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Transient episodes of the syndrome of inappropriate anti-diuresis developped in two severe colchicine poisonings. These are the first cases reported. On patient also developped a reversible periphal neuropathy. The similarity of such accidents with vicristine neuro-toxicity is emphasized.
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We report the result of a study performed in 27 patients taking carbamazepine because of epilepsy or neuralgia, in order to point out subclinical water abnormal retention. We tested serum sodium and potassium levels, plasma and urine osmolarity, free water clearance. The carbamazepine serum level is also reported. We didn't find abnormal values. So in our experience there is not any complication concerning water retention during oral carbamazepine treatment.
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Irrespective of the etiology, a water and electrolyte imbalance provoking a hypo- or hyperosmolar state causes metabolic encephalopathy, as may occur with any metabolic disturbance. The pathophysiology of metabolic encephalopathy relies on a diffuse neuronal dysfunction which occasionally shows a focal maximum. To the clinician it presents in the form of nonspecific symptoms or signs, such as altered level of alertness or awareness of the environment, or impaired attention, cognition or orientation. When the onset of hypo- or hyperosmolality is rapid, delirium may develop or the level of consciousness can decrease to the point of coma. Myoclonic jerks, gait disturbance and focal or generalized fits are additional nonspecific signs. When the water and electrolyte imbalance coincides with or is caused by brain disease, the signs of the two conditions are added. On the other hand, complicating hemorrhages, sinus thrombosis, or brainstem herniation or compression may be taken for a primary structural brain lesion, and the water and electrolyte imbalance may easily be overlooked. Pathophysiology, symptoms and signs, and therapy of hypo- and hyperosmolar states are discussed. Central pontine myelinolysis is considered separately.
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