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INTRODUCTION

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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.

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PATHOPHYSIOLOGY

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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

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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.

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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

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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.

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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.

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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.

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CLINICAL FEATURES

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The spectrum of alteration of mental status ranges from confusion ...

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