The Dementias II - Encephalopathies and Hepatic Coma

Hypoxic encephalopathy: This usually results from conditions producing asphyxia such as drowning, strangulation, aspiration into the respiratory tract, carbon monoxide poisoning, respiratory paralysis secondary to Guillain-Barre syndrome or poliomyelitis and shocked states following myocardial infarction or Cardiac arrest.

Mild degree of hypoxia causes inattentiveness, errors in judgement and confusion which are transitory. Prolonged ands evere hypoxia lasting more than 3 to 5 minutes produce serious and permanent injury to the Brain and leads to coma. In such conditions presence of pupillary reflexes, intact doll's head-eye movement and other brainstem reflexes generally indicate a favorable prognosis. Doll's head-eye movement (Oculo-cephalic reflex) is elicited by turning the head to either sides, when the eyes are seen to deviate to the opposite direction. This sign is absent in conscious individuals. It becomes psotive in the initial stages of coma, but it is lost as the coma deepens. However, when brain stem reflexes are absent with absence of spontaneous respiration, it suggests brain-death. Absence of electrical activity in the EEG (flat EEG) confirms the diagnosis. In less severe hypoxic damage, the patient may recover from coma with some permanent neurological sequelae like dementia, extrapyramidal disturbances, choreoathetosis, ataxia and myoclonus.

HEPATIC

The diagnosis of hypoxic brain damage depends on the clinical setting for hypoxia and arterial oxygen tension (PO2) less than 50 mmHg. The emergency treatment includes provision of a clear airway, cardiopulmonary resuscitation and oxygenation. Intravenous dexamethasone helps in reducing brain edema.

Hypoglycemic encephalopathy: Abnormal lowering of blood sugar leads to confusion, stupor, convulsions or coma depending on the degree of hypoglycemia. Generally, when the blood sugar is 30 mg/dL confusional state sets in and when it is 10mg/dL, the patient becomes comatose.

Causes

1. Accidental overdose of insulin or a long-acting oral anti-diabetic drug.
2. Insulin secreting tumors of the pancreas.
3. Alcoholic bouts
4. Extensive malignant disease like fibrosarcoma.

The effects of hypoglycemia manifest more slowly than those of hypoxia. As the condition progresses, the medullary phase sets in. This is characterized by deep coma, shallow breathing an dilated pupils. Administration of glucose before the onset of the medullary phase results in complete reversal of the neurological lesions. However, once the medullary phase sets in, recovery may be delayed for months or may even be incomplete.

Hyperglycemic encephalopathy: This may be either due to hyperglycemia with ketoacidosis or due to hyperosmolar non-ketotic state. In both conditions, the patient becomes confused, stuporous, and comatose.

Hepatic Coma: Hepatic failure can lead to coma. It is likely that ammonia and other toxic metabolic products formed in the bowel and carried in the portal cicrculation by passing the liver, or not being further metabolized by the failing liver cells, reach the cerebral circulation and impair the metabolism of the brain and vital structures.

The Onset of coma may be precipitated by high protein intake, hematemesis of electrolyte imbalance. It starts with mental confusion, increased psychomotor activity and progressive deterioration of the sensorium to end up in deep comma. During the initial stage, the patient exhibits flapping tremors (asterexis) and this can be brought out when the hands are outstretched. Other signs of hepatic failure may be evident. The EEG reveals characteristic triphasic waves.

Treatment consists of management of the hepatic failure. L-dopa has been found to improve the level of alertness in some cases. With improvement is hepatic function, the neurological syndrome also also improves.

Uremic encephalopathy: Both acute and chronic renal failure can result in confusion and stupor. This is usually due to rising blood levels of toxic nitrogenous products. Muscular twitchings, irregular muscular jerks and occasionally convulsions predominate the clinical picture. The nature of the renal disease determines the prognosis. In chronic irreversible renal disease the condition does not improve without dialysis or renal transplantation. If convulsions occur, anticonvulsants should be given in small doses.

The Dementias II - Encephalopathies and Hepatic Coma

HEPATIC