Pediatric emergency medicine trisk 114

will generally receive EEG testing and CT or MR imaging of the brain.
Consultation with a neurologist who treats children is important to coordinate this
workup (see Chapters 72 Seizures and 97 Neurologic Emergencies ).
The new onset of focal seizures, with or without the presence of fever, should
be evaluated with a head CT scan to determine the presence of a focal lesion such
as a tumor, abscess, or hemorrhage. Only after the results of this study are known
should a lumbar puncture be performed if no lesion predisposing to herniation is
found. If neuroimaging is unavailable and meningitis or encephalitis is a concern,
or if the patient is unstable, empiric treatment for bacterial meningitis or herpetic
encephalitis may be administered and lumbar puncture deferred (see Chapter 94
Infectious Disease Emergencies ).

History of Toxic Ingestions
If no history or physical examination findings suggestive of head trauma or
seizures are present, a toxic ingestion should be considered, especially in toddlers
and adolescents. The availability of any substances capable of depressing CNS
function should be thoroughly explored. In general, coma from toxic ingestions is
of slower onset than that from trauma and may be preceded by delirium or other
abnormal behaviors.
Chapter 102 Toxicologic Emergencies lists major toxidromes that result from
ingestions that produce CNS depression. The pupils of a poisoned comatose
patient are a particularly valuable source of information. Miosis occurs with
ingestions of narcotics, clonidine, organophosphates, gamma-hydroxybutyrate
(GHB), phencyclidine, phenothiazines, and occasionally, barbiturates and ethanol.
Mydriasis is produced by ingestions of anticholinergic agents (e.g., atropine,
antihistamines, and tricyclic antidepressants) and sympathomimetic compounds
(e.g., amphetamines, caffeine, cocaine, LSD, and nicotine). Nystagmus may
indicate the ingestion of barbiturates, ketamine, phencyclidine, or phenytoin.
Pupillary responses are likely to be preserved in toxic or metabolic comas.
Systemic toxins do not cause unequal pupils; anisocoria in the setting of ALOC
should be pursued with neuroimaging.

TABLE 17.5
POISONS UNDETECTED BY TYPICAL DRUG SCREENING THAT
CAUSE COMA/ALTERED LEVEL OF CONSCIOUSNESS
Miosis present
Bromide
Chloral hydrate
Clonidine
Gamma-hydroxybutyrate (GHB)
Methadone, buprenorphine
Organophosphates
Phenobarbital
Pilocarpine and tetrahydrozoline eye drops
Phenothiazines
Valproic acid
Mydriasis present
Anoxia caused by cyanide, carbon monoxide, or methemoglobinemia
LSD
A toxicologic screen of blood and urine should be considered in all children
with coma of unknown origin. The growing legality and popularity of edible
marijuana preparations has produced a rise in pediatric cannabis ingestions
causing ALOC. Table 17.5 lists compounds capable of causing coma that are not
typically detected by routine drug screening, grouped by pupillary effects.
The poisoned patient with depressed consciousness should be intubated with a
cuffed endotracheal tube for airway protection. Naloxone may be administered as
empiric antidotal therapy for coma-producing toxic ingestions involving unknown
medications. Flumazenil should not be given routinely to these patients because
seizures may result. Its use is limited to pure benzodiazepine overdoses in
patients with no history of seizures or drug habituation.

Increased Intracranial Pressure or Focal Neurologic Defect
Nontraumatic causes of increased ICP or focal neurologic deficits include
neoplasms, CSF shunt malfunction, cerebral abscess, and hemorrhage (see
Chapters 97 Neurologic Emergencies and 122 Neurosurgical Emergencies ).


These patients may present with a history of headache, vomiting, confusion,
lethargy, meningismus, focal neurologic dysfunction, or seizure activity, or may
present with sudden onset of deep coma. Initial physical signs of increased ICP
include sluggishly reactive pupils and, in infants, a bulging fontanelle. More
severe and prolonged increases in ICP produce a unilaterally enlarged pupil, other
cranial nerve palsies (III, IV, VI), papilledema, and Cushing triad of hypertension,
bradycardia, and irregular breathing. All may signal impending or progressive
herniation. From the standpoint of the emergency physician, which type of
herniation is present is unimportant; all are life-threatening, and the initial
treatment is identical for all. Endotracheal intubation using rapid sequence
induction is performed to gain airway and breathing control. Evaluation should
parallel that for traumatic head injury, bearing in mind the increased desirability
of using IV contrast for CT imaging. Comatose patients with a CSF shunt may
need their shunt reservoir or ventricle tapped emergently to treat increased ICP.

Fever
Coma accompanied by fever may indicate CNS infection (see Chapters 31 Fever
and 94 Infectious Disease Emergencies ). Resistance to neck flexion is the most
important physical finding in meningitis, the most common infection of this type,
although children younger than 2 years of age may lack this finding. Historical
data may also include a steadily increasing headache, irritability, vomiting, and
worsening oral intake. Kernig and Brudzinski signs may be present. Infants may
exhibit paradoxic irritability, in which crying is worsened by picking up the baby.

Other useful physical clues to CNS infection are the rashes that accompany
meningococcemia, varicella, and Rocky Mountain spotted fever. The historical
and physical findings in encephalitis are similar to those in meningitis;
meningismus may be absent, however. Seizures are particularly common if herpes
simplex is the causative agent.
A history of localized CNS dysfunction, seizures, or a focal infection (e.g.
sinusitis, dental abscess) before the onset of febrile coma or the presence of
concomitant focal neurologic signs may indicate the presence of a focal cerebral
infection such as an abscess or subdural empyema. In addition, either diffuse or
focal infections may present with signs of increased ICP secondary to cerebral
edema or blockage of CSF flow. If this is the case, a head CT scan should be
obtained before lumbar puncture is performed. A contrast-enhanced study is
desirable if concern about focal infection is present. The ill-appearing patient
should receive antibiotics before neuroimaging is performed.
CSF analysis remains the key to establishing the diagnosis of CNS infection.
Abnormalities of CSF white blood cell count (pleocytosis), glucose, and protein


occur in roughly predictable patterns with bacterial or viral meningitis, and
pathogens may be visible using Gram and other stains (see Chapter 94 Infectious
Disease Emergencies ). Rapid testing with agglutination studies or polymerase
chain reaction tests might also be used to identify pathogens. CSF pleocytosis in
encephalitis is variable and, if present, is usually mild (less than 500 cells/mm3),
with normal levels of glucose and protein being common. In the absence of signs
of infection, bloody or xanthochromic CSF under increased pressure indicates
subarachnoid hemorrhage.

Metabolic Abnormalities
The presence of a metabolic disorder leading to coma is usually apparent once the
results of routine laboratory tests are available. These values for glucose, sodium,

potassium, bicarbonate, calcium, magnesium, and phosphorus make any
deficiency or excess of these serum components readily apparent and treatable.
Blood gas analysis for evaluation of acidosis or alkalosis from metabolic or
respiratory causes may also be indicated. Decreased consciousness caused by
diabetic ketoacidosis may initially worsen because of a paradoxical temporary
decrease in CSF pH and/or cerebral edema complicating the disease.
Renal and hepatic functions should be quantified with analysis of blood urea
nitrogen, creatinine, and ammonia. Markedly elevated serum blood urea nitrogen
and creatinine, oliguria, hypertension, anemia, acidosis, and hypocalcemia
indicate the presence of uremic coma as a result of renal failure.
Hyperammonemia with decreased mental status may be caused by hepatic failure,
acetaminophen ingestion with resultant hepatotoxicity, valproic acid toxicity,
Reye syndrome, or inborn metabolic errors. The hyperammonemia of Reye
syndrome is accompanied by a history of antecedent viral illness and likely
treated with aspirin (see Chapter 97 Neurologic Emergencies ). Unremitting
vomiting is soon accompanied by encephalopathy, in the absence of jaundice,
scleral icterus, focal neurologic signs, or meningeal irritation. Hyperammonemia
without accompanying liver failure in the young infant may indicate the presence
of a congenital urea cycle defect.

Coma of Unknown Origin
Patients with coma of unknown origin not falling into any of the diagnostic
categories discussed previously usually benefit from a noncontrast brain CT scan,
CSF analysis, and neurologic consultation, in that order. The emergence of new
infectious diseases such as West Nile virus and eastern equine encephalitis virus
means that diagnosis may require consultation with infectious disease experts and
the Centers for Disease Control. If meningeal irritation is present without fever or