Encephalopathy lead poisoning

The alimentary symptoms may be overshadowed by neuromuscular dysfunction, accompanied by signs of motor weakness that may progress to paralysis of the exterior muscles or the wrist (wrist drop), and less often, of the ankles (foot drop). Encephalopathy, the most serious result of lead poisoning, frequendy occurs in children as a result of pica, ie, ingestion of inorganic lead compounds in paint chips this rarely occurs in adults. Nephropathy has also been associated with chronic lead poisoning (147). The toxic effects of lead may be most pronounced on the developing fetus. Consequendy, women must be particulady cautious of lead exposure (148). The U.S. Center for Disease Control recommends a blood level of less than 10 p.m per 100 mL for children. 

Full Fanconi syndrome has been reported to be present in some children with lead encephalopathy (Chisolm 1968 Chisolm et al. 1955). According to the National Academy of Sciences (NAS 1972), the Fanconi syndrome is estimated to occur in approximately one out of three children with encephalopathy and PbB levels of approximately 150 pg/dL. Aminoaciduria occurs at PbB levels >80 pg/dL in children with acute symptomatic lead poisoning (Chisolm 1962). The aminoaciduria and symptoms of lead toxicity disappeared after treatment with chelating agents (Chisolm 1962). 

Accidental or intentional ingestion of folk remedies containing lead (discussed in Section 5.5) represents another source for potential lead-poisoning in children. Acute lead encephalopathy in early infancy has been reported in a Middle Eastern study for 14 infants following the use of Bint al Thahab, a traditional... 

Suggested Alternatives for Differential Diagnosis Sheep Scrapie, pregnancy toxemia, hypocalcemia, tetanus, listeriosis, tick pyemia, hypocuprosis, rabies, hydatid disease, and various plant poisons. Cattle Malignant catarrhal fever, listeriosis, pseudorabies, bovine spongiform encephalopathy, rabies, hypomagnesemia, hypocalcemia, acute lead poisoning, and certain plant poisons. 

Hunter, B. and G. Wobeser. 1980. Encephalopathy and peripheral neuropathy in lead-poisoned mallard ducks. 

Lead poisoning (with encephalopathy) IM Initially, dimercaprol 4 mg/kg then give dimercaprol 4 mg/kg and calcium EDTA 250 mg/m then 4 hr later and q4h for 5 days. 

Acute inorganic lead poisoning is uncommon today. It usually results from industrial inhalation of large quantities of lead oxide fumes or, in small children, from ingestion of a large oral dose of lead in the form of lead-based paint chips small objects, eg, toys coated or fabricated from lead or contaminated food or drink. The onset of severe symptoms usually requires several days or weeks of recurrent exposure and manifests as signs and symptoms of encephalopathy or colic. Evidence of hemolytic anemia (or anemia with basophilic stippling if exposure has been subacute), and elevated hepatic aminotransferases may be present. 

Higher concentrations of a chemical entity may cause a pharmacological response whereas lower concentrations are incapable of doing so. For example, edetate calcium disodium (9) at a formulated concentration of 20% is indicated as a drug for the treatment of lead poisoning and lead encephalopathy while it can be found commonly present as an excipient in concentrations ranging from 0.01% to 0.1% in parenteral formulations to prevent oxidation of the active ingredient. 

Biochemical changes such as increased aminolaevulinate excretion and inhibition of amino-laevulinate dehydrase may be detected in urine and blood, respectively, at blood lead levels of 0.4 to 0.6 mg mL-1. Anemia is a late feature, however. Neurotoxicity may be detectable at blood lead levels of 0.8 to 1.0 mg mL-1. At blood lead levels greater than 1.2 mg mL-1, encephalopathy occurs. Peripheral nerve palsies are rare, and the foot and wrist drop, which were once characteristic of occupational lead poisoning, only occur after excessive exposure and are now rarely seen. Similarly, seizures and impaired consciousness may result from involvement of the CNS. Bone changes are usually seen in children and are detected as bands at the growing ends of the bones and a change in bone shape. 

Encephalopathy -lead [LEAD COMPOUNDS - INDUSTRIAL TOXICOLOGY] (Vol 15) -from lead poisoning [LEAD COMPOUNDS - LEAD SALTS] (Vol 15)... 

Sodium calciumedetate is the calcium chelate of the disodium salt of ethylenediaminetetra-acetic acid (calcium EDTA). It is effective in acute lead poisoning because of its capacity to exchange calcium for lead the lead chelate is excreted in the urine, leaving behind a harmless amount of calcium. Dimercaprol may usefully be combined with sodium calciumedetate when lead poisoning is severe, e.g. with encephalopathy. 

In severe lead poisoning sodium calciumedetate is commonly used to initiate lead excretion. It chelates lead from bone and the extracellular space and urinary lead excretion of diminishes over 5 days thereafter as the extracellular store is exhausted. Subsequently symptoms (colic and encephalopathy) may worsen and this has been attributed to redistribution of lead from bone to brain. Dimercaprol is more effective than sodium calciumedetate at chelating lead from the soft tissues such as brain, which is the rationale for combined therapy with sodium calciumedetate. More recently succimer (2,3-dimercaptosuccinic acid, DMSA), a water-soluble analogue of dimercaprol, has been increasingly used instead. Succimer has a high affinity for lead, is suitable for administration by mouth and is better tolerated (has a wider therapeutic index) than dimercaprol. It is licenced for such use in the USA but not the UK. 

Exposure to lead in adults has been associated with hypertension, nephropathy, decreased hearing acuity, anemia, peripheral neuropathy, and encephalopathy. Onset of symptoms may be slow with chronic exposure. Anemia, common in chronically exposed adults and children, tends to be more severe in children. The life span of red blood cells decreases when lead concentrations in blood increase. In the past, the morphology of various blood cells was used to diagnose lead poisoning. Zero content is allowed in food (Food and Drug Administration). 

Karp inski FE, Rieders F, Girsh LS Calcium disodium versenate in the therapy of lead encephalopathy. J Pediatr 42 687-699, 1953 Kirkconnell SC, Hicks LE Residual effects of lead poisoning on Denver Developmental Screening Test scores. J Abnorm Child Psychol 8 257-267, 1980 Kotok D Development of children with elevated blood lead levels a controlled study. J Pediatr 80 57-61, 1972... 

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