Inorganic Irritants: Metallic Poisons 451

2. Accidental poisoning may occur in children. • Convulsions

3. Chronic poisoning – industrial hazard. • Retrobulbar neuritis
4. Use to procure criminal abortion. • Ophthalmoplegia
5. Cattle poison. • Peripheral neuropathy.

Thallium Chronic Poisoning

• Alopecia - falling of hairs from head, eyebrows and
Properties axilla are common
• Thallium is soft and pliable metal • Skin rash
• Have tin-white colour but tarnishes the surface on expo- • Acneform eruptions
sure to air due to formation of black thallous oxide • Dystrophy of nails
• Thallium sulfate is odourless and tasteless. • Ascending sensorimotor neuropathy
• Ataxia
Toxic Compounds of Thallium • Optic neuropathy
• Encephalopathy
1. Thallium sulfate • Ptosis
2. Thallium acetate • Nystagmus
3. Thallium iodide • Combination of alopecia and skin rash, painful peripheral
4. Thallium nitrate neuropathy and mental confusion with lethargy is called
5. Thallium carbonate. as thallium triad.1

Uses Management5
1. Dye industry • Gastric lavage with ferric ferrocyanide (Prussian blue).
2. Optical glass Prussian blue binds thallium in the intestine and enhances
3. Imitation jewelry its fecal excretion.
4. Rodenticide • Hemodialysis
5. Depilatory agent • Forced diuresis
6. Fire works. • Supportive measures.

Mechanism3 Autopsy Findings

• Exact mechanism is unclear but postulated that thallium • There may be alopecia
results in ligand formation with protein sulphydryl group • Stomatitis
of enzymes and inhibits cellular respiration. • Fatty degeneration of liver and heart
• It disrupts calcium homeostasis • Tubular necrosis
• Interaction with riboflavin and riboflavin based cofactors. • Pulmonary edema
• Cerebral edema
Clinical Features Fatal dose: 12 mg/kg body weight6
Fatal period: 24 to 30 hours
Acute Poisoning4
• Medicolegal Importance
Toxicology

Pain in abdomen
• Features of gastroenteritis 1. Popular as ideal homicidal agent.
• Hematemesis 2. Also consumed as suicidal agent.
• Hematochezia
•
•
Headache
Confusion
Arsenic B
Section 

• Disorientation Arsenic is a metalloid and per se is not very toxic, however,

• Paraesthesia arsenic salts are toxic.7 The arsenic has inorganic and organic
• Hallucinations compounds. Inorganic compounds are mentioned in Table 36.2.
 452 Principles of Forensic Medicine and Toxicology

Table 36.2: Showing inorganic compounds of

arsenic
Compound Common name Properties
Arsenious oxide Sankhya White crystalline
(Arsenic Somakhar powder
trioxide) White arsenic

Arsenic Manseel Red powder

disulphide Red arsenic
Arsenic Hartal Yellow powder
trisulphide Yellow arsenic (Fig. 36.4)
Orpiment
Sodium - White or grayish
arsenates powder
Potassium -
arsenates
Arsenic acid Arsenic White crystalline
pentoxide powder Fig. 36.4: Arsenic trisulphide (Courtesy: Dr Vaibhav
Arsenic
Sonar Lecturer, Forensic Medicine, GMS, Miraj)
anhydride
Arsenic - Colourless fuming
Sources
trichloride liquid
Arsenic triodide Arsenious Orange colour 1. Rocks and soil
iodide crystals (Fig. 36.5) 2. Hot spring mineral water
Arsine Arseniuretted Colourless and
hydrogen inflammable gas,
3. Drinking water
Arsenic Garlicky odour 4. Sea water
hydride 5. Vegetable, fruits and grains
Sodium arsenite - White powder 6. Sea food
Potassium - White powder 7. Industrial sources
arsenite
Copper arsenite Scheele’s Greenish crystalline Absorption, Excretion and Metabolism
(Fig. 36.6) green powder
Copper Paris green Greenish crystalline • Arsenic is absorbed through all routes viz. through skin,
acetoarsenite powder inhalation, and GIT mucosa. However, cutaneous absorp-
tion is low except in cases of damaged skin. The inor-
ganic pentavalent forms are absorbed at higher rate than
Organic compounds of arsenic are: bivalent forms.8
1. Cacodylic acid • The absorbed inorganic arsenic undergoes methylation
2. Sodium cacodylate mainly in liver to monomethylarsonic acid and dimethy-
3. Atoxyl larsinic acid and excreted in urine.9
• After absorption, arsenic is redistributed to the liver,
Toxicology

4. Stovarsol
lungs, intestinal wall, spleen, and kidneys. It has mini-
Uses mal penetration in blood-brain-barrier.
1. Rodenticide
B 2. Weed killer
Mechanism of Action
• Arsenic reversibly combines with sulphydrl enzymes. It
Section 

3. In alloys
4. Depletory blocks Krebs cycle and interrupts oxidative phosphoryla-
5. Coloring agent tion causing depletion of ATP and death of cell.
 Inorganic Irritants: Metallic Poisons 453

Fig. 36.5: Arsenic triodide Fig. 36.6: Copper arsenite

• It also inhibits transformation of thiamine into acetyl

CoA and Succinyl –CoA resulting in thiamine deficiency.
• It replaces the phosphorus in the bones
• Arsenic is incorporated into hair, nails and skin.
• It causes increased permeability of small blood vessels
with inflammation and necrosis of intestinal mucosa thus
causing manifestation of hemorrhagic gastroenteritis. Table 36.3: Showing difference between arsenic
poisoning and cholera
Clinical Features Features Arsenic poisoning Cholera
Pain in throat Before vomiting After vomiting
Acute poisoning Conjunctiva Inflamed Not inflamed
A patient with acute arsenic consumption may present in Vomitus Contains mucus, It is watery or
1. Fulminant type: collapse and circulatory failure bile and streaks of whey like
blood
2. Gastroenteritis type
Purging Follows vomiting Usually precedes
3. Narcotic form
vomiting
• Metallic taste
• Garlicky odour Stools Rice watery in Rice water
early stages, later liquid,
• Nausea and vomiting
becomes bloody, involuntary jet
• Colicky abdominal pain discharged with
• Profuse diarrhea resembling rice water stool of chol- straining and
era. Difference between arsenic poisoning and chol- tenesmus
era is summarized in Table 36.3 Laboratory 1. Radio-opaque Vibrio cholera
• Circulatory failure examination shadow on X-ray detected on
Toxicology

• Intense thirst of abdomen in microscopic

• Oliguria arsenic trioxide examination
• Uremia poisoning
• Ventricular tachycardia 2. Coproporphyrin
• Headache in urine B
• Vertigo 3. Arsenic
Section 

detected in
• Tremors
chemical analysis
• Convulsions
 454 Principles of Forensic Medicine and Toxicology

• Formication • Nails – become brittle and show Mees’ line. Mees’

• Delirium line are white transverse lines over nails
• Tenderness in muscle • Hairs – dry and may fall off; patchy or diffuse alopecia
• Paralysis • Arsenic dust – flexor eczema, painless perforation
• Hyperpyrexia of nasal septum.
• QT prolongation, tachyarrhythmia including torsades • Liver enlarged (hepatomegaly) and cirrhotic
de pointes may develop within first 24 hours after • Melanosis of neck, eyelids and nipples
ingestion.10 • Bowen’s disease.
3. Third stage
Subacute Poisoning • Headache
• Tingling and numbness of extremities
This results when arsenic is given in small doses at frequent
• Hyperasthesia of skin
intervals. The features are:
• Cramps in muscle and tenderness
• Dyspepsia
• Arthralgia
• Cough
• Knee jerk lost
• Tingling in throat followed by vomiting
• Impotence
• Diarrhea with tenesmus and abdominal pain
• Bone marrow depression with aplstic anemia
• Cramps in muscle
• Interference with folic acid metabolism with defi-
• Restlessness.
ciency
• Hematological abnormalities (Table 36.5).
Chronic Poisoning
4. Fourth stage
The features are exhibited in four stages6 • Peripheral neuropathy
1. First stage • Neuropathy is hallmark of arsenic poisoning. It is
• GIT symptoms dominate usually symmetrical sensorimotor polyneuropathy
• Malaise resembling Guillain-Barre syndrome
• Loss of appetite • Weakness of muscle and atrophy – extensor muscles
• Salivation more commonly affected resulting in wrist drop and
• Colicky abdominal pain foot drop
• Constipation (sometimes diarrhea) • Ataxia
• Vomiting • Tremors
• Gums – red and soft • Emaciation
• Circumscribed edema of ankle • Anemia
• Periorbital edema • Dysuria
2. Second stage • Delusion
• Cutaneous eruptions • Encephalopathy
• Voice – hoarse and husky • Death.
• Rhinorrhea
• Skin – generalized or localized fine mottled pigmenta-
tion of skin (Rain drop pigmentation, see Table 36.4)
Table 36.5: Showing hematological abnormalities
• Epithelial hyperplasia with keratosis – mostly on sole
in arsenic poisoning
and palms
Hematological abnormalities
Toxicology

• Leukopenia
Table 36.4: Displaying differential diagnosis of • Thrombocytopenia
raindrop pigmentation of arsenic • Mild eosinophilia
B Rain drop pigmentation may be mistaken for • Karyorrhexis – manifested by bizarre nuclear forms
• Megaloblastic anemia
Section 

1. Addison’s disease
2. Secondary syphilis • Basophilic stippling
 Inorganic Irritants: Metallic Poisons 455

Differential Diagnosis 4. Muscle

5. Skin
1. Acute poisoning resembles cholera
6. Nails.
2. Alcoholic neuritis
3. Guillain-Barre syndrome.
Medicolegal Importance
10,11
Management 1. Homicidal poison – in past it is considered as ideal homi-
cidal poison. The arsenic is administered in chronic way
Acute poisoning
to a person and the clinical features is manifested for
• Gastric lavage
natural disease
• Administer activated charcoal
2. Used as cattle poison13
• Aggressive fluid resuscitation and cardiovascular support
3. Accidental poisoning: due to
remains the mainstay of initial management.
• Used in indigenous medicine – chronic poisoning
• Chelation – BAL, Succimer (DMSA), or DMPS. Every
• Well water (tube well water) 7
50 mg BAL binds 30 mg of arsenic.
• Adulteration with alcohol drink
• Exchange transfusion
• Mistaken for medicine
• Continuous venovenous hemodiafiltration.
• Arsenophagist – some people take arsenic daily as an
aphrodisiac and are habituated for arsenic.
Disadvantage of BAL
• Have to give as an intramuscular injection Mercury
• Unpredictable bioavailability.
Synonyms: Quick silver. Para
BAL is Contraindicated in:
Features
Patients with glucose-6-phosphate dehydrogenase deficiency
because BAL may cause hemolysis. • Only metal, which is liquid at room temperature
• Metallic mercury is having bright silvery luster and is
Chemical Test for Arsenic Detection volatile at room temperature. The fumes are odourless
and invisible (Fig. 36.7).
1. Reinsch’s test
• It is 13.5 denser than water
2. Marsh’s test
• Metallic mercury is not poisonous if taken by mouth, as
3. Gutzeit test.
it is not absorbed. However, if vapours are inhaled, may
Fatal dose: Arsenious oxide – 180 mg
exert toxic effects.
Fatal period: 12 to 48 hours.
• Mercury exists in three forms:14
1. Elemental mercury – Hgo – vapours are toxic
Autopsy Findings
2. Inorganic mercury
• Rigor mortis last for longer duration 3. Organic mercury.
• Jaundice • Inorganic salts are of two types as:
• GIT – mucosa is congested and edematous. The mucosa 4. Mercuric (bivalent Hg++) – more poisonous
may be reddened or show hemorrhagic gastroenteritis. 5. Mercurous (monovalent Hg+) – less poisonous.
The focal hemorrhages give rise to flea bitten appear-
ance and this appearance is considered as characteristic. Toxic Compounds
The mucosal appearance is described as red velvet like12
Toxicology

• Subendocardial hemorrhages in heart with fatty degen- Inorganic compounds are mentioned in Table 36.6.
eration
• Liver – fatty degeneration. Organic Compounds

B
Organic compounds of mercury are more toxic than inor-
Preserved for Chemical Analysis ganic compounds and are:
Section 

1. Routine viscera 1. Ethyl mercury

2. Long bone – femur 2. Methyl mercury
3. Scalp hairs 3. Mercurochrome.