Lead poisoning in Pediatrics

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  • 1. Lead Poisoning Dr. Abdul Ghaffar Latiffi Pediatric medicine 1st Year Resident FMIC Ab.ghaffar.latiffi@gmail.com Date:06.08.2013
  • 2. “ Lead makes the mind give way.” Greek Physician, 2000 B.C o Heavy, soft, flexible, bluish, tasteless, odorless metal. o wont break down over time, doesn't vaporize. o Φ conduct electricity - resistant to corrosion. o Abundant in the earth's crust (13g/ton or 0.0013% of the earth's crust) o Throughout human history, over 350 million tons of lead have been mined, used and ultimately discarded in the environment Introduction Roman metal
  • 3. Lead Poisoning (Plumbism) "lead poisoning contributed to The decline of the Roman empire “ Jerome Nriagu,geochemist,1983  Lead poisoning is a medical condition caused by increased levels of lead in the body. APP currently defines lead poisoning as a venous BLL ≥ 5μg/dL.  first time lead poisoning in Childhood was reported in Ceylon In 1967 .  Lead paint prohibited in 1922.  UNEP banned global use of leaded gasoline(1995)  Still allowed in 6 nations. Afghanistan, Algeria, Iraq, North Korea, Myanmar and Yemen
  • 4. Epidemiology Approx half million children in the USA have toxic BLL A public health disaster and challenge Children 6 yrs are more susceptible to leads toxic effects  Increased prevalence in inner city children  Children and pregnant women are at double jeopardy due to increased absorption and heavy distribution.  Nutritional deficiencies (Iron ,calcium, zinc, copper, and protein ) result in greater lead absorption
  • 5. August 14, 2007
  • 6. Uses and Sources of Lead  Pigments and paints (pre1978)  Toys and Jewelry  Petrol (antiknock agent ).  Herbal remedies ,Opium  Storage batteries, Weights  Radiations shielding,soldering  drinking-water pipes  Bullets and Ammunition.  lead-glazed tableware
  • 7. Lead ores
  • 8. Pathophysiology Half life of lead in the body compartments • Blood- 25 days •Soft tissues - 40 days •Mineralized tissues- >25 years • Diets high in fat, low in calcium, magnesium, iron, zinc, and copper, increase the absorption of lead. Lead absorbed via the GI , respiratory tract ,skin and transplacentally by the fetus then distribute to the blood, soft tissues and mineralized tissues Lead is not metabolized in the body; it is absorbed, distributed, and excreted 70%-80% 5-10% 1% Distribution Bone Soft tissues Blood
  • 9. Cont…. ► Lead exerts its toxic effect by two mechanisms a) Pb binds to enzymes in the heme synthesis pathway Inhibits ferrochelatase increase level of protoporphyrin in the erythrocyte cause Microcytic anemia Date
  • 10. Cont…. b)Lead as a high potency surrogate is disrupting calcium homeostasis and in interfering with calcium-dependent intracellular functions. Lead interferes with enzymes that help in the synthesis of vitamin D Lead alters the permeability of blood vessels and collagen synthesis Lead exposure has also been associated with a decrease in activity of immune cells such as PMN leukocytes Interferes with mitochondrial oxidative phosphorylation, ATPases enhances oxidation and cell apoptosis.
  • 11. Clinical Presentation  lead exposure often occurs with vague and non specific symptoms, it frequently goes unrecognized  Acute lead poisoning while less common, shows up more quickly and can be fatal.  chronic lead poisoning take time to develop, however. Children can appear healthy despite having high levels of lead in their blood.  Impairment of IQ occur at even lower levels of exposure (1 µg/dL.)
  • 12. Clinical Presentation 1. loss of appetite 2. vomiting 3. weight loss 4. constipation 5. anemia 6. Irritability 7. learning disabilities 8. behavior problems. 1. Cranial nerve paralysis 2. Encephalopathy 3. seizures 4. coma
  • 13. Blood Lead Effects Level Date
  • 14. Degree of Lead Poisoning
  • 15. Diagnosis A. Usually made via screening program B. In suspected cases , must obtain a detailed history • Onset of symptoms • History of Pica • Assessment of potential sources • Family history of lead poisoning C. PhysiCal examination  Pallor and hyperactivity Burton lines on the gums Decreased stature wrist drop, and cognitive dysfunction •signs of elevated iCP Impaired consciousness,Bradycardia Hypertension ,Respiratory depression Papilledema ,Coma
  • 16. Diagnosis Lab and radiographic findings: 1. Increased blood lead level 2. CBC •Microcytic Anemia •Leukocytosis • Basophilic stippling on RBC ( aggregation of ribosomal RNA in the cytoplasm of RBC) 3. Increased FEP concentration 4.CSF changes • high proteins, Lymphocytic pleocytosis 5.Radiodensity at the distal metaphyseal area of long bones (Lead lines ) usually in chronic lead poisoning
  • 17. Long bones radiographs “Lead Lines” in five year old male with radiological growth retardation and blood lead level of 37.7µg/dl “Lead Lines” in 3 yrs old girl with BLL of 10.6 µg/dl
  • 18. Differential Diagnoses  Acute and Chronic Anemia (IDA)  Constipation  Failure to Thrive  Abdominal pain (peptic ulcer ,appendicitis)  Heavy Metal Toxicity  Hydrocarbon Inhalation Injury  Mental retardation  Seizure disorders  Subdural hematoma  Hematologic and CNS neoplasm  Behavior and emotional disorders
  • 19. Treatment & Management Treatment of lead toxicity involves  Prevention of further lead exposure  Decontamination  Chelation  Supportive therapy.
  • 20. Prevention of further lead exposure  Identification and correction of exposure sources is critical  Frequently hands and pacifiers washing.  Use only cold water from the tap ,Hot water may contain more lead.  Avoid using home remedies (such as azarcon, greta, pay-loo- ah,zafron) and cosmetics (such as kohl)  Shower and change clothes after working if your work or hobbies involve working with lead-based products.  Correction of dietary def in iron, calcium, magnesium, and zinc.  Vitamin C is a weak but natural chelating agent
  • 21. Decontamination  May be performed in patients with acute lead ingestion in whom lead paint chips are identified on plain abdominal radiographs.  Polyethylene glycol solution (GoLytely) can be used for lead densities in the stomach and/or small intestine.  Gastric lavage may be performed.  Secure the airway before the initiation of gastric lavage in an obtunded child with acute lead ingestion.  Charcoal binds poorly to lead, and no evidence
  • 22. Chelating Agents
  • 23. Supportive management  Anticonvulsants may be needed.  Mannitol or corticosteroids and volume restriction are indicated in patients with encephalopathy.  A high-calcium, high-phosphorus diet and large doses of vitamin D may remove lead from the blood by depositing it in the bones.
  • 24. Prognosis  The adverse effects of lead are not reversible.  In acute lead poisoning ( seizures and coma), there is a high risk Of permanent brain damage and death.  The long-term effects of lower levels of lead can also be permanent and severe.  Asymptomatic patients tend to have a better prognosis, with good improvement in intellectual functions following lowering of the BLL.  Sequelae of encephalopathy includes seizure disorders, impaired mentation, and rarely
  • 25. REFERENCES 1.Nelson - Textbook Of Pediatrics - 19th Edition 2.Rudolph pediatric 4.http://www.lead.org.au 6. Park’s textbook of preventive and social medicine
  • 26. THANK YOU