Basics
Description
- Lead has multiple mechanisms of toxicity:
- Binds sulfhydryl groups and affects multiple enzymatic processes
- Resembles Ca2+ thereby interfering with Ca2+-dependent processes, such as cell signaling
- May have mutagenic potential and play a role in human carcinogenesis
- Distribution:
- Up to 99% of lead is bound to erythrocytes after initial absorption.
- Ultimately redistributed into bone:
- 95% of total body lead in adults
- 70% of total body lead in children
- High lead levels in the serum compromise the blood " “brain barrier and result in lead entry into the CNS and neurotoxicity.
- Often coexists with iron deficiency; this allows for increased lead absorption in the gut.
- Impairs heme synthesis, leading to elevated free erythrocyte protoporphyrin (FEP); these complex with zinc, resulting in elevated zinc protoporphyrin (ZPP).
- Levels correlate poorly with symptoms:
- Associated with drops in intelligence quotient (IQ) and increase in violent behavior
Etiology
- Acute toxicity:
- Most often due to inhalation of an environmental source or ingestion of substance containing lead
- Pottery glaze
- Certain folk remedies
- Cosmetics
- Jewelry
- Weights
- Home-distilled alcoholic beverages
- Lead dust from ammunition and primer
- Chronic toxicity:
- Occupational exposures (usually via inhalation):
- Battery manufacturing/recycling
- Bridge painting
- Construction workers
- De-leading
- Electronic waste recycling
- Firing range instructors
- Mining and smelting
- Pottery workers
- Welders
- Home exposures (pediatric poisoning):
- Lead-based paint inhalation/ingestion from toys and walls
- Contaminated water from old pipes
- Lead dust from the clothing of a parent exposed at work
- Imported foods
- Folk medicines
Diagnosis
Signs and Symptoms
- Neurologic:
- Seizures (may be prolonged and refractory)
- Encephalopathy
- Learning disabilities
- Psychiatric disturbances
- Cerebral edema
- Peripheral motor neuropathy (wrist drop), classic but rare finding in chronic toxicity
- GI:
- Colicky abdominal pain (lead colic)
- Ileus
- Nausea/vomiting
- Lead lines on gingival line (Burton lines) appear as bluish tint (indication of lifetime burden, not acute exposure).
- Hepatitis/pancreatitis
- Cardiovascular:
- HTN (generally secondary to renal failure)
- Myocarditis and conduction defects
- Renal:
- Chronic renal insufficiency with long-term exposure
- Hematologic:
- Anemia (due to interference with globin chain synthesis)
- Increases RBC fragility, so decreased RBC life span
- Musculoskeletal:
- Lead lines from increased Ca2+ deposition at epiphyses (do not consist of lead itself)
- Decreased bone strength and growth
Essential Workup
Blood lead level (BLL) ‚
Diagnosis Tests & Interpretation
Lab
- Whole-BLL:
- There is no normal BLL
- In pediatric cases, educational interventions begin at BLL ≥10 Ž ¼g/dL
- In pediatric cases, chelation therapy is instituted at BLL ≥45 Ž ¼g/dL
- In adults, chelation therapy is usually considered at BLL ≥70 Ž ¼g/dL
- 100 Ž ¼g/dL may present with severe encephalopathy; cognitive effects increase with rising levels
- Expect that BLL may rise after treatment is completed due to redistribution
- CBC:
- For presence of anemia
- RBC indices and iron studies
- Electrolytes, BUN, creatinine, glucose:
- Transaminases, liver function tests prior to chelation administration
- FEP or ZPP
Imaging
- Plain abdominal radiographs to look for radiopaque foreign body
- Long-bone series to look for lead lines (specifically in children)
- Cranial CT and other studies as indicated by patients condition
Differential Diagnosis
- Acute toxicity:
- Acute appendicitis/colitis/gastroenteritis
- Celiac disease
- Cholera
- Distributive shock
- Encephalopathy
- Toxic ingestions
- Amanita mushroom poisoning
- Cyclic antidepressants or other seizure-inducing toxins
- Organophosphates
- Chronic toxicity:
- Addison disease
- Guillain " “Barre syndrome or other neuropathy
- Vitamin deficiency (B3, B6, or B12)
- Wernicke " “Korsakoff syndrome
Treatment
Pre-Hospital
- Support airway/breathing and circulation
- Cardiac monitoring
- Seizure management
- If possible to do so safely, bring containers in suspected overdose or poisoning.
- Decontaminate skin for obvious dermal exposures.
Initial Stabilization/Therapy
- ABCs:
- Cardiac monitor
- Isotonic crystalloids as needed for hypotension; vasopressors for refractory hypotension
- Naloxone, thiamine, and dextrose (D50W) as indicated for altered mental status
- Cardiovascular:
- Isotonic crystalloids to support BP
- Vasopressors for refractory hypotension (rare)
- Neurologic:
- Treat seizures with benzodiazepines.
- Assist ventilation for respiratory failure due to neuromuscular weakness.
- Renal:
- Hemodialysis for renal failure
- Alimentary:
- Dextrose, enteral, or parenteral feeding may be beneficial
Ed Treatment/Procedures
- Decontamination:
- If opacities are seen on upright abdominal film, institute whole-bowel irrigation at 1 " “2 L/hr of polyethylene glycol until abdominal films are clear
- Activated charcoal is not effective.
- Evaluate need for chelation therapy:
- BLL
- Acuity of exposure
- Clinical symptoms
- Consultation with a medical toxicologist or poison center
Adult Considerations
- Most likely exposures are via inhalation and caused by occupational exposure or ethnic products
- Adults with encephalopathy or those with BLL: >100 mg/dL may need chelation
- Begin with dimercaprol (BAL) and continue for 5 days
- Start edetate calcium disodium (CaNa2 EDTA) after 2nd dose of BAL
- Asymptomatic patients with BLL of 70 " “100 Ž ¼g/dL may be treated with an oral chelating agent, succimer (DMSA)
- Chelation is not indicated for asymptomatic adults with BLL <70 Ž ¼g/dL
- Currently, BLL ≥10 Ž ¼g/dL require investigative and educational interventions:
- Investigation into the cause of the exposure and repeat monitoring must occur
- Parental education should be initiated
- BLL ≥45 Ž ¼g/dL:
- Chelation therapy is initiated
- Asymptomatic children are treated with DMSA
- Symptomatic children or those with BLL ≥70 Ž ¼g/dL are treated with BAL and CaNa2 EDTA
- Consult with medical toxicologist/poison center when chelation therapy is considered
- Much controversy about fetal lead toxicity
- Consult maternal " “fetal medicine and medical toxicologist/poison center in pregnant patients with elevated BLL.
Medication
- Chelating agents:
- Dimercaprol (BAL), 3 mg/kg deep IM q4h for 3 " “5 days if mild to moderate symptoms; 4 mg/kg IM q4h for 5 days for severe symptoms (seizure, encephalopathy):
- Caution: Contraindicated in patients with peanut allergies
- Edetate calcium disodium (CaNa2 EDTA), 50 mg/kg/d as continuous IV infusion (adults and peds) or 1 g/m2/d as continuous IV infusion
- Treat for 5 days and start 4 hr after BAL
- Succimer (DMSA):
- Adults: 10 mg/kg PO q8h for 5 days, then q12h for 14 days
- Peds: 350 mg/m2 q8h for 5 days, then q12h for 14 days
- Dextrose 50%: 25 g (50 mL; peds: 0.5 g/kg D25W) IV for hypoglycemia
- Diazepam: 5 " “10 mg (peds: 0.1 mg/kg) IV for seizure control
- Lorazepam: 2 " “4 mg IV or IM
- Naloxone: 0.4 " “2 mg (peds: 0.1 mg/kg) IV
- Thiamine: 100 mg (peds: 1 mg/kg) IM or IV
Follow-Up
Disposition
Admission Criteria
- Symptomatic lead intoxication
- Children at high risk for re-exposure in their current environment
- Children with difficulty tolerating DMSA
- Pregnant patients with elevated lead levels " ”consult obstetrics and toxicology.
Discharge Criteria
- Asymptomatic patients not requiring IV chelation therapy
- Chronically exposed patients who do not require admission should be referred for outpatient evaluation
- Ensure home environment is safe for patient prior to discharge
- Ensure pediatric patients tolerate oral chelation therapy prior to discharge
Followup Recommendations
Follow up with medical toxicologist or primary care physician. ‚
Pearls and Pitfalls
- Heel sticks may result in falsely elevated BLL; repeat positive blood tests for confirmation
- Secure social worker support to ensure safe home environment prior to discharge
- Inquire and test siblings or family members in a patient with lead toxicity
- Do not give BAL if patient has peanut allergy
Additional Reading
- Binns ‚ HJ, Campbell ‚ C, Brown ‚ MJ. Interpreting and managing blood lead levels of less than 10 microg/dL in children and reducing childhood exposure to lead: Recommendations of the Centers for Disease Control and Prevention Advisory Committee on Childhood Lead Poisoning Prevention. Pediatrics. 2007;120:e1285 " “e1298.
- Centers for Disease Control and Prevention (CDC). Lead poisoning in pregnant women who used Ayurvedic medications from India " “New York City, 2011 " “2012. MMWR Morb Mortal Wkly Rep. 2012;61:641 " “646.
- Henretig ‚ F. Lead. In: Flomenbaum ‚ NE, Goldfrank ‚ LR, Hoffman ‚ RS, et al., eds. Goldfranks Toxicologic Emergencies. 9th ed. New York, NY: McGraw-Hill; 2010.
- Levin ‚ R, Brown ‚ MJ, Kashtock ‚ ME, et al. Lead exposures in U.S. Children, 2008: Implications for prevention. Environ Health Perspect. 2008;116(10):1285 " “1293.
- Lin ‚ CG, Schaider ‚ LA, Brabander ‚ DJ, et al. Pediatric lead exposure from imported Indian spices and cultural powders. Pediatrics. 2010;125:e828 " “e835.
A special thanks goes to Dr. Harry C. Karydes, who contributed to the previous edition. ‚
Codes
ICD9
- 984.0 Toxic effect of inorganic lead compounds
- 984.1 Toxic effect of organic lead compounds
- 984.9 Toxic effect of unspecified lead compound
- 984.8 Toxic effect of other lead compounds
- 984 Toxic effect of lead and its compounds (including fumes)
ICD10
- T56.0X1A Toxic effect of lead and its compounds, accidental, init
- T56.0X4A Toxic effect of lead and its compounds, undetermined, init
SNOMED
- 38342005 toxic effect of lead compound (disorder)
- 78405005 Toxic effect of organic lead compound (disorder)
- 72446009 Toxic effect of inorganic lead compound
- 216777009 Accidental poisoning by lead and its compounds and fumes (event)