Epidural abscess pathophysiology: Difference between revisions
Jump to navigation
Jump to search
Joao Silva (talk | contribs) |
m (Bot: Removing from Primary care) |
||
| (34 intermediate revisions by 3 users not shown) | |||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{{Epidural abscess}} | {{Epidural abscess}} | ||
{{CMG}} | {{CMG}} {{AE}} {{JS}}; {{AG}} | ||
==Overview== | ==Overview== | ||
Epidural abscess pathophysiology differs based on the location of the [[infection]] and responsible organism. The majority of intracranial epidural abscess cases occur as a complication of cranial surgical procedures and [[sinusitis]].<ref name="pmid15043336">{{cite journal| author=Fountas KN, Duwayri Y, Kapsalaki E, Dimopoulos VG, Johnston KW, Peppard SB et al.| title=Epidural intracranial abscess as a complication of frontal sinusitis: case report and review of the literature. | journal=South Med J | year= 2004 | volume= 97 | issue= 3 | pages= 279-82; quiz 283 | pmid=15043336 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15043336 }} </ref> The majority of spinal epidural abscess cases occur as a result of spinal instrumentation, vascular access, and [[IV drug use]].<ref name="pmid24340840">{{cite journal| author=Strauss I, Carmi-Oren N, Hassner A, Shapiro M, Giladi M, Lidar Z| title=Spinal epidural abscess: in search of reasons for an increased incidence. | journal=Isr Med Assoc J | year= 2013 | volume= 15 | issue= 9 | pages= 493-6 | pmid=24340840 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24340840 }} </ref> | |||
==Pathophysiology== | ==Pathophysiology== | ||
Epidural abscess pathophysiology differs based on the location of the [[infection]] and responsible organism. | |||
===Intracranial epidural abscess=== | |||
Intracranial epidural abscess is the result of sequelae of cranial surgical procedures, [[sinusitis]], and [[mastoiditis]]. Cranial [[dura mater]] is adherent to the inner table of the [[skull]] in the [[epidural space]]. This virtual space can become a real space by increasing pressure from a liquid, such as [[pus]] or [[blood]], or a solid mass, such as a [[tumor]]. A tight adherence contributes to the slow progression and typical round-shape appearance of the [[abscess]]. Because the [[dura mater]] is tightly attached to the [[skull]] in the [[foramen magnum]], intracranial epidural abscesses are usually restricted to the [[cranial cavity]]. On the periphery of the [[pus]] collection is a wall of [[inflammation]], which may calcify and is identifiable in imaging studies.<ref name="pmid15043336">{{cite journal| author=Fountas KN, Duwayri Y, Kapsalaki E, Dimopoulos VG, Johnston KW, Peppard SB et al.| title=Epidural intracranial abscess as a complication of frontal sinusitis: case report and review of the literature. | journal=South Med J | year= 2004 | volume= 97 | issue= 3 | pages= 279-82; quiz 283 | pmid=15043336 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15043336 }} </ref><ref name="pmid14519222">{{cite journal| author=Heran NS, Steinbok P, Cochrane DD| title=Conservative neurosurgical management of intracranial epidural abscesses in children. | journal=Neurosurgery | year= 2003 | volume= 53 | issue= 4 | pages= 893-7; discussion 897-8 | pmid=14519222 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14519222 }} </ref> | |||
Pathophysiological pathways for the progression of intracranial epidural abscess include:<ref name="pmid15043336">{{cite journal| author=Fountas KN, Duwayri Y, Kapsalaki E, Dimopoulos VG, Johnston KW, Peppard SB et al.| title=Epidural intracranial abscess as a complication of frontal sinusitis: case report and review of the literature. | journal=South Med J | year= 2004 | volume= 97 | issue= 3 | pages= 279-82; quiz 283 | pmid=15043336 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15043336 }} </ref> | |||
*[[Thrombophlebitis]] of [[diploic veins]], facilitated by the valveless nature of these vessels, allowing for retrograde flow of [[bacteria]] | |||
* | *Direct extension from [[osteomyelitis]] of the [[skull]] | ||
** | *[[Congenital defect]], such as communication between [[sinuses]] and areas of lesion | ||
** | *[[Osteomyelitis]] of the [[skull]] | ||
* | *Extension of [[infection]] from [[otitis]] or [[mastoiditis]] | ||
*Direct inoculation, during a [[surgical procedure]] or [[trauma]] | |||
*Remote [[infection]] sites, through [[haematological]] spread, such as [[respiratory tract infection|respiratory]] and [[urinary tract infections]] | |||
===Spinal Epidural Abscess=== | ===Spinal Epidural Abscess=== | ||
Unlike the | The majority of spinal epidural abscess cases occur as a result of spinal instrumentation, vascular access, and [[IV drug use]].<ref name="pmid24340840">{{cite journal| author=Strauss I, Carmi-Oren N, Hassner A, Shapiro M, Giladi M, Lidar Z| title=Spinal epidural abscess: in search of reasons for an increased incidence. | journal=Isr Med Assoc J | year= 2013 | volume= 15 | issue= 9 | pages= 493-6 | pmid=24340840 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24340840 }} </ref> Unlike the virtual intracranial epidural space, the spinal epidural space is a real space; more specifically, the sequelae occurs in the areas posterior and lateral to the [[spinal cord]], extending down the length of the [[spinal canal]]. This epidural space, which is larger at the [[sacral]] region, contains [[fat]], [[arteries]] and [[venous plexus]]. Because the [[dura mater]] is more adherent to the bony surface of the [[vertebral bodies]], from the [[foramen magnum]] down to the level of L1, the majority of spinal epidural abscesses are located posteriorly, extending to multiple levels.<ref name="pmid3589332">{{cite journal| author=Danner RL, Hartman BJ| title=Update on spinal epidural abscess: 35 cases and review of the literature. | journal=Rev Infect Dis | year= 1987 | volume= 9 | issue= 2 | pages= 265-74 | pmid=3589332 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3589332 }} </ref><ref name="pmid1359381">{{cite journal| author=Darouiche RO, Hamill RJ, Greenberg SB, Weathers SW, Musher DM| title=Bacterial spinal epidural abscess. Review of 43 cases and literature survey. | journal=Medicine (Baltimore) | year= 1992 | volume= 71 | issue= 6 | pages= 369-85 | pmid=1359381 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1359381 }} </ref><ref name="pmid10664371">{{cite journal| author=Akalan N, Ozgen T| title=Infection as a cause of spinal cord compression: a review of 36 spinal epidural abscess cases. | journal=Acta Neurochir (Wien) | year= 2000 | volume= 142 | issue= 1 | pages= 17-23 | pmid=10664371 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10664371 }} </ref> | ||
Pathophysiological pathways for the progression of intracranial epidural abscess include:<ref name="Darouiche2006">{{cite journal|last1=Darouiche|first1=Rabih O.|title=Spinal Epidural Abscess|journal=New England Journal of Medicine|volume=355|issue=19|year=2006|pages=2012–2020|issn=0028-4793|doi=10.1056/NEJMra055111}}</ref> | |||
[[ | *[[neurosurgery|Neurosurgical]] procedures | ||
* | *[[Trauma]] | ||
* | *[[Skin flora]] entering open wounds | ||
**''[[Staphylococcus epidermidis]]'' | |||
* | **''[[Escherichia coli]]'' | ||
**''[[Pseudomonas aeruginosa]]'' | |||
* | **''[[Haemophilus influenzae]]'' | ||
* | **''[[Klebsiella pneumoniae]]'' | ||
As the [[inflammation]] progresses, the extension of the [[abscess]] also increases, | **''[[Listeria monocytogenes]]'' | ||
As the [[inflammation]] progresses, the extension of the [[abscess]] also increases, on average by 3 to 5 [[spinal cord]] segments. However, the degree of damage, associated neurological symptoms, and sequelae are not directly related to the extension of the [[abscess]], as even small abscesses may cause severe [[sequelae]]. The [[abscess]] may contain [[pus]], often observed in acute cases, or [[granulation tissue]], often observed following the surgical intervention. | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
[[Category:Disease]] | [[Category:Disease]] | ||
[[Category:Neurology]] | [[Category:Neurology]] | ||
Latest revision as of 21:36, 29 July 2020
|
Epidural abscess Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Epidural abscess pathophysiology On the Web |
|
American Roentgen Ray Society Images of Epidural abscess pathophysiology |
|
Risk calculators and risk factors for Epidural abscess pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]; Anthony Gallo, B.S. [3]
Overview
Epidural abscess pathophysiology differs based on the location of the infection and responsible organism. The majority of intracranial epidural abscess cases occur as a complication of cranial surgical procedures and sinusitis.[1] The majority of spinal epidural abscess cases occur as a result of spinal instrumentation, vascular access, and IV drug use.[2]
Pathophysiology
Epidural abscess pathophysiology differs based on the location of the infection and responsible organism.
Intracranial epidural abscess
Intracranial epidural abscess is the result of sequelae of cranial surgical procedures, sinusitis, and mastoiditis. Cranial dura mater is adherent to the inner table of the skull in the epidural space. This virtual space can become a real space by increasing pressure from a liquid, such as pus or blood, or a solid mass, such as a tumor. A tight adherence contributes to the slow progression and typical round-shape appearance of the abscess. Because the dura mater is tightly attached to the skull in the foramen magnum, intracranial epidural abscesses are usually restricted to the cranial cavity. On the periphery of the pus collection is a wall of inflammation, which may calcify and is identifiable in imaging studies.[1][3]
Pathophysiological pathways for the progression of intracranial epidural abscess include:[1]
- Thrombophlebitis of diploic veins, facilitated by the valveless nature of these vessels, allowing for retrograde flow of bacteria
- Direct extension from osteomyelitis of the skull
- Congenital defect, such as communication between sinuses and areas of lesion
- Osteomyelitis of the skull
- Extension of infection from otitis or mastoiditis
- Direct inoculation, during a surgical procedure or trauma
- Remote infection sites, through haematological spread, such as respiratory and urinary tract infections
Spinal Epidural Abscess
The majority of spinal epidural abscess cases occur as a result of spinal instrumentation, vascular access, and IV drug use.[2] Unlike the virtual intracranial epidural space, the spinal epidural space is a real space; more specifically, the sequelae occurs in the areas posterior and lateral to the spinal cord, extending down the length of the spinal canal. This epidural space, which is larger at the sacral region, contains fat, arteries and venous plexus. Because the dura mater is more adherent to the bony surface of the vertebral bodies, from the foramen magnum down to the level of L1, the majority of spinal epidural abscesses are located posteriorly, extending to multiple levels.[4][5][6]
Pathophysiological pathways for the progression of intracranial epidural abscess include:[7]
- Neurosurgical procedures
- Trauma
- Skin flora entering open wounds
As the inflammation progresses, the extension of the abscess also increases, on average by 3 to 5 spinal cord segments. However, the degree of damage, associated neurological symptoms, and sequelae are not directly related to the extension of the abscess, as even small abscesses may cause severe sequelae. The abscess may contain pus, often observed in acute cases, or granulation tissue, often observed following the surgical intervention.
References
- ↑ 1.0 1.1 1.2 Fountas KN, Duwayri Y, Kapsalaki E, Dimopoulos VG, Johnston KW, Peppard SB; et al. (2004). "Epidural intracranial abscess as a complication of frontal sinusitis: case report and review of the literature". South Med J. 97 (3): 279–82, quiz 283. PMID 15043336.
- ↑ 2.0 2.1 Strauss I, Carmi-Oren N, Hassner A, Shapiro M, Giladi M, Lidar Z (2013). "Spinal epidural abscess: in search of reasons for an increased incidence". Isr Med Assoc J. 15 (9): 493–6. PMID 24340840.
- ↑ Heran NS, Steinbok P, Cochrane DD (2003). "Conservative neurosurgical management of intracranial epidural abscesses in children". Neurosurgery. 53 (4): 893–7, discussion 897-8. PMID 14519222.
- ↑ Danner RL, Hartman BJ (1987). "Update on spinal epidural abscess: 35 cases and review of the literature". Rev Infect Dis. 9 (2): 265–74. PMID 3589332.
- ↑ Darouiche RO, Hamill RJ, Greenberg SB, Weathers SW, Musher DM (1992). "Bacterial spinal epidural abscess. Review of 43 cases and literature survey". Medicine (Baltimore). 71 (6): 369–85. PMID 1359381.
- ↑ Akalan N, Ozgen T (2000). "Infection as a cause of spinal cord compression: a review of 36 spinal epidural abscess cases". Acta Neurochir (Wien). 142 (1): 17–23. PMID 10664371.
- ↑ Darouiche, Rabih O. (2006). "Spinal Epidural Abscess". New England Journal of Medicine. 355 (19): 2012–2020. doi:10.1056/NEJMra055111. ISSN 0028-4793.