Abstract We report a 39yearold Indian male who presented with

Abstract: We report a 39-year-old Indian male who introduced with the onset of an acute febrile illness with fever, severe myalgia, and generalized fatigue. Dengue fever was confirmed with a optimistic IgM dengue. He was found to have an elevated creatine phosphokinase (CPK) of 290?U/L, leading to a diagnosis of dengue related myalgia. He was aggressively hydrated and had shut monitoring of his day by day fluid intake, urine output, creatinine, and CPK levels. His hospital course was uneventful without the event of acute renal failure.

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This case highlights that extreme myalgia could occur in sufferers with dengue fever and that early and aggressive treatment might prevent extreme issues corresponding to rhabdomyolysis, acute renal failure and death.

Introduction: Dengue fever is an arthropod borne vector disease, caused by domestic feminine Aedes aegypti mosquito, and fewer so, the peri-domestic Aedes albopictus mosquito1. Infection with any one of many 4 serotypes results in numerous scientific manifestations from gentle febrile illness to severe dengue hemorrhagic fever or dengue shock syndrome due to plasma leakage, fluid accumulation, mucosal bleed and multi-organ failure.

Characteristic laboratory findings including leucopenia and thrombocytopenia along with particular antigen detection assist in the early prognosis, acceptable management and prevention of complications. We report a case of dengue fever with neuromuscular complication.

Case Report: A 39-year-old male presented with signs of high-grade fever and generalized myalgia of 7 days duration. He additionally had an related loss of urge for food. There was no history of rashes over his physique. He did not have any previous co-morbidity.

At the time of presentation, there was no history of mucosal bleeding, skin hemorrhages, or hematochezia. There was no history of retro-orbital pain, neck stiffness, or photophobia. There were no urinary symptoms and no history of nausea or vomiting. Clinical examination revealed a temperature of 101°F, pulse price of 82/min, blood pressure 110/80 mm Hg and respiratory fee of 24/min. He was hemodynamically secure with saturation (SPO2) of 98% in room air. The affected person was anicteric. Rest of the overall examination was unremarkable; there was no eschar. On systemic examination, the cardiovascular system had regular heart sounds and no murmur; examination of the chest revealed bilaterally equal air entry with none crepitations or rhonchi; stomach examination revealed a light hepatomegaly. He was conscious and oriented without any focal neurological deficits. There was no proof of any petechiae, purpura, ecchymoses, or rash over the pores and skin. Fundoscopy was unfavorable for retinal hemorrhages. Investigations revealed a gentle leucopenia and thrombocytopenia. His initial urea, creatinine, electrolytes, and coagulation studies have been regular and remained normal throughout his admission. Creatinine degree was 0.8mg/dl on admission and 0.9mg/dl at discharge. Admission aspartate transaminase was 80?U/L (normal 7-32?U/L), ?-glutamyl transferase was 60?U/L (normal 10-70?U/L), and lactate dehydrogenase was 240?U/L (normal 105-200?U/L). These values declined steadily in the course of the admission and ultimately normalized by the time of discharge. His preliminary creatine phosphokinase (CPK) was 290?U/L (normal for a male 22-198?U/L). With early and aggressive therapy, this worth decreased by about 30-50% every day till it was 72?U/L on the time of discharge. Urine microscopy was unfavorable for pink blood cells, casts, or different irregular urinary sediments and urinary myoglobin. Tests for HIV, hepatitis B and C, and leptospirosis were all unfavorable. Dengue IgM became positive on day eight from the onset of fever. This was his first an infection with dengue. We could not detect the serotype of the dengue.

The affected person was given aggressive hydration with intravenous and oral fluids. Input/output charting was accomplished specializing in daily fluid intake and urine output to monitor pH. Urea, creatinine, electrolytes, CPK, and platelet rely had been closely investigated. The patient’s hospital course went uneventful and he was discharged as his myalgia subsided and serum CK levels returned back to normal.

Discussion: Neuromuscular issues of dengue fever are frequent, especially when the spectrum spreads to the hemorrhagic fever or shock syndrome2; three. Muscular indicators of dengue fever are more debilitating since it extends after the febrile interval. Commonest muscular shows of dengue fever embody myalgia, myositis, rhabdomyolysis and hypokalemic paralysis. When a dengue patient presents with muscle ache, tenderness or muscle swelling with associated difficulty in strolling, always rule out dengue related myalgia, because it has been reported in up to 93% of dengue patients4. Diffuse viral invasion into the muscle with subsequent inflammatory changes leads to this myalgia, particularly if contaminated with dengue virus 15. Derangement in EMG or CPK is seen only in minority of cases. These transient self-limiting myalgias don’t want any particular therapy in general, but few circumstances may need analgesics like paracetamol. When a dengue affected person presents with pure motor weak point of four limbs, normal power, normal DTR with markedly elevated CPK and mild myopathic adjustments in EMG, myositis (inflammation of skeletal muscles) secondary to dengue an infection should be suspected. Muscle edema, hemorrhage, metabolic alterations and changes in vascular endothelial cells are responsible for the muscle dysfunction in dengue myositis. It may resolve itself typically, however severe myositis leads to quadriplegia and respiratory insufficiency. Another infrequent muscular complication of dengue is acute, pure, extreme motor paralysis of all of the four limbs with fast falling blood potassium stage. Usually weak point begins 2nd to 5th day of fever over a interval of 24 hours. DTR shall be absent or diminished and potassium might be low (mean-2.23) along with elevated CPK. Quick restoration with potassium infusion is the characteristic characteristic. Hypokalemia induced vasoconstriction and the subsequent muscle ischemia leads to these changes6. The close differentials to dengue associated hypokalemic paralysis embody Guillain Barre Syndrome and first episode of hypokalemic periodic paralysis. The most severe form of muscle involvement in dengue fever is rhabdomyolysis, characterised by myalgia, elevated CPK (10 occasions normal) and myoglobinuria7, eight. Dengue infection induced cytokines are the culprits, which causes injury of muscle cells. Rhabdomyolysis results in acute renal failure and life threatening electrolyte abnormalities. Hydration as a half of dengue remedy itself helps in the recovery of rhabdomyolysis.