arsenic poisoning - FM presentation

1. ARSENIC POISONING
By
PRIYANKA . N (82)

2. OVERVIEW
• Introduction
• Toxic compounds
• Absorption and excretion
• Action
• Acute and chronic poisoning
• Laboratory investigations
• Treatment
• Postmortem findings
• Medico-legal aspects

3. 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.

4. 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

5. Arsenic oxide Copper acetoarsenite
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 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.

8. 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

9. 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

10. 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

11. 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

12. 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

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
• 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

15. 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

16. 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

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
• 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

19. 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.

20. THANK YOU