Metabolic Encephalopathy
Paula D. Ravin
I. BACKGROUND
A. Metabolic encephalopathy is defined as global brain dysfunction caused by a biochemical derangement.
B. There is often a fluctuating level of consciousness with nonfocal signs. Patients can present with the following:
1. Delirium (confusion, inattentiveness, sleeplessness, hallucinosis).
2. Depressed level of consciousness (drowsiness, stupor, coma).
3. Seizures, behavioral disturbances, visual impairment.
C. Metabolic encephalopathy is common in illnesses that cause multiorgan failure (see Table 120-1 for typical patient profiles).
D. The following increase the risk of developing metabolic encephalopathy:
1. Age older than 60 years.
2. Systemic infection.
3. Temperature dysregulation.
4. Chronic disease of the central nervous system (CNS).
5. Organ failure.
6. Endocrine disorders.
7. Multiple CNS-acting drugs.
8. Nutritional deficiency.
9. Alcoholism.
10. History of perinatal injury.
11. Sleep deprivation, sensory deprivation.
E. In cases of a correctible metabolic disorder, prompt treatment may result in reversal of encephalopathy.
F. Progression to stupor or coma may lead to prolonged encephalopathy and complications, with a poor neurologic outcome.
II. ETIOLOGY
A. Drugs and toxins (50%).
B. Hepatic, renal, or pulmonary failure (12%).
C. Endocrine or electrolyte disturbances (8%).
D. Other causes: thiamine deficiency (exacerbated by glucose loading), prolonged hypoglycemia, hypoperfusion during cardiac bypass, hyperthermia (>105°F), hyperammonemia, and severe hypertension.
TABLE 120-1 Patient Profile in Metabolic Encephalopathy | ||
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III. PATHOGENESIS
A. Altered substrate (glucose/oxygen) for neurotransmitter function.
B. CNS-depressant drug accumulation due to abnormal volume of distribution (decreased protein, high lipophilicity).
C. Impaired cerebral blood flow.
D. Abnormal cerebrospinal fluid (CSF) dynamics.
E. Altered neuronal function due to temperature and/or ionic changes.
IV. DIAGNOSIS. Metabolic encephalopathy should be considered when a patient exhibits altered cognition or alertness. The clinical examination should include the following:
A. General physical examination.
1. Vital signs, breathing pattern, and pulse oximetry.
2. Funduscopy, to evaluate for papilledema (increased intracranial pressure), septic emboli.
