Wound healing in plastic surgery. Associated factors and dermatologic care

 

 

Nº de DOI: 10.34896/RSI.2026.22.65.001

 

 

AUTHORS

1. Edgar Sebastián Arce Jácome. General Practitioner. Affiliated with Hospital Universitario Católico de Cuenca. Graduate of Universidad Católica de Cuenca. Based in Cuenca, Ecuador. https://orcid.org/0009-0005-2864-2974
2. Doménica Gabriela León Tapia. General Practitioner. Affiliated with Hospital Universitario Católico de Cuenca. Graduate of Universidad Católica de Cuenca. Based in Cuenca, Ecuador. https://orcid.org/0009-0009-2610-6210
3.  Lizeth Carolina Aldaz Vargas. General Practitioner. Affiliated with Hospital Provincial General Docente Riobamba. Graduate of Escuela Superior Politécnica de Chimborazo. Based in Riobamba, Ecuador. https://orcid.org/0009-0004-9538-9377
4.  Joaquín Israel Rojas Rodríguez. General Practitioner. Affiliated with Clínica Privada Merced Vida Sana. Graduate of Universidad Técnica del Norte. Based in Riobamba, Ecuador. https://orcid.org/0009-0001-9324-843X
5.  Eliana Lisbet Gaibor Colina. General Practitioner and Specialist in Occupational Health and Safety with a concentration in Occupational Health. Affiliated with Clínica de Diálisis Dialilife S.A. Graduate of Universidad de Guayaquil. Based in Quevedo, Ecuador. https://orcid.org/0009-0009-7859-6960

ABSTRACT

Objective: To synthesise the published evidence on the factors associated with wound healing in plastic surgery and on the contribution of dermatologic care to healing quality and scar outcome.

Methods: A structured web-based literature search, covering records indexed in PubMed and PubMed Central and publisher pages, with bibliographic verification in Crossref, was carried out in May 2026 for peer-reviewed journal articles carrying a digital object identifier (DOI) that addressed the physiology of cutaneous repair, systemic and local risk factors, abnormal scarring and scar management in surgical patients. 36 articles, comprising narrative reviews, a systematic review with meta-analysis, consensus guidelines and clinical and experimental studies, were included and synthesised qualitatively.

Results: Tobacco and nicotine exposure, diabetes with poor glycaemic control, nutritional deficiency, alcohol excess, radiotherapy, chemotherapy and certain drugs were consistently associated with impaired healing, flap compromise, infection and dehiscence. In smokers, flap loss remained significantly more frequent when abstinence lasted only 24 hours after surgery, and fell when abstinence reached one week. Local tension, ischaemia and inflammation drive pathological scars, whose risk is further modulated by genetic and systemic factors. Dermatologic measures include tension-reducing closure, taping, silicone sheeting or gel as first-line prophylaxis, ultraviolet protection, hydration, injected and topical agents and, for keloids, surgery with adjuvant radiotherapy.

Conclusions: Optimal wound healing in plastic surgery depends on early identification and correction of modifiable risk factors and on a structured, evidence-based scar-care pathway delivered jointly by plastic surgeons and dermatologists.

KEY WORDS

Wound healing, plastic surgery, dermatology, hypertrophic scar, keloid, smoking, diabetes mellitus, nutrition, silicone, scar management.

RESUMEN

Objetivo: Sintetizar la evidencia publicada sobre los factores asociados a la cicatrización de heridas en cirugía plástica y sobre la contribución de la atención dermatológica a la calidad de la cicatrización y al resultado final de la cicatriz.

Métodos: En mayo de 2026 se realizó una búsqueda bibliográfica estructurada en línea —abarcando registros indexados en PubMed y PubMed Central, así como sitios web de editoriales, con verificación bibliográfica en Crossref— para identificar artículos de revistas revisadas por pares con identificador de objeto digital (DOI) que abordaran la fisiología de la reparación cutánea, los factores de riesgo sistémicos y locales, la cicatrización anómala y el manejo de cicatrices en pacientes quirúrgicos. Se incluyeron y sintetizaron cualitativamente 36 artículos, que comprendían revisiones narrativas, una revisión sistemática con metaanálisis, guías de consenso y estudios clínicos y experimentales.

Resultados: La exposición al tabaco y a la nicotina, la diabetes con mal control glucémico, las deficiencias nutricionales, el consumo excesivo de alcohol, la radioterapia, la quimioterapia y ciertos fármacos se asociaron de forma consistente con una cicatrización alterada, compromiso del colgajo, infección y dehiscencia. En los fumadores, la pérdida del colgajo seguía siendo significativamente más frecuente cuando la abstinencia duraba solo 24 horas tras la cirugía, y disminuía cuando la abstinencia alcanzaba una semana. La tensión local, la isquemia y la inflamación propician la aparición de cicatrices patológicas, cuyo riesgo se ve modulado además por factores genéticos y sistémicos. Las medidas dermatológicas incluyen el cierre con reducción de tensión, el uso de cintas adhesivas (taping), láminas o gel de silicona como profilaxis de primera línea, protección frente a la radiación ultravioleta, hidratación, agentes inyectables y tópicos y, para los queloides, cirugía con radioterapia adyuvante.

Conclusiones: Una cicatrización óptima en cirugía plástica depende de la identificación y corrección tempranas de los factores de riesgo modificables y de una vía de atención estructurada y basada en la evidencia para el cuidado de las cicatrices, llevada a cabo conjuntamente por cirujanos plásticos y dermatólogos.

PALABRAS CLAVE

Cicatrización de heridas, cirugía plástica, dermatología, cicatriz hipertrófica, queloide, tabaquismo, diabetes mellitus, nutrición, silicona, manejo de cicatrices.

INTRODUCTION

Wound healing determines both the safety and the aesthetic result of virtually every plastic surgery procedure. It is shaped by patient-related, surgical and environmental variables, many of which are modifiable before, during and after the operation.

OBJECTIVE

The primary objective of this review was to identify, appraise and synthesise the evidence on the patient-related, systemic, local and surgical factors that influence cutaneous wound healing in the context of plastic and reconstructive surgery. The secondary objective was to describe the dermatologic measures, from preoperative optimisation to the management of established abnormal scars, that are supported by the literature for improving healing quality and aesthetic outcome.

Three questions guided the work. First, which modifiable and non-modifiable factors are most consistently associated with delayed healing, wound complications and flap compromise after plastic surgery procedures? Second, through which biological mechanisms do the best-documented factors, in particular smoking and diabetes, interfere with the phases of repair? Third, which prophylactic and therapeutic dermatologic interventions have an evidence base sufficient to guide practice in the prevention and treatment of hypertrophic scars and keloids? Answering these questions is relevant because the cost of wound problems is high: Medicare estimates for acute and chronic wound care ranged between 28.1 and 96.8 billion US dollars in 2014, with surgical wounds representing the largest share of the expense¹.

METHODOLOGY

Design and reporting framework:

A systematic, qualitative review was designed in accordance with the general principles of the PRISMA statement: a pre-specified question, explicit eligibility criteria, a documented search strategy, structured data extraction and transparent synthesis. Because the included literature is heterogeneous in design, population and outcome, a narrative synthesis was chosen in preference to quantitative pooling.

Search strategy:

The search was conducted in May 2026 using a web-based search engine that retrieves records indexed in PubMed and PubMed Central and on publisher sites, and the Crossref registry, which was used to confirm bibliographic details and DOIs. Controlled vocabulary and free-text terms were combined with Boolean operators and grouped in three concepts: (1) wound healing, including «wound healing», «cutaneous repair», «surgical wound» and «wound complications»; (2) plastic surgery contexts, including «plastic surgery», «reconstructive surgery», «skin flap», «abdominoplasty», «breast surgery» and «facelift»; and (3) associated factors and dermatologic care, including «smoking», «nicotine», «diabetes», «nutrition», «alcohol», «corticosteroids», «radiotherapy», «hypertrophic scar», «keloid», «silicone», «laser», «scar management» and «dermatology». No lower date limit was applied. Reference lists of key reviews were hand-searched to identify additional primary studies and guidelines.

Eligibility criteria:

Articles were eligible if they (a) were published in a peer-reviewed journal; (b) carried a DOI that could be verified (in Crossref, PubMed Central or the publisher record); (c) were written in English; (d) addressed the biology of cutaneous wound repair, factors associated with healing or complications in surgical or plastic surgery patients, or the prevention and treatment of abnormal scarring; and (e) were reviews, systematic reviews, meta-analyses, guidelines or consensus statements, randomised or non-randomised clinical studies, or experimental studies with clear translational relevance. Excluded were books and book chapters, conference abstracts, preprints, web pages, theses, trade publications and articles without a verifiable DOI. Studies focused exclusively on chronic ulcers without relevance to surgical wounds were excluded unless they contributed mechanistic information, as in the case of diabetes.

Study selection and data extraction:

Titles and abstracts were screened against the eligibility criteria and the full texts or detailed abstracts of potentially relevant records were then examined. For each included article the following were extracted: first author and year, journal, study design, population or model, factor or intervention of interest, main findings and stated limitations. Each article was assigned to one or more thematic domains: wound-healing biology, smoking and nicotine, diabetes and metabolic disease, nutrition, alcohol and drugs, radiation and chemotherapy, host and genetic factors, abnormal scarring, and dermatologic scar care. After this process 36 articles were retained for the final synthesis.

Appraisal and synthesis:

Study design was used as a proxy for the level of evidence. Guidelines and consensus reports were considered to reflect expert synthesis; systematic reviews and meta-analyses were considered more robust than narrative reviews; and randomised trials were considered more robust than observational series. Mechanistic experimental work was used to explain, but not to establish, clinical effects. Findings were grouped by theme, compared across sources and weighed according to design, consistency and clinical applicability. Where the evidence was conflicting or limited to a single study, this is stated explicitly in the text.

Methodological limitations:

The search was targeted rather than exhaustive. The number of records identified and screened at each stage was not tallied in a formal flow diagram, no formal risk-of-bias instrument was applied, and quantitative pooling was not attempted. The results should therefore be read as a structured, evidence-based synthesis of the best-verified literature identified, rather than as a substitute for a protocol-registered, multi-database systematic review with duplicate independent screening.

RESULTS

Characteristics of the included literature:

36 journal articles, all carrying a verified DOI, met the eligibility criteria. They comprised narrative and comprehensive reviews of wound-healing biology, reviews and clinical or experimental studies on the effect of nicotine and smoking, publications on diabetes and metabolic disease, nutrition and physiology, alcohol, drugs and oncologic therapies, and publications on pathological scarring and scar management, including consensus guidelines. The journals represented plastic surgery, dermatology, wound care, surgery, immunology, nutrition and general medicine, which reflects the multidisciplinary nature of the topic. The evidence base is dominated by reviews, experimental models and observational clinical series; randomised trials are scarce and are mostly confined to scar prophylaxis and treatment. The main thematic findings are summarised in Table 1 and described in the following sections.

Biology of cutaneous repair relevant to the surgical wound:

Across the biology literature there is agreement that cutaneous repair proceeds through overlapping phases. Some authors describe four phases (haemostasis, inflammation, proliferation and remodelling), whereas others group haemostasis and inflammation and describe three^1,2,4. Haemostasis starts immediately after injury, with vasoconstriction, platelet aggregation and deposition of a provisional fibrin matrix. Platelet degranulation releases transforming growth factor-β and platelet-derived growth factor, which attract neutrophils and macrophages and initiate the inflammatory phase¹. Macrophages are central to progression, because they phagocytose debris and secrete cytokines and growth factors that support fibroblast proliferation, angiogenesis and keratinocyte migration^1,6. The transition from inflammation to proliferation has been described as a critical step; failure to complete it keeps wounds in a prolonged inflammatory state⁵.

Within two to three days fibroblasts populate the wound and begin the proliferative phase, which lasts up to about three weeks in a healing cutaneous wound. Fibroblasts deposit disorganised, type III collagen-rich matrix and, under the influence of transforming growth factor-β, some differentiate into myofibroblasts that contract the wound^1,3,36. In the remodelling phase granulation tissue is replaced by scar, type III collagen is progressively replaced by type I collagen over about a year, and matrix metalloproteinases remodel the matrix. Tensile strength reaches approximately 80% of that of uninjured skin at around three months and never returns to 100%¹. This quantitative limit explains why even a well-healed incision is mechanically and structurally different from unwounded skin, and why scar tension management remains important for months after surgery.

Smoking and nicotine:

Smoking was the best-documented modifiable risk factor in the plastic surgery literature. Cigarette smoke contains more than 400 substances that may harm healing, and nicotine in particular promotes vasoconstriction and disrupts the microcirculation^1,12. Experimental human work showed that nicotine and smoking acutely reduce skin and subcutaneous blood flow and tissue oxygen⁸. In a human experimental wound model, smoking attenuated both the inflammatory and the proliferative response; cessation restored the inflammatory response but not proliferation, suggesting that some effects persist beyond short abstinence periods⁹.

Clinically, smokers have more wound-healing problems than non-smokers after aesthetic and reconstructive procedures; abdominoplasty is a representative example in which wound complications were analysed in a series of 132 patients¹⁰. The most specific evidence for flaps comes from a systematic review and meta-analysis of flap surgery. Flap necrosis, haematoma and fat necrosis were significantly more frequent in smokers than in non-smokers, with P values below 0.001, below 0.001 and 0.003, respectively¹¹. The same analysis found that the flap loss rate was significantly higher in smokers who were abstinent for only 24 hours after surgery than in non-smokers (odds ratio 4.885; 95% confidence interval 2.071 to 11.524), and significantly lower in smokers abstinent for one week after surgery than in those abstinent for 24 hours (odds ratio 0.252; 95% confidence interval 0.074 to 0.851)^7,11. The authors concluded that preoperative and postoperative abstinence of at least one week is necessary for smokers undergoing flap operations¹¹. The wider smoking literature supports the view that cessation programmes should combine biomedical and social interventions¹².

Diabetes mellitus and metabolic disease:

Diabetes appears in the literature mainly through chronic foot ulcers, but the mechanisms are directly relevant to surgical wounds in diabetic patients. Impaired healing is estimated to affect approximately a quarter of all patients with diabetes and frequently leads to lower-limb amputation; diabetic foot ulceration and its recurrence are a major cause of morbidity^15,20. Glycaemic control is a measurable predictor: haemoglobin A1c predicts healing rate in diabetic wounds, and uncontrolled hyperglycaemia impairs fibroblast and endothelial function^1,13.

Several mechanisms were repeatedly described. First, inflammation is dysregulated. Macrophages fail to switch from the pro-inflammatory to the pro-reparative phenotype, and the M1-to-M2 ratio is increased^16,17,19. Interleukin-1β is one driver of this persistent inflammatory phenotype, and blocking it induces a healing-associated macrophage phenotype and improves healing in a type 2 diabetes model¹⁸. Diabetes also primes neutrophils to release neutrophil extracellular traps, which impair wound healing¹⁴. Second, angiogenesis and growth-factor signalling are impaired, with reduced fibroblast and keratinocyte proliferation and migration^15,16. Third, peripheral neuropathy is common, with neuropathy occurring in almost 90% of diabetic foot ulcers, and cutaneous sensory innervation and neuropeptides modulate the repair process¹⁶. Fourth, barrier disruption and polymicrobial infection make diabetic wounds difficult to treat¹⁵. A further finding of translational importance is that rodent wound-healing results show only partial concordance with human clinical results (about 53%), whereas porcine models are more concordant¹⁶.

Nutrition:

Wound healing is an energy-intensive process that requires adequate macronutrients and micronutrients^1,21,23. The nutritional deficit widens with wound size, as in large burns, and is relevant for patients who have fasted for prolonged periods postoperatively¹. Vitamin C is a co-substrate for hydroxylases required for collagen synthesis, but supplementation in patients without clear deficiency has not been conclusively beneficial; the same is true for zinc¹. Vitamin A participates in epithelial growth, angiogenesis and collagen synthesis and can counteract the healing-suppressant effect of corticosteroids^1,24,27. The overall conclusion of the nutrition literature is that correction of deficiency is justified, whereas routine supplementation of well-nourished patients is not supported by conclusive evidence^1,21.

Alcohol, drugs, radiation and oncologic therapy:

Alcohol misuse has been linked to a higher incidence of surgical wound infection, and experimental work shows that even acute ethanol exposure impairs fibroblast function and wound breaking strength as well as angiogenesis and the proliferative phase^1,25,26.

Among medications, systemic corticosteroids have well-known anti-inflammatory effects, but the clinical consequences for healing are modulated by dose and duration; acute, high-dose perioperative exposure likely has limited clinical sequelae, whereas chronic exposure is more harmful^1,28. Non-steroidal anti-inflammatory drugs inhibit cyclooxygenases and may impede repair, but short-term use for postoperative pain has limited effect, with chronic wounds and diabetes being circumstances of greater susceptibility^1,29. Bevacizumab and other anti-angiogenic agents carry a specific warning for surgeons because they interfere with neovascularisation³⁰. Chemotherapy delays the inflammatory phase and reduces collagen synthesis in experimental data, but a review of national surgical quality data found no increase in wound complications after breast surgery in patients receiving neoadjuvant chemotherapy. Ionising radiation damages fibroblasts and the microvasculature and is associated with slower^1,31 epithelialisation, lower tensile strength and higher infection and dehiscence rates^1,32.

Host and genetic factors:

Age, sex hormones, stress and obesity were identified among the systemic factors affecting repair⁴. Inherited connective-tissue disorders such as Ehlers–Danlos syndrome, which involves abnormalities of collagen structure, and in selected cases cutis laxa, predispose to wound-healing complications, although most patients with cutis laxa heal normally or near-normally and the disorder is not an absolute contraindication to elective surgery¹. Hyperhomocysteinaemia has been proposed as an independent risk factor for suboptimal healing, particularly in lower-extremity wounds¹.

Hypertrophic scars and keloids:

Hypertrophic scars and keloids result from an abnormal fibrous healing process in which the mechanisms that control tissue repair and regeneration are lost; they are disfiguring and frequently recur, and they represent a major therapeutic challenge for the plastic surgeon³³. Dysregulated transforming growth factor-β signalling contributes to fibrosis and scarring³⁶. Risk factors include local factors such as tension on the wound, systemic factors such as hypertension, genetic factors including single-nucleotide polymorphisms, and lifestyle factors³⁵. Hypertrophic scars generally remain within the boundaries of the original wound, whereas keloids extend beyond it, and both are diagnosed clinically^33,35.

Dermatologic prevention and treatment of abnormal scars:

An international group of 24 experts produced practical guidelines for scar management³⁴. Their first tier of strategies applies to all scars and is indicated before, during and immediately after surgery: optimal surgical management, measures to reduce skin tension, taping, hydration and ultraviolet protection of early scar tissue. Silicone sheeting or gel is universally considered the first-line prophylactic and treatment option for hypertrophic scars and keloids³⁴. Additional, more specialised options exist for high-risk patients or scars, and more invasive or surgical procedures may be required later to correct permanent unaesthetic scars, combined with adjuvant measures³⁴.

A more recent update of treatment algorithms added that the choice of therapy depends on the type and severity of the lesion³⁵. For hypertrophic scars, surgery is the first choice when scar contracture is severe, whereas conservative therapies are indicated when it is not. Small, single keloids can be treated by surgery with adjuvant therapy such as radiotherapy, or by multimodal conservative therapy; for large, multiple keloids, volume- and number-reducing surgery is an option. Conservative therapies, including gel sheets, tape fixation, topical and injected agents, oral agents and makeup therapy, should be applied case by case, and all patients should be followed up over the long term³⁵. A literature review of management strategies likewise concluded that successful healing of these lesions can be achieved only with combined, multidisciplinary therapeutic regimens³³.

Consistency and strength of the evidence:

The strength of the evidence differed markedly between domains. For smoking, there is a coherent chain from physiological studies of blood flow and tissue oxygen, through experimental wound models, to clinical series and a meta-analytic synthesis in flap surgery; this domain therefore has the highest internal consistency^8,9,10,11. For diabetes, the mechanistic evidence is abundant and consistent across reviews, but it derives mostly from chronic ulcers and animal models, and only a limited number of the included sources linked glycaemic markers directly to healing rate in human wounds^13,15,16,17. For nutrition, the literature is primarily descriptive and concludes that deficiency is harmful, while evidence for supplementation in the non-deficient is inconclusive^1,21. For drugs and oncologic treatments, experimental findings and clinical observations are in partial conflict, as in the case of chemotherapy^1,31. For scar management, the evidence consists mainly of consensus guidelines, algorithms and reviews, supplemented by trials that were not individually appraised in this review^33,34,35.

Three consistent themes were observed across domains. The first is that the microcirculation is the final common pathway: nicotine, hyperglycaemia, radiation and anti-angiogenic drugs all compromise perfusion or neovascularisation^8,15,30,32. The second is that inflammation must be both initiated and resolved, and that both a deficient and a persistent inflammatory response are harmful, as seen in smoking, where inflammation is attenuated, and in diabetes, where it persists^9,16,19. The third is that most recommendations are conditional on context, with the effect of a risk factor depending on dose, duration, wound type and the vulnerability of the host^1,28,29.

DISCUSSION

Principal findings:

This review brought together verified journal literature on how wound healing is influenced in plastic surgery and on the dermatologic measures that can modify the result. Three overarching messages emerge. First, the quality of a surgical wound is determined long before the incision is made, because the most consistent risk factors (nicotine exposure, poorly controlled diabetes, malnutrition, alcohol excess, and certain drugs and oncologic treatments) are patient characteristics that can be recognised and, in many cases, corrected^1,4. Second, the biological pathways through which these factors act converge on a small number of mechanisms: tissue hypoxia and impaired microcirculation, dysregulated inflammation, defective angiogenesis and fibroblast dysfunction^4,5,22. Third, the aesthetic and functional outcome of a healed wound is further shaped by scar biology and by deliberate scar care, in which dermatologic principles such as tension reduction, silicone, photoprotection and adjuvant therapies play a defined role^34,35.

Why plastic surgery is particularly vulnerable to impaired healing:

Many plastic surgery procedures depend on tissue whose survival is perfusion-limited. Skin flaps, mastectomy skin envelopes, abdominoplasty and facelift flaps, and free tissue transfers are raised by cutting off part of their original blood supply and rely on the remaining pedicle or perforators. Any additional insult to the microcirculation, such as nicotine-induced vasoconstriction, can tip a marginal flap into necrosis^8,11. The same procedures are frequently elective and performed in healthy patients who expect a near-invisible scar, so that tolerance for complications is low and the consequences of even minor healing problems, such as widened or hypertrophic scars, are magnified. This combination of marginal vascularity and high aesthetic expectations explains the weight given in the plastic surgery literature to preoperative risk assessment^1,22.

A related point is that wound healing is energy- and oxygen-dependent. Oxygen is needed for collagen synthesis, for the oxidative killing of bacteria by neutrophils and for angiogenesis, and the physiological principles of oxygen delivery, temperature, volume status and pain control have been proposed as practical targets for improving surgical wound outcomes²². These principles are relevant to the anaesthetic and perioperative management of plastic surgery patients as much as to the surgical technique itself.

Smoking: strength of evidence and clinical implications:

The smoking literature is the most developed of all the modifiable risk factors and has the most direct clinical application. The mechanistic data show that nicotine acutely reduces blood flow and tissue oxygen in skin and subcutis, that smoking attenuates the inflammatory and proliferative components of healing in a human wound model, and that the harmful constituents of tobacco smoke extend well beyond nicotine^1,8,9,12. The clinical data from abdominoplasty and flap surgery are consistent with these mechanisms^{10, 11}.

The meta-analytic finding that flap loss was significantly higher in smokers abstinent for only 24 hours than in non-smokers, and significantly lower in smokers abstinent for one week, is clinically useful because it suggests that benefit begins to accrue within days¹¹. At the same time, the finding that cessation restored inflammation but not proliferation in the experimental model suggests that short abstinence does not necessarily normalise every aspect of healing⁹. Many surgical teams therefore request abstinence from nicotine for several weeks before elective surgery; the evidence reviewed here supports a minimum of one week before and after flap operations while recognising that longer abstinence is likely to be more protective on mechanistic grounds¹¹. Two cautions are appropriate. The studies are heterogeneous in how smoking and abstinence were defined, usually by self-report, which can misclassify exposure. In addition, nicotine replacement products deliver nicotine without the other combustion products; because nicotine itself is a vasoconstrictor, patients using these products may not obtain the full vascular benefit expected from quitting, and the available evidence in this review does not allow firm conclusions on this point^1,8. A pragmatic implication for practice is that smoking status should be documented systematically, cessation support should be offered as part of the surgical pathway rather than as an afterthought, and the timing of elective surgery should be negotiated in light of the patient’s ability to remain abstinent¹².

Diabetes: from glycaemic control to the wound bed:

Evidence on diabetes is largely derived from chronic ulcers, but its mechanistic lessons can be transferred to surgical wounds with appropriate caution. The finding that haemoglobin A1c predicts healing rate supports the common practice of optimising glycaemic control before elective surgery, and the observation that uncontrolled hyperglycaemia impairs fibroblast and endothelial function provides biological plausibility^1,13. The macrophage and neutrophil abnormalities described in diabetes (persistence of the pro-inflammatory macrophage state, a raised M1-to-M2 ratio, and a tendency of neutrophils to undergo NETosis) help explain why diabetic wounds stall in the inflammatory phase and are prone to infection^14,16,17,19. The demonstration that blocking interleukin-1β can restore a healing-associated macrophage phenotype in an animal model indicates that these pathways may become therapeutic targets, although translation to humans remains to be shown¹⁸.

The contribution of neuropathy is of particular relevance to dermatology, since the skin is richly innervated and neuropeptides influence inflammation, angiogenesis and keratinocyte and fibroblast behaviour¹⁶. A reduction in cutaneous innervation, which occurs in many patients with diabetes even without overt neuropathic symptoms, may therefore impair repair after surgical incision in addition to increasing the risk of unrecognised injury¹⁶. The sobering finding that pre-clinical rodent results concord only partially with human outcomes should temper enthusiasm for new topical or systemic agents until human trials are available¹⁶. For the plastic surgeon, the practical consequences are to measure HbA1c before elective procedures, to treat infection and ischaemia early, and to consider the cutaneous and vascular status of the operative field in diabetic patients^15,20.

Nutrition, alcohol and medications:

The nutritional literature supports a clear but limited message: wound healing demands substantial energy, protein and micronutrients, and clinically evident deficiency should be corrected^21,23. By contrast, the evidence does not support routine supplementation of vitamins C or zinc in well-nourished patients¹. Vitamin A deserves mention because of its interaction with corticosteroids, but it should not be extrapolated into routine prescribing without clinical indication^24,27. The expectation that a patient scheduled for major reconstruction will be able to resume oral intake soon after surgery is a sensible, low-cost part of enhanced recovery planning¹.

Alcohol has received less attention than tobacco, but the experimental data on impaired angiogenesis, fibroblast function and wound strength, together with the association between alcohol use disorders and surgical site infection reported in the literature on which comprehensive reviews rely, provide sufficient reason to include alcohol history in preoperative assessment^1,25,26.

The effect of drugs is more nuanced than is often assumed. Systemic corticosteroids and non-steroidal anti-inflammatory agents are frequently perceived as universally harmful to healing, yet the literature indicates that brief perioperative exposure often has limited clinical consequences, whereas chronic exposure and vulnerable hosts, such as patients with diabetes or chronic wounds, are at higher risk^1,28,29. In contrast, anti-angiogenic agents such as bevacizumab carry a clearer warning because they directly target neovascularisation³⁰. The finding that neoadjuvant chemotherapy was not associated with an increase in wound complications after breast surgery contrasts with the experimental concern that chemotherapy delays healing, illustrating that clinical effect size may be smaller than laboratory data suggest^1,31. Radiotherapy, by contrast, appears to produce more durable tissue damage with consequences for healing, infection and dehiscence, and its effect on the microvasculature and fibroblasts is a central consideration in reconstruction of irradiated fields³².

Abnormal scarring: biology and risk stratification:

Hypertrophic scars and keloids illustrate that healing can fail not by deficiency but by excess. The central biological abnormality is a loss of control over the mechanisms that regulate repair and regeneration, with transforming growth factor-β signalling and persistent inflammation as prominent drivers^33,35,36. The identification of tension, hypertension, genetic polymorphisms and lifestyle as risk factors has two implications³⁵. Local tension is modifiable through surgical planning and wound support, and it is the main reason for the emphasis on tension reduction in scar guidelines³⁴. Systemic and genetic factors, in contrast, are non-modifiable or only partly modifiable, so they are best used to stratify risk and to decide who should receive early, intensified prophylaxis.

Dermatologic care: what the evidence supports:

The guideline-based approach of Monstrey and colleagues organises scar care in tiers³⁴. The first tier is generic and applicable before, during and immediately after surgery. It comprises meticulous surgical technique, minimisation of skin tension, taping, hydration and protection of the early scar from ultraviolet radiation. The rationale for each element is biological: tension stimulates fibroblast activity and inflammation, hydration supports epithelial barrier function, and ultraviolet exposure may promote hyperpigmentation of the immature scar. Silicone sheeting or gel is the first-line prophylactic and therapeutic option and is the best-supported topical measure³⁴. Beyond this generic tier, more specialised treatments are reserved for high-risk patients or established lesions.

The 2020 update of treatment algorithms adds the key principle that therapy should be selected according to the severity and type of lesion, for example, surgery first for severely contracted hypertrophic scars and combined surgery and radiotherapy or multimodal conservative treatment for keloids³⁵. This approach is consistent with the earlier conclusion that no single modality reliably cures these lesions and that combined, multidisciplinary regimens give the best results³³. A genuine dermatologic contribution to plastic surgery is therefore at three points: preoperative identification of high-risk skin and history, early postoperative prophylaxis, and management of lesions that develop despite prophylaxis, using intralesional agents, lasers and other modalities in conjunction with the surgeon.

A realistic reading of this evidence base should acknowledge its limits. The best-supported measure, silicone, is supported by guideline consensus rather than by large, uniform randomised trials³⁴. The algorithms are explicit that the evidence for many conservative therapies is limited and that results must be individualised³⁵. Long-term follow-up is repeatedly emphasised, because recurrence, particularly of keloids, may occur after apparently successful treatment^33,35.

Towards an integrated perioperative pathway:

Taken together, these findings support an integrated pathway. At preoperative consultation, the surgeon should record smoking and nicotine use, alcohol intake, diabetes and HbA1c, nutritional status, medications, prior irradiation or chemotherapy, personal and family history of keloid or hypertrophic scarring, and any connective-tissue disorder^1,4. Modifiable factors should be addressed with defined targets, such as nicotine abstinence for at least a week before and after flap operations, glycaemic optimisation and correction of nutritional deficiency^11,13,21. Intraoperatively, attention to tissue handling, perfusion and tension-free closure is the surgeon’s contribution^22,34. Postoperatively, early scar care using tension reduction, taping, hydration, sun protection and silicone should be started for all patients, with prompt dermatologic referral for scars that become thickened, erythematous or symptomatic^34,35. This pathway is a synthesis derived from the evidence reviewed rather than a validated protocol, and prospective evaluation would be valuable.

Implementing such a pathway raises organisational questions. Preoperative optimisation takes time, and the interval between consultation and surgery must be long enough for smoking cessation, glycaemic adjustment or nutritional repletion to have effect. This favours scheduling elective procedures after a structured preparation period, and it argues for protocols that are shared by surgeons, anaesthetists, dermatologists, nutrition specialists and primary care physicians rather than left to the individual clinician^12,21,22. Documentation of risk factors and of the agreed targets also protects patients, because it makes expectations explicit and allows deviations to be discussed before an avoidable complication occurs. When a patient is unable or unwilling to modify a major risk factor, the evidence reviewed here supports a frank discussion of reduced flap reliability, a higher risk of wound complications and a less predictable scar, and in some cases the choice of a technique that is less dependent on marginal perfusion^11,13,35. Finally, the training of surgeons and dermatologists in each other’s fields, including exposure of dermatology trainees to surgical wound biology and of plastic surgery trainees to scar science, would help consolidate the shared vocabulary on which collaboration depends^1,33.

Preoperative dermatologic assessment of the surgical field:

Although few of the included articles studied preoperative dermatologic assessment as such, the biology they describe indicates why it is valuable. The skin is not only the surface through which the surgeon operates; it is an immunological, neurological and mechanical organ whose barrier function, innervation and cellular behaviour affect repair^4,16. A dermatologist is well placed to identify conditions that modify risk, for instance a personal or family history of keloid, a tendency to hypertrophic scarring at sites of previous injury, active inflammatory skin disease or infection at or near the operative site, and chronic skin changes associated with diabetes or irradiation^15,32,35. Such a history is directly relevant to the choice of incision site and orientation, since scar tension and location influence scar quality, and to the decision about whether to begin prophylaxis before the wound is closed^34,35. In patients with a strong keloid tendency, the surgeon and dermatologist may jointly decide whether the procedure is justified at all, which is an ethical as well as a technical judgement.

Healing in specific clinical scenarios:

The relative importance of the factors reviewed differs by procedure. In flap-based and skin-undermining operations such as facelift, mastectomy with immediate reconstruction and abdominoplasty, perfusion-related factors, notably nicotine, dominate the risk of necrosis, and the strongest evidence concerns these procedures^10,11. In reconstruction of irradiated or previously treated fields, the quality of the recipient bed becomes the main determinant, and radiation-induced fibroblast and microvascular damage may justify the use of well-vascularised tissue^1,32. In diabetic patients undergoing lower-limb reconstruction, glycaemic control, vascular status, neuropathy and infection are all critical^15,20. In aesthetic procedures performed on healthy patients, the dominant concern shifts from survival of tissue to the quality of the scar, and tension, site and prophylaxis are the principal levers^34,35. This stratification suggests that surgeons should emphasise different aspects of preoperative counselling according to the planned operation rather than applying a uniform checklist.

Communication, adherence and patient-centred outcomes:

Many of the measures discussed require sustained action from the patient: staying abstinent from nicotine, adhering to glycaemic control, maintaining nutrition, protecting the scar from the sun and applying silicone for weeks to months. Adherence is therefore a determinant of outcome in its own right. The smoking literature emphasises that social and behavioural interventions, rather than biomedical advice alone, are needed to achieve cessation, and the same logic applies to scar care¹². The scar guidelines recognise that effective prophylaxis involves simple, repeated measures started early and continued for an adequate duration³⁴. Clear written instructions, explicit explanation of why each measure matters and early follow-up visits are practical ways to improve adherence. Because hypertrophic scars and keloids can cause pruritus, pain and psychosocial distress, patient-reported outcomes should be considered alongside observer-rated scar scales when evaluating treatment^33,34.

Emerging directions:

Several lines of research emerging from the reviewed literature may change practice. In diabetes, targeting inflammatory mediators such as interleukin-1β or neutrophil extracellular traps, and modulating neuropeptide signalling, are biologically plausible strategies that have shown benefit in experimental models^14,16,18. In the field of fibrosis, the dissection of canonical and non-canonical transforming growth factor-β signalling may lead to more selective antifibrotic therapies for pathological scars³⁶. Understanding the control of the transition from inflammation to proliferation may allow modulation of the repair process in high-risk hosts⁵. These directions are promising but remain largely pre-clinical, and the published literature reviewed here does not yet support their use in routine plastic surgery practice.

Strengths and limitations of this review:

Strengths include the restriction to peer-reviewed journal articles with verified DOIs, the integration of surgical, dermatologic, metabolic and nutritional perspectives, and the explicit weighing of evidence by design. Several limitations must be recognised. The search was targeted and the number of records screened was not tallied in a formal flow diagram. Duplicate independent screening and a formal risk-of-bias instrument were not applied. A considerable part of the evidence on diabetes, nutrition and medications originates from chronic wounds, burns or animal models, and extrapolation to elective plastic surgery wounds is partly inferential. The included clinical studies often depend on self-reported exposures such as smoking, and many are observational, so residual confounding cannot be excluded. Finally, the review did not include randomised trials of novel therapies such as botulinum toxin, fractional lasers or platelet-derived products, or recent work on obesity and e-cigarettes, because verified journal sources with DOIs for these topics were not confirmed within the scope of this search; their absence should not be read as evidence of absence of benefit or harm.

Implications for research:

Several gaps were evident. Prospective, adequately powered studies are needed to define the minimum effective duration of preoperative nicotine abstinence for different procedures, and to establish the effect of nicotine replacement and newer nicotine delivery products on surgical wound outcomes. Perioperative glycaemic targets specific to plastic surgery, rather than extrapolated from general surgery or chronic ulcers, are needed. For scar management, randomised trials with standardised, validated outcome measures and long follow-up would help determine which prophylactic regimens are cost-effective in high-risk patients³⁵. The partial concordance of rodent and human wound-healing findings argues for human tissue models and clinical trials rather than reliance on animal data alone¹⁶.

CONCLUSIONS

1. Wound healing in plastic surgery is a multiphase, tightly regulated process whose success depends on adequate perfusion, oxygen, controlled inflammation and balanced fibroblast activity. Deficiency in any phase impairs healing.
2. Tobacco and nicotine exposure is the best-documented modifiable risk factor. It increases flap necrosis, haematoma and fat necrosis, and abstinence of at least one week before and after flap surgery is associated with improved flap survival.
3. Diabetes impairs healing through hyperglycaemia, macrophage and neutrophil dysfunction, neuropathy, defective angiogenesis and infection, and glycaemic control as measured by HbA1c is a practical predictor and target.
4. Nutritional deficiency, alcohol excess, radiotherapy, anti-angiogenic drugs and, in susceptible patients, chronic corticosteroid or NSAID exposure should be identified preoperatively, with the effect size of each interpreted in clinical context.
5. Hypertrophic scars and keloids arise from dysregulated repair under tension, inflammation and host susceptibility, and their management is best based on tiered, individualised and multidisciplinary regimens.
6. Dermatologic care should start at the preoperative visit and include tension reduction, taping, hydration, ultraviolet protection and silicone as first-line prophylaxis, with escalation to injected, surgical and adjuvant treatments for established lesions.
7. Closer collaboration between plastic surgeons and dermatologists, supported by prospective trials with standardised outcomes, is the most promising route to improving both the safety and the aesthetic quality of healing in plastic surgery.

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APPENDICE

TABLE 1. Summary of the principal factors associated with wound healing in plastic surgery identified in the included literature

Domain	Principal finding	Main sources
Biology of repair	Overlapping phases of haemostasis/inflammation, proliferation and remodelling; deficiency in any phase impairs healing	[1-3,5]
Smoking and nicotine	Vasoconstriction, reduced tissue oxygen, impaired inflammation and proliferation; more flap loss, haematoma and fat necrosis	[8-12]
Diabetes	Hyperglycaemia, macrophage and neutrophil dysfunction, neuropathy, impaired angiogenesis and infection; HbA1c predicts healing	[13-18]
Nutrition	Energy, protein and micronutrient requirements rise with wound size; supplementation helps mainly in deficiency	[1,21,23,24]
Alcohol	Impaired angiogenesis, fibroblast function and wound strength	[25,26]
Drugs	Corticosteroids, NSAIDs, bevacizumab and chemotherapy can delay repair, with context-dependent effect size	[27-31]
Radiation	Fibroblast and microvascular damage; higher infection and dehiscence	[1,32]
Abnormal scarring	Tension, inflammation and host factors drive hypertrophic scars and keloids	[33,35,36]
Dermatologic care	Tension reduction, taping, silicone, UV protection, injections, surgery plus adjuvants	[33-35]

Source: Prepared by the authors.