Wound healing is a sophisticated biological process encompassing hemostasis, inflammation, proliferation and remodeling. Any disruption in these tightly regulated phases can lead to chronic wounds or wound dehiscence, both of which pose significant clinical challenges [1].

Mechanisms of Wound Healing

The initial hemostatic phase is marked by platelet aggregation, thrombus formation and cytokine release. Platelet-Derived Growth Factors (PDGF) and transforming growth factor-beta (TGF-β) orchestrate the recruitment of inflammatory cells necessary for the subsequent phase [2]. The inflammatory phase, lasting 2–3 days, involves macrophages and neutrophils clearing debris and secreting cytokines to initiate tissue repair [3].

The proliferative phase is characterized by fibroblast proliferation, collagen deposition, angiogenesis and re-epithelialization. Granulation tissue forms as a hallmark of this phase [4]. Finally, the remodeling phase involves collagen maturation, predominantly the transition from type III to type I collagen, resulting in tensile strength restoration over several months [4].

Classification of Wounds

Surgical wounds are classified based on contamination risk. Class I wounds are clean with no entry into respiratory or alimentary tracts. Class II wounds involve controlled entry into these systems. Class III wounds are contaminated, while Class IV wounds are dirty-infected, often involving pre-existing infection or necrotic tissue [5].

Factors Influencing Wound Healing

Wound oxygenation is critical, as hypoxia impairs fibroblast function, collagen synthesis and neovascularization [6]. Infection, notably by biofilm-forming bacteria such as Pseudomonas aeruginosa, disrupts healing by prolonging inflammation and degrading extracellular matrix proteins [7].

Age-related changes include delayed macrophage infiltration, impaired angiogenesis and diminished collagen deposition [8]. Diabetes mellitus exacerbates these challenges through impaired leukocyte function, reduced neovascularization and chronic hypoxia [9]. Certain medications, including glucocorticoids and chemotherapeutic agents, impair healing through suppression of fibroblast proliferation and inhibition of angiogenesis [10].

Nutritional deficiencies also impede healing. Protein, vitamins C and A and minerals such as zinc and iron are indispensable for collagen synthesis, immune function and cellular proliferation [11].

Wound Dehiscence

Wound dehiscence, defined as partial or complete disruption of a surgical incision, is typically observed between the fifth and eighth postoperative day. Risk factors include infection, ischemia, obesity, diabetes, malnutrition and technical failures in wound closure [12]. Minor dehiscence may be managed conservatively with abdominal binders and careful monitoring [13]. However, full-thickness dehiscence, particularly with evisceration, constitutes a surgical emergency requiring immediate operative intervention [14].

The introduction of wound Vacuum-Assisted Closure (VAC) devices has revolutionized the management of complex and dehisced wounds. By applying negative pressure, VAC therapy reduces edema, enhances perfusion and stimulates granulation tissue formation, significantly improving healing rates [15].

Understanding the intricacies of wound healing mechanisms, identifying modifiable risk factors and applying evidence-based management strategies are essential for minimizing postoperative wound complications and optimizing surgical outcomes.

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