Lead Poisoning

Dr. Abdul Ghaffar LatiffiPediatric medicine 1st Year Resident

FMICAb.ghaffar.latiffi@gmail.com

Date:06.08.2013

“ 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 Introduction

Roman metal

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

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

August 14, 2007

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

Lead ores

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

Cont….

► Lead exerts its toxic effect by two mechanismsa) Pb binds to enzymes in the heme synthesis pathway

Inhibits ferrochelatase increase level of protoporphyrin in the erythrocyte cause Microcytic anemia

Date

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 DLead alters the permeability of blood vessels and collagen synthesisLead exposure has also been associated with a decrease in activity of immune cells such as PMN leukocytesInterferes with mitochondrial oxidative phosphorylation, ATPasesenhances oxidation and cell apoptosis.

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.)

Clinical Presentation

1. loss of appetite2. vomiting3. weight loss4. constipation5. anemia6. Irritability7. learning disabilities8. behavior problems.

1. Cranial nerve paralysis 2. Encephalopathy3. seizures 4. coma

Blood Lead Effects Level

Date

Degree of Lead Poisoning

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 hyperactivityBurton lines on the gums Decreased staturewrist drop, and cognitive dysfunction•Signs of Elevated ICPImpaired consciousness,BradycardiaHypertension ,Respiratory depressionPapilledema ,Coma

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

Long bones radiographs 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

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

Treatment & Management

Treatment of lead toxicity involves

Prevention of further lead exposure Decontamination Chelation Supportive therapy.

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

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 supports its use in acute lead ingestion.

Chelating Agents

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.

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 blindness and hemiparesis.

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

THANK YOU