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3.4– 11% of medical ICU admissions
12–33% of multiple-organ dysfunction pts
With predisposing conditions (e.g., hepatic insufficiency), risk of developing or exacerbating metabolic encephalopathy
Increasing severity of preexisting encephalopathy
Worsening hepatic insufficiency causing hepatic encephalopathy
Diabetics becoming hypoglycemic or with DKA/hyperosmolar coma
Postop hyponatremia
Deteriorating renal insufficiency leading to uremic encephalopathy
Preexisting encephalopathy may be exacerbated by anesthetics (e.g., benzodiazepines) in hepatic encephalopathy
Postpartum, especially with preeclampsia, eclampsia; PRES
Undiagnosed sepsis, hypothermia, high fever, CNS-acting drugs, including overdose
CNS cause: Brainstem CVA, meningitis, occult head trauma, encephalitis, brain tumor
Altered sensorium, stupor, or coma without any other explanation in the setting of a metabolic disturbance.
Process affects global cortical function by altering brain biochemistry.
Distinguished from structural lesions by a nonfocal neurologic exam.
EEG shows diffuse background slowing, triphasic waves in hepatic encephalopathy.
Increased spontaneous motor activity: Restlessness, asterixis, myoclonus, tremors, rigidity.
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