Lead poisoning, clinical examination, diagnosis

Lead poisoning

1. Lead poisoning Abdulla Mohammed Tabsheer Roll no. 3

2. Introduction Heavy, soft, flexible, bluish, tasteless, odorless metal. wont break down over time, doesn't vaporize. conduct electricity- resistant to corrosion. Abundant in the earth's crust (13g/ton or 0.0013% of the earth's crust) Throughout human history, over 350 million tons of lead have been mined, used and ultimately discarded in the environment

3. Lead poisoning Lead poisoning is a medical condition caused by increased levels of lead in the body In 2012 the center for diseases control and prevention designated 5 µg/ dl as the "reference value based on the 97.5th percentile of the population of US children aged 1-5 years.”

4. Epidemiology Approx half million children in the USA have toxic BLL 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 Increased prevalence in inner city children

5. Source of exposure It readily crosses placenta Paint chips Toys Jewelry Lead plumbing(pollutes water) Herbal remedies Petrol(antiknocking agent) Soldering in Canned foods

6. Source of lead

7. Pathophysiology Lead is absorbed by 1)Inhalation 2)Ingestion 3)Skin Lead absorbed via the Gl, respiratory tract, skin and transplacentally by the fetus then distribute to the blood, soft tissues and mineralized tissues Ninety per cent of the ingested lead is excreted in the faeces. Lead absorbed from the gut enters the circulation, and 95 per cent enters the erythrocytes. It is then transported to the liver and kidneys finally transported to the bones where it is laid down with other minerals. Although bone lead is thought to be 'metabolically inactive, it may be released to the soft tissues again under conditions of bone resorption.

8. Pathophysiology 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 B)Lead as a high potency surrogate is disrupting calcium homeostasis and in interfering with calcium-dependent intracellular functions.

9. Other effects 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 I nterferes with mitochondrial oxidative phosphorylation, ATPases Enhances oxidation and cell apoptosis.

10. 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.)

11. Clinical Presentation

12. Clinical Presentation

13. 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

14. Diagnosis 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

15. Diagnosis Lab 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)

16. Diagnosis Radiographic Findings 5.Radiodensity at the distal metaphyseal area of long bones (Lead lines) usually in chronic lead poisoning

17. Treatment &Manag ement Treatment of lead toxicity involves Prevention of further lead exposure Decontamination Chelation Supportive therapy.

18. Prevention of further lead exposure Identification and correction of exposure sources is critical Frequently hand washing Avoid using home remedies and cosmetics which is suspected for containing lead Shower and change clothes after working if your work or hobbies involve working with lead-based products Correction of dietary deficiency in iron, calcium,magnesium, and zinc. Vitamin C is a weak but natural chelating agent

19. Decontamination May be performed in patients with acute lead ingestion in whom lead paint chips are identified on plain abdominal radiographs. 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, thus there is no use of it

20. Chelating Agent