Aims: The dengue virus causes a mosquito born viral disease with an estimate of about 390 million people infected each year. The clinical manifestations include a feverish period, arthralgia and myalgia. Guillain-Barre Syndrome (GBS) caused by dengue fever has been reported in very few occasions. Presentation of case: A 46-year-old male with no relevant medical history presented with progressive flaccid quadriparesis, dysautonomy, dysphagia and facial paresia. Ten days before seeking medical attention the patient had fever, myalgia, arthralgia, rash, thrombocytopenia and a positive NS1 dengue antigen. GBS was suspected and immunoglobulin was started while nerve conduction studies confirmed an acute motor axonal polyradiculoneuropathy. …show more content…
The patient presented stable vital signs. On physical examination he was alert, oriented, with normal pupils reflex and cranial nerves preserved; muscle strength in upper limbs was 4/5 and 1/5 in lower limbs, osteotendinous reflexes abolished in lower limbs and normal muscle reflexes in upper limbs, no sensitive abnormalities and negative Babinski reflex. Abdominal exploration reported distended bladder and a Foley catheter was placed. The rest of the physical exploration was normal. According to the initial presentation of the patient and local epidemiology, the acute lower limb weakness and findings compatible with dysautonomia led to the diagnostic approach to common viral and bacterial diseases with antigenic capacity that would lead to the appearance of autoimmune neuropathy. Such is the cause of the Zika virus, Dengue and Epstein-Barr virus (EBV); on the other hand infections by enterobacteria like Campylobacter Jejuni and Yersinia Pestis. Upon intentional questioning, the patient denied all gastrointestinal symptoms. Laboratory showed complete blood count, biochemical profile, C-reactive protein, globular sedimentation rate and creatine phosphokinase within normal range. Anti-zika IgG were positive and IgM were negative; anti-Dengue IgG and IgM antibodies were positive. Antinuclear and heterophile antibodies were negative. As a first diagnostic impression, GBS was suspected due to clinical characteristics and findings compatible with physical examination. Therefore, a therapeutic start was given to this entity, as well as the continuation of auxiliary diagnostic tests for confirmation. The patient was treated with intravenous fluids, gastric protection and strict monitoring of vital signs. Immunoglobulin was started at of 0.4g/kg/day (30g/day) at an infusion rate of 10g/hour for 5 days. Nerve conduction studies confirmed an acute motor axonal polyradiculoneuropathy with abolished H reflex and absence of F wave in lower and upper limbs.