METALLIC
POISONS
Arsenic
Lead
Mercury
Dr.Abhishek Karn
Asst.Professor, Dept. of Forensic
Medicine & Toxicology, CMC
Poisonous compounds of arsenic are as follows:
1. Arsenious oxide / Arsenic Trioxide (sankhya of
somalkhar) /white arsenic
2. Copper compounds of As- coloring agents for wall paper,
toys etc
3. Sulfides of As
4. Arsenical compounds of Pb, Na & K- weed killer,
insecticide, fungicide
5. Arsine gas- industry and laboratory
MECHANISM OF ACTION
Arsenic interferes with cellular respiration
by combining with the -SH groups of
mitochondrial enzymes.
Locally acts on the mucous membrane
causing irritation and remotely acts on the
nervous system.
Fulminant type
- Massive dose 3 5gm cause death in 1 3
hours due to peripheral vascular failure
and shock
- It also has direct action on heart muscle.
acute poisoning
(resembles bacterial food poisoning and
symptoms starts in half to 1 hour)
a. Metallic test, garlic odour in breath, dysphagia
b. Severe n/v, colicky abdominal pain and profuse
diarrhoea with rice-water stools.
c. Intense thirst
d. Painful cramps in the legs
e. Multi-organ damage, delayed cardiomyopathy,
convulsions or coma leads to death
Chronic poisoning
accidentalingestion of repeated small doses by
those working with the metal or by taking food
or drink.
homicidal nature due to repeated small doses.
GIT symptoms
Loss of weight & appetite
Salivation, colicky pain
Vomiting
Tongue is coated with thin, white silvery fur
Circumscribed edema of lower eyelids & ankles
Skin symptoms
persistent erythematous flush leading to hyperkeratotic
skin and desquamation
Patchy pigmentation (rain drop on a dusky road)
Diffuse desquamation of the palms and soles
Mees line in finger nails
Anemia and leucopenia
Normocytic and normochromic
Peripheral neuropathy
Tolerance
Some people take arsenic daily as tonic or as
an aphrodisiac and they acquire tolerance up
to 0.3gm or more in one does.
Such people are known as Arsenophagists .
FD:- 0.1-0.2 gm
FP:- 1-2 days
S.N TRAITS ARSENIC POISONING CHOLERA
.
1 Pain in throat Before vomiting After
2 Purging After vomiting Before
3 Stools Dark-colored & Rice-watery, not
bloody, later rice- bloody
watery
4 Tenesmus & + -
anal irritation
5 Vomitted Mucus, bile & blood Watery
matter
6 Voice Not affected Rough & whistling
7 Conjuctivae inflamed Not
8 Analysis of As + Cholera vibrio +
excreta
9 Circumscribed Of As poisoning + Other cases in locality
evidence
Diagnosis
Tests
1. Marsh test
2. Reinschs test
Treatment
1. Gastric lavage repeatedly
2. Butter or fatty substance prevent absorption
3. Freshly precipitated hydrated ferric oxide
(arsenic antidote)
The antidote is prepared by mixing 45 ml of
tincture ferric perchlorate with 5gm magnesium
oxide or potassium carbonate in a glass of
water
4. BAL (british antilewisite)
400800 mg on first day, 200400 mg 2nd and 3rd
day in divided doses 4 hourly then 100200mg BD
for 1 week
5. Penicillamine 100mg/kg q.i.d for 5 days
6. DMSA (dimercapto Succinic acid)10gm/kg
orally t.d.s for 5 days then same dose BD for 2
weeks.
Post mortem Appearances:
Externally:
Pigmentation of the skin and Mees lines in finger nails
Rigor mortis lasts longer
Shrunken appearance- body, eye ball
Cyanosed
Internally:
Garlicky odor
Inflamed & congested- GI mucosa
Petechial hemorrhages under the endocardium of the left
ventricle
Patchy fatty degenerative changes- liver, spleen & kidney
POST MORTEM IMBIBITION OF ARSENIC
In exhumation- possibility of imbibitions
from stomach to viscera's and surrounding
earth or from surround earth to body is
possible
Poisonous compounds of Lead:
Pb acetate (sugar of Pb)- astringent & local
sedative for sprains
Pb carbonate (white Pb)- paints
Pb tetraoxide (red lead or vermilion)- sindoor
Tetraethyl lead- in petrol
Lead oleate- abortifacient
Mechanism of action
It has affinity for cell membranes and mitochondria
interferes with mitochondrial oxidative
phosphorylation and Na, K, and Ca ATPase
Lead depresses enzyme responsible for haem
synthesis and shortens erythrocyte life-span
leading to anemia.
Acute lead poisoning
Rare
Symptoms are similar to acute arsenic poisoning,
except diarrhoea is replaced by constipation and
stool is blackened (lead sulphide) and offensive.
Fatal dose- 10gm/70 kg body wt
Fatal period- 24 hrs in severe cases
2-3 days usually
MANAGEMENT
Emesis
Gastric lavage with magnesium prevents
absorption of insoluble lead sulphide
For elimination of absorbed part-EDTA, DMSA
Some prefer BAL with EDTA
Chronic lead poisoning (plumbism or
saturnism)
Occurs in industrial environment due to
inhalation of lead dust or vapor.
Drinking water supplied in lead pipes
Due to food preserved in lead containers
Prolonged use of lead cosmetics
People who handle petrol or gasoline
Clinical features
1. Facial Pallor
2. Anemia with Punctuate basophilia or basophilic stippling
Hypochromic, microcytic type with increased count of
reticulocytes and basophilic stippled RBC
3. Lead line or Burtonian line
bluish- black discoloration of gingivae at the junction
with teeth
4. Retinal stippling
Greyish glistening lead particles
5. Colic and Constipation
6. Lead palsy
Peripheral demyelination- prolonged nerve
conduction- paralysis, usually of extensor
muscles of hand and feet (wrist drop and foot
drop)
7. Encephalopathy
Changes in personality, restlessness, fatigability
and mental dullness
Convulsion, delirium and coma
8. Effects on renal system- chronic interstitial
nephritis & renal failure
9. Effect on CVS- hypertension & hypertensive
cardiopathy
Treatment
Gaaef Protocol
1) Severe acute poisoning with Encephalopathy
-BAL 4mg/kg stat repeated 4hrly till BL<40ug/100 ml, then
12mg/kg/day in 3 divided doses.
-EDTA 75mg/kg/day i.v. till asymptomatic.
-Then oral chelation with DMSA 10mg/kg t.d.s for 20 days.
2) Severe poisoning without Encephalopathy (BL= >70
ug/100ml)BAL 12mg/kg/day & EDTA 50mg/kg/day till
BL<40ug/100 ml then discontinue BAL but continue EDTA for
5 more days. Then oral chelation
3) Moderate poisoning (BL b/w 45-70ug/100ml)--
EDTA 50mg/kg/day till BL<40ug/100 ml then oral chelation.
4) Mild poisoning (20-35ug/100ml)DMSA 10mg/kg
t.d.s for 20 days.
Supportive measures
I. Thiamine 10-50mg/kg for neurological manifestation
II. iv calcium gluconate for lead colic
III. Correct iron deficiency
Post mortem findings
Blue lines may be seen in the gums
Paralyzed muscles show fatty degeneration
Stomach and Intestine may show ulcerative and
hemorrhagic changes and are contracted and
thickened.
The brain is pale and greatly swollen.
Heart maybe hypertrophied
Poisonous compounds of mercury and their sources
Mercuric chloride (corrosive sublimate)-in lab as
preservative and in industries (most common)
Mercurous chloride (calomel)-used as purgatives
for human consumption in therapeutic dose.
Medicinal preparations of organic compounds as
diuretics
Dental amalgam- for restoration
Fatal Dose: 1-2 gm of mercuric chloride
Fatal Period: 3-5 days
Acute poisoning
Corrosive action
Metallic taste, increased salivation
Abdominal pain, vomiting and diarrhoea
Renal tubular necrosis with oliguria,
proteinuria, hematuria and progressive renal
failure
Leucocytosis in peripheral smear
Chronic poisoning (hydrargyrism)
Metallic taste, gingivitis, halitosis, loosening of teeth
Anorexia, insomnia, abnormal sweating, headache
Mercuria lentis- discoloration of the anterior capsule
of the lens of the eye
Neurological toxicity
Danbury Tremors occurs in hand, then progresses
to lips, tongue and finally involves arms and legs.
Moderately coarse and is interspersed by jerky
movent
Hatters Shake or glass blowers shakes- common
in persons working in glass blowing industries. The
patient cannot dress himself and cannot walk
properly
Mecurial erethism
is seen in person working with mercury in
mirror manufacturing firms.
psychological effects - anxiety, depression,
shyness, timidity, irritability, loss of confidence,
delusion, hallucination or suicidal melancholia or
maniac depressive psychosis
Acrodynia or pink disease generalized body rash,
irritation in hands and feet usually followed by
desquamation, loss of hair, hyperkeratosis
Gastric wash with milk or water.
100 ml of 5% sodium sulphate I.V. to help
anuria
Sodium bicarbonate- for acidosis
Chelating agents
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