He was electively paralyzed and intubated. is a rare but possible neurological sequel following dengue fever. In areas where dengue is definitely hyperendemic, screening for dengue illness may be important in individuals showing with acute flaccid paralysis. strong class=”kwd-title” Keywords: Dengue fever, Guillan-Barr syndrome, Respiratory failure, Sri Lanka Background Dengue is an arboviral illness generally showing with fever, arthralgia, headache, and rashes. It is a major global general public heath challenge. Neurological manifestations of dengue fever are rare but have been reported in the medical literature. Guillain-Barr syndrome (GBS) is definitely a demyelinating polyneuropathy which regularly follows gastrointestinal or respiratory infections. Although rare, few instances of GBS have been causally linked to serologically confirmed dengue illness in the medical literature. Etiopathogenesis of GBS following dengue is not yet full explained. But the molecular mimicry causing immune assault on myelin and axons, and pro-inflammatory cytokines such as tumor necrosis element (TNF), interleukins, and matches participating in immune response are postulated as you possibly can mechanisms. Plasma exchange and intravenous immunoglobulins are equally effective and a mainstay of management. Individuals with dengue fever can develop acute flaccid paralysis like a complication. In areas where dengue is definitely hyperendemic, screening for dengue illness may be important in patients showing with acute flaccid paralysis. Case demonstration A 60-year-old Sri Lankan man was admitted in April 2017 having a 2-day time history of fever Danicopan with arthralgia, myalgia, headache, and generalized malaise. He complained of numbness and pain of the bilateral top limbs and lower limbs, with weakness of both lower limbs. He was unable to walk as typical or get up from a squatting position. He could pass urine without difficulty and experienced no difficulty in deep breathing and coughing. He denied recent diarrheal, respiratory illness or recent vaccinations. He was previously apparently well with no significant comorbidities. On exam, he was conscious, rational, and experienced normal vital guidelines. Cardiovascular, respiratory and abdominal examinations were normal. A limb exam exposed hypotonia and reduced power in the bilateral lower limbs. His top limbs were normal. His lesser limb tendon reflexes were absent with encouragement and his top limb reflexes were diminished. All his sensory modalities were intact. Although he had a good cough reflex, his neck muscle mass power was reduced. A cranial nerve exam was normal. On admission, his spontaneous tidal volume Danicopan (STV) was 400 mL. A provisional analysis of Guillan-Barr syndrome was made. The complete blood count on admission showed a white cell count of 4.2 106/microL, Platelets of 166 103/microL and a hematocrit of 40. Hus nonstructural protein 1 (NS1) antigen result was positive on admission. With the compatible history, positive dengue antigen, leukopenia and thrombocytopenia, a analysis of dengue fever was made. Serology results for HIV, hepatitis B and a throat swab for influenza were negative. Nerve conduction studies exposed grossly delayed nerve conduction in common peroneal and posterior tibia nerves. F waves were delayed. Ulnar nerve conduction was delayed with BIMP3 absent F waves. It was compatible with a severe demyelinating polyneuropathy. A cerebrospinal fluid study done later on day time 11 of his illness showed albumincytological dissociation (protein 70 g/dL, cell count – lymphocytes 5/cumm and no polymorphs). Our individual was started on intravenous immunoglobulins (IvIG) 0.4 g/kg/day time (30 g with this 75 kg weighing man) on admission. On Danicopan the second day time of hospital stay, our patient deteriorated neurologically. He was having poor respiratory effort.
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