What is the treatment for yellow phosphorus (YP) consumption?

Treatment of Yellow Phosphorus Poisoning

There is no specific antidote for yellow phosphorus poisoning; management is entirely supportive, focusing on aggressive fluid resuscitation, correction of coagulopathy, management of acute liver failure, and early consideration for liver transplantation in patients who develop fulminant hepatic failure. 1, 2, 3

Immediate Management

Decontamination and Initial Stabilization

• Remove any contaminated clothing and perform thorough dermal decontamination with copious soap and water irrigation if external exposure occurred, using appropriate personal protective equipment to prevent caregiver contamination 4
• Gastric lavage may be considered in early presentation (within 1-2 hours), though efficacy is limited given rapid absorption from the gastrointestinal tract 5
• Activated charcoal is generally ineffective as yellow phosphorus is poorly adsorbed 2

Supportive Care (Cornerstone of Treatment)

• Aggressive intravenous fluid resuscitation to maintain hemodynamic stability and support renal perfusion 2, 3
• Correct coagulopathy aggressively with fresh frozen plasma, cryoprecipitate, and vitamin K as acute liver failure with coagulopathy develops in virtually all significant exposures 1, 2
• Monitor and manage electrolyte abnormalities, particularly hypocalcemia and hypophosphatemia that may paradoxically occur 2
• Provide nutritional support and glucose supplementation to prevent hypoglycemia in the setting of hepatic failure 3

Organ-Specific Management

Hepatic Failure Management

• Monitor hepatic enzymes, coagulation parameters (INR/PT), ammonia levels, and lactate as markers of hepatic injury and prognosis 1, 2, 3
• Manage hepatic encephalopathy with lactulose and rifaximin if it develops 3
• Consider N-acetylcysteine despite lack of specific evidence for yellow phosphorus, as it may provide antioxidant support in acute liver failure 3

Renal Support

• Initiate continuous renal replacement therapy (CRRT) for acute kidney injury, volume overload, or severe metabolic acidosis 3
• CRRT may also help remove circulating toxins and serve as a bridge to transplantation 3

Cardiovascular Support

• Monitor for cardiotoxicity with serial ECGs and cardiac biomarkers, as myocardial injury can occur 3
• Provide vasopressor support (norepinephrine preferred) if hypotension persists despite adequate fluid resuscitation 2

Advanced Therapies

Extracorporeal Support

• Plasmapheresis or plasma exchange has been used with limited success as a bridge to transplantation in patients with severe coagulopathy and hepatic failure 3
• Cytosorb hemoadsorption may be considered in select cases as a bridge to transplant, though evidence is limited 3

Liver Transplantation

• Early referral to a transplant center is critical for any patient developing signs of acute liver failure (encephalopathy, coagulopathy, lactic acidosis) 2, 3
• Liver transplantation is the definitive treatment for fulminant hepatic failure due to yellow phosphorus and has shown good outcomes in both adults and children when performed without contraindications 3
• Separate listing criteria should be applied to ensure rapid listing of critical patients, as deterioration can be swift 3
• Transplantation should not be delayed in appropriate candidates, as mortality approaches 100% in untreated fulminant hepatic failure 6, 2, 3

Monitoring Protocol

Essential Laboratory Monitoring

• Serial hepatic function tests (AST, ALT, bilirubin, alkaline phosphatase) every 6-12 hours initially 2
• Coagulation studies (PT/INR, fibrinogen) every 6-12 hours 1, 2
• Renal function (creatinine, BUN) and electrolytes daily 2
• Arterial blood gas and lactate to assess metabolic acidosis and tissue perfusion 3
• Complete blood count to monitor for neutropenia 3
• Creatine kinase to assess for rhabdomyolysis 3

Clinical Course and Prognosis

Expected Presentation Pattern

• Patients typically present with initial gastrointestinal symptoms (nausea, vomiting, abdominal pain, diarrhea) within hours of ingestion 1, 6, 2
• A "honeymoon period" may occur where symptoms temporarily improve 2
• Hepatic failure develops typically within 2-5 days, characterized by jaundice, coagulopathy, and encephalopathy 1, 2
• Mean presentation to hospital is often delayed to 5 days, which worsens prognosis 2

Prognostic Factors

• Dose ingested correlates directly with severity and outcome 6, 5
• Early presentation and aggressive supportive care improve survival 2, 3
• Development of multi-organ dysfunction (hepatorenal failure, cardiovascular collapse) is associated with near-certain mortality without transplantation 6, 2
• Lower doses may cause only gastrointestinal symptoms with spontaneous recovery 3

Critical Pitfalls to Avoid

• Do not delay transplant evaluation in patients showing signs of hepatic failure—early referral is essential as deterioration is rapid 2, 3
• Do not underestimate the severity based on initial presentation, as the "honeymoon period" can be misleading 2
• Do not rely on specific antidotes—none exist, and management is purely supportive 1, 2
• Ensure adequate personal protective equipment during decontamination to prevent secondary exposure to healthcare workers 4