Postoperative Polyuria following Craniotomy
In the past ten years, we have experienced 27 patients who developed post-craniotomy polyuria with daily output more than 3000 ml. These lesions are localized in the neighbourhood of the pituitary gland e.g. frontal base, third ventricle. In 23 cases, polyuria was relatively easy of control, but in...
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Veröffentlicht in: | Neurologia medico-chirurgica 1973, Vol.13 (1), p.144-144 |
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Sprache: | jpn |
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Zusammenfassung: | In the past ten years, we have experienced 27 patients who developed post-craniotomy polyuria with daily output more than 3000 ml. These lesions are localized in the neighbourhood of the pituitary gland e.g. frontal base, third ventricle. In 23 cases, polyuria was relatively easy of control, but in 4 cases polyuria was refractory to any therapy, as a result they died of pulmonary edema. When the hourly urinary output exceeded 200 ml postoperatively, uptake by intravenous fluid was increased in proportional to the degree of polyuria, and supplemental electrolytes were added accordingly if the patient was not able to drink enough due to impaired conscousness or nausea. When the polyuria persisted and urinary specific gravity dropped below 1.005, 2.5 units of Pitressin tannate in oil was given intramuscularly. 23 cases responded well to either the Pitression or the oral Chlorpropamide. Remaining 4 cases were refractory; those are postoperative patients with craniopharyngioma, chronic subdural hematome, aqueduct stenosis and an aneurysm at the anterior communicating artery. Within 24 hours upon the appearance of polyuria, the Pitressin was given to all these cases. Responses are variable. In one group there was no response. In the other group effect of administered Pitressin was transient. Repeated Pitressin injections were employed in the hope that patients would be responsive in the future, but unexpectedly urinary output increased gradually and finally reached several thousand milliliter per hour. These patients developed disturbed conscousness and died of pulmonary edema. In 3 cases hyponatremia was found. It is felt that these polyuria is not a result of genuine diabetes insipidus due to shortage of ADH, but of the other cousative metabolic disturbance such as inappropriate intravenous fluid therapy. At present, our regimen for polyuria is the close observation of intake and output without the immediate administration of Pitressin until significant changes in vital signs take place and careful initiation of supplemental fluid therapy. |
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ISSN: | 0470-8105 |