Clinical toxicology (Philadelphia, Pa.) · 2007
Reversible myocardial injury associated with aluminum phosphide poisoning.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Akkaoui Mostafa, Achour Sanae, Abidi Khalid, Himdi Btissam, Madani Aoupe, Zeggwagh Amine Ali, Abouqal Redouane
Аннотация
BACKGROUND: Aluminum phosphide poisoning has high mortality resulting from cardiac impairment and hemodynamic disorders. We report two cases of aluminum phosphide associated with reversible myocardial injury.
CASES REPORTS: A 19-year-old woman and a 28-year-old man were admitted to hospital following ingestion of aluminum phosphide. The clinical course was characterized by the development of a shock syndrome requiring the use of vasoactive amines in the woman. However, the arterial hypotension in the man was improved by fluid filling and vasoactive drugs. The myocardial injury was objectively documented in both cases. The electrocardiogram showed ST-segment elevations and diffusely abnormal repolarization. The plasma concentrations of cardiac enzymes were elevated. In the second case, echocardiography showed similar myocardial involvement with left ventricular hypokinesis (left ventricle ejection fraction 30%). In both cases, there was progressive improvement in hemodynamic status, cardiac traces, and biochemical values. A simultaneous improvement was observed in echocardiogram of the second case (left ventricle ejection fraction increased to 50%).
CONCLUSION: Reversible myocardial injury following aluminum phosphide poisoning has been described in few cases. We objectively documented progressive clinical and electrical improvement in two cases.
CASES REPORTS: A 19-year-old woman and a 28-year-old man were admitted to hospital following ingestion of aluminum phosphide. The clinical course was characterized by the development of a shock syndrome requiring the use of vasoactive amines in the woman. However, the arterial hypotension in the man was improved by fluid filling and vasoactive drugs. The myocardial injury was objectively documented in both cases. The electrocardiogram showed ST-segment elevations and diffusely abnormal repolarization. The plasma concentrations of cardiac enzymes were elevated. In the second case, echocardiography showed similar myocardial involvement with left ventricular hypokinesis (left ventricle ejection fraction 30%). In both cases, there was progressive improvement in hemodynamic status, cardiac traces, and biochemical values. A simultaneous improvement was observed in echocardiogram of the second case (left ventricle ejection fraction increased to 50%).
CONCLUSION: Reversible myocardial injury following aluminum phosphide poisoning has been described in few cases. We objectively documented progressive clinical and electrical improvement in two cases.