ACMT Toxicology Visual Pearl – Black Vomit, Big Problem

4. Zinc Phosphide

Background [1-3]

Zinc and aluminum phosphide rodenticides are available in pellet form and, when ingested, cause a rapid toxidrome with nausea and vomiting of dark emesis with a garlicky or fishy odor and a high risk of cardiovascular collapse.  Poisoning with metal phosphides is relatively rare in North America; however, in agricultural regions of South Asia, the Middle East, and North Africa, it represents a leading cause of mortality due to their widespread use and low cost.  Case fatality rates range from 30% to 70% secondary to refractory shock.

What are metal phosphides? [1,2]

• Inorganic compounds made of phosphorus bound to a metal, most commonly zinc and aluminum
• Can be solid pellets, tablets, or granules, which are typically used as rodenticides for mice, rats, or gophers, and as agricultural fumigants, especially in stored grains for shipping
• When exposed to water or acid, metal phosphides release highly toxic phosphine gas.
  • Aluminum phosphide (Al P) + 3H₂O —–> Phosphine gas (PH₃) + aluminum hydroxide (Al (OH₃))

How do metal phosphides cause illness? [1-4]

• Toxicity is secondary to the released phosphine gas which is colorless and easily absorbed via the lungs or the GI tract.
• Phosphine gas
  • Inhibits mitochondrial oxidative phosphorylation
  • Disrupts electron transport
  • Causes cellular hypoxia despite normal oxygen delivery
  • Leads to oxidative stress and membrane damage
• The myocardium is especially vulnerable, resulting in:
  • Profound shock
  • Myocarditis
  • Arrhythmias
  • Rapid cardiovascular collapse
• Phosphine gas can be generated for hours after ingestion and can expose health care workers via secretions, emesis, or stool.

What is the clinical presentation after ingestion of metal phosphide? [1-3]

• Symptom onset is almost immediate due to rapid production of phosphine gas.
  • Headache and dizziness
  • Nausea, vomiting, and abdominal pain
  • Vomitus can smell garlicky or fishy.
  • Significant gastrointestinal irritation results in mucosal damage and bleeding, leading to coffee-ground or black emesis.
• Patients may initially appear stable but often decompensate rapidly.
• Serious toxicity presents within six hours:
  • Myocardial depression leading to heart failure
  • Pulmonary edema
  • Metabolic acidosis
  • Hypotension, often severe and refractory
  • Cardiac arrhythmias
• Most deaths occur within the first 12 – 24 hours.
  • Mortality approaches 30 – 70% in patients who have this toxicity.
• Patients surviving the initial phase will often develop complications such as acute kidney injury, liver injury, ARDS, and persistent cardiogenic shock within 24 – 72 hours after ingestion.
  • Survival beyond 72 hours is a favorable prognostic sign.

How can you diagnose metal phosphide toxicity? [4-7]

• History and exam are imperative to recognize this toxicity.
• Ask about occupational exposures, rodenticide or fumigant use.
  • If an exposure occurs, it is important to determine timing, route, concentration, and amount ingested if possible.
• Garlic or fishy smell can be suggestive, as well as dark colored emesis.
• Silver nitrate paper often reacts with phosphine gas, changing color to dark gray or black.
  • May be used on breath or vomitus to detect the presence of phosphine gas.
• Laboratory testing often demonstrates severe acidosis with an elevated lactate.
• Metal phosphides may be radiopaque on X-ray.
• ECG findings may display nonspecific arrhythmias, heart blocks, and STEMI mimics.
• Pulmonary edema is often seen on chest x-rays.
• Bedside echo may demonstrate hypokinesia and a significantly reduced ejection fraction.

What is the management of metal phosphide toxicity? [3-10]

• It is imperative to ensure bedside teams have appropriate PPE and handle waste with care, as phosphine gas can be inhaled and is highly toxic even at low concentrations.
  • Recommended PPE includes skin, eye, and respiratory protection.
  • If there is concern for off-gassing, then rubber gloves, chemical-resistant suits, and full-face respirators are recommended.
  • Ensure adequate room ventilation; consider a negative-pressure room if there is a large ingestion or a high-risk procedure.
  • Place bodily fluids in sealed containers when able.
• Be aware that phosphine gas can continue to be generated for hours after ingestion.
• There is no antidote, and supportive care is the cornerstone of management.
• GI decontamination can be considered early in presentation.
  • Emerging studies show that GI decontamination with oils such as paraffin oil can reduce mortality and the need for intubation by encapsulating metal phosphide pellets and decreasing phosphine gas production. [9, 10]
• Secure the patient’s airway if there is significant vomiting, agitation, or respiratory concerns.
• IV fluid resuscitation
• Cardiac monitoring for arrhythmias
• Correction of electrolyte abnormalities
• Early vasopressors and hemodynamic monitoring are crucial.
• In severe refractory shock, ECMO and CRRT may be utilized if available.
• Some exploratory treatments such as Vitamin E, NAC, high-dose insulin, Coenzyme Q, and pralidoxime have been tried; however, results are variable, and more studies are needed.

Bedside Pearls

• Metal phosphides are rodenticides or agricultural fumigants that release phosphine gas upon interaction with water or acid.
• Globally, they are one of the leading causes of suicide-related poisoning.
• Clinical presentations include early GI symptoms with garlicy smelling and black colored emesis followed by profound shock, cardiac arrhythmias, and severe metabolic acidosis.
• No antidote is available; the quality of resuscitation affects overall survival.
• Emerging studies suggest that GI decontamination with oil can improve outcomes.
• Off-gassing of phosphine gas in the patient’s vomit, secretions and other bodily fluids may occur, and treatment teams must ensure they have appropriate PPE.