ARSENIC POISONING
By
PRIYANKA . N (82)
OVERVIEW
• Introduction
• Toxic compounds
• Absorption and excretion
• Action
• Acute and chronic poisoning
• Laboratory investigations
• Treatment
• Postmortem findings
• Medico-legal aspects
INTRODUCTION
• Arsenic is a heavy metallic irritant poison.
• Metallic arsenic is not poisonous ,as it is not absorbed
from GIT.
• It is a normal constituent of all animal tissues.
• Soil, water and some sea fish are the natural sources
of arsenic.
• The most common reason for long-term exposure is
contaminated drinking water.
• Long term exposure to arsenic from drinking-water
and food can cause cancer and skin lesions.
TOXIC COMPOUNDS
• Arsenious oxide or arsenic trioxide – most toxic form, no
taste or smell and is sparingly soluble in water. Used in fruit
sprays, insecticides, rat poisons, weed-killers etc.,
• Copper arsenite (Scheele's green)
• Copper acetoarsenite (Paris green or emerald green)
• Sodium and potassium arsenate
• Arsenic sulfide
• Arsine- colorless gas with garlic-like odor
Arsenic oxide Copper acetoarsenite
Arsenic sulfide
ABSORPTION AND EXCRETION
• It is absorbed orally, topically, by inhalation or
parenterally.
• Arsenic is found in greatest quantity in the liver, followed
by kidneys and spleen.
• In cases in which life is prolonged, it is found in the
muscles for days, in the bones, keratin tissues, hair, nails
and skin for years.
• It is excreted mainly by the kidneys but also in the faeces,
bile, sweat, milk, nails and hair.
ACTION
• Arsenic compounds act by inactivating the sulphydryl groups of
mitochondrial enzymes which inturn interfere with cellular
metabolism resulting in decreased production of ATP.
• It inhibits cellular glucose uptake, gluconeogenesis, fatty acid
oxidation and further production of acetyl CoA.
• Its particular target is vascular endothelium, leading to increased
permeability, tissue oedema and hemorrhage, especially in the
intestinal canal.
• Locally it causes irritation of the mucous membranes and
remotely depression of the nervous system.
ACUTE POISONING
• Acute exposures- cholera like gastrointestinal symptoms,
respiratory failure and pulmonary edema
• Fulminant type- dose- > 3g, death in 1-3 hr from shock and
peripheral vascular failure. GIT symptoms are absent
• Narcotic type- GIT symptoms are less. Giddiness, formication,
tenderness of the muscles, delirium , coma and death.
• Arsine gas exposure – hemolysis , hemoglobinuria , renal failure
and depresses the CNS.
• Fatal dose – inorganic arsenic : 0.6mg/kg/day
arsenic trioxide :120-200mg(adults)
2mg/kg(children)
• Fatal period – 1-2 days
Difference between Arsenic poisoning and cholera
FEATURE ARSENIC POISONING CHOLERA
Pain in throat Before vomiting After vomiting
Purging Purging follows vomiting Vomiting follows purging
Vomitus Contains mucus, bile and blood Watery, without mucus,
bile or blood
Stools Rice-watery, may contain blood Rice-watery, not bloody
and passed in continuous
involuntary jet
Tenesmus and
anal irritation
present Absent
Voice Not affected Rough and whistling
Conjunctiva Inflamed Not inflamed
Analysis of
excreta
Arsenic present Vibrio cholerae present
Circumstantial
evidence
Of arsenic poisoning may be
present
Other cases of cholera in
locality
CHRONIC POISONING
• Chronic exposure – black foot disease characterized by
diabetes, vasospasm and peripheral vascular insufficiency
• GIT disturbances – gradual weight loss, malnutrition,
fatigue, nausea, vomiting
• Catarrhal changes – running nose, headache, conjunctivitis
• Skin rashes – rain drop pigmentation, hyperkeratosis of skin
of palm and soles
• Nervous disturbances
CLINICOPATHOLOGICAL FINDINGS
SYSTEM ACUTE CHRONIC
Skin Skin rash, eruptions ,delayed
hair loss
Melanosis, hyperkeratosis,
cutaneous cancer
Nails - Brittle, Aldrich-Mees lines
Neurologic Hyperthermia, convulsions,
tremors, coma
Encephalopathy,
polyneuropathy, axonal
degeneration
GI tract Abdominal pain, dysphagia,
vomiting, rice-water diarrhea,
mucosal erosions
Nausea, vomiting, diarrhea,
anorexia, weight loss
Liver Fatty infiltration Hepatomegaly, jaundice,
cirrhosis
Renal Oliguria , uremia Chronic nephritis
Hematologic - Bone marrow hypoplasia,
anemia, thrombocytopenia,
leukemia
SYSTEM ACUTE CHRONIC
Cardiovascular Hypotension, ARDS,
circulatory collapse
Hypertension,
ischemic heart disease
Respiratory - Cough, hoarseness of
voice, dyspnea
Musculoskeletal Pain in limbs, weakness -
Ocular Congestion, photophobia -
Aldrich-Mees linesHyperkeratosis
LABORATORY INVESTIGATIONS
• Urine - >50µg/l in 24hr urine, metabolites may be recovered.
• Blood - >0.9µg/dl, microcytic hypochromic anemia.
• Hair - >75µg%, 1.0-3.0 mg/kg(acute) and 0.1-0.5mg/kg(chronic).
• Nails - >100µg%
• Chemical test- Reinsch’s test, Marsh’s test, Gutzeit’s test.
• Abdominal X-ray
• ECG
• Neutron activation analysis
• Atomic absorption spectroscopy
TREATMENT
Acute poisoning
• Gastric lavage with warm water and milk.
• Demulcents and purgatives.
• Whole bowel irrigation
• Antidote-BAL- 3-5mg/kg IM 4 hourly for 2 days,
6 hourly for 1 day and then 12 hourly for 10 days
- DMSA-10mg/kg every 8 hourly for 10 days
- DMPS- 200mg iv 4 hourly
• Glucose-saline with sodium bicarbonate
• Hemodialysis or exchange transfusion
TREATMENT
Chronic poisoning
• Remove the patient from the source of exposure and
administer BAL in usual doses.
• Vitamin B complex and sodium thiosulfate are useful
• Symptomatic treatment
POSTMORTEM FINDINGS
Acute poisoning
External-Body looks emaciated.
-Rigor mortis appears early and putrefaction is delayed.
-Eye balls are sunken and skin is cyanosed.
-Blood tinged vomitus and fecal matter on body and clothes.
Internal- Mucous membrane of small intestine are inflamed
-Stomach- red velvety appearance
-Liver, kidney and heart: congested, enlarged and fatty
degeneration may be seen
POSTMORTEM FINDINGS
Chronic poisoning
External
Emaciation, pigmentation, keratosis, alopecia, white
streaks on nails, jaundice, wasting of muscles and
ulceration of nasal septum.
Internal
Stomach - patchy inflammatory redness
Small intestine - reddish with thickened mucosa
Liver - hepatomegaly, fatty degeneration
Kidney - tubular necrosis
Heart - myocardial necrosis
Bone marrow histopathology - hypoplasia
MEDICO-LEGAL ASPECTS
• Arsenic is the most popular homicidal poison.
• Suicide is rare
• Accidental death- admixture with food or improper
medicinal use.
• Occupational exposure
• Environmental contamination
• It is sometimes used in abortion sticks
REFERENCE :
• Biswas G. Inorganic Metallic Irritants- Arsenic, In:
Review of Forensic Medicine and Toxicology, 4th edition,
Jaypee Brothers Medical Publishers (P) Ltd,
2019.p.492-496.
• Reddy N. Metallic Poisons,In: The Essentials of Forensic
Medicine & Toxicology, 34th edition, Jaypee Brothers
Medical Publishers (P) Ltd,2017.p.501-504.
• Rao N G. Irritant poison,In: Textbook of forensic
medicine & toxicology, 2nd edition, Jaypee Brothers
Medical Publishers (P) Ltd, 2010.p.463-466.
THANK YOU

Arsenic poisoning roll no.82

  • 1.
  • 2.
    OVERVIEW • Introduction • Toxiccompounds • Absorption and excretion • Action • Acute and chronic poisoning • Laboratory investigations • Treatment • Postmortem findings • Medico-legal aspects
  • 3.
    INTRODUCTION • Arsenic isa heavy metallic irritant poison. • Metallic arsenic is not poisonous ,as it is not absorbed from GIT. • It is a normal constituent of all animal tissues. • Soil, water and some sea fish are the natural sources of arsenic. • The most common reason for long-term exposure is contaminated drinking water. • Long term exposure to arsenic from drinking-water and food can cause cancer and skin lesions.
  • 4.
    TOXIC COMPOUNDS • Arseniousoxide or arsenic trioxide – most toxic form, no taste or smell and is sparingly soluble in water. Used in fruit sprays, insecticides, rat poisons, weed-killers etc., • Copper arsenite (Scheele's green) • Copper acetoarsenite (Paris green or emerald green) • Sodium and potassium arsenate • Arsenic sulfide • Arsine- colorless gas with garlic-like odor
  • 5.
    Arsenic oxide Copperacetoarsenite Arsenic sulfide
  • 6.
    ABSORPTION AND EXCRETION •It is absorbed orally, topically, by inhalation or parenterally. • Arsenic is found in greatest quantity in the liver, followed by kidneys and spleen. • In cases in which life is prolonged, it is found in the muscles for days, in the bones, keratin tissues, hair, nails and skin for years. • It is excreted mainly by the kidneys but also in the faeces, bile, sweat, milk, nails and hair.
  • 7.
    ACTION • Arsenic compoundsact by inactivating the sulphydryl groups of mitochondrial enzymes which inturn interfere with cellular metabolism resulting in decreased production of ATP. • It inhibits cellular glucose uptake, gluconeogenesis, fatty acid oxidation and further production of acetyl CoA. • Its particular target is vascular endothelium, leading to increased permeability, tissue oedema and hemorrhage, especially in the intestinal canal. • Locally it causes irritation of the mucous membranes and remotely depression of the nervous system.
  • 8.
    ACUTE POISONING • Acuteexposures- cholera like gastrointestinal symptoms, respiratory failure and pulmonary edema • Fulminant type- dose- > 3g, death in 1-3 hr from shock and peripheral vascular failure. GIT symptoms are absent • Narcotic type- GIT symptoms are less. Giddiness, formication, tenderness of the muscles, delirium , coma and death. • Arsine gas exposure – hemolysis , hemoglobinuria , renal failure and depresses the CNS. • Fatal dose – inorganic arsenic : 0.6mg/kg/day arsenic trioxide :120-200mg(adults) 2mg/kg(children) • Fatal period – 1-2 days
  • 9.
    Difference between Arsenicpoisoning and cholera FEATURE ARSENIC POISONING CHOLERA Pain in throat Before vomiting After vomiting Purging Purging follows vomiting Vomiting follows purging Vomitus Contains mucus, bile and blood Watery, without mucus, bile or blood Stools Rice-watery, may contain blood Rice-watery, not bloody and passed in continuous involuntary jet Tenesmus and anal irritation present Absent Voice Not affected Rough and whistling Conjunctiva Inflamed Not inflamed Analysis of excreta Arsenic present Vibrio cholerae present Circumstantial evidence Of arsenic poisoning may be present Other cases of cholera in locality
  • 10.
    CHRONIC POISONING • Chronicexposure – black foot disease characterized by diabetes, vasospasm and peripheral vascular insufficiency • GIT disturbances – gradual weight loss, malnutrition, fatigue, nausea, vomiting • Catarrhal changes – running nose, headache, conjunctivitis • Skin rashes – rain drop pigmentation, hyperkeratosis of skin of palm and soles • Nervous disturbances
  • 11.
    CLINICOPATHOLOGICAL FINDINGS SYSTEM ACUTECHRONIC Skin Skin rash, eruptions ,delayed hair loss Melanosis, hyperkeratosis, cutaneous cancer Nails - Brittle, Aldrich-Mees lines Neurologic Hyperthermia, convulsions, tremors, coma Encephalopathy, polyneuropathy, axonal degeneration GI tract Abdominal pain, dysphagia, vomiting, rice-water diarrhea, mucosal erosions Nausea, vomiting, diarrhea, anorexia, weight loss Liver Fatty infiltration Hepatomegaly, jaundice, cirrhosis Renal Oliguria , uremia Chronic nephritis Hematologic - Bone marrow hypoplasia, anemia, thrombocytopenia, leukemia
  • 12.
    SYSTEM ACUTE CHRONIC CardiovascularHypotension, ARDS, circulatory collapse Hypertension, ischemic heart disease Respiratory - Cough, hoarseness of voice, dyspnea Musculoskeletal Pain in limbs, weakness - Ocular Congestion, photophobia - Aldrich-Mees linesHyperkeratosis
  • 13.
    LABORATORY INVESTIGATIONS • Urine- >50µg/l in 24hr urine, metabolites may be recovered. • Blood - >0.9µg/dl, microcytic hypochromic anemia. • Hair - >75µg%, 1.0-3.0 mg/kg(acute) and 0.1-0.5mg/kg(chronic). • Nails - >100µg% • Chemical test- Reinsch’s test, Marsh’s test, Gutzeit’s test. • Abdominal X-ray • ECG • Neutron activation analysis • Atomic absorption spectroscopy
  • 14.
    TREATMENT Acute poisoning • Gastriclavage with warm water and milk. • Demulcents and purgatives. • Whole bowel irrigation • Antidote-BAL- 3-5mg/kg IM 4 hourly for 2 days, 6 hourly for 1 day and then 12 hourly for 10 days - DMSA-10mg/kg every 8 hourly for 10 days - DMPS- 200mg iv 4 hourly • Glucose-saline with sodium bicarbonate • Hemodialysis or exchange transfusion
  • 15.
    TREATMENT Chronic poisoning • Removethe patient from the source of exposure and administer BAL in usual doses. • Vitamin B complex and sodium thiosulfate are useful • Symptomatic treatment
  • 16.
    POSTMORTEM FINDINGS Acute poisoning External-Bodylooks emaciated. -Rigor mortis appears early and putrefaction is delayed. -Eye balls are sunken and skin is cyanosed. -Blood tinged vomitus and fecal matter on body and clothes. Internal- Mucous membrane of small intestine are inflamed -Stomach- red velvety appearance -Liver, kidney and heart: congested, enlarged and fatty degeneration may be seen
  • 17.
    POSTMORTEM FINDINGS Chronic poisoning External Emaciation,pigmentation, keratosis, alopecia, white streaks on nails, jaundice, wasting of muscles and ulceration of nasal septum. Internal Stomach - patchy inflammatory redness Small intestine - reddish with thickened mucosa Liver - hepatomegaly, fatty degeneration Kidney - tubular necrosis Heart - myocardial necrosis Bone marrow histopathology - hypoplasia
  • 18.
    MEDICO-LEGAL ASPECTS • Arsenicis the most popular homicidal poison. • Suicide is rare • Accidental death- admixture with food or improper medicinal use. • Occupational exposure • Environmental contamination • It is sometimes used in abortion sticks
  • 19.
    REFERENCE : • BiswasG. Inorganic Metallic Irritants- Arsenic, In: Review of Forensic Medicine and Toxicology, 4th edition, Jaypee Brothers Medical Publishers (P) Ltd, 2019.p.492-496. • Reddy N. Metallic Poisons,In: The Essentials of Forensic Medicine & Toxicology, 34th edition, Jaypee Brothers Medical Publishers (P) Ltd,2017.p.501-504. • Rao N G. Irritant poison,In: Textbook of forensic medicine & toxicology, 2nd edition, Jaypee Brothers Medical Publishers (P) Ltd, 2010.p.463-466.
  • 20.