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Coma in many cases is a symptom of a potentially life-threatening condition that requires swift and prompt assessment and intervention simultaneously. No single algorithm is currently available for clinician to follow because of the wide spectrum of conditions causing coma. A basic sequential approach is suggested, consisting of initial stabilization, emergent diagnostic evaluation and intervention if needed, and then focusing on detailed evaluation and etiology-specific management as summarized in Figure 31-1.
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Initial Stabilization
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Regardless of the etiology, any child presenting with decreased level of consciousness should receive Airway, Breathing, Circulation, Disability, and Exposure (ABCDE) evaluation. Intervention should be done as quickly as possible for initial stabilization. No studies have evaluated the risk of airway obstruction and decreased rate of breathing with decreased mental status in children. In a pediatric near-drowning case series, 50% of children were apneic when their GCS was 3 or 4.49 The airway should be opened for signs of obstruction and oxygen should be provided if oxygen saturation is less than 95%. Bag-mask ventilation should be done for persistent hypoxemia, decreasing breathing rate, ineffective breathing, or apnea. Cervical spine injury should be assumed, especially in trauma patients because neck pain and tenderness are difficult to assess in patients with decreased mental status. Immobilization of the cervical spine should be done until definitive diagnosis is established. Endotracheal (ET) intubation should be considered with apnea, oxygen saturation below 92% despite airway positioning and bag-mask ventilation, GCS lower than 8 and loss of airway protective (cough and gag) reflexes, signs of raised intracranial pressure, shock state, and need for ongoing resuscitation. ET intubation should be done by the most experienced person available, especially in cases of trauma with possible C-spine injury or raised intracranial pressure. Hypotension and signs of poor perfusion (eg, capillary refill > 2 s, mottled extremities, diminished peripheral pulses, and decreased urine output) should be promptly treated with rapid IV normal saline boluses or blood depending upon presentation; hypotonic IV fluids should be avoided.50 A majority of patients with traumatic brain injury with intracranial hemorrhage, brain edema, or raised intracranial pressure will have hypertension on presentation most likely due to a stress response to maintain cerebral perfusion pressure. In the setting of traumatic or nontraumatic brain injury, hypertension should not be treated emergently except in patients with hypertensive encephalopathy coma. Laboratory tests, including blood glucose and electrolytes mentioned in Table 31-5, should be quickly checked. Complete patient exposure should be done to evaluate for signs of injuries and the GCS should be assessed for changes every 15 minutes in the initial few hours.
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Narcotic ingestion or overdose and hypoglycemia are common findings in children with coma of an unknown etiology, and their immediate reversal can improve consciousness quickly. If raised intracranial pressure is suspected, mannitol or 3% saline should be given during stabilization. Doses and indications of some helpful initial medications for coma patients are listed in Table 31-7.
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Immediately after hemodynamic stabilization, a head CT scan should be obtained in all children with coma and suspicion of structural cause or in otherwise unclear cases. Subsequently, a detailed history and physical examination should be obtained, and etiology-specific workup, including but not limited to lumbar puncture, EEG, or MRI, should be done along with appropriate consultation and transfer arrangements.
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Specific Etiology Management
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It is impossible to discuss the management of all the specific etiologies of coma in this chapter. There are a few common and important situations that clinicians managing pediatric patients with coma need to know. These are briefly discussed here.
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Patients with Increased ICP
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If raised ICP is suspected with traumatic or nontraumatic cause, treatment should be started immediately, especially if signs of herniation are identified. Detailed guidelines for traumatic brain injury management have been published.51 General measures include ET intubation and mechanical ventilation and avoiding hypoxemia and hyperventilation, elevation of the head of the bed to 30 to 45°, maintaining neutral neck position, and aggressively reducing fever. In cases of impending herniation, hyperventilation can be used for short duration until other measures are taken to decrease intracranial pressure. Since hyperventilation raises intrathoracic pressure and may impair venous return, it is important to avoid hypotension, hence blood pressure should be frequently monitored. Bolus fluid administration will often restore venous return to maintain a cerebral perfusion pressure greater than 50 mm Hg.52 Hyperosmolar therapy with either mannitol or 3% saline53 should be started immediately and subsequently continued guided by cerebral perfusion pressure and ICP, if available. Immediate neuroimaging with CT scan and neurosurgical consult should be obtained for surgical lesions. Patients should be subsequently managed in pediatric intensive care units. ICP monitoring and management can improve outcome following TBI, but has not been effective in improving outcome in patients with brain edema and raised ICP due to hypoxic ischemic brain injury.54
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Patients with Meningitis and/or Severe Sepsis
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In patients with strong suspicion of CNS infection or severe systemic infection, in addition to the general measures discussed above, emergent broad-spectrum antimicrobial administration is crucial. Although lumbar puncture is considered the gold standard to confirm the diagnosis of meningitis, antibiotic therapy should never be delayed for obtaining a CSF sample. Clinical decision rules have been published to help clinicians manage children with meningeal signs.41 Patients with meningitis and low GCS, abnormal pupillary reflexes, focal neurological signs, or posturing should undergo a CT scan to rule out increased ICP before lumbar puncture. Steroid therapy with dexamethasone, 0.15 mg/kg, before or with the first dose of antibiotics decreases mortality and neurological sequelae in bacterial meningitis in adults but its utility in children is still debated.55
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Patients with Convulsive or Nonconvulsive Status Epilepticus
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Patients with convulsive status are easy to identify and require prompt management with anticonvulsants. In refractory cases, emergent neurologist consultation and an EEG should be obtained. Electrolytes like serum sodium, calcium, and magnesium should be checked, especially in infants, and corrected if abnormal. Often patients will remain unconscious due to a post-ictal state for up to 1 hour. In general, if consciousness is not recovered by 30 minutes after seizure activity ends without any apparent reason, nonconvulsive status should be ruled out by obtaining an urgent EEG along with other neuroimaging. Children with refractory status epilepticus should be admitted to the PICU for induction of general anesthesia and EEG burst suppression.
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Patients with Coma Due to Toxins
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Patients with suspicion of drug ingestion or intoxication and coma should be stabilized with general measures first. If signs and symptoms of narcotics, benzodiazepines, or anticholinergics are present, antidotes like naloxone, flumazenil, or physostigmine respectively, could be used to improve consciousness. Sodium bicarbonate is suggested in cases of tricyclic antidepressent toxicity. Activated charcoal should be given to decrease systemic absorption, although this should be done only after securing the airway in the comatose child. Doses of these medications are given in Table 31-7.
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Patients with Coma Due to Metabolic Causes
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Although the list of metabolic diseases resulting in coma is very long, some common ones are hypoglycemia, diabetic ketoacidosis, hyperammonemia (eg, from hepatic failure, organic acidurias, urea cycle defects, amino acid transport defects, or Reye syndrome), and nonhyperglycemic ketacidosis (eg, from organic acidopathies, amino acidopathies, fatty acid oxidation defects, and mitochondrial diseases). After initial patient stabilization with general measures, emergent consult with endocrine and metabolic disease experts should be obtained. Patients with severe hyperammonemia may require emergent dialysis for correction. Special laboratory test like plasma lactate levels, plasma amino acids profile, urinary amino acid, and organic acid profile should be sent to delineate the diagnosis.