Reversal of Acute Lead Encephalopathy in a Child

Treatment of Lead-exposed Children

PEDIATRICS ◽

10.1542/peds.98.1.161a ◽

1996 ◽

Vol 98 (1) ◽

pp. 161-162

Author(s):

Steven M. Marcus

Keyword(s):

Lead Poisoning ◽

Lead Exposure ◽

Treatment Guidelines ◽

Clinical Symptoms ◽

Double Blind ◽

Developmental Abnormalities ◽

Lead Encephalopathy

I am writing in response to the recommendations in the statement "Treatment Guidelines for Lead Exposure in Children," by the Committee on Drugs, reported in the July 1995 issue of Pediatrics. The Committee did an admirable job in reviewing the various aspects of treating lead poisoning; however, there are several points that were made that need to be clarified. Although no one would argue that treatment is indicated for lead encephalopathy, there have been no studies, to my knowledge, of a double-blind, controlled nature, showing that treatment of lead poisoning, in the absence of clinical symptoms, is of any use in either reversing any neurologic or developmental abnormalities or, in fact, in prevention of such.

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Letters to the Editor

PEDIATRICS ◽

10.1542/peds.41.2.536b ◽

1968 ◽

Vol 41 (2) ◽

pp. 536-536

Author(s):

David L. Knox

Keyword(s):

Letters To The Editor ◽

Lead Encephalopathy

We appreciate Dr. Hart's compliments and his reminder of acute lead encephalopathy as a cause of VI palsy.

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CHRONIC LEAD ENCEPHALOPATHY

PEDIATRICS ◽

10.1542/peds.25.2.309 ◽

1960 ◽

Vol 25 (2) ◽

pp. 309-315

Author(s):

Harry H. White ◽

Fred D. Fowler

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Pediatric Patients ◽

Early Recognition ◽

Central Nervous System Involvement ◽

Fast Screening ◽

The Central Nervous System ◽

Lead Encephalopathy ◽

Urinary Coproporphyrin

Chronic lead encephalopathy must be considered in the differential diagnosis of pediatric patients who present with manifestations of schizophrenia, behavior disorders or degenerative diseases of the central nervous system. Determination of urinary coproporphyrin is a simple, fast screening procedure applicable to office practice. The prognosis for normal mental development following encephalopathy is poor. It is hoped that early recognition of the more subtle signs of central nervous system involvement will allow treatment to be instituted soon enough to prevent the crippling mental deterioration which is so often a sequela of lead poisoning.

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Lead encephalopathy presenting as a posterior fossa mass

Journal of Neurosurgery ◽

10.3171/jns.1986.65.5.0713 ◽

1986 ◽

Vol 65 (5) ◽

pp. 713-715 ◽

Cited By ~ 8

Author(s):

J. Frederick Harrington ◽

Timothy B. Mapstone ◽

Warren R. Selman ◽

Pamela Galloway ◽

Carl Bundschuh

Keyword(s):

Computerized Tomography ◽

Posterior Fossa ◽

Content Type ◽

Lead Encephalopathy ◽

Fine Print

✓ A case of lead encephalopathy with clinical and computerized tomography evidence of a midline posterior fossa mass is presented. The pathophysiology and the predilection for posterior fossa involvement are discussed.

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Fatal lead encephalopathy following the ingestion of fishing weights (“sinkers”)

Clinical Toxicology ◽

10.1080/15563650.2021.1994985 ◽

2021 ◽

pp. 1-1

Author(s):

Allister Vale ◽

Nicola Barlow ◽

Sally Bradberry

Keyword(s):

Lead Encephalopathy

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Screening to Prevent Lead Poisoning

PEDIATRICS ◽

10.1542/peds.54.5.626 ◽

1974 ◽

Vol 54 (5) ◽

pp. 626-628

Author(s):

Richard W. Moriarty

Keyword(s):

Natural History ◽

Lead Poisoning ◽

Diagnostic Tests ◽

Chelating Agents ◽

Clinical Evidence ◽

Clinical Symptoms ◽

Blood Lead ◽

Blood Lead Levels ◽

Lead Levels ◽

Lead Encephalopathy

The absence of fully effective treatment for lead encephalopathy, and the suggestive evidence that lead poisoning may cause brain damage even in the absence of overt encephalopathy, have led to massive efforts to prevent such damage. These preventive efforts have been directed toward screening to identify children who have absorbed an undue amount of lead from their environment, reducing their further exposure to lead, and removing already absorbed lead from those most in danger of developing ill effects. This approach has been codified in the Surgeon General's Report of 19701 which makes the following recommendations: 1. All young children who live in or visit old dilapidated buildings should have periodic blood lead determinations. 2. Any child with repeated blood lead levels over 40µg/100 ml whole blood should be considered to be at risk of lead poisoning, h ave current sources of exposure to lead investigated and corrected, and be followed closely to ensure that he does not develop higher blood lead levels or clinical symptoms. 3. All children with blood lead levels between 50 and 79µg/100 ml should have diagnostic tests for metabolic and clinical evidence of lead poisoning and be treated immediately if such evidence is present. 4. All children with blood lead levels over 80µg/100 ml should be hospitalized immediately and treated with chelating agents. Many aspects of this approach are subjects of current controversey, and the last word will not be written until much better knowledge of the natural history and ecology of lead poisoning is available.

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