Lead toxicity

1. Dr. Saikat Saha
Assistant Professor
MMC&H

2. Physical Forms
Sugar of Lead, therapeutic use.
Lead Acetate
01
Lead Carbonate
02
Colouring agent in Ceramic Industry
Lead Oxide
03
Cosmetic- Surma
Lead Sulphide
06
White pigment- Paint.
Sindur
Lead tetraoxide
05
Anti shock- to prevent detonation
Tetra Ethyl Lead
04

3. Our Team Style
Sugar of Lead Lead Sulphide Lead Carbonate Lead Tetraoxide

4. Automobile exhaust (0.56gm/Lt), Drug abuse, Soil,
Water
.
Environmental
Ceramic, Coloured picture books,
Contaminated flour, Cosmetics, Health
foods, House paints, Indigenous
medicines, Pencil, Toys.
Domestic
Source of Lead Exposure
Auto repair works, Battery making, Glass
and plastic manufacture, Mining, Plumbing,
Pottery, Printing, Rubber industry,
Soldering (electronic), Steel welding
Occupational

5. Absorbs through all portal of
entry
1. inhalation
2. ingestion
3. skin contact
Stored in bone as phosphate and
carbonate ( 70% in children and
95% in adult) at growing end.
Releases in blood in acidosis,
fever, sunlight exposure and
alcohol intake.
Unretained lead excreted through
urine(65%) and bile(35%).
Toxicokinetics

6. Uncertain, usually 2 to 3 days
Fatal Period
Fatal Dose:
Lead acetate – 20 gm.
Lead tetraethyl – 100mg/kg; usually
uncertain.
Lead carbonate – 40 gm.
Absorption of more than 0.5 mg/day.

7. Mechanism of Action
Learning Disorder
Lower IQ
Oedema
Increased
Psychomotor Activity
.
a.ALA dehydrase
b.ALA synthatase
c.coproporphyrinogen
oxidase
d. ferrochelatase
.
Inhibit SH-
enzymes
Inhibit Heme
Synthesis
Haemolysis CNS CVS
a. Reticuloctosis
b. Basophilic stippled
cell (Pyrimidine 5
neucleotidase)
.
Kidney
Fanconi Syndrome
.

8. Adult – ingest 300 microgm and inhale 15 microgm
per day. (only 10% absorbs but in children 50%
absorption occurs)
Accepted level- 10 microgram/100 ml
Blood Lead
Permissible
level
Adverse Effect
Haemopoetic System>10 microgram/100 ml,
CNS>25 microgram/100 ml

9. Clinical Features
Acute Poisoning
Metallic taste,
Abdominal pain,
Constipation or diarrhea ( blackish
stool), Vomiting,
Hyperactivity or lethargy,
Ataxia,
Behavioral changes,
Convulsion and coma.

10. Plumbism or Saturnism
Mild Toxicity (BL 40 to 60 mcg/100ml)
. myalgia
. paraesthesia
. fatigue
. irritibility
. abdominal discomfort
.
Chronic Poisoning
Moderate toxicity – (BL 60 TO 100mcg/100ml)
Nocturnal arthralgia
Muscular exhaustibility
. Tremor
. Headache
. Diffuse abdominal pain
. Anorexia,, metallic taste, vomiting
. Constipation
. Weight loss
. Hyertension
.
Severe toxicity – (BL more than
100 mcg/100ml)
a. Lead palsy: wrist drop,
foot drop
b. Bartons line
c. Lead colic ( dry gripes)
d. Circum oral facial pallor
e. Anaemia
Clinical Features

11. Mortality – 25%
more in children in organic lead
poisoning
Recovers with features of
permanent brain damage like
mental retardation,
cerebral palsy,
optic neuropathy,
hyperkinesis and periodic
convulsion
sudden onset of features –
Vomiting,
Irritability, headache,
Ataxia, vertigo,
Convulsiuon,
Psychotic manifestation,
Coma, death
Clinical Features
Lead
Encephalopathy

12. Lab Diagnosis
Blood
lead
FEP:ZNP
Blood Count
And
Smear
05
Normal:10:9
If ZnP raised
than measure
blood lead level
Blood lead level detected
on 1st birthday and every
year until 6 year.
If 20 microgm/100ml –
therapeutic interventation
if 70 microgm/100ml –
medical emergency
Normocytic
Hypochromic
Basophilic Stippling
Urine
ALA and Coproporphyrin
Lead – above 150 microgm/lt is
significant
Calcium disodium EDTA
mobilisation test ( between BL 25-
49 microgm/100ml
Bones
Lead Lines

13. Basophilic Stippling
Lead Lines

14. Treatment
1. BAL 4mg/kg - immediately in children 2. CT scan – cerebral edema
3. KUB – lead chips in GIT
4. For convulsion – diazepam or phenobarbitone
5. Foley’s catheter/ urine lead level
6.CaNa2 EDTA – 75 mg/kg/day i.V.
7. BAL – repeate 4 hourly until BL below 40microgm/100ml than reduce 2
mg/kg/day in 3 divided doses.
8. Reduce cana2 EDTA – 50 mg/kg/day i.V.
9. Continue until asymptomatic than start oral chelation with D- penicillami
ne or DMSA
Graef Protocol
Severe poisoning with Encephalopathy

15. Treatment
1. BAL 12 mg/kg/day
2. EDTA 50mg/kg/day
3. Discontinue BAL when BL is less than 40microgm/100ml but continue
EDTA for 5 days
4. Start oral chelation until BL level less than15microgm/100ml or 3 month.
Graef Protocol
Severe poisoning without Encephalopathy
Bl Lead > 70 mcg/ 100 ml

16. Treatment
1. EDTA 50mg/kg/day
2. Start oral chelation until BL level less than15microgm/100ml or 3 month.
Graef Protocol
Moderate Poisoning
Bl Lead- 45- 70 mcg/ 100 ml

17. Treatment
d-penicillmine 30mg/kg/day in 3 divided doses, start with 1/4th dose and dou
ble after 7 days, double again after 7 days, continue utill blood lead level bel
ow 15 microgm/100ml or 3 month.
Graef Protocol
Mild Poisoning
Bl Lead < 35 mcg/ 100 ml

18. Treatment
Remove the patient from the source of exposure
1. Thiamine- 10-50mg/kg
2. In acute poisoning or in radio-opacity in GIT in x-ray stomach wash - 1%
magnesium sulphate or sodium sulphate or warm water and simple emetics s
hould be administered
3. Lead colic – i.V. Ca gluconate
4. Correct iron deficiency anemia
5. I.V. Fluid
6. Maintain ICP by mannitol or steroid
7. Organic lead chelation – managed symptomatically
8. Repeate BL after 2 week and repeat chelation; if required Rebounds are c
ommon
9. Succimer
Supportive Measure

19. Pale Mucosa, Conjucntiva, skin
PM
Findings
Emaciation
Lead Line in X-Ray
Hypertrophy of Heart
Ulceration and
Haemorrhage at
Mucosa
Swollen and Pale

20. Thank You
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