Rat Poisoning

Introduction and Classification

• Rodenticide poisoning is a highly significant pediatric emergency in India, ranking as a leading cause of toxic hepatotoxicity and multi-organ failure.
• Exposure is typically accidental in toddlers due to the sweet paste formulation of rodenticides, and intentional in adolescents.
• Early identification of the active compound is critical as clinical features and treatments are highly substance-specific.

Table 1: Classification of Common Rodenticides in India

Table 2: Overview of Major Rodenticides

1. Yellow Phosphorus (YP) Poisoning

Pathophysiology and Kinetics

• Yellow phosphorus is a highly lipophilic, protoplasmic cellular toxin.
• It is commonly marketed as a 3% paste (e.g., Ratol®) or used in fireworks.
• It causes rapid inhibition of protein synthesis and cellular energy failure, leading to microvesicular steatosis and hepatocyte necrosis.
• Hypocalcemia can occur due to the binding of calcium with excessive phosphorus in the bloodstream.

Triphasic Clinical Stages

• Stage 1: Gastrointestinal Phase (0 to 24 hours):
  • Manifests as abdominal pain, nausea, severe vomiting, and diarrhea.
  • Vomitus and feces may be luminescent ("smoking stool") and carry a strong garlic-like odor.
• Stage 2: Latent Phase (24 to 72 hours):
  • The child experiences a temporary resolution of gastrointestinal symptoms.
  • Serum transaminases (AST, ALT) and bilirubin begin to rise progressively.
• Stage 3: Hepato-Renal Phase (Greater than 72 hours):
  • Fulminant acute liver failure (ALF) develops, accompanied by hepatic encephalopathy and coma.
  • Coagulopathy, bleeding diathesis, acute kidney injury (renal tubular necrosis), and arrhythmias emerge.
  • Circulatory shock and cardiovascular collapse are the primary causes of death.

Management Protocol

• Gastric Decontamination:
  • Perform gastric lavage using a 1:1000 potassium permanganate ((KMnO_4)) solution.
  • This oxidizes toxic elemental phosphorus into non-toxic phosphates.
  • Administer single-dose activated charcoal ((1\text{ g/kg})) to bind remaining enteral toxin.
• Hepatoprotective Strategy:
  • Initiate an intravenous N-acetylcysteine (NAC) infusion protocol to replenish glutathione stores and mitigate oxidative injury.
• Therapeutic Plasma Exchange (TPE):
  • TPE acts as a vital non-transplant option or bridge to transplantation.
  • Early standard volume TPE (initiated within 15–18 hours of ingestion) removes fat-soluble toxins, clears inflammatory cytokines, and corrects coagulopathy.
• Definitive Cure:
  • Emergency liver transplantation is the only curative intervention for patients progressing to fulminant hepatic failure.

2. Metal Phosphide Poisoning (Aluminium / Zinc Phosphide)

Pathophysiology

• These are inorganic metallic salts used widely as agricultural fumigants and household rodenticides.
• Upon contact with gastric hydrochloric acid or moisture, they release highly toxic phosphine gas.
• Phosphine halts oxidative phosphorylation by binding to cytochrome c oxidase, causing severe cellular anoxia.
• It triggers lipid peroxidation, destroying cellular membranes in vital organ systems.

Clinical Features and Systemic Toxicity

• Gastrointestinal: Intractable vomiting, severe epigastric pain, and a distinct garlic breath odor.
• Cardiovascular: Circulatory collapse, profound refractory shock, toxic myocarditis, pericarditis, and congestive heart failure.
• Pulmonary: Severe dyspnea, chest tightness, acute pulmonary edema, and ARDS.
• Metabolic: Widespread metabolic acidosis, severe hypoglycemia, and electrolyte imbalances (including hypo- or hypermagnesemia).

Management Protocol

• Decontamination Safety:
  • Gastric lavage with water is strictly contraindicated as it accelerates phosphine gas release and endangers healthcare staff.
  • Lavage with vegetable oils (such as coconut oil) can be considered to reduce the release and dissolution of phosphine.
  • Instill activated charcoal to limit systemic absorption.
• Hemodynamic and Intensive Care Support:
  • Transfer the pediatric patient immediately to an intensive care unit (ICU).
  • Aggressively treat shock with intravenous crystalloids and vasoactive infusions (epinephrine, norepinephrine, or dopamine).
  • Closely monitor and correct metabolic acidosis (via sodium bicarbonate), hypoglycemia, and dyselectrolytemia.
  • Provide prompt mechanical ventilation for respiratory failure or acute pulmonary edema.

3. Anticoagulant Rodenticides (LAARs / Superwarfarins)

Pathophysiology

• Includes long-acting agents like brodifacoum, bromadiolone, and indanedione derivatives.
• These compounds inhibit vitamin K1 epoxide reductase, stopping the cyclic regeneration of active Vitamin K.
• This leads to a severe failure of gamma-carboxylation of Vitamin K-dependent clotting factors: Factor II, VII, IX, and X.
• Due to the extremely long half-lives of superwarfarins, coagulopathy persists for weeks to months.

Clinical Features

• Symptoms are typically delayed for 24 to 48 hours until pre-existing clotting factors deplete below 30% of normal.
• Manifests as mucocutaneous bleeding, epistaxis, hematuria, gastrointestinal bleeding, ecchymoses, and large hematomas.
• Intracranial hemorrhage is the most feared and fatal complication.

Diagnostic Investigations

• Universal prolongation of Prothrombin Time (PT) and International Normalized Ratio (INR), along with activated Partial Thromboplastin Time (aPTT).
• Coagulation factor assays confirm a decrease in factors II, VII, IX, and X.

Antidotal and Hemostatic Management

• Antidotal Therapy (Vitamin K1):
  • Phytomenadione (Vitamin K1) is the specific antidote.
  • Active Bleeding: Administer Vitamin K1 at (10 - 20\text{ mg}) via slow intravenous (IV) infusion.
  • No Active Bleeding (INR elevation only): Administer Vitamin K1 at (5 - 10\text{ mg}) IV or orally.
  • Maintenance dosing of (10 - 120\text{ mg/day}) must be continued for several weeks based on serial INR monitoring.
• Hemostatic Resuscitation:
  • Transfuse fresh frozen plasma (FFP) or prothrombin complex concentrates (PCC) to restore active clotting factors during major hemorrhagic crises.
  • Therapeutic Plasma Exchange (TPE) is highly effective in removing brodifacoum due to its low volume of distribution and high protein-binding capacity, especially if the child develops an anaphylactic reaction to Vitamin K.

4. Other Chemical Rodenticides

Table 3: Summary of Niche Rodenticide Toxins