eMedicine Specialties > Emergency Medicine > Toxicology
Toxicity, Lead: Differential Diagnoses & Workup
Updated: Aug 10, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Differential Diagnoses
| Anemia, Acute | Guillain-Barré Syndrome |
| Anemia, Chronic | Sickle cell disease |
| Constipation | Toxicity, Heavy Metals |
| Depression and Suicide | Toxicity, Mercury |
| Gout |
Other Problems to Be Considered
Neuropathies
Workup
Laboratory Studies
- The criterion standard is a whole blood lead level (BLL). Any BLL above 10 micrograms/dL is considered positive and consequential. Patients with lead levels between 10 and 20 micrograms/dL require removal from the exposure, repeated testing, and follow-up.
- The blood must be drawn in an anticoagulated and lead-free tube. Only one tube is certified by the manufacturer as being lead free. Trace metal tubes and anticoagulated tubes are available, but aside from the certified tube, they all tend to give high-biased levels.
- The result may not be immediately available at all institutions because of laboratory limitations.
- A baseline hemogram may be indicated to look for the presence of a microcytic hypochromic anemia.
- Lead toxicity causes what appears to be a typical pattern of iron-deficiency anemia with hypochromia and microcytosis. Iron deficiency does frequently coexist. Assessing iron storage status (ferritin) in all cases of lead poisoning is important.
- In pregnant women, some evidence suggests that lead also causes a decrease in erythropoietin production and a depression in red cell production.
- Lead is a surface-acting poison and may produce increased red cell fragility and acute hemolytic anemias.
- Lead interferes with the enzyme ferrochelatase, blocking the incorporation of iron into the protoporphyrin molecule; thus, a free erythrocyte protoporphyrin (EP) level may be useful in demonstrating the degree of biological abnormalities that exist. EP can also be used to help distinguish recent acute lead exposure from chronic exposure.
- A chemistry profile including renal studies, liver studies, and a uric acid is advisable.
- Children often have low uric acids and leak uric acid into their urine.
- Adults, because of the disturbance of enzymatic amino hydrolases, manifest elevated uric acid levels and, possibly, clinical gout.
- Lead may produce subtle nephrogenic effects, which, if unappreciated, may lead to treatment failures or complications.
- For example, a child may appear to have a mild degree of dehydration based on decreased urine output, increased urine specific gravity, and poor appetite.
- This may be the predictor of impending inappropriate secretion of antidiuretic hormone and should lead to a careful analysis of fluid intake, plasma volume, and, perhaps, fluid restriction.
Imaging Studies
Obtain a radiograph of the abdomen in children with suspected elevated lead levels.
The presence of radio-opaque foreign bodies throughout the GI tract may highlight the diagnosis and prompt immediate intervention. A radiograph also helps guide therapy as to the prevention of further absorption through GI decontamination.
Abdominal flat plate showing multiple radio-opaque foreign bodies including paint chips and an earring.
A radiodensity in the distal metaphyseal plate is a frequent occurrence in children with chronic lead poisoning of a moderate degree. These findings are unlikely to be observed in adults.
Radiographs of the long bones in growing children may reveal the characteristic lead lines. These lines, actually growth arrest lines, are not pathognomonic but are associated with lead levels in excess of 40 mcg/dL over a protracted period of time.
Growth arrest lines, also known as lead lines, in bones of a child who recovered from lead poisoning.
If an alteration of mental status is present, consider a CT scan of the head or MRI to rule out cerebral edema or structural lesions.
Other Tests
- A spinal tap may be needed in evaluation of patients with altered mental status. However, it is contraindicated in patients with lead encephalopathy due to possible risk of herniation resulting from elevated intracranial pressure.
- A provocative chelation test was used in the past in order to provide additional information (total body burden). Urine was collected after administering a dose of chelator. Calcium disodium edetate was the most commonly used chelator for this test. Recently, the potential dangers of such provocative chelation have decreased the frequency of its use and it is not recommended as the standard of care.
More on Toxicity, Lead |
| Overview: Toxicity, Lead |
Differential Diagnoses & Workup: Toxicity, Lead |
| Treatment & Medication: Toxicity, Lead |
| Follow-up: Toxicity, Lead |
| Multimedia: Toxicity, Lead |
| References |
| « Previous Page | Next Page » |
References
Lanphear BP, Hornung R, Khoury J, Yolton K, Baghurst P, Bellinger DC, et al. Low-level environmental lead exposure and children's intellectual function: an international pooled analysis. Environ Health Perspect. Jul 2005;113(7):894-9. [Medline].
Murata K, Iwata T, Dakeishi M, Karita K. Lead toxicity: does the critical level of lead resulting in adverse effects differ between adults and children?. J Occup Health. 2009;51(1):1-12. [Medline].
Jones RL, Homa DM, Meyer PA, Brody DJ, Caldwell KL, Pirkle JL, et al. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 years, 1988-2004. Pediatrics. Mar 2009;123(3):e376-85. [Medline].
Morgan BW, Todd KH, Moore B. Elevated blood lead levels in urban moonshine drinkers. Ann Emerg Med. Jan 2001;37(1):51-4. [Medline].
Herman SS, Geraldine M, Venkatesh T. Influence of minerals on lead-induced alterations in liver function in rats exposed to long-term lead exposure. J of Hazardous Materials. In press.
[Guideline] Lead exposure in children: prevention, detection, and management. Pediatrics. Oct 2005;116(4):1036-46. [Medline]. [Full Text].
[Guideline] Interpreting and managing blood lead levels < 10 microg/dL in children and reducing childhood exposures to lead: recommendations of CDC's Advisory Committee on Childhood Lead Poisoning Prevention. MMWR Recomm Rep. Nov 2 2007;56:1-16. [Medline]. [Full Text].
[Guideline] Centers for Disease Control and Prevention (CDC). Preventing lead poisoning in young children. Aug 2005;[Full Text].
[Guideline] U.S. Preventive Services Task Force (USPSTF). Rockville (MD): Agency for Healthcare Research and Quality (AHRQ). Screening for elevated blood lead levels in children and pregnant women: recommendation statement. Dec 12 2006;[Full Text].
Chisolm JJ Jr. Evaluation of the potential role of chelation therapy in treatment of low to moderate lead exposures. Environ Health Perspect. Nov 1990;89:67-74. [Medline].
Canfield RL, Henderson CR Jr, Cory-Slechta DA, Cox C, Jusko TA, Lanphear BP, et al. Intellectual impairment in children with blood lead concentrations below 10 microg per deciliter. N Engl J Med. Apr 17 2003;348(16):1517-26. [Medline].
Cory-Slechta DA, Weiss B, Cox C. Mobilization and redistribution of lead over the course of calcium disodium ethylenediamine tetraacetate chelation therapy. J Pharmacol Exp ther. 1987;243:804-13. [Medline].
Seaton CL, Lasman J, Smith DR. The effects of CaNa(2)EDTA on brain lead mobilization in rodents determined using a stable lead isotope tracer. Toxicol Appl Pharmacol. Sep 15 1999;159(3):153-60. [Medline].
Sanchez-Fructuoso AI, Cano M, Arroyo M, Fernandez C, Prats D, Barrientos A. Lead mobilization during calcium disodium ethylenediaminetetraacetate chelation therapy in treatment of chronic lead poisoning. Am J Kidney Dis. Jul 2002;40(1):51-8. [Medline].
Chisolm JJ Jr. The use of chelating agents in the treatment of acute and chronic lead intoxication in childhood. J Pediatr. Jul 1968;73(1):1-38. [Medline].
Smith DR, Markowitz ME, Crick J, Rosen JF, Flegal AR. The effects of succimer on the absorption of lead in adults determined by using the stable isotope 204Pb. Environ Res. Oct 1994;67(1):39-53. [Medline].
Cremin JD Jr, Luck ML, Laughlin NK, Smith DR. Oral succimer decreases the gastrointestinal absorption of lead in juvenile monkeys. Environ Health Perspect. Jun 2001;109(6):613-9. [Medline].
Varnai VM, Piasek M, Blanusa M, Saric MM, Kostial K. Succimer treatment during ongoing lead exposure reduces tissue lead in suckling rats. J Appl Toxicol. Sep-Oct 2001;21(5):415-6. [Medline].
Flora SJ, Pande M, Mehta A. Beneficial effect of combined administration of some naturally occurring antioxidants (vitamins) and thiol chelators in the treatment of chronic lead intoxication. Chem Biol Interact. Jun 15 2003;145(3):267-80. [Medline].
Varnai VM, Piasek M, Blanusa M, Juresa D, Saric M, Kostial K. Ascorbic acid supplementation does not improve efficacy of meso-dimercaptosuccinic acid treatment in lead-exposed suckling rats. Pharmacol Toxicol. Oct 2003;93(4):180-5. [Medline].
Thomas DJ, Chisolm J Jr. Lead, zinc and copper decorporation during calcium disodium ethylenediamine tetraacetate treatment of lead-poisoned children. J Pharmacol Exp Ther. Dec 1986;239(3):829-35. [Medline].
Besunder JB, Super DM, Anderson RL. Comparison of dimercaptosuccinic acid and calcium disodium ethylenediaminetetraacetic acid versus dimercaptopropanol and ethylenediaminetetraacetic acid in children with lead poisoning. J Pediatr. Jun 1997;130(6):966-71. [Medline].
Blank E, Howieson J. Lead poisoning from a curtain weight. JAMA. Apr 22-29 1983;249(16):2176-7. [Medline].
Canfield RL, Henderson CR Jr, Cory-Slechta DA, Cox C, Jusko TA, Lanphear BP. Intellectual impairment in children with blood lead concentrations below 10 microg per deciliter. N Engl J Med. Apr 17 2003;348(16):1517-26. [Medline].
Ciriza C, Garcia L, Suarez P, Jimenez C, Romero MJ, Urquiza O. What predictive parameters best indicate the need for emergent gastrointestinal endoscopy after foreign body ingestion?. J Clin Gastroenterol. Jul 2000;31(1):23-8. [Medline].
Cocco P, Hua F, Boffetta P, Carta P, Flore C, Flore V. Mortality of Italian lead smelter workers. Scand J Work Environ Health. Feb 1997;23(1):15-23. [Medline].
Farrell SE, Vandevander P, Schoffstall JM, Lee DC. Blood lead levels in emergency department patients with retained lead bullets and shrapnel. Acad Emerg Med. Mar 1999;6(3):208-12. [Medline].
Fergusson JA, Malecky G, Simpson E. Lead foreign body ingestion in children. J Paediatr Child Health. Dec 1997;33(6):542-4. [Medline].
Glotzer DE, Weitzman M. Commonly asked questions about childhood lead poisoning. Pediatr Ann. Dec 1995;24(12):630-2, 637-9. [Medline].
Hotz M, Kniepmann K, Kohn L. Occupational therapy in pediatric lead exposure prevention. Am J Occup Ther. Jan 1998;52(1):53-9. [Medline].
Kostial K, Blanusa M, Piasek M, Restek-Samarzija N, Jones MM, Singh PK. Combined chelation therapy in reducing tissue lead concentrations in suckling rats. J Appl Toxicol. May-Jun 1999;19(3):143-7. [Medline].
Lioy PJ, Yiin LM, Adgate J, Weisel C, Rhoads GG. The effectiveness of a home cleaning intervention strategy in reducing potential dust and lead exposures. J Expo Anal Environ Epidemiol. Jan-Mar 1998;8(1):17-35. [Medline].
Macgregor D, Ferguson J. Foreign body ingestion in children: an audit of transit time. J Accid Emerg Med. Nov 1998;15(6):371-3. [Medline].
McKinney PE. Acute elevation of blood lead levels within hours of ingestion of large quantities of lead shot. J Toxicol Clin Toxicol. 2000;38(4):435-40. [Medline].
Mowad E, Haddad I, Gemmel DJ. Management of lead poisoning from ingested fishing sinkers. Arch Pediatr Adolesc Med. May 1998;152(5):485-8. [Medline].
Osorio AM, Melius J. Lead poisoning in construction. Occup Med. Apr-Jun 1995;10(2):353-61. [Medline].
Perazella MA. Lead and the kidney: nephropathy, hypertension, and gout. Conn Med. Sep 1996;60(9):521-6. [Medline].
Rosen JF. Adverse health effects of lead at low exposure levels: trends in the management of childhood lead poisoning. Toxicology. 1995;97:11-7. [Medline].
Ruprecht J. Scientific Monograph Dimaval (DMPS). In: Investigators Brochure. Houston, Tex: Heyltex Corporation: 1997.
Sun JB, Wang JP. Recommended diagnostic criteria for occupational chronic lead poisoning. Biomed Environ Sci. Dec 1995;8(4):318-29. [Medline].
Trachtenbarg DE. Getting the lead out: when is treatment necessary?. Postgrad Med. Mar 1996;99(3):201-2, 207-18. [Medline].
Winneke G, Lilienthal H, Kramer U. The neurobehavioural toxicology and teratology of lead. Arch Toxicol Suppl. 1996;18:57-70. [Medline].
Further Reading
Keywords
lead toxicity, lead poisoning, lead consumption, lead poisoning causes, lead poisoning treatment, adult lead poisoning, pediatric lead poisoning, effects of lead poisoning, lead contamination, lead paint, lead exposure, childhood lead exposure, childhood lead poisoning, lead-related occupations, lead-pigmented paint, iron deficiency






Differential Diagnoses & Workup: Toxicity, Lead