Year : 2013 | Volume
: 6 | Issue : 3 | Page : 365--366
Acute hypokalemic quadriparesis in dengue fever
Shyam Chand Chaudhary, Deepali Mohanty, Satyendra Kumar Sonkar, Abhinav Gupta, Preeti Singla, Rajesh Kumar Arya
Department of Medicine, C.S.M. Medical University and Sahara Hospital, Lucknow, Uttar Pradesh, India
Shyam Chand Chaudhary
Department of Medicine, C.S.M. Medical University and Sahara Hospital, Lucknow, Uttar Pradesh
Dengue fever is an acute mosquito-borne infection caused by dengue viruses belonging to the family Flaviviridae. It is an important public health problem in tropical and subtropical climates. Acute motor quadriparesis during the course of dengue infection is quite unusual and uncommonly reported. We hereby report two cases of acute motor quadriparesis during the course of dengue infection due to hypokalemia.
|How to cite this article:|
Chaudhary SC, Mohanty D, Sonkar SK, Gupta A, Singla P, Arya RK. Acute hypokalemic quadriparesis in dengue fever.Ann Trop Med Public Health 2013;6:365-366
|How to cite this URL:|
Chaudhary SC, Mohanty D, Sonkar SK, Gupta A, Singla P, Arya RK. Acute hypokalemic quadriparesis in dengue fever. Ann Trop Med Public Health [serial online] 2013 [cited 2020 Feb 27 ];6:365-366
Available from: http://www.atmph.org/text.asp?2013/6/3/365/121013
Dengue fever is the most common mosquito-borne arboviral infection found in tropical and sub-tropical climates. It can lead to dire consequences if not identified and treated at appropriate time. Dengue virus can affect any Organ or system of the body including the brain, spinal cord, spinal roots, peripheral nerves, and muscles. Various neurological manifestations including acute motor quadriparesis have been reported but there are only few case reports of hypokalemic quadriparesis during dengue fever. 
A 30-year-old male presented with high grade fever for 4 days and acute onset weakness of all four limbs for 2 days. There was no history of trauma, vomiting and diarrhea, rash, bleeding manifestation, back pain, intramuscular injection or recent vaccination, and no personal or family history of such weakness in past. His vitals were stable and general examination was unremarkable. On neurological examination, he was conscious, had normal higher mental functions and intact cranial nerves. He had hypotonia, decreased power in all four limbs (2/5), absent deep tendon reflexes and flexor plantars response bilaterally. There was no sensory or bladder/bowel involvement. Investigation revealed hemoglobin 11.8g%, total leukocyte count 3300/mm 3 and platelet count 42,000/mm 3 . Other routine blood tests were absolutely normal except serum potassium level which was found to be low (2.2 mEq/L). Electrocardiogram was also suggestive of hypokalemia. Urine examination including sodium and potassium levels was normal. NS1 antigen at admission and IgM antibody for dengue done on 7 th day was positive. On subsequent work-up his nerve conduction study was found to be normal. In view of clinical features and investigations, he was diagnosed as a case of dengue fever with pure motor flaccid quadriparesis due to hypokalemia. He was started on potassium chloride injection to which he showed marked response and discharged without any neurological sequalae after 7 days of hospitalization.
Second case was a 27 year young male who had similar complaints of continuous high grade fever for 2 days and gradual onset weakness of all four limbs for 1 day. There was no significant antecedent history. His vitals were stable and general examination was unremarkable. This patient also had hypotonia, decreased power in all four limbs (1/5), absent deep tendon reflexes and flexor plantars response bilaterally without sensory or bladder/bowel involvement. Investigation revealed hemoglobin 14.8 g%, total leukocyte count 4000/mm 3 and platelet count 92,000/mm 3 . Serum biochemistry was within normal limits except that the potassium level was found to be very low (1.5mEq/L). Electrocardiogram was suggestive of severe hypokalemia. Urine examination was unremarkable. NS1 antigen was positive. IgM antibody for dengue was not done due to financial constrain. Electrophysiological studies were found to be absolutely normal. He was also diagnosed as a case of dengue fever with pure motor flaccid quadriparesis due to hypokalemia. He was treated like the previous case to which he showed gradual response and discharged after 7 days without any neurological sequalae.
Dengue infections are usually asymptomatic but can present with classic dengue fever, dengue hemorrhagic fever, or dengue shock syndrome. Neurological manifestation of dengue includes encephalitis, encephalopathy, aseptic meningitis, mononeuropathies, Guillain-Barre syndrome, myelitis, intracranial hemorrhage, and thrombosis.  However, there is a paucity of literature documenting intriguing association of motor weakness in dengue infection. Of the 16 patients with dengue fever with quadriparesis evaluated by Kalita and colleagues,  in seven motor quadriparesis was due to myositis. Guillain-Barre syndrome complicating dengue infection has also been documented. ,, In a large study from India, it was observed that neurological manifestations of dengue fever were presented in two major categories, encephalopathy and pure motor quadriparesis but the quadriparesis was due to myositis.  Our two patients with quadriparesis were due to hypokalemia.
The two with hypokalemia were investigated to rule out other causes of hypokalemic paralysis such as urinary potassium wasting syndromes (Bartter's, Gitelman's syndromes, and acute tubular necrosis), thyrotoxicosis, GI losses, and drugs (diuretics). Familial periodic paralysis was unlikely because there was no family history of such illness and the age of presentation in both the cases was more than 25 years. There was no history of either heavy physical exertion followed by rest or heavy carbohydrate intake before the episode. The possible mechanisms of hypokalemia could be due to either redistribution of potassium into the cells, renal tubular abnormalities leading to increased urinary potassium wasting that occur transiently during the course of the infection, anabolic states following rapid cell regrowth after treatment in patient with neutropenia  or hyperreninemia.  Redistribution of potassium occurs due to increased catecholamines in response to stress of the infection and secondary insulin release. All of these causes can work together in causing hypokalemia with one predominating over another.
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