Lead poisoning natural history, complications and prognosis: Difference between revisions
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{{Lead poisoning}} | {{Lead poisoning}} | ||
{{CMG}}; {{AE}} | {{CMG}}; {{AE}}{{AKS}} | ||
==Overview== | ==Overview== | ||
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===Complications=== | ===Complications=== | ||
*Common complications of [[lead poisoning]] include: | *Common complications of [[lead poisoning]] include: | ||
** [[gastrointestinal]] | **[[gastrointestinal]] | ||
**[[neuromuscular]] | **[[neuromuscular]] | ||
**[[neurological]] | **[[neurological]] | ||
[[Central nervous system]] and neuromuscular symptoms usually result from intense exposure, while [[gastrointestinal symptoms]] usually result from exposure over longer periods.<ref name="Brunton07-31"/> 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 | [[Central nervous system]] and [[neuromuscular symptoms]] usually result from intense exposure, while [[gastrointestinal symptoms]] usually result from exposure over longer periods.<ref name="Brunton07-31"/> 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.<ref name="Patrick06"/>{{ums|date=December 2017}} [[Fatigue]], problems with sleep, [[headaches]], [[stupor]], [[slurred speech]], and [[anemia]] are also found in chronic lead poisoning.<ref name="Pearce07-EurNeurol"/> A "lead hue" of the skin with [[pallor]] and/or [[lividity]] is another feature of [[chronic lead poisoning]].<ref name="Andrews">James, William; Berger, Timothy; Elston, Dirk (2005). ''Andrews' Diseases of the Skin: Clinical Dermatology''. (10th ed.). Saunders. {{ISBN|0-7216-2921-0}}. {{Rp|859}}</ref><ref name="El SafouryAbd El Fatah2009">{{cite journal|last1=El Safoury|first1=OmarSoliman|last2=Abd El Fatah|first2=DinaSabry|last3=Ibrahim|first3=Magdy|title=Treatment of periocular hyperpigmentation due to lead of kohl (surma) by penicillamine: A single group non-randomized clinical trial|journal=Indian Journal of Dermatology|volume=54|issue=4|year=2009|pages=361|issn=0019-5154|doi=10.4103/0019-5154.57614|pmid=20101339}}</ref> 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.<ref name="Rambousek08-177">[[#CITEREFRambousek08|Rambousek (2008)]] p.177</ref> Children with chronic poisoning may refuse to play or may have [[Hyperkinetic disorder|hyperkinetic]] or aggressive behavior disorders.<ref name="Pearce07-EurNeurol"/> Visual disturbance may present with gradually progressing [[blurred vision]] as a result of [[central scotoma]], caused by [[toxic optic neuritis]].<ref>{{cite journal|last1=Fintak|first1=David R.|title=Wills Eye Resident Case Series|date=30 January 2007|url=http://www.revophth.com/content/d/wills_resident_case_series/i/1297/c/24966/|deadurl=no|archiveurl=https://web.archive.org/web/20140714181927/http://www.revophth.com/content/d/wills_resident_case_series/i/1297/c/24966/|archivedate=14 July 2014|df=}}</ref> | ||
===Prognosis=== | ===Prognosis=== | ||
*Prognosis is generally | *Prognosis is generally related to the extent and duration of lead exposure.<ref name="Chisolm04-223">[[#CITEREFChisolm04|Chisolm (2004)]] p. 223</ref> | ||
Effects of lead on the physiology of the kidneys and blood are generally reversible; its effects on the central nervous system are not.<ref name="Rubin08-267"/> 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.<ref name="Bellinger04-Pedi">{{cite journal|last1=Bellinger|first1=DC|title=Lead|journal=Pediatrics|volume=113|issue=4 Suppl|pages=1016–22|year=2004|pmid=15060194|doi=10.1542/peds.113.4.S1.1016|doi-broken-date=2018-05-20}}</ref> Children with lead poisoning may thus have adverse health, cognitive, and behavioral effects that follow them into adulthood.<ref name="Woolf07-PedClin">{{cite journal|last1=Woolf|first1=AD|last2=Goldman|first2=R|last3=Bellinger|first3=DC|title=Update on the clinical management of childhood lead poisoning|journal=Pediatric clinics of North America|volume=54|issue=2|pages=271–94, viii|year=2007|pmid=17448360|doi=10.1016/j.pcl.2007.01.008}}</ref> | |||
==References== | ==References== | ||
Latest revision as of 15:15, 15 August 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya Stevasarova, M.D.
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]
Prognosis
- Prognosis is generally related to the extent and duration of lead exposure.[8]
Effects of lead on the physiology of the kidneys and blood are generally reversible; its effects on the central nervous system are not.[9] 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.[10] Children with lead poisoning may thus have adverse health, cognitive, and behavioral effects that follow them into adulthood.[11]
References
- ↑ 1.0 1.1 1.2
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5
- ↑
- ↑ 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.
- ↑ Chisolm (2004) p. 223
- ↑
- ↑ 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.