INTRODUCTION
Aluminum phosphide (ALP) is a rodenticide and insecticide used in pest control during grain storage (1). ALP is utilized in the form of clay-emulsified aluminum phosphide tablets (2). Solid ALP reacts with moisture in the air or water in the environment, releasing phosphine gas, which is originally responsible for its toxicity (3). Upon contact with gastric fluid following oral ingestion, the release of this PH3 gas typically produces a characteristic garlic odor (2). There is no specific antidote for ALP poisoning, and mortality rates are quite high (4). Toxic dose is above 150 mg, and lethal dose is above 1000 mg (5). While most cases of ALP poisoning reported in the literature are due to intentional oral ingestion, toxicity can also occur accidentally through inhalation, although respiratory-related ALP intoxications are rare (1, 6).
This case presentation describes a case of ALP poisoning through respiratory exposure presenting to the emergency department.
CASE
A 21-year-old female patient presented to our emergency department with chest pain. In her history, it was revealed that four days prior to her presentation, she was exposed to aluminum phosphide through inhalation while with her family, which led to her presenting to the emergency department with this complaint. Subsequently, she was admitted to the Intensive Care Unit for observation but left against medical advice on the 3rd day of her stay. The patient’s general condition was fair, and her vital signs were stable. Physical examination was unremarkable. Her electrocardiogram showed normal sinus rhythm with no other pathological findings detected. Laboratory values from her complete blood count were as follows: hemoglobin 11.4 g/dL, hematocrit 35.4%, white blood cell count 5.76 x 10^3/μL, and platelet count 237 x 10^3/μL. Biochemical tests revealed normal levels of aspartate aminotransferase (14 U/L), alanine aminotransferase (20 U/L), blood urea nitrogen (9 mg/dL), and creatinine (0.57 mg/dL). Serum ethanol level was <10 mg/dL, international normalized ratio (INR) was 1.06, and high-sensitive troponin was within normal limits at 5.11 ng/L. Venous blood gas analysis showed partial pressure of carbon dioxide (PCO2) of 37.8 mmHg, partial pressure of oxygen (PO2) of 37.6 mmHg, carboxyhemoglobin (COHb) of 1.4%, bicarbonate (HCO3) of 26.3 mmol/L, lactate of 1.3 mmol/L, and a pH of 7.451. Chest X-ray revealed no abnormalities. Echocardiography showed no pathology, and cardiac-related chest pain was not considered. Despite no pathology detected during follow-up in the emergency department and resolution of her symptoms, the patient chose to leave the emergency department against medical advice without further observation.
DISCUSSION
Following the first reported cases of intoxication in the 1980s, ALP has become a commonly used agent for suicide, particularly among individuals involved in agriculture (4). While it is seen as the second most common cause of organophosphate poisoning, most cases result from intentional oral ingestion for self-harm purposes, although toxicity can rarely occur due to respiratory exposure as well (1, 2, 6).
ALP is a colorless and odorless substance in its natural state. When combined with hydrochloric acid in the stomach, it releases phosphine gas, which is lethal, and is rapidly absorbed from the gastrointestinal system (GIS) (1, 7-9). When phosphine gas, produced by the moisture layer formed on phosphide, is inhaled, it is quickly absorbed from the lungs (4). Exposure to phosphine gas at concentrations above 50 ppm in ambient air or at a dose of 1400 mg/m3 for 30 minutes can be fatal (6, 10). Phosphine gas disrupts oxidative phosphorylation by inhibiting the cytochrome-c oxidase enzyme and causes tissue damage via free oxygen radicals (11).
Since there is no specific laboratory test for diagnosis of ALP poisoning, clinical suspicion and history of drug intake are crucial (4). The gastrointestinal system, respiratory system, heart, and kidneys can be affected (7-9). Symptoms that may occur in patients include nausea, vomiting, dysphagia, abdominal pain, palpitations, shock, cardiac arrhythmias, pulmonary edema, dyspnea, cyanosis, and sensory changes, which can develop within a few hours after ingestion (2). In our case, the primary complaint during both initial and subsequent presentations was chest pain.
The amount and form of intake, the purpose of intake (accidental or intentional), and the timing of presentation to medical care are factors that influence the clinical course of ALP poisonings. While mortality is low in accidental ingestions, it can rise up to 85% in intentional ingestions, especially among young adults. Early complications often include cardiovascular collapse, pulmonary edema, acute respiratory distress syndrome, central nervous system depression, and coma, whereas late complications involve hepatotoxicity and nephrotoxicity (1).
Less common complications include intravascular hemolysis, acute adrenal insufficiency, pancreatitis, hypo-hyperglycemia, hypo-hypermagnesemia, methemoglobinemia, microangiopathic hemolytic anemia, and disseminated intravascular coagulation (12). In our patient, however, no complications related to ALP poisoning were detected.
Early presentation and prompt initiation of treatment are associated with a good prognosis, while treatment-resistant hypotension and acidosis are indicators of a poor prognosis. In early-stage ALP poisonings following oral ingestion, gastric lavage and administration of activated charcoal are crucial for survival. However, in cases of poisoning due to respiratory exposure, supportive therapies constitute the mainstay of treatment. The first step in treatment is intravenous hydration, with aggressive fluid resuscitation being the most important aspect of treatment in patients with unstable hemodynamics.
In cases where fluid therapy is ineffective, vasoactive agents such as norepinephrine, phenylephrine, dopamine, and dobutamine are added to the treatment regimen. Studies have shown that the early use of inotropes may not be very beneficial and may even increase myocardial oxygen consumption and arrhythmia frequency. Due to the prominent role of free oxygen radicals in ALP poisoning, antioxidant drugs such as N-acetylcysteine (NAC), calcium gluconate, pralidoxime, trimetazidine, and magnesium sulfate have been suggested to be beneficial in treatment.
In the literature, treatments such as hemodialysis, hemodiafiltration, and extracorporeal membrane oxygenation have been applied in limited cases. Cases benefiting from continuous renal replacement therapy and extracorporeal membrane oxygenation have also been reported. In some cases where intravenous fluid and inotropic therapies are ineffective, intra-aortic balloon pump has been used.
CONCLUSION
In cases of ALP poisoning, which carry a high mortality rate, a thorough history of drug intake should be carefully considered. It is essential to remember that clinical suspicion plays a crucial role in diagnosis, and early treatment can increase survival rates.
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