Poisoning - FMT Exam Comprehensive Notes

1. DEFINITION & CLASSIFICATION OF POISONS

Classification of Poisons (Medico-legal)

2. IDEAL HOMICIDAL POISON

3. TREATMENT OF POISONING (General Principles)

A. Life-Saving Measures - ABCD

• Airway: Open/clear airway; endotracheal intubation if needed
• Breathing: Supplemental oxygen via ventimask/ET tube; arterial blood gas monitoring
• Circulation: IV fluid administration
• Depression of CNS: Correct; place unconscious patient in recovery position (lateral)

B. Removal of Unabsorbed Poison

• Useful within 2 hours of ingestion
• Use Ewald's tube or Boa's tube
• Volume: 200-300 mL warm water/normal saline per cycle, total 3-5 liters
• Contraindications: Corrosive poisoning, unconscious patient without intubation (risk of aspiration), kerosene/petroleum products (risk of aspiration pneumonia), convulsions

• Contraindicated in: Corrosives, unconscious patients, petroleum products, strychnine (may precipitate convulsions), infants under 6 months

C. Chemical Antidotes (Local)

• Dose: 60-100 g adults; 15-30 g children
• Effective for: Barbiturates, atropine, benzodiazepines, strychnine, phenothiazines, digitalis, organophosphates, theophylline, antidepressants
• NOT effective for: Corrosives, heavy metals, cyanide, hydrocarbons, alcohol, iron

• Creates concentration gradient between blood and gut lumen
• Loading: 1-2 g/kg; Repeat: 0.5-1 g/kg every 4-6 hours
• Useful for: Opium, cyanide, phenobarbital - significantly decreases half-life

D. Enhanced Elimination

• Forced diuresis: Alkaline diuresis for salicylates, barbiturates
• Hemodialysis: Methanol, ethylene glycol, salicylates, lithium
• Charcoal hemoperfusion: Useful for highly protein-bound substances

4. ORGANOPHOSPHORUS (OP) POISONING - HIGH YIELD

Mechanism

Types

• Alkyl phosphates: Malathion, TEPP, HETP, Demeton
• Aryl phosphates: Parathion (Folldol), Methyl-parathion (Metacide), Diazinon, Chlorthion

Routes of Absorption

Clinical Features (3 types)

• Salivation, Lachrymation, Urination, Defecation, GI distress, Emesis
• Bronchoconstriction + secretions, bradycardia, miosis, urinary incontinence, hypotension

• Muscle fasciculations, weakness, paralysis (persistent depolarization)
• Sympathetic ganglia: Hypertension, tachycardia, pallor, mydriasis
• Seen in only 10-20% of cases

• Restlessness, confusion, ataxia, convulsions, coma
• Depression of respiratory and cardiovascular centers

Special Syndromes

• Intermediate Syndrome: After 1-4 days, motor cranial nerve palsies, neck flexor weakness, respiratory paresis. Does NOT respond to oximes or atropine.
• Delayed Peripheral Neuropathy: 1-5 weeks after exposure to certain compounds

Treatment of OP Poisoning

1. Atropine - antidote for muscarinic effects
   • Initial: 2-4 mg IV, repeated every 5-15 min until atropinized
   • Average requirement: 40 mg/day (up to 1000 mg/day)
   • Goal: Dry secretions (not just tachycardia - tachycardia is NOT a contraindication)
   • Give oxygen BEFORE atropine if cyanotic (hypoxia + atropine = ventricular arrhythmias)
2. Pralidoxime (2-PAM) / Oximes - cholinesterase reactivators
   • Dose: 1-2 g IV over 5-30 min; repeat in 1 hour if needed; then every 6-12 hours for 24-48 hours
   • Max: 12 g/24 hours
   • Act at nicotinic sites, improve muscle strength within 10-40 min
   • Do NOT cross blood-brain barrier
   • Must be used EARLY; pralidoxime and atropine work synergistically
   • Ineffective against: Dimefox, dimethoate, phorate, schradan
3. DAM (Diacetyl monoxime): Crosses BBB; regenerates CNS cholinesterase

5. CORROSIVE POISONS

Mineral Acids (Mechanism)

Sulfuric Acid (H2SO4 - Oil of Vitriol)

• Pure: Heavy, odorless, colorless, nonfuming, hygroscopic, oily liquid
• Causes superficial burns in 1 sec, full thickness burns in 30 sec
• Signs: Swollen/excoriated lips, brown-black streaks from angles of mouth, corrosion of mucous membranes, epigastric pain, brown/black strongly acid vomit
• Commonly used in "acid attacks"

Nitric Acid (HNO3)

• Stains tissues yellow (xanthoproteic reaction)
• Vomit and staining are distinctly yellowish

Hydrochloric Acid (HCl)

• Burns are white/grayish in color

Oxalic Acid

• Forms calcium oxalate crystals in urine/kidneys
• Causes hypocalcemia (tetany, convulsions)
• Leaves white crystalline deposit

Carbolic Acid (Phenol)

• Characteristic smell
• Urine turns dark (carbol-melanuria)
• Causes CNS depression and cardiac arrhythmias

Caustic Alkalis

• Cause liquefaction necrosis (no eschar formation - penetrate deeply)
• More dangerous than acids for the esophagus
• NaOH (lye/caustic soda), KOH, Ammonia

6. ARSENIC POISONING - HIGH YIELD

Forms

• Metallic arsenic: Black, NON-toxic (not absorbed)
• Arsenious oxide (As2O3) / White arsenic: Most common toxic form; no taste, no smell, floats on water despite being heavier

Fatal Dose

• Arsenic trioxide: 120-180 mg

Clinical Features (Acute)

• GI: Vomiting, rice-water stools, intense abdominal pain, gastroenteritis
• Systemic: Cyanosis, hypotension, shock, "garlic odor" from breath

Chronic Arsenic Poisoning (Mees' Lines)

• Mees' lines: White transverse lines on nails (also seen in other heavy metal poisonings)
• Skin: Raindrop pigmentation, hyperkeratosis
• Peripheral neuropathy, Aldrich-Mees lines in hair (using XRF analysis)

Autopsy Findings

• Stomach mucosa: Red velvet appearance (edematous, hemorrhagic), congestion along rugae crests
• Particles of arsenic may be seen in mucous mass covering stomach

Detection

• Reinsch's test: Copper spiral turns black/silver in acid solution
• Marsh test: Formation of arsenic mirror (arsine gas passed over heated tube)
• Arsenic detectable even in putrefied bodies

Treatment

• BAL (British Anti-Lewisite / Dimercaprol): Chelating agent of choice
  • Dose: 3 mg/kg IM every 4 hours for 2 days, then every 6 hours for 7-10 days
• DMSA (Succimer) or DMPS: Superior to BAL; can be used instead
• Penicillamine: 100 mg/kg daily for 5 days
• Castor oil/MgSO4 to prevent intestinal absorption
• Hemodialysis if renal failure

7. CARBON MONOXIDE (CO) POISONING

Characteristics

Fatal Level

Mechanism of Action

1. CO affinity for hemoglobin is 230-270 times greater than O2 → forms carboxyhemoglobin (COHb)
2. Causes left shift of oxyhemoglobin dissociation curve (O2 not released to tissues)
3. Inhibits mitochondrial cytochrome oxidase → cellular hypoxia
4. Activates guanyl cyclase + displaces NO from platelets → vasodilation → hypotension

Postmortem Signs

• Classic cherry-red/carmine discoloration of skin, blood, and organs
• COHb remains stable for years in preserved tissues

Treatment

• 100% oxygen by tight-fitting mask (most important) - displaces CO
• Hyperbaric oxygen (HBO): For COHb > 25%, unconscious patients, pregnant women, children
• Carboxyhemoglobin normal: 1-5% (up to 7-8% in smokers)

8. OPIATES AND OPIOID POISONING

Classification

• Natural: Morphine, Codeine
• Semisynthetic: Heroin (diacetylmorphine), Pholcodeine, Hydromorphone
• Synthetic: Fentanyl, Methadone, Pethidine, Tramadol, Propoxyphene

Mechanism

Duration of Action

• Minutes-hours: Fentanyl, alfentanil
• 2-4 hours: Pethidine, Pentazocine
• 4-8 hours: Morphine, Codeine, Heroin
• 8 hours: Methadone, Buprenorphine

Signs of Acute Poisoning (Classic Triad)

1. Pinpoint pupils (miosis)
2. Coma/unconsciousness
3. Respiratory depression

• Also: cyanosis, bradycardia, hypotension, reduced bowel sounds

Stages

1. Stage of Excitement (brief or absent): euphoria, flushed face, talkativeness
2. Stage of Narcosis: Progressive CNS depression, stupor, coma, slow/shallow breathing

Treatment

• Naloxone (Narcan): Opioid antagonist - dose 0.4-2 mg IV, repeat every 2-3 min as needed. Caution: shorter half-life than most opioids, re-sedation can occur.

9. CYANIDE POISONING

Sources

Mechanism

Features

• Bitter almond smell (characteristic)
• Rapid onset: excitement → convulsions → coma → death within minutes to hours
• Paradox: Venous blood bright red (like arterial blood - tissues cannot extract O2)

PM Findings

• Cherry-pink discoloration of blood/organs (similar to CO)
• Smell of bitter almonds from stomach contents

Treatment

• Dicobalt edetate (co-EDTA): 300 mg IV - drug of choice
• Amyl nitrite (inhale) + Sodium nitrite (300 mg IV) + Sodium thiosulfate (12.5 g IV) - classic triad
• Mechanism: Nitrites form methemoglobin → combines with CN to form cyanmethemoglobin; Thiosulfate + CN → thiocyanate (excreted in urine)
• Hydroxocobalamin (Cyanokit): 5 g IV

10. KEY FORENSIC TOXICOLOGY CONCEPTS

Specimens for Analysis (Priority Order)

1. Blood - specimen of choice; best indication of quantity of drug at time of death
2. Urine - concentrates poison; good for single spot tests
3. Bile - useful for some drugs
4. Vitreous humor - resistant to decomposition
5. Muscle (thigh) - best preserved in decomposition; levels more accurately reflect blood levels

Postmortem Redistribution

• Drugs diffuse from stomach into liver (mainly left lobe) after death
• Also affects: base of left lung, spleen, pericardial fluid
• Peripheral blood (femoral) preferred over central blood to minimize PM redistribution artifact

Causes of Failure to Detect Poison

1. Eliminated by vomiting/diarrhea (irritant poisons)
2. Evaporation from lungs (volatile poisons)
3. Complete detoxification and elimination
4. Rapid metabolism
5. Decomposition products mask the poison
6. Wrong/insufficient material sent for analysis

Poisons Identifiable Even in Putrefied Bodies

Bedside Clinical Tests

11. IMPORTANT LAWS (India)

12. QUICK EXAM MNEMONICS