Case Reports

Indian Pediatrics 1999;36: 1161-1163

Pleural Effusion_A Rare Complication of Aluminium Phosphide Poisoning

From the Department of Pediatrics, Bal Chikitsalya, R.N.T. Medical College, Udaipur, Rajasthan, India.
Reprint requests: Dr. R.L. Suman, 23-C Madhuban, Udaipur, Rajasthan 313 001, India.
Manuscript Received: April 15, 1999; Initial review completed: June 6, 1999;
Revision Accepted: June 21, 1999

Aluminium phosphide (ALP) poisoning (Celphos) has emerged as a common cause of accidental poisoning in children with mortality ranging from 37-100%(1). It usually presents with gastrointestinal upset and shock followed by adult respiratory distress syndrome (ARDS) and central nervous system manifestations. Common complicatins of celphos poisoning include hemorrhage, acute renal failure, disseminated intravascular coagulation and arrhythmia's(1,2). We recently managed a case of ALP (celphos) poisoning who developed pleural effusion which forms the subject of this communication.

Case Report

A previously healthy 12-year-girl was admitted with history of accidental ingestion of one fresh celphos (3 g) tablet. Within 10-15 minutes, she developed persistent vomiting and was hospitalized after 30 minutes of ingestion. On examination, she was irritable, restless, cyanosed with cool extremities. Heart rate was 170/min with absent peripheral pulses, respiratory rate was 52/min, axillary tempera-ture was 96°F, BP was not recordable and oxgen saturation by pulse oximetry was 86%.

Resuscitative measures for shock were started immediately after taking samples for investigation. Two boluses of Ringer lactate (20 ml/kg each) were given quickly along with oxygenation, gastric wash was done with KMnO₄ and then activated charcoal tablets were left in the stomach. Hydrocortisone and ceftriaxone were also started. After one hour, BP was 60 mm of Hg and cyanosis and respiratory distress improved. Because of low BP, Dopamine infusion was started at the rate of 10 mg/kg/min but even after 2 hours, BP was 70 mm of Hg. Hence Dobutamine was added in the dose of 5 mg/kg/min. The BP rose to 86/50 mm Hg and the child stabilized in the next 2 hours, as evidenced by a SaO₂ of 93% and disappearance of cyanosis. Meanwhile, Chest X-ray showed diffuse pulmonary edema. Other investigations revealed blood urea-25 mg/dl, serum creatinine - 1.1 mg/dl, blood sugar - 130 mg/dl, serum sodium - 136 mEq/L and serum potassium - 4.4 mEq/L. Routine investigations were within normal limits. EKG showed tachycardia with ST elevation. On second day, the child was stable except for a mild tachypnea (RR 34 min). On third day, there was diminution of breath sounds on right infrascapular area with a dull note. Repeat Chest X-ray revealed pleural effusion. Needle aspiration showed 7 ml pale yellow colored fluid with protein 3.6 g/dl and glucose 56 mg/dl. On microscopy, cell count was 800 cells/mm³ with 80% lymphocytes and 20% polymorphs. Gram's staining was negative. Culture was negative for pyogenic organism. Serum protein was 5.8 g/dl with albumin fraction of 3.8 g/dl. There was no family history of tuberculosis and Mantoux test was negative  at 72 hours. Injection Gentamicin was added to Ceftriaxone. The child was discharged afer 10 days and was normal at one month of follow-up.

Discussion

This patient presented with the usual features of ALP poisoning, namely, gastrointestinal upset and shock. Subsequently, the child developed ARDS with right sided pleural effusion. The pleural fluid was exudative in type, i.e., pleural fluid to serum protein ratio was >0.5.

A possible explanation for the exudative pleural effusion might be that when ALP comes in contact with moisture, it releases phosphines (PH₃) gas which is absorbed by simple diffusion. This phosphine gas due to non competitive inhibition of cytochrome oxidase system of mitochondria or damage by free radicals causes global hypoxia(3). This global hypoxia leads to an increase in capillary permeability that could lead to pleural effusion.

Furthermore, this phosphine gas is eliminated through the lungs, hence due to high concentration in the respiratory alveoli, it is responsible for direct alveolar damage(3). This alveolar damage (acute lung injury) causes ARDS. Studies in the past have shown increased levels of inflammatory markers (cytokines and interleukins) in ARDS(4,5) which increase the capillary permeability. This combined effect of increase in capillary permeability due to global hypoxia and ARDS could be responsible for the exudative effusion seen predominantly in the pleural cavity and not in other serous cavities.

Autopsy studies have proved that phosphine is a systemic poison causing congestion in all the organs of the body. Lungs may be primarily affected after inhalation/exhalation of phos-phine after ALP ingestion, when pulmonary edema is a prominent feature(6,7). Pleural effusion along with congestive changes in other organs of the body have been reported on autopsy of a 2 year old child who died due to acute phosphine poisoning(8).

To conclude, in cases of ALP (Celphos) poisoning, when patient is having persistent cough, respiratory distress. cyanosis or features of hypoxemia, along with ARDs, pleural effusion should also be kep in mind as a possible complication.

References

1. Chugh SN, Arora BB, Malhotra GC. Incidence and outcome of aluminium phosphide poisoning in a hospital study. Indian J Med Res 1991; 94: 232-235.

2. Singh UK, Chakraborty B, Prasad R. Aluminium phosphide poisoning: A growing concern in pediatric population. Indian Pediatr 1997; 34: 650-651.

3. Chefurka W, Kashi KP, Bond EJ. The effect of phosphine on electron transport of mitochondria. Physiol 1976; 6: 65-84.

4. Goodman RB, Strieter RM, Martin DR, Seattle VA, Arbor A. Inflammatory cytokines in patients with persistence of the ARDS. Am J Respir Crit Care Med 1996; 154: 602-611.

5. Miller EJ. Cochen AB, Matthay MA. Increased Interleukin-8 concentrations in the pulmonary edema fluid of patients with ARDS from sepsis. Crit Care Med 1996; 24: 1448-1454.

6. Siwach SB, Yadav DR, Arora B, Dalal S. Acute aluminium phosphide poisoning_An epidemio-logical, clinical and histopathological study. J Assoc Phys India 1988; 36: 594-596.

7. Koley TP. Aluminium phosphide poisoning. Indian J Clin Pract 1998; 9: 14-22.

8. Wilson R, Lovejoy FH, Jaegar RJ, Landrigen PL. Acute phosphine poisoning abroad on a grain freighter. Epidemiological, clinical, pathological findings. JAMA 1980; 244: 148-150.