Lead poisoning natural history, complications and prognosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya Stevasarova, M.D.. Leena Josephin Jetty, M.B.B.S[2]
Overview
If left untreated, 100% of patients with [lead poisoning] may progress to develop seizures, unconsciousness and death.
Natural History, Complications, and Prognosis
Natural History
- Symptoms of acute lead poisoning usually develop in the first 3 year of life, and start with symptoms such as pain, muscle weakness, numbness and tingling, and, rarely, symptoms associated with encephalitis.[1] Abdominal pain, nausea, vomiting, diarrhea, and constipation are other acute symptoms.[2] Lead's effects on the mouth include astringency and a metallic taste.[2] Gastrointestinal problems, such as constipation, diarrhea, poor appetite, or weight loss, are common in acute poisoning. Absorption of large amounts of lead over a short time can cause circulatoryshock due to loss of water from the gastrointestinal tract.[2] Hemolysis due to acute poisoning can cause anemia and hemoglobinuria.[2] Damage to kidneys can cause changes in urination such as oliguria.[2]
Complications
- Common complications of lead poisoning include:
Central nervous system and neuromuscular symptoms usually result from intense exposure, while gastrointestinal symptoms usually result from exposure over longer periods.[2] Signs of chronic exposure include loss of short-term memory or concentration, depression, nausea], abdominal pain, loss of coordination, and numbness and tingling in the extremities.[3][unreliable medical source?] Fatigue, problems with sleep, headaches, stupor, slurred speech, and anemia are also found in chronic lead poisoning.[1] A "lead hue" of the skin with pallor and/or lividity is another feature of chronic lead poisoning.[4][5] A blue line along the gum with bluish black edging to the teeth, known as a Burton line, is another indication of chronic lead poisoning.[6] Children with chronic poisoning may refuse to play or may have hyperkinetic or aggressive behavior disorders.[1] Visual disturbance may present with gradually progressing blurred vision as a result of central scotoma, caused by toxic optic neuritis.[7]
- Studies conducted in the recent past have confirmed that long term exposure of low levels of lead, which were previously determined to be safe are a major risk factor for atherosclerotic cardiovascular disease in adults and cognitive deficits in children. The effects of exposure to lead on long term basis varies in children and adults.
Complications
- Low level lead poisoning in children was found to be a risk factor for :
- In adults it is associated with :
Effects on Growth and Development
- Lead exposure is found to be a risk factor for preterm birth ,a 10 microgram elevation in blood lead levels is associated with 70 % increase in preterm birth.For those with Vitamin D deficiency this risk is even more elevated.
- Lead exposure is associated with reduced I.Q ,with higher reductions occurring at relatively low levels of exposure.[8]
- Childhood exposure to Lead is a known risk factor for anti social disorders ,including
- In Adults:
- Higher blood or bone levels are found to be congruently associated with accelerated cognitive decline; especially in those withAPOE4 alleles, drawing suspicion that it may have a role as a risk factor for late onset Alzheimer’s disease.
CVS
- Lead causes cellular changes that are characteristic for hypertension and atherosclerosis.Is is a leading risk factor for death from cardiovascular disease. *Laboratory studies revealed endothelial cells incubated in lead for 72 hours at concentrations of 0.14 to 8.2 μg per liter showed signs of membrane damage , which is the earliest finding in the natural history of atherosclerosis.
- Studies revealed that the risk of death from cardiovascular disease and coronary artery disease increased sharply at levels below 50 μg per liter, when adjusted for other risk factors.
Hypertension
- The incidence of hypertension in the U.S decreased tremendously during the phaseout of leaded gasoline.
- The usual factors like smoking, antihypertensive medicines, obesity, or even the larger size of the cuff used to measure blood pressure in persons with obesity — did not explain the decline.but it was observed that the median blood lead levels dropped by 100 μg per litre over a period of 18 years, which point towards the role of Lead in the causation of hypertension[9]
CVS
- Lead causes cellular changes that are characteristic for hypertension and atherosclerosis.Is is a leading risk factor for death from cardiovascular disease. *Laboratory studies revealed endothelial cells incubated in lead for 72 hours at concentrations of 0.14 to 8.2 μg per liter showed signs of membrane damage , which is the earliest finding in the natural history of atherosclerosis.
- Studies revealed that the risk of death from cardiovascular disease and coronary artery disease increased sharply at levels below 50 μg per liter, when adjusted for other risk factors.
Hypertension
- The incidence of hypertension in the U.S decreased tremendously during the phaseout of leaded gasoline.
- The usual factors like smoking, antihypertensive medicines, obesity, or even the larger size of the cuff used to measure blood pressure in persons with obesity — did not explain the decline.but it was observed that the median blood lead levels dropped by 100 μg per litre over a period of 18 years, which point towards the role of Lead in the causation of hypertension[9]
Prognosis
- Prognosis is generally related to the extent and duration of lead exposure.[10]
Effects of lead on the physiology of the kidneys and blood are generally reversible; its effects on the central nervous system are not.[11] While peripheral effects in adults often go away when lead exposure ceases, evidence suggests that most of lead's effects on a child's central nervous system are irreversible.[12] Children with lead poisoning may thus have adverse health, cognitive, and behavioral effects that follow them into adulthood.[13]
References
- ↑ 1.0 1.1 1.2 Invalid
<ref>tag; no text was provided for refs namedPearce07-EurNeurol - ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Invalid
<ref>tag; no text was provided for refs namedBrunton07-31 - ↑ Invalid
<ref>tag; no text was provided for refs namedPatrick06 - ↑ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders. ISBN 0-7216-2921-0. :859
- ↑ El Safoury, OmarSoliman; Abd El Fatah, DinaSabry; Ibrahim, Magdy (2009). "Treatment of periocular hyperpigmentation due to lead of kohl (surma) by penicillamine: A single group non-randomized clinical trial". Indian Journal of Dermatology. 54 (4): 361. doi:10.4103/0019-5154.57614. ISSN 0019-5154. PMID 20101339.
- ↑ Rambousek (2008) p.177
- ↑ Fintak, David R. (30 January 2007). "Wills Eye Resident Case Series". Archived from the original on 14 July 2014.
- ↑ Canfield RL, Henderson CR, Cory-Slechta DA, Cox C, Jusko TA, Lanphear BP (April 2003). "Intellectual impairment in children with blood lead concentrations below 10 microg per deciliter". N Engl J Med. 348 (16): 1517–26. doi:10.1056/NEJMoa022848. PMC 4046839. PMID 12700371.
- ↑ 9.0 9.1 Wright JD, Stevens J, Poole C, Flegal KM, Suchindran C (June 2010). "The impact of differences in methodology and population characteristics on the prevalence of hypertension in US adults in 1976-1980 and 1999-2002". Am J Hypertens. 23 (6): 620–6. doi:10.1038/ajh.2010.40. PMC 5774853. PMID 20339353.
- ↑ Chisolm (2004) p. 223
- ↑ Invalid
<ref>tag; no text was provided for refs namedRubin08-267 - ↑ Bellinger, DC (2004). "Lead". Pediatrics. 113 (4 Suppl): 1016–22. doi:10.1542/peds.113.4.S1.1016 (inactive 2018-05-20). PMID 15060194.
- ↑ Woolf, AD; Goldman, R; Bellinger, DC (2007). "Update on the clinical management of childhood lead poisoning". Pediatric clinics of North America. 54 (2): 271–94, viii. doi:10.1016/j.pcl.2007.01.008. PMID 17448360.