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Miller Fisher Variant of Guillain-Barré Syndrome Triggered by Ventilator-Associated Pneumonia.
BACKGROUND: Miller Fisher syndrome (MFS), a triad of ophthalmoplegia, areflexia and ataxia, is one of the regional variants of Guillain-Barré syndrome (GBS) that might account for a quarter of all cases of GBS, especially in Asian countries. There is history of an antecedent upper respiratory tract infection in up to two thirds of MFS cases. However, association of MFS in adults and pneumonia is rarely reported and in those cases causative pathogen was Mycoplasma pneumonia e . To our knowledge, association of MFS and ventilator-associated pneumonia has never been reported. So, we hereby report the first case of MFS which followed ventilator-associated pneumonia (VAP).
CASE REPORT: We report case of a 22-year-old male who was known to have temporal lobe epilepsy and mental retardation. He presented with status epilepticus. He was sedated and put on mechanical ventilation. Two days later, he developed a fever associated with increased tracheobronchial secretions and new infiltrates on chest X-ray. Diagnosis of VAP was made. Upon improvement, he was extubated and shifted out of ICU. Ten days after the onset of fever, he developed gradual onset bulbar weakness and ataxia. On examination, he had generalized areflexia and ataxia. CSF analysis showed cytoalbuminic dissociation. Antibodies against ganglioside complex were elevated. Diagnosis of sero-negative MFS was made, and intravenous immunoglobulin (IVIG) was started. He improved remarkably within two days.
CONCLUSION: MFS is immune-mediated entity which is usually triggered by upper respiratory tract infection but in rare cases it can be consequence of pneumonia including VAP. Further research is needed to establish link between MFS and VAP.
CASE REPORT: We report case of a 22-year-old male who was known to have temporal lobe epilepsy and mental retardation. He presented with status epilepticus. He was sedated and put on mechanical ventilation. Two days later, he developed a fever associated with increased tracheobronchial secretions and new infiltrates on chest X-ray. Diagnosis of VAP was made. Upon improvement, he was extubated and shifted out of ICU. Ten days after the onset of fever, he developed gradual onset bulbar weakness and ataxia. On examination, he had generalized areflexia and ataxia. CSF analysis showed cytoalbuminic dissociation. Antibodies against ganglioside complex were elevated. Diagnosis of sero-negative MFS was made, and intravenous immunoglobulin (IVIG) was started. He improved remarkably within two days.
CONCLUSION: MFS is immune-mediated entity which is usually triggered by upper respiratory tract infection but in rare cases it can be consequence of pneumonia including VAP. Further research is needed to establish link between MFS and VAP.
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