| Abstract|| |
Renal excretion and cellular uptake of potassium play key roles in the body's defense mechanism against hyperkalemia. Intra-operative hyperkalemia is an uncommon life-threatening complication during elective renal transplant surgery. We report herewith a non-insulin dependent diabetic kidney transplant recipient with prolonged pre-operative fasting, in whom, despite pre-operative hemodialysis, unforeseen high serum potassium level suddenly presented as wide-complex bradycardia during the surgery. The patient responded well to medical therapy of the hyperkalemia and the surgery was completed uneventfully. It is difficult to single out the exact cause of hyperkalemia in our patient. Prolonged pre-operative fasting for about nine hours, associated with insulinopenia and hyperglycemia, in the presence of β-blockade and metabolic acidosis, have probably collectively resulted in efflux of potassium from intra-cellular stores. This potentially catastrophic complication should be remembered in diabetic patients undergoing any type of surgery.
Keywords: Surgery, Kidney transplant, Complication, Hyperkalemia.
|How to cite this article:|
Gautam P L, Kathuria S, Singh A, Aulakh BS, Sandhu K. Unforeseen Intra-operative Hyperkalemia in a well Dialyzed Patient during Renal Transplantation. Saudi J Kidney Dis Transpl 2001;12:45-8
|How to cite this URL:|
Gautam P L, Kathuria S, Singh A, Aulakh BS, Sandhu K. Unforeseen Intra-operative Hyperkalemia in a well Dialyzed Patient during Renal Transplantation. Saudi J Kidney Dis Transpl [serial online] 2001 [cited 2022 Jan 25];12:45-8. Available from: https://www.sjkdt.org/text.asp?2001/12/1/45/33885
| Case Report|| |
A 61-year-old male patient, weighing 78 kg was scheduled for elective renal transplantation for end-stage renal disease (ESRD) following non-insulin dependent diabetes mellitus (NIDDM). He was a known diabetic for 18 years, on regular treatment with tolbutamide 0.5 gm thrice daily. He was also a known hypertensive for one and a half years and his blood pressure was well controlled with amlodipine 5 mg, metoprolol 50 mg and prazocin 5 mg, all administered orally, once daily. His daily urine output ranged between 300 to 1000 ml during the month prior to transplantation. His past history revealed head injury ten years earlier, which was managed conservatively. There was no history suggestive of muscular dystrophy, neuropathy or ischemic heart disease.
The general physical and systemic examinations were normal. Pre-operative investigations showed: hemoglobin, 87 gm/L; hematocrit, 0.26; total serum proteins, 75.8 gm/L; serum albumin, 43 gm/L; alkaline phosphatase, 75.7 units; aspartate aminotransferase, 18 units/L; alanine aminotransferase, 24 units/L; serum creatinine, 789.4 µmol/L; HbsAg and HIV were non-reactive. Chest X-ray and electrocardiogram (ECG) showed no abnormality. An esophagogastroscopy was normal. Echocardiography showed good left ventricular function (ejection fraction-71%) with concentric left ventricular hypertrophy and no regional wall motion abnormality. The pre-dialysis serum potassium was 5.2 mmol/L. He underwent heparin free hemodialysis for four hours, 12 hours before surgery. The post-dialysis serum potassium was 4.4 mmol/L and fasting blood sugar was 8.05 mmol/L.
The patient was kept nil per orally after midnight. Routine dose of anti-hypertensives, along with tab. diazepam 5 mg were given in the morning. Epidural catheter 18G was placed through 16G Tuohy's needle and 15 ml of 2% xylocaine was given. As there was a patchy effect, anesthesia was converted to general anesthesia. After preoxygenation with 100% oxygen for three minutes, anesthesia was induced with thiopentone sodium 250 mg and atracurium 50 mg intravenously. Oral endotracheal intubation was done with 8.5 mm OD, cuffed endotracheal tube. Anesthesia was maintained with oxygen and nitrous oxide (50: 50) and isoflurane 0.4-0.8%. Analgesia was supplemented with 4.0 mg morphine sulphate given intravenous (i.v.). Intraoperative monitoring included heart rate, blood pressure, continuous three lead ECG, arterial oxygen hemoglobin saturation (SpO2), end-tidal carbon dioxide (EtCO2) and central venous pressure. The patient remained hemodynamically stable throughout, except for the heart rate, which remained on the lower side i.e. 60-65 beats/min, probably due to beta-blockade effect.
After two hours of commencing surgery, the ECG suddenly showed wide-complex bradycardia with loss of P-waves, which did not respond to atropine 1.2 mg i.v.. Arterial blood gas analysis showed: pH7.44, Pco2-5.05 kPa, Po 2 -11.97 kPa, base excess-3.0 mmol/L and standard bicarbonate-24 mmol/L. Complete electrolyte profile revealed high levels of serum potassium (> 9.0 mmol/L) and random blood sugar was 12.65 mmol/L. It was immediately managed with calcium gluconate (10%) 20 ml, sodium bicarbonate (7.5%) 50 ml and dextrose (20%) 100 ml containing 10 units of soluble insulin. Arterial blood gas analysis done after half an hour showed: pH-7.30, Pco2-7.26 kPa, Po2-9.95 kPa and serum potassium-7.2 mmol/L. Surgery was continued uninterruptedly. He was given inj. hydrocortisone hemisuccinate 400 mg and frusemide 100 mg i.v.. After the release of vascular clamps, the graft function picked up immediately and the patient produced about one litre of urine in the first hour. Two hours after surgery, the ECG reverted back to regular sinus rhythm and the serum potassium level at that time was 4.6 mmol/L. He was transfused one unit of whole blood in the recovery room. The post-operative course remained uneventful.
| Discussion|| |
Besides anemia, the other significant complications of end-stage renal disease (ESRD) are coagulopathies, hypertension, left ventricular hypertrophy, volume overload and electrolyte disturbances. ,, Although potassium is an intra-cellular anion, 1.5-2.0% of its extra-cellular presence contributes a major role in maintaining normal cardiac conduction and pacemaker functions.
Hyperkalemia is well known during kidney transplantation after declamping, due to the flushing of acid metabolites and the preservative Collin's solution, which contains 115 mmol/litre of potassium, into the main vascular pool. However, occurrence of high serum potassium levels before release of vascular clamps during elective renal transplant surgery is rare. Other factors leading to high serum potassium level under anesthesia include transfusion of old stored blood, use of suxamethonium, muscular dystrophies, prolonged pre-operative fasting in diabetic patients, extensive use of electrocautery, administration of potassium containing drugs or fluids, β-blockers, massive dose of steroids and metabolic acidosis. 
Our patient had a baseline heart rate on the lower side of the normal range, probably because of β-blockers. Two hours after induction of general anesthesia, he suddenly developed wide-complex bradycardia and severe hyperkalemia. This was despite the fact that patient was well prepared for an elective renal transplant with hemodialysis for four hours, the night before surgery.
The serum potassium level can rise 0.5-0.7 mmol/L following the injection of succinylcholine in both normal and uremic patients. However, succinylcholine was not used in our patient. Also, our patient did not give any history suggestive of muscular dystrophy or weakness and neither was blood transfusion or potassium containing fluids used. Although electrocautery was used in our patient, hyperkalemia after electrocoagulation has been reported only after prolonged use and muscle dissection, especially with high-voltage current.
Prolonged pre-operative fasting can be another important contributing factor, leading to hyperkalemia in diabetic patients. Prolonged fasting coupled with omitting a dose of insulin can result in insulinopenia, which in turn, leads to efflux of potassium from intra-cellular stores. Insulin deficiency and the hyper-osmolality caused by hyperglycemia, can lead to hyperkalemia even in patients with marked potassium depletion. Hyper-osmolality results in osmotic movement of water from the cells into the extra-cellular fluid, along with potassium drag. The loss of intra-cellular water raises the intra-cellular potassium concentration further favoring the passive potassium efflux. The friction forces between water and the solute can further result in movement of potassium out along with water, through the water pores in the cell membrane. ,,
β-adrenergic blockers interfere with β-adrenergic facilitation of potassium uptake by the cells. However, this effect is associated with only a minor increase in plasma potassium concentration (< 0.5 mmol/L). Metabolic acidosis can also lead to transcellular shift of potassium in exchange for hydrogen ions, to maintain electroneurality. Another cause of hyperkalemia in these settings can be type-4 renal tubular acidosis following hypoaldosteronism in diabetic nephropathy. However, it is often associated with mild metabolic acidosis, acidic urine and hypochloremia.
Although it is difficult to single out the exact cause of hyperkalemia in our patient, prolonged pre-operative fasting for about nine hours, associated with insulinopenia and hyperglycemia, in the presence of β-blockade and metabolic acidosis, has probably caused this catastrophic complication.
Another interesting feature in our patient was the abrupt appearance of ECG changes, without any warning signs of hyperkalemia. Severe hyperkalemia has been reported to lead to typical ECG changes leading to death due to arrhythmias. However, there are substantial reports where hyperkalemia has been found without ECG changes and the patients have survived, in spite of very high serum potassium levels. ,
To conclude, hyperkalemia under anesthesia can present as abrupt ECG changes with catastrophic arrhythmias. Hence, it is important to be vigilant for hyperkalemia in a patient with ESRD undergoing elective renal transplantation under general anesthesia, even if there are no apparent leading etiological factors. Secondly, one should be cautious about prolonged period of preoperative fasting in diabetic patients before renal transplantation.
| References|| |
|1.||Hirshman CA, Edelstein G. Intraoperative hyperkalemia and cardiac arrests during renal transplantation in an insulin dependent diabetic patient. Anesthesiology 1979;51(2):161-2. |
|2.||Kim HJ. Combined effect of bicarbonate and insulin with glucose in acute therapy of hyperkalaemia in end-stage renal disease patients. Nephron 1996;72(3):476-82. |
|3.||Conte G, Dal Canton A, Imperatore P, et al. Acute increase in plasma osmolality as a cause of hyperkalemia in patients with renal failure. Kidney Int 1990;38(2):301-7. |
|4.||Robert MB. Disorders of plasma sodium and potassium. In: Ripple JM et al (ed). Intensive care medicine, 3rd Edition, Little Brown & Co., New York 1996;976. |
|5.||Gifford JD, Rutsky EA, Kirk KA, McDaniel HG. Control of serum potassium during fasting in patients with end-stage renal disease. Kidney Int 1989;35(1):90-4. |
|6.||Allon M, Dansby L, Shanklin N. Glucose modulation of the disposal of an acute potassium load in patients with endstage renal disease. Am J Med 1993;94(5):475-82. |
|7.||Martinez Ved-A, Bardaji A, Garcia C, Oliver JA. Severe hyperkalemia with minimal electrocardiographic manifestations: a report of seven cases. J Electrocardiol 1999;32(1):45-9. |
|8.||Hylander B. Survival of extreme hyper-kalemia. Acta Med Scand 1987;221(1): 121-3. |
P L Gautam
50-G, Kitchlu Nagar, Ludhiana - 141001, Punjab