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Renal failure in a patient with postpolio syndrome and a normal creatinine level
American Journal of Emergency Medicine (2012) 30, 247.e1–247.e3
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Case Report Renal failure in a patient with postpolio syndrome and a normal creatinine level Abstract Patients with renal failure who are taking trimethoprim have an increased risk of developing hyperkalemia, which can cause muscle weakness. In patients with postpolio syndrome, a normal creatinine level could be abnormally high, renal failure is possible because of lack of creatinine production, and the muscle weakness from resultant hyperkalemia could be more severe because of their underlying condition. This abnormally high creatinine level has been termed from this point relative renal failure. The objective of the study was to review a case in which relative renal failure and hyperkalemia caused muscle weakness that manifested as shortness of breath and confusion with electrocardiographic changes. A dehydrated patient with relative renal failure and postpolio syndrome had taken trimethoprim-sulfamethoxazole that caused symptomatic hyperkalemia. The patient presented with muscle weakness, shortness of breath, and confusion, with her postpolio syndrome compounding the situation and likely making the muscle weakness more severe. A patient on trimethoprim with renal failure is at an increased risk of developing hyperkalemia. Patients with postpolio syndrome could have severe muscle weakness from the hyperkalemia and could have renal failure even with a normal creatinine level. This case report will remind treating physicians to evaluate such patients for hyperkalemia if they present with muscle weakness, especially if the patient has renal failure and is on trimethoprim. Postpolio syndrome is a residual denervation of motor neurons caused by the polio virus. Polio virus enters the body through the gastrointestinal tract and travels to the bloodstream where it concentrates at the motor end-plates of nerves. The virus then travels retrograde up the motor neuron and enters the central nervous system, causing damage to the nerve cell. A period of denervation and reinnervation occurs; and eventually, there is an inability to compensate for the lost neurons, leading to chronic muscular weakness or atrophy [1]. Trimethoprim/sulfamethoxazole (TMP/SMX) work synergistically to treat urinary tract infections (UTIs) [2]. Trimeth0735-6757/$ – see front matter © 2012 Elsevier Inc. All rights reserved.
oprim is known to cause hyperkalemia in patients with renal insufficiency [3]. It is hypothesized that TMP blocks the amiloride-sensitive sodium channels in the distal nephrons, thereby causing hyperkalemia and occasionally hyponatremia. We discuss a patient with a history of postpolio syndrome and a subacute UTI who presented with renal failure secondary to dehydration and therefore TMP-induced hyperkalemia with a normal serum creatinine level. This patient is an 80-year-old woman with a medical history of postpolio syndrome with muscular atrophy, hypertension, diabetes, hypoparathyroidism, polyneuropathy, and prior UTI who presented to the emergency department with weakness, shortness of breath, and confusion. The patient had recently been diagnosed with a UTI and placed on TMP/SMX. She was also taking lisinopril, amlodipine besylate, latanoprost ophthalmic drops, and dorzolamide/timolol ophthalmic drops. Physical examination showed an elderly, obese, somnolent woman in no acute distress. The result of head/ears/eyes/ nose/throat examination was within normal limits (WNL). Cardiovascular examination revealed an irregularly irregular heartbeat, a well-healed pacemaker scar over her left chest, no murmurs/rubs/gallops, and no evidence of jugular venous distension. The patient had bilateral breath sounds with decreased air movement. The result of her abdominal examination was WNL. She had motor strength of 1/5 in bilateral lower extremities extending to the hips and 1/5 motor strength in the right upper extremity. The patient was unable to move the left upper extremity except for a slight flexor action of the wrist. Marked QRS widening (QRS = 0.206 seconds) was noted on the patient's electrocardiogram (EKG) in Fig. 1. The patient's laboratory values were as follows: sodium, 144 mM/L; potassium, 9.2 mM/L (range, 3.5-5.0); chloride, 116 mM/L (range, 100-112); bicarbonate, 21 mM/L (range, 24-32), blood urea nitrogen level, 51 mg/dL (range, 8-22); creatinine, 0.8 mg/dL (range, 0.7-1.3), with a baseline creatinine of 0.3 mg/dL 7 months before this hospitalization; glucose, 113 mg/dL; white blood cell count, 3.8; hemoglobin, 12.9 g/dL; platelets, 198; and lactate, 0.7 mM/L. The results of cardiac enzymes, urinalysis, and blood cultures were all WNL. The patient was treated for hyperkalemia with calcium gluconate, nebulized albuterol, glucose, insulin, and sodium polystyrene (Kayexalate). After treatment, the patient's
247.e2
Case Report
Fig. 1
The initial EKG before treatment with peaked T waves and widened QRS interval.
repeated EKG showed narrow QRS complexes (QRS = 0.159 seconds) in Fig. 2. Her motor strength, shortness of breath, confusion, and somnolence all improved. Repeated potassium was 8.7 mM/L (3 hours after triage), 6.6 mM/L (6.5 hours after triage), and 4.5 mM/L (12 hours after triage). Trimethoprim/sulfamethoxazole was discontinued, and the patient's potassium level during her hospital stay continued to be WNL without further treatments. This is the first reported case of a patient with postpolio syndrome who presented with a normal creatinine level in renal failure due to dehydration, and hyperkalemia likely secondary to TMP. As noted above, the patient's baseline
Fig. 2
creatinine was 0.3 mg/dL; and therefore, a rise 3-fold from her baseline level upon emergency department presentation led to a diagnosis of renal failure, with resultant hyperkalemia that was potentially life threatening. The patient's weakness was unlikely to be from postpolio muscle weakness because of short onset of muscle weakness and improvement with electrolyte normalization [4]. In a study by Mori et al [5], it was shown that potassium levels tend to increase in patients with renal dysfunction (measured by creatinine) while taking TMP. The incidence of hyperkalemia was shown to be 85.7% in the population with renal dysfunction and 17.5% in the population without
After treatment of hyperkalemia with narrowed QRS intervals and improved T waves.
Case Report renal impairment. There was no association found between age or sex and TMP-induced hyperkalemia. In a prospective chart review study by Alappan and colleagues [6], there was no significant correlation between diabetes and the incidence or severity of TMP-induced hyperkalemia. It is possible that our patient's postpolio syndrome with resultant muscle atrophy placed her at a risk for dehydration, thus causing relative renal failure. In turn, TMP-induced hyperkalemia from her renal failure may have worsened her condition. The patient's shortness of breath may have been due to diaphragmatic muscle weakness [1]. This is supported by improvement in her muscle weakness and shortness of breath once her potassium was lowered to 5.5 mM/L. This case suggests that in patients with postpolio syndrome and resultant low baseline creatinine levels, it may be advisable to evaluate for relative acute renal failure and hyperkalemia, especially when the patient is prescribed TMP.
Acknowledgment We thank Cynthia JT Clendenin, Medical Editor for Academic Affairs and Research, for her assistance with our manuscript.
247.e3 Melissa K. Leming MD Michael J. Breyer MD Department of Emergency Medicine Christiana Care Health System Newark, DE 19718, USA E-mail address: [email protected] doi:10.1016/j.ajem.2010.07.026
References [1] Thorsteinsson G. Management of postpolio syndrome. Mayo Clin Proc 1997;72:627-38. [2] Levine BJ, editor. Genitourinary: 2009 EMRA antibiotic guide. Texas: Irving; 2009. p. 45. [3] Velazquez H, Perazella MA, Wright FS, et al. Renal mechanism of trimethoprim-induced hyperkalemia. Ann Intern Med 1993;119: 296-301. [4] Jubelt BA, James C. Characteristics and management of postpolio syndrome. JAMA 2000;284:412-4. [5] Mori H, Kuroda Y, Imamura S, et al. Hyponatremia and/or hyperkalemia in patients treated with the standard dose of trimethoprimsulfamethoxazole. Intern Med 2003;42:665-9. [6] Alappan RP, Mark A, Buller GK. Hyperkalemia in hospitalized patients treated with trimethoprim-sulfamethoxazole. Ann Intern Med 1996;124: 316-20.
www.elsevier.com/locate/ajem
Case Report Renal failure in a patient with postpolio syndrome and a normal creatinine level Abstract Patients with renal failure who are taking trimethoprim have an increased risk of developing hyperkalemia, which can cause muscle weakness. In patients with postpolio syndrome, a normal creatinine level could be abnormally high, renal failure is possible because of lack of creatinine production, and the muscle weakness from resultant hyperkalemia could be more severe because of their underlying condition. This abnormally high creatinine level has been termed from this point relative renal failure. The objective of the study was to review a case in which relative renal failure and hyperkalemia caused muscle weakness that manifested as shortness of breath and confusion with electrocardiographic changes. A dehydrated patient with relative renal failure and postpolio syndrome had taken trimethoprim-sulfamethoxazole that caused symptomatic hyperkalemia. The patient presented with muscle weakness, shortness of breath, and confusion, with her postpolio syndrome compounding the situation and likely making the muscle weakness more severe. A patient on trimethoprim with renal failure is at an increased risk of developing hyperkalemia. Patients with postpolio syndrome could have severe muscle weakness from the hyperkalemia and could have renal failure even with a normal creatinine level. This case report will remind treating physicians to evaluate such patients for hyperkalemia if they present with muscle weakness, especially if the patient has renal failure and is on trimethoprim. Postpolio syndrome is a residual denervation of motor neurons caused by the polio virus. Polio virus enters the body through the gastrointestinal tract and travels to the bloodstream where it concentrates at the motor end-plates of nerves. The virus then travels retrograde up the motor neuron and enters the central nervous system, causing damage to the nerve cell. A period of denervation and reinnervation occurs; and eventually, there is an inability to compensate for the lost neurons, leading to chronic muscular weakness or atrophy [1]. Trimethoprim/sulfamethoxazole (TMP/SMX) work synergistically to treat urinary tract infections (UTIs) [2]. Trimeth0735-6757/$ – see front matter © 2012 Elsevier Inc. All rights reserved.
oprim is known to cause hyperkalemia in patients with renal insufficiency [3]. It is hypothesized that TMP blocks the amiloride-sensitive sodium channels in the distal nephrons, thereby causing hyperkalemia and occasionally hyponatremia. We discuss a patient with a history of postpolio syndrome and a subacute UTI who presented with renal failure secondary to dehydration and therefore TMP-induced hyperkalemia with a normal serum creatinine level. This patient is an 80-year-old woman with a medical history of postpolio syndrome with muscular atrophy, hypertension, diabetes, hypoparathyroidism, polyneuropathy, and prior UTI who presented to the emergency department with weakness, shortness of breath, and confusion. The patient had recently been diagnosed with a UTI and placed on TMP/SMX. She was also taking lisinopril, amlodipine besylate, latanoprost ophthalmic drops, and dorzolamide/timolol ophthalmic drops. Physical examination showed an elderly, obese, somnolent woman in no acute distress. The result of head/ears/eyes/ nose/throat examination was within normal limits (WNL). Cardiovascular examination revealed an irregularly irregular heartbeat, a well-healed pacemaker scar over her left chest, no murmurs/rubs/gallops, and no evidence of jugular venous distension. The patient had bilateral breath sounds with decreased air movement. The result of her abdominal examination was WNL. She had motor strength of 1/5 in bilateral lower extremities extending to the hips and 1/5 motor strength in the right upper extremity. The patient was unable to move the left upper extremity except for a slight flexor action of the wrist. Marked QRS widening (QRS = 0.206 seconds) was noted on the patient's electrocardiogram (EKG) in Fig. 1. The patient's laboratory values were as follows: sodium, 144 mM/L; potassium, 9.2 mM/L (range, 3.5-5.0); chloride, 116 mM/L (range, 100-112); bicarbonate, 21 mM/L (range, 24-32), blood urea nitrogen level, 51 mg/dL (range, 8-22); creatinine, 0.8 mg/dL (range, 0.7-1.3), with a baseline creatinine of 0.3 mg/dL 7 months before this hospitalization; glucose, 113 mg/dL; white blood cell count, 3.8; hemoglobin, 12.9 g/dL; platelets, 198; and lactate, 0.7 mM/L. The results of cardiac enzymes, urinalysis, and blood cultures were all WNL. The patient was treated for hyperkalemia with calcium gluconate, nebulized albuterol, glucose, insulin, and sodium polystyrene (Kayexalate). After treatment, the patient's
247.e2
Case Report
Fig. 1
The initial EKG before treatment with peaked T waves and widened QRS interval.
repeated EKG showed narrow QRS complexes (QRS = 0.159 seconds) in Fig. 2. Her motor strength, shortness of breath, confusion, and somnolence all improved. Repeated potassium was 8.7 mM/L (3 hours after triage), 6.6 mM/L (6.5 hours after triage), and 4.5 mM/L (12 hours after triage). Trimethoprim/sulfamethoxazole was discontinued, and the patient's potassium level during her hospital stay continued to be WNL without further treatments. This is the first reported case of a patient with postpolio syndrome who presented with a normal creatinine level in renal failure due to dehydration, and hyperkalemia likely secondary to TMP. As noted above, the patient's baseline
Fig. 2
creatinine was 0.3 mg/dL; and therefore, a rise 3-fold from her baseline level upon emergency department presentation led to a diagnosis of renal failure, with resultant hyperkalemia that was potentially life threatening. The patient's weakness was unlikely to be from postpolio muscle weakness because of short onset of muscle weakness and improvement with electrolyte normalization [4]. In a study by Mori et al [5], it was shown that potassium levels tend to increase in patients with renal dysfunction (measured by creatinine) while taking TMP. The incidence of hyperkalemia was shown to be 85.7% in the population with renal dysfunction and 17.5% in the population without
After treatment of hyperkalemia with narrowed QRS intervals and improved T waves.
Case Report renal impairment. There was no association found between age or sex and TMP-induced hyperkalemia. In a prospective chart review study by Alappan and colleagues [6], there was no significant correlation between diabetes and the incidence or severity of TMP-induced hyperkalemia. It is possible that our patient's postpolio syndrome with resultant muscle atrophy placed her at a risk for dehydration, thus causing relative renal failure. In turn, TMP-induced hyperkalemia from her renal failure may have worsened her condition. The patient's shortness of breath may have been due to diaphragmatic muscle weakness [1]. This is supported by improvement in her muscle weakness and shortness of breath once her potassium was lowered to 5.5 mM/L. This case suggests that in patients with postpolio syndrome and resultant low baseline creatinine levels, it may be advisable to evaluate for relative acute renal failure and hyperkalemia, especially when the patient is prescribed TMP.
Acknowledgment We thank Cynthia JT Clendenin, Medical Editor for Academic Affairs and Research, for her assistance with our manuscript.
247.e3 Melissa K. Leming MD Michael J. Breyer MD Department of Emergency Medicine Christiana Care Health System Newark, DE 19718, USA E-mail address: [email protected] doi:10.1016/j.ajem.2010.07.026
References [1] Thorsteinsson G. Management of postpolio syndrome. Mayo Clin Proc 1997;72:627-38. [2] Levine BJ, editor. Genitourinary: 2009 EMRA antibiotic guide. Texas: Irving; 2009. p. 45. [3] Velazquez H, Perazella MA, Wright FS, et al. Renal mechanism of trimethoprim-induced hyperkalemia. Ann Intern Med 1993;119: 296-301. [4] Jubelt BA, James C. Characteristics and management of postpolio syndrome. JAMA 2000;284:412-4. [5] Mori H, Kuroda Y, Imamura S, et al. Hyponatremia and/or hyperkalemia in patients treated with the standard dose of trimethoprimsulfamethoxazole. Intern Med 2003;42:665-9. [6] Alappan RP, Mark A, Buller GK. Hyperkalemia in hospitalized patients treated with trimethoprim-sulfamethoxazole. Ann Intern Med 1996;124: 316-20.