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Lead Poisoning, Emergency Medicine

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

- 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

- 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

- Chronic toxicity: - Addison disease - Guillain " “Barre syndrome or other neuropathy - Vitamin deficiency (B3, B6, or B12) - Wernicke " “Korsakoff syndrome

- 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

- 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

  • Lead has multiple mechanisms of toxicity:Binds sulfhydryl groups and affects multiple enzymatic processesResembles Ca2+ thereby interfering with Ca2+-dependent processes, such as cell signalingMay 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 adults70% of total body lead in childrenHigh 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 leadPottery glazeCertain folk remediesCosmeticsJewelryWeightsHome-distilled alcoholic beveragesLead dust from ammunition and primer
  • Chronic toxicity:Occupational exposures (usually via inhalation):Battery manufacturing/recyclingBridge paintingConstruction workersDe-leadingElectronic waste recyclingFiring range instructorsMining and smeltingPottery workersWeldersHome exposures (pediatric poisoning):Lead-based paint inhalation/ingestion from toys and wallsContaminated water from old pipesLead dust from the clothing of a parent exposed at workImported foodsFolk medicines

Diagnosis

Signs and Symptoms

  • Neurologic:Seizures (may be prolonged and refractory)EncephalopathyLearning disabilitiesPsychiatric disturbancesCerebral edemaPeripheral motor neuropathy (wrist drop), classic but rare finding in chronic toxicity
  • GI:Colicky abdominal pain (lead colic)IleusNausea/vomitingLead 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 BLLIn pediatric cases, educational interventions begin at BLL ≥10 Ž ¼g/dLIn pediatric cases, chelation therapy is instituted at BLL ≥45 Ž ¼g/dLIn adults, chelation therapy is usually considered at BLL ≥70 Ž ¼g/dL100 Ž ¼g/dL may present with severe encephalopathy; cognitive effects increase with rising levelsExpect that BLL may rise after treatment is completed due to redistribution
  • CBC:For presence of anemiaRBC 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/gastroenteritisCeliac diseaseCholeraDistributive shockEncephalopathyToxic ingestionsAmanita mushroom poisoningCyclic antidepressants or other seizure-inducing toxinsOrganophosphates
  • Chronic toxicity:Addison diseaseGuillain " “Barre syndrome or other neuropathyVitamin 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 monitorIsotonic 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 BPVasopressors 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 clearActivated charcoal is not effective.
  • Evaluate need for chelation therapy:BLLAcuity of exposureClinical symptomsConsultation 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 chelationBegin with dimercaprol (BAL) and continue for 5 daysStart 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 occurParental education should be initiated
  • BLL ≥45 Ž ¼g/dL:Chelation therapy is initiatedAsymptomatic children are treated with DMSASymptomatic children or those with BLL ≥70 Ž ¼g/dL are treated with BAL and CaNa2 EDTAConsult 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 allergiesEdetate calcium disodium (CaNa2 EDTA), 50 mg/kg/d as continuous IV infusion (adults and peds) or 1 g/m2/d as continuous IV infusionTreat for 5 days and start 4 hr after BALSuccimer (DMSA):Adults: 10 mg/kg PO q8h for 5 days, then q12h for 14 daysPeds: 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)