# Wound Care and Surgical Complications ## Year 4: Sub-Internship Surgery --- ## Learning Objectives By the end of this seminar, students will be able to: 1. Describe the phases of wound healing and identify factors that impair tissue repair 2. Perform systematic wound assessment and recognize early signs of wound complications 3. Classify and appropriately manage surgical site infections at different tissue levels 4. Recognize and respond to wound dehiscence including the emergency management of evisceration 5. Apply appropriate dressing selection and wound care techniques including negative pressure therapy 6. Identify and manage systemic complications of surgery including sepsis and thromboembolic disease --- ## Section I: Wound Healing Physiology Wound healing proceeds through four overlapping phases that restore tissue integrity following injury. Hemostasis begins immediately upon tissue disruption as platelets aggregate at the injury site and the coagulation cascade generates fibrin to stabilize the clot. This platelet plug serves as a provisional matrix and releases growth factors that initiate subsequent phases. Vasoconstriction limits initial blood loss, followed by vasodilation that brings inflammatory cells to the wound. The hemostatic phase establishes the foundation for tissue repair and typically completes within minutes to hours of injury. The inflammatory phase mobilizes immune cells to clear debris and prevent infection. Neutrophils arrive within hours and predominate during the first two to three days, phagocytosing bacteria and releasing proteases that begin matrix breakdown. Macrophages become the predominant cell type by days three through five, continuing debris clearance while secreting growth factors that drive the transition to proliferation. The inflammatory response is essential for normal healing; its prolongation by infection, foreign bodies, or chronic disease impairs repair. Clinical manifestations include erythema, warmth, swelling, and pain at the wound site during this period. Proliferation rebuilds the tissue defect through coordinated cellular activities spanning approximately days four through twenty-one. Fibroblasts migrate into the wound and synthesize collagen, creating the extracellular matrix that provides structural integrity. Angiogenesis generates new blood vessels to supply the metabolically active healing tissue, creating the characteristic red, granular appearance of granulation tissue. Epithelialization resurfaces the wound as keratinocytes migrate from wound edges and skin appendages. Wound contraction reduces the defect size through myofibroblast activity. These simultaneous processes progressively close the wound and restore barrier function. Remodeling continues for months to years after wound closure, progressively strengthening and reorganizing the repair. Collagen turnover replaces the initial type III collagen with stronger type I collagen. Cross-linking between collagen fibers increases tensile strength, which reaches approximately eighty percent of unwounded tissue by three months but never fully recovers to normal. The wound transitions from raised and red to flat and pale as vascularity decreases and collagen matures. Excessive remodeling produces hypertrophic scars or keloids, while inadequate repair leaves weak scars prone to dehiscence or hernia. ![Wound healing physiology. Panel A: Hemostasis phase with platelet aggregation, fibrin clot formation, vasoconstriction, and growth factor release. Panel B: Inflammatory phase showing neutrophil and macrophage activities with clinical manifestations. Panel C: Proliferation phase elements including fibroblast collagen synthesis, angiogenesis, epithelialization, and contraction. Panel D: Remodeling phase with collagen turnover, cross-linking, strength recovery, and scar maturation.](images/wound_complications_section1.png) --- ## Section II: Factors Affecting Wound Healing Local wound factors directly impact the tissue environment and healing capacity. Infection prolongs the inflammatory phase, consumes nutrients, and produces tissue-damaging toxins and enzymes. Foreign bodies, including retained suture material or debris, perpetuate inflammation and may harbor bacteria. Tissue ischemia from vascular disease, pressure, or tension impairs oxygen and nutrient delivery essential for cellular activities. Radiation induces fibrosis and damages vasculature, creating chronic wounds that resist healing. Local tissue edema increases diffusion distances and may compress microvessels. Repeated trauma from dressing changes or patient manipulation disrupts the healing process. Systemic conditions affect healing capacity throughout the body. Diabetes mellitus impairs multiple aspects of wound healing including inflammatory cell function, collagen synthesis, and angiogenesis; additionally, neuropathy prevents recognition of injury and vascular disease limits perfusion. Malnutrition deprives wounds of protein for matrix synthesis, vitamins for enzymatic processes, and calories for energy-demanding cellular work. Immunosuppression, whether from disease or medications, increases infection risk and may impair normal inflammatory signaling. Age-related changes slow all phases of healing and reduce physiologic reserve for complications. Smoking causes vasoconstriction, reduces oxygen delivery, and impairs collagen synthesis. Medications can significantly impair or support wound healing. Corticosteroids suppress inflammation, impair fibroblast function, and reduce collagen synthesis; chronic steroid use substantially increases wound complications. Non-steroidal anti-inflammatory drugs may impair early healing by suppressing the inflammatory phase. Chemotherapeutic agents affect rapidly dividing cells including those involved in wound repair. Anticoagulants increase hematoma risk, which can compromise wounds mechanically and serve as infection medium. Conversely, supplemental vitamin C supports collagen synthesis, and zinc supplementation may benefit deficient patients. Wound classification predicts infection risk and healing potential. Clean wounds involve no entry into respiratory, gastrointestinal, or genitourinary tracts and have less than two percent infection risk. Clean-contaminated wounds involve controlled entry into hollow viscera without spillage and carry three to ten percent infection risk. Contaminated wounds include gross spillage, traumatic wounds, or major breaks in technique with fifteen to twenty percent infection risk. Dirty wounds have established infection, devitalized tissue, or fecal contamination with greater than thirty percent infection risk. Classification guides antibiotic use, closure decisions, and patient counseling about expected outcomes. ![Factors affecting wound healing. Panel A: Local factors including infection, foreign bodies, ischemia, radiation, edema, and trauma with mechanisms of impairment. Panel B: Systemic conditions including diabetes, malnutrition, immunosuppression, age, and smoking with healing impacts. Panel C: Medication effects on healing for steroids, NSAIDs, chemotherapy, and anticoagulants. Panel D: Wound classification from clean through dirty with infection rates and examples.](images/wound_complications_section2.png) --- ## Section III: Wound Assessment Systematic daily wound examination detects complications early and documents healing progress. Wound edges are assessed for approximation, noting whether edges meet as intended or show separation suggesting early dehiscence. Tissue color indicates perfusion and viability: pink tissue suggests healthy perfusion, pale tissue may indicate ischemia, and dark tissue raises concern for necrosis. Edge eversion, maintained by proper suturing technique, promotes healing, while inversion creates a potential dead space. Sutures or staples are evaluated for tension, loosening, or tissue reaction. The overall wound trajectory, whether improving or worsening compared to previous examinations, guides management decisions. Drainage assessment provides important information about wound status. Amount is characterized as none, scant, small, moderate, or large, with trends over time more meaningful than single measurements. Character is described as serous (clear or straw-colored), sanguinous (bloody), serosanguinous (pink, mixing blood and serum), or purulent (thick, opaque, potentially colored). Serous or serosanguinous drainage is expected in early healing, while purulent drainage indicates infection. Increasing drainage after initial decrease suggests developing complication. Odor should be absent; foul smell strongly suggests anaerobic infection. Drainage through drain sites versus through the incision itself has different implications. Periincisional tissue examination extends assessment beyond the wound itself. Erythema is characterized by extent, measuring the distance from wound edge, and by quality, whether fading gradually or sharply demarcated. Expanding erythema over time indicates spreading cellulitis requiring treatment. Warmth accompanies inflammation and may be normal immediately post-operatively but persisting warmth suggests infection. Induration describes firmness of surrounding tissue, which may indicate cellulitis, hematoma, or seroma. Crepitus, the sensation of air in tissues, constitutes an emergency suggesting necrotizing infection. Fluctuance indicates fluid collection requiring drainage. Documentation creates a medical-legal record and enables tracking of wound trajectory. Description includes all assessed elements in consistent format allowing comparison over time. Measurements of wound dimensions and erythema extent provide objective data. Photography supplements written description for complex wounds and provides visual comparison over time. The care performed, including dressing changes and drainage procedures, is recorded. Any changes in management prompted by assessment findings are documented with clinical reasoning. Clear, thorough documentation communicates wound status to other providers and supports continuity of care. ![Wound assessment. Panel A: Wound edge evaluation including approximation, tissue color, eversion, and suture status. Panel B: Drainage characterization by amount categories, character types, odor significance, and trajectory interpretation. Panel C: Periincisional examination for erythema extent, warmth, induration, crepitus, and fluctuance. Panel D: Documentation elements including descriptions, measurements, photography, care performed, and rationale.](images/wound_complications_section3.png) --- ## Section IV: Surgical Site Infection Surgical site infection classification determines management approach and guides treatment intensity. Superficial incisional infections involve only skin and subcutaneous tissue above the fascia, typically presenting with localized erythema, warmth, tenderness, and purulent drainage from the incision. Deep incisional infections extend to fascia or muscle layers and present with deeper pain, systemic symptoms, and potentially drainage from deeper tissues through the incision or through drains. Organ-space infections occur in any manipulated space deep to the fascia and may present as abscesses, anastomotic leaks, or other deep collections. The distinction guides both antibiotic selection and the extent of surgical intervention required. Diagnosis of surgical site infection relies primarily on clinical findings rather than laboratory tests. Purulent drainage from the incision confirms superficial infection without need for culture. Erythema, warmth, and tenderness surrounding the incision suggest infection but may also reflect normal inflammation. Wound dehiscence may result from or be complicated by infection. Systemic signs including fever, elevated white blood cell count, and tachycardia support the diagnosis, particularly for deep or organ-space infections. Imaging with CT scan identifies deep collections not apparent on examination. Culture of purulent drainage guides antibiotic selection but is not required for diagnosis or initial treatment. Risk factors for surgical site infection include both patient and procedural characteristics. Patient factors include diabetes with poor glycemic control, obesity, smoking, immunosuppression, and malnutrition. Procedural factors include wound classification, operative duration, blood loss, inadequate antibiotic prophylaxis, and breaks in sterile technique. Pre-operative risk is assessed using validated tools such as the National Surgical Quality Improvement Program risk calculator. Modifiable factors should be addressed before elective surgery when possible. Post-operative glycemic control, maintaining normothermia, and appropriate wound care reduce infection risk. Management depends on infection depth and severity. Superficial infections require opening the wound to allow drainage, which often resolves infection without antibiotics. The wound is packed with moist gauze and heals by secondary intention. Antibiotics are added for surrounding cellulitis, systemic symptoms, or immunocompromised patients. Deep incisional infections require wound opening, debridement of devitalized tissue, and antibiotics. Organ-space infections typically require drainage, either percutaneous under imaging guidance or surgical. Antibiotic selection initially covers expected organisms based on the procedure; culture results guide subsequent narrowing. Duration is typically seven to ten days but may be extended for deep infections. ![Surgical site infection. Panel A: Classification by depth showing superficial incisional, deep incisional, and organ-space infections with typical presentations. Panel B: Diagnostic criteria including purulent drainage, clinical signs, systemic findings, imaging, and culture role. Panel C: Risk factors categorized as patient factors and procedural factors with examples of each. Panel D: Management approach by infection type including wound opening, debridement, drainage, and antibiotic guidance.](images/wound_complications_section4.png) --- ## Section V: Wound Dehiscence Wound dehiscence encompasses a spectrum from superficial skin separation to fascial disruption to evisceration. Superficial dehiscence involves separation of skin and subcutaneous tissue while the fascial closure remains intact. Fascial dehiscence indicates failure of the musculofascial layer, creating a significant defect even if skin remains closed. Evisceration represents the most severe form, with bowel or other abdominal contents protruding through the wound. Each level carries different implications and requires distinct management. Early recognition allows intervention before progression to more severe categories. Multiple factors contribute to dehiscence risk. Malnutrition, particularly protein deficiency, impairs collagen synthesis needed for tissue repair. Obesity creates wound tension and is associated with poorer tissue perfusion. Infection, whether clinical or subclinical, directly damages healing tissue and prolongs inflammation. Technical factors including excessive tension, ischemia from tight sutures, and inadequate fascial bites affect closure integrity. Increased intra-abdominal pressure from coughing, straining, or ileus stresses the closure. Steroids and other immunosuppressive medications impair wound healing. Emergency surgery allows less optimal conditions than elective procedures. The presentation of dehiscence typically occurs between post-operative days five and ten, though timing varies. Serosanguinous or salmon-colored drainage from the wound often precedes visible dehiscence and should prompt urgent wound examination. Visible wound separation indicates superficial dehiscence. A palpable fascial defect beneath intact skin or through a partial wound opening indicates fascial dehiscence. Evisceration presents dramatically with bowel or omentum visible or protruding through the wound. Patients may report a popping sensation or sudden gush of fluid. The finding of evisceration constitutes a surgical emergency. Management depends on dehiscence severity and patient condition. Superficial dehiscence is managed with wound care, typically wet-to-dry dressings, allowing healing by secondary intention. Fascial dehiscence requires operative repair to restore abdominal wall integrity and prevent evisceration. Evisceration management begins immediately: the exposed bowel is covered with saline-soaked sterile gauze to prevent desiccation; the patient is kept NPO and volume resuscitated; and emergent operative repair is arranged. Intraoperatively, the bowel is inspected for injury, the wound is irrigated, and the fascia is closed, often with retention sutures for additional security. ![Wound dehiscence. Panel A: Spectrum from superficial skin separation through fascial disruption to evisceration with anatomic diagrams. Panel B: Risk factors including malnutrition, obesity, infection, technical factors, IAP increase, and steroids. Panel C: Presentation features including serosanguinous drainage, visible separation, palpable defect, and evisceration recognition. Panel D: Management by type including wound care for superficial, operative repair for fascial, and emergency protocol for evisceration.](images/wound_complications_section5.png) --- ## Section VI: Wound Fluid Collections Seroma represents accumulation of serous fluid in a surgical dead space. Disruption of lymphatics during dissection creates fluid leakage that accumulates when not adequately drained. Procedures involving extensive tissue dissection, particularly lymph node dissection, mastectomy, and hernia repair, carry higher seroma risk. Presentation includes fluctuant swelling at the surgical site without erythema, warmth, or systemic symptoms. Small seromas may be observed and often resolve spontaneously with compression. Larger seromas causing discomfort or wound tension benefit from needle aspiration with sterile technique. Recurrent seromas may require placement of a drain or sclerotherapy. Hematoma results from inadequate hemostasis or post-operative bleeding into the surgical site. Early hematomas develop within hours of surgery from vessel bleeding not controlled during the procedure. Delayed hematomas may result from anticoagulation resumption or dislodgement of clots. Presentation includes painful swelling, ecchymosis, and potentially visible bulging at the surgical site. Small, stable hematomas may be observed as the body resorbs the collection. Expanding hematomas require surgical evacuation to achieve hemostasis and prevent wound compromise. Large hematomas increase infection risk and should generally be evacuated. Hematomas compressing vital structures, such as neck hematomas compromising the airway, require emergent evacuation. Abscess represents a walled-off collection of purulent material requiring drainage for resolution. Surgical site abscesses may develop at the incision or in deeper spaces manipulated during surgery. Presentation includes localized pain, fever, erythema, and fluctuance; deeper abscesses may present with fever and elevated white count without localizing examination findings. CT scan identifies deep abscesses and guides drainage approach. Superficial abscesses are drained by opening the wound. Deep abscesses may be drained percutaneously under CT or ultrasound guidance or may require operative drainage when not accessible percutaneously. Antibiotics supplement drainage but cannot replace it; antibiotic therapy alone for undrained abscess leads to treatment failure. Lymphocele specifically refers to lymphatic fluid collection, typically following procedures involving lymph node dissection such as axillary dissection, groin dissection, or retroperitoneal procedures. Unlike seroma, which may contain mixed fluid, lymphocele contains pure lymph. Presentation resembles seroma with fluctuant collection at the surgical site. Initial management involves observation for small collections and aspiration for larger or symptomatic ones. Recurrence is common after aspiration alone. Definitive management options include prolonged closed suction drainage, sclerotherapy with agents such as doxycycline, or surgical marsupialization creating a window for drainage into the peritoneal cavity. ![Wound fluid collections. Panel A: Seroma pathophysiology, risk procedures, presentation, and management from observation through aspiration to drainage. Panel B: Hematoma causes, early versus delayed timing, presentation, and management based on size and stability. Panel C: Abscess formation, presentation with superficial versus deep considerations, imaging role, and drainage principles. Panel D: Lymphocele following lymph node procedures with management options including observation, aspiration, sclerotherapy, and marsupialization.](images/wound_complications_section6.png) --- ## Section VII: Advanced Wound Care Dressing selection matches wound characteristics to promote optimal healing. Dry gauze provides simple protection for closed, healing incisions. Wet-to-dry dressings, applied moist and allowed to dry before removal, provide mechanical debridement for wounds with necrotic tissue, though they may damage healthy tissue. Non-adherent dressings protect granulating tissue from trauma during dressing changes. Foam dressings absorb moderate drainage while maintaining moisture balance. Alginate dressings, derived from seaweed, absorb heavy drainage and conform to wound contours. Hydrocolloid dressings maintain moist environments for autolytic debridement of minimal slough. Silver-impregnated dressings provide antimicrobial activity for contaminated or infected wounds. Matching dressing to wound phase and drainage level optimizes healing. Negative pressure wound therapy (wound VAC) accelerates healing of complex wounds through multiple mechanisms. Continuous or intermittent subatmospheric pressure removes wound fluid and edema. Mechanical forces promote granulation tissue formation and wound contraction. Reduced bacterial load lowers infection risk. Indications include complex wounds with tissue loss, wounds healing by secondary intention, open abdominal wounds, and skin graft bolstering. Contraindications include untreated infection, necrotic tissue requiring debridement, exposed vessels or organs, and malignancy in the wound. Typical settings range from negative seventy-five to negative one hundred twenty-five mmHg. Dressing changes occur every forty-eight to seventy-two hours or when seal is lost. Debridement removes necrotic tissue that impairs healing and harbors bacteria. Sharp debridement uses scalpel or scissors to excise devitalized tissue, providing immediate and precise removal. Mechanical debridement with wet-to-dry dressings physically removes debris with dressing changes, though this method is less selective. Enzymatic debridement applies collagenase or other enzymes that selectively digest necrotic tissue while sparing viable tissue. Autolytic debridement uses occlusive dressings to promote the body's own enzymatic breakdown of devitalized tissue, appropriate for wounds with minimal necrosis. Biological debridement with sterile maggots selectively consumes necrotic tissue and secretes antimicrobial substances. Selection depends on wound characteristics, patient tolerance, and clinical urgency. Wound closure techniques address wounds that cannot or should not close primarily. Healing by secondary intention allows open wounds to granulate from the base and epithelialize from the edges. This approach suits contaminated wounds and those with tissue loss. Delayed primary closure (tertiary intention) leaves the wound open initially for observation or drainage, then closes it surgically once infection is controlled or wound character improves. Skin grafts provide coverage for wounds with adequate granulation base but insufficient tissue for primary closure. Split-thickness grafts, harvested with a dermatome, require a healthy recipient bed and provide durable coverage. Flaps transfer tissue with its blood supply to cover complex defects including exposed bone, tendon, or hardware. ![Advanced wound care. Panel A: Dressing selection guide matching wound type with appropriate dressing including dry gauze, foam, alginate, and silver options. Panel B: Negative pressure wound therapy mechanisms, indications, contraindications, settings, and change frequency. Panel C: Debridement methods comparing sharp, mechanical, enzymatic, autolytic, and biological approaches. Panel D: Closure options including secondary intention, delayed primary closure, skin grafts, and flaps with indications for each.](images/wound_complications_section7.png) --- ## Section VIII: Thromboembolic Complications Deep venous thrombosis risk increases substantially following surgery. Virchow's triad elements converge in surgical patients: stasis from immobility, endothelial injury from positioning and surgical manipulation, and hypercoagulability from surgical stress response. Procedure-specific risks vary, with orthopedic and pelvic surgery carrying highest risk. Patient factors including prior VTE, malignancy, obesity, advanced age, and inherited thrombophilias compound procedural risk. Risk assessment tools stratify patients into categories guiding prophylaxis intensity. The combination of surgical and patient factors creates a period of elevated risk extending beyond hospitalization. DVT presentation may be subtle or dramatic. Unilateral leg swelling represents the most common finding, with asymmetric calf or thigh circumference. Pain, often described as cramping or tightness, may be present. Warmth and erythema along the venous distribution occur with significant thrombosis. Homans' sign, calf pain with dorsiflexion, is neither sensitive nor specific and should not guide diagnosis. Palpable venous cord indicates superficial thrombophlebitis. Upper extremity DVT, increasingly common with central venous catheter use, presents with arm swelling. Asymptomatic DVT is common, underscoring the importance of prophylaxis rather than relying on clinical detection. Pulmonary embolism represents the most feared complication of DVT. Sudden dyspnea, often the presenting symptom, results from pulmonary vascular obstruction and ventilation-perfusion mismatch. Pleuritic chest pain reflects pleural irritation from peripheral emboli. Tachycardia occurs as the heart compensates for increased pulmonary vascular resistance. Hypoxia may be present, though oxygen saturation may be normal with smaller emboli. Hemodynamic instability with hypotension and shock indicates massive PE with significant obstruction. Clinical probability assessment using tools such as the Wells criteria guides diagnostic testing. CT pulmonary angiography provides definitive diagnosis in most cases. Prevention employs both mechanical and pharmacologic approaches tailored to risk level. Mechanical prophylaxis with sequential compression devices enhances venous return and stimulates fibrinolysis; these devices apply to virtually all surgical patients and begin in the operating room. Early ambulation remains the most effective intervention when feasible. Pharmacologic prophylaxis adds anticoagulant protection proportional to VTE risk; options include unfractionated heparin, low-molecular-weight heparin, and fondaparinux. Higher-risk patients may receive extended prophylaxis beyond hospitalization. Treatment of established VTE requires therapeutic anticoagulation; options include heparin, low-molecular-weight heparin, and direct oral anticoagulants. Duration depends on circumstances surrounding the VTE. Inferior vena cava filter placement is reserved for patients who cannot receive anticoagulation. ![Thromboembolic complications. Panel A: DVT risk factors from Virchow's triad, procedure-specific risks, and patient factors. Panel B: DVT presentation with leg swelling, pain, warmth, and consideration of upper extremity DVT. Panel C: Pulmonary embolism presentation including dyspnea, chest pain, tachycardia, hypoxia, and hemodynamic instability. Panel D: Prevention and treatment with mechanical prophylaxis, pharmacologic options, early ambulation, and treatment anticoagulation.](images/wound_complications_section8.png) --- ## Section IX: Anastomotic Complications Anastomotic leak represents failure of a surgical connection between hollow viscera. Risk factors include technical issues such as tension, inadequate blood supply, or improper technique. Patient factors including malnutrition, steroid use, diabetes, and prior radiation impair tissue healing. Emergency surgery increases risk compared to elective procedures. Anatomic location affects leak rate, with colorectal anastomoses carrying higher risk than small bowel connections. Perioperative factors including hypotension, hypoxia, and hypothermia may compromise anastomotic healing. Recognizing high-risk patients allows appropriate monitoring and potentially protective interventions such as proximal diversion. The presentation of anastomotic leak varies from subtle to dramatic. Persistent tachycardia without clear explanation may be the earliest sign, occurring before fever or other symptoms develop. Fever develops as the body responds to extravasated contents and developing infection. Abdominal pain, particularly if out of proportion to expected post-operative discomfort, warrants concern. Peritonitis with diffuse tenderness, guarding, and rebound indicates free perforation. Prolonged ileus beyond expected recovery suggests intra-abdominal process. Output from drains, if present, may show enteric contents. Sepsis with hemodynamic instability indicates severe leak with overwhelming contamination. Diagnosis of suspected anastomotic leak employs clinical assessment and imaging. CT scan with oral and intravenous contrast represents the imaging modality of choice, demonstrating extraluminal fluid, air, or contrast extravasation. Contrast study through a nasogastric tube or rectum can demonstrate leak directly but may miss contained or small leaks. Laboratory findings including elevated white blood cell count, elevated lactate, and new or worsening renal function support the diagnosis. Clinical suspicion remains paramount; imaging may be falsely negative, particularly early in the course. When clinical suspicion is high despite negative imaging, close monitoring or operative exploration may be warranted. Management depends on leak severity and patient condition. Contained leaks with minimal peritonitis may be managed non-operatively with bowel rest, broad-spectrum antibiotics, and percutaneous drainage of any collection. Close monitoring for deterioration is essential. Free perforation with peritonitis requires operative intervention with washout, repair or resection of the anastomosis, and often proximal diversion or end ostomy. Septic patients may require damage control approach with staged return to OR. Nutrition support, typically parenteral, sustains patients during the extended recovery period. The mortality of anastomotic leak is substantial, making prevention through meticulous technique and appropriate patient selection paramount. ![Anastomotic complications. Panel A: Leak risk factors including technical, patient, emergency status, anatomic location, and perioperative factors. Panel B: Presentation spectrum from persistent tachycardia through fever, pain, peritonitis, and ileus to sepsis. Panel C: Diagnostic approach with CT findings, contrast study indications, laboratory abnormalities, and clinical suspicion role. Panel D: Management stratified by contained versus free leak with non-operative, operative, and nutritional support components.](images/wound_complications_section9.png) --- ## Section X: Systemic Complications Sepsis following surgery requires prompt recognition and aggressive management. Surgical causes include wound infection, anastomotic leak, abscess, and device-related infection. Recognition employs screening tools such as qSOFA (respiratory rate greater than or equal to twenty-two, altered mental status, systolic blood pressure less than or equal to one hundred) and SOFA scores for organ dysfunction. Sepsis bundles improve outcomes through standardized care: obtain lactate and blood cultures, administer broad-spectrum antibiotics, and provide volume resuscitation within the first hour. Source control, addressing the surgical cause of sepsis, remains essential; antibiotics alone cannot cure undrained abscess or ongoing leak. De-escalation of antibiotics based on culture results limits resistance development. Multi-organ dysfunction syndrome represents progressive organ failure following severe insult. Respiratory failure manifests as acute respiratory distress syndrome requiring mechanical ventilation. Renal failure presents as oliguria and rising creatinine, potentially requiring renal replacement therapy. Hepatic dysfunction elevates bilirubin and impairs synthetic function. Cardiovascular failure requires vasopressor support despite adequate volume resuscitation. Hematologic dysfunction includes disseminated intravascular coagulation with both clotting and bleeding. Neurologic dysfunction presents as encephalopathy and altered mental status. Management addresses each failing organ while treating the underlying cause. Prognosis worsens with each additional organ involved. Intensive care unit management of the critically ill surgical patient addresses multiple interrelated systems. Ventilator management follows lung-protective strategies with low tidal volumes and appropriate PEEP. Nutrition, preferably enteral, supports healing and immune function. Sedation is minimized with daily awakening trials to reduce delirium and ventilator time. Infection prevention bundles target ventilator-associated pneumonia, catheter-related bloodstream infection, and catheter-associated urinary tract infection. Stress ulcer prophylaxis reduces gastrointestinal bleeding risk. DVT prophylaxis continues throughout the ICU stay. Glycemic control targets below one hundred eighty milligrams per deciliter. Mortality predictors help set expectations and guide goals-of-care discussions. Age strongly predicts outcomes, with elderly patients facing higher surgical mortality. ASA physical status class quantifies baseline health and correlates with complications. Emergency surgery carries substantially higher mortality than elective procedures. Surgical complexity and operative findings affect prognosis. Post-operative complications, particularly when severe or multiple, substantially increase mortality. Comorbidity burden, particularly when involving multiple organ systems, reduces physiologic reserve. These factors inform conversations with patients and families about prognosis, treatment intensity, and care goals. When recovery becomes unlikely, transition to comfort-focused care honors patient values and dignity. ![Systemic complications. Panel A: Sepsis recognition with surgical sources, screening tools, bundle elements, and source control principles. Panel B: Multi-organ dysfunction affecting respiratory, renal, hepatic, cardiovascular, hematologic, and neurologic systems. Panel C: ICU management elements including ventilation, nutrition, sedation, infection prevention, and prophylaxis bundles. Panel D: Mortality predictors including age, ASA class, emergency status, complications, and comorbidities informing goals discussions.](images/wound_complications_section10.png) --- ## Summary Wound healing proceeds through hemostasis, inflammation, proliferation, and remodeling phases, each essential for restoration of tissue integrity. Local factors including infection, ischemia, and foreign bodies, along with systemic conditions including diabetes, malnutrition, and smoking, impair healing and must be optimized when possible. Systematic wound assessment evaluates approximation, drainage, periincisional tissue, and trajectory, with thorough documentation enabling care coordination. Surgical site infections are classified by depth as superficial, deep incisional, or organ-space, with management ranging from simple wound opening to surgical debridement and drainage. Wound dehiscence spans superficial separation to fascial disruption to evisceration; the latter constitutes an emergency requiring immediate wet dressing coverage and operative repair. Fluid collections including seroma, hematoma, and abscess are managed with observation, aspiration, or drainage depending on size and symptoms. Advanced wound care matches dressings to wound characteristics and employs negative pressure therapy for complex wounds, with debridement removing necrotic tissue that impairs healing. Thromboembolic complications are prevented through risk-stratified mechanical and pharmacologic prophylaxis; DVT presents with leg swelling while PE presents with dyspnea and may cause hemodynamic collapse. Anastomotic leak presents with tachycardia, fever, and abdominal pain, requiring imaging confirmation and management ranging from non-operative treatment of contained leaks to operative intervention for free perforation. Systemic complications including sepsis and multi-organ dysfunction require intensive care support while addressing the underlying surgical cause. --- ## Key Terms **SSI (Surgical Site Infection)**: Infection occurring within thirty days of surgery (or within one year for implants) involving the incision or deep tissue manipulated during the procedure. **Dehiscence**: Separation of wound layers, which may be superficial (skin only), fascial (musculofascial layer), or complete (evisceration with bowel exposure). **Evisceration**: Surgical emergency in which abdominal contents protrude through a disrupted wound, requiring immediate wet dressing coverage and emergent operative repair. **Seroma**: Collection of serous fluid in a surgical dead space, typically presenting as fluctuant swelling without inflammatory signs. **Wound VAC (Vacuum-Assisted Closure)**: Negative pressure wound therapy applying subatmospheric pressure to promote granulation, reduce edema, and accelerate healing of complex wounds. **Anastomotic Leak**: Failure of a surgical connection between hollow viscera, allowing extravasation of luminal contents and causing peritonitis or contained abscess. **Incarcerated Hernia**: Hernia in which contents cannot be reduced into the abdominal cavity, potentially progressing to strangulation with vascular compromise. **Strangulated Hernia**: Hernia with vascular compromise of contents causing ischemia and requiring emergent surgical intervention. --- *This content is subject to the [MIT License](https://opensource.org/licenses/MIT). © 2024–2026 Hibbert School of Medicine.*