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Arsenic - Metallic Poison (Forensic Medicine & Toxicology)

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1. Introduction & Historical Significance

• Tasteless, colorless, and odorless
• Easily administered in food and drink
• Symptoms mimicked cholera (a common disease of the era)
• Difficult to detect before 19th century

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2. Chemical Forms & Compounds

Metallic Arsenic

• Black colored; non-toxic when ingested (not absorbed from GI tract)
• When volatilized by heat, unites with oxygen to form poisonous arsenic trioxide vapor

Poisonous Compounds (in order of importance)

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3. Sources of Arsenic

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4. Mechanism of Action

1. Sulphydryl (–SH) group inhibition - reversibly combines with SH groups of mitochondrial enzymes (especially pyruvate oxidase), blocking cellular respiration
2. Enzyme inhibition - interferes with multiple enzyme systems essential for cellular metabolism
3. Capillary endothelial damage - dilates and damages capillaries → increased permeability → tissue edema, hemorrhage, fluid transudation into bowel lumen
4. Oxidative phosphorylation uncoupling (arsenate form) - interferes with glycolysis
5. Fatty degeneration of liver
6. Renal tubular necrosis
7. Peripheral axonal neuropathy - disintegration of axis cylinder, fragmentation and resorption of myelin

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5. Fatal Dose and Fatal Period

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6. Signs & Symptoms

Acute Arsenic Poisoning

• Metallic taste in mouth + slight garlicky odor to breath
• Xerostomia (dry mouth) and dysphagia
• Burning pain, throat constriction, increased salivation
• Intense thirst

• Severe nausea and projectile vomiting (dark brown/yellow, contains mucus, bile, blood)
• Severe colicky abdominal pain
• Profuse diarrhea with rice-water stools (due to mucosal vesicle formation, sloughing, and plasma transudation into bowel lumen)
• Tenesmus and anal irritation

• Dehydration: skin cold and clammy, sunken eyes, face pale
• Muscle cramps (calf muscles), restlessness
• Oliguria, proteinuria, hematuria (renal damage)
• Periorbital edema, severe headache, vertigo
• Hyperpyrexia, acute hemolysis

• Acute cardiomyopathy, subendocardial hemorrhages
• ECG: prolonged QT interval, non-specific ST-T changes
• Hypoxia, convulsions, encephalopathy
• Acute tubular necrosis (shock-related)
• Death from irreversible circulatory insufficiency

• Hair loss (alopecia)
• Mee's lines (Aldrich-Mees lines) - white transverse lines on nail plates
• Sensorimotor peripheral neuropathy (usually 2-8 weeks after exposure)

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Chronic Arsenic Poisoning

• Weight loss, anorexia, salivation
• Colicky pain, constipation, vomiting, diarrhea
• Soft red gums, coated tongue (thin white silvery fur)
• Edema of eyelids and ankles
• Raised temperature and pulse

• Cutaneous eruptions; catarrh of larynx and bronchial tubes
• Hoarseness, coryza, cough with bloody expectoration
• Photophobia and conjunctivitis

• Raindrop pigmentation - finely mottled brown change on skin flexures, temples, eyelids, neck
• Hyperkeratosis of palms and soles
• Irregular thickening of nails + Aldrich-Mees lines (white transverse lines in fingernails)

• CNS: polyneuritis, paresthesias, anesthesias, encephalopathy
• GI: nausea, vomiting, abdominal cramps
• Liver: hepatomegaly, jaundice, cirrhosis
• Kidneys: chronic nephritis, renal failure
• CVS: cardiac failure, dependent edema
• Blood: bone marrow suppression, anemia, thrombocytopenia, leukemia
• Cancer: lung cancer, skin cancer (arsenic is a carcinogen/teratogen)

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7. Difference: Arsenic Poisoning vs. Cholera

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8. Post-Mortem Appearances

Acute Arsenic Poisoning

• Body appears dehydrated and cyanosed
• Sunken eyeballs, wrinkled skin
• Skin may be jaundiced
• Rigor mortis lasts longer than usual

• Stomach (classic sign): "Red velvet" appearance - mucosa red, edematous, swollen in patches corresponding to arsenic deposits; covered with tenacious blood-tinged mucus; small ulcerations or large erosions at pyloric end; submucous petechial hemorrhages
• Small intestine: Inflamed upper part, dilated, reddened, thickened mucosa; may form a pseudomembrane
• Large intestine: Rectum most prone to inflammation; caecum inflamed, mucosa flabby
• Heart: Petechial hemorrhages under endocardium of left ventricle (comparatively common)
• Liver: Patchy fatty degenerative changes, necrosis with jaundice
• Kidneys: Tubular necrosis, enlarged and congested
• Lungs: Congested, edematous, subpleural ecchymoses
• Brain: Congested; ventricles full of serum
• Spleen: Enlarged and congested
• Note: Decomposition is NOT significantly retarded in acute poisoning

Chronic Arsenic Poisoning (PM Findings)

• Retardation of decomposition is evident (hallmark of chronic poisoning)
• Progressive emaciation, anemia
• Fatty degenerative changes in heart muscle, liver, and kidneys
• Congestion of gastrointestinal tract
• Microscopy: peripheral neuropathy
• Skin changes (raindrop pigmentation, hyperkeratosis)
• Arsenic deposited at the end of long bones (lower end of femur is suitable for analysis)

Arsine Gas Poisoning (PM Findings)

• Skin is dirty yellow
• Mucous membrane of stomach and intestine is yellow and inflamed
• Liver: small or enlarged, fatty degeneration
• Spleen: destruction of blood, blood pigment deposition
• Kidneys: enlarged, congested, tubular necrosis
• Lungs: congested, edematous

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9. Distribution & Excretion

• Normal blood arsenic: <4 mg/L; normal urine: <0.03 µg/L
• Acute poisoning: 24-hour urine excretion >100 µg
• Normal hair: <0.05/100 g; >1 mg/100 g = poisoning

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10. Chemical Tests for Detection

Note: Marsh's and Reinsch's tests are now considered obsolete (Reddy, 2026). Current detection uses atomic absorption spectroscopy.

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11. Medico-Legal / Forensic Importance

Why Arsenic is a Popular Homicidal Poison:

1. Cheap and easily obtained
2. Colorless, odorless, nearly tasteless
3. Can be administered in food or drink without suspicion
4. Small quantity required for death
5. Onset of symptoms is gradual
6. Symptoms simulate cholera (natural disease)

Disadvantages for the Poisoner (Forensic Detection):

1. Delays putrefaction (chronic poisoning) - body preserved for analysis
2. Can be detected in completely decomposed bodies
3. Found in bones, hair, nails for several years - detectable long after burial
4. Detectable even in charred bones or ashes
5. Detectable in exhumed bodies

Modes of Administration:

• Homicide: mixed with sweets, bread, milk, tea, cold drinks; mass poisoning via well/food supply
• Suicide: rare (causes much pain)
• Accidental: admixture with food, improper medicinal use, drinking arsenic-contaminated well water

Post-Mortem Imbibition (Defense Plea):

• Post-mortem imbibition follows an anatomical course (left side predominantly)
• Signs of inflammation and ulceration of stomach are ABSENT in post-mortem imbibition
• Arsenic from soil is in insoluble form and cannot percolate into a cadaver

Exhumation:

• Arsenic from soil cannot percolate into the cadaver (insoluble)
• Hair and nails may have higher contamination from soil externally
• Soil at burial site must be taken for chemical analysis as a control

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12. Samples for Chemical Analysis (Forensic)

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13. Treatment

1. Remove from source / remove poison from GI tract (emetics, gastric lavage)
2. Gastric lavage with freshly prepared ferric oxide in water (forms ferric arsenite, insoluble and harmless) or 1% sodium thiosulfate
3. Whole bowel irrigation; nasogastric suction (arsenic is re-secreted into GI tract)
4. Antidote: BAL (British Anti-Lewisite / Dimercaprol)
   • 400-800 mg day 1; 200-400 mg days 2-3; then 100-200 mg twice daily for 7-10 days
   • Chelates arsenic by forming stable ring complexes with SH groups
   • Stop when 24-hr urine arsenic falls below 50 µg
5. Oral Penicillamine 100 mg/kg/day in 4 divided doses for 4-8 days after initial BAL
6. DMSA (succimer) or DMPS - superior to BAL; used if available
7. IV normal saline for dehydration
8. Morphine for pain, castor oil/MgSO₄ to reduce intestinal absorption

Note: Alkalis should NOT be given as they increase arsenic solubility. Copper sulfate or tartar emetics should NOT be used as emetics.

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