ABSTRACT
Plasma renin activity (PRA) was estimated in 30 patients with aluminium phosphide (AIP) poisoning (study group) admitted in shock. Ten patients in shock other than due to AIP poisoning (Group II A) and 20 normal healthy subjects (Group II B) served as controls. The PRA was significantly higher in the study group and group II A as compared to normal healthy subjects (p less than 0.001). Significantly higher PRA was found in the study group as compared to Group II A (p less than 0.001). The initial higher PRA continued to rise further in the study group but it started decreasing in Group II A as the duration of shock advanced. Continuation of shock in AIP poisoning was probably due to slow release of toxic PH3 gas, which was detected by positive silver nitrate paper test. The rise in PRA was directly proportional to the dose of pesticide consumed. There was direct relationship of mortality with increased PRA. Angiotensin converting enzyme inhibitors may have a role in combating shock in AIp poisoning.
Subject(s)
Adolescent , Adult , Aluminum Compounds , Child , Dose-Response Relationship, Drug , Female , Humans , Male , Pesticides/administration & dosage , Phosphines/administration & dosage , Renin/blood , Shock/bloodABSTRACT
Mixed heart rate response has been observed in shock due to aluminium phosphide poisoning. Bradycardia observed in 9 of 30 cases studied indicated transient vagotonia and it reversed with atropine. Both tachycardiac bradycardiac responses were associated with significant increase in the mortality.