Orris

GROUP – A (LAQ-15 MARKS) 1. A person is brought to the emergency at 10 pm with pain abdomen. History reveals that he had such episodes on and off for last one month along with constipation. He also complains that there is weakness of his hands and feets and he was having cramps and tremors & numbness over hands and legs before the actual weakness started. On physical examination, his blood pressure was raised along with facial pallor. Further enquiry revealed that he is working in a paint industry for last 30 years. i. What poisoning may cause the above noted presentation ? ii. Describe the usual and expected hematological features in a case of such poisoning ? iii. How will you proceed to conifrm the diagnosis and manage such a case of poisoning ? [2+4+(4+5)] [ESIC JOKA] 2. A worker of a battery industry is hospitalized with a history of sudden onset dysphagia, pain abdomen, vomiting, constipation & headache. On examination, he has anemia, fine tremors, & wrist drop. Name the probable poison. Mention another 3 common sources of this poison causing human exposure. What are the expected findings in a peripheral blood smear? Mention the biochemical markers in blood & urine. What is the reason behind anemia in this case? Mention the other clinical manifestations of chronic poisoning with this poison. Mention the specific therapeutic measure for acute involvement of the central nervous system in this substance poisoning. (2+2.5+1.5+2+2 = 10) [JNM] 3. One labour was admitted at a peripheral Medical College with history of fatigue, irritability and weight loss. Clinical examination revealed a blue line over his gum and wrist drop. What are the differential diagnoses of this case? What are the other clinical features of this case? How will you confirm the diagnosis? How will you manage this case? (2 + 5 + 3 + 5 = 15) [NRS] 4. During autopsy, an autopsy surgeon found evidence of bluish discoloration of stomach & duodenum mucosa with yellowish discoloration of skin. a) What may be the suspected cause of death in this case? b) What are the clinical signs & symptoms of this case? c) Enumerate the specific treatment of this case. d) Mention the method of preservation of viscera in this case. (1+3+3+3=10) [RGKAR] 5. A person presented in emergency at 10 pm with pain abdomen. History reveals that he had such episodes on and off for last one month. He also complains that there is weakness of his hands and feet and he was having tremors, numbness and cramps over hands and legs before the actual weakness starts. On enquiry it was found that he is working in a paint industry for last 30 years. What are the different causes of chronic lead poisoning? Describe the clinical features of chronic lead poisoning? Describe the hematological findings in a case of Chronic lead poisoning? Outline the management of a case of chronic lead poisoning. (2+5+3+5=15) [MJNMCH] 6. A male worker working in an industry since long time presented to the emergency with complain of diffuse skin pigmentation over the back of body along with features of wrist and foot drop. a) What is your provisional diagnosis? b) What are the investigation to be done for confirmation of diagnosis? c) Write down the steps of management. d) Describe the autopsy findings you will get in this case. (2+4+6+3=15) [JALPAIGURI] 7. A 30-year-old painter by occupation, presents to the Medicine OPD with history of vomiting headache, visual disturbances, restlessness and convulsion. On examination, patient is anaemic with facial paleness, blue line on the gums and left wrist drop. a) Explain the various clinical manifestations of the suspected poison. b) Discuss in detail about treatment protocol in a case of acute poisoning by the same. c) What are the samples you will preserve during autopsy in such a case? (5+5+5=15) [CMSDH]

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I have enough information. Now let me write the comprehensive answers for all 7 questions.

LEAD POISONING - Complete Answers to All 7 Questions

All seven questions revolve around Lead Poisoning (Plumbism). Q4 describes autopsy findings consistent with arsenic (bluish stomach + yellowish skin/jaundice), which is addressed separately below.

QUESTION 1 (ESIC JOKA) - [2+4+(4+5)]

i. What poisoning may cause the above presentation? (2 marks)

Chronic Lead Poisoning (Plumbism)
The clinical triad of:
  • Pain abdomen + constipation (lead colic)
  • Peripheral neuropathy (weakness, tremors, cramps, numbness preceding actual weakness)
  • Raised BP + facial pallor
  • Occupation: paint industry for 30 years (classic lead exposure source)
...is pathognomonic of chronic lead poisoning.

ii. Hematological Features of Lead Poisoning (4 marks)

Lead is a potent inhibitor of the heme synthesis pathway, producing characteristic blood findings:
1. Peripheral Blood Smear Changes:
  • Basophilic stippling (punctate basophilia) - pathognomonic of plumbism. Discrete dark-blue pinhead-sized particles in the cytoplasm of RBCs, seen at blood lead levels of 60-80 μg/100 mL. Due to aggregation/clumping of ribosomes.
  • Polychromasia and polychromatophilia (early stages)
  • Reticulocytosis - compensatory increase
  • Poikilocytosis and anisocytosis
  • Nucleated red cells (sideroblasts)
  • Decreased polymorphonuclear cells and platelets
  • Under UV light: 75-100% fluorescent red cells due to increased protoporphyrin
2. Type of Anaemia:
  • Early stages: Polycythemia with polychromatophilia
  • Late stages: Microcytic or normocytic anaemia (NOT macrocytic)
3. Mechanism of Anaemia:
  • Inhibition of heme synthesis: Lead inhibits delta-aminolevulinic acid dehydratase (ALAD) and ferrochelatase, blocking incorporation of iron into protoporphyrin
  • Decreased RBC lifespan: RBCs become mechanically more fragile → shortened survival
4. Porphyrin Disturbances:
  • Elevated erythrocyte protoporphyrin (EP) / zinc protoporphyrin (ZPP) in blood
  • Increased coproporphyrin III (CPIII) in urine (>150 μg/L) - detectable as reddish fluorescence under UV lamp
  • Delta-aminolevulinic acid (ALA) in urine >5 mg/L indicates lead absorption

iii. Confirmation of Diagnosis + Management (4+5 marks)

A. Confirming the Diagnosis (4 marks):
  1. History: Occupational exposure (paint industry) for 30 years; symptoms of colic, constipation, neuropathy
  2. Clinical Features: Blue gum line (Burtonian/Lead line), facial pallor, hypertension, wrist drop / peripheral neuropathy
  3. Laboratory Tests:
    • Blood lead level (BLL): Normal = 0.03 mg/100 mL; BLL >70 μg/100 mL = clinical symptoms; 0.1-0.6 mg/100 mL = diagnostic of poisoning
    • Urine lead: >0.8 mg/L (normal: 0.2-0.8 mg/L)
    • ALA in urine: >5 mg/L indicates lead absorption
    • Coproporphyrin in urine (CPU): >150 μg/L in exposed individuals
    • Peripheral blood smear: Basophilic stippling - sensitive and pathognomonic
    • X-ray of long bones (esp. in children): Radio-opaque "lead lines" at metaphyses
  4. Chelation challenge test (EDTA mobilization test): Increased urinary lead excretion after EDTA administration confirms significant body burden
B. Management (5 marks):
Step 1 - Remove from exposure: Immediate removal from the paint industry / source of exposure
Step 2 - Decontamination/Prevent further absorption:
  • Gastric lavage with 1% magnesium sulphate or sodium sulphate
  • Oral magnesium or sodium sulphate (8-12 g) - converts unabsorbed lead to insoluble lead sulphate
Step 3 - Supportive Treatment:
  • Calcium gluconate IV - for colic relief
  • Morphine or atropine - for severe pain
  • High calorie diet; 3 pints of milk/day (alkalosis to fix lead in bones)
  • Thiamine 10-50 mg/kg - helps neurological manifestations
Step 4 - Chelation Therapy (based on BLL and severity):
SeverityBlood Lead LevelTreatment
Severe with encephalopathy>70 μg/100 mLBAL 4 mg/kg IM q4h + CaNa₂EDTA 75 mg/kg/day IV
Severe without encephalopathy>70 μg/100 mLBAL + EDTA; stop BAL when BLL <40 μg/100 mL
Moderate45-75 μg/100 mLEDTA alone 50 mg/kg/day
Mild20-35 μg/100 mLD-penicillamine or DMSA (oral)
  • CaNa₂EDTA (Calcium Disodium Versenate): 5 mL of 20% solution in 250-500 mL NS/5%D, slow IV drip over 1 hour, twice daily for 5 days. Increases urinary lead excretion 50-fold
  • BAL (British Anti-Lewisite/Dimercaprol): 4 mg/kg IM q4h. Give at least 4 hours BEFORE EDTA. Chelates lead both intracellularly and extracellularly. Drug of choice with renal impairment
  • D-Penicillamine: 10 mg/kg/day oral; useful in children
  • DMSA (Succimer/Dimercaptosuccinic acid): 10 mg/kg three times daily for 20 days; more effective and less toxic than penicillamine
Step 5 - Prevention of recurrence:
  • Adequate ventilation and industrial hygiene
  • Regular BLL monitoring of workers
  • Workers should be removed if BLL persistently elevated

QUESTION 2 (JNM) - (2+2.5+1.5+2+2 = 10)

Name the probable poison (2 marks)

Lead (Pb) - Chronic Lead Poisoning
History: battery industry worker + dysphagia, abdominal pain, vomiting, constipation, headache + anemia + fine tremors + wrist drop = classic plumbism.

3 Other Common Sources of Lead Exposure (2.5 marks)

  1. Paint industry - inhalation of lead dust/fumes (most common occupational source)
  2. Gasoline/petroleum - environmental lead from automobile exhaust (leaded petrol)
  3. Drinking water - from water stored in lead pipes or lead-lined cisterns
  4. Tinned food - contaminated through lead solder
  5. Printing/compositing industry, rubber industry, lead smelters, glass manufacturing
  6. Vermilion (sindoor) - applied to scalp by Hindu married women; absorbed through skin with hair oil

Expected Peripheral Blood Smear Findings + Biochemical Markers (1.5 marks)

Blood smear:
  • Basophilic stippling (punctate basophilia) - pathognomonic
  • Reticulocytosis, polychromasia, anisocytosis, poikilocytosis
  • Nucleated RBCs (sideroblasts), decreased polymorphs and platelets
Biochemical markers:
  • Blood: BLL >70 μg/100 mL (normal <0.03 mg/100 mL); elevated erythrocyte protoporphyrin (EP)/ZPP
  • Urine: ALA (delta-aminolevulinic acid) >5 mg/L; Coproporphyrin III >150 μg/L; Lead >0.8 mg/L

Reason Behind Anaemia (2 marks)

Two mechanisms:
  1. Inhibition of heme synthesis: Lead inhibits ALA dehydratase and ferrochelatase, blocking incorporation of iron into protoporphyrin IX to form heme. This causes iron to accumulate in RBC mitochondria as ringed sideroblasts.
  2. Decreased RBC lifespan: Lead makes RBCs mechanically more fragile, shortening their survival time (hemolytic component).
  3. Inhibition of globin synthesis also contributes.
Result: Microcytic/normocytic anemia with sideroblasts.

Other Clinical Manifestations of Chronic Lead Poisoning (2 marks)

  • Facial pallor (earliest and most consistent sign, due to vasospasm around mouth)
  • Lead line / Burtonian line: Bluish-black line on gums (due to lead sulphide formation from H₂S)
  • Lead colic: Severe colicky abdominal pain, usually nocturnal, in 85% cases; constipation
  • Lead palsy: Wrist drop (radial nerve; extensor muscle weakness), foot drop (anterior tibial muscles)
  • Lead encephalopathy: Insomnia, headache, vomiting, restlessness, delirium, convulsions, coma
  • Cardiovascular/renal: Hypertension, arteriolar degeneration, chronic interstitial nephritis
  • Reproductive: Menstrual disturbances, infertility, abortion at 3-6 months, fetal abnormalities
  • Other: Anorexia, weight loss, alopecia, vertigo, metallic taste

Specific Therapeutic Measure for Acute CNS Involvement (2 marks)

BAL (British Anti-Lewisite / Dimercaprol) + CaNa₂EDTA combination:
  • BAL: 4 mg/kg IM every 4 hours (in children). Repeat until BLL falls below 40 μg/100 mL. Given FIRST, at least 4 hours before EDTA.
  • CaNa₂EDTA: 75 mg/kg/day as IV infusion (for encephalopathy). Reduce to 50 mg/kg/day as condition improves. Continue until patient is asymptomatic.
  • Then transition to oral chelation: D-penicillamine 10 mg/kg/day OR DMSA (succimer) 10 mg/kg TDS for 20 days.
  • Supportive: Control seizures with diazepam/phenobarbitone; manage cerebral edema; corticosteroids may be used for brain edema.

QUESTION 3 (NRS) - (2+5+3+5 = 15)

Differential Diagnoses (2 marks)

Key features: Fatigue, irritability, weight loss + blue line on gums + wrist drop
  1. Chronic Lead Poisoning - most likely (Burton's line + wrist drop)
  2. Chronic Mercury Poisoning (Mercurialism) - can cause gum discoloration, tremors, neuropsychiatric features (but blue line is characteristic of lead)
  3. Chronic Arsenic Poisoning - fatigue, weight loss, neuropathy (but features like Mees' lines, skin pigmentation more typical)
  4. Alcoholic peripheral neuropathy - wrist/foot drop but no gum line
  5. Other heavy metal poisoning - bismuth, copper can cause gum line

Other Clinical Features (5 marks)

A. General/Systemic:
  • Facial pallor (especially around mouth, due to vasospasm) - earliest and most consistent sign
  • Anorexia, emaciation, weight loss, alopecia
  • Metallic/sweetish taste in mouth
B. Gastrointestinal:
  • Lead colic - severe colicky pain, usually nocturnal, occurring in 85% cases; abdominal wall rigid/contracted; relieved by pressure
  • Obstinate constipation (constant feature)
  • Vomiting and nausea may occur
C. Hematological:
  • Anaemia (microcytic/normocytic), basophilic stippling
  • Facial pallor
D. Neurological - Lead Palsy:
  • Tremors, cramps, numbness, hyperesthesia PRECEDE actual weakness
  • Wrist drop (extensor muscles of wrist; radial nerve affected) - commonest
  • Foot drop (anterior tibial muscles affected)
  • Deltoid and biceps may be affected
  • Purely motor paralysis; recovery slow but may be complete
E. Lead Encephalopathy:
  • Insomnia, headache, visual disturbances, irritability, restlessness
  • Delirium, hallucinations, convulsions, coma - can be fatal
  • Present in some form in almost every case
  • More common in children; often irreversible (85% permanent brain damage)
F. Cardiovascular/Renal:
  • Hypertension (vascular constriction)
  • Chronic arteriosclerotic nephritis, interstitial nephritis
G. Reproductive:
  • Menstrual disturbances, sterility, abortion, fetal abnormalities

Confirming the Diagnosis (3 marks)

  1. Detailed occupational history - type and duration of exposure
  2. Blood lead level (BLL):
    • Normal: 0.03 mg/100 mL; BLL >70 μg/100 mL = clinical symptoms
    • Diagnostic in poisoning: 0.1-0.6 mg/100 mL
  3. Urine tests:
    • ALA (aminolevulinic acid): >5 mg/L = significant lead absorption
    • Coproporphyrin III: >150 μg/L (normal <150); detected as reddish fluorescence under UV lamp with acetic acid and ether
    • Urine lead: >0.8 mg/L
  4. Peripheral blood smear: Basophilic stippling, sideroblasts
  5. X-ray long bones (children): Radio-opaque lead lines at metaphyses
  6. Zinc protoporphyrin (ZPP): Elevated (>35 μg/L)

Management (5 marks)

(Same as Q1 management - refer above for full details)
Key points:
  1. Remove from exposure immediately
  2. Prevent further absorption: Gastric lavage (MgSO₄ solution), saline purgative
  3. Supportive: Calcium gluconate IV for colic; high calorie diet with milk; morphine for pain; thiamine for neuropathy
  4. Chelation (as per severity):
    • With encephalopathy: BAL 4 mg/kg IM q4h + CaNa₂EDTA 75 mg/kg/day IV
    • Without encephalopathy but BLL >70: BAL + EDTA; stop BAL when <40 μg/100 mL
    • Moderate (45-75): EDTA alone
    • Mild: Oral D-penicillamine or DMSA
  5. Prevent recurrence: Occupational hygiene, ventilation, periodic medical screening
  6. Lead poisoning is a notifiable and compensatable disease in India (since 1924)

QUESTION 4 (RGKAR) - (1+3+3+3 = 10)

a. Suspected Cause of Death (1 mark)

Bluish discoloration of stomach/duodenum mucosa + yellowish skin discoloration at autopsy:
  • Yellowish skin = jaundice (hepatic damage)
  • Bluish/dark discoloration of stomach and duodenum = characteristic of Arsenic Poisoning
Suspected cause: Acute Arsenic Poisoning
Note: The bluish-grey discoloration of the gastric and duodenal mucosa with yellowish jaundice is the classic autopsy picture of arsenic. (In lead autopsy, the stomach is contracted and thickened, mucosa softened/eroded; the blue line is on the gums.)

b. Clinical Signs and Symptoms (3 marks)

Acute Arsenic Poisoning:
GI Phase (within 30 min - few hours):
  • Metallic/garlic taste in mouth
  • Burning in throat and esophagus
  • Severe nausea and projectile vomiting (rice-water or blood-stained)
  • Profuse watery diarrhea ("rice-water" stools resembling cholera)
  • Violent abdominal cramps and colicky pain
Systemic Phase:
  • Dehydration, hypotension, circulatory collapse
  • Oliguria → anuria, renal failure
  • Jaundice (hepatic damage - yellow skin)
  • Muscle cramps and weakness
  • Mees' lines (transverse white lines on fingernails - in chronic cases)
  • CNS: Headache, convulsions, coma
Chronic/Subacute:
  • Skin: Diffuse hyperpigmentation ("rain-drop pigmentation"), keratosis of palms/soles
  • Peripheral neuropathy: "Stocking and glove" sensory neuropathy
  • Alopecia, Mees' lines
  • Marrow suppression, pancytopenia

c. Specific Treatment (3 marks)

  1. Remove from source - stop exposure immediately
  2. Decontamination:
    • Gastric lavage with warm water or freshly prepared ferric hydroxide (antidote for arsenic)
    • Activated charcoal
    • Saline cathartic
  3. Specific Antidote - Chelation Therapy:
    • BAL (Dimercaprol): Drug of choice. 3-5 mg/kg IM every 4 hours for 2 days, then 2-3 mg/kg IM q6h for 2 more days, then 2-3 mg/kg IM daily for 7 days
    • DMSA (Succimer): 10 mg/kg oral TDS for 5 days - safer alternative
    • D-penicillamine: 250 mg oral QID as follow-up chelation
  4. Supportive:
    • IV fluids and electrolyte replacement (manage dehydration/shock)
    • Treat renal failure (dialysis if needed)
    • Manage hepatic failure
    • Pain relief

d. Method of Preservation of Viscera (3 marks)

In cases of suspected metallic/inorganic poisoning (including arsenic), the standard method is Saturated Common Salt (NaCl) solution - NOT formalin (which is organic).
Organs to be preserved and method:
Organ/SampleContainerPreservative
Stomach + contentsWide-mouth glass jarSaturated NaCl solution (30%)
Portion of small intestine (jejunum + ileum) + contentsSeparate glass jarSaturated NaCl solution
Portion of liver (250 g)Glass jarSaturated NaCl solution
One kidney (half)Glass jarSaturated NaCl solution
Urine (100 mL)Clean glass bottleNo preservative / plain
Blood (50 mL)Clean bottleSodium fluoride (NaF) as preservative
Hair and nailsPaper envelopeNone (dry)
Bone (rib/femur segment)Dry containerNone
Key rule: Use glass containers (not plastic), clean and new (to avoid contamination). Each container sealed and labeled. No formalin as it is an organic preservative and interferes with chemical analysis. Saturated salt solution is used for all metallic poisons.

QUESTION 5 (MJNMCH) - (2+5+3+5 = 15)

Different Causes / Sources of Chronic Lead Poisoning (2 marks)

Occupational Sources:
  1. Paint industry (pigments - lead carbonate/white lead, red lead)
  2. Battery industry (lead plates)
  3. Printing and compositing industry
  4. Plumbing industry (lead pipes)
  5. Glass and enamel manufacture
  6. Lead smelting, rubber industry
  7. Electric light workers
  8. Petrol/gasoline industry (lead tetraethyl)
Non-Occupational Sources:
  1. Drinking water from lead pipes or lead-lined cisterns
  2. Tinned food contaminated with lead from solder
  3. Ghee stored in tin-lined brass/copper vessels (oleate of lead formed)
  4. Sindoor/vermilion applied to scalp by Hindu women (absorbed through skin with hair oil)
  5. Children chewing/licking lead-painted toys, walls, furniture
  6. Environmental pollution from automobile exhaust (leaded petrol)
  7. Food cooked in lead vessels

Clinical Features of Chronic Lead Poisoning (5 marks)

1. Facial Pallor
  • The earliest and most consistent sign
  • Particularly around the mouth
  • Independent of degree of anaemia
  • Due to vasospasm
2. Anaemia
  • Occurs at BLL 70-80 μg/100 mL
  • Microcytic or normocytic (not macrocytic)
  • Associated features: basophilic stippling, reticulocytosis, poikilocytosis
3. Lead Line (Burtonian Line)
  • Present in 50-70% of cases
  • Blue/bluish-black line on gums at the junction with teeth
  • Only near dirty/carious teeth, especially in upper jaw
  • Appears within a week of exposure
  • Due to lead sulphide formation from H₂S (decomposed food bacteria in mouth)
  • Metallic/sweetish taste in mouth
4. Colic and Constipation ("Dry belly-ache")
  • Late symptom; occurs in 85% of cases
  • Intestinal, ureteral, uterine colic
  • Usually nocturnal, very severe
  • Abdominal wall rigid and contracted; relief by firm pressure
  • Attacks last few minutes, recur over days/weeks
  • Constipation is constant; diarrhea and vomiting may occur
5. Lead Palsy
  • Late feature, in <10% cases
  • Tremors, hyperesthesia, numbness, cramps PRECEDE actual weakness
  • Commonest: Wrist drop (extensor muscles; radial nerve; C7)
  • Others: Foot drop (anterior tibial muscles), deltoid, biceps
  • Purely motor paralysis; axonal degeneration of nerve with muscle atrophy
  • Recovery is slow but may be complete
6. Lead Encephalopathy
  • Present in almost all cases in some form
  • More common in children
  • Symptoms: Insomnia, headache, vomiting, visual disturbances, irritability, restlessness, delirium, hallucinations, convulsions, coma → death
  • Usually irreversible; 85% permanent brain damage; 25% mortality
7. Cardiovascular and Renal
  • Hypertension (vascular constriction)
  • Arteriolar degeneration, arteriosclerosis
  • Chronic interstitial nephritis, nephrosclerosis
8. Reproductive System
  • Menstrual irregularities, sterility
  • Abortion at 3-6 months of gestation
  • Fetal abnormalities, stillbirths
9. Miscellaneous
  • Coproporphyrinuria (porphyrin excreted in urine ~500 μg/day)
  • Anorexia, emaciation, alopecia, vertigo

Hematological Findings in Chronic Lead Poisoning (3 marks)

  1. Basophilic Stippling (Punctate Basophilia) - pathognomonic
    • Discrete dark-blue pinhead-size particles in RBC cytoplasm
    • Seen at BLL 60-80 μg/100 mL
    • Due to aggregation of ribosomes (ribosomal RNA) - lead inhibits pyrimidine-5'-nucleotidase
    • Under UV light: 75-100% fluorescent cells due to increased protoporphyrin
  2. Anaemia: Microcytic/normocytic (not macrocytic)
    • Early: Polycythemia with polychromatophilia
    • Late: Anaemia with reticulocytosis
  3. Reticulocytosis - compensatory response
  4. Morphological changes: Poikilocytosis, anisocytosis, polychromasia
  5. Nucleated RBCs / Sideroblasts (ringed sideroblasts in bone marrow)
  6. Decreased polymorphs and platelets
  7. Elevated erythrocyte protoporphyrin (EP) / Zinc protoporphyrin (ZPP) - elevated in blood
  8. Mechanism of anaemia:
    • Lead inhibits ALAD and ferrochelatase → block in heme synthesis
    • Decreased RBC survival (mechanical fragility)

Management of Chronic Lead Poisoning (5 marks)

(Refer to Q1 management above - complete details provided)
Summary outline:
  1. Remove from exposure (workplace)
  2. Decontamination - saline purgative/lavage
  3. Alkaline diet - milk, calcium gluconate IV (immobilizes lead in bones)
  4. Chelation therapy based on BLL:
    • Encephalopathy: BAL + EDTA IV
    • Severe (no encephalopathy): BAL + EDTA
    • Moderate: EDTA alone
    • Mild: D-penicillamine oral / DMSA oral
  5. Symptomatic: Ca-gluconate for colic, thiamine for neurology, morphine for pain
  6. Occupational rehabilitation + periodic monitoring
  7. Notifiable disease in India

QUESTION 6 (JALPAIGURI) - (2+4+6+3 = 15)

a. Provisional Diagnosis (2 marks)

Chronic Lead Poisoning (Plumbism) with Arsenic poisoning also in differential
The features pointing to lead:
  • Long industrial exposure
  • Wrist drop and foot drop (lead palsy)
The feature of diffuse skin pigmentation over back of body is more suggestive of Chronic Arsenic Poisoning ("rain-drop pigmentation" / melanosis). However, combined with wrist drop and foot drop from industrial exposure, this may also suggest combined or arsenic poisoning.
Most likely: Chronic Arsenic Poisoning (diffuse pigmentation is pathognomonic of arsenic, not lead)
Alternative: Chronic Lead Poisoning (wrist/foot drop) - but pigmentation is less typical.

b. Investigations for Confirmation (4 marks)

For Arsenic:
  1. Urine arsenic: >50 μg/L (normal <50 μg/L); >1000 μg/L in acute poisoning
  2. Blood arsenic level: Elevated
  3. Hair and nail arsenic: Mees' bands on nails; hair arsenic (Reinsch's test, atomic absorption spectroscopy)
  4. Urine: ALA, coproporphyrins (if lead component)
Confirming peripheral neuropathy:
  • Nerve conduction velocity (NCV) studies
  • Electromyography (EMG)
Blood tests:
  • CBC: Pancytopenia (arsenic), anemia + basophilic stippling (lead)
  • LFTs, RFTs (liver/kidney involvement)
  • Blood lead level, ZPP
Imaging:
  • X-ray long bones: Lead lines if lead
  • Chest X-ray
Skin biopsy: Melanocyte hyperactivity in arsenic

c. Steps of Management (6 marks)

Step 1 - Remove from exposure: Immediate transfer away from the industry; sick leave
Step 2 - Decontamination:
  • If recent ingestion: Gastric lavage
  • Activated charcoal
  • Saline cathartic (MgSO₄)
Step 3 - Specific Chelation Therapy:
If Arsenic:
  • BAL (Dimercaprol): 3-5 mg/kg IM q4h × 2 days → 2-3 mg/kg IM q6h × 2 days → 2-3 mg/kg/day for 7 days
  • DMSA (Succimer): 10 mg/kg orally TDS × 5 days (safer, fewer side effects)
  • D-penicillamine: 250 mg oral QID as follow-up
If Lead:
  • BAL + EDTA (as per BLL-guided protocol above)
Step 4 - Supportive Treatment:
  • IV fluid and electrolyte replacement
  • Analgesics for pain
  • Anticonvulsants if seizures (diazepam)
  • Calcium gluconate IV for colic
  • Thiamine for neuropathy
  • Treatment of hepatic/renal failure
  • Corticosteroids if encephalopathy/cerebral edema
Step 5 - Symptomatic Management of Neuropathy:
  • Physiotherapy and rehabilitation for wrist drop/foot drop
  • Wrist/foot splints
  • Vitamin B complex supplementation
Step 6 - Occupational and Legal Measures:
  • Notify appropriate authorities (both lead and arsenic poisoning are notifiable in India)
  • Industrial hygiene assessment
  • Workplace ventilation improvement
  • Protective equipment for co-workers
  • Periodic medical surveillance
Step 7 - Follow-up:
  • Serial blood/urine heavy metal levels
  • NCV monitoring
  • Skin examination (for malignant changes in arsenic - risk of Bowen's disease, squamous cell carcinoma)

d. Autopsy Findings (3 marks)

If Lead Poisoning:
  1. Blue/Burtonian line visible on gums
  2. Stomach and intestines contracted and thickened; gastric mucosa softened, eroded, thickened
  3. Liver and kidneys contracted and shrunken
  4. Brain pale and swollen (cerebral edema in encephalopathy)
  5. Heart hypertrophied with atheroma of aorta
  6. Bone marrow: Hyperplasia of leukoblasts and erythroblasts
  7. Peripheral nerves: Axonal degeneration, muscle atrophy
If Arsenic Poisoning:
  1. Subicteric or jaundiced skin (yellowish discoloration)
  2. Stomach/duodenum mucosa: Bluish-grey/dark discoloration, congested, hemorrhagic erosions
  3. Garlic odor from all organs
  4. Liver: Fatty changes (yellow/pale), centrizonal necrosis
  5. Kidneys: Congested, tubular necrosis
  6. Skin: Pigmentation changes
  7. Hair/nails: Mees' lines on nails; arsenic detectable by Marsh's test
  8. Body well-preserved (arsenic has antiseptic properties - classic "embalming" effect; body preserved even after exhumation)

QUESTION 7 (CMSDH) - (5+5+5 = 15)

(Painter - vomiting, headache, visual disturbances, restlessness, convulsion + anaemia + facial pallor + blue line on gums + left wrist drop)

a. Clinical Manifestations of Lead Poisoning (5 marks)

Summarized systematically:
I. General:
  • Facial pallor (earliest sign, due to vasospasm)
  • Anorexia, weight loss, fatigue, emaciation, alopecia
II. Oral/GI:
  • Blue lead line (Burtonian line) on gums (50-70% cases; upper jaw near carious teeth)
  • Sweetish metallic taste
  • Lead colic (85% cases): severe nocturnal colicky abdominal pain, rigid contracted abdomen
  • Obstinate constipation (constant feature)
III. Hematological:
  • Microcytic/normocytic anaemia
  • Basophilic stippling (pathognomonic)
  • Reticulocytosis, poikilocytosis, sideroblasts
  • Pallor, fatigue
IV. Neurological - Lead Palsy:
  • Tremors, cramps, numbness, hyperesthesia PRECEDE weakness
  • Wrist drop (radial nerve - C7; extensors of wrist)
  • Foot drop (anterior tibial muscle)
  • Deltoid and biceps involvement possible
  • Purely motor; axonal degeneration with muscle atrophy
V. Lead Encephalopathy (most dangerous):
  • Insomnia → Headache → Vomiting → Visual disturbances → Irritability → Restlessness → Delirium → Hallucinations → Convulsions → Coma → Death
  • More common in children; often irreversible (85%)
  • Mortality ~25%
VI. Cardiovascular/Renal:
  • Hypertension (vascular constriction)
  • Interstitial nephritis, nephrosclerosis
  • Arteriosclerosis
VII. Reproductive:
  • Menstrual irregularities, abortion, fetal abnormalities

b. Treatment of Acute Lead Poisoning (5 marks)

Immediate Measures:
  1. Admit to ICU (this is acute encephalopathy with convulsions)
  2. Remove from source of exposure (stop painting/industrial work)
  3. ABC - Airway, Breathing, Circulation
  4. Control seizures: Diazepam IV (0.3 mg/kg) or phenobarbitone
Decontamination: 5. If recent oral ingestion: Gastric lavage with 1% magnesium sulphate 6. Activated charcoal (if recent ingestion <1 hour) 7. MgSO₄ or Na₂SO₄ orally to convert unabsorbed lead to insoluble form
Specific Antidotes - Chelation Therapy (for acute encephalopathy: BLL >70 μg/100 mL): 8. BAL (Dimercaprol) - FIRST LINE for encephalopathy:
  • 4 mg/kg IM every 4 hours
  • Give at LEAST 4 hours before starting EDTA
  • Continue until BLL falls below 40 μg/100 mL
  1. CaNa₂EDTA (Calcium Disodium Versenate):
    • 75 mg/kg/day as IV infusion (severe with encephalopathy)
    • 5 mL of 20% solution in 500 mL NS/5%D, slow IV drip, twice daily × 5 days
    • Reduces to 50 mg/kg/day as condition improves
  2. Sequential oral chelation after IV:
    • D-penicillamine: 10 mg/kg/day
    • OR DMSA (Succimer): 10 mg/kg TDS × 20 days
    • Continue until BLL <15 μg/100 mL
Supportive Measures: 11. Manage cerebral edema: Mannitol, dexamethasone 12. Calcium gluconate IV (10-20 mL of 10%): For colic/spasm 13. High-calorie diet + 3 pints of milk daily (induces alkalosis, immobilizes lead in bones) 14. Morphine/atropine for severe pain 15. Thiamine 10-50 mg/kg for neurological improvement 16. Monitor BP, urine output, renal function, BLL
Treatment Summary Table (from Essentials of FMT, 36th ed):
SeverityBLLTreatment
Severe + encephalopathy>70 μg/100 mLBAL + EDTA IV → then oral DMSA/penicillamine
Severe - encephalopathy>70 μg/100 mLBAL + EDTA; stop BAL at <40
Moderate45-75 μg/100 mLEDTA alone
Mild20-35 μg/100 mLOral DMSA or penicillamine

c. Samples to Preserve During Autopsy (5 marks)

In case of suspected lead (or any inorganic metallic) poisoning:
Preservative Rule: Use SATURATED COMMON SALT (NaCl) solution - NOT formalin
  • Formalin is an organic compound and interferes with chemical analysis
  • All containers must be clean, new, wide-mouth glass (not plastic)
SampleAmountContainerPreservative
Stomach + contentsEntireWide-mouth glass jarSaturated NaCl
Part of small intestine (upper + lower) + contents~30 cm eachSeparate glass jarSaturated NaCl
Part of large intestine + contents~30 cmGlass jarSaturated NaCl
Liver500 g from central portionGlass jarSaturated NaCl
One kidney (whole or half)~150 gGlass jarSaturated NaCl
Portion of brain250-500 gGlass jarSaturated NaCl
Blood50-100 mLClean glass bottleSodium fluoride (NaF) as anticoagulant/preservative
UrineAll availableClean glass bottleNone / plain
HairMultiple strands from occiputPaper envelopeNone (dry)
NailsClippingsPaper envelopeNone (dry)
Bone (femur / rib segment)~5 cm pieceDry glass/cardboardNone
Vitreous humor2 mLPlain vialNone
Additional points:
  • Each container individually labeled: name of deceased, date of PM, case number, organ
  • Sealed with wax/tape and signed by autopsy surgeon
  • Chain of custody maintained
  • Sent to Chemical Examiner (Forensic Science Laboratory)
  • Control blank sent alongside (same container with same preservative, no biological material)
Sources: The Essentials of Forensic Medicine and Toxicology, 36th ed. (KS Narayana Reddy, 2026) | PC Dikshit Textbook of Forensic Medicine and Toxicology | Park's Textbook of Preventive and Social Medicine | KS Narayana Reddy - Chapter 27 (Lead Poisoning)
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