The lateral decubitus position is frequently used for operative procedures on the hip. This position is usually well tolerated by the patient, and complications involving the internal organs are uncommon. We report the case of a patient who had postoperative acute tubular necrosis of a transplanted cadaveric kidney that had been functioning well. This unusual complication followed a left total hip replacement and was thought to be secondary to a positioning device that caused obstruction of the blood supply to the cadaveric kidney.
*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.
†Departments of Anesthesiology (T. D. C. and P. A. S.) and Surgery (H. K.), University of Kentucky Hospital, 800 Rose Street, Lexington, Kentucky 40536. E-mail address for Dr. Sloan: psloan@uky.campus.mci.net.
A thirty-seven-year-old man who had steroid-related bilateral degenerative hip disease was scheduled for a left total hip replacement. Five years earlier, a successful transplant of a cadaveric kidney had been performed because of renal failure secondary to poorly controlled hypertension. The kidney had been functioning well, with a usual baseline creatinine level of 1.6 milligrams per deciliter (141 micromoles per liter) (normal range, 0.6 to 1.2 milligrams per deciliter [fifty-three to 106 micromoles per liter]). The patient also had a remote history of coronary angioplasty, had smoked for twenty years, and had hypertension, which was controlled with the use of antihypertensives. His usual medications included Vasotec (enalapril maleate), Procardia (nifedipine), Imuran (azathioprine), cyclosporin A, prednisone, and aspirin.
The results of the physical examination before the hip replacement were unremarkable except for the bilateral dysfunction of the hip. The patient weighed sixty kilograms and was 180 centimeters tall. The allograft kidney was easily visible in the left lower quadrant of the abdomen and was non-tender to palpation. Apart from the mildly elevated level of creatinine, the laboratory values were within normal limits.
Induction of general anesthesia with five milligrams of midazolam, 500 micrograms of fentanyl, 120 milligrams of succinylcholine, and 400 milligrams of Pentothal (thiopental) was uneventful. The maintenance anesthetics were oxygen and nitrous oxide with isoflurane. One hundred milligrams of hydrocortisone and two grams of cefazolin were administered after the induction of anesthesia. The patient was then positioned in the right lateral position with use of the Montreal Hip Positioner (Orthopaedic Systems, Union City, California) (Fig. 1). All pressure points, particularly on the extremities and the axilla, were padded appropriately. Special attention was given to the relationship of the hip positioner to the abdominal kidney. On initial positioning, the allograft kidney was noted to be free from outside pressure. The operation proceeded uneventfully, and a catheter in the bladder drained clear urine at a rate of approximately fifty milliliters per hour for the first two hours of the operation. With an estimated blood loss of only 300 milliliters and two liters of normal saline maintenance fluid having been given, the output of urine stopped abruptly. A one-liter challenge of normal saline solution was given with no effect. The bladder catheter was checked, flushed, and noted to drain well. The patient was hemodynamically stable throughout the operation, with the blood pressure averaging 110/70 millimeters of mercury (14.66/9.33 kilopascals) and a heart rate of eighty beats per minute. The position of the patient was rechecked, and we noted that he had shifted position so that the transplanted kidney was compressed by the hip positioner. Repositioning freed the kidney from pressure, and the operation was finished as quickly as possible. There was no additional output of urine for the remainder of the operation. A total of four liters of saline solution was given throughout the operation, but the patient remained anuric. Thirty milligrams of furosemide was administered intraoperatively without effect. At the conclusion of the operation, the anesthesia was discontinued, and the patient awakened uneventfully in the operating room.
In the immediate postoperative period, a consultant nephrologist administered several liters of a crystalloid to rule out hypovolemic anuria and large doses of diuretics were administered intravenously. This treatment resulted in a negligible output of urine and congestive heart failure. The pulmonary symptoms resolved with emergency dialysis, and the patient recovered from the operation with no additional complications. A renal ultrasound showed mild dilation of the collecting system secondary to possible obstruction, and a renal scan showed good blood flow and a poorly functioning pelvic kidney. A renal biopsy showed acute tubular necrosis of the cadaveric kidney. The patient required dialysis for three weeks postoperatively, during which time the output of urine returned to normal. He was then discharged home with baseline levels of blood urea nitrogen of sixty-three milligrams per deciliter (22.5 millimoles per liter) and creatinine of 5.7 milligrams per deciliter (504 micromoles per liter). Over the subsequent months, the patient continued to do well. He had improved function of the kidney, and the creatinine level returned to the preoperative level of 1.6 milligrams per deciliter (141 micromoles per liter). At the time of the most recent follow-up, the patient had returned to work at full capacity, the transplanted kidney continued to function well, and no additional renal treatment had been necessary.
Acute renal failure is common in hospitalized patients, with a reported prevalence of 4.9 per cent (109) of 2216 such patients according to one prospective study3. In that study, 54 per cent (fifty-nine) of 109 cases of acute renal failure were believed to be iatrogenic, and 59 per cent (thirty-five) of those fifty-nine cases were related to operations or trauma, or both. Acute renal failure is a life-threatening condition with a reported mortality rate ranging from 25 to 100 per cent in series of eleven to 1542 patients5. This high rate of death occurs regardless of etiology or treatment.
The etiology of acute renal failure is often categorized as pre-renal, intrinsic renal, or post-renal. Pre-renal failure is predominantly secondary to states of hypoperfusion, with the most common cause being extracellular fluid-volume contraction. Other conditions that cause pre-renal failure are those that result in decreased cardiac output, including myocardial infarction, valvular heart disease, constrictive pericarditis, and cardiac tamponade. Causes of intrinsic renal failure are categorized by the site in the nephron that is affected (the glomeruli, vessels, or tubules). Of the many causes of acute renal failure secondary to intrinsic disease, acute tubular necrosis probably accounts for more than 75 per cent of the cases in critically ill individuals4. The two principal causes of acute tubular necrosis in critically ill patients are ischemia and nephrotoxins. Ischemic acute tubular necrosis is caused by hypovolemic states or the interruption of the renal vasculature secondary to an operative procedure. Nephrotoxic acute tubular necrosis may be caused by antibiotics, contrast medium, anesthetic drugs such as methoxyflurane, heavy metals, organic solvents, chemotherapeutic agents, or pigments such as myoglobin and hemoglobin.
The lateral decubitus position is generally considered safe but may be associated with several complications. For example, damage to the eye, neck pain, and peripheral neuropathy have been reported following operations performed with the patient in the lateral decubitus position. We believe that the etiology of the acute tubular necrosis in our patient was direct trauma to the pelvic kidney, and the important contributing factor in the development of renal failure was compression of the pelvic renal artery by the hip positioner. To our knowledge, this is the first reported case of acute tubular necrosis in a transplanted kidney secondary to operative positioning. Rejection of the transplanted kidney by the patient is a possible explanation of the intraoperative renal failure; however, there was no preoperative evidence of any ongoing rejection. The anesthetic agents methoxyflurane2 and sevoflurane have both been suggested as possible causes of renal damage, but neither was used in our patient. There was no hemodynamic evidence of a hypovolemic state during the operation to suggest this as a contributing factor in the development of acute tubular necrosis.
Advances in immunosuppressive therapy have led to increased expectations with regard to the longevity of both a patient who has had a transplant and the transplanted kidney. Operations for conditions unrelated to the kidney have been shown to be generally safe in this population of patients and have not been associated with adverse effects on the transplanted kidney1. Bakkaloglu et al. measured serum levels of creatinine in nineteen patients who had had a renal transplant and were being managed with an operation unrelated to the kidney. They reported that, when compared with control levels (mean, 1.8 milligrams per deciliter [159 micromoles per liter]), there was no significant change in serum creatinine levels (mean, 1.7 milligrams per deciliter [150 micromoles per liter]) as long as four weeks postoperatively. A repeat study of a larger sample would be helpful to confirm this observation. Our patient had a substantial increase in the levels of both blood urea nitrogen and creatinine, reflecting acute damage to the kidney. The effect of this single episode of acute tubular necrosis on the life of the transplanted kidney cannot be known.
In conclusion, acute injury of a transplanted kidney as a result of an operation and anesthesia is life-threatening. To decrease the possibility of such an injury related to pressure by a hip positioner, we recommend careful positioning of the patient in the lateral decubitus position, adequate padding of the pelvic kidney, and frequent verification of positioning throughout the operation to avoid pressure on the transplanted kidney. Alternatively, to avoid use of the Montreal-type hip positioner, the operation could be performed through an anterior or direct lateral approach. In addition, the output of urine should be measured every fifteen minutes, with a high index of suspicion in the event of a sudden decrease in drainage from the bladder.