Medical School · Year 3 · General Surgery · includes a quiz and discussion video

Seminar 02: Surgical Wound Healing

Year 3: General Surgery Clerkship

Learning Objectives

By the end of this seminar, students will be able to:

1. Describe the phases of normal wound healing
2. Classify surgical wounds by contamination level
3. Identify factors affecting wound healing
4. Recognize wound healing complications
5. Apply principles of wound closure techniques
6. Describe surgical site infection prevention

Seminar Outline

I. Phases of Wound Healing

The hemostasis phase begins immediately upon tissue injury and represents the body's initial response to prevent exsanguination through a coordinated cascade of vascular and cellular events. Vasoconstriction occurs within seconds as smooth muscle in injured vessel walls contracts, transiently reducing blood flow to the wounded area. Platelets rapidly adhere to exposed collagen and subendothelial matrix, becoming activated and releasing adenosine diphosphate, thromboxane A2, and other factors that recruit additional platelets to form an initial hemostatic plug. The coagulation cascade is simultaneously triggered through both intrinsic and extrinsic pathways, ultimately generating thrombin that converts fibrinogen to fibrin, creating a stable clot that provides the provisional matrix for subsequent wound healing phases.

The inflammatory phase spans approximately the first four days following injury and establishes the foundation for tissue repair through recruitment of inflammatory cells and initiation of debridement. Neutrophils are the first leukocytes to arrive, typically within hours of injury, drawn by chemotactic signals released during hemostasis and serving primarily to phagocytose bacteria and debris. Macrophages subsequently become the dominant cell type, arriving around forty-eight to seventy-two hours post-injury and playing a critical coordinating role in wound healing through secretion of growth factors, cytokines, and matrix metalloproteinases. The cardinal signs of inflammation including rubor, calor, tumor, and dolor reflect the vascular permeability changes, vasodilation, and mediator release that characterize this phase and are essential for normal healing progression.

The proliferative phase extends from approximately day four through day twenty-one and encompasses the formation of granulation tissue, angiogenesis, epithelialization, and wound contraction. Fibroblasts migrate into the wound, proliferate, and begin synthesizing collagen, initially producing type III collagen that will later be replaced by stronger type I collagen during remodeling. Angiogenesis produces the rich capillary network visible as red, granular tissue that characterizes a healthy healing wound and is driven primarily by vascular endothelial growth factor and fibroblast growth factor. Epithelialization occurs as keratinocytes at the wound edges proliferate and migrate across the wound surface, while myofibroblasts with contractile properties draw wound edges together, reducing the overall wound size.

The remodeling phase represents the longest phase of wound healing, beginning around three weeks post-injury and continuing for up to two years as the wound matures and strengthens. Type III collagen is progressively replaced by type I collagen through a balanced process of synthesis and degradation mediated by matrix metalloproteinases and their inhibitors. Collagen fibers become increasingly organized and cross-linked, progressively increasing wound tensile strength that reaches approximately eighty percent of normal tissue strength by three months. The scar tissue never fully regains the strength of uninjured tissue, and the healed wound remains more susceptible to re-injury than surrounding intact skin throughout the patient's lifetime.

<image>Panel A: A four-quadrant timeline diagram showing the overlapping phases of wound healing from hemostasis through remodeling with key cellular and molecular events labeled at each stage. Panel B: A microscopic cross-section illustration showing platelet plug formation during hemostasis with fibrin mesh entrapping red blood cells and platelets visible. Panel C: A histological representation of granulation tissue formation during the proliferative phase showing new capillary formation, fibroblast infiltration, and collagen deposition. Panel D: A graph displaying wound tensile strength over time from injury through one year, showing rapid initial increase followed by gradual plateau at approximately eighty percent of normal tissue strength.</image>

II. Types of Wound Healing

Primary intention healing, also known as primary closure, occurs when wound edges are directly approximated using sutures, staples, or adhesive materials, resulting in rapid healing with minimal scar formation. This approach is appropriate for clean surgical incisions, traumatic lacerations that are debrided and closed within the golden period, and wounds without significant contamination or tissue loss. The absence of a tissue gap allows epithelialization to occur rapidly, typically within twenty-four to forty-eight hours, sealing the wound from external contamination. Primary closure results in faster healing times, superior cosmetic outcomes, and lower infection rates compared to other closure methods when appropriately applied to suitable wounds.

Secondary intention healing allows wounds to close spontaneously through granulation tissue formation, wound contraction, and epithelialization without surgical approximation of wound edges. This approach is indicated for wounds that are heavily contaminated, have significant tissue loss, contain foreign bodies that cannot be fully removed, or are associated with abscess cavities. The wound fills progressively from the base and edges with granulation tissue as new blood vessels and fibroblasts populate the provisional matrix. Secondary intention healing requires significantly longer time frames than primary closure, results in larger and often cosmetically inferior scars, but provides advantages in contaminated situations by allowing drainage and preventing enclosed infection.

Tertiary intention healing, also called delayed primary closure, represents a planned approach combining features of both primary and secondary healing to optimize outcomes in contaminated wounds. The wound is initially left open for a period of several days, typically three to five days, allowing debridement, drainage, and reduction of bacterial bioburden before surgical closure. This approach is commonly employed for contaminated traumatic wounds, abscesses after incision and drainage, and surgical wounds at high risk for infection due to contamination during the procedure. When the wound appears clean with healthy granulation tissue and no signs of infection, delayed primary closure can be performed with healing rates and outcomes approaching those of primary closure.

Surgical wound classification according to CDC categories provides a framework for predicting surgical site infection risk and guiding perioperative antibiotic decisions. Clean wounds, designated Class I, include surgical procedures that do not enter the gastrointestinal, respiratory, or genitourinary tracts and are performed under sterile conditions with no breaks in technique, carrying surgical site infection rates of less than two percent. Clean-contaminated wounds, Class II, involve controlled entry into hollow viscera with minimal spillage, with infection rates of five to ten percent. Contaminated wounds, Class III, include major breaks in technique, gross spillage from gastrointestinal tract, or traumatic wounds less than four hours old, with infection rates of ten to twenty percent. Dirty or infected wounds, Class IV, involve established infection, perforated viscera, or old traumatic wounds with devitalized tissue, carrying infection rates of twenty to forty percent.

<image>Panel A: A side-by-side comparison of primary, secondary, and tertiary intention healing showing cross-sectional wound appearance at initial presentation and after healing completion with scar characteristics. Panel B: A photographic progression of secondary intention wound healing showing granulation tissue formation over weeks from an open wound base. Panel C: A surgical field demonstrating delayed primary closure technique with wound packed open initially then closed after granulation tissue formation. Panel D: The CDC surgical wound classification system displayed with visual examples of each category from clean through dirty-infected with corresponding infection rate ranges.</image>

III. Factors Affecting Wound Healing

Local factors directly impact the wound environment and include infection as the most significant impediment to healing, with bacterial loads exceeding one hundred thousand organisms per gram of tissue generally preventing wound closure. Tissue ischemia and hypoxia compromise healing by limiting oxygen delivery essential for fibroblast function, collagen synthesis, and bacterial killing by neutrophils, making adequate perfusion critical for wound healing. Foreign bodies within wounds perpetuate the inflammatory response, provide nidus for bacterial proliferation, and prevent epithelialization until removed. Excessive wound tension leads to ischemia at wound edges, dehiscence risk, and widened scars, emphasizing the importance of proper suture technique and tension-relieving measures when closing wounds under stress.

Systemic factors affecting wound healing include diabetes mellitus, which impairs neutrophil function, reduces angiogenesis, and causes microvascular disease that limits tissue perfusion and predisposes to wound complications. Malnutrition significantly impairs wound healing through multiple mechanisms including reduced protein availability for collagen synthesis, deficiencies of vitamins and minerals essential for enzymatic processes, and impaired immune function. Corticosteroid therapy inhibits the inflammatory phase, reduces fibroblast proliferation, and impairs collagen synthesis, with these effects potentially reversible through vitamin A supplementation. Smoking causes vasoconstriction that reduces tissue perfusion, while carbon monoxide displaces oxygen from hemoglobin, and smoking cessation at any time before surgery improves wound healing outcomes.

Nutritional requirements for optimal wound healing include adequate protein intake, typically requiring one to one-and-a-half grams per kilogram daily in surgical patients, as amino acids provide the building blocks for collagen synthesis. Vitamin C serves as an essential cofactor for prolyl and lysyl hydroxylase enzymes that catalyze collagen cross-linking, and deficiency results in scurvy characterized by impaired wound healing and wound dehiscence. Vitamin A promotes epithelialization and can partially counteract the wound healing impairment caused by corticosteroids, making supplementation beneficial in patients on chronic steroid therapy. Zinc plays important roles in protein synthesis and cell proliferation, and deficiency should be corrected though supplementation in zinc-replete individuals does not enhance healing.

Tissue oxygenation represents a critical determinant of wound healing success, with adequate oxygen delivery supporting fibroblast collagen production, bacterial killing by neutrophils, and angiogenesis. Tissue oxygen tension of at least thirty to forty millimeters of mercury is required for fibroblast function and collagen synthesis, while neutrophil oxidative killing mechanisms require even higher oxygen levels to function optimally. Factors reducing tissue oxygenation include vasoconstriction from smoking, hypothermia, hypovolemia, and sympathetic stimulation, as well as systemic hypoxemia and anemia. Perioperative strategies to optimize tissue oxygenation include maintaining normothermia, adequate fluid resuscitation, supplemental oxygen administration, and smoking cessation.

<image>Panel A: A diagram illustrating the various local factors affecting wound healing including infection, ischemia, foreign bodies, and tension with arrows indicating their impact on the wound environment. Panel B: A comparison of wound healing in diabetic versus non-diabetic patients showing delayed closure, reduced granulation tissue, and increased infection risk in the diabetic wound. Panel C: A nutritional requirements infographic for wound healing displaying protein, vitamins A and C, zinc, and caloric requirements with food sources and recommended daily intakes. Panel D: An oxygen tension diagram showing the relationship between tissue oxygen levels and cellular functions including collagen synthesis at thirty mmHg and optimal neutrophil killing above fifty mmHg.</image>

IV. Wound Healing Complications

Seroma formation occurs when serous fluid accumulates within the wound, typically in dead space created during surgical dissection or resulting from disruption of lymphatic channels. These collections commonly occur following procedures involving extensive tissue mobilization such as mastectomy, hernia repair, and abdominoplasty. Seromas present as fluid-filled, non-tender swellings at the surgical site without the warmth and erythema characteristic of infection. Management includes observation for small asymptomatic collections, percutaneous aspiration for symptomatic or large seromas, and compression dressings to prevent reaccumulation, with prevention strategies focusing on elimination of dead space through layered closure and drain placement when indicated.

Hematoma represents collection of blood within the wound and typically results from inadequate hemostasis during surgery, postoperative bleeding from a vessel, or coagulopathy. Hematomas increase the risk of wound infection by providing culture medium for bacteria and separating wound edges, while large hematomas may cause wound necrosis through pressure effects. Clinical presentation includes swelling, ecchymosis, and pain at the surgical site, with tension on the wound potentially leading to dehiscence. Small hematomas may be observed and allowed to resorb, while large or expanding hematomas require surgical evacuation with identification and control of the bleeding source.

Surgical site infection is defined by CDC criteria as infection occurring within thirty days of surgery for superficial and deep incisional infections or within ninety days for infections involving implants or organ spaces. Superficial incisional infections involve only the skin and subcutaneous tissue and present with erythema, warmth, tenderness, and purulent drainage from the incision. Deep incisional infections extend to the fascia and muscle layers and may present with wound dehiscence, abscess formation, or systemic signs of infection. Organ-space surgical site infections involve any anatomic site other than the incision itself that was opened or manipulated during surgery, such as intra-abdominal abscess following bowel surgery.

Wound dehiscence represents separation of wound layers after closure and may involve superficial layers only or extend to complete fascial separation with or without evisceration. Risk factors include infection, increased intra-abdominal pressure from coughing or vomiting, malnutrition, obesity, and technical factors in closure. The classic presentation involves serosanguinous discharge from the wound, typically occurring between postoperative days five and ten when wound strength is at its nadir before collagen cross-linking increases tensile strength. Fascial dehiscence with evisceration of abdominal contents constitutes a surgical emergency requiring immediate coverage of exposed viscera with moist sterile dressings and urgent return to the operating room for abdominal wall closure.

<image>Panel A: A clinical photograph showing seroma formation as a fluctuant subcutaneous collection following mastectomy with needle aspiration being performed. Panel B: A cross-sectional diagram comparing small hematoma managed conservatively versus large hematoma requiring surgical evacuation with visible blood clot separating tissue layers. Panel C: The three types of surgical site infection displayed anatomically showing superficial incisional infection limited to skin and subcutaneous tissue, deep incisional infection involving fascia and muscle, and organ-space infection as an intra-abdominal abscess. Panel D: A wound dehiscence with evisceration showing exposed bowel loops through a separated abdominal incision with moist saline dressings being applied as initial management.</image>

V. Abnormal Wound Healing

Hypertrophic scars represent excessive collagen deposition that remains confined within the boundaries of the original wound and typically develop within weeks to months after injury. These raised, erythematous, firm scars result from an imbalance between collagen synthesis and degradation during the remodeling phase, with excessive type III collagen production and inadequate matrix metalloproteinase activity. Hypertrophic scars occur most commonly in wounds crossing joints, wounds closed under tension, and in areas of repeated motion or stress. Unlike keloids, hypertrophic scars tend to improve spontaneously over time, typically over one to two years, and respond to treatment modalities including pressure therapy, silicone gel sheeting, and intralesional corticosteroid injection.

Keloids represent pathologic scar formation in which collagen deposition extends beyond the boundaries of the original wound, invading surrounding normal tissue in a tumor-like fashion. These lesions occur more frequently in individuals with darker skin pigmentation and demonstrate familial clustering suggesting genetic predisposition, with common locations including the earlobes, shoulders, chest, and upper back. Keloids characteristically do not regress spontaneously and have high recurrence rates after surgical excision alone, often exceeding fifty percent. Multimodal treatment approaches combining excision with adjuvant therapies such as intralesional corticosteroid injection, radiation therapy, or pressure earrings for earlobe keloids offer improved outcomes compared to single-modality treatment.

Chronic wounds are defined as wounds that fail to progress through the normal healing sequence within expected timeframes, typically three months for most wounds. Venous ulcers represent the most common chronic lower extremity wounds, occurring in the gaiter distribution of the medial malleolus and resulting from venous hypertension causing tissue damage and impaired healing. Arterial ulcers occur in the context of peripheral arterial disease, typically located distally on the toes or lateral ankle, presenting as painful punched-out lesions with pale or necrotic bases. Diabetic ulcers develop at pressure points on the foot, often in the setting of peripheral neuropathy that prevents patients from sensing tissue damage, combined with impaired healing mechanisms and increased susceptibility to infection.

Wound healing failure occurs when multiple factors combine to prevent progression through normal healing phases, requiring systematic evaluation to identify and correct contributing factors. Infection must be ruled out and treated when present, as biofilm formation in chronic wounds creates persistent bacterial presence that impedes healing despite topical antimicrobial therapy. Tissue perfusion assessment using ankle-brachial index, toe pressures, or transcutaneous oxygen measurement helps determine whether revascularization is necessary to support healing. Nutritional status, glycemic control in diabetics, offloading of pressure in diabetic foot ulcers, and compression therapy for venous disease represent additional modifiable factors that must be optimized for chronic wound healing.

<image>Panel A: A clinical comparison of hypertrophic scar confined to the original wound boundary versus keloid scar extending beyond the wound margins into surrounding normal skin. Panel B: A lower extremity diagram showing typical locations and characteristics of venous ulcers at the medial malleolus, arterial ulcers at the lateral ankle and toes, and diabetic ulcers at pressure points on the plantar foot. Panel C: Silicone gel sheet application and pressure garment use for hypertrophic scar treatment with before and after photographs demonstrating improvement. Panel D: A chronic wound evaluation algorithm flowchart showing systematic assessment of infection, perfusion, nutrition, offloading, and compression with treatment pathways for each factor.</image>

VI. Wound Closure Techniques

Suture materials are classified as absorbable or non-absorbable and monofilament or braided, with selection based on tissue requirements, healing time, and desired characteristics. Absorbable sutures including polyglactin, poliglecaprone, and polydioxanone undergo degradation through hydrolysis or enzymatic action and are used for deep tissue layers that will not be removed. Non-absorbable sutures such as nylon, polypropylene, and silk provide permanent tensile strength and are typically used for skin closure where they can be removed or for applications requiring permanent suture such as vascular anastomosis. Monofilament sutures slide through tissue more easily and harbor fewer bacteria than braided sutures, while braided sutures have better knot security and handling characteristics.

Suture size selection follows the principle of using the smallest suture that will adequately hold tissue under expected tension, as larger sutures cause more tissue reaction and leave larger needle tracks. Fascial closure typically requires heavy sutures such as zero or two-zero to provide strength through the early healing period before collagen deposition increases wound tensile strength. Subcutaneous closure uses intermediate sizes such as three-zero or four-zero absorbable sutures to eliminate dead space and reduce tension on the skin closure. Skin closure with three-zero to five-zero sutures depends on location, with face and eyelid requiring five-zero or six-zero sutures for optimal cosmesis while scalp and trunk may use larger sutures.

Closure techniques include simple interrupted sutures as the most versatile method, providing good wound edge eversion and the ability to remove individual sutures if wound complications develop. Running or continuous sutures allow more rapid closure and distribute tension evenly along the wound but require removal of the entire suture line if infection develops. Vertical mattress sutures provide excellent wound edge eversion and are particularly useful in skin that tends to invert or in thick skin where simple sutures may not adequately approximate deep layers. Horizontal mattress sutures are useful for high-tension closures but may cause more ischemia at wound edges if tied too tightly. Subcuticular running sutures provide excellent cosmesis by placing suture entirely within the dermis without surface marks.

Alternative closure methods include surgical staples, which allow rapid wound closure and are commonly used for scalp lacerations and surgical incisions where cosmesis is less critical. Tissue adhesives such as octyl-cyanoacrylate provide a rapid, painless closure method for clean, low-tension wounds, forming a protective barrier that sloughs off as the wound heals. Adhesive strips such as Steri-Strips may be used as primary closure for superficial, low-tension wounds or as adjuncts to support sutured wounds after suture removal. Negative pressure wound therapy creates a controlled subatmospheric environment that promotes wound healing through removal of excess fluid, reduction of edema, and stimulation of granulation tissue formation.

<image>Panel A: A comparison display of common suture materials showing absorbable versus non-absorbable and monofilament versus braided categories with examples and primary uses for each type. Panel B: A diagram showing proper suture size selection by anatomic layer from fascia using zero or one suture through subcutaneous using three-zero to four-zero to skin using four-zero to five-zero. Panel C: Step-by-step illustrations of closure techniques including simple interrupted, running, vertical mattress, horizontal mattress, and subcuticular sutures with cross-sectional views showing tissue bite patterns. Panel D: Alternative closure methods displayed including staple application, tissue adhesive application, adhesive strip placement, and negative pressure wound therapy device application.</image>

VII. Surgical Site Infection Prevention

The CDC surgical site infection prevention bundle encompasses evidence-based interventions that when implemented together significantly reduce infection rates compared to individual measures. Prophylactic antibiotics must be administered within sixty minutes before incision to achieve adequate tissue concentrations, with the specific agent selected based on expected organisms for the surgical site and patient-specific factors such as allergies and MRSA colonization. Hair removal should be avoided when possible, and when necessary should be performed with clippers immediately before surgery rather than razors that cause microscopic skin injury harboring bacteria. Perioperative glucose control targeting blood glucose below one hundred eighty milligrams per deciliter reduces infection risk, particularly in diabetic patients and those undergoing cardiac surgery.

Antibiotic prophylaxis selection follows established guidelines that match antimicrobial spectrum to expected wound flora for each surgical procedure. Cefazolin serves as the first-line agent for most clean and clean-contaminated procedures, providing coverage against staphylococci and streptococci that represent the predominant skin flora. Colorectal and other gastrointestinal procedures require additional anaerobic coverage, typically achieved by adding metronidazole to cefazolin or using a single agent with broad spectrum such as ertapenem or piperacillin-tazobactam. Patients colonized with methicillin-resistant Staphylococcus aureus or those with beta-lactam allergies require alternative agents such as vancomycin. Duration of prophylaxis should not exceed twenty-four hours postoperatively, as extended antibiotic courses do not reduce infection rates and promote antimicrobial resistance.

Intraoperative measures for infection prevention include meticulous sterile technique with all team members adhering to principles of asepsis throughout the procedure. Gentle tissue handling minimizes devitalization that creates ischemic tissue susceptible to bacterial colonization and impairs local immune defenses. Maintenance of hemostasis prevents hematoma formation that serves as culture medium for bacteria and separates tissue layers. Dead space elimination through appropriate suture techniques and drain placement when indicated removes potential fluid collection sites. Wound irrigation, particularly for contaminated cases, dilutes bacterial load though the benefit of antibiotics added to irrigation solutions remains controversial.

Postoperative wound care begins with application of a sterile dressing at the conclusion of surgery, which should remain in place and undisturbed for twenty-four to forty-eight hours while initial epithelialization creates a barrier against bacterial invasion. Hand hygiene before and after any wound contact represents the single most important measure for preventing healthcare-associated infection transmission. Daily wound inspection allows early detection of infection, with patients educated to monitor for signs including increasing redness, warmth, swelling, drainage, or fever. Uncomplicated surgical wounds may be left open to air and showered after forty-eight hours, with evidence indicating that this does not increase infection risk.

<image>Panel A: The CDC surgical site infection prevention bundle displayed as interconnected elements including appropriate antibiotic timing, hair removal technique, glucose control, and normothermia maintenance. Panel B: A surgical prophylaxis antibiotic selection guide organized by procedure type from clean through dirty with recommended agents and timing for each category. Panel C: An operating room scene demonstrating infection prevention principles including sterile technique, gentle tissue handling, meticulous hemostasis, and irrigation. Panel D: A postoperative wound care timeline showing sterile dressing application, first dressing change at twenty-four to forty-eight hours, transition to showering, and patient education regarding infection warning signs.</image>

VIII. Surgical Drains

The purposes of surgical drain placement include removal of anticipated fluid collections such as seroma or blood, monitoring for complications such as anastomotic leak or bleeding, decompression of organs or cavities, and obliteration of dead space to prevent fluid accumulation. Prophylactic drains are placed in anticipation of expected fluid accumulation, while therapeutic drains address established collections. The decision to place a drain requires weighing the benefits of fluid removal against the risks of drain-related complications including infection, erosion into adjacent structures, and pain. Evidence-based evaluation of drain utility has led to reduced drain use in many surgical procedures where routine drainage was previously standard practice.

Passive drains rely on gravity and capillary action to remove fluid and include the Penrose drain, a flat latex tube placed in the wound with the external end covered by dressings that absorb drainage. Passive drains function as open systems that may allow bidirectional flow, creating a potential pathway for bacterial entry into the wound. Active drains utilize closed suction systems that create negative pressure to evacuate fluid, with examples including Jackson-Pratt drains featuring a grenade-shaped bulb and Blake drains with a flat channel design. Closed suction drainage systems reduce infection risk compared to open systems by preventing external contamination and maintaining continuous negative pressure that collapses dead space.

Drain management requires monitoring of output volume, color, and character to assess wound healing and detect complications. Output should be recorded at regular intervals, typically every eight to twelve hours, with significant changes in volume or character prompting clinical evaluation. Bloody output is expected initially after surgery and should progressively decrease and transition to serosanguinous then serous drainage. High-volume serous output may indicate seroma formation, while bilious or enteric-appearing drainage suggests anastomotic leak or injury requiring urgent evaluation. Drain site care includes keeping the insertion site clean and dry, securing the drain to prevent dislodgement, and maintaining patency of closed suction systems.

Evidence regarding drain utility varies by surgical procedure, with some long-standing practices not supported by contemporary literature. Cholecystectomy typically does not require routine drain placement, with multiple randomized trials demonstrating no benefit and potential harm from drains. Thyroidectomy drain placement has declined as evidence suggests drains do not prevent clinically significant hematoma and may increase pain and length of stay. Colorectal anastomoses present ongoing controversy, with some surgeons favoring selective drainage for low pelvic anastomoses while omitting drains for higher colorectal connections. Pancreatic surgery generally warrants drain placement given the consequences of uncontrolled pancreatic fistula, though early drain removal based on amylase levels can reduce complications.

<image>Panel A: A diagram showing the various purposes of surgical drain placement including evacuation of seroma and blood, detection of anastomotic leak, and obliteration of dead space with visual examples of each scenario. Panel B: A comparison of passive Penrose drain and active closed suction Jackson-Pratt drain showing mechanism of action, advantages, and infection risk profiles. Panel C: A drain output recording chart showing expected progression from bloody to serosanguinous to serous drainage with alert indicators for concerning output characteristics. Panel D: A summary of evidence-based drain recommendations by surgical procedure showing procedures where drains are rarely needed, selectively used, and routinely indicated.</image>

IX. Wound Dressings

The functions of wound dressings extend beyond simple protection to include maintenance of optimal moisture balance, absorption of excess exudate, provision of compression for hemostasis, and facilitation of autolytic debridement. The moist wound healing paradigm recognizes that epithelialization proceeds more rapidly in a moist environment, and dressings that maintain appropriate moisture levels optimize healing rates. Excessive moisture leads to maceration of surrounding skin and increased bacterial proliferation, while desiccation causes cell death and impairs migration of epithelial cells across the wound surface. The ideal dressing maintains a balance appropriate for the specific wound, with various products designed for wounds producing different amounts of exudate.

Traditional gauze dressings remain widely used for their availability, low cost, and versatility in wound packing, coverage, and absorption. Non-adherent gauze and petroleum-impregnated gauze prevent disruption of newly formed epithelium during dressing changes and are particularly appropriate for superficial wounds and skin graft donor sites. Hydrocolloid dressings contain gel-forming agents that absorb exudate while maintaining moisture, creating an occlusive environment that promotes autolytic debridement of necrotic tissue. Alginate dressings derived from seaweed absorb large amounts of exudate and are appropriate for heavily draining wounds, while foam dressings provide moderate absorption with cushioning properties suitable for wounds overlying bony prominences.

Negative pressure wound therapy applies controlled subatmospheric pressure to the wound through an airtight dressing connected to a vacuum source. This modality promotes wound healing through multiple mechanisms including removal of excess wound fluid, reduction of bacterial load, stimulation of granulation tissue formation through mechanical stretch of cells, and enhancement of perfusion at wound edges. Indications include complex wounds with large tissue defects, wounds with extensive undermining, exposed bone or tendon, and wounds in the open abdomen. Negative pressure wound therapy is contraindicated over exposed blood vessels, in the presence of untreated osteomyelitis, over malignant tissue, and in wounds with unexplored fistulas to body cavities.

Wound care principles emphasize maintaining appropriate moisture levels and removing necrotic tissue to promote healing progression. Sharp debridement using scalpel or scissors provides rapid removal of devitalized tissue but requires procedural skill and may cause pain and bleeding. Enzymatic debridement using collagenase preparations offers a selective, painless alternative that digests necrotic tissue over time. Autolytic debridement occurs naturally under occlusive dressings as endogenous enzymes in wound fluid liquefy necrotic material. The underlying cause of chronic wounds must be addressed for healing to proceed, with compression for venous disease, revascularization for arterial insufficiency, offloading for diabetic foot ulcers, and control of infection representing essential components of comprehensive wound management.

<image>Panel A: A visual guide to dressing selection based on wound exudate level showing low-exudate wounds managed with hydrocolloids, moderate exudate with foams, and high exudate with alginates. Panel B: The negative pressure wound therapy system displayed with foam dressing applied to wound, transparent adhesive seal, and connection to vacuum device with canister for collecting wound fluid. Panel C: A comparison of debridement methods including sharp debridement with scalpel, enzymatic debridement with collagenase, and autolytic debridement under occlusive dressing. Panel D: A wound care algorithm showing assessment of wound characteristics, selection of appropriate dressing, frequency of dressing changes, and criteria for transitioning to different dressings as wound healing progresses.</image>

X. Special Wound Situations

Contaminated wounds from trauma require systematic evaluation including assessment of mechanism, time since injury, tetanus status, and presence of foreign bodies or devitalized tissue. Wound irrigation with copious volumes of saline or water under low pressure reduces bacterial load and removes debris, with high-pressure irrigation potentially causing additional tissue damage and driving bacteria deeper into tissues. Debridement of devitalized tissue removes substrates for bacterial growth and is essential for healing, though careful judgment is required to preserve viable tissue and important structures. Delayed primary closure after three to five days of open wound management with dressing changes allows contaminated wounds to declare themselves as either clean, permitting closure, or infected, requiring continued open management.

Animal bites present unique challenges based on the mechanism of injury and microbiology of oral flora for different species. Dog bites cause crushing injuries from powerful jaws with mixed aerobic and anaerobic flora, and may be closed primarily when located on the face but are often left open elsewhere due to moderate infection risk. Cat bites create deep puncture wounds that seed bacteria into deep tissues, carry high infection risk approaching fifty percent, and are generally not closed primarily. Human bites carry high infection risk from oral flora including Eikenella corrodens and should not be closed primarily, with clenched-fist injuries from teeth striking the hand representing a particularly high-risk pattern requiring careful evaluation of tendon and joint involvement.

Burns are classified by depth, which determines healing potential and need for surgical intervention. Superficial burns involve only the epidermis, appear erythematous and painful, and heal within three to five days without scarring. Superficial partial thickness burns extend into the papillary dermis, form blisters over moist pink painful tissue, and heal in seven to fourteen days with good cosmetic outcomes. Deep partial thickness burns extend into the reticular dermis, appear pale with decreased sensation, heal in two to four weeks with scarring, and may benefit from excision and grafting. Full thickness burns destroy the entire dermis, appear waxy or leathery with absent sensation, will not heal spontaneously, and require excision and skin grafting.

Pressure ulcers result from sustained pressure over bony prominences that exceeds capillary closing pressure, causing tissue ischemia and necrosis. Staging ranges from Stage 1 with intact skin and non-blanchable erythema through Stage 4 with full-thickness tissue loss exposing bone, muscle, or tendon. Prevention through frequent repositioning, pressure-redistribution surfaces, and optimization of nutrition represents the most effective management strategy. Treatment of established pressure ulcers requires offloading of pressure as the fundamental intervention, along with optimization of nutrition, treatment of infection, debridement of necrotic tissue, and appropriate wound dressing selection, with surgical reconstruction reserved for deep ulcers that fail conservative management.

<image>Panel A: A contaminated wound management flowchart showing initial irrigation and debridement, assessment of contamination level, decision for primary versus delayed primary closure, and tetanus prophylaxis guidelines. Panel B: A comparison of bite wound characteristics and management for dog, cat, and human bites including mechanism, infection risk, microbiology, and closure recommendations. Panel C: Burn depth classification displayed as cross-sectional skin diagrams showing superficial, superficial partial thickness, deep partial thickness, and full thickness burns with clinical appearance and healing characteristics. Panel D: Pressure ulcer staging from Stage 1 through Stage 4 shown over a bony prominence with tissue layers indicating depth of injury and corresponding treatment approaches for each stage.</image>

Summary

• Wound healing progresses through four overlapping phases: hemostasis occurring immediately, inflammation over days one through four, proliferation from days four through twenty-one, and remodeling from three weeks up to two years
• Primary intention closure approximates wound edges for rapid healing; secondary intention allows wounds to granulate and contract; tertiary intention uses delayed closure after initial open management
• Surgical wound classification predicts infection risk: Clean less than two percent, Clean-contaminated five to ten percent, Contaminated ten to twenty percent, and Dirty twenty to forty percent
• Local factors impairing healing include infection, ischemia, foreign bodies, and excessive tension; systemic factors include diabetes, malnutrition, steroid use, and smoking
• Nutritional support for wound healing requires adequate protein, vitamin C for collagen cross-linking, vitamin A for epithelialization, and zinc for cell proliferation
• Wound complications include seroma requiring aspiration, hematoma requiring evacuation if large, surgical site infection requiring drainage and antibiotics, and dehiscence requiring surgical repair
• Suture selection matches material to tissue with absorbable sutures for deep layers and appropriate size being the smallest that maintains adequate strength
• SSI prevention bundles include antibiotic prophylaxis within sixty minutes, clipping rather than shaving, glucose control below one hundred eighty, and maintenance of normothermia
• Drain placement should be selective based on evidence, with removal when output decreases and no longer serves the original purpose
• Negative pressure wound therapy promotes healing of complex wounds through fluid removal, bacterial reduction, and stimulation of granulation tissue

Key Terms

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