Journal of Clinical Anesthesia (2012) xx, xxx–xxx
Correspondence
Intraoperative hyperkalemia induced by administration of trimethoprim-sulfamethoxazole in a patient receiving angiotensin receptor blockers To the Editor: Perioperative hyperkalemia is occasionally a lifethreatening condition due to its effect on cardiac conductivity. Hyperkalemic events during surgery should be detected as soon as possible by closely monitoring the electrocardiogram (ECG) and potassium concentration, if needed. A 76 year old woman was scheduled to undergo tympanomastoidectomy for chronic otitis media. She had been taking an angiotensin receptor blocker (ARB) and aspirin for 6 months since being diagnosed with hypertension. She had also been prescribed trimethoprim-sulfamethoxazole as a perioperative antibiotic for two weeks. A recent preoperative blood test was performed two weeks before surgery and showed no notable findings, including potassium level. Electrocardiogram was normal and showed only sinus tachycardia, while chest radiography was unremarkable. In the operating room, her initial vital signs were stable with normal sinus rhythm. Anesthesia was induced with intravenous (IV) administration of 0.2 mg of glycopyrrolate, 80 mg of propofol, and 50 mg of rocuronium. Endotracheal intubation was achieved shortly after mask ventilation. During the operation, 4% to 6% of desflurane was administered in a 50:50 air/oxygen mixture. Remifentanil was continuously infused at 0.4 1 μg/kg/min intravenously. Electrocardiogram, noninvasive blood pressure (BP), heart rate, peripheral oxygen saturation, capnogram, and body temperature were monitored during surgery. After anesthesia was induced, the patient’s BP fluctuated significantly from 81/46 mmHg to 155/99 mmHg. For arterial blood gas (ABG) analysis and continuous monitoring of BP, a 20-gauge catheter was inserted into the left dorsalis pedis artery. Small doses of esmolol or ephedrine were used to control BP. About one hour after induction, ECG suddenly changed (QRS widening with tall T waves) and fluctuations in BP became worse. An ABG showed pH 7.315, PaCO2 0952-8180/© 2014 Elsevier Inc. All rights reserved.
36.3 mmHg, PaO2 208.2 mmHg, base excess − 7.4 mEq/L, potassium 6.99 mEq/L, and calcium 1.11 mEq/L at FIO2 of 0.5. First, 600 mg of IV calcium chloride was injected to stabilize the heart from the effects of potassium. Dextrose and regular insulin were loaded by 200 mL (1000 mL of 10% dextrose mixed with 20 units of regular insulin) and continually infused at a rate of 100 mL/hr along with the injection of 50 mEq of sodium bicarbonate. After about 30 minutes, the potassium level was 6.54 mEq/L and ECG remained unchanged. Then 20 mg of IV furosemide was injected. At the end of surgery, the patient started spontaneous respiration with glycopyrrolate 0.4 mg and pyridostigmine 15 mg. She was subsequently extubated and transferred to a Postanesthesia Care Unit. In the recovery room, her potassium level normalized and tall T waves on ECG resolved. The patient was discharged from the hospital roughly one week after the operation. Hyperkalemia is a potentially life-threatening condition during surgery and is one of the main causes that extend hospitalization. Serum potassium homeostasis is comprised of two mechanisms. First, potassium excretion out of the body is regulated primarily by the kidney and to a lesser extent by intestinal excretion. Second, the potassium equilibrium between extracellular and intracellular compartments is affected by the sympathetic system and insulin secretion [1]. Perioperative hyperkalemia is caused by migration of intracellular potassium ions into plasma, decreased renal function, or increased potassium intake [2]. Patients with renal insufficiency commonly experience hyperkalemia. In individuals with normal renal function, hyperkalemia rarely occurs and is easily missed. The present patient had no medical history significant for renal dysfunction. She was receiving ARBs as an antihypertensive drug. Drugs such as cyclooxygenase inhibitors, angiotensin-converting enzyme inhibitors (ACEIs), and ARBs interfere with the renin-aldosterone system to potentially cause hyperkalemia [3]. In addition, trimethoprim structurally resembles the potassium-sparing diuretic amiloride and impairs renal potassium excretion [4]. Administration of trimethoprim-sulfamethoxazole to elderly patients receiving therapy with either ACEIs or
2
Correspondence
ARBs was strongly associated with hyperkalemia-related hospitalization in a population-based study [5]. Furthermore, the patient was in a slightly dehydrated condition due to fasting before the surgery. Dehydration may aggravate hyperkalemia with drugs that reduce potassium excretion. In conclusion, an intraoperative hyperkalemic episode associated with trimethoprim-sulfamethoxazole therapy coprescribed with an ARB is presented. Anesthesiologists should carefully monitor ECG and potassium levels while evaluating the effective circulatory volume during surgery when patients are treated with medications that impair potassium excretion. Sang-Wook Lee MD (Resident) Sung-Wook Park MD, PhD (Assistant Professor of Anesthesia) Department of Anesthesia and Pain Medicine Kyung Hee University Hospital Kyung Hee University Seoul, 130–701, Korea
Jong-Man Kang MD, PhD (Associate Professor of Anesthesia) Department of Anesthesiology and Pain Medicine Kyung Hee University Hospital at Gangdong Kyung Hee University Seoul, 134–090, Korea E-mail address: [email protected] http://dx.doi.org/10.1016/j.jclinane.2014.03.003
References [1] Ahmed J, Weisberg LS. Hyperkalemia in dialysis patients. Semin Dial 2001;14:348-56. [2] Alfonzo AV, Isles C, Geddes C, Deighan C. Potassium disorders–clinical spectrum and emergency management. Resuscitation 2006;70:10-25. [3] Halperin ML, Kamel KS. Potassium. Lancet 1998;352(9122):135-40. [4] Eiam-Ong S, Kurtzman NA, Sabatini S. Studies on the mechanism of trimethoprim-induced hyperkalemia. Kidney Int 1996;49:1372-8. [5] Antoniou T, Gomes T, Juurlink DN, Loutfy MR, Glazier RH, Mamdani MM. Trimethoprim-sulfamethoxazole-induced hyperkalemia in patients receiving inhibitors of the renin-angiotensin system: a population-based study. Arch Intern Med 2010;170:1045-9.
Correspondence
Intraoperative hyperkalemia induced by administration of trimethoprim-sulfamethoxazole in a patient receiving angiotensin receptor blockers To the Editor: Perioperative hyperkalemia is occasionally a lifethreatening condition due to its effect on cardiac conductivity. Hyperkalemic events during surgery should be detected as soon as possible by closely monitoring the electrocardiogram (ECG) and potassium concentration, if needed. A 76 year old woman was scheduled to undergo tympanomastoidectomy for chronic otitis media. She had been taking an angiotensin receptor blocker (ARB) and aspirin for 6 months since being diagnosed with hypertension. She had also been prescribed trimethoprim-sulfamethoxazole as a perioperative antibiotic for two weeks. A recent preoperative blood test was performed two weeks before surgery and showed no notable findings, including potassium level. Electrocardiogram was normal and showed only sinus tachycardia, while chest radiography was unremarkable. In the operating room, her initial vital signs were stable with normal sinus rhythm. Anesthesia was induced with intravenous (IV) administration of 0.2 mg of glycopyrrolate, 80 mg of propofol, and 50 mg of rocuronium. Endotracheal intubation was achieved shortly after mask ventilation. During the operation, 4% to 6% of desflurane was administered in a 50:50 air/oxygen mixture. Remifentanil was continuously infused at 0.4 1 μg/kg/min intravenously. Electrocardiogram, noninvasive blood pressure (BP), heart rate, peripheral oxygen saturation, capnogram, and body temperature were monitored during surgery. After anesthesia was induced, the patient’s BP fluctuated significantly from 81/46 mmHg to 155/99 mmHg. For arterial blood gas (ABG) analysis and continuous monitoring of BP, a 20-gauge catheter was inserted into the left dorsalis pedis artery. Small doses of esmolol or ephedrine were used to control BP. About one hour after induction, ECG suddenly changed (QRS widening with tall T waves) and fluctuations in BP became worse. An ABG showed pH 7.315, PaCO2 0952-8180/© 2014 Elsevier Inc. All rights reserved.
36.3 mmHg, PaO2 208.2 mmHg, base excess − 7.4 mEq/L, potassium 6.99 mEq/L, and calcium 1.11 mEq/L at FIO2 of 0.5. First, 600 mg of IV calcium chloride was injected to stabilize the heart from the effects of potassium. Dextrose and regular insulin were loaded by 200 mL (1000 mL of 10% dextrose mixed with 20 units of regular insulin) and continually infused at a rate of 100 mL/hr along with the injection of 50 mEq of sodium bicarbonate. After about 30 minutes, the potassium level was 6.54 mEq/L and ECG remained unchanged. Then 20 mg of IV furosemide was injected. At the end of surgery, the patient started spontaneous respiration with glycopyrrolate 0.4 mg and pyridostigmine 15 mg. She was subsequently extubated and transferred to a Postanesthesia Care Unit. In the recovery room, her potassium level normalized and tall T waves on ECG resolved. The patient was discharged from the hospital roughly one week after the operation. Hyperkalemia is a potentially life-threatening condition during surgery and is one of the main causes that extend hospitalization. Serum potassium homeostasis is comprised of two mechanisms. First, potassium excretion out of the body is regulated primarily by the kidney and to a lesser extent by intestinal excretion. Second, the potassium equilibrium between extracellular and intracellular compartments is affected by the sympathetic system and insulin secretion [1]. Perioperative hyperkalemia is caused by migration of intracellular potassium ions into plasma, decreased renal function, or increased potassium intake [2]. Patients with renal insufficiency commonly experience hyperkalemia. In individuals with normal renal function, hyperkalemia rarely occurs and is easily missed. The present patient had no medical history significant for renal dysfunction. She was receiving ARBs as an antihypertensive drug. Drugs such as cyclooxygenase inhibitors, angiotensin-converting enzyme inhibitors (ACEIs), and ARBs interfere with the renin-aldosterone system to potentially cause hyperkalemia [3]. In addition, trimethoprim structurally resembles the potassium-sparing diuretic amiloride and impairs renal potassium excretion [4]. Administration of trimethoprim-sulfamethoxazole to elderly patients receiving therapy with either ACEIs or
2
Correspondence
ARBs was strongly associated with hyperkalemia-related hospitalization in a population-based study [5]. Furthermore, the patient was in a slightly dehydrated condition due to fasting before the surgery. Dehydration may aggravate hyperkalemia with drugs that reduce potassium excretion. In conclusion, an intraoperative hyperkalemic episode associated with trimethoprim-sulfamethoxazole therapy coprescribed with an ARB is presented. Anesthesiologists should carefully monitor ECG and potassium levels while evaluating the effective circulatory volume during surgery when patients are treated with medications that impair potassium excretion. Sang-Wook Lee MD (Resident) Sung-Wook Park MD, PhD (Assistant Professor of Anesthesia) Department of Anesthesia and Pain Medicine Kyung Hee University Hospital Kyung Hee University Seoul, 130–701, Korea
Jong-Man Kang MD, PhD (Associate Professor of Anesthesia) Department of Anesthesiology and Pain Medicine Kyung Hee University Hospital at Gangdong Kyung Hee University Seoul, 134–090, Korea E-mail address: [email protected] http://dx.doi.org/10.1016/j.jclinane.2014.03.003
References [1] Ahmed J, Weisberg LS. Hyperkalemia in dialysis patients. Semin Dial 2001;14:348-56. [2] Alfonzo AV, Isles C, Geddes C, Deighan C. Potassium disorders–clinical spectrum and emergency management. Resuscitation 2006;70:10-25. [3] Halperin ML, Kamel KS. Potassium. Lancet 1998;352(9122):135-40. [4] Eiam-Ong S, Kurtzman NA, Sabatini S. Studies on the mechanism of trimethoprim-induced hyperkalemia. Kidney Int 1996;49:1372-8. [5] Antoniou T, Gomes T, Juurlink DN, Loutfy MR, Glazier RH, Mamdani MM. Trimethoprim-sulfamethoxazole-induced hyperkalemia in patients receiving inhibitors of the renin-angiotensin system: a population-based study. Arch Intern Med 2010;170:1045-9.
![[Intraoperative anaphylaxis due to beta-lactams in a hypertensive patient on angiotensin ii receptor antagonists and beta-blockers].](/assets/img/hold.png)
