Ver el código de «Aluminum phosphide poisoning»

==Background==
*Aluminum phosphide (AlP) poisoning is one of the most lethal forms of self-poisoning worldwide.
*Upon contact with moisture or gastric acid, AlP liberates phosphine gas (PH₃), which inhibits mitochondrial cytochrome C oxidase, causing profound cellular hypoxia, refractory cardiovascular collapse, and multiorgan failure.<ref name="Gurjar2011">Gurjar M, et al. Managing aluminum phosphide poisonings. ''J Emerg Trauma Shock''. 2011;4(3):378-384. doi:10.4103/0974-2700.83868</ref> There is no specific antidote; mortality ranges from 37-100%.<ref name="Wahab2008">Wahab A, Zaheer MS, Wahab S, Khan RA. Acute aluminium phosphide poisoning: an update. ''Hong Kong J Emerg Med''. 2008;15:152-155.</ref>
*Aluminum phosphide is sold as tablets or pellets (3 g each, containing approximately 56% AlP) under trade names including Celphos, Quickphos, Phostoxin, and Fumitoxin
*Known colloquially as "rice tablet" in parts of India and Iran
*Used worldwide as a grain fumigant and rodenticide, especially in developing countries
*AlP is unstable — releases phosphine gas rapidly on contact with moisture, making it more acutely lethal than [[Zinc phosphide poisoning|zinc phosphide]]<ref name="Trakul2017">Trakulsrichai S, et al. Clinical characteristics of zinc phosphide poisoning in Thailand. ''Ther Clin Risk Manag''. 2017;13:335-340.</ref>
* Lethal dose: 150-500 mg (as little as one-tenth of a standard 3 g tablet can be fatal)<ref name="Gurjar2011"/>
*Deaths from cardiovascular toxicity typically occur within the '''first 12-24 hours'''<ref name="Turkmen2016">Turkmen YH, et al. Successful Management of Aluminium Phosphide Poisoning Resulting in Cardiac Arrest. ''Turk J Anaesthesiol Reanim''. 2016;44(3):155-157. doi:10.5152/TJAR.2016.96168</ref>
*Most poisoning cases are intentional (self-harm) in young adults in agricultural regions of South Asia, the Middle East, and Africa<ref name="Ethiopia2021">Teshome Z, et al. Clinical Profile and Treatment Outcome of Aluminum Phosphide Poisoning in Felege Hiwot Referral Hospital, Northwest Ethiopia. ''Open Access Emerg Med''. 2021;13:223-230. doi:10.2147/OAEM.S313181</ref>

===Mechanism of toxicity===
*AlP + gastric HCl/moisture → phosphine gas (PH₃)
*Phosphine inhibits cytochrome C oxidase (complex IV of mitochondrial electron transport chain) → blocks oxidative phosphorylation → cellular energy crisis<ref name="Gurjar2011"/>
*Generates highly reactive hydroxyl radicals → lipid peroxidation, glutathione depletion → oxidative cellular injury
* Myocardium is the primary target — cell membrane dysfunction, impaired glucose utilization, oxidative stress → cardiogenic shock (most common cause of death)<ref name="Nature2025">Aluminum phosphide poisoning and its clinical management. ''Nature Research Intelligence''. 2025.</ref>
*Also targets lungs, liver, kidneys, adrenals, and GI tract
*Phosphine may also be exhaled by the patient and released from vomitus — posing a risk to healthcare workers

===Healthcare worker safety===
* Phosphine gas is hazardous to staff — vomitus, gastric aspirate, and exhaled air may contain phosphine
*Treat in a well-ventilated area or negative-pressure room
*PPE including respiratory protection is recommended
*Exposure at 1400 mg/m³ for 30 minutes can be fatal<ref name="Turkmen2016"/>
*Handle gastric lavage effluent as hazardous material

==Clinical features==
*Onset is rapid (minutes to hours), in contrast to the more delayed presentation of zinc phosphide<ref name="Trakul2017"/>
*The cardinal feature is profound, refractory hypotension (present in 50-100% of severe cases)<ref name="Gurjar2011"/>

===Gastrointestinal===
*Nausea, vomiting (most common presenting symptom; 74% of cases)<ref name="Ethiopia2021"/>
*Severe epigastric and abdominal pain
*Diarrhea
*Hematemesis (from erosive gastropathy)
* Garlic or decaying fish odor from breath/vomitus (classic but not always present)

===Cardiovascular (primary cause of mortality)===
* Refractory hypotension and [[Cardiogenic shock|cardiogenic shock]]
*Myocarditis, pericarditis, subendocardial infarction
*ECG abnormalities: ST-segment elevation/depression, T-wave inversion, QTc prolongation, conduction blocks, ventricular tachycardia, atrial fibrillation<ref name="Gurjar2011"/>
* Cardiac arrest (often within 12-24 hours of ingestion)
*Elevated troponin

===Respiratory===
*Dyspnea, tachypnea
*[[Acute pulmonary edema]] (cardiogenic and non-cardiogenic)
*[[ARDS]]
*Respiratory failure requiring intubation

===Metabolic===
* Severe metabolic acidosis (high anion gap; elevated lactate) — most sensitive marker of severity and strongest predictor of mortality<ref name="Gurjar2011"/>
*Hyperkalemia (from cellular injury and acidosis)
*Hypomagnesemia (associated with increased mortality)
*Hypoglycemia (poor prognostic sign)

===Hepatic===
*Hepatocellular injury (elevated AST, ALT)
*Hepatic failure with coagulopathy

===Renal===
*[[Acute kidney injury]]
*Oliguria/anuria

===Neurologic===
*Agitation, restlessness, anxiety
*Altered mental status, delirium, coma
*Seizures

===Other===
*[[Methemoglobinemia]] (less common)
*[[DIC|Disseminated intravascular coagulation]]
*Adrenal insufficiency

==Differential diagnosis==
*[[Zinc phosphide poisoning]] (slower onset, lower mortality)
*[[Organophosphate poisoning]]
*[[Acute myocardial infarction]] or [[Myocarditis|myocarditis]] (other causes)
*[[Septic shock]]
*[[Acute gastroenteritis]] (early presentation)
*[[Iron toxicity]]
*[[Arsenic poisoning]]
*[[Cyanide poisoning]] (similar mechanism of cytochrome oxidase inhibition)
*[[Calcium channel blocker toxicity]] (refractory hypotension with cardiogenic shock)


{{Toxic gas exposure DDX}}

==Evaluation==
===Workup===
* Silver nitrate test: simple bedside diagnostic test<ref name="Gurjar2011"/>
**Expose filter paper impregnated with silver nitrate solution to the patient's gastric aspirate, vomitus, or exhaled breath
**Positive test: paper turns black (silver phosphide formation) — confirms phosphine exposure
* ABG/VBG: metabolic acidosis with elevated lactate — severity correlates directly with mortality
* ECG: continuous monitoring; look for ST changes, QTc prolongation, arrhythmias, conduction blocks
* CBC, BMP, hepatic function panel, coagulation studies (PT/INR)
* Cardiac biomarkers: troponin (serial), BNP
* Serum magnesium, calcium, phosphorus
* Blood glucose (monitor frequently; hypoglycemia is a poor prognostic indicator)
* Chest radiograph: pulmonary edema, ARDS
* Echocardiography: assess myocardial function; may show global hypokinesis in severe myocarditis
* Abdominal radiograph: AlP tablets are not reliably radiopaque (unlike zinc phosphide)
* Methemoglobin level if cyanosis present
* Salicylate, acetaminophen, ethanol levels if intentional co-ingestion suspected

===Diagnosis===
*Primarily clinical: history of ingestion of fumigant/rodenticide tablet + garlic odor + rapid-onset refractory shock + metabolic acidosis
* Silver nitrate test on gastric aspirate or breath is the most accessible confirmatory test
*Phosphine gas levels are not routinely available
* Poor prognostic indicators:<ref name="Gurjar2011"/><ref name="Ethiopia2021"/>
**Shock or hypotension at presentation
**Severe metabolic acidosis (pH <7.2) or elevated lactate
**Cardiac arrhythmias
**Hyperkalemia
**Hypoglycemia
**Need for vasopressors or mechanical ventilation
**Amount ingested >1.5 g

==Management==
No specific antidote exists. Management is aggressive supportive care and GI decontamination.<ref name="Gurjar2011"/>

===GI decontamination===
* Gastric lavage with potassium permanganate (KMnO₄ 1:10,000) — oxidizes phosphine to non-toxic phosphate<ref name="Gurjar2011"/>
* Coconut oil (100-200 mL via NG tube) — forms a protective mucosal barrier and may reduce phosphine liberation; reported to decrease absorption even up to 6 hours after ingestion<ref name="Shadnia2005">Shadnia S, et al. Successful treatment of acute aluminium phosphide poisoning: possible benefit of coconut oil. ''Hum Exp Toxicol''. 2005;24(4):215-218.</ref>
* Sodium bicarbonate (NaHCO₃ 7.5%) added to lavage fluid — neutralizes gastric acid to reduce phosphide-to-phosphine conversion<ref name="Agrawal2015">Agrawal VK, et al. Aluminum phosphide poisoning: possible role of supportive measures in the absence of specific antidote. ''Indian J Crit Care Med''. 2015;19(2):113-115. doi:10.4103/0972-5229.151019</ref>
*'''Do NOT use plain water''' for lavage — promotes phosphine gas formation
* Activated charcoal: limited evidence of benefit (phosphine is a gas and poorly adsorbed); may be given if co-ingestant suspected
*'''Do NOT induce emesis''' — re-exposure risk and aspiration hazard

===Cardiovascular support (core of management)===
* Aggressive IV fluid resuscitation
* Vasopressors: norepinephrine or dopamine for refractory hypotension; high doses frequently required<ref name="Gurjar2011"/>
* Intra-aortic balloon pump (IABP): case reports of use as rescue therapy for refractory cardiogenic shock<ref name="Siddaiah2009">Siddaiah L, et al. Intra-aortic balloon pump in toxic myocarditis due to aluminium phosphide poisoning. ''J Med Toxicol''. 2009;5(2):80-83.</ref>
* Hyperinsulinemia-euglycemia therapy (HIE): emerging evidence suggests benefit by shifting myocardial metabolism from beta-oxidation to glycolysis, improving contractility<ref name="Nature2025"/>
**Insulin 1 IU/kg/h with dextrose infusion to maintain euglycemia
* ECMO (extracorporeal membrane oxygenation): may be considered as bridge therapy in refractory cardiogenic shock in centers with capability
* Continuous cardiac monitoring — arrhythmias are common and frequently fatal
*For ventricular tachycardia or [[Torsades de pointes]]: magnesium sulfate, lidocaine, defibrillation
** Avoid class IA (procainamide, quinidine), IC, and III antiarrhythmics — risk of further QTc prolongation

===Magnesium sulfate===
* IV magnesium sulfate — membrane stabilizer, antioxidant (restores glutathione), cardioprotective<ref name="Gurjar2011"/>
*Multiple dosing regimens described; one protocol: 1 g IV q1h for 3 hours, then 6 g/day infusion for 3-5 days<ref name="Agrawal2015"/>
*Studies suggest improved survival, particularly in patients with hypomagnesemia<ref name="Gurjar2011"/>
*Monitor for magnesium toxicity (loss of DTRs, respiratory depression)

===Sodium bicarbonate===
*IV sodium bicarbonate for correction of metabolic acidosis
*Also used in gastric lavage (see above)
*May help stabilize myocardial membranes

===Antioxidant therapy===
* N-acetylcysteine (NAC): hepatoprotective, replenishes glutathione; loading dose 140 mg/kg, maintenance 70 mg/kg for 17 additional doses<ref name="Nature2025"/>
* Vitamin C: 1 g IV q8h (antioxidant; limited evidence)
* Vitamin E: 100 IU q12h (antioxidant; limited evidence)

===Additional supportive measures===
* Hydrocortisone: IV stress-dose steroids for refractory shock (relative adrenal insufficiency may contribute)<ref name="Ethiopia2021"/>
* Calcium gluconate: for hypocalcemia
* Hemodialysis: not effective at removing phosphine (protein-bound), but essential for supportive management of AKI, hyperkalemia, and refractory acidosis<ref name="Turkmen2016"/>
* Blood products: as needed for coagulopathy/DIC
* Intubation and mechanical ventilation for respiratory failure

==Medication Dosing==
{{MedicationDose
| drug = Magnesium sulfate
| dose = 4g IV over 20min, then 6g over 12hr infusion
| route = IV
| context = Cardioprotective, may reduce mortality
| indication = Aluminum phosphide poisoning
| population = Adult
}}
{{MedicationDose
| drug = Sodium bicarbonate
| dose = 1-2mEq/kg IV bolus, then infusion to maintain pH >7.2
| route = IV
| context = Correct metabolic acidosis
| indication = Aluminum phosphide poisoning
| population = Adult
}}

==Disposition==
*'''All patients with confirmed or suspected AlP ingestion must be admitted to the ICU''' — even if initially stable<ref name="Gurjar2011"/>
* Continuous cardiac monitoring for a minimum of 72 hours — most deaths occur within 12-24 hours, but delayed deterioration can occur
*Serial ABGs, ECGs, cardiac biomarkers, LFTs, renal function, electrolytes, and blood glucose every 4-6 hours during the first 48 hours
* Death typically occurs from refractory cardiogenic shock within 24 hours in severe cases<ref name="Turkmen2016"/>
*Survivors of the acute phase generally recover fully if organ failure is supported
* All intentional ingestions: psychiatric evaluation mandatory prior to discharge
*Contact [[Poison control]] (1-800-222-1222 in the US) for all cases
*Key differences from [[Zinc phosphide poisoning|zinc phosphide poisoning]]:

{| class="wikitable"
|-
! Feature !! Aluminum phosphide !! Zinc phosphide
|-
| Onset of systemic toxicity || Rapid (minutes to hours) || Delayed (hours to >12 hours)
|-
| Stability of compound || Unstable; rapid phosphine release || Relatively stable
|-
| Radiopaque on X-ray || No (not reliably) || Yes (zinc component)
|-
| Mortality rate || Higher (37-100%) || Lower (~7-37%)
|-
| Primary cause of death || Cardiogenic shock || Cardiogenic shock/hepatic failure
|-
| Hepatic failure || Less prominent || More prominent (delayed)
|}

==See Also==
*[[Zinc phosphide poisoning]]
*[[Organophosphate poisoning]]
*[[Cyanide poisoning]]
*[[Carbon monoxide poisoning]]
*[[Calcium channel blocker toxicity]]
*[[Methemoglobinemia]]
*[[Cardiogenic shock]]
*[[Acute kidney injury]]
*[[Torsades de pointes]]

==External Links==
*[https://pmc.ncbi.nlm.nih.gov/articles/PMC3162709/ J Emerg Trauma Shock — Managing aluminum phosphide poisonings (2011)]
*[https://pmc.ncbi.nlm.nih.gov/articles/PMC4339895/ Indian J Crit Care Med — Aluminum phosphide poisoning: possible role of supportive measures (2015)]
*[https://pmc.ncbi.nlm.nih.gov/articles/PMC4917145/ Turk J Anaesthesiol Reanim — Successful Management of AlP Poisoning Resulting in Cardiac Arrest (2016)]
*[https://pmc.ncbi.nlm.nih.gov/articles/PMC8216064/ Open Access Emerg Med — Clinical Profile and Treatment Outcome of AlP Poisoning, Ethiopia (2021)]
*[https://pmc.ncbi.nlm.nih.gov/articles/PMC12309822/ Turk J Emerg Med — Aluminum phosphide: Toxicological profiles, health risks, and management protocols (2025)]

==References==
<references/>

[[Category:Toxicology]]