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      Can E-Cigarettes Cause Free Flap Failure? A Case of Arterial Vasospasm Induced by Electronic Cigarettes Following Microsurgical Breast Reconstruction

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      , MD, Mphil, , MD, , MD
      Plastic and Reconstructive Surgery Global Open
      Wolters Kluwer Health

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          Abstract

          Sir: The vasoconstrictive effects of cigarettes is well documented and routinely discussed with patients seeking microsurgical breast reconstruction. It is generally accepted that patients stop smoking 2–4 weeks before the planned reconstruction to avoid vasoconstriction and to prevent issues with wound healing. Although studies have documented the consequences of cigarette smoking on flap failure and wound healing, no prior study has documented the potential consequence of free flap failure after the use of electronic cigarettes (e-cigarette). 1 A 48-year-old woman with right intraductal carcinoma was presented in May 2015 for delayed autologous breast reconstruction. She is a former cigarette smoker who confirmed that she had stopped smoking before scheduling surgery. The patient underwent a bilateral muscle-sparing free transverse rectus abdominis musculocutaneous flap reconstruction without any intraoperative complications. The following morning, the Vioptix Tissue Oximeter (Fremont, Ca) reading on the left breast dropped to 35% with deteriorating clinical examination. Bedside evaluation 20 minutes later revealed a clinically healthy appearing flap with a 77% Vioptix signal (Fig. 1). Transient vasospasm was suspected. On postoperative day 2, the Vioptix reading on the left breast dropped to 3% with progressive flap deterioration. The decision was made to return to the operating room for an exploration. During transport to the operating room, the Vioptix reading returned to baseline; however, the decision to explore the anastomosis was maintained. Exploration revealed widely patient arterial and venous anastomoses without any kinks or twists of the pedicle. Nifedipine (10 mg per os daily) was started for presumed vasospasm. The patient then had an uneventful hospital course and was discharged home on postoperative day 4. It was later revealed to the plastic surgery team by the patient’s mother that the patient had been smoking e-cigarettes until the day of surgery. Fig. 1. Photograph of the patient and corresponding Vioptix readings (left flap is top reading, right flap is bottom reading) when initially called to see patient by nursing staff after a drop in the Vioptix reading to 35% on the left side. Upon examining the patient, her left flap appeared clinically healthy and the Vioptix reading rebounded to 77% spontaneously. E-cigarettes are battery-powered, vaporized nicotine delivery devices introduced into the U.S. in 2007 as a safe alternative to traditional tobacco-based cigarette smoking. 2 The use of e-cigarettes has increased in popularity to more than 6% of the population in the U.S. with nearly one third of current smokers reporting to have ever used e-cigarettes. 3 E-cigarettes are unregulated by the U.S. Food and Drug Administration and can be bought over the counter or online with no limit on the nicotine content. The vascular consequences of smoking traditional cigarettes/cigars are widely published and routinely counseled to patients; however, few providers discuss the use of e-cigarettes. Although e-cigarettes are free from many of the carbon monoxide, carcinogens, and tobacco present in traditional cigarettes/cigars, they contain variable amounts of nicotine that can cause peripheral vasoconstriction and inhibition of endothelial-dependent vasodilation, which can have devastating effects on free flaps. 4 There are few publications about the consequences of e-cigarettes in the plastic surgery literature. 5 This case example will help surgeons to advise patients on the risks of all tobacco products including e-cigarettes during the preoperative workup. DISCLOSURES M.Y.N. is a consultant for LifeCell. The other authors have no financial interest to declare in relation to the content of this article. The Article Processing Charge was paid for by Dr. Nahabedian. PATIENT CONSENT Patient provided consent for the use of her images and there are no patient identifiers in the images used.

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          Wound healing and infection in surgery: the pathophysiological impact of smoking, smoking cessation, and nicotine replacement therapy: a systematic review.

          The aim was to clarify how smoking and nicotine affects wound healing processes and to establish if smoking cessation and nicotine replacement therapy reverse the mechanisms involved. Smoking is a recognized risk factor for healing complications after surgery, but the pathophysiological mechanisms remain largely unknown. Pathophysiological studies addressing smoking and wound healing were identified through electronic databases (PubMed, EMBASE) and by hand-search of articles' bibliography. Of the 1460 citations identified, 325 articles were retained following title and abstract reviews. In total, 177 articles were included and systematically reviewed. Smoking decreases tissue oxygenation and aerobe metabolism temporarily. The inflammatory healing response is attenuated by a reduced inflammatory cell chemotactic responsiveness, migratory function, and oxidative bactericidal mechanisms. In addition, the release of proteolytic enzymes and inhibitors is imbalanced. The proliferative response is impaired by a reduced fibroblast migration and proliferation in addition to a downregulated collagen synthesis and deposition. Smoking cessation restores tissue oxygenation and metabolism rapidly. Inflammatory cell response is reversed in part within 4 weeks, whereas the proliferative response remains impaired. Nicotine does not affect tissue microenvironment, but appears to impair inflammation and stimulate proliferation. Smoking has a transient effect on the tissue microenvironment and a prolonged effect on inflammatory and reparative cell functions leading to delayed healing and complications. Smoking cessation restores the tissue microenvironment rapidly and the inflammatory cellular functions within 4 weeks, but the proliferative response remain impaired. Nicotine and nicotine replacement drugs seem to attenuate inflammation and enhance proliferation but the effect appears to be marginal.
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            Arterial blood nicotine concentration and coronary vasoconstrictive effect of low-nicotine cigarette smoking.

            Low-nicotine cigarettes have been advertised to the public as less harmful to the cardiovascular system. We studied the effects of smoking two low-nicotine cigarettes on arterial and venous blood nicotine levels, hemodynamics, and coronary vascular tone in 12 patients referred for diagnostic coronary arteriography. All were chronic smokers as evidenced by their elevated baseline arterial and venous cotinine blood levels (139 +/- 30 ng/ml and 155 +/- 34 ng/ml, respectively). High-resolution coronary angiograms were evaluated "blindly" before and after smoking. An electronic caliper was used to measure the diameter of disease-free coronary segments of the left anterior descending and circumflex arteries. Arterial nicotine levels rose from 5 +/- 1 ng/ml at baseline to 37 +/- 7 ng/ml (p less than 0.01) after the first cigarette was smoked and to 45 +/- 8 ng/ml (p less than 0.01) after the second cigarette. Venous nicotine levels rose from 8 +/- 2 ng at baseline to 15 +/- 3 ng/ml (p less than 0.05) after the first cigarette and to 20 +/- 3 ng/ml (p less than 0.01) after the second cigarette. After the first cigarette heart rate increased 8 +/- 2 beats/min (p less than 0.003) and double product 1229 +/- 400 beats/min x mm Hg (p less than 0.02). Compared to baseline values, after the second cigarette heart rate increased 9 +/- 1 beats/min (p less than 0.001) and double product 1767 +/- 486 beats/min x mm Hg (p less than 0.01). Systolic, diastolic, and mean blood pressure did not change significantly after either the first or second cigarette.(ABSTRACT TRUNCATED AT 250 WORDS)
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              Electronic cigarettes: have you asked your patients about vaping?

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                Author and article information

                Journal
                Plast Reconstr Surg Glob Open
                Plast Reconstr Surg Glob Open
                GOX
                Plastic and Reconstructive Surgery Global Open
                Wolters Kluwer Health
                2169-7574
                January 2016
                18 January 2016
                : 4
                : 1
                : e596
                Affiliations
                Department of Plastic Surgery, Georgetown University Hospital, Wash., D.C.
                Author notes
                Correspondence to Maurice Y. Nahabedian, MD, Department of Plastic Surgery, Georgetown University Hospital, 3800 Reservoir Road, Washington, DC 20007, drnahabedian@ 123456aol.com
                Article
                00010
                10.1097/GOX.0000000000000576
                4801098
                27104095
                74678ecd-a09a-444d-a691-6f70512bd4bd
                Copyright © 2016 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The American Society of Plastic Surgeons. All rights reserved.

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially.

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