Brodie abscess pathophysiology: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
No edit summary |
||
| Line 5: | Line 5: | ||
Local [[trauma]] and [[bacteremia]] lead to increased susceptibility to bacterial seeding of the [[metaphysis]]. History of trauma is reported in 30% of patients. | Local [[trauma]] and [[bacteremia]] lead to increased susceptibility to bacterial seeding of the [[metaphysis]]. History of trauma is reported in 30% of patients. | ||
==Pathophysiology== | ==Pathophysiology== | ||
*Local [[trauma]] and [[bacteremia]] lead to increased susceptibility to bacterial seeding of the [[metaphysis]]. History of [[trauma]] is reported in 30% of patients. Brodie abscess arises where the [[bacteria]] and the [[host]] [[defenses]] are equally | *Local [[trauma]] and [[bacteremia]] lead to increased susceptibility to bacterial seeding of the [[metaphysis]]. History of [[trauma]] is reported in 30% of patients. Brodie abscess arises where the [[bacteria]] and the [[host]] [[defenses]] are equally balanced. Bacteria proliferate in bone and cause [[inflammation]] and [[necrosis]]. It spreads through the [[haversian]] [[system]] or [[medullary]] cavity within the shaft and to [[periosteum]]. To reduce the [[systemic]] response, the abscess is walled-off. An [[osseous]] [[infection]] can be caused by [[hematogenous]] spread of [[pathogens]] to bone or by direct inoculations by bacteria. The [[organisms]] reach the bone from a disrupted site else where in the body such as a [[skin]] [[pustule]], [[furuncles]], [[impetigo]], infected [[blisters]] and [[burns]], or secondary to an infection of another organ system ([[urogenital]] [[infections]], [[enteritis]], [[cholangitis]] or [[endocarditis]]. <ref name="pmidDOI:10.5334/jbr-btr.145">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=DOI:10.5334/jbr-btr.145 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10 }} </ref> | ||
== References == | == References == | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Latest revision as of 08:24, 4 February 2023
|
Brodie abscess Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Brodie abscess pathophysiology On the Web |
|
American Roentgen Ray Society Images of Brodie abscess pathophysiology |
|
Risk calculators and risk factors for Brodie abscess pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Abdulkerim Yassin, M.B.B.S[2]
Overview
Local trauma and bacteremia lead to increased susceptibility to bacterial seeding of the metaphysis. History of trauma is reported in 30% of patients.
Pathophysiology
- Local trauma and bacteremia lead to increased susceptibility to bacterial seeding of the metaphysis. History of trauma is reported in 30% of patients. Brodie abscess arises where the bacteria and the host defenses are equally balanced. Bacteria proliferate in bone and cause inflammation and necrosis. It spreads through the haversian system or medullary cavity within the shaft and to periosteum. To reduce the systemic response, the abscess is walled-off. An osseous infection can be caused by hematogenous spread of pathogens to bone or by direct inoculations by bacteria. The organisms reach the bone from a disrupted site else where in the body such as a skin pustule, furuncles, impetigo, infected blisters and burns, or secondary to an infection of another organ system (urogenital infections, enteritis, cholangitis or endocarditis. [1]
References
- ↑ Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMID DOI:10.5334/jbr-btr.145 Check
|pmid=value (help).