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Hypodipsic hypernatremia and diabetes insipidus following anterior communicating artery aneurysm clipping: diagnostic and therapeutic challenges in the amnestic rehabilitation patient.

Hypodipsic hypernatremia (HH) represents a pathological increase in serum sodium due to a lack of thirst and defect in hypothalamic osmoreceptors. While 15% of patients with HH have a vascular aetiology, few cases have been described. Moreover, the presence of such abnormalities in the amnestic patient can have particularly threatening implications, as HH tends to recur unless the patient complies with a regimen of water intake. This study reports the case of a 46-year-old male admitted for rehabilitation of functional deficits following subarachnoid haemorrhage (SAH), with clipping of an anterior communicating artery (ACoA) aneurysm. Clinical examination was remarkable for profound short-term memory loss and inability to retain new information. Blood chemistry on admission showed a serum sodium level of 160 mEq/L, increasing to 167 mEq/L the following day. The patient denied thirst, and showed no clinical signs of dehydration. Neuroendocrine evaluation revealed diabetes insipidus (DI) and HH. Treatment initially included DDAVP and intravenous hydration, later supplemented with chlorpropramide. Stabilization of serum sodium and osmolality did not ensue until the treatment regimen included hydrochlorothiazide and supervision of enforced fluid intake. Endocrine abnormalities may be encountered among patients with vascular lesions adjacent to the hypothalamus. Rehabilitation interventions include establishing a structured medication regimen with fluid administration in the amnestic patient with hypothalamic dysfunction.

Amnesia, Anterograde↗

Type II diabetes: some problems in diagnosis and treatment.

This case is a rather typical presentation of a patient with mild, type II diabetes. His case illustrates some of the pitfalls in the dietary management of diabetes, in treating the glucose abnormality and hypertension, and in diagnosing the mental obtundation that can occur in type II disease. This patient¿s glucose abnormality can probably be treated adequately with a normal- or low-calorie diet that is appropriately high in carbohydrates and low in fats. His hypertension must be treated adequately, preferably with lower doses of diuretics or, if other drugs are necessary, one other than a beta-adrenergic blocking drug. Clearly, his cholesterol should be treated too, but the high-carbohydrate, low-fat diet now prescribed for diabetics will probably be adequate to reduce this risk factor for cardiovascular disease. Finally, the last major risk factor for cardiovascular disease, namely smoking, should unquestionably be removed.

Blood Glucose↗