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==Overview== | ==Overview== | ||
==Pathophysiology== | The process leading to the formation of [[empyema]] involves migration of organisms into the pleural cavity. Lung parenchymal infection stimulates local pleural immune activation, [[neutrophil]] migration and release of inflammatory cellular components and toxic oxygen species, such as [[IL-6]], [[IL-8]] and [[tumour necrosis factor]] (TNF)-α.<ref name="pmid8144895" /><ref name="pmid1416405" /><ref name="pmid9387973" /> | ||
These mediators promotes endothelial injury resulting in increased pleural membrane permeability and increased osmotic pressure.<ref name="pmid2480911" /> With persistent inflammation, increased permeability of vascular and mesothelial membranes results in increased plasma leakage into the pleural cavity. Coagulation cascade when activated within the pleural cavity contributes to the development of a “fibrinopurulent” or “complicated” [[parapneumonic effusion]]. Fibrin is deposited over the pleural surfaces with fibrinous septae producing loculated effusions.<ref name="pmid12953144">{{cite journal| author=Mohammed KA, Nasreen N, Hardwick J, Van Horn RD, Sanders KL, Antony VB| title=Mycobacteria induces pleural mesothelial permeability by down-regulating beta-catenin expression. | journal=Lung | year= 2003 | volume= 181 | issue= 2 | pages= 57-66 | pmid=12953144 | doi=10.1007/s00408-003-1006-1 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12953144 }} </ref><ref name="pmid11404254">{{cite journal| author=Mohammed KA, Nasreen N, Hardwick J, Logie CS, Patterson CE, Antony VB| title=Bacterial induction of pleural mesothelial monolayer barrier dysfunction. | journal=Am J Physiol Lung Cell Mol Physiol | year= 2001 | volume= 281 | issue= 1 | pages= L119-25 | pmid=11404254 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11404254 }} </ref> | |||
==Pathophysiology == | |||
===Pathogenesis=== | ===Pathogenesis=== | ||
The process leading to the formation of empyema involves migration of organisms into the pleural cavity. This may be via direct extension/contiguous route. Lung parenchymal infection stimulates local pleural immune activation, neutrophil migration and release of inflammatory cellular components and toxic oxygen species, such as IL-6, IL-8 and tumour necrosis factor (TNF)-α.<ref name="pmid8144895">{{cite journal| author=Broaddus VC, Boylan AM, Hoeffel JM, Kim KJ, Sadick M, Chuntharapai A et al.| title=Neutralization of IL-8 inhibits neutrophil influx in a rabbit model of endotoxin-induced pleurisy. | journal=J Immunol | year= 1994 | volume= 152 | issue= 6 | pages= 2960-7 | pmid=8144895 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8144895 }} </ref><ref name="pmid1416405">{{cite journal| author=Broaddus VC, Hébert CA, Vitangcol RV, Hoeffel JM, Bernstein MS, Boylan AM| title=Interleukin-8 is a major neutrophil chemotactic factor in pleural liquid of patients with empyema. | journal=Am Rev Respir Dis | year= 1992 | volume= 146 | issue= 4 | pages= 825-30 | pmid=1416405 | doi=10.1164/ajrccm/146.4.825 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1416405 }} </ref><ref name="pmid9387973">{{cite journal| author=Kroegel C, Antony VB| title=Immunobiology of pleural inflammation: potential implications for pathogenesis, diagnosis and therapy. | journal=Eur Respir J | year= 1997 | volume= 10 | issue= 10 | pages= 2411-8 | pmid=9387973 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9387973 }} </ref> | The process leading to the formation of [[empyema]] involves migration of organisms into the pleural cavity. This may be via direct extension/contiguous route. Lung parenchymal infection stimulates local [[pleural]] immune activation, [[neutrophil]] migration and release of inflammatory cellular components and toxic oxygen species, such as [[IL-6]], [[IL-8]] and [[tumour necrosis factor]] (TNF)-α.<ref name="pmid8144895">{{cite journal| author=Broaddus VC, Boylan AM, Hoeffel JM, Kim KJ, Sadick M, Chuntharapai A et al.| title=Neutralization of IL-8 inhibits neutrophil influx in a rabbit model of endotoxin-induced pleurisy. | journal=J Immunol | year= 1994 | volume= 152 | issue= 6 | pages= 2960-7 | pmid=8144895 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8144895 }} </ref><ref name="pmid1416405">{{cite journal| author=Broaddus VC, Hébert CA, Vitangcol RV, Hoeffel JM, Bernstein MS, Boylan AM| title=Interleukin-8 is a major neutrophil chemotactic factor in pleural liquid of patients with empyema. | journal=Am Rev Respir Dis | year= 1992 | volume= 146 | issue= 4 | pages= 825-30 | pmid=1416405 | doi=10.1164/ajrccm/146.4.825 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1416405 }} </ref><ref name="pmid9387973">{{cite journal| author=Kroegel C, Antony VB| title=Immunobiology of pleural inflammation: potential implications for pathogenesis, diagnosis and therapy. | journal=Eur Respir J | year= 1997 | volume= 10 | issue= 10 | pages= 2411-8 | pmid=9387973 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9387973 }} </ref> | ||
These mediators promotes endothelial injury resulting in increased pleural membrane permeability and increased osmotic pressure.<ref name="pmid2480911">{{cite journal| author=Strange C, Tomlinson JR, Wilson C, Harley R, Miller KS, Sahn SA| title=The histology of experimental pleural injury with tetracycline, empyema, and carrageenan. | journal=Exp Mol Pathol | year= 1989 | volume= 51 | issue= 3 | pages= 205-19 | pmid=2480911 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2480911 }} </ref> The resultant empyema may spontaneously burrowed through the parietal pleura into the chest wall to form a subcutaneous abscess that may eventually rupture through the skin leading to formation of empyema necessitans.<ref name="pmid17301589">{{cite journal| author=Ahmed SI, Gripaldo RE, Alao OA| title=Empyema necessitans in the setting of pneumonia and parapneumonic effusion. | journal=Am J Med Sci | year= 2007 | volume= 333 | issue= 2 | pages= 106-8 | pmid=17301589 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17301589 }} </ref> | These mediators promotes [[endothelial]] injury resulting in increased pleural membrane permeability and increased [[osmotic pressure]].<ref name="pmid2480911">{{cite journal| author=Strange C, Tomlinson JR, Wilson C, Harley R, Miller KS, Sahn SA| title=The histology of experimental pleural injury with tetracycline, empyema, and carrageenan. | journal=Exp Mol Pathol | year= 1989 | volume= 51 | issue= 3 | pages= 205-19 | pmid=2480911 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2480911 }} </ref> The resultant empyema may spontaneously burrowed through the parietal pleura into the chest wall to form a [[subcutaneous]] [[abscess]] that may eventually rupture through the skin leading to formation of empyema necessitans.<ref name="pmid17301589">{{cite journal| author=Ahmed SI, Gripaldo RE, Alao OA| title=Empyema necessitans in the setting of pneumonia and parapneumonic effusion. | journal=Am J Med Sci | year= 2007 | volume= 333 | issue= 2 | pages= 106-8 | pmid=17301589 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17301589 }} </ref> Mesothelial cells release TNF-α and concurrently antifibrinolytic mediator function is enhance, example [[plasminogen]] activator inhibitor-1 and -2<ref name="pmid2064128">{{cite journal| author=Idell S, Girard W, Koenig KB, McLarty J, Fair DS| title=Abnormalities of pathways of fibrin turnover in the human pleural space. | journal=Am Rev Respir Dis | year= 1991 | volume= 144 | issue= 1 | pages= 187-94 | pmid=2064128 | doi=10.1164/ajrccm/144.1.187 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2064128 }} </ref>. | ||
Mycobacteria bacille Calmette–Guerin infection of pleural cells lead to enhanced [[VEGF]] release.<ref name="pmid12953144" /> Mycobacteria bacille Calmette–Guerin ([[BCG]]) and [[Staphylococcus aureus|S. aureus]] infections increase permeability across the mesothelial membrane, partly via [[downregulation]] of [[β-catenin]]. <ref name="pmid12953144" /><ref name="pmid11404254" /> | |||
=== Genetics === | |||
S. aureus infection of the pleura have been found to result in pleural mesothelial cells expression of early response genes c-fos and c-jun, followed by the expression of pro-apoptotic genes Bak and Bad during later stage of infection.<ref name="pmid17929089">{{cite journal| author=Mohammed KA, Nasreen N, Antony VB| title=Bacterial induction of early response genes and activation of proapoptotic factors in pleural mesothelial cells. | journal=Lung | year= 2007 | volume= 185 | issue= 6 | pages= 355-65 | pmid=17929089 | doi=10.1007/s00408-007-9046-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17929089 }} </ref> This results in apoptosis of [[mesothelial tissue]] and impaired membrane integrity, which may contribute to loss of the normal [[fibrinolytic]] function of the pleura. | |||
===Microscopic Pathology=== | |||
=== | With persistent inflammation, increased permeability of vascular and [[mesothelial]] membranes results in increased plasma leakage into the pleural cavity. Coagulation cascade when activated within the pleural cavity contributes to the development of a “fibrinopurulent” or “complicated” [[parapneumonic effusion]]. Fibrin is deposited over the pleural surfaces with [[fibrinous]] septae producing loculated effusions.<ref name="pmid12953144" /><ref name="pmid11404254">{{cite journal| author=Mohammed KA, Nasreen N, Hardwick J, Logie CS, Patterson CE, Antony VB| title=Bacterial induction of pleural mesothelial monolayer barrier dysfunction. | journal=Am J Physiol Lung Cell Mol Physiol | year= 2001 | volume= 281 | issue= 1 | pages= L119-25 | pmid=11404254 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11404254 }} </ref> | ||
==References== | ==References== | ||
Latest revision as of 17:28, 16 January 2017
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Empyema Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]
Overview
The process leading to the formation of empyema involves migration of organisms into the pleural cavity. Lung parenchymal infection stimulates local pleural immune activation, neutrophil migration and release of inflammatory cellular components and toxic oxygen species, such as IL-6, IL-8 and tumour necrosis factor (TNF)-α.[1][2][3] These mediators promotes endothelial injury resulting in increased pleural membrane permeability and increased osmotic pressure.[4] With persistent inflammation, increased permeability of vascular and mesothelial membranes results in increased plasma leakage into the pleural cavity. Coagulation cascade when activated within the pleural cavity contributes to the development of a “fibrinopurulent” or “complicated” parapneumonic effusion. Fibrin is deposited over the pleural surfaces with fibrinous septae producing loculated effusions.[5][6]
Pathophysiology
Pathogenesis
The process leading to the formation of empyema involves migration of organisms into the pleural cavity. This may be via direct extension/contiguous route. Lung parenchymal infection stimulates local pleural immune activation, neutrophil migration and release of inflammatory cellular components and toxic oxygen species, such as IL-6, IL-8 and tumour necrosis factor (TNF)-α.[1][2][3] These mediators promotes endothelial injury resulting in increased pleural membrane permeability and increased osmotic pressure.[4] The resultant empyema may spontaneously burrowed through the parietal pleura into the chest wall to form a subcutaneous abscess that may eventually rupture through the skin leading to formation of empyema necessitans.[7] Mesothelial cells release TNF-α and concurrently antifibrinolytic mediator function is enhance, example plasminogen activator inhibitor-1 and -2[8].
Mycobacteria bacille Calmette–Guerin infection of pleural cells lead to enhanced VEGF release.[5] Mycobacteria bacille Calmette–Guerin (BCG) and S. aureus infections increase permeability across the mesothelial membrane, partly via downregulation of β-catenin. [5][6]
Genetics
S. aureus infection of the pleura have been found to result in pleural mesothelial cells expression of early response genes c-fos and c-jun, followed by the expression of pro-apoptotic genes Bak and Bad during later stage of infection.[9] This results in apoptosis of mesothelial tissue and impaired membrane integrity, which may contribute to loss of the normal fibrinolytic function of the pleura.
Microscopic Pathology
With persistent inflammation, increased permeability of vascular and mesothelial membranes results in increased plasma leakage into the pleural cavity. Coagulation cascade when activated within the pleural cavity contributes to the development of a “fibrinopurulent” or “complicated” parapneumonic effusion. Fibrin is deposited over the pleural surfaces with fibrinous septae producing loculated effusions.[5][6]
References
- ↑ 1.0 1.1 Broaddus VC, Boylan AM, Hoeffel JM, Kim KJ, Sadick M, Chuntharapai A; et al. (1994). "Neutralization of IL-8 inhibits neutrophil influx in a rabbit model of endotoxin-induced pleurisy". J Immunol. 152 (6): 2960–7. PMID 8144895.
- ↑ 2.0 2.1 Broaddus VC, Hébert CA, Vitangcol RV, Hoeffel JM, Bernstein MS, Boylan AM (1992). "Interleukin-8 is a major neutrophil chemotactic factor in pleural liquid of patients with empyema". Am Rev Respir Dis. 146 (4): 825–30. doi:10.1164/ajrccm/146.4.825. PMID 1416405.
- ↑ 3.0 3.1 Kroegel C, Antony VB (1997). "Immunobiology of pleural inflammation: potential implications for pathogenesis, diagnosis and therapy". Eur Respir J. 10 (10): 2411–8. PMID 9387973.
- ↑ 4.0 4.1 Strange C, Tomlinson JR, Wilson C, Harley R, Miller KS, Sahn SA (1989). "The histology of experimental pleural injury with tetracycline, empyema, and carrageenan". Exp Mol Pathol. 51 (3): 205–19. PMID 2480911.
- ↑ 5.0 5.1 5.2 5.3 Mohammed KA, Nasreen N, Hardwick J, Van Horn RD, Sanders KL, Antony VB (2003). "Mycobacteria induces pleural mesothelial permeability by down-regulating beta-catenin expression". Lung. 181 (2): 57–66. doi:10.1007/s00408-003-1006-1. PMID 12953144.
- ↑ 6.0 6.1 6.2 Mohammed KA, Nasreen N, Hardwick J, Logie CS, Patterson CE, Antony VB (2001). "Bacterial induction of pleural mesothelial monolayer barrier dysfunction". Am J Physiol Lung Cell Mol Physiol. 281 (1): L119–25. PMID 11404254.
- ↑ Ahmed SI, Gripaldo RE, Alao OA (2007). "Empyema necessitans in the setting of pneumonia and parapneumonic effusion". Am J Med Sci. 333 (2): 106–8. PMID 17301589.
- ↑ Idell S, Girard W, Koenig KB, McLarty J, Fair DS (1991). "Abnormalities of pathways of fibrin turnover in the human pleural space". Am Rev Respir Dis. 144 (1): 187–94. doi:10.1164/ajrccm/144.1.187. PMID 2064128.
- ↑ Mohammed KA, Nasreen N, Antony VB (2007). "Bacterial induction of early response genes and activation of proapoptotic factors in pleural mesothelial cells". Lung. 185 (6): 355–65. doi:10.1007/s00408-007-9046-6. PMID 17929089.