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Year : 2010  |  Volume : 58  |  Issue : 4  |  Page : 592-594

Dengue infection causing acute hypokalemic quadriparesis

Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, UP, India

Date of Acceptance01-Feb-2010
Date of Web Publication24-Aug-2010

Correspondence Address:
Sanjeev Jha
Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, UP
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.68657

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 » Abstract 

Dengue infection is endemic to India and an important public health problem. We report three confirmed cases of dengue infection with acute, pure motor, reversible quadriparesis due to hypokalemia. Clinicians should be aware of such an association and consider the clinical possibility in the differential diagnosis while evaluating acute quadriparesis in patients with dengue fever, especially in endemic areas.

Keywords: Dengue, Guillain-Barre syndrome, hypokalemia, quadriparesis

How to cite this article:
Jha S, Ansari M K. Dengue infection causing acute hypokalemic quadriparesis. Neurol India 2010;58:592-4

How to cite this URL:
Jha S, Ansari M K. Dengue infection causing acute hypokalemic quadriparesis. Neurol India [serial online] 2010 [cited 2022 Dec 3];58:592-4. Available from: https://www.neurologyindia.com/text.asp?2010/58/4/592/68657

 » Introduction Top

Dengue is the most important mosquito-borne, arboviral infection found in tropical and sub-tropical climates, mostly in urban and semi-urban areas. Clinical presentation varies from a severe flu-like illness to a potentially lethal dengue hemorrhagic fever. There are only a few isolated case reports and case series documenting acute pure motor quadriparesis in dengue fever. [1],[2],[3] We report acute pure motor reversible quadriparesis due to hypokalemia in three confirmed cases of dengue infection. To the best of our knowledge such an atypical manifestation of dengue infection has not been reported earlier.

 » Case Reports Top

Case 1

A 26-year-old male presented with high grade, continuous fever of four days duration and acute onset symmetric quadriparesis of one day prior to admission. Weakness progressed to maximum over five to six hours. There was no history of sensory symptoms, neck pain, bladder, bowel or bulbar involvement, respiratory distress, recent vaccination or diarrhoeal illness. There was no family history of episodic weakness or any similar episodes of weakness in past. Except for oral temperature of 101΀ F, other vitals were stable and the general examination was unremarkable. Neurological examination revealed a conscious and alert patient with normal higher mental functions and intact cranial nerves. There was hypotonia and motor power was grade 1/5 in all the group of muscles in all the four limbs and deep tendon reflexes were diminished with, bilateral flexor plantar response. The sensory examination was normal. Blood biochemistry revealed serum potassium of 1.9 mEq/L, sodium of 140 mEq/L, and creatine kinase (CK) of 167 U/L. The arterial blood gas analysis revealed: pH of 7.38, bicarbonate 22.6 mmol/L and anion gap 1.0 mmol/L. Serum creatinine was 1.2 mg/dL and urinary pH was 6.3. Liver and thyroid function tests were normal. Spot urinary sodium, potassium and calcium were within normal range. The electro cardiogram revealed flattening of T waves and prominant U waves. The total leukocyte count was 3000/mm 3 with 50% lymphocytes and platelets were 30,000/ mm 3 . The dengue antigen ELISA was positive. Nerve conduction studies and needle electromyogram was normal.

For hypokalemic motor paralysis, patient was treated with 40 mEq potassium chloride infusion in 500 ml of 5% dextrose. There was significant improvement in the motor power within two to three hours and complete recovery over six hours. Repeat serum potassium was 4.8 mEq/L and repeat electro-cardiogram also revealed no U waves. The platelet counts and total leukocyte counts remained in the lower normal range for the initial three days and later gradually increased to normal values. The hospital stay was uneventful. After seven days, a challenge test performed with heavy carbohydrates diet and strenuous exercise, followed by rest, failed to produce any weakness. For the challenge test, the patient was hospitalized, procedure explained to him and informed consent was taken. It was undertaken in intensive care setting. In the fasting state he was given 50 grams of glucose in 150 ml water orally every hour and monitored every 30 minutes for muscle strength or any subjective complaints of muscle weakness. His vitals were kept under continuous monitoring including electrocardiogram and oxygen saturation. Electrolytes were monitored every 30 minutes for three hours and then hourly for the next two hours. During the test procedure patient neither developed motor weakness nor there was any fall in serum potassium values. The test was interpreted as negative. [4] For exercise challenge test, the patient was subjected to 30 minutes of bicycle exercise test followed by absolute rest in bed and then he was evaluated for muscle strength or any subjective complaints of weakness. [5]

Case 2

A 48-year-old male presented with high grade intermittent fever of five days duration and one-day history of acute onset symmetrical quadriparesis. On examination, he was febrile (101°F). The motor power was grade 3/5 in all the group of muscles in all the four limbs. Deep tendon reflexes were absent and sensory examination was normal. Laboratory tests were: serum potassium 2.8 mEq/L. total leukocyte count 5000/mm 3 and platelet count 80 thousand/mm 3 . serum CK 758 U/L. Renal, liver and thyroid profiles were normal. The antigen ELISA for dengue was positive. Patient was managed conservatively with potassium supplements. Reversal of weakness was achieved after 10 -12 hours with the correction of serum potassium. The platelet and total leucocyte counts also improved over the next few days.

Case 3

A 26-year-old male presented with high grade continuous fever and acute onset, symmetrical quadriparesis of two days duration. On examination, vitals were stable and general examination was unremarkable. Motor power was 2/5 in all the group of muscles in all the four limbs. The deep tendon reflexes were diminished in both the lower limbs and were absent in the upper limbs. Sensory examination was normal. Laboratory tests were: serum potassium 1.8 mEq/L. total leukocyte count8000/mm 3 and platelet count 45000/mm 3 , and serum CK 140 U/L. The antigen ELISA for dengue was positive. Weakness improved over 4 hours with potassium supplementation. The platelet improved to normal value over a week.

 » Discussion Top

Neurological manifestation of dengue include: encephalitis, encephalopathy, aseptic meningitis, mononeuropathies, polyneuropathies, Guillain-Barre syndrome, myelitis, intracranial haemorrhage and thrombosis. [6] However, there is paucity of literature documenting intriguing association of motor weakness and dengue infection. Of the sixteen patients with dengue fever with quadriparesis evaluated by Kalita and colleagues, [1] in seven the motor quadriparesis was due to myositis. Guillain-Barre syndrome complicating dengue infection had also been documented. [2],[3] In all our three patients the pure motor quariparesis was due to hypokalemia and all the three patients had dramatic recovery with the supplementation of potassium. We investigated the patients to excluded the other causes hypokalemic paralysis such as thyrotoxicosis, alcohol, drugs (diuretics), gastrointestinal loss and urinary potassium wasting syndrome (Bartter's, Gitelman's syndromes and acute tubular necrosis) by clinical examination and relevant investigations. Familial periodic paralysis was unlikely because there was no family history of episodic motor weakness and this being their first episode. All the three patients were aged above 25 years and there was no history of either heavy physical exertion followed by rest, or heavy carbohydrate intake and in the first patient neither of these challenge tests, reproduced the weakness.

Hypokalemia in association with infectious diseases, dengue fever in particular, have been reported and documented in up to 28% of serologically proven cases of dengue infection. [7],[8] Hypokalemic paralysis secondary to chikungunya fever has also been documented. [9] The putative mechanism of the hypokalemia in our patients could be either due to redistribution of potassium in cells or transient renal tubular abnormalities leading to increased urinary potassium wasting. Preliminary investigations were not suggestive of renal tubular abnormalities. However, transient self limiting renal tubular defects secondary to infections cannot be ruled out. Increased catecholamine levels in response to stress of the infection and secondary insulin release may result in intracellular shift of potassium and hypokalemia. Anabolic states following rapid cell regrowth in patients of pernicious anemia treated with vitamin B 12 and in patients with neutropenia after treatment with granulocyte-macrophage colony stimulating factor can result in hypokalemia due to potassium shift into cells. [10] All our three patients had neutropenia that resolved without any specific treatment. Endogenous granulocyte macrophage - colony stimulating factors (GM-CSF) and related cytokines in response to neutropenia may be another putative factor leading to intracellular potassium shift and hypokalemia. It may not be possible to attribute a single definite pathophysiological basis and rather it may be postulated that probably these putative mechanisms together may be responsible for the hypokalemia in dengue infection. Of the three patients described, only Case 2 had elevated total CK levels, however, electrodiagnostic evaluation was normal in all of them. Thus, it may be postulated that besides myositis and Guillain-Barre syndrome, hypokalemia may be another putative mechanism for the acute pure motor quadriparesis in patients with dengue infection.

The report warrants further documentation and studies of acute pure motor weakness in infections like dengue and chikungunya. Clinicians should be aware of such an association especially in endemic areas and consider hypokalemia in the differential diagnosis while evaluating fever and acute quadriparesis.

 » References Top

1.Kalita J, Misra UK, Mahadevan A, Shankar SK. Acute pure motor quadriparesis: is it dengue myositis? Electromyogr Clin Neurophysiol 2005;45:357-61.  Back to cited text no. 1  [PUBMED]    
2.Esack A, Teelucksingh S, Singh N. The Guillain-Barre syndrome following dengue fever. West Indian Med J 1999;48:36-7.  Back to cited text no. 2  [PUBMED]    
3.Santos NQ, Azoubel AC, Lopes AA, Costa G, Bacellar A. Guillain-Barre syndrome in the course of dengue: case report. Arq Neuropsiquiatr 2004;62:144-6.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]  
4.Gamstorp I. Disorders characterised by spontaneous attacks of weakness connected with changes of serum potassium. In: Bartsocas CS, editor. Genetics of neuromuscular disorders: Alan R. Liss Inc; 1989. p. 175-95.  Back to cited text no. 4      
5.Kantola IM, Tarssanen LT. Diagnosis of familial hypokalemic periodic paralysis: role of the potassium exercise test. Neurology 1992;42:2158-61.  Back to cited text no. 5  [PUBMED]    
6.Gulati S, Maheshwari A. Atypical manifestations of dengue. Trop Med Int Health 2007;12:1087-95.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]  
7.Widodo D, Setiawan B, Chen K, Nainggolan L, Santoso WD. The prevalence of hypokalemia in hospitalized patients with infectious diseases problem at Cipto Mangunkusumo Hospital, Jakarta. Acta Med Indones 2006;38:202-5.   Back to cited text no. 7  [PUBMED]  [FULLTEXT]  
8.Ying RS, Tang XP, Zhang FC, Cai WP, Chen YQ, Wang J, et al. Clinical characteristics of the patients with dengue fever seen from 2002 to 2006 in Guangzhou. Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi 2007;21:123-5.  Back to cited text no. 8  [PUBMED]    
9.Rampal, Sharda M, Meena H. Hypokalemic paralysis following Chikungunya fever. J Assoc Physicians India 2007;55:598.   Back to cited text no. 9  [PUBMED]    
10.Singer GG, Brenner BM. Fluid and electrolyte disturbances. In: Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscalzo J, editors. Harrison's principles of internal medicine. 17th ed. New York: Mcgraw-Hill Companies; 2008. p. 274-85.  Back to cited text no. 10      

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