**9. Diagnosis**

350 Toxicity and Drug Testing

red cell magnesium concentrations to be normal. Concentrations were increased in the brains, lungs, hearts, livers, kidneys, and stomachs of fatalities but later studies showed this to be the result of magnesium administration and not phosphide toxicity (Siwach, et al, 1995). Clearly, these studies cannot all be correct and the analytical method used to generate the results may be an important factor. The results of a study (Siwach, et al, 1994) carry particular weight because they used atomic absorption spectroscopy, a technique that is superior to the colorimetric method published in 1977 and used (Singh, et al, 1991) and the titan yellow method employed (Chugh, et al, 1991) despite it being claimed that results obtained using the former method correlated extremely well with those from atomic absorption spectroscopy (Khayam-Bashi, et al, 1977). If these studies (Siwach, et al, 1994) are considered the most reliable, there is no choice but to accept that neither hypomagnesemia nor hypermagnesemia is a feature of aluminium phosphide poisoning, though confirmation

Although phosphine causes Heinz body formulation and hemoglobin oxidation *in vitro*  (Chin, et al, 1992; Potter, et al, 1991), intravascular hemolysis and methemoglobinaemia are unusual complications of phosphide poisoning in humans. Nine individuals with intravascular hemolysis after ingestion of aluminium phosphide have been identified from the literature. Three were glucose-6-phosphate dehydrogenase deficient (Srinivas, et al, 2007), including one young man who had previously developed haemolysis when given primaquine (Sood, et al, 1997). Two others had no history to suggest this possible predisposing disorder (Aggarwal, et al, 1999; Lakshmi, 2002) and in the remaining four the issue was not addressed (Chugh, et al, 1991). Intravascular hemolysis was associated with renal failure and severe metabolic acidosis to which 3 days of vomiting and diarrhea may have partly contributed (Memis, et al, 2007). In addition to hemolysis one man was found to have methemoglobinaemia of 17% 32 h post-ingestion (Lakshmi, 2002) while another developed Heinz bodies (Srinivas, et al, 2007), a further indicator of damage to hemoglobin. Rats given aluminium phosphide had methemoglobin concentrations measured at 10 and 30 min intervals. They increased simultaneously with those of malonyldialdehyde suggesting that methemoglobinaemia was secondary to increased oxygen free radical generation (Lall, et al, 2000). A study revealed that there is a significant association between blood level of methemoglobin and mortality in patients with aluminium phosphide intoxication (Mostafazadeh, et al, 2010). Disseminated intravascular coagulation was present in six out of

Unusual complications of phosphide ingestion include atrial infarction (Jain, et al, 1992), pleural effusion (Bayazit, et al, 2000; Suman & Savani, 1999), ascites (Bayazit, et al, 2000), skeletal muscle damage (Khosla, et al, 1988), rhabdomyolysis (Abder-Rahman, 1999), a bleeding diathesis (Gupta, et al, 1990), adrenocortical congestion, hemorrhage and necrosis (Arora, et al, 1995), pancreatitis (Sarma, et al, 1996), and renal failure (Chugh, et al, 1991; Singh, et al, 1996; Bayazit, et al, 2000; Gupta, et al, 2000). Acute pericarditis has also been reported infrequently (Wander, et al, 1990; Chugh & Malhotra, 1992) though pericardial fluid was detected by echocardiography in a third of patients in one study (Bhasin, et al, 1991). Subendocardial infarction complicated the recovery of a 16-year-old male (Kaushik, et al, 2007) and a 26-year-old woman who had recovered from aluminium phosphide ingestion

418 patients poisoned with aluminium phosphide (Chugh, et al, 1991).

by another independent study would be welcome.

**8.6 Hematological toxicity**

**8.7 Uncommon features**

A positive history of ingestion is the basis of diagnosis in most cases. The presence of typical clinical features, garlicky odour from the mouth and highly variable arrhythmias in a young patient with shock and no previous history of cardiac disease points towards aluminium phosphide poisoning. Aluminium phosphide poisoning risk is low down in the following instances, When taking patient's history should be special attention to these points: If the patient uses the expired one

If aluminum phosphide is dissolved in water before use

If the patient experiences immediate vomiting

Confirmation can be done by the Silver Nitrate Test (Chugh, et al, 1989). In this test, 5 ml of gastric aspirate and 15 ml of water are put in a flask and the mouth of the flask is covered by filter paper impregnated with silver nitrate. The flask is heated at 50oC for 15 to 20 min. If phosphine is present the filter paper turns black. For performing the test on exhaled air, the silver nitrate impregnated filter paper is placed on the mouth of the patient and the patient is asked to breath through it for 15-20 minutes, blackening of the paper indicates the presence of phosphine in breath. The sensitivity of the test is 100%. However the most specific and sensitive method for detecting the presence of PH3 in blood/air is gas chromatography (Vins Jansen A, Thrane, 1978). For spot sampling of phosphine in air, detector tubes and bulbs are available commercially (International Programme on Chemical Safety, 1998; Leesch, 1982).
