• Definition: The process by which materials (especially metals) are slowly destroyed by chemical reactions with substances in their surroundings (oxygen, moisture, acids, salts, etc.)
• Electrochemical nature: Most metallic corrosion involves electron transfer - the metal acts as an anode and loses electrons (oxidation), while another site acts as a cathode (reduction)
• Common example: Rusting of iron: 4Fe + 3O₂ + 6H₂O → 4Fe(OH)₃ → Fe₂O₃·nH₂O (rust)
• Types:
  • Uniform corrosion - even attack across the surface
  • Galvanic corrosion - two dissimilar metals in contact in an electrolyte
  • Pitting corrosion - localized holes/pits on the surface
  • Crevice corrosion - in confined spaces with stagnant solution
  • Intergranular corrosion - along grain boundaries
  • Stress corrosion cracking - combined effect of stress and corrosive environment
• Prevention methods: Painting/coating, galvanizing (zinc coating), cathodic protection, use of corrosion-resistant alloys (stainless steel), adding inhibitors

Corrosion in Forensic Toxicology

Definition

"A corrosive poison fixes, destroys and erodes the surface with which it comes in contact. These act by extracting water from the tissues, coagulate cellular proteins, and convert hemoglobin into hematin."

• The Essentials of Forensic Medicine and Toxicology, 36th ed. (2026)

Classification of Corrosive Poisons

Mechanism/Mode of Action

1. Act locally only - no remote/systemic effects in most cases
2. Extract water from tissues
3. Fix, destroy and erode tissues - causing coagulation necrosis (precipitation of proteins)
4. Convert haemoglobin into haematin (brownish color)
5. When strong mineral acids contact moist skin, an exothermic reaction occurs - the heat + corrosion together cause coagulation necrosis
6. The crust formed may limit deeper penetration, but acid can still absorb systemically causing acidosis, haemolysis, and reduced cardiac output
7. Oesophagus is relatively resistant; stomach (especially pyloric region) is most susceptible
8. Complications develop from 3 weeks to 3 months after ingestion
9. When diluted - act as irritants; when well diluted - act as stimulants

1. Absorb water from tissues
2. Precipitate proteins
3. Combine with proteins to form proteinases and with fats to form soaps
4. Produce soft, necrotic, deeply penetrating areas - more dangerous than acids as they penetrate deeper

Acids vs. Alkalis - Key Difference

Signs and Symptoms

• Corrosive Acids: Brownish/blackened scars, charring of mucosa, vomit is acidic, intense pain in mouth/throat/abdomen
• Corrosive Alkalis:
  • Soft, oedematous, translucent, swollen, reddish-brown scar formation
  • No charring (unlike acids)
  • Vomited matter is alkaline
  • Frequent purging; mucus and blood in stools
  • Blistering and discolouration of lips and mouth
  • If ammonia vapours inhaled: eye congestion, sneezing, choking, possible death from glottal oedema

General Treatment Principles (Forensic Relevance)

1. No stomach wash (risk of perforation) - though a Levin tube can be used cautiously within 30 minutes
2. Dilution with water or milk
3. No emetics
4. Neutralization (with caution - exothermic reactions can worsen injury)
5. Supportive care; monitor for complications (stricture, perforation, mediastinitis, sepsis)

Medico-legal Significance

• Corrosive poisoning is seen in homicidal, suicidal, and accidental contexts
• Acid attacks (vitriolage) - throwing of corrosive acids on victims - is a recognized medico-legal entity
• Post-mortem findings: Charred/eroded mucosa, brownish discoloration, perforation of stomach
• Identification: Corrosive mineral acids and alkalis are identified only in the gastrointestinal content
• No trace of acid may be found if the victim survives for more than 2 days

• The Essentials of Forensic Medicine and Toxicology, 36th ed. (2026), Chapter 26
• P C Dikshit Textbook of Forensic Medicine and Toxicology, Chapter 37

Diagnosis of Poisoning in Living Persons

Key Principle

"There is no single symptom, and no definite group of symptoms, which are absolutely characteristic of poisoning. The closest resemblance to disease may be produced by thallium poisoning."

• The Essentials of Forensic Medicine and Toxicology, 36th ed. (2026)

1. Circumstances Arousing Suspicion of Poisoning

1. Symptoms appear suddenly in a previously healthy person
2. Symptoms appear immediately or shortly after eating, drinking, or taking medication
3. Symptoms are uniform in character and rapidly increase in severity
4. Several persons eating or drinking from the same source are affected simultaneously with similar symptoms (e.g., food poisoning)
5. Poison is detected in food, vomit, or excreta - strong proof of poisoning
6. Sudden illness in a person with a history of psychiatric problems (especially depression)
7. Onset of illness during work with chemicals (occupational exposure)
8. Persons arriving from foreign countries or arrested who may be body packers/stuffers (concealing drugs in body cavities)

2. History Taking

• From the patient (if conscious): nature of substance taken, time, quantity, route
• From relatives/bystanders: behavioral changes, available medications, social media posts (self-harm plans often described there), recent life events
• Prescription Monitoring Programs (PMP): reveal controlled substance use
• Review of belongings/scene: suicide note, drug containers, chemical labels
• Occupational history: Safety Data Sheets (SDS) from worksite
• Imprint codes on pills and chemical labels can help identify the poison

3. Physical Examination

Vital Signs (assess repeatedly - critical)

• Pulse, blood pressure, respiratory rate, pulse oximetry, temperature
• Core temperature is especially important - elevation is the most reliable predictor of poor outcome in stimulant poisoning or drug withdrawal

Characterize the Physiologic State

Specific Examination Points

• Eyes: Pupil size and reactivity, nystagmus
• Skin: Burns, bullae, color, warmth, moisture, pressure sores, puncture/injection marks
• Abdomen: Bowel sounds, bladder distension
• Breath/vomitus odor: Many poisons have characteristic smells (see below)
• All orifices: Examine for burns, drug packets
• Neurological: Dyskinesia, dystonia, fasciculations, myoclonus, rigidity, tremors
• Note: Focal neurological findings are uncommon in poisoning - their presence should prompt evaluation for a structural CNS lesion

4. Toxidromes (Poison Syndromes)

5. Characteristic Odors (Diagnostic Clues)

6. Samples to Collect (Medico-legal Importance)

7. Symptoms Suggestive of Poisoning

1. Sudden onset of abdominal pain, nausea, vomiting, diarrhoea and collapse
2. Sudden coma with constriction of pupils (miosis)
3. Sudden onset of convulsions
4. Delirium with dilated pupils (mydriasis)
5. Paralysis, especially lower motor neurone type
6. Jaundice and hepatocellular failure
7. Oliguria with proteinuria and haematuria
8. Persistent cyanosis
9. Rapid neurological or GI illness in persons known to be occupationally exposed to chemicals

8. Symptoms of Chronic Poisoning (Special Scenario)

1. Symptoms exaggerated after taking suspected food/fluid/medicine
2. Malaise, cachexia, depression, gradual deterioration
3. Repeated attacks of diarrhoea, vomiting
4. Symptoms disappear when patient is removed from usual surroundings
5. Traces of poison found in urine, stool, or vomit

9. Ancillary Investigations

• X-ray abdomen: Radio-opaque shadows in arsenic/lead poisoning; transverse bands at bone ends in chronic heavy metal poisoning (arsenic, lead, iron)
• ECG: Arrhythmias (antidepyclic antidepressants, digoxin, calcium channel blockers)
• Blood investigations: ABG, LFT, RFT, electrolytes, glucose, coagulation profile
• Specific toxicology screens: Blood/urine drug levels, serum paracetamol, salicylate, ethanol, carboxyhaemoglobin levels

• The Essentials of Forensic Medicine and Toxicology, 36th ed. (2026)
• P C Dikshit Textbook of Forensic Medicine and Toxicology
• Parikh's Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
• Harrison's Principles of Internal Medicine, 22nd ed. (2025)

Gastric Lavage in Non-Oral Poisoning

The Core Principle

"Appropriate antidote should be given to neutralize the poisonous compound even despite gastric lavage and emesis, as some poisons are secreted again into the stomach after having been absorbed."

• P C Dikshit, Textbook of Forensic Medicine and Toxicology

Why This Happens: The Physiological Basis

1. Concentration gradient - the blood concentration may be higher than the gastric content, driving passive diffusion back into the stomach lumen
2. Gastric secretion - the gastric mucosa actively or passively secretes certain compounds (e.g., morphine/opioids, some alkaloids) into gastric juice
3. Ion trapping - basic (alkaline) drugs like morphine become ionised in the acidic gastric environment, get "trapped" in the stomach, and cannot easily diffuse back into blood - making lavage effective even hours after injection

Classic Examples Where Gastric Lavage is Done Despite Non-Oral Route

Important Conditions Where Gastric Lavage is Extended Beyond the Usual Time

• Salicylates (aspirin) - slow gastric emptying, bezoar formation
• Tricyclic antidepressants - delayed gastric emptying due to anticholinergic effect
• Carbamazepine - enterohepatic recirculation
• Barbiturates - delayed absorption
• Sustained-release medications - prolonged absorption

The Gastric Lavage Fluid Used (by Poison Type)

Contraindications to Gastric Lavage (Do NOT Perform)

1. Corrosive poisoning (except carbolic acid) - risk of perforation
2. Convalescent poisons
3. Comatose patient - risk of aspiration (unless intubated)
4. Volatile poisons - risk of inhalation injury
5. Hypothermia

1. Oesophageal varices or other alimentary tract disease
2. Ingestion of alkalis
3. Advanced pregnancy
4. Haemorrhagic diathesis
5. Recent surgical operation

Complications of Gastric Lavage

1. Laryngeal spasm
2. Aspiration pneumonitis
3. Perforation of stomach or oesophagus
4. Sinus bradycardia and ST elevation on ECG