Objective:To identify the impact of clindamycin use on mortality and amputation rates in patients with necrotizing fasciitis.Design:Retrospective review.Setting:Level 1 trauma center, single-center study.Patients/Participants:All patients from 2008 to 2019 with a diagnosis of necrotizing fasciitis. One hundred ninety patients were included in statistical analysis.Intervention:Use of clindamycin in the initial antibiotic regimen in the treatment of necrotizing soft tissue infection.Main Outcome Measurements:Amputation and mortality rates.Results:Patients who received clindamycin had 2.92 times reduced odds of having an amputation when compared with their counterparts, even when American Society of Anesthesiologist scores, comorbidities, smoking, drug use, alcohol consumption, race, ethnicity, sex, and age were controlled for and regardless of other antibiotics started (P = 0.015). There was no significant difference in mortality rate between those patients who did and did not receive clindamycin as part of their initial antibiotic regimen (8.3% vs. 11.6%, respectively; P = 0.453).Conclusion:The use of clindamycin in the initial antibiotic regimen for treatment of NSTI was shown to significantly decrease rates of amputation but not mortality.Level of Evidence:Therapeutic Level III. See Instructions for Authors for a complete description of levels of evidence.
Peripheral artery disease is a matter of global concern that affects 200 million people and is associated with decreased arterial perfusion in the extremities. The most plausible pathomechanism involves the formation of atheromas which subsequently cause occlusive atherosclerosis that impinge blood supply. Atheroma formation involves endothelial dysfunction with an accumulation of LDL (Low-density lipoprotein) that subsequently become oxidized and consumed by macrophages to form foam cells. The foam cells will release factors such as MMPs (Matrix metalloproteinases) and PDGF (platelet derived growth factor) that induce the proliferation and migration of smooth muscle cells, forming atheroma. Furthermore, endothelial cell damage can cause a loss of protective mechanisms, such as a reduction in the release of protective vasodilatory prostaglandins and Nitric Oxide. Atherosclerosis formation also decreases oxygen diffusion to the arterial media, resulting in atrophy in the vessel wall and ischemia. Additionally, chronic transmural inflammation cyclically releases increased MMPs and elastases that expand the arterial wall while degrading the protective collagen.
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