Guan-Hsing Chen1, Ja-Liang Lin, Yao-Kuang Huang. 1. Poison Center, Chang Gung Memorial Hospital, Lin-Kou Medical Center, Chang Gung Medial College and University, Taipei, Taiwan, Republic of China.
Abstract
OBJECTIVE: To report a severe case of paraquat poisoning successfully treated with repeated-pulse therapy of methylprednisolone. DESIGN: Case study. SETTING: University Hospital, Lin-Kou Medical Center, Taipei, Taiwan, Republic of China. PATIENTS: A 60-yr-old man with paraquat poisoning with severe acute renal failure (serum creatinine level of 11.8 mg/dL and serum paraquat level of 3.66 microg/mL at 10 hrs after ingestion) and severe hypoxemia (Pao2, 66.6 mm Hg). INTERVENTION: Repeated 3-day pulse therapy with methylprednisolone, one course of 2-day cyclophosphamide, and a high dose of dexamethasone for 33 days. MEASUREMENTS AND MAIN OUTCOME: Arterial blood gas analysis was obtained regularly. A chest radiography was obtained every week. The arterial blood oxygen concentrations dramatically elevated from 66 mm Hg to 97 mm Hg, and the chest radiographs markedly improved after repeated-pulse therapy with anti-inflammatory agents and cyclophosphamide. CONCLUSIONS: We successfully treated a severe paraquat poisoned patient with repeated methylprednisolone pulse therapy and prolonged dexamethasone treatment. This case demonstrates that the severe inflammation, not the fibrosis, of the lungs plays a major role in the lethal hypoxemia of patients with paraquat poisoning during the subacute period and confirms our previous hypotheses. Clearly, the use of anti-inflammatory therapy to treat paraquat-poisoned patients needs further evaluation; however, anti-inflammatory therapy may be an effective treatment after failure of standard therapies.
OBJECTIVE: To report a severe case of paraquat poisoning successfully treated with repeated-pulse therapy of methylprednisolone. DESIGN: Case study. SETTING: University Hospital, Lin-Kou Medical Center, Taipei, Taiwan, Republic of China. PATIENTS: A 60-yr-old man with paraquat poisoning with severe acute renal failure (serum creatinine level of 11.8 mg/dL and serum paraquat level of 3.66 microg/mL at 10 hrs after ingestion) and severe hypoxemia (Pao2, 66.6 mm Hg). INTERVENTION: Repeated 3-day pulse therapy with methylprednisolone, one course of 2-day cyclophosphamide, and a high dose of dexamethasone for 33 days. MEASUREMENTS AND MAIN OUTCOME: Arterial blood gas analysis was obtained regularly. A chest radiography was obtained every week. The arterial blood oxygen concentrations dramatically elevated from 66 mm Hg to 97 mm Hg, and the chest radiographs markedly improved after repeated-pulse therapy with anti-inflammatory agents and cyclophosphamide. CONCLUSIONS: We successfully treated a severe paraquat poisoned patient with repeated methylprednisolone pulse therapy and prolonged dexamethasone treatment. This case demonstrates that the severe inflammation, not the fibrosis, of the lungs plays a major role in the lethal hypoxemia of patients with paraquat poisoning during the subacute period and confirms our previous hypotheses. Clearly, the use of anti-inflammatory therapy to treat paraquat-poisoned patients needs further evaluation; however, anti-inflammatory therapy may be an effective treatment after failure of standard therapies.