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A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
Published on: April 28, 2019
Beyond Hemorrhage: A Case of Acute Dengue Infection Presenting with Budd-Chiari Syndrome and Bilateral Sensory
Krushna Keshav Dalvi1, Priya Khaire, Mohammed Hassan Shaik
1Department of General Medicine, Dr. D. Y. Patil Medical College, Hospital and Research Centre, Pune, Maharashtra, India.
Abstract:
Budd-Chiari syndrome (BCS) is a rare hepatic vascular disorder characterized by hepatic venous outflow obstruction with an incidence of 1-2 per million population annually. While dengue fever is primarily associated with hemorrhagic complications, thrombotic events are rarely reported. To our knowledge, this represents the first documented case of BCS occurring in association with dengue fever. A 22-year-old male from a rural area presented with a 4-day history of abdominal pain, fever, vomiting, and loose stools. Physical examination revealed hepatomegaly, ascites, and mild dehydration. Laboratory investigations confirmed dengue IgM positivity with thrombocytopenia (104,000/mm3) and elevated liver enzymes. Thrombophilia screening revealed deficiencies in protein C, protein S, and antithrombin III. Imaging studies, including ultrasonography, computed tomography with contrast, and color Doppler, demonstrated hepatic vein thrombosis, inferior vena cava narrowing, and caudate lobe hypertrophy, establishing the diagnosis of BCS. Upper gastrointestinal endoscopy revealed grade II esophageal varices consistent with portal hypertension. During admission, the patient also developed severe bilateral lower limb pain refractory to strong analgesics, and nerve conduction studies confirmed sensory polyneuropathy in both lower limbs. The patient was managed with supportive care and careful anticoagulation therapy using low-molecular-weight heparin (LMWH), followed by warfarin 4 mg daily. Despite initial thrombocytopenia, anticoagulation was successfully initiated with close monitoring for bleeding complications. The patient showed an excellent clinical response, with complete resolution of hepatic vein thrombosis, normalization of liver function, and resolution of ascites at follow-up. At 6-month follow-up, repeat thrombophilia assays performed after stopping warfarin and bridging with LMWH revealed normal levels of protein C, protein S, and antithrombin III, indicating no true inherited deficiency. This case highlights a novel association between dengue fever, BCS, and sensory polyneuropathy in a patient with apparent but transient thrombophilia. Early recognition, appropriate anticoagulation, and careful neurological evaluation can lead to favorable outcomes despite concurrent thrombocytopenia.
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