Emergency management of acute coma in children

Emergency management of acute coma in children

Hector E. James

Definitions of the various levels in disturbance of consciousness are not uniform. In this discussion, the term “lethargy” applies to the patient who is sleepy but arousable and capable of responding to verbal commands and tactile stimuli; “stupor” means that the child falls asleep when left alone but can be aroused by verbal or painful stimuli, and “obtundation” describes the patient who is unconscious but responds to extreme stimuli by crying out or moaning. The term “coma” is used to describe the state in which a patient cannot, regardless of stimulation, open his or her eyes, given verbal responses or obey commands.

The Glasgow Coma Scale (GCS) was developed as a system for categorizing the severity of central nervous system impairment and predicting the outcome for head-injured adults.[1] According to the GCS, the best indicators of outcome in the patient with an acute brain insult are the ability to open the eyes and the ability to respond to verbal or tactile stimulation (Table 1). In initial studies of head-injured adults (mean age: 33 years),[1] 64 percent of the patients who did not spontaneously open their eyes within 24 hours of injury were dead or in a vegetative state at six months; in contrast, 65 percent of the patients who were responsive within 24 hours had a good recovery.


Glasgow Coma Scale

Activity Best response Score

Eye opening Spontaneous 4

To verbal stimuli 3

To pain 2

None 1

Verbal Oriented 5

Confused 4

Inappropriate words 3

Nonspecific sounds 2

None 1

Motor Follows commands 6

Localizes pain 5

Withdraws in response 4

to pain

Flexion in response 3

to pain

Extension in response 2

to pain

None 1

Total score = Sum of eye opening, verbal

and motor scores

Maximum score (best): 15

Minimum score (worst): 3

In pediatric head injuries, however, the GCS has recently been shown to lack predictive accuracy.[2] Nevertheless, most regional trauma centers use the scale as a means of documenting the severity of the patient’s condition.[3] Since verbal assessment is limited in infants, it cannot be graded effectively in this age group. Consequently, we have modified the GCS for infants and use it as a means of communicating the patient’s clinical status (Table 2).[4] However, the prognostic value of this modified scale has not been studied.


Modified Glasgow Coma Scale for Infants

Activity Best response Score

Eye opening Spontaneous 4

To speech 3

To pain 2

None 1

Verbal Coos, babbles 5

Irritable, cries 4


Cries to pain 3

Moans to pain 2

None 1

Motor Normal spontaneous 6


Withdraws to touch 5

Withdraws to pain 4

Abnormal flexion 3

Abnormal extension 2

None 1

Total score = Sum of eye opening, verbal

and motor scores

Maximum score (best): 15

Minimum score (worst): 3

From Traumer DA, James HE. The Glasgow Coma

Score. In: James HE, Anas NG, Perkin RM, eds. Brain

insults in infants and children. Orlando, Fla.: Grune

& Stratton, 1985:179-82. Used with permission.

Initial Management

Many conditions can be responsible for coma or other alterations of consciousness. However, because management is often started before the cause has been identified, and because the initial measures are usually the same regardless of etiology, a treatment protocol is described in this article before a discussion of specific causes. Table 3 summarizes the initial approach to the child with coma.


Initial Support and Evaluation of a Child with Acute Coma

Initial measures

Stabilize cervical spine.

Ensure airway and hemodynamic stability (intravenous access).

Obtain screening laboratory tests, including toxicology screen.

Administer 25 percent glocuse, 2 to 3 mL per kg intravenously,


hypoglycemia is cause of coma.

Administer naloxone (Narca), 0.01 mg per kg, if drug ingestion

is cause

of coma.

Obtain cranial computed tomographic scan.

Secondary evaluation

Perform lumbar puncture if meningitis is suspected.

Obtain electroencephalogram if seizures have occurred.

Other measures

Insitute hyperventilation and/or administer mannitol, 0.5 to 1.0

g per kg,

if intracranial hypertension is suspected.

Place bladder catheter if mannitol is given.

Place central venous or pulmonary arterial line to monitor



In managing a child with a sudden deterioration of consciousness, the physician should be prepared to resuscitate the patient with airway control and ventilation. Children with impaired consciousness often develop upper airway obstruction, due either to pharyngeal hypotonia or to the inability to clear pharyngeal secretions. Obstruction of air flow, with resultant hypoxemia and respiratory acidosis, aggravates or promotes intracranial hypertension,[5] may potentiate pulmonary hypertension (particularly in infants with a reactive pulmonary vascular bed[6]) and interferes with oxygen delivery to vital organ systems.

Since assisted ventilation and oxygenation are most easily controlled with the use of an artificial airway, endotracheal intubation is recommended for the following categories of patients with impaired consciousness: (1) those with seizures that are difficult to control; (2) those with any abnormality of respiratory rate or rhythm that interferes with gas exchange, and (3) those with a GCS score of 8 or less (Table 1 and 2).

In terms of preserving brain function, the importance of maintaining “adequate” cardiac output to ensure sufficient cerebral blood flow cannot be overemphasized. Administration of fluids to support circulation is critical. Hypotonic fluids should be avoided because excessive free water may augment existing brain edema. Hypotension may result in inadequate cerebral perfusion and therefore must be treated immediately, utilizing appropriate fluid infusion and inotropic agents if necessary. Hypovolemia in childhood head injury is most commonly due to blood loss from abdominal, pelvic or long-bone trauma and not to intracranial hemorrhage. A central venous or pulmonary arterial catherter to determine cardiac function may guide management in a hemodynamically unstable child. Naloxome (Narcan), 0.01 mg per kg, or 25 percent glucose (2 to 3 mL per kg), can be administered intravenously if drug ingestion or hypoglycemia is the cause of coma.

All pathophysiologic factors that are known to increase intracranial pressure or diminish cerebral perfusion should be avoided in the initial phases of brain resuscitation. The patient’s head should be placed in the midline position and elevated at a 15- to 20-degree angle to maximize cerebral venous drainage. Hyperthemia, seizure activity, hyponatremia, hypoglycemia and metabolic acidosis must be treated.[7]

If intracranial hypertension is suspected, diagnostic and therapeutic maneuvers must be instituted promptly. Intracranial hypertension should be suspected in any child with a brain insult and one or more of the following: a GCS score of 8 or less; difficult-to-control seizure activity; abnormalities in vital signs, such as systemic hypertension, bradycardia or abnormal respiratory patterns; dilated, unreative pupils, or decerebrate or decorticate posturing[8] (Figure 1). However, no definitive test is available for the diagnosis of intractional hypertension.

The most rapid way to reduce intracranial hypertension is to intubate the patient and institute hyperventilation, which reduces cerebral blood volume.[9] One should aim for a reduction of the arterial [Pco.sub.2] to 25 to 30 mm Hg. Osmotic agents, such as intravenous mannitol, 0.5 to 1.0 g per kg, may also be administered once a bladder catheter has been placed.[9]

As soon as these initial steps have been performed, a computed tomographic (CT) study of the brain should be obtained to rule out a surgically treatable lesion.[8] If the CT scan is consistent with brain swelling alone, the patient should be moved to a pediatric intensive care unit for the secondary phases of brain resuscitation, including intracranial pressure monitoring.[10]

Differential Diagnosis

The five categories of brain lesions that produce alterations in the level of consciousness are supratentorial mass lesions, infratentorial mass lesion, metabolic abnormalities, infections and vascular anomalies. The primary care physician may determine the underlying problem by evaluating the neurologic findings and the acid-base state at the time of presentation.[9-12]


The important causes of supratentorial mass lesions that produce progressive deterioration in children include cerebral hyperemia secondary to head trauma,[9] epidural and subdural hematomas, intracerebral hemorrhage, acute hydrocephalus and subdural empyema. In most instances, patients with these lesions present with evidence of increased intracranial pressure.

The most common clinical situations associated with acute supratentorial lesions in children are head trauma, severe systemic hypertension, obstruction of an existing ventriculoperitoneal shunt and bleeding from an arteriovenous malformation.

Surgical decompression is the definitive treatment when cerebral hemorrhage results in brain shift, a herniaton syndrome or acute hydrocephalus.


Infratentorial (posterior fossa) lesions may cause coma through compression of the blood supply to the ascending reticular activating system. Cona due to a posterior fossa lesion is difficult to distinguish from coma due to a supratentorial lesion unless localizing brainstem signs have preceded the onset of coma. Important infratentorial lesions to consider are head trauma, cerebellar hemorrhage or tumor with secondary hemorrhage or tumor with encephalitis. Midbrain or pontine lesions may lead to abrupt coma, central neurogenic hyperventilation, absent oculovestibular and oculocephalic reflexes (doll’s eyes), pinpoint pupils and decerebrate rigidity.[11]


Metabolic disorders constitute the majority of nontraumatic causes of acute coma in children (Tables 4 and 5). Table 6 summarizes key signs and findings associated with coma due to metabolic abnormalities.


Differential Diagnosis

of Metabolic Coma in Infants

Hypoxic-ischemic conditions

Respiratory failure

Shock syndromes

Severe anemia

Apnea of infancy

Carbon monoxide poisoning

Cerebral vasculitis (“cerebritis”)





Postictal state


Nonendocrine organ failure



Endocrine organ failure







Types and Causes of Acid-Base

Imbalance in the Comatose Child

Metabolic acidosis

Lactic acidosis (hypoxic-ischemic insult; septic


Diabetic ketoacidosis

Renal failure

Organic acidurias

Ingestions (e.g., methanol, ethylene glycol)

Salicylate poisoning (late)


Respiratory acidosis (apnea or hypoventilation)

Supratential or infratentorial lesions

Ingestions (e.g., narcotics, clonidine [Catapres])

Respiratory muscle fatigue; neuromuscular


Metabolic encephalopathies

Generalized seizure activity

Respiratory alkalosis (hyperventilation)

Intracranial hypertension

Septic shock (early)

Hepatic failure

Salicylate poisoning (early)

Reye’s syndrome

Brainstem dysfunction


Characteristics of Coma

Due to Metabolic Abnormalities

Stupor or coma precedes motor signs (decorticate

or decerebrate positioning).

Motor signs are usually symmetrically depressed.

Pupillary reactions are preserved.

Acid-base imbalance is common.

Seizures or abnormal motor movements are

common findings.

Derived from Lockman.[12]

Changes in mental status are early signs of metabolic encephalopathy. Hypoglycemia is an important cause of coma and is readily treated. Hyponatremia may occur because of excessive free water, inadequate salt intake or inappropriate secretion of antidiuretic hormone. Hepatic or renal failure is rarely responsible for an acute change in mental status. Reye’s syndrome, however, can cause diffuse brain swelling, intracranial hypertension and coma.[8]

Bacterial meningitis can cause coma. If cranial CT scanning reveals no mass effect in a child with fever and altered consciousness, and it intracranial hypertension is not suspected, lumbar puncture must be performed.

Generalized seizures are another cause of prolonged unresponsiveness. If the postictal state persists for more than one hour, an electroencephalogram should be obtained to rule out clinically silent seizure activity.

Ingestion to toxic agents should always be considered in a comatose child who has previously been well, and the medications available in the home should be reviewed. Pupillary size and reactivity should be noted, and a toxicology screen, serum electrolytes and blood gases should be obtained.

Child Abuse Syndrome

Child abuse is often a diagnostic challenge.[12-15] Factors that can make the diagnosis difficult include the absence of a history of trauma, a vague clinical presentation and, frequently, the paradox of significant intracranial bleeding without external signs of trauma to the head and face.[13,14]

Severe head injuries in the first year of life are usually the result of child abuse.[12] A shaking injury is frequently the cause. Shaking injuries are particularly devastating because they are associated with a significant risk of death, as well as a high incidence of mental retardation and neurologic deficit.[13-15] Unfortunately, the signs and symptoms of this form of head trauma are not always specific.[13] The findings may suggest infection, intoxication or metabolic abnormalities. Diagnosis depends on a high index of suspicion and the physical findings of a bulging fontanelle, head circumference greater than the 90th percentile and retinal hemorrhage.[14] Bloody fluid from a lumbar or subdural puncture is also highly suggestive.[14] Cranial CT findings may confirm the diagnosis.[4,13,14,16]

The diagnosis must be considered in comatose infants with decerebrate posturing or flaccidity, dilated pupils, apnea or bradypnea, and tense fontanelle. These children require immediate intubation and hyperventilation. Consideration should be given to tapping the lateral margins of the fontanelle with a 19- or 21-gauge spinal needle. Usually, bloody, nonclotting fluid can be obtained from either side. This maneuver often produces a dramatic improvement in the neurologic state.

The patient should then be transported (with monitoring) for a CT scan. Less severely affected infants presenting with full fontanelle, retinal hemorrhage and altered neurologic state should also undergo CT scanning without delay.

Regardless of the initial presentation, infants with acute head injuries must be carefully observed because secondary brain swelling may occur. The primarily care physician must be alert to this possibility so that therapy can be started promptly.


[1.] Jennett B. Teasdale G, Braakman R, Minderhoud J. Knill-Jones R. Predicting outcome in individual patients after severe head injury. Lancet 1976;1(7968):1031-4. [2.] Lieh-Lai MW, Theodorou AA, Sarnaik AP, Meert KL, Moyland PM, Canady AI. Limitations of the Glasgow Coma Scale in predicting outcome in children with traumatic brain injury. J Pediatr 1992;120(2 Pt 1):195-9. [3.] Johnson DL, Duma C, Sivit C. The role of immediate operative intervention in severely head-injured children with a Glasgow Coma Scale score of 3. Neurosurgery 1992;30:320-4. [4.] Trauner DA, James HE. The Glasgow Coma Score. In: James HE, Anas NG, Perkin RM, eds. Brain insults in infants and Children: pathophysiology and management Orlando, Fla.: Grune & Stratton, 1985:179-82. [5.] Shapiro HM. Intracranial hypertension: therapeutic and anesthetic considerations. Anesthesiology 1975;43:445-71. [6.] Perkin RM, Anas NG. Pulmonary hypertension in pediatric patients. J Pediatr 1984;105:511-22. [7.] Bruce DA. Cerebrovascular dynamics. In: James HE, Anas NG, Perkin RM, eds. Brain insults in infants and children: pathophysiology and management. Orlando, Fla.: Grune & Stratton, 1985:53-7. [8.] James HE. Coma in infants, children and adolescents. In: Nussbaum E, ed. Pediatric intensive care. Mount Kisco, N.Y.: Futura, 1989:25-37. [9.] Bruce DA, Raphaely RC, Goldberg AI, et al. Pathophysiology, treatment and outcome following severe and injury in children. Child’s Brain 1979;5:174-91. [10.] Miller JD, Becker DP, Ward JD, Sullivan HG, Adams WE, Rosner MJ. Significance of intracranial hypertension in severe head injury. J Neurosurg 1977;47:503-16. [11.] Marshall SB, et al. Neuroscience critical care. Philadelphia: Saunders, 1990:85-113. [12.] Lockman LA, Coma. In: Swaiman KF, Wright PS, eds. The practice of pediatric neurology. St. Louis: Mosby, 1982. [13.] Zimmerman RA, Bilaniuk LT, Bruce DA, Schut L, Uzzell B, Goldberg HI. Computed tomography of craniocerebral injury in the abused child. Radiology 1979;130:687-90. [14.] Ludwig S, Warman M. Shaken baby syndrome: a review of 20 cases. Ann Emerg Med 1984;13:104-7. [15.] Spaide RF, Swengel RM, Scharre DW, Mein LE. Shaken baby syndrome. Am Fam Physician 1990;41:1145-52. [16.] Merten DF, Osborne DR. Craniocerebral trauma in the child abuse syndrome. Pediatr Ann 1983; 12:882-7.

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