Case Reports  |   November 2000
Intraoperative Hemodialysis during Emergency Laparotomy
Author Affiliations & Notes
  • James R. Cooper, B.S.N.
  • Stephen B. Kurtz, M.D.
  • Mark D. Sawyer, M.D.
  • Bradly J. Narr, M.D.
  • *Student Nurse Anesthetist, Mayo School of Health-Related Sciences, †Associate Professor of Medicine, Division of Hypertension and Nephrology, ‡Assistant Professor of Surgery, Department of Surgery, §Assistant Professor of Anesthesiology, Department of Anesthesiology.
Article Information
Case Reports
Case Reports   |   November 2000
Intraoperative Hemodialysis during Emergency Laparotomy
Anesthesiology 11 2000, Vol.93, 1356-1357. doi:
Anesthesiology 11 2000, Vol.93, 1356-1357. doi:
MANY patients with advanced organ system dysfunction present for anesthesia and surgery. The incidence of renal failure that requires dialysis has increased dramatically in the past decade. 1 We describe two cases in which intraoperative hemodialysis was performed for refractory hyperkalemia.
Case Reports
Case 1
A 61-yr-old man had a history of aortic and mitral valve replacement, chronic renal insufficiency (baseline creatinine level 2.2 mg/dl), ascites, and a known umbilical hernia. Long-term medications included furosemide, aldactone, digoxin, warfarin, and losartan. He presented with fever, emesis, and painful bulging of the hernia defect. A presumptive diagnosis of strangulated umbilical hernia was made. Initial laboratory evaluation showed a potassium (K+) concentration of 7.6 mEq/l. Intravenous administration of 50 ml dextrose, 50%, 10 U regular insulin, and 1 g calcium chloride were followed by a repeat K+of 6.8 mEq/l. In addition, blood urea nitrogen level was 86 mg/dl (baseline 53), creatine level was 2.6 mg/dl, glucose level was 134 mg/dl, and arterial blood gases with room air showed an arterial oxygen tension (Pao2) of 89 mmHg, an arterial carbon dioxide tension (Paco2) of 37 mmHg, HCO3of 22 mEq/l, and a pH 7.39. An electrocardiogram showed sinus bradycardia with left bundle-branch block and was unchanged from 3 months before. He received 4 units fresh frozen plasma to reverse chronic anticoagulation.
He arrived in the operating room with a pulse of 85 beats/min, a blood pressure of 140/70 mmHg, and a respiratory rate of 18 breaths/min. A right internal jugular dialysis catheter (Mahurkar 11.5-French dual lumen; Sherwood Medical Company, St. Louis, MO) and an arterial catheter were placed while the patient was awake. All intravenous infusions were normal saline. A modified rapid sequence induction was performed, and, 15 min later, dialysis was begun. K+concentration at that time was 6.5 mEq/l. His pulse rate gradually decreased during the first hour of hemodialysis to 50 beats/min, and his blood pressure remained stable at 120–145/55–75 mmHg throughout the procedure. The hernia sac was dissected, and, after incision of the surrounding fascia, the bowel that had looked ischemic regained viability. More than 2 l ascites were removed from the abdomen, and the hernia was repaired. He was given 2 more units fresh frozen plasma and a total of 1,250 ml normal saline during 2 h anesthesia. Muscle relaxant was reversed, and the patient was extubated while dialysis continued. He underwent dialysis for a total of 1 h and 45 min against a dialysate with a K+concentration of 1 mEq/l. No fluid was removed during hemodialysis. Urine production was negligible. When transferred to the intensive care unit, he was breathing spontaneously, alert, and oriented, with a K+concentration of 5.0 mEq/l. Five h postoperatively, arterial blood gases showed a partial pressure of oxygen (Po2) of 132, a partial pressure of carbon dioxide (Pco2) of 46, a pH of 7.36, and 25 mEq/l HCO3on 3 l oxygen/min administered via  nasal cannulae. Aldactone was held postoperatively for 3 days. He produced 350 ml urine during the first 12 h after the procedure, and urine flow continued to be adequate. No further dialysis was performed during his hospital stay. At discharge, creatinine concentration was 1.9 mg/dl, and K+concentration was 4.5 mEq/l. His usual medical regimen was restarted, and he has continued to do well.
Case 2
A 29-yr-old woman with an 18-yr history of insulin-dependent diabetes was involved in an automobile collision while driving to a dialysis center for her triweekly hemodialysis treatment. At admission to the emergency room, the patient was conscious, oriented, and reporting severe abdominal pain. Abdominal computed tomography showed diffuse fluid throughout the retroperitoneum and air within the mesentery. A diagnosis of small bowel rupture was considered. Arterial blood gas evaluation showed a hemoglobin concentration of 8.7 g/dl (baseline 10.3 g/dl 1 week previously), a sodium (Na+) concentration of 133 mEq/l, a K+concentration of 6.9 mEq/l (baseline 3.9 mEq/l 1 week previously), a glucose concentration of 278 mg/dl, a Pao2of 129, a Paco2of 42, and a pH of 7.37. She had an arteriovenous fistula for chronic hemodialysis in the right arm. She was administered intravenous insulin and prepared for arrival to the operating room.
At arrival in the operating room, her pulse was 105 beats/min, with a blood pressure of 124/72 mmHg. Electrolytes obtained just before incision showed an Na+concentration of 131, a K+concentration of 5.4 mEq/l, a glucose concentration of 111 mg/dl, and an ionized calcium (Ca2+) concentration of 3.88 mg/dl. Calcium chloride, 500 mg, was administered intravenously. Hemodialysis was initiated 30 min after induction, using the existing right arteriovenous fistula. Vital signs were stable, with a gradual decrease in pulse rate to 75 beats/min and blood pressures of 100–120/60–75 mmHg. During 21/2 h dialysis, she underwent transfusion of 2 units packed red cells via  the dialysis machine, and no fluid was removed. Laboratory tests after dialysis revealed a K+concentration of 3.3 mEq/l, a glucose concentration of 138 mg/dl, and a Ca2+concentration of 4.3 mg/dl. The duodenal perforation was repaired, and the patient was taken to the intensive care unit. She was extubated 12 h later and had hemodialysis every 24 h for the next 3 days to remove fluid. Her recovery was otherwise uneventful.
Modern anesthetic care allows many procedures to be performed, even in the patient with no renal function. Traditionally, the logistics of providing hemodialysis required that this therapy be provided preoperatively or postoperatively in intensive care units or special dialysis units. However, emergency hemodialysis treatments no longer necessitate systemic anticoagulation, and new dialysis membranes are well-tolerated hemodynamically and cause minimal systemic disturbance. If appropriate equipment and personnel can be mobilized, intraoperative dialysis is not an anesthetic challenge. Some intravascular volume will be lost when blood replaces the priming fluid in the dialyzer, but this has minimal effects. Our impression was that immediate surgical intervention with perioperative dialysis during the procedures was in the patient’s best interest. We have continuous coverage in our hospital for emergency dialysis by a nephrology team that was available for intraoperative care.
Indications for intraoperative hemodialysis should be limited to severe electrolyte abnormalities and some types of volume overload. In patients with no renal function in whom immediate surgical intervention is necessary, ultrafiltration can be used to remove fluid without dialysis. However, vasodilators, ventilatory assistance with positive end-expiratory pressure, and inotropic support are more common treatments. Hemodynamically unstable patients with ongoing blood loss may not tolerate dialysis. Patients who have surgical diagnoses that allow for preoperative optimization should be treated medically or should undergo dialysis in a more traditional environment.
Hyperkalemia is a life-threatening disorder. Medical interventions to shift K+into cells (hyperventilation, intravenous sodium bicarbonate, glucose, and insulin infusion) that mitigate the effect of hyperkalemia on electrically excitable tissues (intravenous calcium) or removal of K+from the body (cation exchange resins via  the gut or dialysis) are treatment options. As these cases show, we used several of these treatments. Hemodialysis is an efficient mechanism for treating hyperkalemia. 2 A case has been reported in which severe hyperkalemia occurred after transfusion in a patient with end-stage renal disease. He underwent dialysis intraoperatively to correct the electrolyte abnormality. 3 Our patients were hemodynamically stable, without active hemorrhage. We could not use the gut for cation exchange resins, and they both had the potential for further exacerbation of K+homeostasis. To correct hyperkalemia in this setting, we chose hemodialysis.
Hemodialysis is the most efficient means of decreasing serum K+, with the bulk of the loss occurring during the first hour. The normal dialysate consists of an Na+concentration of 140 mEq/l and a K+content ranging from 0 to 4 mEq/l. Because hemodialysis can rapidly decrease K+levels, hypokalemia can become a concern. Holter studies indicate that patients whose K+levels decrease to below 3.5 mEq/l and who have left ventricular hypertrophy or are prescribed digoxin are at risk for ventricular arrhythmias. 2 Patients other than these have undergone dialysis to low serum K+levels without adverse consequences. 4 
Intraoperative hemodialysis can be used to treat severe hyperkalemia and allow simultaneous surgical intervention. This has the potential to improve patient outcomes when ischemia of bowel can be reversed or peritoneal contamination can be limited by rapid surgical intervention. By choosing to use dialysis intraoperatively, we prevented further increases in serum K+levels and the complications that potentially accompany it. Hemodynamically stable patients can undergo dialysis safely during general anesthesia.
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