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.

The acute toxicity of paraphenylenediamine (PPD) has been associated with several histopathological changes. In humans, acute PPD poisoning is known to cause rhabdomyolisis and particularly myocardial lysis. However, its toxicity for the fetus has never been reported in the literature. We report a case of myocardial lysis in a fetus expelled by a 22-year-old mother after apparent ingestion of an unknown amount of PPD. The patient was admitted to our intensive care unit with acute onset of respiratory distress and rhabdomyolysis. The pelvic ultrasonography on admission showed a normally progressing pregnancy of 23–24 weeks. On day 9 post-ingestion, the patient spontaneously expelled a non-viable fetus. The fetal examination did not show any external or macroscopic abnormalities. However, the histopathological exam showed an important heart and lung congestion. There was also some interstitial edema and inflammation at the base of the lingua, in addition to a chorionic villus thrombosis and abruptio placentae. The histopathology of the myocardium showed lysis of the cardiac muscle. This observation suggests that the PPD was most likely responsible for the myocardial injury in the fetus.