Household Poisoning Notes

Corrosives

Corrosives are substances that destroy body tissues upon contact.

Types of Corrosives

  • Acids: Give hydrogen ions.

    • Inorganic: HCl, nitric acid, sulfuric acid.

    • Organic: Carbolic, oxalic, acetic acids.

  • Alkalis: Receive hydrogen ions. Examples include Potassium hydroxide KOH, Sodium hydroxide NaOH, Ammonia (NH_4OH).

  • Other: Salts of heavy metals, k permanganate, Iodine, Hydrogen peroxide (H2O2), Cationic detergent.

Pathophysiology

Local Effects

  • Acids: Coagulative necrosis, forming a protective eschar, primarily affecting the stomach.

  • Alkalis: Liquefactive necrosis, causing penetrating injuries, commonly affecting the esophagus and oropharynx.

Systemic Effects

  • Some organic acids (e.g., phenol) have systemic effects.

Clinical Presentation

  • Severe pain from mouth to stomach.

  • Oropharyngeal burns.

  • Swelling of lips, tongue edema, dysphagia, hoarseness, drooling.

  • Vomiting, hematemesis, and melena.

  • Inhalation: Cough, dyspnea, stridor, wheezing, chemical pneumonitis, ARDS.

  • Eye exposure: Pain, redness, conjunctivitis, keratitis, blindness.

  • Dermal exposure: Pain, burn.

Complications

Acute

  • Respiratory: Laryngeal edema, ARDS.

  • GIT: Hemorrhage, perforation.

  • Shock: Hemorrhagic, neurogenic, septic.

  • DIC, Renal failure.

Delayed

  • Sloughing: Mediastinitis, Pericarditis, Tracheoesophageal fistula, Pleurisy.

  • Scarring: Esophageal obstruction, Pyloric stenosis, Malnutrition, dehydration, cachexia.

Investigations

  • Upper GI endoscopy (within 12-24 hours) unless perforation, airway edema, or shock is present.

  • Labs: ABG, Electrolytes, glucose, CBC, Coagulation profile, Liver enzymes, kidney functions.

  • Radiography: Chest x-ray (mediastinal air), Abdominal x-ray (free abdominal air), CT scan (perforation), Barium swallow (stenosis).

Treatment

  • Stabilization: ABCD.

  • No antidotes.

  • Decontamination: NO Gastric lavage, Emesis, Activated charcoal, Catharsis, Neutralization.

  • Dilution therapy: Milk or water (if alert, no airway compromise, no vomiting, no abdominal pain, no hematemesis).

  • Supportive: Pain killers, H_2 blockers or PPIs, Antibiotics, Steroids (controversial).

  • Feeding: Gastrostomy, jejunostomy, TPN.

  • Surgical intervention: Emergency (hemorrhage, perforation), Elective (Esophageal bypass, Dilatation, Repair of fistula, Gastrostomy).

Carbolic Acid (Phenol)

  • Disinfectant; organic acid.

  • Local: Mild corrosive, local anesthetic, coagulative necrosis.

  • Systemic: CNS stimulation then depression, Respiratory depression, Myocardial depression, Hemolysis, Acute renal failure. Urine turns dark green.

  • Causes of death: Early (CNS depression), Late (Renal complications).

Treatment

  • ABCD.

  • No antidote.

  • Decontamination: Gastric lavage within 1 hour (controversial), wash skin.

  • Supportive: Hemodialysis, Methylene blue (Methemoglobinemia), Alkalinization of urine and blood transfusion (Hemolysis).

Kerosene

Pathophysiology

Low viscosity, high volatility, and low surface tension leading to aspiration. Destroys surfactant, causing respiratory tract injury.

Clinical Picture

  • GIT: Nausea, vomiting, diarrhea, abdominal pain.

  • Pulmonary: Chemical pneumonitis, respiratory distress, dyspnea, tachypnea, bronchospasm, non-cardiogenic pulmonary edema.

  • Neurologic: Dizziness, stupor, hyporeflexia, coma, central respiratory depression.

  • Cutaneous: Mild erythema, dermatitis.

Causes of Death

Early: Respiratory failure, ventricular arrhythmia. Delayed: Bronchopneumonia, non-cardiogenic pulmonary edema.

Investigations

  • ABG.

  • Chest x-ray (after 6 hours).

  • Lab investigations for toxic additives.

Treatment

  • Emergency Measures: ABCD, Oxygen, bronchodilators.

  • No specific antidote.

  • Decontamination:

    • Cutaneous: Wash with soap and water.

    • Gastric lavage (if toxic additives are present) after intubation.

    • No activated charcoal.

  • Symptomatic: Care of chemical pneumonitis, antibiotics (if bacterial pneumonia), corticosteroids (controversial).

Insecticides

Types

Organophosphates, Carbamates, Pyrethroids

Mechanism of Action (Organophosphates)

Inhibition of acetyl choline esterase enzyme, accumulation of acetyl choline neurotransmitters, stimulation of nicotinic, muscarinic and CNS cholinergic receptors; irreversible if 24 hours pass without treatment

Clinical Picture

Muscarinic Stimulation (DUMBLES)

Diarrhea, Urination, Miosis, Bradycardia, Bronchospasm, Bronchorrhea, Lacrimation, Emesis, Salivation and Sweating

Nicotinic Stimulation (MATCH)

Muscle Fasciculation, Adrenal Medullary Hyperactivity, Tachycardia, Cramps, Hypertension

Central Effects

Confusion, Tremors, Convulsions, Coma

Complications

  • Intermediate Syndrome: Muscle weakness involving respiratory muscles, 2-5 days after acute cholinergic crises.

  • Delayed Neuropathy: Sensory and motor neuropathy, 2-3 weeks later.

  • Cardiotoxicity: Prolonged QT interval, ventricular tachycardia.

Causes of Death

Respiratory failure (Bronchorrhea, Bronchospasm, Respiratory muscle paralysis, Respiratory center inhibition), Ventricular Arrhythmia

Investigations

  • ABG, Electrolytes, Glucose.

  • Renal and Liver Functions.

  • ECG.

  • Cholinesterase enzyme level.

Treatment

  • Emergency Treatment: ABCD, Atropine.

  • Antidotes:

    • Atropine: Competitively antagonizes Ach at muscarinic receptors; does not antagonize nicotinic receptors. Administer until full atropinization (dryness of chest).

    • Cholinesterase Reactivators (Oximes): Pralidoxime, Obidoxime; reactivate Ach esterase enzyme; give within first 48 hours before aging of the enzyme.

  • Decontamination and Elimination:

    • Skin: Remove clothes, wash with soap and water.

    • Ingestion: Gastric lavage with endotracheal intubation, activated charcoal. Avoid emesis.

  • Supportive Treatment: Management of arrhythmia, convulsions (diazepam), and complications.

Carbamates

  • Inhibit Ach E by carbamylation; milder picture; no CNS manifestations.

  • Enzyme recovery in 1-2 days.

  • Less atropine needed; no oximes are needed.

Phosphides

Types

Zinc phosphide (rodenticide), Aluminum phosphide (grain fumigant)

Mechanism of Action

Contact with water or gastric juice releases phosphine gas, which inhibits cytochrome oxidase leading to inhibition of aerobic respiration, metabolic acidosis, and cellular death.

Clinical Picture

Three Phases

  • First Phase (1-24 h):

    • Vomiting, diarrhea, dehydration, metabolic acidosis, toxic cardiomyopathy, arrhythmia, shock, pulmonary edema, and ARDS.

  • Second Phase (24-48h): Apparent recovery.

  • Third Phase:_

    • Toxic hepatitis, renal tubular necrosis, and anuria.

Investigations

  • ABG (metabolic acidosis).

  • ECG (arrhythmias).

  • Liver and Kidney function tests.

  • Detection of phosphine gas in breath.

Treatment

  • Stabilization (ABCD).

  • No antidote available.

  • Decontamination: Gastric Lavage using NaHCO_3 if within 1 hour, paraffin oil.

  • Supportive Treatment: IV fluids, vasopressors, treatment of acid-base and electrolyte disturbances, antiarrhythmics.