After urgent relief of upper urinary tract blockage, patients with bilateral obstruction or obstruction of a solitary kidney are at risk for postobstructive diuresis. The chronically obstructed patient with signs and symptoms of fluid overload including pedal edema, congestive heart failure, increased abdominal girth, weight gain, and azotemia is more likely to have this problem (Gulmi et al. 2002). Postobstructive diuresis is classified as physiologic, pathologic, or iatrogenic. In the physiologic form, the diuresis is caused by retained free water, sodium, and urea. The pathologic form is associated with impairment in renal concentrating ability or sodium reabsorption. When patients are given high volumes of intravenous fluid containing dextrose, glucose reabsorption in the proximal tubule can be exceeded, leading to the iatrogenic type of postobstruc-
tive diuresis. While postobstructive diuresis can be thought of as these three types, the reality is that many patients experience mixed patterns. In addition, the development of postobstructive diuresis after relief of upper tract obstruction is relatively rare. Furthermore, most patients that develop the problem have a physiologic-type diuresis that rapidly returns to normal. In fact, providing the patient access to free water and avoiding the use of intravenous fluids usually is enough to remedy the situation (Gulmi et al. 2002).
Nonetheless, it is important to identify patients at risk for postobstructive diuresis after relief of upper tract obstruction. Following the drainage procedure, urine output should be carefully monitored, especially for patients with evidence of chronic obstruction and fluid overload. When urine outputs are higher than 200 ml/h for 2 consecutive hours, urine and plasma osmo-lality should be obtained to determine the type of diuresis. In the presence of low or iso-osmolar urine, the alert patient with access to water will typically normalize the serum creatinine and blood urea nitrogen within 1 or 2 days. Until the diuresis is corrected, urine output should be carefully monitored (every 2 h), the patient should be weighed daily, and serum electrolytes should be checked twice daily (Gulmi et al. 2002). Furthermore, it is important to assess the adequacy of hydration while the postobstructive diuresis is being treated. To achieve this goal, postural vital sign assessments should be utilized at a minimum of every 8 h as the patient is being treated for the postobstructive diuresis.
In situations where the diuresis continues for more than 2 days and the urine persists with a low osmolari-ty, concern for a pathologic type of diuresis is increased. The alert patient continues with oral intake, but if serum electrolytes show unchanged elevations in creatinine and blood urea nitrogen, intravenous fluid (0.45% sodium chloride with 5% dextrose) should additionally be started. In most instances, urine output is replaced with the intravenous fluid as a ratio 0.5 cc of saline to 1.0 cc of urine output and this treatment is continued with frequent monitoring until the diuresis stops. This type of pathologic diuresis is related to a water diuresis secondary to damage in the distal tubules. In the rarest form of pathologic postobstructive diuresis, significant sodium loss also occurs secondary to distal tubule damage. Correction of this diuresis involves 1: 1 replacement of urinary sodium with intravenous saline. In this form of diuresis, patients are at risk of volume depletion and vascular collapse (Gulmi et al. 2002). Faced with issues of postobstructive diuresis in a patient with fluid overload and uremia, nephrologic consultation is advised.
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