Cases reported "Oliguria"

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1/9. Compartmental syndrome and its relation to the crush syndrome: A spectrum of disease. A review of 11 cases of prolonged limb compression.

    A review of 11 cases of prolonged limb compression usually following drug overdose, revealed a spectrum of disease from isolated compartmental syndromes to full crush syndromes with renal failure. Residual limb contractures were moderate or severe in 80 per cent of the extremities involved. Five of the 11 patients demonstrated significant, systematic manifestations, Stage II or Stage III crush syndrome by our definition. The severity of the systemic manifestations is related to the amount of muscle tissue being subjected to elevated pressure and the length of time this pressure is maintained. Delay in hospitalization, delay in diagnosis, and delay in treatment prolong this period. The diagnosis should be made on the basis of the histroy of prolonged immobilization and the finding of a swollen extremity. Fasciotomy should be performed immediately, both to minimize residual limb contracture and to prevent the crush syndrome from developing secondary to myonecrosis.
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2/9. The management of acute quinidine intoxication.

    A 16-year-old patient survived severe intoxication with quinidine. hypotension, rapidly progressing to oliguria and shock, was resistant to the usual therapeutic interventions but responded favorably to the use of an intra-aortic balloon pump. Some hemodynamic implications are discussed. pulmonary edema occurred and was treated with positive end-expiratory pressure. Electrocardiographic disturbances in conduction, transient bradycardia and recurrent ventricular arrhythmias characterized the initial 36-hour critical period. Unexplained electrolyte abnormalities occurred and further complicated management.
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3/9. oliguria from high intra-abdominal pressure secondary to ovarian mass.

    oliguria in association with elevated intra-abdominal pressure developed in a patient with an ovarian mass. Operative decompression of the abdomen reversed the oliguric state. Clinically, laparotomy may be indicated in the presence of decreasing urinary output and elevated intra-abdominal pressure.
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4/9. Isolated ultrafiltration in the therapy of volume overload accompanying oliguric vascular shock states.

    Isolated ultrafiltration (removal of plasma water and solute without dialysis) was used as a "last resort" therapy in three patients with diuretic and pressor resistant oliguria complicating severe volume overload and vascular shock. The improvement in clinical and hemodynamic parameters is reported and the possible mechanisms of action (decreased pulmonary capillary wedge pressure and increased colloid osmotic pressure) are discussed.
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5/9. The measurement of intra-abdominal pressure as a criterion for abdominal re-exploration.

    Acute elevation of intra-abdominal pressure above 30 mmHg caused oliguria in 11 postoperative patients. Operative re-exploration and decompression in seven patients resulted in immediate diuresis. Four patients who were not re-explored developed renal failure and died. If intra-abdominal pressure rises above 25 mmHg in the early postoperative period and is associated with oliguria and normal blood pressure and cardiac index, the patient should undergo re-exploration and decompression of the abdomen.
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6/9. minoxidil treatment of malignant hypertension. Recovery of renal function.

    We treated eight severely hypertensive, long-term hemodialysis patients who failed to respond to ultrafiltration or conventional medication with minoxidil rather than with bilateral nephrectomy. Control of blood pressure and relief of symptoms was achieved in all eight. In addition, three of the patients, who were all severely oliguric, recovered sufficient renal function to allow the discontinuation of dialysis. Two are presently doing well, while one died of causes unrelated to uremia or minoxidil therapy. We presently reserve bilateral nephrectomy for those hypertensive dialysis patients who are awaiting transplantation.
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7/9. Lipoid nephrosis appearing as acute oliguric renal failure.

    Acute oliguric renal failure previously was reported to develop in patients with preexisting idiopathic nephrotic syndrome in association with clinical evidence of vascular volume depletion. We describe an 81-year-old man without recent proteinuria or evidence of preexisting nephrotic syndrome in whom acute oliguric renal failure developed. Renal biopsy disclosed minimal change disease. Nephrotic range proteinuria without severe hypoalbuminemia was detected during the 25-day course of oliguric renal failure. Renal vein thrombosis was excluded. urine sodium concentration and fractional sodium excretion were reduced, yet left ventricular filling pressure was not subnormal and could be increased to supernormal levels without improvement in glomerular filtration rate. oliguria and azotemia were corrected following initiation of glucocorticoid therapy. This case suggests that lipoid nephrosis can appear as acute oliguric renal failure without historical or physical evidence of preexisting nephrotic syndrome.
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8/9. Reversible renal failure in malignant hypertension.

    Acute renal failure requiring dialysis to sustain life may be due to malignant hypertension. If the blood pressure is controlled during a period of dialysis, then it is possible that the renal lesions may heal, with some recovery of renal function. This report describes eight patients with acute renal failure due to malignant hypertension who required temporary dialysis. In all eight cases adequate control of blood pressure was achieved and all recovered renal function such that dialysis could be discontinued. The longest period of follow-up was five years, and one patient achieved a creatinine clearance of 23 ml/min. Renal histology, available in five cases, showed changes of malignant hypertension only, with no evidence of other renal lesions. A review of the literature is presented and the potentially reversible nature of acute oliguric renal failure due to malignant hypertension is emphasized.
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9/9. Postresuscitative hypertension: a reappraisal.

    New concepts of cause and therapy for postresuscitative hypertension (PRH) were evaluated in four patients with PRH. Each patient had severe injury and shock, and received an average of 28.3 transfusions, 15.4 L of electrolyte solution, and 1.4 L of plasma by the end of surgery for control of bleeding. Near the end of the sequestration phase, PRH developed. In two patients, PRH (190/100 mm Hg and 180/90 mm Hg) responded to previously recommended therapy; blood pressure fell to about 135/90 mm Hg. Shortly thereafter, bradycardia developed and both patients died. In the latter two patients, PRH (205/115 mm Hg and 150/120 mmHg) was treated less aggressively, maintaining intravenous fluids to keep urine output at a minimum of 50 mL/hr. Postresuscitative hypertension persisted for five and six days as both patients improved, continued to mobilize sequestered fluid, and maintained good organ perfusion. Postresuscitative hypertension may be a cell-mediated protective response to a need for increased capillary hydrostatic pressure to facilitate mitochondrial oxygenation. Fluid replacement should be guided by careful monitoring of cardiac, pulmonary, and renal function.
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