Pediatric emergency medicine trisk 112

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 2
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