Lead poisoning diagnosis

Hu-Howard. Knowledge of Diagnosis and Reproductive History among Survivors of Childhood Plumbism. American Journal of Public Health. 81 (Aug. 1991) 1070-1072. Source for third-generation effects of lead poisoning. 

Kohler PF Tulane University School of Medicine, New Orleans, LA To determine lead poisoning process to evaluate the use of the oral chelator of lead, Succimer, in the diagnosis and treatment of lead poisoning in adults National Center for Research Resources ... 

Piomelli S, Graziano J. 1980. Laboratory diagnosis of lead poisoning. Pediatr Clin North Am 27 843-853. 

Suggested Alternatives for Differential Diagnosis Salmonellosis, pasteurellosis, enterotox-emia due to . coli, rabies, pregnancy toxemia, polioencephalomalatia, acute rumen impaction, louping-ill hypocalcemia, hypomagnesemia, and acute lead poisoning. 

Suggested Alternatives for Differential Diagnosis In pigs Nipah virus, Aujeszky s disease, brucellosis, porcine reproductive and respiratory syndrome (PRRS) virus, Classical swine fever, parvovirus. In horses Equine encephalomyelitis (Western, Eastern, and Venezuelan), Rabies, Borna disease, Lead poisoning, Tetanus. 

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. 

Diagnosis of lead poisoning IM,IV 500 mg/m. Maximum 1 g/mVday divided in equal doses 8-12 hr apart for 5 days, skip 2-4 days and repeal course if needed. 

Buneaux F, Protin P, Besson-leaud M, Fabiani P. Role du laboratoire dans le diagnostic et la traitement d une intoxication par le plomb. [Role of the laboratory in the diagnosis and treatment of lead poisoning.] Eur J Toxicol Environ Hyg 1976 9(3) 165-70. 

Reference intervals are given in Table 32-3. Total erythrocyte porphyrin concentrations are increased in EPP, CEP, the rare homozygous variants of the autosomal dominant porphyrias, iron deficiency, hemolytic anemia, some other forms of anemia, and lead poisoning. A normal total porphyrin concentration excludes the diagnosis of EPP. Distinction between EPP and other causes of increased erythrocyte total porphyrin concentration requires differentiation between protoporphyrin and its zinc chelate because the acidic condition of this assay dissociates the zinc chelate and provides only a measure of total porphyrin. 

The determination of PbB is of prime importance with respect to the diagnosis of lead poisoning and to the assessment of hazardous conditions both in occupationally exposed people and in the general population. It is generally agreed that the concentrations of lead in air. food and water are less relevant for assessing health hazards for humans than the amount of lead actually absorbed and this is what actually is reflected by PbB (WHO, 1977, 1980). 

The diagnosis of acute lead poisoning may be difficult, since the symptoms often simulate a number of disorders of the gastrointestinal system, including acute appendicitis. In children... 

E. Other tests. Nonspecific laboratory findings that support the diagnosis of lead poisoning include anemia (normocytic or microcytic), and basophilic stippling of erythrocytes, a useful but insensitive clue. Acute high-dose exposure may sometimes be associated with transient azotemia (elevated BUN and serum creatinine) and mild to moderate elevation in serum transaminases. Recently ingested lead paint, glazes, chips, or solid lead objects may be visible on abdominal x-rays. CT or MRI of the brain often reveals cerebral edema in patients with lead encephalopathy. Because iron deficiency increases lead absorption, iron status should be evaluated. 

The myth that only poor inner-city minority children can be lead poisoned has resulted in the delayed diagnosis of numerous cases of lead poisoning. 

A problem inherent in the study of lead poisoning is that the symptoms are largely non-specific (Table 7.10). This can lead to difficulties in the diagnosis of cases of over-exposure to lead. The first consequence of exposure to lead to be considered is its effect on the blood itself. 

Barltrop D (1965) The relationship between some parameters employed in the diagnosis of lead poisoning in childhood with special reference to the excretion of delta-amino laevul ini c acid. Thesis. University of London... 

American Academy of Pediatrics, 1969. Prevention, diagnosis, and treatment of lead poisoning in childhood. Pediatrics 44, 291-298. 

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