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Acute Paralysis in a Uremic Patient
CLINICAL COMMUNICATION TO THE EDITOR
Acute Paralysis in a Uremic Patient To the Editor: Acute paralysis is a rare but critical presentation of hyperkalemia, reflecting extremely high serum potassium concentration and necessitating prompt treatment.
CASE REPORT The patient was a 53-year-old Chinese man with a medical history of end-stage renal disease and regular hemodialysis who presented with muscular weakness progressing to paralysis of both lower limbs for 6 hours. On admission, he was alert and fully oriented. Neurologic examination of both lower limbs revealed a muscle strength of grade 1/5 and hyporeflexia. In the upper limbs, the muscle strength was grade 4/5, and the reflexes were normal. Sensory and cranial nerve function were intact. An electrocardiogram (ECG) showed T-wave elevation, PR-interval prolongation, and QRS-complex widening (Figure 1). Laboratory tests revealed a markedly elevated serum potassium level of 7.5 mmol/L (not hemolyzed). Other laboratory test results were as follows: blood urea nitrogen 92 mg/dL, serum creatinine 10.1 mg/dL, sodium 135 mmol/L, chloride 102 mmol/L, total calcium 2.7 mmol/L, and creatinine phosphokinase 50 IU/L. Emergency hemodialysis rapidly normalized serum potassium and dramatically reversed all neuromuscular symptoms within 4 hours, without any sequelae. A repeat ECG showed normalized PR, QRS interval, and T wave compared with the initial ECG (Figure 2). The patient was discharged after hemodialysis with repeated exhortations to avoid a high potassium diet.
DISCUSSION Hyperkalemia, also called the “silent killer,” is usually asymptomatic even at fatal levels.1 The symptoms of hyperkalemia are essentially limited to muscle weakness and Funding: None. Conflict of Interest: None of the authors have any conflicts of interest associated with the work presented in this manuscript. Authorship: All authors had access to the data and played a role in writing this manuscript. All authors meet the criteria for authorship, including acceptance of responsibility for the scientific content of the article. Requests for reprints should be addressed to Chia-Chao Wu, MD, PhD, Division of Nephrology, Department of Medicine, Tri-Service General Hospital, Number 325, Section 2, Cheng-Kung Road, Neihu 114, Taipei, Taiwan. E-mail address: [email protected]
Figure 1 Initial ECG showing sinus rhythm with prolonged PR interval, tall T wave, and widening of the QRS complex.
abnormal cardiac conduction, which can lead to potentially fatal dysrhythmia. Cardiac toxicity typically precedes neuromuscular manifestations. Despite marked hyperkalemia, this uremic patient did not report any cardiac symptoms. Several mechanisms were proposed to explain why cardiac manifestations are less intense in uremic patients. First, the myocardial cells of patients with chronic renal failure seem to tolerate higher levels of serum potassium without ECG changes.2 Second, hypercalcemia, which is frequently found in uremic patients, may stabilize the myocardium and counteract the hyperkalemic cardiotoxicity.2,3 Uremic patients are particularly susceptible to hyperkalemia2 because of predialytic metabolic acidosis, impaired cellular potassium uptake, and defective urinary potassium excretion.2,4 Any additional potassium input would result in a large increase in the serum potassium concentration. In any given month, 5% to 10% of uremic patients have varying degrees of hyperkalemia.3 The ECG findings of hyperkalemia may be less prominent in uremic patients,2 which may result in postponement of treatment and a disastrous outcome if hyperkalemia is not recognized. Mortality due to hyperkalemia has been estimated at 3.1 per 1000 patientyears for uremic patients.3 The muscular weakness was the sole symptom of lifethreatening hyperkalemia in this patient. Less commonly, severe hyperkalemia may affect the skeletal muscles profoundly. Neuromuscular manifestations vary from paresthesia, mild motor weakness, paraparesis, ascending paraplegia, to tetraplegia. The paralysis usually starts distally with an ascending course and often mimics Guillain–Barré syn-
0002-9343/$ -see front matter Crown Copyright © 2010 Published by Elsevier Inc. All rights reserved.
e8
The American Journal of Medicine, Vol 123, No 6, June 2010
CONCLUSIONS Hyperkalemic paralysis should be kept in mind in the differential diagnosis of acute paralysis. Early recognition with prompt treatment not only completely reverses paralysis but also prevents fatal complications of hyperkalemia. Chih-Chiang Wang, MDa,b Chia-Chao Wu, MD, PhDa Jeng-Chuan Shiang, MDb Ming-Kai Tsai, MDb I-Hung Chen, MDb a
Figure 2 Post-treatment ECG showing normal sinus rhythm and normalized PR, QRS interval, and T wave.
Division of Nephrology, Department of Internal Medicine Tri-Service General Hospital Taipei, Taiwan, ROC b Division of Nephrology, Department of Internal Medicine Kaohsiung Armed Forces General hospital Kaohsiung, Taiwan, ROC
doi:10.1016/j.amjmed.2009.10.008
References drome. The diaphragm, cranial nerves, and sensory function are usually unaffected.3 Muscular weakness typically develops when the plasma potassium concentration exceeds 7 meq/L.5 Therefore, hyperkalemic paralysis reflects a lifethreatening condition that necessitates early recognition. Before starting time-consuming examinations, ECG findings should be promptly checked in patients with acute paralysis to recognize not only hyperkalemia but also hypokalemia.
1. Weiner ID, Wingo CS. Hyperkalemia: a potential silent killer. J Am Soc Nephrol. 1998;9:1535-1543. 2. Ahmed J, Weisberg LS. Hyperkalemia in dialysis patients. Semin Dial. 2001;14:348-356. 3. Putcha N, Allon M. Management of hyperkalemia in dialysis patients. Semin Dial. 2007;20:431-439. 4. Knoll GA, Sahgal A, Nair RC, et al. Renin-angiotensin system blockade and the risk of hyperkalemia in chronic hemodialysis patients. Am J Med. 2002;112:110-114. 5. Evers S, Engelien A, Karsch V, et al. Secondary hyperkalaemic paralysis. J Neurol Neurosurg Psychiatry. 1998;64:249-252.
Acute Paralysis in a Uremic Patient To the Editor: Acute paralysis is a rare but critical presentation of hyperkalemia, reflecting extremely high serum potassium concentration and necessitating prompt treatment.
CASE REPORT The patient was a 53-year-old Chinese man with a medical history of end-stage renal disease and regular hemodialysis who presented with muscular weakness progressing to paralysis of both lower limbs for 6 hours. On admission, he was alert and fully oriented. Neurologic examination of both lower limbs revealed a muscle strength of grade 1/5 and hyporeflexia. In the upper limbs, the muscle strength was grade 4/5, and the reflexes were normal. Sensory and cranial nerve function were intact. An electrocardiogram (ECG) showed T-wave elevation, PR-interval prolongation, and QRS-complex widening (Figure 1). Laboratory tests revealed a markedly elevated serum potassium level of 7.5 mmol/L (not hemolyzed). Other laboratory test results were as follows: blood urea nitrogen 92 mg/dL, serum creatinine 10.1 mg/dL, sodium 135 mmol/L, chloride 102 mmol/L, total calcium 2.7 mmol/L, and creatinine phosphokinase 50 IU/L. Emergency hemodialysis rapidly normalized serum potassium and dramatically reversed all neuromuscular symptoms within 4 hours, without any sequelae. A repeat ECG showed normalized PR, QRS interval, and T wave compared with the initial ECG (Figure 2). The patient was discharged after hemodialysis with repeated exhortations to avoid a high potassium diet.
DISCUSSION Hyperkalemia, also called the “silent killer,” is usually asymptomatic even at fatal levels.1 The symptoms of hyperkalemia are essentially limited to muscle weakness and Funding: None. Conflict of Interest: None of the authors have any conflicts of interest associated with the work presented in this manuscript. Authorship: All authors had access to the data and played a role in writing this manuscript. All authors meet the criteria for authorship, including acceptance of responsibility for the scientific content of the article. Requests for reprints should be addressed to Chia-Chao Wu, MD, PhD, Division of Nephrology, Department of Medicine, Tri-Service General Hospital, Number 325, Section 2, Cheng-Kung Road, Neihu 114, Taipei, Taiwan. E-mail address: [email protected]
Figure 1 Initial ECG showing sinus rhythm with prolonged PR interval, tall T wave, and widening of the QRS complex.
abnormal cardiac conduction, which can lead to potentially fatal dysrhythmia. Cardiac toxicity typically precedes neuromuscular manifestations. Despite marked hyperkalemia, this uremic patient did not report any cardiac symptoms. Several mechanisms were proposed to explain why cardiac manifestations are less intense in uremic patients. First, the myocardial cells of patients with chronic renal failure seem to tolerate higher levels of serum potassium without ECG changes.2 Second, hypercalcemia, which is frequently found in uremic patients, may stabilize the myocardium and counteract the hyperkalemic cardiotoxicity.2,3 Uremic patients are particularly susceptible to hyperkalemia2 because of predialytic metabolic acidosis, impaired cellular potassium uptake, and defective urinary potassium excretion.2,4 Any additional potassium input would result in a large increase in the serum potassium concentration. In any given month, 5% to 10% of uremic patients have varying degrees of hyperkalemia.3 The ECG findings of hyperkalemia may be less prominent in uremic patients,2 which may result in postponement of treatment and a disastrous outcome if hyperkalemia is not recognized. Mortality due to hyperkalemia has been estimated at 3.1 per 1000 patientyears for uremic patients.3 The muscular weakness was the sole symptom of lifethreatening hyperkalemia in this patient. Less commonly, severe hyperkalemia may affect the skeletal muscles profoundly. Neuromuscular manifestations vary from paresthesia, mild motor weakness, paraparesis, ascending paraplegia, to tetraplegia. The paralysis usually starts distally with an ascending course and often mimics Guillain–Barré syn-
0002-9343/$ -see front matter Crown Copyright © 2010 Published by Elsevier Inc. All rights reserved.
e8
The American Journal of Medicine, Vol 123, No 6, June 2010
CONCLUSIONS Hyperkalemic paralysis should be kept in mind in the differential diagnosis of acute paralysis. Early recognition with prompt treatment not only completely reverses paralysis but also prevents fatal complications of hyperkalemia. Chih-Chiang Wang, MDa,b Chia-Chao Wu, MD, PhDa Jeng-Chuan Shiang, MDb Ming-Kai Tsai, MDb I-Hung Chen, MDb a
Figure 2 Post-treatment ECG showing normal sinus rhythm and normalized PR, QRS interval, and T wave.
Division of Nephrology, Department of Internal Medicine Tri-Service General Hospital Taipei, Taiwan, ROC b Division of Nephrology, Department of Internal Medicine Kaohsiung Armed Forces General hospital Kaohsiung, Taiwan, ROC
doi:10.1016/j.amjmed.2009.10.008
References drome. The diaphragm, cranial nerves, and sensory function are usually unaffected.3 Muscular weakness typically develops when the plasma potassium concentration exceeds 7 meq/L.5 Therefore, hyperkalemic paralysis reflects a lifethreatening condition that necessitates early recognition. Before starting time-consuming examinations, ECG findings should be promptly checked in patients with acute paralysis to recognize not only hyperkalemia but also hypokalemia.
1. Weiner ID, Wingo CS. Hyperkalemia: a potential silent killer. J Am Soc Nephrol. 1998;9:1535-1543. 2. Ahmed J, Weisberg LS. Hyperkalemia in dialysis patients. Semin Dial. 2001;14:348-356. 3. Putcha N, Allon M. Management of hyperkalemia in dialysis patients. Semin Dial. 2007;20:431-439. 4. Knoll GA, Sahgal A, Nair RC, et al. Renin-angiotensin system blockade and the risk of hyperkalemia in chronic hemodialysis patients. Am J Med. 2002;112:110-114. 5. Evers S, Engelien A, Karsch V, et al. Secondary hyperkalaemic paralysis. J Neurol Neurosurg Psychiatry. 1998;64:249-252.