**8. Clinical features**

Aluminium phosphate poisoning affects the most organs and a variety of signs and symptoms appear in patients. Early symptoms include nausea, vomiting, retrosternal and epigastric pain, dyspnea, anxious, agitation and smell of garlic (Popp, et al, 2002; Aggarwal, et al, 1999; Sood, et al, 1997). on the breath. Moreover shock and peripheral circulatory failure are mainly imperative early signs of toxicity. Mortalities in past studies have ranged from 40–77% and in one survey 55% occurred within 12 h of ingestion and 91% within 24 h (Singh, et al, 1991).

#### **8.1 Cardiac toxicity**

Cardiac toxicity comprises circulatory failure (Alter, et al, 2001) hypotension (Bayazit, et al, 2000; Ragone, et al, 2002), congestion of the heart, separation of myocardial fibres by edema, fragmentation of fibres, non-specifc vacuolation of myocytes, focal necrosis, neutrophil and eosinophil infiltration were found in autopsy (Akkaoui, et al, 2007; Sinha, et al, 2005; Chugh, et al, 1991, Katira, et al, 1990). Also, significantly increasing left ventricular dimensions (Bajaj, et al, 1988), hypokinesia of the left ventricle and septum, akinesia, ejection fractions reduction (Bhasin, et al 1991), severe hypotension, raised systemic venous pressure, normal pulmonary artery wedge pressure, inadequate systemic vasoconstriction and ECG abnormalities (ST and T-wave changes) (Kalra, et al, 1991) are other signs and symptoms.

#### **8.2 Respiratory toxicity**

Tachypnea, dyspnea, crepitations, and rhonchi were present on examination in 192 out of 418 cases (46%) of phosphide poisoning (Chugh, et al, 1991) and have been found by others (Gupta, et al, 2000). Pulmonary edema is common but it is not always clear whether it is cardiogenic or non-cardiogenic in etiology. It tends to develop 4–48 h after ingestion and the finding of a reduced arterial pressure of O2 without an increase in pulmonary artery wedge pressure, suggested it was non-cardiogenic (Kalra, et al, 1991). Others have confidently diagnosed adult respiratory distress syndrome (Singh, et al, 1991, Bajaj, et al, 1988, Gupta, et al, 1995, Chugh, et al 1989) and non-specifed pulmonary edema (Singh, et al, 1996, Chugh, et al, 1998). The edema fluid may be protein-rich and hemorrhagic (Singh, et al, 1996).

#### **8.3 Gastrointestinal toxicity**

Hematemesis (Gupta, et al, 2000), corrosive lesions of the esophagus and stomach (Madan, et al, 2006, Tiwari, et al, 2003), vomiting, epigastric pain, severe gastric erosions, duodenal erosions, esophageal strictures tracheo-oesophageal fistulae,dysphagia (Darbari, et al, 2007). Dysphagia may be apparent as soon as 3 or 4 days after ingestion of aluminium phosphide (Madan, et al, 2006, Darbari, et al, 2007) but is more usual about 2 weeks later.

#### **8.4 Hepatic toxicity**

Transient elevations of alanine aminotransferase and aspartate aminotransferase activities are not infrequent after ingestion of metal phosphides (Frangides & Pneumatikos, 2002;

these reactions support the involvement of erythrocytes in the biotransformation of

Aluminium phosphate poisoning affects the most organs and a variety of signs and symptoms appear in patients. Early symptoms include nausea, vomiting, retrosternal and epigastric pain, dyspnea, anxious, agitation and smell of garlic (Popp, et al, 2002; Aggarwal, et al, 1999; Sood, et al, 1997). on the breath. Moreover shock and peripheral circulatory failure are mainly imperative early signs of toxicity. Mortalities in past studies have ranged from 40–77% and in one survey 55% occurred within 12 h of ingestion and 91% within 24 h

Cardiac toxicity comprises circulatory failure (Alter, et al, 2001) hypotension (Bayazit, et al, 2000; Ragone, et al, 2002), congestion of the heart, separation of myocardial fibres by edema, fragmentation of fibres, non-specifc vacuolation of myocytes, focal necrosis, neutrophil and eosinophil infiltration were found in autopsy (Akkaoui, et al, 2007; Sinha, et al, 2005; Chugh, et al, 1991, Katira, et al, 1990). Also, significantly increasing left ventricular dimensions (Bajaj, et al, 1988), hypokinesia of the left ventricle and septum, akinesia, ejection fractions reduction (Bhasin, et al 1991), severe hypotension, raised systemic venous pressure, normal pulmonary artery wedge pressure, inadequate systemic vasoconstriction and ECG abnormalities (ST and T-wave changes) (Kalra, et al, 1991) are other signs and symptoms.

Tachypnea, dyspnea, crepitations, and rhonchi were present on examination in 192 out of 418 cases (46%) of phosphide poisoning (Chugh, et al, 1991) and have been found by others (Gupta, et al, 2000). Pulmonary edema is common but it is not always clear whether it is cardiogenic or non-cardiogenic in etiology. It tends to develop 4–48 h after ingestion and the finding of a reduced arterial pressure of O2 without an increase in pulmonary artery wedge pressure, suggested it was non-cardiogenic (Kalra, et al, 1991). Others have confidently diagnosed adult respiratory distress syndrome (Singh, et al, 1991, Bajaj, et al, 1988, Gupta, et al, 1995, Chugh, et al 1989) and non-specifed pulmonary edema (Singh, et al, 1996, Chugh, et

al, 1998). The edema fluid may be protein-rich and hemorrhagic (Singh, et al, 1996).

(Madan, et al, 2006, Darbari, et al, 2007) but is more usual about 2 weeks later.

Hematemesis (Gupta, et al, 2000), corrosive lesions of the esophagus and stomach (Madan, et al, 2006, Tiwari, et al, 2003), vomiting, epigastric pain, severe gastric erosions, duodenal erosions, esophageal strictures tracheo-oesophageal fistulae,dysphagia (Darbari, et al, 2007). Dysphagia may be apparent as soon as 3 or 4 days after ingestion of aluminium phosphide

Transient elevations of alanine aminotransferase and aspartate aminotransferase activities are not infrequent after ingestion of metal phosphides (Frangides & Pneumatikos, 2002;

phosphine in vivo in humans (Stewart, et al, 2003).

**8. Clinical features** 

(Singh, et al, 1991).

**8.1 Cardiac toxicity**

**8.2 Respiratory toxicity**

**8.3 Gastrointestinal toxicity**

**8.4 Hepatic toxicity**

Akkaoui, et al, 2007; Bayazit, et al, 2000; Memis, et al, 2007) but jaundice secondary to liver damage (Chugh, et al, 1998) is much less common. It was present in 12 out of 92 cases (Singh, et al, 1991) and was said to be common in another series of 15 patients (Singh, et al, 1985) but confirmatory laboratory data were not provided. Jaundice was alleged to be present in 16 (52%) members of the crew of a grain freighter who inhaled phosphine after an accidental release (Wilson, et al, 1980) but, in the six tested, serum bilirubin concentrations were normal and transaminase activities only minimally disturbed, casting doubt on the clinical observation. Acute hepatic failure and encephalopathy was considered to be the cause of death in one man (Chittora, et al, 1994), while a 12-yearold girl died from a combination of acute hepatic failure and encephalopathy with renal failure (Bayazit, et al, 2000). Portal edema, congestion of the portal tract and central veins, and vacuolization of hepatocytes are the most frequent findings at autopsy (Saleki, et al, 2007).

#### **8.5 Electrolyte and metabolic abnormalities**

Hypokalemia. metabolic acidosis, mixed metabolic acidosis and respiratory alkalosis, and acute renal failure are reported frequently. Also,Hypoglycemia and hypomagnesemia have been reported in several studies (Chugh, et al, 2000; Dueñas, et al, 1999). Hypokalemia is common soon after ingestion of metal phosphides and is probably secondary to vomiting, though catecholamine release could also contribute. It is thought to be the result of impaired gluconeogenesis and glycogenolysis (Frangides & Pneumatikos, 2002) possibly secondary to adrenal gland damage and low circulating cortisol concentrations (Chugh, et al, 2000). Hyperglycemia (Abder-Rahman, 1999) appears to be rare. The main controversy relates to the existence or otherwise of disturbances of magnesium homeostasis. In 1989, prompted by reports of the empirical use of magnesium sulphate to treat phosphide toxicity, this study (Singh, et al, 1989; Singh & Sharma, 1991) demonstrated that serum magnesium concentrations were increased, possibly secondary to release from damaged cardiac myocytes and hepatocytes, and confirmed the findings in subsequent studies (Singh, et al, 1991; Singh, et al, 1990). Unfortunately, other studies have found the converse, that is serum and erythrocyte concentrations were reduced rather than increased. Chugh, et al, (1991) compared serial serum and erythrocyte magnesium concentrations in four groups of people. One comprised patients poisoned with aluminium phosphide who had resulting shock and cardiotoxicity while the second included those poisoned but without shock or cardiac features. The remaining two groups acted as controls, the first being patients in shock secondary to trauma or hemorrhage but without other features of cardiac toxicity and the second, normal volunteers. The only significant finding in admission samples was that cell and serum concentrations were lower in shocked, cardiotoxic patients (mean serum and RBC concentrations 0.9 and 3.7 mEq/L respectively compared with 1.8 and 5.2 mEq/L in volunteers). Since, first, hypomagnesemia was found in toxic shocked patients but not in those with non-toxic shock and secondly, 75% of those in the toxic/shock group had ECG changes, it was concluded that the evidence supported a causal relationship between hypomagnesemia and phosphide induced shock. Without intervention both serum and cell values returned to normal by about 24 h. The authors confirmed their findings in a later study (Chugh, et al, 1994) and thought the hypomagnesemia secondary to consumption in combating free radical stress (Chugh, et al, 1997). Hypomagnesemia has also been found in a recent single case of phosphine inhalation from aluminium phosphide (Dueñas, et al, 1999). The situation became even more complicated when, in 1994, a study (Siwach, et al, 1994) found themselves unable to agree with either. They found pre-treatment mean serum and

Aluminium Phosphide Poisoning 351

suffered an intracranial hemorrhage 5 days after the event. No explanation other than the

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

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

Laboratory evaluation is often performed to assess the prognosis. Leucopenia indicates severe toxicity. Increased aspartate aminotransferase or alanine aminotransferase and metabolic acidosis indicate moderate to severe ingestional poisoning. Electrolyte analysis shows decreased magnesium while potassium may be increased or decreased (Chugh, et al, 1990). Measurement of plasma renin is significant as its level in blood carries a direct relationship with mortality and is raised in direct proportion to the dose of pesticide. The serum level of cortisol is usually found to be decreased in severe poisoning (Chugh, et al, 1989). Chest X-ray may reveal hilar or perihilar congestion if ARDS develops. Electrocardiogram shows various manifestations of cardiac injury (ST depression or elevation, bundle branch block, ventricular tachycardia, ventricular fibrillation) (Jain, et al, 1985; Katira, et al, 1990; Siwach, et al, 1998; Singh, et al, 1989). Wall motion abnormalities, generalised hypokinesia of the left ventricle, decreased ejection fraction and pericardial

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

instances, When taking patient's history should be special attention to these points:

poison was found (Dave, et al, 1994).

If the patient uses the expired one

Safety, 1998; Leesch, 1982).

**11. Prognostic markers** 

**10. Laboratory investigations** 

If aluminum phosphide is dissolved in water before use

effusion can be seen in echocardiography (Chugh, 1995).

If the patient experiences immediate vomiting

**9. Diagnosis** 

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 by another independent study would be welcome.
