**8.6 Hematological toxicity**

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

#### **8.7 Uncommon features**

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 suffered an intracranial hemorrhage 5 days after the event. No explanation other than the poison was found (Dave, et al, 1994).
