eMedicine Specialties > Neurology > Neurotoxicology

Lead Encephalopathy: Differential Diagnoses & Workup

Author: Adam K Rowden, DO, Assistant Professor of Emergency Medicine, Thomas Jefferson University; Director, Division of Toxicology, Department of Emergency Medicine, Albert Einstein Medical Center; Consulting Toxicologist, Children's Hospital of Philadelphia
Coauthor(s): Christopher P Holstege, MD, Associate Professor of Emergency Medicine and Pediatrics, University of Virginia; Director, Division of Medical Toxicology, Center of Clinical Toxicology; Medical Director, Blue Ridge Poison Ctr, Associate Medical Toxicology Fellowship Director, VA Dept of Health; J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center; Rika Nagakuni O'Malley, MD, Fellow, Division of Toxicology, Department of Emergency Medicine, Albert Einstein Medical Center
Contributor Information and Disclosures

Updated: Oct 26, 2009

Differential Diagnoses

Confusional States and Acute Memory Disorders
Diabetic Neuropathy
Epileptic and Epileptiform Encephalopathies
Frontal Lobe Syndromes
Organic Solvents
Radial Mononeuropathy

Other Problems to Be Considered

Attention deficit hyperactivity disorder
Learning disorder
Developmental delay
Language disorder
Peripheral neuropathy
Autism/pervasive developmental disorder

Workup

Laboratory Studies

  • Venous blood lead level: Although not an accurate measure of the whole-body burden of lead, the blood lead level is a reasonable approximation of lead exposure10 , as levels decline in a predictable manner after removal from the source of lead. Capillary (ie, finger-stick) blood levels do provide a reliable measurement if performed correctly, though samples improperly collected may be contaminated by lead dust on the skin or from the collecting equipment.
    • Levels above 70 mcg/dL (ie, class V) are considered medical emergencies, regardless of whether neurological symptoms are present. Risk of encephalopathy is high and treatment is required. However, lead levels should be reviewed in the context of the clinical exam and history.
    • For example, a child can swallow a lead foreign body and have a documented level above 70 mcg/dL within 2 days, but the total body burden would be low (the lead would be predominantly within the blood compartment in this scenario). Encephalopathy would not be expected in this scenario. However, a child with chronic ingestion of lead paint dust may have a lower lead level, but with a much higher body burden and subsequent neurological findings (the lead has had time to redistribute amongst all the compartments).
    • Levels ranging from 45-69 mcg/dL (ie, class IV) warrant chelation therapy, according to CDC criteria, and a medical evaluation including further blood testing and possibly abdominal radiograph looking for lead paint chips. Removal from the source of lead exposure is paramount.
    • Levels ranging from 20-44 mcg/dL (ie, class III) require medical evaluation including further lab testing and possible abdominal radiographs. Removal of the source of lead and an environmental evaluation are also required. There is no good evidence that treatment with chelation agents for lead levels below 45 mcg/dL is of benefit (in fact, the evidence tends to point to potential harm by chelating at lower levels).11
    • Levels ranging from 15-19 mcg/dL (ie, class II) require repeat blood lead level screening and lead prevention education. If elevated levels persists in this range or rise over a 3-month period, treat patient as above (levels 20-44 mcg/dL).
    • Levels ranging from 10-14 mcg/dL (ie, class I) require no further treatment other than lead prevention education, but periodic screening in young children should continue.
  • Free erythrocyte protoporphyrin (FEP): This provides a good estimate of the acuity of exposure. If FEP in normal in the context of high blood lead levels, the exposure is more likely acute; if both are elevated, the exposure is more likely chronic. FEP elevation lags behind the blood lead elevation that causes it.
  • Hemogram: Significantly elevated blood lead levels are associated with a microcytic anemia. Iron deficiency, also associated with anemia, may produce an elevation of FEP, confounding the significance of FEP measurement.
  • These work-up guidelines are based on the recommendations from the CDC Advisory Committee on Childhood Lead Poisoning Preventions, the National Center of Environmental Health/Agency for Toxic Substances and Disease Registry, and the American Academy of Pediatrics Committee on Environmental Health.12

Imaging Studies

  • Neuroimaging (eg, MRI, CT) does not play an important role in the diagnosis of lead poisoning. However, cerebral edema and microhemorrhages may be seen in patients presenting with acute encephalopathy on both CT and MRI. With chronic exposure to lead, patchy calcifications may be seen. Atrophy and white matter changes may be present with chronic exposures. Atre et al reported a case of lead encephalopathy with MRI findings of symmetric occipital lobe lesions that were bright on T2-weighted and fluid-attenuated inversion recovery images and hypointense on T1-weighted images.13 These lesions disappeared after chelation therapy with clinical laboratory improvement.
  • Classic findings of lead lines on radiographs of long bones are seen rarely, as most cases of lead poisoning in children are due to exposures to low or moderate amounts of lead. Obtaining radiographs in search of lead lines is not recommended by the CDC.
  • In selected cases, abdominal radiographs may demonstrate lead-containing paint chips or other lead-containing objects. Retained lead objects within the gastrointestinal tract are an acute emergency and should prompt referral for potential removal.
  • EEG findings can be normal or show nonspecific findings and are generally not helpful in the diagnosis.

Other Tests

Formal neuropsychological testing provides the best measure of a patient's cognitive impairment. This is effective in tracking improvement in attention, visual-spatial abnormalities, and memory as a result of treatment and in establishing the extent and nature of long-term impairment.

Staging

The CDC has established 5 stages of lead toxicity, based upon blood lead levels. These are discussed under Lab Studies.

More on Lead Encephalopathy

Overview: Lead Encephalopathy
Differential Diagnoses & Workup: Lead Encephalopathy
Treatment & Medication: Lead Encephalopathy
Follow-up: Lead Encephalopathy
References
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References

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Further Reading

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Keywords

lead encephalopathy, lead poisoning, lead toxicity, plumbism, lead-based paint, lead absorption, effects of lead poisoning, lead exposure

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Contributor Information and Disclosures

Author

Adam K Rowden, DO, Assistant Professor of Emergency Medicine, Thomas Jefferson University; Director, Division of Toxicology, Department of Emergency Medicine, Albert Einstein Medical Center; Consulting Toxicologist, Children's Hospital of Philadelphia
Adam K Rowden, DO is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, American College of Osteopathic Emergency Physicians, American Osteopathic Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Christopher P Holstege, MD, Associate Professor of Emergency Medicine and Pediatrics, University of Virginia; Director, Division of Medical Toxicology, Center of Clinical Toxicology; Medical Director, Blue Ridge Poison Ctr, Associate Medical Toxicology Fellowship Director, VA Dept of Health
Christopher P Holstege, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Association for the Advancement of Science, American College of Emergency Physicians, American College of Medical Toxicology, American Medical Association, Medical Society of Virginia, Society for Academic Emergency Medicine, Society of Toxicology, and Wilderness Medical Society
Disclosure: Nothing to disclose.

J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Rika Nagakuni O'Malley, MD, Fellow, Division of Toxicology, Department of Emergency Medicine, Albert Einstein Medical Center
Disclosure: Nothing to disclose.

Medical Editor

Jonathan S Rutchik, MD, MPH, Assistant Professor, Department of Occupational and Environmental Medicine, University of California at San Francisco
Jonathan S Rutchik, MD, MPH is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Occupational and Environmental Medicine, and Society of Toxicology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Richard J Caselli, MD, Professor, Department of Neurology, Mayo Medical School, Rochester, MN; Chair, Department of Neurology, Mayo Clinic of Scottsdale
Richard J Caselli, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, American Neurological Association, and Sigma Xi
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Tarakad S Ramachandran, MBBS, FRCP(C), FACP, Professor of Neurology, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Chair, Department of Neurology, Crouse Irving Memorial Hospital
Tarakad S Ramachandran, MBBS, FRCP(C), FACP is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners, American College of International Physicians, American College of Managed Care Medicine, American College of Physicians, American Heart Association, American Stroke Association, Royal College of Physicians, Royal College of Physicians and Surgeons of Canada, Royal College of Surgeons of England, and Royal Society of Medicine
Disclosure: Abbott Labs  Honoraria Consulting; Teva Marion Honoraria Consulting; Boeringer-Ingelheim Honoraria Speaking and teaching

 
 
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