Release of antidiuretic hormone is a natural response to perioperative stressors, thus it should be expected that urine output will decrease during and after major surgery. Alpert and Roizen showed in 1984 that the lowest intraoperative UOP has absolutely no correlation with post-operative creatinine changes (137 patients undergoing vascular surgery) [Alpert RA et al. Surgery 95: 707, 1984].
Treatment of “low urine output” in a patient who is intravascularly volume-depleted is controversial, with evidence both for and against. Importantly, there are no prospective, randomized trials designed to specifically address this. The results of the SPARK II trial, a phase II randomized blinded controlled trial of the effect of furosemide in critically ill patients with early acute kidney injury, should be available in December 2011 and offer additional guidance. In the meantime, two separate trials of pediatric patients undergoing cardiopulmonary bypass have identified furosemide as an independent risk factor for injury [Chiravuri SD et al. Paediatr Anaesth 21: 880, 2011; Moffett BS et al. Pediatr Crit Care Med. 2011 (Epub ahead of print)], although outside the context of a RCT it is impossible to say whether or not this can be attributed to furosemide itself. The FACTT trial, which was designed to test the efficacy of diuretics in acute lung injury, showed a benefit associated with diuretic administration, although this may have been due to favorable changes in volume status [Grams ME et al. Clin J Am Soc Nephrol 6: 966, 2011]
Choice of vasopressor may affect urine output, with alpha agonists generally decreasing blood flow to the kidneys and urine output. Vasopressin, by contrast, allows for a relative increase in renal blood flow and consequently relatively increased urine output.