**11. Prognostic markers**

Development of refractory shock, acute respiratory distress syndrom, aspiration, pneumonitis, anaemia, metabolic acidosis, electrolyte imbalance, coma, severe hypoxia, gastrointestinal bleeding, and pericarditis are associated with poor prognosis. The outcome correlates best with the number of vomiting the patient gets after ingestion and the severity of hypotension the patient develops (Singh, et al, 1998) 95% of the patients die within 24

1998).

**12.3 Magnesium supplementation** 

additional studies are necessary.

aluminium phosphide poisoning (Bogle, et al, 2006).

**12.4 N-acetylcysteine** 

**12.5 Pralidoxime** 

**13. Conclusions** 

Aluminium Phosphide Poisoning 353

All types of ventricular arrhythmias are seen in these patients and the management is the same as for arrhythmias in other situations (International Programme on Chemical Safety,

The problematic decision is whether or not supplemental magnesium should be given. If magnesium depletion does not occur such a course would appear illogical but single cases have been reported where magnesium administration appeared to terminate atrial fibrillation (Chugh, et al, 1989) and supra ventricular tachycardia and ventricular tachycardia (Chugh, et al, 1991). On the other hand, magnesium sulphate 3 g given intravenously over 30 min did not abolish very frequent ventricular ectopic beats and bigeminy though it restored a normal magnesium concentration (Dueñas, et al, 1999). Only a few studies have attempted to assess the value of magnesium sulphate in large groups of patients and their results are conflicting. In a study, 50 patients after aluminium phosphide ingestion were given high doses of magnesium and the result compared with the control group that was not treated. The result showed (42%) of those given supplemental magnesium survived compared with (40%) not so treated. In addition, treatment did not considerably improve survival at any dose (number of tablets) consumed. As you see magnesium supplementation was of no value in this study (Siwach, et al, 1994). Chugh et al. (2004) obtained opposite results in a case control study. The authors showed survival remarkably improved after each dose ingested for those patients treated by magnesium (Chugh, et al, 2004). To illuminate the potential benefit of magnesium supplementation,

Different studies in rats (Hsu, et al, 2000, 2002) and humans (Chugh, et al, 1997) showed glutathione concentrations reduction after treating with N-acetylcysteine in patients with

There is experimental and clinical evidence that phosphine (Potter, et al, 1993) and aluminium (Marquis & Lerrick, 1982, 1983) inhibit acetylcholinesterase. A study (Mittra, et al, 2001) investigated the benefit of administering atropine 1 mg/kg and pralidoxime 5 mg/kg parenterally to rats dosed with aluminium phosphide 10 mg/kg (5.55 × LD50) 5 min previously. Treatment increased the survival time by 2.5-fold in nine out of 15 animals and resulted in the survival of the six remaining animals. There were no survivors in the two

Acute poisoning with metal phosphides, particularly aluminium phosphide, is a worldwide problem most commonly encountered in the Indian Sub-Continent. The clinical features have been well described though it is only recently that the mechanisms of toxicity have been more clearly understood. Poisoning from phosphides is mediated by phosphine which has been shown to rapidly perturb mitochondrial morphology, inhibit oxidative respiration, and cause a severe drop in mitochondrial membrane potential. This failure of cellular

control groups. Further studies are required to confirm the benefit of oximes.

hours and the commonest cause of death in this group is arrhythmia. Death after 24 hours is due to shock, acidosis, acute respiratory distress syndrom and arrhythmia. The mortality rate is highly variable, ranging from 37-100% and can reach more than 60% even in experienced and well equipped centres.
