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, den-
gue 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 manifesta-
tions 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 ten-
dency. 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: pratibhas.dr@gmail.com
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 flat-
tened T wave and prominent U wave. Arterial blood gas
analysis, serum creatine phosphokinase (CPK), urinary potas-
sium level, thyroid profile, abdominal ultrasound, nerve con-
duction 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 sup-
plementation 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 in-
fection, or can be immune mediated (Murthy 2010).
Hypokalemic paralysis is considered as a systemic complica-
tion 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 rele-
vant 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 uri-
nary 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.
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