What is the recommended acute management for yellow phosphorus poisoning?

Yellow Phosphorus Poisoning: Acute Management

There is no specific antidote for yellow phosphorus poisoning; immediate aggressive supportive care with early consideration for liver transplantation is the cornerstone of management, as this toxin causes severe acute liver failure with high mortality. 1, 2

Immediate Initial Management

Gastrointestinal Decontamination

• Perform gastric lavage followed by activated charcoal administration (1 g/kg orally in a slurry) via nasogastric tube if the patient presents early after ingestion. 3, 2
• This should be done as soon as possible after presentation, ideally within the first few hours of ingestion. 2

Aggressive Fluid Resuscitation

• Initiate aggressive intravenous fluid resuscitation immediately to address gastrointestinal losses and maintain hemodynamic stability. 3, 2
• Yellow phosphorus poisoning causes severe vomiting and diarrhea leading to significant volume depletion. 1

Intensive Care Management

Monitoring and Supportive Care

• Admit all patients with confirmed or suspected yellow phosphorus ingestion to an intensive care unit for close monitoring of hepatic function, coagulation parameters, acid-base status, and multi-organ function. 2
• Monitor for development of hepatic encephalopathy, coagulopathy, lactic acidosis, cardiotoxicity, rhabdomyolysis, and neutropenia—all well-documented complications. 1, 2
• Serial MELD scores should be calculated to track disease progression and guide transplant decisions. 4

Extracorporeal Therapies

Therapeutic plasma exchange (TPE) should be initiated early in patients developing acute liver failure, as it significantly improves transplant-free survival and can serve as a bridge to either recovery or transplantation. 2, 4, 5, 6

TPE Protocol Details:

• Perform low-volume TPE (1.3 to 1.5 plasma volumes) for three consecutive days, with three additional sessions if needed. 4
• Replace with 0.9% normal saline, 5% human albumin solution, and fresh frozen plasma based on clinical parameters. 4
• Early initiation is critical—delay in starting TPE is an independent predictor of mortality. 4
• TPE works by removing the toxin, its metabolites, and inflammatory mediators. 5

Continuous renal replacement therapy (CRRT) should be used for patients developing acute kidney injury or severe metabolic acidosis. 1, 2

Liver Transplantation Considerations

All patients developing acute liver failure from yellow phosphorus poisoning should be immediately listed for emergency liver transplantation, as this is often the only definitive lifesaving treatment. 1, 2

Transplant Listing Criteria:

• Development of hepatic encephalopathy (any grade). 2, 6
• Progressive coagulopathy despite fresh frozen plasma. 2
• Lactic acidosis. 1, 2
• Refractory shock requiring vasopressor support. 4
• Rising MELD score despite maximal medical therapy. 4

Important Transplant Considerations:

• Liver transplantation has excellent outcomes in yellow phosphorus-induced ALF when performed before irreversible multi-organ failure develops. 1
• Success rates are very promising in both adult and pediatric patients, provided there are no contraindications to transplant. 1
• TPE can serve as a bridge to transplantation in critically ill patients awaiting organ availability. 2, 5, 6

Predictors of Poor Outcome

The following are independent predictors of mortality and should trigger immediate escalation of care:

• Refractory shock requiring high-dose vasopressors. 4
• Delay in initiating extracorporeal therapies. 4
• Severe metabolic acidosis. 4
• MELD score >35. 4

Critical Pitfalls to Avoid

• Do not wait for "spontaneous recovery" in patients with evidence of acute liver failure—yellow phosphorus causes unpredictable and rapid deterioration. 2
• Do not delay TPE initiation while waiting for transplant evaluation—early TPE improves outcomes regardless of eventual need for transplantation. 4, 6
• Do not underestimate lower-dose ingestions—even smaller amounts can cause significant hepatic injury requiring intensive monitoring. 1
• Do not discharge patients who appear stable initially—clinical deterioration can occur rapidly over 24-48 hours after ingestion. 2