J. Neurovirol. (2014) 20:103–104 DOI 10.1007/s13365-014-0232-z
CASE REPORT
Acute hypokalemic quadriparesis: an atypical neurological manifestation of dengue virus Rajendra Singh Jain & Rahul Handa & Swayam Prakash & Kadam Nagpal & Pankaj Gupta
Received: 19 November 2013 / Accepted: 2 January 2014 / Published online: 24 January 2014 # Journal of NeuroVirology, Inc. 2014
Introduction Dengue is the most common arboviral disease worldwide which is caused by four virus serotypes (Gulati and Maheshwari 2007). In India, cases of dengue have steadily increased over the past decade with almost 50,000 people affected in the year 2012 (Chaudhuri 2013). Clinically, dengue fever can be asymptomatic, or present as undifferentiated fever or as dengue haemorrhagic fever. As more and more people are being affected with dengue fever, many atypical manifestations are being witnessed. Neurological manifestations are not reported frequently and their exact incidence remains unknown. Acute onset quadriparesis in dengue fever could be due to myositis, Guillain-Barre Syndrome (GBS), or hypokalemia (Murthy 2010). We herein report a case of acute onset rapidly progressive quadriparesis due to hypokalemia in a confirmed case of dengue fever.
Case report A 32-year-old male presented with high-grade continuous fever since 3 days followed by 1-day history of acute onset rapidly progressive quadriparesis without bowel bladder or cranial nerve abnormality. Weakness progressed rapidly over 4 to 5 h to involve all the four limbs. There was no history of diarrhea, respiratory tract infection, vaccination, or jaundice in the preceding 1 month. There was no past history of similar illness in the patient or in his family. On examination, the patient was febrile with no signs of increased bleeding tendency. Cardiovascular, gastrointestinal, and respiratory R. S. Jain : R. Handa (*) : S. Prakash : K. Nagpal : P. Gupta Department of Neurology, SMS Medical College, Jaipur, Rajasthan, India e-mail: [email protected]
system examinations were unremarkable. Nervous system examination showed normal higher mental functions with no cranial nerve deficit including fundus. Motor examination revealed hypotonia, motor power grade 2/5 (MRC grade) with diminished reflexes in all four limbs, and bilateral flexor plantar response. Sensory examination was normal. Thus, a clinical diagnosis of pure motor, lower motor neuron (LMN) quadriparesis was made, and the patient was investigated for possible causes. Laboratory investigations revealed platelet count of 50K per microliter and low potassium level of 2.5 mEq/L. Patient’s ELISA for dengue antigen was positive. ECG showed flattened T wave and prominent U wave. Arterial blood gas analysis, serum creatine phosphokinase (CPK), urinary potassium level, thyroid profile, abdominal ultrasound, nerve conduction study, and electromyography were normal. Urine for porphobilinogen was negative. Thus, a final diagnosis of hypokalemic paralysis with dengue fever was made. The patient was managed conservatively with oral potassium supplementation and showed dramatic improvement and the muscle power recovered completely over the next 24 h. His serum potassium was measured every 4 h and showed steady improvement and normalized within 24 h. His platelet count improved over the next 3 days and he was discharged 4 days after admission in a stable condition.
Discussion Neurological manifestations seen in dengue fever can be due to neurotrophic effect, systemic complications of dengue infection, or can be immune mediated (Murthy 2010). Hypokalemic paralysis is considered as a systemic complication of dengue infection. GB syndrome and myositis are widely known causes of LMN quadriparesis in patients with dengue fever; however, quadriparesis secondary to
104
hypokalemia has been reported only recently from India as few case reports (Jha and Ansari 2010). In our patient, we investigated other possible causes of LMN quadriparesis including GBS and myositis. Patient’s serum CPK, nerve conduction study, and electromyography were normal, whereas his serum potassium was low. He responded well and became asymptomatic within 24 h of starting oral potassium supplementation. Secondary causes of hypokalemia like thyrotoxicosis, gastrointestinal loss, and urinary potassium wasting syndromes were excluded by relevant investigations. Hypokalemic paralysis has also been reported in other infectious diseases like Leptospirosis and Chikungunya (Gutch et al. 2012). The exact mechanism of hypokalemia in dengue fever is not known. Possible mechanisms suggested by Jha and Ansari were redistribution of potassium in cells or transient renal tubular abnormality leading to increased urinary potassium wasting (Jha and Ansari 2010). However, urinary potassium level was normal in our patient. Thus, it may be postulated that besides GBS and myositis, hypokalemia could be a possible cause of quadriparesis in patients of dengue fever. This case highlights the association of hypokalemic paralysis and dengue fever and clinicians
J. Neurovirol. (2014) 20:103–104
should be aware of this association, especially in endemic areas like India where atypical manifestations of dengue fever are now commonly being encountered so that such a condition can be treated promptly. Acknowledgments This study was not sponsored by any organization. Conflict of interest The authors have no conflict of interest.
References Chaudhuri M (2013) What can India do about dengue fever? BMJ 346: f643. doi:10.1136/bmj.f643 Gulati S, Maheshwari A (2007) Atypical manifestations of dengue. Trop Med Int Health 12(9):1087–1095. doi:10.1111/j.1365-3156.2007. 01891 Gutch M, Agarwal A, Amar A (2012) Hypokalemic quadriparesis: an unusual manifestation of dengue fever. J Nat Sci Biol Med 3(1):81– 83. doi:10.4103/0976-9668.95976 Jha S, Ansari MK (2010) Dengue infection causing acute hypokalemic quadriparesis. Neurol India 58(4):592–594. doi:10.4103/00283886.68657 Murthy JM (2010) Neurological complications of dengue infection. Neurol India 58(4):581–584. doi:10.4103/0028-3886.68654
CASE REPORT
Acute hypokalemic quadriparesis: an atypical neurological manifestation of dengue virus Rajendra Singh Jain & Rahul Handa & Swayam Prakash & Kadam Nagpal & Pankaj Gupta
Received: 19 November 2013 / Accepted: 2 January 2014 / Published online: 24 January 2014 # Journal of NeuroVirology, Inc. 2014
Introduction Dengue is the most common arboviral disease worldwide which is caused by four virus serotypes (Gulati and Maheshwari 2007). In India, cases of dengue have steadily increased over the past decade with almost 50,000 people affected in the year 2012 (Chaudhuri 2013). Clinically, dengue fever can be asymptomatic, or present as undifferentiated fever or as dengue haemorrhagic fever. As more and more people are being affected with dengue fever, many atypical manifestations are being witnessed. Neurological manifestations are not reported frequently and their exact incidence remains unknown. Acute onset quadriparesis in dengue fever could be due to myositis, Guillain-Barre Syndrome (GBS), or hypokalemia (Murthy 2010). We herein report a case of acute onset rapidly progressive quadriparesis due to hypokalemia in a confirmed case of dengue fever.
Case report A 32-year-old male presented with high-grade continuous fever since 3 days followed by 1-day history of acute onset rapidly progressive quadriparesis without bowel bladder or cranial nerve abnormality. Weakness progressed rapidly over 4 to 5 h to involve all the four limbs. There was no history of diarrhea, respiratory tract infection, vaccination, or jaundice in the preceding 1 month. There was no past history of similar illness in the patient or in his family. On examination, the patient was febrile with no signs of increased bleeding tendency. Cardiovascular, gastrointestinal, and respiratory R. S. Jain : R. Handa (*) : S. Prakash : K. Nagpal : P. Gupta Department of Neurology, SMS Medical College, Jaipur, Rajasthan, India e-mail: [email protected]
system examinations were unremarkable. Nervous system examination showed normal higher mental functions with no cranial nerve deficit including fundus. Motor examination revealed hypotonia, motor power grade 2/5 (MRC grade) with diminished reflexes in all four limbs, and bilateral flexor plantar response. Sensory examination was normal. Thus, a clinical diagnosis of pure motor, lower motor neuron (LMN) quadriparesis was made, and the patient was investigated for possible causes. Laboratory investigations revealed platelet count of 50K per microliter and low potassium level of 2.5 mEq/L. Patient’s ELISA for dengue antigen was positive. ECG showed flattened T wave and prominent U wave. Arterial blood gas analysis, serum creatine phosphokinase (CPK), urinary potassium level, thyroid profile, abdominal ultrasound, nerve conduction study, and electromyography were normal. Urine for porphobilinogen was negative. Thus, a final diagnosis of hypokalemic paralysis with dengue fever was made. The patient was managed conservatively with oral potassium supplementation and showed dramatic improvement and the muscle power recovered completely over the next 24 h. His serum potassium was measured every 4 h and showed steady improvement and normalized within 24 h. His platelet count improved over the next 3 days and he was discharged 4 days after admission in a stable condition.
Discussion Neurological manifestations seen in dengue fever can be due to neurotrophic effect, systemic complications of dengue infection, or can be immune mediated (Murthy 2010). Hypokalemic paralysis is considered as a systemic complication of dengue infection. GB syndrome and myositis are widely known causes of LMN quadriparesis in patients with dengue fever; however, quadriparesis secondary to
104
hypokalemia has been reported only recently from India as few case reports (Jha and Ansari 2010). In our patient, we investigated other possible causes of LMN quadriparesis including GBS and myositis. Patient’s serum CPK, nerve conduction study, and electromyography were normal, whereas his serum potassium was low. He responded well and became asymptomatic within 24 h of starting oral potassium supplementation. Secondary causes of hypokalemia like thyrotoxicosis, gastrointestinal loss, and urinary potassium wasting syndromes were excluded by relevant investigations. Hypokalemic paralysis has also been reported in other infectious diseases like Leptospirosis and Chikungunya (Gutch et al. 2012). The exact mechanism of hypokalemia in dengue fever is not known. Possible mechanisms suggested by Jha and Ansari were redistribution of potassium in cells or transient renal tubular abnormality leading to increased urinary potassium wasting (Jha and Ansari 2010). However, urinary potassium level was normal in our patient. Thus, it may be postulated that besides GBS and myositis, hypokalemia could be a possible cause of quadriparesis in patients of dengue fever. This case highlights the association of hypokalemic paralysis and dengue fever and clinicians
J. Neurovirol. (2014) 20:103–104
should be aware of this association, especially in endemic areas like India where atypical manifestations of dengue fever are now commonly being encountered so that such a condition can be treated promptly. Acknowledgments This study was not sponsored by any organization. Conflict of interest The authors have no conflict of interest.
References Chaudhuri M (2013) What can India do about dengue fever? BMJ 346: f643. doi:10.1136/bmj.f643 Gulati S, Maheshwari A (2007) Atypical manifestations of dengue. Trop Med Int Health 12(9):1087–1095. doi:10.1111/j.1365-3156.2007. 01891 Gutch M, Agarwal A, Amar A (2012) Hypokalemic quadriparesis: an unusual manifestation of dengue fever. J Nat Sci Biol Med 3(1):81– 83. doi:10.4103/0976-9668.95976 Jha S, Ansari MK (2010) Dengue infection causing acute hypokalemic quadriparesis. Neurol India 58(4):592–594. doi:10.4103/00283886.68657 Murthy JM (2010) Neurological complications of dengue infection. Neurol India 58(4):581–584. doi:10.4103/0028-3886.68654
