Pediatric toxic ingestions are often unwitnessed and are usually complicated by the young patient’s inability to provide information on the quantity or identity of the substance ingested (see Chapter 102 Toxicologic Emergencies ) Table 17.2 lists many drug classes that cause coma with overdose Exogenous toxins may impair neuronal function directly or by causing hypoxia, acidosis, enzyme inhibition, hypoglycemia, or seizures ALOC can occur after direct intrathecal injection of medication such as baclofen resulting from intrathecal pump malfunction Metabolic Alterations Abnormal serum concentrations of any substrate or product involved in neuronal metabolism can produce ALOC leading to coma Hypoglycemia is the most common disorder in this category, especially in infants and young children, whose capacity for hepatic gluconeogenesis is limited Disorders known to produce hypoglycemia include serious bacterial infections, sepsis, dehydration, and toxic ingestions (especially ethanol, beta blockers, and oral hypoglycemics) Diabetes mellitus, especially of new onset, may present with profoundly depressed consciousness from the combination of hyperosmolarity, dehydration, hypotension, and metabolic acidosis Patients under treatment for diabetic ketoacidosis may also develop cerebral edema and ALOC Patients with type diabetes may have coma as part of hyperglycemic hyperosmolar nonketotic syndrome, which can be complicated by malignant hyperthermia Metabolic acidosis or alkalosis of sufficient degree produces ALOC The most common disorder of this type in children is severe dehydration leading to metabolic acidosis Abnormal concentrations of any serum electrolyte, including sodium, calcium, magnesium, and phosphorus, can also produce altered mental status Hyponatremia, from either dehydration or dilution from excess water, and hypernatremic dehydration, are among the most common causes of ALOC in infants The degree of resulting neurologic compromise will be affected by the duration and severity of the electrolyte disturbance and concurrent disorders Severe dehydration alone may also produce profound lethargy in infants and children, even in the absence of significant electrolyte abnormalities Other causes of metabolic coma in the pediatric age group include kidney or hepatic failure, both of which may result in progressive apathy, confusion, and lethargy Urea cycle defects may present with ALOC and hyperammonemia in young infants (see Chapter 95 Metabolic Emergencies ) Acute toxic encephalopathy (Reye syndrome) is a rare but devastating illness caused by mitochondrial injury of unknown origin that affects all organs of the body, particularly the brain and liver (see Chapter 97 Neurologic Emergencies ) An epidemiologic association exists between the disorder and an antecedent viral illness (including varicella) from which a patient is recovering Patients with Reye syndrome typically develop severe vomiting, followed by combative delirium that progresses to coma Cerebral edema, increased ICP, and central herniation may occur Miscellaneous Conditions Other causes of coma or ALOC in children are less easily categorized Children with intussusception, the most common cause of bowel obstruction in childhood, may present with significant apathy and lethargy As a result, they may be treated for dehydration, sepsis, or meningitis before the appropriate diagnosis is discovered CNS involvement in hemolytic uremic syndrome may produce a comatose state because of cerebral infarction, most commonly in the basal ganglia Breastfed infants of vegan mothers have presented in coma from severe vitamin B12 deficiency Children with adrenoleukodystrophy may present acutely with coma due to CNS neuron demyelination Psychiatric disorders may produce a true stuporous or catatonic state More commonly, neurologically intact behavioral health patients may appear unresponsive, and be remarkably successful at remaining immobile despite painful stimuli The nature of their illness may be discovered by a detailed neurologic examination Conscious patients will usually avoid hitting their face with a dropped arm, may resist eyelid opening, will raise their heart rate to auditory or painful stimuli, and will have intact deep tendon, oculovestibular, and oculocephalic reflexes EVALUATION AND DECISION An approach for the evaluation of pediatric patients presenting with coma is summarized in Figure 17.1 All patients need rapid assessment of their airway, breathing, and circulation, followed by a focused history, physical examination with careful neurologic evaluation, and consideration of laboratory and imaging studies This approach is based on the selective use of the following critical clinical and laboratory findings: (i) Vital signs; (ii) a history of recent head trauma, seizure activity, or ingestion; (iii) signs of increased ICP or focal neurologic abnormality; (iv) fever; (v) laboratory results; (vi) brain CT scan results; and (vii) CSF analysis The evaluation of the comatose patient should follow an orderly series of steps, addressing the more life-threatening problems of hypoxia, hypotension, or increased ICP before investigating less urgent disorders If one or more of the former are present, immediate resuscitative efforts are begun Point-of-care testing for glucose, sodium, blood gas analysis, and hemoglobin should be performed immediately History and Physical Examination Focused, goal-directed questioning pertaining to suspected diagnoses is required to treat coma quickly Caregivers should be specifically queried regarding current medications, medications and substances available to ingest, seizures, fever, headache, irritability, vomiting, changes in gait, and behavioral abnormalities The most important historical finding in a comatose patient is a history of recent head trauma If no history of head trauma is present, it should continue to be considered as a potential cause of ALOC, since many cases are unwitnessed and patients with nonaccidental trauma may have a misleading history A patient’s vital signs will reveal the presence of fever, hypotension, or hypertension The consciousness of a neurologically impaired patient may initially be evaluated using a simple AVPU scale, representing four major levels of alertness: Alert, responsive to Verbal stimuli, responsive to Painful stimuli, and Unresponsive Elements of a more detailed neurologic evaluation are discussed in the following section The patient should be carefully examined for physical findings consistent with head trauma, including retinal hemorrhage, hemotympanum, CSF otorrhea or rhinorrhea, postauricular hematoma (Battle sign), palpable or visual damage to scalp or skull, and periorbital hematoma (“raccoon eyes”) Child abuse should be suspected if unexplained bruising is present or the stated mechanism of injury is disproportionate to the degree of physical damage present or to the child’s developmental level (e.g., 1-month-old “rolled off bed”) Bruising on the face, neck, head, or ears in nonambulatory children is of great concern for abusive head trauma (“those who don’t cruise, rarely bruise”) Other significant physical findings include anisocoria, absent or reduced pupil reactivity, papilledema, and nuchal rigidity Purpuric or varicelliform rashes may signify the presence of systemic infections with CNS involvement Incontinence of urine or stool may indicate that an unwitnessed seizure has occurred FIGURE 17.1 Evaluation of the comatose child CT, computed tomography; CSF, cerebrospinal fluid; CNS, central nervous system; ALOC, altered level of consciousness; ICP, intracranial pressure Neurologic Examination and Scoring ... oculovestibular, and oculocephalic reflexes EVALUATION AND DECISION An approach for the evaluation of pediatric patients presenting with coma is summarized in Figure 17.1 All patients need rapid assessment