**2. Classifications and healing of surgical wounds**

The global volume of surgery was estimated to be 312.9 million procedures in 2012, which represented an increase of 38.2% from a prior estimate in 2004 [3]. Almost all of these surgical procedures begin with the creation of an incisional wound to provide

access to the organ or anatomy of interest and end with the closure of the incision. Surgical incisions can be made at any location on the body, be of any length, variable depths, and different shapes. With over fourteen surgical specialties creating multiple types of incisions, classifying these wounds can be complex [4]. There are however, two classification systems for surgical wounds that are widely used [5, 6].

In the first, surgical wounds are classified preoperatively into one of four categories according to the likelihood and degree of wound contamination at the time of operation [5]. The Centers for Disease Control and Prevention (CDC), using an adaptation of the American College of Surgeons' wound classification schema, divides surgical wounds into four classes [5]. Class I or clean wounds are defined as uninfected operative wounds in which no inflammation is encountered and the respiratory, alimentary, genital, or uninfected urinary tracts are not entered [5]. Class II or clean-contaminated wounds are defined as operative wounds in which the respiratory, alimentary, genital, or urinary tracts are entered under controlled conditions and without unusual contamination [5]. Operations involving the biliary tract, appendix, vagina, and oropharynx are included in this category provided no evidence of infection or major break in sterile technique is encountered [5]. Class III or contaminated wounds are defined as open, fresh, accidental wounds. In addition, operations with major breaks in sterile technique (e.g., open cardiac massage) or gross spillage from the gastrointestinal tract, and incisions in which acute, nonpurulent inflammation is encountered [5]. Class IV or dirty-infected wounds are defined as old traumatic wounds with retained devitalized tissue and those that involve existing clinical infection or perforated viscera [5]. This definition suggests that the organisms causing postoperative infection were present in the operative field before the operation [5].

The second classification system for surgical wounds is determined postoperatively and refers to when and how they are closed and will heal. Primary wound closure refers to the immediate closure of a surgical incision (usually within 4–8 h) and is also known as healing by primary intention [6]. Wounds that heal by primary intention are those with little or no tissue loss in which the wound edges can be easily approximated or brought together [6]. Primary intention healing occurs via epithelization and connective tissue deposition [7]. Most incised surgical wounds will heal by primary intention [6]. Secondary wound closure, also known as healing by secondary intention, applies to wounds with significant tissue loss in which the wound edges cannot be approximated. Secondary intention healing requires a granulation tissue matrix to form and fill the defect prior to epithelialization of the surface [7]. Less frequently, surgical wounds are managed by tertiary or delayed primary closure, also known as healing by tertiary intention [6]. This approach is usually taken in wounds where there is not significant tissue loss but an elevated risk or presence of infection [7]. Examples include traumatic injuries such as animal bites or lacerations involving foreign bodies. These wounds can usually be surgically closed, or skin grafted after thorough cleansing, debridement of any necrotic tissue, and observation for up to 7 days to ensure adequate tissue viability and perfusion [8].

Wound healing, whether in chronic wounds or acute wounds like closed surgical incisions involves a complex series of molecular and cellular events that culminate in fibrotic repair or a scar [9]. These wound healing events can be described as four overlapping phases of hemostasis, inflammation, proliferation (collagen formation) and maturation (collagen remodeling) [9]. Hemostasis begins at the moment of incision with a complex series of enzymatic events that result in the formation of a fibrin clot [9]. The clot establishes a temporary extracellular matrix and subsequent platelet mediated stimuli recruit neutrophils to the wound environment to initiate the

#### *Surgical Wound Closure and Healing DOI: http://dx.doi.org/10.5772/intechopen.105978*

inflammatory phase with the initial function of defending against bacterial infection [9]. Within 2–3 days, monocytes from the bloodstream enter the tissues and transition into macrophages [9]. Early wound macrophages phagocytize dead neutrophils, bacteria, and tissue debris [9]. Later these macrophages take on an anti-inflammatory role in preparation for tissue repair and begin to secrete a variety of growth factors to stimulate fibroblast migration and activation [9]. The acute inflammatory phase can last 3–7 days dependent on tissue type [7]. During this phase of healing, a surgical incision does not gain appreciable tensile strength, and is dependent upon the wound closure material to hold it in approximation [7]. The arrival of fibroblasts signals the beginning of the proliferative phase [9]. The fibroblasts and endothelial cells begin to produce a highly vascularized extracellular matrix composed of glycosaminoglycans, proteoglycans, and collagen called granulation tissue [9]. The ratio of type III to type I collagen in granulation tissue is higher than in unwounded tissue or mature/ remodeled scar and it accounts for the weaker tissue strength in a healing wound [9]. Although collagen deposition by fibroblasts is at its maximal level around 3 weeks after injury, wound strength is still at a minimum [9]. Surgical incisional wounds have minimal to no tissue loss, so the proliferative phase may be attenuated with lower volume of granulation tissue relative to wounds with significant tissue loss. Epithelial cells resurface the wound only after granulation in wounds with tissue loss, however in incisional wounds with close wound edge approximation, epithelization is complete within about 48–72 h [10]. The maturation phase begins after proliferation subsides and involves remodeling of the newly deposited matrix with changes in collagen fibril orientation and a shift toward a higher proportion of type I to type III collagen [9]. This remodeling process results in a mature scar that can regain up to 80% of the strength of normal skin after 3–4 months [9]. Remodeling involves reorganization of extracellular matrix by matrix metalloproteinases and collagenases and is accompanied by decreased cellularity and vascularity of scar tissue [7]. Epithelial appendages such as hair follicles, sweat glands, and sebaceous glands are not reformed, so a healed scar is an acellular arrangement of epithelialized extracellular matrix composed primarily of collagen [9].

There are many elements of an operative procedure that can impact the surgical wound healing process [7]. The patient's overall health status will affect the duration of healing with many factors to be considered, including but not limited to age, BMI, nutrition, hydration, diabetes, tobacco use, blood supply, polypharmacy, and immunodeficiencies [7]. Likewise, there are factors related to the surgical procedure itself, such as the length and orientation of the incision, dissection technique, tissue handling, elimination of dead space, closing tension, and the choice of wound closure materials [7].
