**12.1 Decontamination**

Gastric lavage is probably best avoided after ingestion of phosphides as it might increase the rate of disintegration of the pesticide and increase toxicity (Maitai, et al, 2002). To reduce the absorption of phosphine, gastric lavage with potassium permanganate (1:10,000) is done. Permanganate is used as it oxidizes PH3 to form non-toxic phosphate. This is followed by a slurry of activated charcoal (approximately 100 gm) given through a nasogastric tube. In vitro studies suggested that vegetable oil and liquid paraffin inhibit phosphine release from phosphides (Goswami, et al, 1994) but these oils have not been tested in clinical practice. However, vomiting may make the administration of charcoal difficult. Although the administration of sodium bicarbonate via a gastric tube to decrease gastric hydrochloric acid has been proposed in the belief that hydrochloric acid assists the conversion of phosphide to phosphine, there is no experimental support for its use. Moreover, based on an understanding of the mechanisms of toxicity of metal phosphides, this strategy is unlikely to reduce morbidity and mortality. Removal of victims of phosphine inhalation from the contaminated atmosphere will have been carried out by the emergency service first on scene. Supplemental oxygen may be given if necessary but further measures for airway control are unlikely to be required.

#### **12.2 Supportive care**

Many patients will die from metal phosphide poisoning despite intensive care. Supportive measures are all that can be offered and should be implemented as required by clinical developments. The most important factor for success is resuscitation of shock and institution of supportive measures as soon as possible. Intravenous access should be established and 2- 3 litres of normal saline are administered within the first 8-12 hr guided by central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP). The aim is to keep the CVP at around 12-14 cm of water (Siwach, et al, 1997). Some workers have recommended rapid infusion of saline (3-6 litres) in the initial 3 hr (Kalra, et al, 1991). Low dose dopamine (4-6 μg/kg/min) is given to keep systolic blood pressure >90 mm Hg. The other vasopressures such as norepinephrine may be usefull in critical patients. The use of high doses of glucagon may benefit in the treatment of aluminum phosphide poisoning; the likely mechanism of action is the increase of cAMP in the myocardium, effectively bypassing the β-adrenergic second messenger system. Oxygen is given for hypoxia. Acute respiratory distress syndrom requires intensive care monitoring and mechanical ventilation. The blood glucose concentration should be measured in every case and hypoglycemia corrected if found. Similarly, hypokalemia should be sought and, if clinically indicated, at least partially corrected; cardiac features have resolved in occasional patients on correction of potassium concentrations (Kochar, et al, 2000). It must be remembered, however, that the onset of acidosis, renal failure and cell damage may produce life-threatening hyperkalemia. Metabolic acidosis should be managed conventionally. Bicarbonate level less than 15 mEq/L requires bicarbonate in a dose of 50-100 mEq intravenously every 8 hour (Singh, et al, 1989).

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

Gastric lavage is probably best avoided after ingestion of phosphides as it might increase the rate of disintegration of the pesticide and increase toxicity (Maitai, et al, 2002). To reduce the absorption of phosphine, gastric lavage with potassium permanganate (1:10,000) is done. Permanganate is used as it oxidizes PH3 to form non-toxic phosphate. This is followed by a slurry of activated charcoal (approximately 100 gm) given through a nasogastric tube. In vitro studies suggested that vegetable oil and liquid paraffin inhibit phosphine release from phosphides (Goswami, et al, 1994) but these oils have not been tested in clinical practice. However, vomiting may make the administration of charcoal difficult. Although the administration of sodium bicarbonate via a gastric tube to decrease gastric hydrochloric acid has been proposed in the belief that hydrochloric acid assists the conversion of phosphide to phosphine, there is no experimental support for its use. Moreover, based on an understanding of the mechanisms of toxicity of metal phosphides, this strategy is unlikely to reduce morbidity and mortality. Removal of victims of phosphine inhalation from the contaminated atmosphere will have been carried out by the emergency service first on scene. Supplemental oxygen may be given if necessary but further measures for airway

Many patients will die from metal phosphide poisoning despite intensive care. Supportive measures are all that can be offered and should be implemented as required by clinical developments. The most important factor for success is resuscitation of shock and institution of supportive measures as soon as possible. Intravenous access should be established and 2- 3 litres of normal saline are administered within the first 8-12 hr guided by central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP). The aim is to keep the CVP at around 12-14 cm of water (Siwach, et al, 1997). Some workers have recommended rapid infusion of saline (3-6 litres) in the initial 3 hr (Kalra, et al, 1991). Low dose dopamine (4-6 μg/kg/min) is given to keep systolic blood pressure >90 mm Hg. The other vasopressures such as norepinephrine may be usefull in critical patients. The use of high doses of glucagon may benefit in the treatment of aluminum phosphide poisoning; the likely mechanism of action is the increase of cAMP in the myocardium, effectively bypassing the β-adrenergic second messenger system. Oxygen is given for hypoxia. Acute respiratory distress syndrom requires intensive care monitoring and mechanical ventilation. The blood glucose concentration should be measured in every case and hypoglycemia corrected if found. Similarly, hypokalemia should be sought and, if clinically indicated, at least partially corrected; cardiac features have resolved in occasional patients on correction of potassium concentrations (Kochar, et al, 2000). It must be remembered, however, that the onset of acidosis, renal failure and cell damage may produce life-threatening hyperkalemia. Metabolic acidosis should be managed conventionally. Bicarbonate level less than 15 mEq/L requires bicarbonate in a dose of 50-100 mEq intravenously every 8 hour (Singh, et al, 1989).

experienced and well equipped centres.

control are unlikely to be required.

**12.2 Supportive care** 

**12. Management 12.1 Decontamination**  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, 1998).

### **12.3 Magnesium supplementation**

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, additional studies are necessary.

#### **12.4 N-acetylcysteine**

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

#### **12.5 Pralidoxime**

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