The evaluation and treatment of the comatose child fall into two phases. During the immediate phase, treatment precedes establishment of a diagnosis, and its most important aspects include stabilizing the child and protecting him or her from sustaining further brain damage. An evaluation of etiologic possibilities for the coma follows. After providing immediate treatment to the comatose child, the physician must be prepared to manage the potential complications of a prolonged altered state of consciousness. Knowledge of the probable prognosis for recovery or long-term impairment will facilitate provision of patient care and will improve communication with the child’s parents.

During the initial phase of treatment, the physician must ensure that the patient’s brain is receiving adequate substrate for energy production. The airway must be maintained, and sufficient oxygen and ventilation must be provided; a child with inadequate respiratory effort needs intubation and respirator assistance. The patient’s cardiac output must be evaluated, and cardiac dysrhythmias and hypotension must be treated appropriately. Treatment also should include control of body temperature, especially in children with hyperthermia (greater than 42°C), to prevent irreversible damage to the CNS. The possibility of reversible hypoglycemic encephalopathy being present should be considered, and immediate treatment of the patient (after blood is obtained for determination of the serum glucose level) should include the administration of 1 mg/kg of concentrated glucose solution (50% dextrose).

Recurrent or prolonged seizures can produce brain damage; iatrogenic paralysis and ventilation do not protect against this damage. Therefore, status epilepticus requires emergency treatment (see Chapter 402).

During the initial treatment period, a rapid physical examination should be performed to search for signs of trauma that could necessitate performing immediate laboratory testing and surgical or neurosurgical intervention. The child should be evaluated for signs of increased intracranial pressure (ICP), keeping in mind that papilledema may not be apparent for hours after the onset of ICP. Loss of venous pulsations may be helpful in the early identification of ICP. If intracranial hypertension is present, immediate therapy, including hyperventilation to reduce the partial pressure of carbon dioxide to 25 to 30 mm Hg and elevation of the head, should be initiated. (For further therapeutic measures for intracranial hypertension, see Chapter 399.)

After immediate assessment and treatment have been performed, further historical information should be obtained. The diagnostic workup should include measurement of serum electrolyte, arterial blood gas, and serum calcium levels, along with liver and renal function tests and a complete white blood cell count. Lumbar puncture should be considered in the presence of signs of meningeal irritation, such as nuchal rigidity, to evaluate for such possibilities as meningitis or subarachnoid hemorrhage. Signs of meningeal irritation may be absent in young children or infants. When the history is suggestive or the cause of coma is not clear, blood and urine evaluations for toxicologic studies should be performed.

The general physical examination can provide clues to the cause of coma. Of particular importance are signs of trauma and vital signs, including respiratory pattern, heart rate and rhythm, and blood pressure. The neurologic examination must include particular attention given to pupillary size and reactivity, ocular motility, respiratory rate and pattern, and motor response to pain.

Once the child’s condition has been stabilized, a more exhaustive search for a cause of the coma may be necessary. In general, the causes of coma can be divided into two major categories: traumatic and nontraumatic.

Blunt trauma to the head is a common occurrence in childhood. Alteration of consciousness that lasts less than 24 hours after blunt trauma is termed concussion. The neuropathologic implication of concussion is that no microscopic or gross change in the brain has resulted. If the period of unresponsiveness lasts longer than 24 hours, the clinical diagnosis is contusion of the brain. The neuropathologic changes associated with contusion include focal hemorrhage and necrosis of brain tissue. The magnitude of alteration caused in brain function after blunt trauma depends on several variables, including the amount of force exerted on the skull, the area of the skull involved, the direction of force against the skull, the relative mobility of the skull, and the angular velocity of the brain after the trauma. The frontal, temporal, and occipital lobes are especially prone to injury caused by rotational acceleration forces when rotation and flexion of the skull on the neck have occurred. Flexion and rotational acceleration may cause brainstem injury.

Radiologic evaluation of pediatric head trauma should begin with a noncontrast computed tomography (CT) scan, followed by a magnetic resonance imaging (MRI) scan if significant neurologic deficits are found on examination. Even in children with only mild alteration in consciousness (GCS score of 13 to 14), the incidence of intracerebral hemorrhage was shown in one study to be approximately 19% (30 of 135 patients). Depressed skull fractures may be associated with laceration of the brain and dura, and they should be identified and evaluated quickly. Fractures across the middle meningeal artery groove may be associated with tearing of the meningeal artery and subsequent epidural hemorrhage. Epidural hematoma frequently is associated with a biphasic clinical presentation: an initial episode of coma occurring immediately after the injury, followed by a lucid interval, after which loss of consciousness ensues as the hematoma enlarges. Periorbital ecchymosis, cerebrospinal fluid (CSF) rhinorrhea, and hemorrhage behind the tympanic membrane are signs of basilar skull fracture. Acute subdural hematoma may develop after laceration of the dura associated with depressed skull fracture occurs.