Acute Toxic-Metabolic Encephalopathy

Background

• Acute toxic-metabolic encephalopathy refers to global neurological dysfunction in absence of structural or electrophysiological neurological injuries with diverse causes including organ dysfunction, malnutrition, electrolyte imbalances, infection, metabolic imbalances, endocrine disorders, sepsis, hyperammonemia, medication ingestion, and other toxins.
• Presentation varies from mental confusion to fluctuating levels of attentiveness or arousal (delirium) to coma.
• Pathogenesis includes disruption in attention and arousal centers in the brain regardless of etiology.
• It is most commonly encountered in critically ill patients, especially in the intensive care unit and in older persons.

Evaluation

• Onset may be acute or subacute and concordant with organ dysfunction, and clinical presentation varies from subtle changes in behavior to severe disturbances in consciousness.
• Neurological signs and symptoms may be focal or global with changes in mental status or behavior within prior 24 hours illustrated by inability to focus attention, disorganized thinking, and altered levels of consciousness (agitation, drowsiness, lethargy, stupor or coma).
• Blood tests can identify potential underlying metabolic, endocrine, nutritional, and chemical imbalances causing encephalopathy.
  • Arterial blood gas is often the first blood test to assess for hypercarbia and hypoxemia; obtain with carbon monoxide oximetry if carbon monoxide exposure is suspected.
  • Additional blood tests may include complete blood count, electrolytes, bicarbonate, glucose, calcium, magnesium, phosphorus, blood urea nitrogen, creatinine, liver function tests, thyroid function tests, drug screen, ammonia level, cortisol, thiamine, vitamin B12, and blood cultures if sepsis is suspected.
• Consider a urine toxicology screen if there is suspected toxin exposure.
• Neuroimaging should be considered in patients with focal neurologic deficits.
  • Head computed tomography (CT) or magnetic resonance imaging (MRI) can rule out organic lesions.
  • Electroencephalography (EEG) may detect presence of convulsive and nonconvulsive seizures.
  • Lumbar puncture may be considered in patients with fever and meningismus or in patients predisposed to central nervous system infections (such as patients who have undergone a neurosurgical procedure).

Management

• Initial management includes the following:
  • ensuring adequate respiration and circulation, even while evaluating for a cause of encephalopathy
  • treatment of seizure when present or suspected
  • IV thiamine 100 mg, administered ideally before glucose drip or carbohydrate load, may be considered for prevention of Wernicke encephalopathy
• Patients presenting to emergency department or who have been hospitalized and develop acute toxic-metabolic encephalopathy are best managed in a higher level of care, such as an intensive care unit.
• For patients with epileptic seizure, benzodiazepine is considered first-line treatment.
• For patients with coma or acute altered consciousness of unknown cause, treatment includes correction of hypoglycemia or hyperglycemia and antagonists of benzodiazepine or opiates in case of overdose.
• Cause-specific treatment should be given if etiology is defined.