Altered mental status in children is characterized by the failure to respond to verbal or physical stimulation in a manner appropriate to the child’s developmental level. The ED incidence of altered mental status in children varies widely depending on the type of institution reporting, the patient population served, and the specific definition of altered mental status used.^1,2 Children with altered mental status require simultaneous stabilization, diagnosis, and treatment. The objectives of treatment are to sustain life and prevent irreversible CNS damage. Once the patient is resuscitated, the goal is to determine the cause and stop disease progression.

Altered mental status is caused by abnormalities of the ascending reticular activating system or the cerebral cortex. The ascending reticular activating system is located in the brainstem and modulates wakefulness in response to the environment, as well as homeostasis and cardiovascular and respiratory functions. Neural pathways from the ascending reticular activating system project to the cerebral cortices, producing awareness. Altered mental status occurs through dysfunction of the neurons or bilateral cerebral cortices.^3,4

There are many factors that can cause dysfunction in the ascending reticular activating system and cerebral hemispheres, including inadequate substrate for metabolic demand, insufficient blood flow, presence of toxins or metabolic waste products, or alterations of body temperature.⁴ Typical causes of bilateral cortical impairment are toxic and metabolic states that deprive the brain of normal substrates.

The pathologic conditions that affect awareness and arousal can be divided into three broad pathologic categories: supratentorial mass lesions, subtentorial mass lesions, and metabolic encephalopathy.⁵

Supratentorial mass lesions compress the brainstem and/or diencephalon. Signs and symptoms of this type of lesion include focal motor abnormalities, which are often present from the onset of the altered level of consciousness. The progression of neurologic dysfunction is from rostral to caudal, with sequential failure of midbrain, pontine, and medullary functions. When compromise due to supratentorial lesions is present, the fast component of nystagmus is in a direction away from a cold stimulus during caloric testing.

Subtentorial mass lesions lead to reticular activating system dysfunction, in which prompt loss of consciousness is generally the rule. Cranial nerve abnormalities are frequent, and abnormal respiratory patterns, such as Cheyne-Stokes respiration, neurogenic hyperventilation, and ataxic breathing, are common. With brainstem injury, asymmetric and/or fixed pupils are found. No eye movements occur despite cold water irrigation of both auditory canals.

Metabolic encephalopathy usually causes depressed consciousness before motor signs become depressed. Motor signs are typically symmetric. Respiratory abnormalities are usually secondary to acid-base imbalance. Pupillary reflexes are generally preserved. Pupils may be sluggish, but pupil responses are intact and symmetric, except in the case of profound anoxia or poisoning with cholinergics, anticholinergics, opiates, or barbiturates.

The spectrum of alteration of mental status ranges from confusion or delirium (disorders in perception) to lethargy, stupor, and coma (states of decreased awareness). A lethargic child has decreased awareness of self and the environment. Patients may be aroused from an apparent deep sleep, but they immediately relapse into a state of minimal responsiveness. A stuporous child has decreased eye contact, decreased motor activity, and unintelligible vocalization. Stuporous patients can be aroused with vigorous noxious stimulation. Comatose patients are unresponsive and cannot be aroused by verbal or physical stimulation, such as phlebotomy, arterial catheterization, or lumbar puncture.⁶

Take a methodical and comprehensive history (Table 137-1). Ask about the prodromal events before the change in consciousness as well as recent illnesses or infectious exposures, and determine the likelihood of trauma, abuse, or ingestion. Inquire about antecedent fever, headache, head tilt, abdominal pain, vomiting, diarrhea, gait disturbance, seizures, drug ingestion, palpitations, weakness, hematuria, weight loss, and rash. For infants and young children, review developmental milestones. The medical, immunization, and family histories are important in children of all ages. Be alert for any inappropriate responses, inconsistencies, or delays in seeking care that may arouse the suspicion of child abuse.^6,7

Proceed with a general examination only after respiratory, cardiac, and cerebral stabilization. The objectives of the examination are to identify occult infection, trauma, toxicity, or metabolic disease. The neurologic examination should document the child’s response to sensory input, motor activity, pupillary reactivity, oculovestibular reflexes, and respiratory pattern. Although several coma scales have been published, such as the Modified Pediatric Glasgow Coma Scale (GCS) (Table 137-2), the most simplified and functional in an emergency setting is the AVPU scale (Table 137-3).