INTRODUCTION

There are two kinds of pesticide which are used to protect grains and rice from pests and rodents in household that are known as rice tablet. One of them is an herbal product and poisoning with it, is not dangerous but the other one is aluminum phosphide (AlP), a fumigant which release phosphine gas when comes in contact with water or hydrochloric acid in stomach (Mehrpour and Abdollahi, 2010). Phosphine is a mitochondrial poison (Abdollahi et al., 2004) and interferes with protein and enzyme synthesis (Mehrpour and Singh, 2010; Shadnia et al., 2005, 2009). Impairment of oxidative phosphorylation and shock due to AlP poisoning may lead to multi organ dysfunction especially hypoxic damages (Mehrpour et al., 2008a).

Reported mortality rate due to AlP poisoning is too high (60-80%) and it is an emergency situation in emergency departments (Pajoumand et al., 2002; Shadnia et al., 2009; Mehrpour and Abdollahi, 2010). Although, some compounds have been introduced as decontaminant from gastrointestinal tract (Shadnia et al., 2005) but there is no specific antidote for AlP poisoning (Nikfar et al., 2011). Cardiogenic shock still remains the most common cause of death in AlP poisoning (Shadnia et al., 2011), so theoretically; treatment of cardiogenic shock may result in recovery because of digoxin cardiotonic potential in this poisoning as hypothesized by Sanaei-Zadeh and Farajidana (2011). Here a case of severe acute AlP poisoning with major cardiotoxicity who was successfully survived by use of digoxin is reported.

CASE REPORT

An 18 years old female was admitted to emergency Department of Emam-Khomeini Hospital as the main referral hospital for poisoned patients located in Ardabil, west of Iran (Mehrpour and Singh, 2010), about 4 h post ingestion of one 3 g tablet of AlP. After intentionally ingestion of AlP at the home, she complained vomiting, epigastric pain and thirst, when she was transferred to a local hospital where received gastric lavage and 100 g charcoal. Then, the patient was referred to Emam-Khomeini Hospital for better management.

Table 1:	Clinical and laboratory investigation of our patient with aluminum phosphide poisoning
*International Normalized Ratio (INR)

The patient did not have history of chronic disease or taking any medications or illicit drugs. At admission, she was agitated with Glasgow Consciousness Scale (GCS) of 14. Her Blood Pressure (BP) was not detected but others were as follow: pulse rate: 120 min^-1 and filiform, respiratory rate: 17, oral temperature: 35.8°C with cold and clammy extremities. Investigations revealed hematocrit: 40 and white blood cell counts: 11500. Arterial Blood Gas (ABG) analysis revealed ever metabolic acidosis with pH: 7.162; serum O₂ pressure (PO₂): 59 mmHg; serum CO₂ pressure (PCO₂): 31.7 mmHg; serum HCO₃: 11.1 mmol L^-1 and O₂ saturation of 92%. Her electrocardiogram was normal except for sinus tachycardia. Blood biochemistry revealed serum sodium (Na): 142 meq mL^-1, serum potassium (K): 3.9 meq mL^-1, serum calcium (Ca): 7.9 mg dL^-1, serum magnesium (Mg): 1.5 mg dL^-1; Blood Urea Nitrogen (BUN): 18 mg dL^-1, creatinine: 1 mg dL^-1 and blood glucose: 212 mg dL^-1 (Table 1). Electrocardiogram (ECG) showed sinus tachycardia with no ST-T changes. Troponin I (TPI) was negative. Her bedside echocardiogram showed severe Left Ventricular (LV) systolic dysfunction (EF = 25%), global hypokinesia, mitral valve regurgitation (MR) and increased mean pulmonary artery pressure (PAP = 26). End-diastolic size of LV was 55 mm and end-systolic size of LV was 45 mm. Left atrial size was 37 mm. Then when she was transferred to ICU, she received endotracheal intubation and mechanical ventilation and gastric decontamination with sodium bicarbonate (44 mEq, orally), permanganate potassium (1:10,000) and activated charcoal (1 g kg^-1, orally). Then she was treated with magnesium sulfate 6 g by IV infusion daily, calcium gluconate 4 g by IV infusion daily and adequate hydration. Due to severe metabolic acidosis she received 6 vials of sodium bicarbonate (44 mEq) stat that continued by 6 vials daily. Due to acute left heart failure and severe hypotension, dopamine (10 μg kg^-1 min^-1) was started. Additionally, she received digoxin 0.5 mg initially followed by 0.5 mg every 6 h during the first day. Digital continued by 0.25 mg daily. At day 2, her blood pleasure and pH significantly increased (Table 1). At day 3, INR were increased till 2. Echocardiography on day 3 was normal. At that time due to better condition of patient she was extubated. At day 4 of admission, she was transferred to the poisoning ward. At day 6, infusion of digoxin was stopped. She was discharged 10 days after admission, with full recovery.