Lead poisoning symptomatic

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). 

Chronic lead nephropathy in moonshiners, more often than not, is accompanied by gout and hypertension, in accord with 19 century descriptions of plumbism and reports from Austraha [1]. A statistically significant odds ratio of 2.4 has been reported for moonshine consumption and end-stage renal disease, suggesting a causal association with lead in fhe absence of symptomatic lead poisoning [31]. 

In summary, chelation therapy is justified in cases of symptomatic lead poisoning or when the blood lead exceeds about 80 pg/dL. When no symptom end-point... 

Ruff HA, Bijur PE, Markowitz M, et al Declining blood lead levels and cognitive changes in moderately lead-poisoned children. JAMA 269 1641-1646,1993 Rnmmo JH, Routh DK, Rnmmo NJ, et al Behavioral and neurological effects of symptomatic and asymptomatic lead exposure in children. Arch Environ Health 34 120-124, 1979... 

Edetate calcium disodium, a metal-chelating agent, is indicated in the treatment of symptomatic lead poisoning without encephalopathy and blood lead concentrations less than 100 mcg/dL, or in the treatment of severe lead poisoning with symptoms of encephalopathy and/or blood lead concentrations greater than 100 mcg/dL. 

Because the onset of lead poisoning usually is insidious, it often is desirable to estimate the body burden of lead in individuals who are exposed to an environment that is contaminated with the metal. In the past, the edetate calcium disodium (CaNaJlDTA) provocation test was used to determine whether there is an increased body burden of lead in those for whom exposure occurred much earlier. The provocation test is performed by intravenous administration of a single dose of CaNa DTA (50 mg/kg) followed by collection of urine for 8 hours. The test is positive for children when the lead excretion ratio (pg of lead excreted in the urine per mg of CaNa DTA administered) is >0.6 it also may be useful for therapeutic chelation in children with blood levels of 25 5 pg/dL. This test is not used in symptomatic patients or in those whose concentration of lead in blood is >45 pg/dL because these patients require the proper therapeutic regimen with chelating agents (see below). 

Treatment of organic lead poisoning is symptomatic. Chelation therapy will promote excretion of the inorganic lead produced from the metabolism of organic lead, but the increase is not dramatic. 

It does, however alleviate overt symptoms in the extremely rare case when lead poisoning is so severe as to be symptomatic. It also prevents the disease from progressing. Older children (4 to 6 years old) are more difficult to chelate because the lead stored in their bones has become part of the bony matrix and more tightly bound than in a younger child (1 to 2 years old). ... 

A multiplicity of terms exists to describe lead poisoning. Strictly speaking frank means unmistakable, clinical is recognisable by a physician and classic as described in a textbook. Symptomatic is in the presence of well-defined symptoms and asymptomatic in the presence of an elevated blood lead without obvious symptoms. Other terms include subclinical and intoxication in which effects of lead are assumed but not yet proven. 

Many papers have attempted to define a normal blood lead level and seem to imply that values not diagnostic of lead poisoning are normal. Indeed, most papers equate the lowest symptomatic blood lead level with the upper limit of normal. A level not associated with overt clinical evidence of toxicity is not necessarily normal. However, most children with increased and therefore abnormal blood leads are reported as asymptomatic. This may be due to the absence of classical symptoms and the failure to recognize other less obvious clinical features. The evidence supporting low lead toxicity is nevertheless slight and is prone to criticism, as other variables, e.g. genetic, perinatal, nutritional and socioeconomic factors may be just as relevant in causing the sequelae detected. 

In summary, pertinent literature demonstrates that lead poisoning with encephalopathy results in a greatly increased incidence of permanent neurological and cognitive impairments. Also, several studies showed that children with overt, symptomatic lead intoxication in the absence of encephalopathy experience persisting neurological and behavioural impairments. 

Rummo, J.H. (1974). Intellectual and behavioral effects of lead poisoning in children [dissertation]. Chapel Hill, NC University of North Carolina. Available from University Microfilms, Ann Arbor, MI publication no. 74-26, 930 Rummo, J.H., Routh, D.K., Rummo, N.J. and Brown, J.F. (1979). Behavioral and neurological effects of symptomatic and asymptomatic lead exposure in children. Arch. Environ. Health, 34, 120-124... 

Answer D. The symptoms of cholinergic excess seen in this child are indicative of exposure to insecticides such as the organophosphate parathion, which cause irreversible inhibition of acetylcholinesterase. Other symptoms may include CNS excitation and stimulation of the skeletal NMJ, ultimately leading to paralysis of respiratory musdes— DUMB-BELSS. In addition to symptomatic support, management of AChE inhibitor poisoning involves the use of atropine and 2-PAM. 

Hair lead levels do not accurately reflect blood lead levels and only help make the diagnosis in extreme cases of symptomatic poisoning (Roper et al. 1993). Research continues in the field of hair lead, but the bulk of work appeared in the 1970s and 1980s (Rimland and Larson 1983). 

Although chelation therapy effectively reverses acute lead nephropathy and the preclinical renal dysfunction of occupational lead nephropathy, there is no evidence that such therapy reverses established interstitial nephritis due to lead. The partial remissions achieved among moonshiners and symptomatic lead workers may represent reversal of acute poisoning superimposed on chronic lead nephropathy. No improvement in renal function can be expected once ad-... 

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