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Acquired Metabolic Encephalopathies

Hypoxic-ischemic encephalopathy. An acute lack of oxygen (Pao2 < 40mmHg), severe hypotension (< 70mmHg systolic), or a combination of the two causes loss of consciousness within minutes. The most important causes of hypoxic and ischemic states are an inadequate pumping function of the heart (as in myocardial infarction, shock, and cardiac arrhythmia), suffocation, carbon monoxide poisoning, respiratory muscle paralysis (as in spinal trauma, Guil-lain-Barré syndrome, and myasthenia), and inadequate ventilation (as in opiate intoxication). Permanent damage usually does not occur if the partial pressure of oxygen and the blood pressure can be brought back to normal in 3-5 minutes. Longer periods of hypoxia and ischemia are rarely tolerated (except under conditions of hypothermia or barbiturate intoxication); brain damage usually ensues, and may be permanent. Persistent coma (p. 118) with absent brain stem reflexes (pp. 26,118) once the circulation is restored indicates a poor prognosis; the probable outcome is then a persistent vegetative state or death (p. 120). Patients who regain consciousness may develop various postanoxic syndromes, e.g., dementia, visual agnosia, parkinsonism with personality changes, choreoathetosis, cerebellar ataxia, intention or action myoclonus (Lance-Adams syndrome), and Korsakoff syndrome. Delayed postanoxic syndrome occurs 1-4 weeks after the initial recovery from anoxia and is characterized by behavioral changes (apathy, confusion, restlessness) that may either regress or worsen, perhaps to coma. These changes may be accompanied by gait impairment and parkinsonism. Hypercapnia (t)PaCO2) due to chronic hypoventilation (as in emphysema, fibrosing alveolitis, or central hypoventilation) causes headache, behavioral disturbances, impairment of consciousness (p. 116 ff), asterixis (p. 68), fasciculations, and bilateral papilledema. Hypoglycemia. If the blood glucose concentration acutely falls below 40mg/dl, behavioral changes occur (restlessness, hunger, sweating, anxiety, confusion). Any further decrease leads to unconsciousness (grand mal seizure, dilated pupils, pale skin, shallow breathing, bradycar-dia, decreased muscle tone). Glucose must be given intravenously to prevent severe brain damage. Subacute hypoglycemia produces slowed thinking, attention deficits, and hypothermia. Chronic hypoglycemia produces behavioral changes and ataxia (p. 324); it is rarely seen (e. g., in pancreatic islet cell tumors). Hyperglycemia (p. 324). Diabetic ketoacidosis is characterized by dehydration, headache, fatigue, abdominal pain, Kussmaul respiration (deep, rhythmic breathing at a normal or increased rate). Blood glucose > 350mg/dl (C pH, C pCO2, C HCO3 ). In hyperosmolar nonketotic hyperglycemia, the blood glucose concentration is > 600 mg/dl and there is little or no ketoacidosis. The persons at greatest risk are elderly patients being treated with corti-costeroids and/or hyperosmolar agents to reduce edema around a brain tumor. Hepatic/portosystemic encephalopathy occurs by an unknown pathogenetic mechanism in patients with severe liver failure (hepatic en-cephalopathy) and/or intrahepatic or extrahe-patic venous shunts (portosystemic en-cephalopathy). Venous shunts can develop spontaneously (e. g., hepatic cirrhosis) or be created surgically (portocaval anastomosis, transjugular intrahepatic stent). Clinical features (see Table 50, p. 387): Behavioral changes, variable neurological signs (increased or decreased reflexes, Babinski reflex, rigidity, decreased muscle tone, asterixis, dysarthrophonia, tremor, hepatic coma), and EEG changes (generalized symmetric delta/triphasic waves). The diagnosis is based on the clinical findings, the exclusion of other causes of encephalopathy (such as intoxication, sepsis, meningoencephalitis, and electrolyte disorders), and an elevated arterial serum ammonia concentration. Repeated episodes of hepatic coma may lead to chronic encephalopathy (head tremor, asterixis, choreoathetosis, ataxia, behavioral changes); this can be prevented by timely liver transplantation.

Brain atrophy

Normal Slow waves EEG

Brain atrophy

Normal Slow waves EEG

Coma

Seizure Loss of brain function jm/iwi/M

- Decrease in blood sugar level

EEG changes in hypoglycemia

Hypoxic-ischemic encephalopathy

(apallic syndrome; axial CT scan)

Cutaneous and scleral jaundice

Palmar erythema

Hepatic cirrhosis (ascites, gynecomastia, absence of chest and axillary hair)

Normal EEG Somnolence, stupor

Coma Loss of brain function

-Declining liver function ■

Palmar Erythema

Hepatic encephalopathy

Kayser-Fleischer ring (Wilson disease)

Hepatic encephalopathy

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