Suppurative thrombophlebitis pathophysiology: Difference between revisions
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{{Suppurative thrombophlebitis}} | {{Suppurative thrombophlebitis}} | ||
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==Overview== | |||
The pathophysiology of suppurative thrombophlebitis depends on the subtype. [[Lemierre's syndrome]] is initiated by an infection of the head and neck region. During the primary infection, ''[[Fusobacterium necrophorum]]'' colonizes the infection site and the infection spreads to the parapharyngeal space. The bacteria then invade the peritonsillar blood vessels where they can spread to the [[internal jugular vein]]. In this vein, the bacteria cause the formation of a [[thrombus]] containing these bacteria.<ref name=abc> Lemierre Syndrome. Wikipedia. https://en.wikipedia.org/wiki/Lemierre%27s_syndrome#Pathophysiology Accessed on October 19, 2015</ref> The pathogenesis of pelvic vein suppurative thrombophlebitis is thought to include injury to the intima of the pelvic vein caused by a spreading uterine infection, [[bacteremia]], and [[endotoxin]]s, which can also occur secondary to the trauma of delivery or surgery.<ref name="pmid17485796">{{cite journal| author=Garcia J, Aboujaoude R, Apuzzio J, Alvarez JR| title=Septic pelvic thrombophlebitis: diagnosis and management. | journal=Infect Dis Obstet Gynecol | year= 2006 | volume= 2006 | issue= | pages= 15614 | pmid=17485796 | doi=10.1155/IDOG/2006/15614 | pmc=PMC1581461 | http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17485796 }} </ref> Pylephlebitis is due to an abdominal infection that drains into the portal venous system. The most commonly isolated organism is ''[[Bacteroides fragilis]]'', which facilitates [[coagulation]] via the capsular and surface components. Capsular polysaccharides activate [[macrophage]]s therefore initiating the clotting cascade while the surface component accelerates [[fibrin]] cross-linking.<ref name="pmid23882407">{{cite journal| author=Wong K, Weisman DS, Patrice KA| title=Pylephlebitis: a rare complication of an intra-abdominal infection. | journal=J Community Hosp Intern Med Perspect | year= 2013 | volume= 3 | issue= 2 | pages= | pmid=23882407 | doi=10.3402/jchimp.v3i2.20732 | pmc=PMC3716219 | http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23882407 }} </ref> | |||
==Pathophysiology== | ==Pathophysiology== | ||
=== | ===Lemierre syndrome=== | ||
Lemierre's syndrome is initiated by an infection of the head and neck region. During the primary infection, ''[[Fusobacterium necrophorum]]'' colonizes the infection site and the infection spreads to the parapharyngeal space. The bacteria then invade the peritonsillar blood vessels where they can spread to the [[internal jugular vein]]. In this vein, the bacteria cause the formation of a [[thrombus]] containing these bacteria. Furthermore, the [[internal jugular vein]] becomes inflamed. This septic [[thrombophlebitis]] can give rise to septic [[Septic embolism|microemboli]] that disseminate to other parts of the body where they can form abscesses and septic infarctions. The first [[capillary|capillaries]] that the emboli encounter where they can nestle themselves are the pulmonary capillaries. As a consequence, the most frequently involved site of septic metastases are the lungs, followed by the joints (knee, hip, [[sternoclavicular articulation|sternoclavicular joint]], shoulder and elbow). In the lungs, the bacteria cause abscesses, nodulary and cavitary lesions. Pleural effusion is often present. Other sites involved in septic metastasis and abscess formation are the muscles and soft tissues, liver, spleen, kidneys and nervous system (intracranial abscesses, meningitis). Production of bacterial toxins such as [[lipopolysaccharide]] leads to secretion of [[cytokines]] by white blood cells which then both lead to symptoms of [[sepsis]]. ''[[Fusobacterium necrophorum]]'' produces [[hemagglutinin]] which causes platelet aggregation that can lead to [[diffuse intravascular coagulation]] and [[thrombocytopenia]].<ref name=abc> Lemierre Syndrome. Wikipedia. https://en.wikipedia.org/wiki/Lemierre%27s_syndrome#Pathophysiology Accessed on October 19, 2015</ref> | |||
===Pelvic Thrombophlebitis=== | |||
The pathogenesis of pelvic vein suppurative thrombophlebitis is thought to include injury to the intima of the pelvic vein caused by a spreading uterine infection, bacteremia, and endotoxins, which can also occur secondary to the trauma of delivery or surgery. In this setting, Virchow’s triad is completed due to the contribution of pregnancy as a well-known hypercoagulable state, and the reduction of blood flow in dilated uterine and ovarian veins during the postpartum period which causes venous stasis.<ref name="pmid17485796">{{cite journal| author=Garcia J, Aboujaoude R, Apuzzio J, Alvarez JR| title=Septic pelvic thrombophlebitis: diagnosis and management. | journal=Infect Dis Obstet Gynecol | year= 2006 | volume= 2006 | issue= | pages= 15614 | pmid=17485796 | doi=10.1155/IDOG/2006/15614 | pmc=PMC1581461 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17485796 }} </ref> [[Pelvis|Pelvic]] [[infection]] leads to infection of the [[vein]] wall and intimal damage, leading to [[Thrombogenicity|thrombogenesis]]. The [[clot]] is then invaded by [[microorganism]]s.<ref> Septic pelvic thrombophlebitis. Wikipedia. https://en.wikipedia.org/wiki/Septic_pelvic_thrombophlebitis Accessed on October 19, 2015</ref> | |||
===Pylephlebitis=== | |||
Pylephlebitis is due to an abdominal infection that drains into the portal venous system. The most commonly isolated organism is ''[[Bacteroides fragilis]]'', which facilitates [[coagulation]] via the capsular and surface components. Capsular polysaccharides activate [[macrophage]]s therefore initiating the clotting cascade while the surface component accelerates [[fibrin]] cross-linking.<ref name="pmid23882407">{{cite journal| author=Wong K, Weisman DS, Patrice KA| title=Pylephlebitis: a rare complication of an intra-abdominal infection. | journal=J Community Hosp Intern Med Perspect | year= 2013 | volume= 3 | issue= 2 | pages= | pmid=23882407 | doi=10.3402/jchimp.v3i2.20732 | pmc=PMC3716219 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23882407 }} </ref> | |||
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==References== | ==References== | ||
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[[Category:Emergency medicine]] | [[Category:Emergency medicine]] | ||
[[Category:Disease]] | [[Category:Disease]] | ||
Latest revision as of 00:21, 30 July 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Maliha Shakil, M.D. [2]
Overview
The pathophysiology of suppurative thrombophlebitis depends on the subtype. Lemierre's syndrome is initiated by an infection of the head and neck region. During the primary infection, Fusobacterium necrophorum colonizes the infection site and the infection spreads to the parapharyngeal space. The bacteria then invade the peritonsillar blood vessels where they can spread to the internal jugular vein. In this vein, the bacteria cause the formation of a thrombus containing these bacteria.[1] The pathogenesis of pelvic vein suppurative thrombophlebitis is thought to include injury to the intima of the pelvic vein caused by a spreading uterine infection, bacteremia, and endotoxins, which can also occur secondary to the trauma of delivery or surgery.[2] Pylephlebitis is due to an abdominal infection that drains into the portal venous system. The most commonly isolated organism is Bacteroides fragilis, which facilitates coagulation via the capsular and surface components. Capsular polysaccharides activate macrophages therefore initiating the clotting cascade while the surface component accelerates fibrin cross-linking.[3]
Pathophysiology
Lemierre syndrome
Lemierre's syndrome is initiated by an infection of the head and neck region. During the primary infection, Fusobacterium necrophorum colonizes the infection site and the infection spreads to the parapharyngeal space. The bacteria then invade the peritonsillar blood vessels where they can spread to the internal jugular vein. In this vein, the bacteria cause the formation of a thrombus containing these bacteria. Furthermore, the internal jugular vein becomes inflamed. This septic thrombophlebitis can give rise to septic microemboli that disseminate to other parts of the body where they can form abscesses and septic infarctions. The first capillaries that the emboli encounter where they can nestle themselves are the pulmonary capillaries. As a consequence, the most frequently involved site of septic metastases are the lungs, followed by the joints (knee, hip, sternoclavicular joint, shoulder and elbow). In the lungs, the bacteria cause abscesses, nodulary and cavitary lesions. Pleural effusion is often present. Other sites involved in septic metastasis and abscess formation are the muscles and soft tissues, liver, spleen, kidneys and nervous system (intracranial abscesses, meningitis). Production of bacterial toxins such as lipopolysaccharide leads to secretion of cytokines by white blood cells which then both lead to symptoms of sepsis. Fusobacterium necrophorum produces hemagglutinin which causes platelet aggregation that can lead to diffuse intravascular coagulation and thrombocytopenia.[1]
Pelvic Thrombophlebitis
The pathogenesis of pelvic vein suppurative thrombophlebitis is thought to include injury to the intima of the pelvic vein caused by a spreading uterine infection, bacteremia, and endotoxins, which can also occur secondary to the trauma of delivery or surgery. In this setting, Virchow’s triad is completed due to the contribution of pregnancy as a well-known hypercoagulable state, and the reduction of blood flow in dilated uterine and ovarian veins during the postpartum period which causes venous stasis.[2] Pelvic infection leads to infection of the vein wall and intimal damage, leading to thrombogenesis. The clot is then invaded by microorganisms.[4]
Pylephlebitis
Pylephlebitis is due to an abdominal infection that drains into the portal venous system. The most commonly isolated organism is Bacteroides fragilis, which facilitates coagulation via the capsular and surface components. Capsular polysaccharides activate macrophages therefore initiating the clotting cascade while the surface component accelerates fibrin cross-linking.[3]
References
- ↑ 1.0 1.1 Lemierre Syndrome. Wikipedia. https://en.wikipedia.org/wiki/Lemierre%27s_syndrome#Pathophysiology Accessed on October 19, 2015
- ↑ 2.0 2.1 Garcia J, Aboujaoude R, Apuzzio J, Alvarez JR (2006). "Septic pelvic thrombophlebitis: diagnosis and management". Infect Dis Obstet Gynecol. 2006: 15614. doi:10.1155/IDOG/2006/15614. PMC 1581461. PMID 17485796. Unknown parameter
|http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=ignored (help) - ↑ 3.0 3.1 Wong K, Weisman DS, Patrice KA (2013). "Pylephlebitis: a rare complication of an intra-abdominal infection". J Community Hosp Intern Med Perspect. 3 (2). doi:10.3402/jchimp.v3i2.20732. PMC 3716219. PMID 23882407. Unknown parameter
|http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=ignored (help) - ↑ Septic pelvic thrombophlebitis. Wikipedia. https://en.wikipedia.org/wiki/Septic_pelvic_thrombophlebitis Accessed on October 19, 2015