelitis of the skull, or following neurosurgical procedures or penetrating skull injuries. Epidural abscess has also been reported as a complication of fetal scalp monitoring.

The source for spinal epidural abscess is usually hematogenous spread of infection from skin, soft tissue, bone, or the respiratory or urinary tract. Direct extension from local osteomyelitis, retropharyngeal, retroperitoneal, or abdominal abscess is another potential source. Penetrating injury and spinal surgery are also potential sources.

Yogev R: Focal suppurative infections of the central nervous system. In Long SS, Pickering LK, Prober CG (eds): Principles and Practice of Pediatric Infectious Diseases. New York, Churchill Livingstone, 2003, pp 302–312.

27 What are some of the clues that can help identify brain abscesses?

Unfortunately, the presentation of brain abscess in children is often nonspecific initially. Common initial symptoms include headache, fever, and vomiting. Seizures, mental status change, coma, focal neurologic deficits, papilledema, meningeal signs, and hemiparesis are other clues. Unfortunately, most of these occur in less than half of patients with brain abscess and may not manifest themselves initially. As unilateral headache is unusual in children, its presence should also raise concern for the presence of brain abscess.

Yogev R: Focal suppurative infections of the central nervous system. In Long SS, Pickering LK, Prober CG (eds): Principles and Practice of Pediatric Infectious Diseases. New York, Churchill Livingstone, 2003, pp 302–312.

28 Describe the laboratory findings in focal suppurative intracranial infections.

Common blood test indicators of infection and inflammation, such as leukocytosis, left shift, and elevated erythrocyte sedimentation rates (ESR) and CRP levels, are of limited usefulness in diagnosing or excluding the presence of suppurative intracranial infections. An elevated CRP level may be a better indicator of infection in this setting than leukocytosis or elevated ESR; however, elevated CRP levels, like elevated WBC counts and ESR, are not specific to intracranial infection, limiting its use. Although blood cultures are positive in only about 10% of cases, they should be considered.

CSF can be normal or nonspecifically abnormal (mild to moderately elevated WBC count, neutrophil predominance, low glucose and elevated protein levels). The rate of positive cultures in brain abscess may be as low as 10%; the exceptions are concurrent meningitis or abscess rupture into the subarachnoid space. Moreover, if focal intracranial infection is suspected, lumbar puncture is contraindicated until CT or magnetic resonance imaging (MRI) has excluded increased ICP.

Yogev R: Focal suppurative infections of the central nervous system. In Long SS, Pickering LK, Prober CG (eds): Principles and Practice of Pediatric Infectious Diseases. New York, Churchill Livingstone, 2003, pp 302–312.

29 What is the diagnostic modality of choice for focal suppurative central nervous system (CNS) infections?

CT (contrast-enhanced) or MRI is mandatory if the clinician is considering a focal suppurative CNS infection. MRI is superior to CT for both intracranial and spinal investigation. Consultation with a radiologist is helpful in choosing the correct study for a specific patient.

Stevens JM, Hall-Craggs MA, “Kling” Chong WK, et al: Cranial and intracranial pathology (2): Infections; AIDS; inflammatory, demyelinating and metabolic diseases. In Grainger & Allison’s Diagnostic Radiology: A Textbook of Medical Imaging, 4th ed. New York, Churchill Livingstone, 2001, pp 2377–2391.

Yogev R: Focal suppurative infections of the central nervous system. In Long SS, Pickering LK, Prober CG (eds): Principles and Practice of Pediatric Infectious Diseases. New York, Churchill Livingstone, 2003, pp 302–312.

30 What is the treatment for focal suppurative CNS infections?

The ABCs are the first priority, along with institution of measures to control increased ICP. It is important to obtain the assistance of infectious disease and neurosurgical consultants. Antibiotics are indicated in all cases. The initial choice of antibiotics may be driven by knowledge of predisposing conditions and therefore likely pathogens. The extent of surgical treatment will depend on the specific site of infection and other aspects of each individual case. Corticosteroids may be indicated in limited instances for brain abscess, specifically in cases where edema has resulted in increased ICP or neurologic deterioration.

Yogev R: Focal suppurative infections of the central nervous system. In Long SS, Pickering LK, Prober CG (eds): Principles and Practice of Pediatric Infectious Diseases. New York, Churchill Livingstone, 2003, pp 302–312.

31 What are some causes of stroke in children?

General etiologic categories include cardiac abnormalities, hematologic abnormalities, coagulopathies, vascular anomalies, venous infarcts, metabolic disorders, vasculitides, vasospastic events, and trauma. Sickle cell disease and cardiovascular disease are the most common causes of childhood stroke. When considering hemorrhagic stroke alone, arteriovenous malformation is the most common cause.

Carlin TM, Chanmugam A: Stroke in children. Emerg Med Clin North Am 20:671–685, 2002.

Gorelick MH, Blackwell CD: Neurologic emergencies. In Fleisher GR, Ludwig S, Henretig F (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 759–781.

32 What is the initial evaluation for suspected stroke?

Noncontrast head CT is a reasonable first study in the emergency department (ED) because it will identify hemorrhage. Unfortunately, it may not detect an ischemic event in its early stages and provides limited evaluation of the posterior fossa. MRI is a better study in both regards and should be performed if the noncontrast CT is normal.

33 What are the next steps in the diagnostic work-up for stroke?

The work-up that follows the initial evaluation above is directed at identifying the cause for the hemorrhage or ischemia. Such an evaluation may include additional brain imaging (magnetic resonance angiography/magnetic resonance venography/transfontanel Doppler), cardiovascular evaluation (electrocardiography, chest radiography, echocardiography, transesophageal echocardiography, bubble contrast echocardiography), and laboratory evaluation (complete blood count, electrolytes, drug screen, prothrombin time/partial thromboplastin time/international normalized ratio, anticardiolipin antibodies, lupus anticoagulants, ESR, antinuclear antibody, and screening for antithrombin III, protein C and protein S deficiencies, factor V Leiden mutation, and prothrombin 20210 polymorphism).

Carlin TM, Chanmugam A: Stroke in children. Emerg Med Clin North Am 20:671–685, 2002.

Gorelick MH, Blackwell CD: Neurologic emergencies. In Fleisher GR, Ludwig S, Henretig F (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 759–781.

34 What is the treatment for stroke?

The ABCs are the first priority. Control seizures and hyperthermia. Avoid free water overload if fluid resuscitation is required. Avoid hypoglycemia and hyperglycemia. Additional treatment depends on the type of stroke and specific etiology. Neurosurgical intervention may be necessary in cases of hemorrhagic stroke.

Carlin TM, Chanmugam A: Stroke in children. Emerg Med Clin North Am 20:671–685, 2002.

Gorelick MH, Blackwell CD: Neurologic emergencies. In Fleisher GR, Ludwig S (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 759–781.

35 What are the common signs and symptoms of nontraumatic spinal cord compression in the pediatric patient?

Back pain is an important clue. Weakness, increased or absent tendon reflexes, extensor Babinski reflex, symmetric loss of sensation with a sensory level, and sphincter abnormalities (late) are common signs of cord compression from a space-occupying lesion. Conus medullaris and cauda equina compression may also be associated with abnormalities in sensory-motor function, tendon reflexes, Babinski reflex, and sphincter function.

Rheingold SR, Lange, BJ: Oncologic emergencies. In Pizzo PA, Poplack DG (eds): Principles and Practice of Pediatric Oncology, 4th ed. Philadelphia, Lippincott Williams & Wilkins, 2002, pp 1177–1203.

Schiff D: Spinal cord compression. Neurol Clin 21:67–86, 2003.

36 What is the ED approach to suspected nontraumatic spinal cord compression?

A space-occupying lesion must be ruled out if spinal cord compression is suspected. As such, imaging is the cornerstone of the initial evaluation of such patients. Plain films are not sensitive enough in this setting. Emergent MRI is the preferred diagnostic tool. If a tumor is identified and there has been rapid progression of symptoms or there is a clear cord-level deficit, initiate high-dose corticosteroids without delay. Consultation with a neurosurgeon and an oncologist are crucial. Spinal epidural abscess and subdural abscess mandate the immediate involvement of a neurosurgeon as well.

Rheingold SR, Lange BJ: Oncologic emergencies. In Pizzo PA, Poplack DG (eds): Principles and Practice of Pediatric Oncology, 4th ed. Philadelphia, Lippincott Williams & Wilkins, 2002, pp 1177–1203.

Schiff D: Spinal cord compression. Neurol Clin 21:67–86, 2003.

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