It is axiomatic in anesthesiology that abundant, or at least physiologically normal, intraoperative urine output (UOP) is essential to good postoperative renal outcome. Although it is true that the best monitor of intraoperative renal function is UOP, this is unfortunately true only in the sense that there is no other monitor of even passable use. One should not confuse poor data from a bad monitor with excellent data (such as from end-tidal capnography) from a monitor that demands action. Unfortunately, the differential diagnosis of intraoperative oliguria is not hypovolemia alone.

Clearly, slavish devotion to producing a UOP of 3 mL/kg/hour in an anuric renal failure patient during a lengthy bowel procedure will predictably produce pulmonary edema and ultimately congestive heart failure. A more probable situation is that in which large volumes of fluid are administered to a physiologically normal patient in an attempt to correct presumed hypovolemia in an oliguric patient who in fact has a kinked Foley catheter or an unsuspected urinary tract injury in the surgical field. In the first case, delayed diagnosis of the kinked catheter and volume resuscitation will result in an overdistended bladder and ultimately obstructive renal failure. In the second, renal function may be unaffected.

It has been frequently observed that patients undergoing laparoscopic surgery have lower-than-expected intraoperative UOP. Aggressive volume resuscitation in these patients may or may not increase their UOP. Euvolemia or slight relative hypervolemia may be necessary to ensure adequate blood pressure in this setting (because of increased intrathoracic pressure reducing return to the right heart). But does the reduced UOP reflect a danger to the kidney? Early laparoscopists thought this was the case—that pneumoperitoneum caused renal vein and parenchymal compression, which resulted in oliguria and eventually renal injury. There is now good evidence to show otherwise. In multiple studies in animal models, pneumoperitoneum of 15 mm Hg or less (the upper limit for most laparoscopic procedures is 15 mm Hg) predictably reduces UOP but does not result in significant changes in ultrasound, pathologic, or chemical indicators of renal function. This question has also been evaluated in humans. As laparoscopic gastric bypass was being developed, Nguyen et al. reported on renal physiology in more than 100 patients assigned randomly to either laparoscopic or open gastric bypass. Despite longer operative time and 64% lower intraoperative UOP in
the laparoscopic group, there was no significant difference in postoperative blood urea nitrogen (BUN), creatinine, antidiuretic hormone (ADH), aldosterone, or renin levels, strongly suggesting that the reduced UOP reflects a reversible noninjurious physiologic consequence of pneumoperitoneum.