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Year : 2019  |  Volume : 22  |  Issue : 4  |  Page : 519-520

Hypokalemic quadriparesis: A rare manifestation of dengue fever

1 Department of Medicine, S P Medical College, Bikaner, Rajasthan, India
2 Department of Emergency Medicine, S P Medical College, Bikaner, Rajasthan, India

Date of Submission17-Dec-2018
Date of Acceptance30-Jan-2019
Date of Web Publication25-Oct-2019

Correspondence Address:
Dr. Harish Kumar
Department of Emergency Medicine, PBM Hospital, Bikaner, Rajasthan - 334 001, India. B-3 Shastri Nagar, Bikaner, Rajasthan - 334 001
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aian.AIAN_512_18

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How to cite this article:
Singh VB, Kumar H. Hypokalemic quadriparesis: A rare manifestation of dengue fever. Ann Indian Acad Neurol 2019;22:519-20

How to cite this URL:
Singh VB, Kumar H. Hypokalemic quadriparesis: A rare manifestation of dengue fever. Ann Indian Acad Neurol [serial online] 2019 [cited 2020 Sep 26];22:519-20. Available from:


Dengue fever is endemic in India, caused by dengue virus (DENV1-4). It is the most common acute viral disease transmitted by Aedes mosquitoes, arthropod-borne disease. Neurological manifestation of dengue is rare. Herein, we are presenting a case report of hypokalemic quadriparesis with dengue fever.

This 25-year non-diabetic, old male was admitted with acute onset of weakness of all four limbs. Patient has the history of high-grade fever for 2 days; on third day, he developed sudden onset of weakness of both lower limbs, which was progressed to both upper limbs over a period of 5–6 h. No history suggestive of bladder and bowl dysfunction, trauma, recent strenuous exercise, and vaccination. There was no history of similar history in past or family.

At admission, he was febrile with the temperature of 101.5°F by axilla. Conscious and oriented with normal vitals. There was no erythematous rash. Power in all four limbs was 2/5 with hyporeflexia. Planters were flexor. Cranial nerves and sensory examination were normal. Respiratory and cardiovascular examinations were normal.

Laboratory examination revealed Hb% of 12.6 g%, total leucocyte count 3,900/mm 3, platelet count 59,000/mm 3, random blood glucose 89 mg/dL, blood urea 30.1 mg/dL, and serum creatinine was 1.15 mg/dL with normal electrolytes. The hematocrit on first day was 42%, which was progressively decreased to 35% on third day. As patient improved after 4 days, hematocrit become in normal limit. There were no edema feet. CSF examination was normal.

On first day, Dengue NS1 antigen was reactive, which become immunoglobulin M (IgM)-positive (33.80 units) and immunoglobulin G (IgG)-positive (30.80 units) on fifth day. Peripheral blood smear did not reveal malarial parasite. IgM leptospira and IgM chikungunya were negative. Electrocardiogram revealed U waves.

A diagnosis of dengue fever with thrombocytopenia and acute hypokalemic quadriparesis was made. Patient was given 40 mEq/L of intravenous 15% potassium chloride (KCl) infusion in 500 mL of Normal saline for 2 days. Fever was treated with oral paracetamol.

He improved to normal power on fifth day, whereas serum potassium improved (4.83 mEq/L) on fourth day. Patient was observed for any bleeding diathesis. Periodic platelet count monitoring did not show deterioration and platelet count reached 1.34 lakhs/mm 3 on fifth day. Patient was discharged after full recovery with no recurrence at follow-up.

Dengue infection present as classic dengue fever, dengue hemorrhagic fever, or dengue shock syndrome. Atypical presentation of dengue fever are hepatic failure, acalculous cholecystitis, pancreatitis, febrile diarrhea, renal failure, myocarditis, pericarditis, conduction abnormalities, and acute respiratory distress syndrome. Affection of endothelium by immunopathological mechanisms leading to increased vascular permeability, and coagulation disorder is the main cause of all atypical manifestation. In this case, neurological manifestation was observed in association with dengue fever. The associations of neurological manifestation with dengue fever are not clearly mentioned in the literature. However, in the last few years, many cases of dengue-associated hypokalemic paralysis and numerous neurological complications related to dengue fever have been reported specially from endemic area.[1],[2],[3],[4] Neurological complications lead to significant morbidity and mortality. Guillain-Barre syndrome is the single most important differential diagnosis of hypokalemic paralysis. The differentiation of dengue-associated Guillain-Barre syndrome with dengue-associated hypokalemic paralysis is crucial because the treatment of both the clinical entity is different. Dengue-associated hypokalemic paralysis is quickly improved soon after potassium is administered. In this case, patient was fully recovered after potassium administration. Neurological complications occur in 0.5%–6% of the cases with dengue fever.[5] Both direct (neurotropism) and immunological mechanisms are responsible for neurological manifestations in dengue infection. In this case, weakness was most likely due to direct effect of dengue virus (viremia) because weakness occurred in the first 3 days. Neurological complication, such as dengue encephalopathy, Guillain–Barre syndrome, acute disseminated encephalomyelitis, and neuralgic amyotrophy, are explained on the basis of autoimmunity, molecular mimicry, or nonspecific activation of autoreactive T-cell clones leading to destruction of the myelin sheath/self-antigens.[6],[7] The exact cause of hypokalemic paralysis in dengue infection is not known. Various mechanisms described in the literature are as follows: redistribution of potassium into the cells, transient renal tubular abnormalities leading to increased urinary potassium wasting, increased catecholamine levels secondary to infections, secondary insulin resistance leading to intracellular shift of potassium, endogenous granulocyte macrophage colony-stimulating factor and related cytokines in response to neutropenia may be another putative factor leading to intracellular potassium shift and hypokalemia, and loss of potassium due to vomiting and diarrhea in febrile phase of dengue fever.[1]

Quadriparesis has been reported in various infectious conditions. In our patient, other infectious causes, such as malaria, Chikungunya, and leptospira, have been excluded by blood investigation. Now, Guillain–Barre syndrome considered as differential diagnosis, but fever with sudden onset of quadriparesis, hypokalemia with U wave in ECG, and prompt improvement after administration of potassium and normal CSF exclude the diagnosis of Guillain–Barre syndrome (GBS). Our patient recovered immediately with potassium supplementation. Absence of family history of episodic motor weakness and this being first episode of motor weakness that the patient suffered, familial periodic paralysis can be excluded.

Dengue fever can result in various neurological manifestations. Dengue infection should be suspected as a differential diagnosis and properly investigated in patients presenting with fever, associated with various neurological disorders without obvious etiology; hypokalemic quadriparesis secondary to dengue fever should be considered as a differential diagnosis in a case of acute febrile illness with muscle weakness in tropical countries like India especially in rainy season. This case report is to increase the awareness of clinician to a treatable entity.

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There are no conflicts of interest.

   References Top

Sanjeev Jha, Ansari MK. Dengue infection causing acute hypokalemic quadriparesis. Neurol India 2010;58:592-4.  Back to cited text no. 1
Wasay M, Channa R, Jumani M, Shabbir G, Azeemuddin M, Zafar A. Encephalitis and myelitis associated with dengue viral infection clinical and neuroimaging features. Clin Neurol Neurosurg 2008;110:635-40.  Back to cited text no. 2
Misra UK, Kalita J, Syam UK, Dhole TN. Neurological manifestations of dengue virus infection. J Neurol Sci 2006;244:117-22.  Back to cited text no. 3
Solomon T, Dung NM, Vaughn DW, Kneen R, Thao LT, Raengsakulrach B, et al. Neurological manifestations of dengue infection. Lancet 2000;25:1053-9.  Back to cited text no. 4
Hendarto SK, Hadinegoro SR. Dengue encephalopathy. Acta Paediatr Jpn 1992;34:350-7.  Back to cited text no. 5
Carod-Artal FJ, Wichmann O, Farrar J, Gascón J. Neurological complications of dengue virus infection. Lancet Neurol 2013;12:906-19.  Back to cited text no. 6
Varatharaj A. Encephalitis in the clinical spectrum of dengue infection. Neurol India 2010;58:585-91.  Back to cited text no. 7
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