We present a 15 year old with hypotrophic right kidney due to vesicoureteral reflux and hypertension of renal etiology presenting for laparoscopic simple right nephrectomy, developing unexpected intraoperative hyperkalemia, significant lactic acidosis, and increase in serum creatinine.
Induction, intravenous catheter, and arterial line placement were uneventful. Vital signs were stable. Blood pressure was maintained without pressors at about 10% below baseline (136/88 preoperatively). Four hours after incision peaked T waves on ECG prompted an arterial blood gas, which revealed serum potassium (K+) of 6.6 and lactate of 2.2. At baseline, K+ was 3.7, pH 7.37 and lactic acid 0.9.
Hyperkalemia was treated with calcium chloride, albuterol, hyperventilation, bicarbonate, insulin and glucose. The potassium fell to 6, then 4.1, then to 2.6 within an hour and normalized within 8 hours. Lactic acid increased to a maximum of 10.8 about 4 hours after the hyperkalemic event, and normalized within 12 hours. The lowest pH was 7.19, resolved within 7 hours. 20 minutes after the diagnosis of hyperkalemia, the blood pressure drifted within 5 minutes from 120 systolic to 100 then briefly low 80’s, and improved rapidly with phenylephrine 300 mcg total.
After discussion with surgeon, laparoscopic examination was performed, with no intestinal ischemia or injury noted. Liver function, creatine kinase, and creatinine were tested. The only abnormal result was creatinine, increased to 1.69 from 0.94 baseline, normalized within 11 hours. The patient was taken intubated to ICU due to concern for unexplained worsening lactic acidosis and extubated uneventfully the next day, with resolution of lab abnormalities.
It is unclear why this routine nephrectomy patient developed hyperkalemia and then worsening lactic acidosis with renal injury. Surgery was uneventful, save for the brief (1-minute) episode of 80/40 BP. Independently of the BP change, the right kidney was perfused retrograde through the venous system for 40 minutes while the artery was clamped and the surgical team waited for a larger clamp for the renal vein. These were the two notable events during surgery, but neither appears sufficient to produce this situation.
Compression of the renal arteries might cause acute kidney failure, but patient positioning and surgical approach were normal. Postoperative Doppler study showed increased resistive indices in the interlobar arteries, so kidney perfusion may have been less than systemic pressures would indicate due to a combination of unsuspected increased resistance and intraperitoneal pressure (CO2 insufflation). Lactic acidosis has been reported after treatment with albuterol for asthma, so hyperkalemia treatment with albuterol in a hyperadrenergic state might explain the lactic acidosis [1], but not the initial hyperkalemia. Rhabdomyolysis has been described in nephrectomy cases, but laboratory values were normal [2].
1. Koul PB, et al. Lactic acidosis in children with acute exacerbation of severe asthma. Eur J Emerg Med 2007; 14:56–8
2. van Dellen D, et al. Intraoperative hyperkalemia complicating hand-assisted live-donor nephrectomy. Exp Clin Transplant 2011;9:417–20
