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Eloessar flap

The Eloessar flap is a surgical procedure developed by Dr. Leo Eloesser in 1935 at the San Francisco General Hospital.[1] It was originally intended to aide with drainage of tuberculous empyemas, since at the time there were no effective medications to treat tuberculosis. The procedure was used extensively[2] until the development of effective chemotherapy for tuberculosis in the late 1940s and early 1950s.[3] It is still used occasionally for chronic empyemas.[4][5]

Technique

As originally described by Dr. Eloessar, the procedure started with cutting a 2 inch wide, U-shaped flap of skin on the side of the chest wall underneath the axilla and scapula. The section of rib under the top of the flap was also removed. The finger-like skin flap was then inserted into the cavity made in the chest wall and sown into the inner pleural lining of the chest. The edges of the incision are then brought together.[1] The flap allows for 1) passive drainage of the pleural space and 2) negative pressure to develop in the thoracic cavity due to it being easier for air to escape than to enter the chest. The lung can then expand to the chest wall and seal the inner opening of the flap.[3] Other surgeons have subsequently proposed modifications to the procedure.[6]

Modern use

The Eloesser flap is still utilized for patients with chronic empyemas who have not improved despite being treated with antibiotics and first line surgical procedures to remove pus and re-expand the lung such as decortication or video-assisted thoracoscopic surgery.[4] Often they are thought to be too ill for more definitive procedures such as a major thoracotomy or muscle flap transposition.[5] In a recent case series, the most common reasons to need an Eloessar flap were parapneumonic effusions and postresection empyemas, with only 9% done for tuberculosis.[4]

Complications

A downside to the procedure are that a permanent drainage path from the thoracic cavity is made and will need prolonged wound care and dressing changes.[5][4] Complications can also include sepsis.[4]

History

Prior to the development of the Eloessar flap in the 1930s, the main surgical treatments for chronic tuberculous empyema were an open thoracotomy or chest tube drainage. In his original published description of the procedure, Dr. Eloesser wrote that he felt that those options were "unsatisfactory" as he felt they led to secondary infection and death.[1] Another option included removing the infected fluid with a needle through the chest wall (percutaneous drainage) but it often quickly reaccumulated. Dr. Eloessar explained that when developing his procedure he wished to maintain drainage as with a chest tube to allow the lung to re-expand but without the presence of the chest tube that he felt "tends to keep up fever and sepsis."[1]

Finegoldia

Finegoldia are gram positive aerobic cocci of the class clostridia, with finegoldia magna being the type species.[7] Finegoldia magna was formerly known, along with several other gram positive anaerobic cocci (GPACs), as peptostreptococcus magna but was moved into its own genus in 1999.[8][9] The name is in honor of Sydney M. Finegold, an American microbiologist, while magna is latin for large.[7] It is an opportunistic human pathogen that normally colonizes skin and mucous membranes.[10] It is often seen in biofilms on chronic ulcers such as in diabetic foot or decubitus ulcers.[9] Most surveys have found it to be susceptible to penicillins, carbapenems and metronidazole, though resistant strains have been identified.[11] Resistance to clindamycin is common and has been seen in over 10% of isolates in the US.[12][9] One review stated that "The combination of diminished antimicrobial susceptibility, its prevalence, and the described virulence factors gives F. magna a special position among the GPAC."[11]

H37Rv

Tuberculosis strain H37Rv is the most studied strain of tuberculosis in research laboratories.[13] It was first isolated by Dr. Edward R. Baldwin in 1905.[14] The strain came from a 19 year old patient with chronic pulmonary tuberculosis at the Trudeau Sanatorium in Saranac Lake, New York.[15] It was maintained for many years by serial passage of cultures as strain H37 at the Trudeau Sanatorium but was found to have variable virulence based on which medium it was grown on. Strains with different virulence were produced with H37R being grown in acidic media having less virulence and H37S was grown in alkaline media and became more virulent in guinea pigs.[15] The virulent strain was later renamed H37Rv, with R for rough morphology and v for virulent.[14] The strain was used for many laboratory studies and became the standard for tuberculosis. It was later designated as the neotype for the species.[14] It is unclear how related it might be to the original tubercle bacillus that was described by Koch in 1892 when he discovered of the cause of tuberculosis. H37Rv has continued to be the strain of tuberculosis most used in laboratories, and was the first to have its complete genome published in 1998.[16] It is unclear how much H37Rv may have evolved in its more than 100 years in laboratories from strains that infect humans, but its genome is similar to a strain isolated from a 19th century grave in Yorkshire.[17] However it does have some characteristics, such as not causing caseous necrosis in rabbits that are seen in modern clinical isolates.[18]

  1. ^ a b c d ELOESSER, L. (1935-10-01). "An operation for tuberculous empyema". Chest. 1 (8): 8–23. doi:10.1378/chest.1.8.8. ISSN 0012-3692.
  2. ^ Brown, A.Lincoln. "Simple drainage of intrathoracic suppurations". The American Journal of Surgery. 62 (2): 169–184. doi:10.1016/s0002-9610(43)90247-8.
  3. ^ a b Eloesser, Leo. "Of an Operation for Tuberculous Empyema". The Annals of Thoracic Surgery. 8 (4): 355–357. doi:10.1016/s0003-4975(10)66250-9.
  4. ^ a b c d e Thourani, Vinod H; Lancaster, R.Todd; Mansour, Kamal A; Miller, Joseph I. "Twenty-six years of experience with the modified eloesser flap". The Annals of Thoracic Surgery. 76 (2): 401–406. doi:10.1016/s0003-4975(03)00470-3.
  5. ^ a b c Denlinger, Chadrick E. "Eloesser Flap Thoracostomy Window". Operative Techniques in Thoracic and Cardiovascular Surgery. 15 (1): 61–69. doi:10.1053/j.optechstcvs.2010.03.003.
  6. ^ Symbas, Panagiotis N.; Nugent, Jeffrey T.; Abbott, Osier A.; Logan, William D.; Hatcher, Charles R. "Nontuberculous Pleural Empyema in Adults : The Role of a Modified Eloesser Procedure in Its Management". The Annals of Thoracic Surgery. 12 (1): 69–78. doi:10.1016/s0003-4975(10)65095-3.
  7. ^ a b "Finegoldia". www.bacterio.net. Retrieved 2016-01-06.
  8. ^ Murdoch, D. A; Shah, H. N (1999-10-01). "Reclassification of Peptostreptococcus magnus (Prevot 1933) Holdeman and Moore 1972 as Finegoldia magna comb. nov. and Peptostreptococcus micros (Prevot 1933) Smith 1957 as Micromonas micros comb. nov". Anaerobe. 5 (5): 555–559. doi:10.1006/anae.1999.0197.
  9. ^ a b c "Anaerobic Cocci and Anaerobic Gram-Positive Nonsporulating Bacilli". Mandell, Douglas, and Bennett's principles and practice of infectious diseases. ISBN 978-1-4557-4801-3.
  10. ^ de Moreuil, Claire; Héry-Arnaud, Geneviève; David, Charles-Henri; Provost, Bastien; Mondine, Philippe; Alavi, Zarrin; de Saint Martin, Luc; Bezon, Eric; Berre, Rozenn Le (2015-04-01). "Finegoldia magna, not a well-known infectious agent of bacteriemic post-sternotomy mediastinitis". Anaerobe. 32: 32–33. doi:10.1016/j.anaerobe.2014.11.012.
  11. ^ a b Veloo, A. C. M.; Welling, G. W.; Degener, J. E. (2011-03-01). "Antimicrobial Susceptibility of Clinically Relevant Gram-Positive Anaerobic Cocci Collected over a Three-Year Period in the Netherlands". Antimicrobial Agents and Chemotherapy. 55 (3): 1199–1203. doi:10.1128/AAC.01771-09. ISSN 0066-4804. PMC 3067104. PMID 21189338.
  12. ^ Brazier, J. S.; Hall, V.; Morris, T. E.; Gal, M.; Duerden, B. I. (2003-08-01). "Antibiotic susceptibilities of Gram-positive anaerobic cocci: results of a sentinel study in England and Wales". Journal of Antimicrobial Chemotherapy. 52 (2): 224–228. doi:10.1093/jac/dkg316. ISSN 0305-7453. PMID 12837734.
  13. ^ Camus, Jean-Christophe; Médigue, Claudine; Cole, Stewart T.; Pryor, Melinda J. (2002-10-01). "Re-annotation of the genome sequence of Mycobacterium tuberculosis H37Rv". Microbiology. 148 (10): 2967–2973. doi:10.1099/00221287-148-10-2967.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  14. ^ a b c KUBICA, G. P.; KIM, T. H.; DUNBAR, F. P. (1972-04-01). "Designation of Strain H37Rv as the Neotype of Mycobacterium tuberculosis". International Journal of Systematic Bacteriology. 22 (2): 99–106. doi:10.1099/00207713-22-2-99.
  15. ^ a b Steenken, W.; Oatway, W. H.; Petroff, S. A. (1934-09-30). "BIOLOGICAL STUDIES OF THE TUBERCLE BACILLUS : III. DISSOCIATION AND PATHOGENICITY OF THE R AND S VARIANTS OF THE HUMAN TUBERCLE BACILLUS (H(37))". The Journal of Experimental Medicine. 60 (4): 515–540. ISSN 0022-1007. PMC 2132400. PMID 19870319.
  16. ^ Cole, S. T.; Brosch, R.; Parkhill, J.; Garnier, T.; Churcher, C.; Harris, D.; Gordon, S. V.; Eiglmeier, K.; Gas, S. (1998-06-11). "Deciphering the biology of Mycobacterium tuberculosis from the complete genome sequence". Nature. 393 (6685): 537–544. doi:10.1038/31159. ISSN 0028-0836.
  17. ^ Bouwman, Abigail S.; Kennedy, Sandra L.; Müller, Romy; Stephens, Richard H.; Holst, Malin; Caffell, Anwen C.; Roberts, Charlotte A.; Brown, Terence A. (2012-11-06). "Genotype of a historic strain of Mycobacterium tuberculosis". Proceedings of the National Academy of Sciences. 109 (45): 18511–18516. doi:10.1073/pnas.1209444109. ISSN 0027-8424. PMC 3494915. PMID 23091009.
  18. ^ Shammari, Basim Al; Shiomi, Takayuki; Tezera, Liku; Bielecka, Magdalena K.; Workman, Victoria; Sathyamoorthy, Tarangini; Mauri, Francesco; Jayasinghe, Suwan N.; Robertson, Brian D. (2015-08-01). "The Extracellular Matrix Regulates Granuloma Necrosis in Tuberculosis". Journal of Infectious Diseases. 212 (3): 463–473. doi:10.1093/infdis/jiv076. ISSN 0022-1899. PMC 4539912. PMID 25676469.
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