[Acute polyneuropathy and encephalopathy caused by arsenic poisoning]. / Encefalopatía y polineuropatía agudas causadas por arsénico.

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.

Encefalopatía y polineuropatía agudas causadas por arsénico / Acute polyneuropathy and encephalopathy caused by arsenic poisoning

Introducción. La intoxicación por arsénico inorgánico es una enfermedad multisistémica con derrames pericárdico y pleural, síntomas gastrointestinales y pancitopenia. La complicación neurológica más frecuente es la aparición de una polineuropatía distal simétrica. Caso clínico. Se describe la evolución de un paciente con un cuadro sistémico de tres meses de evolución, consistente fundamentalmente en sintomatología abdominal, que desarrolló una tetraparesia rápidamente progresiva asociada a una polineuropatía aguda desmielinizante, atribuida en un primer momento a un síndrome de Guillain-Barré (SGB) postinfeccioso. La aparición de un cuadro encefalopático asociado hizo descartar otras posibilidades diagnósticas; entre ellas, la intoxicación por metales pesados, y se detectaron unos niveles elevados de arsénico en el pelo, las uñas y la orina. A pesar del tratamiento quelante, el paciente falleció por complicaciones respiratorias. Conclusiones. La confusión diagnóstica con un SGB en la polineuropatía por arsénico no es infrecuente. La progresión atípica obliga a descartar intoxicación por metales pesados, entre otras patologías. En nuestro caso, la aparición de un cuadro encefalopático fue clave para el diagnóstico. Las neuropatías por arsénico, tanto desde el punto de vista electrodiagnóstico como anatomopatológico, pueden ser de tipo axonal o desmielinizante, según la dosis y el tiempo de exposición al mismo. Se postula la interferencia con el ciclo de Krebs como mecanismo fisiopatológico (AU)

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 (AU)