Intoxication and drug overdose as suicidal attempt are rare in pregnancy. We report here the case of aluminum phosphide poisoning in a pregnant lady through oral and intravaginal administration which was managed with aggressive supportive measures without resorting to extracorporeal life support.
We report the case of a 35-year-old female who was admitted to our intensive care unit for aluminum phosphide (AlP) poisoning. She was found unresponsive beside empty AlP vials in her home before being brought to our ICU.
Upon admission in the ED (the exact time of the ingestion is unknown), she was unconscious with a Glasgow Coma Scale of 7 (eye opening 1/4, verbal response 2/5, and motor response 4/6), hypothermic with central temperature of 33°C, and had mottled and cold extremities. She was hypotensive with a blood pressure of 70/40 mmHg, with a heart rate of 50 beats per minute, and had shallow breathing with SpO2 at 60% on 10 liters on rebreathing mask. The remainder of the physical examination was remarkable for a distended abdomen with a fundal height above the umbilicus. A bedside point-of-care ultrasound was performed, showing global hypokinesia with an EF of 20%, a collapsed inferior vena cava (IVC), and at the pelvis, the fetus was with negative heart activity.
Resuscitation was commenced according to our department’s protocol for the management of AlP poisoning [
Bedside chest X-ray (Figure
Admission Chest X-ray showing bilateral infiltrates.
Admission EKG.
Chest X-ray found bilateral infiltrates with a normal cardiac silhouette.
Blood results found abnormal renal function tests: urea: 0.58 g/l, creatinine: 18 mg/l, and high troponine TnIc: 6.71 ng/ml (Table
ABG and biological values evolution throughout the stay.
Value | Normal range | Admission | Two hours after admission | Day 2 | Day 7 (discharge) |
---|---|---|---|---|---|
pH | 7.38–7.42 | 7.01 | 7.12 | 7.25 | 7.34 |
HCO3− | 22–26 | 11 | 13 | 17 | 23 |
PaO2 | >75 mmHg | 32 | 70 | 72 | 62 |
PaCO2 | 35–45 mmHg | 22 | 25 | 35 | 32 |
PaO2/FiO2 ratio | >300 | 80 | 140 | 144 | 310 |
Troponin I-C | <0.04 ng/ml | 6.71 | 8.02 | 5.04 | 0.06 |
Urea | 0.1–0.4 g/l | 0.58 | 0.63 | 0.87 | 0.43 |
Creatinine | 7–14 mg/l | 18 | 19 | 19 | 15 |
Admission EKG showed diffuse negative T wave, sinus bradycardia, and Osborn waves consistent with hypothermia.
Admission ABG: pH: 7.01, HCO3−: 11 mmol/l, PaCo2: 22 mmHg, and PaO2: 32 mmHg with a PaO2/FiO2 ratio of 80.
Toxicologic tests found evidence of phosphine using the silver nitrate test on the gastric content.
On admission to our ICU, the patient was still hypothermic with a temperature of 35°C with an improved hemodynamic status on 15 mcg/kg/min dobutamine (BP: 94/52 mmHg). She remained, however, oliguric and hypoxic with SpO2 reaching only 80% on 100% FiO2.
We decided to withhold labor induction after consulting with the hospital obstetricians. A control beside echo showed a slightly improved contractility on dobutamine with an EF of 30%, an ITV of 14, and an IVC measured at 20 cm. We decided to add norepinephrine 0.3 mcg/kg/min with a furosemide infusion. A better hemodynamic status was obtained with a mean arterial pressure >65 mmHg and acceptable diuresis (0.6 cc/kg/h).
However, with persistent hypoxia despite hemodynamic improvement, we considered ARDS and ventilated the patient subsequently with a SpO2 reaching 90%.
Upon hemodynamic and respiratory improvement, we decided to induce labor with intravaginal misoprostol after consulting with the obstetricians on the third day after admission. A male fetus was vaginally delivered the following day. Weaning from catecholamines, mechanical ventilation was started, and the patient was extubated on the fifth day under both low norepinephrine and dobutamine. She was discharged two days later after proper psychiatric counseling and weaning from catecholamines. A week later, the patient came back for a post-ICU consult, she was conscious, eupneic, stable, and exhibiting no signs of neither cardiac nor respiratory failure. She was followed up with the hospital psychiatry ward which deemed she could be treated as an outpatient.
AlP poisoning is common especially in underdeveloped countries. AlP is the main compound of a rodenticide (PHOSTOXIN©) used to protect crops. It is formulated as a dark-gray 3 g-tablet having the smell of decaying fish. Its toxicity stems from the liberation of phosphine gas (PH3), produced upon contact with atmosphere or the gastric hydrochloric acid [
As there is no specific antidote for Alp, the treatment is supportive and consists on thorough decontamination, hemodynamic, and respiratory support. Following ingestion, gastric lavage, following airway protection when deemed necessary, should be performed with bicarbonate and potassium permanganate KMnO4(1 : 10000), and the latter oxidizes phosphine to nontoxic phosphate [
Our patient presented with multiple organ failure: respiratory, hemodynamic, neurologic, and renal failure. Aggressive and early management were paramount in the evolution. There is yet no antidote for aluminum phosphide [
Alp poisoning remains fatal and common in underdeveloped countries. The keystone of recovery is early supportive hemodynamic and respiratory management, which should be tailored to every patient and to the equipment and therapies available in each institution.
The authors declare no conflicts of interest.