INTRODUCTION: Acute arsenic toxicity is a multisystemic disease with pleural and pericardial effusions, gastrointestinal symptoms and pancytopenia. The most frequent neurological complication of inorganic arsenic intoxication is a distal symmetrical polyneuropathy. CASE REPORT: We report here a patient who developed a systemic illness followed with severe acute polyneuropathy. Electrophysiological findings suggested a Guillain-Barré syndrome (GBS). Finally an acute encephalopathy appeared which led to reconsideration of the diagnosis. A 24-hour heavy metal urine, nail and hair analysis was performed. A diagnosis of arsenic toxicity was made. Instead of chelating therapy patient died due to respiratory failure. CONCLUSIONS: A misdiagnosis of GBS in inorganic arsenic polyneuropathy is not infrequent. Atypical progression compels to rule out arsenic or heavy metal intoxication. In our case the appearance of the encephalopathy was the key to the diagnosis. It has been suggested that axonal degeneration and segmental demyelination might be equally prominent pathological features of the neuropathy, depending on the dosage and the length of time of exposure to arsenic. The exact pathophysiology of arsenic polyneuropathy remains unclear and a interference with pyruvate oxidation has been postulated.
INTRODUCTION: Acute arsenic toxicity is a multisystemic disease with pleural and pericardial effusions, gastrointestinal symptoms and pancytopenia. The most frequent neurological complication of inorganic arsenic intoxication is a distal symmetrical polyneuropathy. CASE REPORT: We report here a patient who developed a systemic illness followed with severe acute polyneuropathy. Electrophysiological findings suggested a Guillain-Barré syndrome (GBS). Finally an acute encephalopathy appeared which led to reconsideration of the diagnosis. A 24-hour heavy metal urine, nail and hair analysis was performed. A diagnosis of arsenic toxicity was made. Instead of chelating therapy patient died due to respiratory failure. CONCLUSIONS: A misdiagnosis of GBS in inorganic arsenic polyneuropathy is not infrequent. Atypical progression compels to rule out arsenic or heavy metal intoxication. In our case the appearance of the encephalopathy was the key to the diagnosis. It has been suggested that axonal degeneration and segmental demyelination might be equally prominent pathological features of the neuropathy, depending on the dosage and the length of time of exposure to arsenic. The exact pathophysiology of arsenic polyneuropathy remains unclear and a interference with pyruvate oxidation has been postulated.