Table 1. Demographic profile of five patients with polyserositis following aluminum phosphide ingestion.

Cases

Age

Sex

Dose

Onset of manifestations

Nausea/

vomiting

Palpitation

Dyspnea

Altered   mental status

1

23

F

1.5 g (0.5 tab)

30 min.

+

+

-

-

2

32

M

9.0 g (3 tabs)

+

+

-

+

3

27

F

1.5 g (0.5 tab)

+

+

+

-

4

26

M

3.0 g (1 tab)

+

+

-

-

5

30

M

3.0 g (1 tab)

+

+

-

-

M; Male, F; Female

All these patients had multiple episodes of vomiting and were in shock at the time of presentation. All except one had no respiratory distress at presentation and developed respiratory distress after 12 hours of admission. One patient was irritable and confused at the time of admission but was not hypoxic (Table 2). All 35 patients were managed initially with a standard treatment protocol including gastric decontamination, intravenous fluids, and inotropic support with dopamine and noradrenalin. 20 patients died within first 12 hours after admission and out of the rest, 14 patients could be discharged while only a patient died on the 3rd day post-ingestion. The baseline clinical and paraclinical parameters of all cases with polyserosits are described in the table 3.

During admission (median: 3.8 days post-ingestion), five patients developed respiratory distress requiring endotracheal intubation and mechanical ventilation. The mean duration of ventilatory support for these patients was 3.4 days. All these patients had bilateral pleural effusion (median: 3.6 days post-ingestion) and ascites (median: 4.6 day post-ingestion). The pleural effusion was tapped and was transudative in nature. Three patients developed pericardial effusion on day 5. Ultrasonography and echocardiography was done in all 20 patients. It showed systolic dysfunction with low ejection fraction and mild pericardial effusion in three patients with polyserositis (Table 3). Aggressive management with mechanical ventilation was continued in all patients developing polyserositis and four patients could be successfully weaned from ventilator and discharged. The median period of hospitalization was 10 days.

DISCUSSION

Aluminum phosphide is a solid fumigant pesticide, commonly used as a food grain preservative, in India. It is available in 3 gram tablets and pellets. The ingredients of the tablets are aluminum phosphide and ammonium carbonate (commonly marketed in India as Celphos and Quickphos tablets). These compounds are cheap, easily available, and effective grain fumigants with little residue. These properties made them ideal for poisoning. Use of AlP products has tremendously increased over last decade due to the increasing need of grain storage (1). 

Following exposure to the air and moisture, this compound generates a highly toxic phosphine gas, which dissipate very rapidly into the air and leaves very little residue on the food grains. The chemical reaction of this compound will be enhanced in the presence of acidic medium, so the liberation of this gas increases due to the presence of hydrochloric acid in the stomach (ALP +3H2O ¦ Al(OH)3 + PH3) (2,8). The phosphine gas, after absorption through the mucosal layer, enters into blood circulation and causes immediate both local and systemic manifestations. Consequently, extensive complications with cardiopulmonary instability may occur which lead to high mortality ranging from 37 to 100% (1,9).

Phosphine gas can cause toxicity by ingestion (more common mode of toxicity) and inhalation route. The exact pathophysiology of the toxicity of this compound is not clear. After absorption through the gastrointestinal tract by simple diffusion, it is mainly excreted through kidneys and lungs. It has been postulated that in case of high concentration of phosphine gas in the lungs, direct alveolar damage might occur. This may produce acute respiratory distress syndrome (ARDS) like picture (5,9,10). Phosphine causes non-competitive inhibition of the cytochrome oxidase system of the mitochondria, inhibition of cellular respiration (by inhibiting oxidative phosphorylation) and inhibition of catalase. This results in damages due to free oxygen radicals and furthermore, produces a state of cellular or global hypoxia (11,12). Multi-organ failure and shock following AlP poisoning, which are seen in majority of such patients, are likely to be due to direct extensive cytotoxic oxidative damage by phosphine (12,13). 

We propose that hypoxic injury causes endothelial dysfunction and cellular apoptosis which lead to increased capillary permeability and leakage of fluid into third space, a mechanism similar to systemic capillary leak syndrome (14). The increased capillary permeability will thus lead to bilateral pleural effusion, ascites with mild pericardial effusion, as were seen in our patients. Since majority of patients with severe AlP poisoning dies, the evidence of capillary leak could be under-reported.  

However, diffuse hemorrhages and edema of all the major organs have been commonly reported in autopsy studies (15,16). Correspondingly, diffuse congestion and hemorrhage of lungs, liver, spleen, kidney and heart along with evidence of free fluid in pericardial, peritoneal and pleural cavity was found in one patient who died in our study. 

Pleural effusion (6,17), and coexisting ascites (7), have been reported in a few patients with severe AlP poisoning to date. Our study is the first study reporting the development of polyserositis in patients with aluminum phosphide poisoning and its correlation with mortality. Although unusual, polyserositis should be actively considered for and managed in patients with severe poisoning. 

LIMITATIONS

The inability to demonstrate pathological evidence of capillary leak and endothelial damage is the major limitation of our study. 

CONCLUSION