Suppurative thrombophlebitis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Lemierre syndrome=== | ===Lemierre syndrome=== | ||
Lemierre's syndrome is initiated by an infection of the head and neck region. During the primary infection, ''F. 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]] | Lemierre's syndrome is initiated by an infection of the head and neck region. During the primary infection, ''F. 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]]. ''F. necrophorum'' produces [[hemagglutinin]] which causes platelet aggregation that can lead to [[diffuse intravascular coagulation]] and [[thrombocytopenia]]. | ||
Production of bacterial toxins such as [[lipopolysaccharide]] leads to secretion of [[cytokines]] by white blood cells which then both lead to symptoms of [[sepsis]]. ''F. necrophorum'' produces [[hemagglutinin]] which causes platelet aggregation that can lead to [[diffuse intravascular coagulation]] and [[thrombocytopenia]]. | |||
==References== | ==References== | ||
Revision as of 15:55, 19 October 2015
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Lemierre syndrome
Lemierre's syndrome is initiated by an infection of the head and neck region. During the primary infection, F. 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. F. necrophorum produces hemagglutinin which causes platelet aggregation that can lead to diffuse intravascular coagulation and thrombocytopenia.