|Year : 2016 | Volume
| Issue : 1 | Page : 76-78
Dengue fever presenting as hypokalemic muscle weakness
Laxmikant Ramkumarsingh Tomar, Alpana Raizada, Anil Yadav, Sunil Agarwal
Department of Medicine, University College of Medical Sciences and Guru Teg Bahadur Hospital, University of Delhi, Delhi, India
|Date of Web Publication||17-Dec-2015|
Laxmikant Ramkumarsingh Tomar
Department of Medicine, University College of Medical Sciences and Guru Teg Bahadur Hospital, University of Delhi, Dilshad Garden, Delhi - 110 095
Dengue fever has emerged as a major public health problem in India. In recent years, there has been an upsurge of neurological manifestations in dengue. Here, we report reversible acute motor weakness due to hypokalemia in two confirmed cases of dengue infection. Over a course of few hours following administration of potassium, both the patients recovered without any residual neurological deficit.
Keywords: Dengue, hypokalemia, paraplegia, quadriparesis
|How to cite this article:|
Tomar LR, Raizada A, Yadav A, Agarwal S. Dengue fever presenting as hypokalemic muscle weakness. Trop J Med Res 2016;19:76-8
| Introduction|| |
Dengue fever is a viral exanthematous febrile illness which has emerged as a major public health problem in India. In the year 2012 alone, India had reported 47,209 cases and 242 deaths from dengue. Neurological manifestations of dengue that have been reported include encephalitis, aseptic meningitis, Guillain-Barre syndrome (GBS), myelitis, intracranial haemorrhage, etc., However, there is paucity of literature documenting association of reversible pure motor weakness and dengue infection. We report reversible acute pure motor weakness due to hypokalemia in two confirmed cases of dengue infection.
| Case Reports|| |
A 30-year-old male presented with complaints of high grade, continuous fever of 3 days duration, and acute onset symmetric weakness of lower limbs that ascended to affect the upper limbs within an interval of 2-3 h 1 day prior to admission. There was no history of neck pain, sensory symptoms, bladder and bowel involvement, recent vaccination, diarrheal illness, headache, or vomiting. There was no history of excessive intake of heavy carbohydrate diet, any excessive exercise before development of limb weakness or family history of episodic weakness. On examination the patient was febrile with an oral temperature of 102°F, with other vitals being within normal limits. There was a generalized erythematous rash all over the body and non-tender hepatomegaly of 2-3 cm below the costal margin was noted. Neurological examination revealed a conscious and alert patient with normal higher mental functions, no signs of meningismus and normal cranial nerve examination. There was hypotonia and power was grade 2/5 in all the group of muscles in all the four limbs, and deep tendon reflexes were depressed with bilateral equivocal plantar response. The sensory system examination was normal. Single breath count was 28 per min. Rest of systemic examination was within normal limits.
Initial haemogram revealed haemoglobin of 11 g/dL, total leucocyte count of 3,500 per cu mm and platelet count of 43,000 per cu mm. Blood biochemistry revealed serum potassium of 2.8 mEq/L, and serum sodium of 140 mEq/L. Arterial blood gas analysis showed a pH of 7.33, bicarbonate of 18.2 mmol/L and an anion gap of 5.4 mmol/L. Creatine kinase (CK) and thyroid function tests (TFT) were within the reference range as well. Urine analysis showed a pH of 6.4, specific gravity was within the expected limits, and there was no proteinuria or glycosuria. Spot urinary sodium, potassium, calcium levels were within normal limits. NS1 antigen enzyme-linked immunosorbent assay (ELISA) and IgM antibodies for dengue were positive. An electrocardiogram (ECG) showed ventricular premature complexes, flattening of “T waves” and formation of “U” waves [Figure 1]. His nerve conduction velocity (NCV) and electromyography (EMG) were completely normal. A diagnosis of fever with thrombocytopenia with hypokalemic paralysis was made and it was managed with potassium supplements, antipyretics, and other supportive management. The motor power and ECG changes reverted to normal after 5 h of treatment. On the second day of treatment, his repeat serum potassium was 4.8 mmol/L. The platelet counts and total leukocyte counts gradually increased to normal values during next few days and the patient did not require any platelet transfusions. The hospital stay was uneventful.
After ten days, a heavy carbohydrate was given to patient and strenuous exercise was performed followed by rest but he did not develop weakness., For this challenge test, written consent was taken from patient. He was given a challenge of 50 g of glucose in 150 ml water orally every hour with monitoring of muscle strength or weakness every 30 min. Vitals were monitored along with electrolytes, ECG and oxygen saturation monitoring. During the procedure, he neither developed motor weakness nor hypokalemia. Bicycle exercise test was performed for 30 min to look for any muscle weakness, but the patient easily continued exercise without any weakness.
A 25-year-old male presented with complaints of high grade, continuous fever of 3 days duration and acute onset symmetric weakness of lower limbs 1 day prior to admission. On examination the patient was febrile with an oral temperature of 103°F, with other vitals being stable. Neurological examination revealed a conscious and alert patient with normal higher mental functions, no signs of meningismus and intact cranial nerves. There was hypotonia and motor power was grade 0/5 in all the group of muscles in bilateral lower limbs. The deep tendon reflexes were absent bilaterally and the plantar reflex was equivocal. The sensory system examination was normal.
Haemogram revealed haemoglobin of 15 g/dL, total leucocyte count of 2,500 per cu mm and platelet count of 23,000 per cu mm. Blood biochemistry revealed serum potassium of 2.5 mEq/L, and serum sodium of 143 mEq/L. Arterial blood gas analysis showed pH of 7.34, bicarbonate 20 mmol/L and anion gap 5.3 mmol/L. CK, TFT, and urine examination were normal. ECG showed flattening of “T waves.” NS-1 antigen ELISA and IgM dengue serology were positive. NCV and EMG revealed normal study. The patient was managed with potassium supplements, antipyretics, and other supportive management. Motor functions recovered in about 3 h after commencement of therapy. The platelet counts and total leukocyte counts gradually increased to normal values during next few days and the patient did not require any platelet transfusions. The hospital stay was uneventful. A similar challenge test was performed as stated above and both tests were negative.
| Discussion|| |
Though the first recognized epidemics of dengue fever were known as early as 1780s, the neurological manifestations of the disease have been reported over the last two decades only. With dengue fever assuming epidemic proportions in India, more and more atypical manifestations of the disease are coming to light. Neurological involvement described in dengue can be attributed to direct neuropathic involvement of the central nervous system (CNS) during the acute phase manifesting as encephalitis, meningitis, myelitis, etc., or could manifest as acute disseminated encephalomyelitis, neuromyelitisoptica, optic neuritis, and GBS in the post-infectious period. In one of the largest case series of sixteen patients of dengue fever with quadriparesis by Kalita et al., myositis was found to be the commonest cause.
Both our patients had acute pure motor weakness due to hypokalemia which responded well to potassium supplements. The commonly attributed cause like myositis was ruled out by documenting normal CK and EMG. GBS was ruled out by history, examination, and a normal NCV. We investigated the patients to exclude other causes of hypokalemia like thyrotoxicosis, alcohol, drugs (diuretics), gastrointestinal loss, and urinary potassium loss by clinical examination and relevant investigations. Both the patients were aged above 25 years and there was no history of either heavy physical exertion followed by rest, or heavy carbohydrate meal prior to onset of weakness so the hypothesis that it could be the first episode of hypokalemic periodic paralysis was negated. Some authors reported that dengue fever can precipitate an attack of hypokalemic periodic paralysis which responded well to potassium supplements.,, Prevalence of hypokalemia in dengue fever varies from 14% to 28% according to different studies.,,
The proposed mechanism of hypokalemia could be either due to redistribution of potassium in cells or transient renal tubular abnormalities leading to increased urinary potassium wasting. In our case preliminary investigations did not suggest renal tubular abnormalities but transient self-limiting renal tubular defects secondary to infection cannot be ruled out. Increased catecholamine levels in response to stress due to infection may also result in hypokalemia. Another possible mechanism for hypokalemia is that endogenous granulocyte macrophage-colony stimulating factors (GM-CSF) and related cytokines in response to neutropenia may lead to shift of potassium intracellularly. It is possible that probably more than one mechanism may be responsible for the hypokalemia in dengue infection.
| Conclusion|| |
Dengue fever should be kept in mind while constructing the differential diagnosis of acute motor weakness in a febrile patient. Hypokalemia is a potentially life-threatening complication of dengue fever and is easily reversible if the appropriate therapy is initiated in a timely manner.
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