2. Soft Tissue Infections, Wound Infections, NPWT, and Antibiotic Prophylaxis

I. Soft Tissue Infections

• Soft tissue infection: Infection of skin, subcutaneous tissue, fascia and/or muscle
• Spectrum → Folliculitis → Furuncle/carbuncle → Cellulitis/phlegmon → Abscess → Necrotizing fasciitis/gangrene
• Key exam question → Is there pus? Is there necrosis? Is there systemic toxicity?

Abscess

• Abscess: Localized, encapsulated pus-filled lesion in tissue
• Etiology → Usually Staphylococcus aureus; can be anaerobes/mixed flora depending on site
• Pathomechanism → Infection → Neutrophil infiltration → Tissue liquefaction → Pus cavity + capsule
• Clinical features → Calor, rubor, tumor, dolor, functio laesa
• Typical sign → Fluctuant, tender, warm mass
• May have surrounding cellulitis, fever, leukocytosis

Diagnosis

• Usually clinical
• US → If deep, unclear fluctuation, obese patient, foreign body suspicion
• Culture pus → Recurrent abscess, severe infection, immunosuppression, failed treatment, hospital-acquired infection

Treatment

1. Analgesia/local anesthesia
2. Incision and drainage (I&D) → Gold standard
3. Break loculations, evacuate pus
4. Irrigation + dressing/packing only if needed
5. Antibiotics only if indicated

• Indications for antibiotics → Large/deep abscess, extensive cellulitis, systemic signs/SIRS, immunosuppression, diabetes, difficult anatomical site, recurrent abscess, failed drainage alone
• MRSA risk → Previous MRSA, recent hospitalization/antibiotics, IVDU, severe purulent infection

Empyema

• Empyema: Collection of pus within a naturally occurring anatomical cavity
• Examples → Pleural empyema, gallbladder empyema, joint empyema
• Treatment principle → Drainage + antibiotics + source control

Phlegmon / Cellulitis

• Phlegmon: Diffuse, spreading acute purulent inflammation of soft tissue without a well-defined pus cavity
• Deeper pyogenic infiltration than simple superficial infection
• Cellulitis → Diffuse infection of dermis/subcutis, usually ill-defined margins
• Etiology → Streptococci, S. aureus, anaerobes/mixed flora depending on site
• Pathomechanism → Skin barrier defect → Bacterial spread in dermis/subcutis → Edema + inflammatory infiltration
• Can progress → Phlegmon/cellulitis → Abscess or necrotizing infection

Clinical Features

• Redness, warmth, swelling, tenderness
• Ill-defined border in cellulitis/phlegmon
• More systemic symptoms than simple abscess → Fever, chills, fatigue, headache
• Lymphangitis → Red streaking along lymphatic vessels
• Lymphadenitis → Tender regional lymph nodes

Diagnosis

• Usually clinical
• Blood culture/swab not routine in mild typical cases
• Culture if severe, immunosuppressed, bite, immersion injury, necrosis, postoperative infection, treatment failure
• US/CT/MRI if abscess, foreign body, deep infection or necrotizing fasciitis suspected

Treatment

1. Rest + elevation of affected limb
2. Treat portal of entry → Toe web maceration, ulcer, eczema, wound
3. Empirical antibiotics
4. Drainage if abscess develops
5. Surgical exploration if deterioration / necrotizing infection suspicion

• Mild non-purulent cellulitis → Streptococcal coverage
• Moderate/systemic signs → Systemic antibiotics, often cover MSSA too
• Severe/SIRS/MRSA risk/penetrating trauma → MRSA + streptococcal coverage; broad-spectrum if very severe

Erysipelas

• Erysipelas: Acute spreading bacterial infection of upper dermis + superficial lymphatics
• Special form of cellulitis/phlegmon with sharply demarcated raised border
• Etiology → Mainly Streptococcus pyogenes; sometimes S. aureus
• Risk factors → Skin break, lymphedema, venous insufficiency, obesity, diabetes, tinea pedis

Clinical Features

• Bright erythematous, hot, tender, edematous, painful skin
• Very sharp, raised border
• Usually unilateral
• Fever, chills, shivering can precede skin signs
• Common sites → Face, lower limb

Complications

• Lymphangitis and lymphadenitis
• Abscess formation
• Necrotizing fasciitis if rapidly progressive/deep tissue involvement
• Recurrent erysipelas → Chronic lymphedema → More recurrence
• Sepsis in severe cases

Treatment

• Antibiotics active against streptococci
• Elevation, analgesia, antipyretics
• Treat entry lesion and predisposing factors
• Debridement only if necrosis/abscess/necrotizing infection is present

Folliculitis, Furuncle, Carbuncle

Folliculitis

• Folliculitis: Infection/inflammation of hair follicle
• Etiology → Usually S. aureus; also fungi, virus, hot-tub Pseudomonas
• Clinical features → Tender red follicular papule, often with surface pustule
• Treatment → Hygiene, local antiseptic/topical antibiotic; PO antibiotics or antifungal if extensive/special cause

Furuncle and Carbuncle

• Furuncle: Deep bacterial folliculitis with perifollicular abscess
• Carbuncle: Cluster of furuncles connected subcutaneously, multiple draining openings
• Etiology → Usually S. aureus
• Risk → Diabetes, obesity, immunosuppression, poor hygiene, nasal S. aureus carriage
• Treatment → Drainage if fluctuant; antibiotics if large, cellulitis/systemic signs, immunosuppression or high-risk site

Gangrene and Necrotizing Infection

Dry Gangrene

• Ischemic necrosis without major infection
• Typical → Peripheral arterial disease, diabetic ischemic foot
• Clinical features → Dry, black, mummified tissue; demarcation line
• Treatment → Vascular assessment/revascularization if possible + amputation/debridement of necrotic tissue

Wet Gangrene

• Ischemic tissue + bacterial infection
• Rapidly spreading, swollen, foul-smelling soft tissue necrosis
• Emergency → Sepsis risk
• Treatment → Urgent radical debridement/amputation + broad-spectrum IV antibiotics + resuscitation

Gas Gangrene / Clostridial Myonecrosis

• Caused by Clostridium perfringens and other clostridia
• Usually after contaminated trauma, devitalized muscle, ischemia
• Pathomechanism → Anaerobic spores germinate → Toxin production → Myonecrosis + hemolysis + shock
• Clinical features → Severe pain, swelling, crepitus, brown/foul discharge, systemic toxicity, hemodynamic instability
• X-ray/CT → Gas in tissue supports diagnosis but do not delay surgery
• Treatment → Emergency surgical exploration + radical debridement/amputation + high-dose IV penicillin + clindamycin after clostridia confirmed
• Hyperbaric oxygen → Adjunct only in selected centers; never delay surgery

Necrotizing Fasciitis

• Rapidly progressive infection of fascia/subcutaneous tissue with thrombosis and necrosis
• Fatal without early treatment
• Warning signs → Pain out of proportion, rapid spread, systemic toxicity, bullae, skin anesthesia, crepitus, necrosis, shock
• Etiology → Polymicrobial aerobic-anaerobic infection or group A streptococcus / S. aureus
• Treatment → Immediate surgical consultation + radical debridement + broad-spectrum IV antibiotics + ICU resuscitation

II. Wound Infections

• Wound infection: Infection of a surgical or traumatic wound caused by bacterial colonization/invasion + tissue inflammation
• Can affect acute surgical wounds, traumatic wounds, chronic ulcers and burn wounds
• Colonization alone is not infection → Infection needs inflammatory tissue response and/or systemic signs
• Important rule → Antibiotics do not replace drainage/debridement/source control

Classification by Etiology

1. Surgical Site Infection (SSI)

• Infection related to an operation at/near the surgical incision or operated organ/space
• Usually occurs within 30 days after operation
• If implant/prosthesis involved → Follow-up period may be longer in surveillance definitions

Classification by Depth

• Superficial incisional SSI → Skin + subcutaneous tissue
• Deep incisional SSI → Deep soft tissue: fascia + muscle
• Organ/space SSI → Any manipulated organ/space deeper than incision

2. Traumatic Wound Infection

• Infection after traumatic wound
• Risk → Delay, devitalized tissue, foreign body, soil/feces/saliva contamination, crush injury, bite, puncture wound

3. Chronic Wound Infection

• Examples → Diabetic foot ulcer, pressure ulcer, venous leg ulcer, arterial ulcer
• Often colonized; infection means invasion + clinical inflammatory signs
• Biofilm → Delayed healing, recurrent inflammation, reduced antibiotic effect

4. Burn Wound Infection

• Loss of skin barrier + necrotic tissue → High infection risk
• Pathogens → S. aureus, streptococci, Gram-negative rods, Pseudomonas, fungi in extensive burns
• Severe sign → Conversion of partial thickness to full thickness, discoloration, eschar separation, systemic sepsis

Classification by Surgical Wound Contamination

Pathogens

• Most common in skin/clean SSI → S. aureus, coagulase-negative staphylococci, streptococci
• GI/perineal/female genital operations → Gram-negative rods + anaerobes
• Common organisms → E. coli, enterococci, Enterobacter, Pseudomonas aeruginosa, anaerobes
• Implants/foreign material → Staphylococci + biofilm
• Hospital-acquired/recurrent infection → Consider MRSA and resistant Gram-negative bacteria

Typical Pathogens by Surgical Field

• Orthopedic / prosthesis → S. aureus, coagulase-negative staphylococci
• Appendectomy, colorectal, biliary → Gram-negative bacilli + anaerobes
• Gastroduodenal → Gram-negative bacilli + streptococci
• Vascular → S. aureus, Gram-negative bacilli
• Head and neck / oral cavity → Staphylococci, streptococci, anaerobes
• Obstetrics/gynecology → Gram-negative bacilli, enterococci, anaerobes
• Urology → Gram-negative bacilli, enterococci depending on field/urine culture

Risk Factors for Wound Infection / SSI

1. Host Factors

• Local → Decreased tissue perfusion, ischemia, necrosis, edema, hematoma, seroma, foreign body, contamination
• Systemic → Older age, obesity, malnutrition, diabetes, anemia, malignancy, immunosuppression, sepsis, smoking
• Colonization → Nasal S. aureus/MRSA carriage

2. Surgical / Hospital Factors

• Poor tissue handling, dead space, inadequate hemostasis, tension, excessive electrocautery
• Prolonged operation
• Prolonged perioperative hospitalization
• Intraoperative contamination / break in sterile technique
• Implants, drains, foreign material
• Hypothermia, hypoxia, poor perfusion, hyperglycemia

3. Antibiotic Resistance Factors

• Unnecessary antibiotic prescribing
• Wrong timing, wrong spectrum, prolonged prophylaxis
• Poor patient adherence
• Previous hospitalization or recent antibiotic exposure

Diagnosis of Wound Infection

Symptoms and Signs

• Redness/erythema around wound
• Swelling, warmth, induration
• Pain or tenderness increasing over time
• Purulent discharge → Yellow, green or foul-smelling pus
• Delayed wound healing
• Wound dehiscence → Edges separating
• Localized abscess/fluctuance if collection forms
• Fever or chills → Systemic involvement

Assessment

1. Inspect wound → Redness, swelling, pus, necrosis, dehiscence, odor
2. Assess depth → Superficial vs deep fascia/muscle vs organ/space
3. Look for source control problem → Abscess, hematoma, foreign body, dead tissue
4. Assess systemic severity → Fever, tachycardia, hypotension, confusion, oliguria
5. Labs if moderate/severe → CBC, CRP, renal function, glucose, lactate if sepsis
6. Microbiology → Pus/deep tissue culture after opening/debridement; blood cultures if septic
7. Imaging → US for fluid collection; CT/MRI for deep infection, gas, organ/space abscess

Treatment of Wound Infection

1. Assess patient first → Sepsis? ABCDE, IV access, fluids if unstable
2. Analgesia/local or general anesthesia
3. Open and investigate wound → Depth, pus, necrosis, damaged tissues, foreign body
4. Take samples → Pus/deep tissue for microbiology before antibiotics if feasible and not delaying treatment
5. Mechanical cleaning → Saline irrigation, remove debris/foreign material
6. Drainage → Evacuate abscess/hematoma/seroma
7. Debridement → Remove necrotic/devitalized tissue
8. Empirical antibiotics if systemic signs, cellulitis, deep infection, immunosuppression, dirty wound, necrotizing infection or organ/space infection
9. Closure decision → Primary, delayed primary, secondary intention, or reconstruction
10. Tetanus prophylaxis according to wound type and vaccination status

Empirical vs Definitive Antibiotics

• Empirical therapy → Start broad enough for likely field flora if systemic/deep infection is present
• Definitive therapy → Narrow after culture and sensitivity results
• Topical antiseptics/antibacterial dressings can help selected superficial/chronic wounds, but do not replace debridement
• Hydrogen peroxide is not routine for healthy granulating wounds because it can damage viable tissue; use mainly irrigation/cleansing according to local practice

Closure Logic

• Clean wound → Refresh wound edges + primary closure if viable and low infection risk
• Contaminated wound → Debridement + irrigation; delayed primary closure after 3-5 days if clean
• Bite, puncture, gunshot, crush, dirty wound → Often leave open; frequent dressing changes; delayed closure/reconstruction
• Established infection/pus/necrosis → Do not close primarily until source controlled

Management of Contaminated Acute Wounds

1. Irrigation + adequate debridement
2. Primary closure may be possible after proper debridement in selected fresh traumatic wounds
3. Do not primarily close high-risk wounds → Bite wound, crushed/ischemic tissue, delayed presentation, heavy contamination, immunosuppression/high-dose steroids
4. Use monofilament skin sutures when suturing contaminated-risk wounds
5. Check contaminated wounds within 24-48 h after closure
6. If doubt exists → Leave open and use delayed primary closure

Management of Contaminated Chronic Wounds

1. Debridement → Excision, curettage, repeated dressing changes
2. Control underlying cause → Diabetes, ischemia, venous hypertension, pressure
3. Systemic antibiotics only if clinical infection, cellulitis, osteomyelitis or sepsis
4. Topical antibacterial dressing/cream in selected locally infected or burn wounds
5. Biological dressing/allograft/xenograft may be used in selected wounds/burns
6. Final closure → Secondary intention, skin graft, flap, or NPWT-assisted preparation

III. Negative Pressure Wound Therapy (NPWT / VAC)

• NPWT: Wound dressing system applying continuous or intermittent subatmospheric pressure to a sealed wound dressing
• Also called VAC → Vacuum-assisted closure
• System → Foam/gauze dressing + occlusive film + tubing + canister + vacuum pump
• Can be continuous or intermittent depending on wound and goal

Mechanism

• Removes excess fluid and wound exudate
• Decreases edema
• Improves local perfusion and oxygenation
• Promotes granulation tissue formation
• Reduces bacterial burden after adequate debridement/source control
• Approximates wound edges / wound contraction
• Creates controlled moist wound environment

Indications

• Chronic wounds not healing with standard treatment
• Diabetic foot ulcer, pressure ulcer, venous ulcer after assessment/debridement
• Post-debridement wounds
• Infected or contaminated wounds after initial source control
• Trauma wounds with soft tissue loss
• Open surgical wounds / dehisced wounds
• Fasciotomy wounds
• Skin graft fixation and graft bed preparation

Contraindications / Cautions

• Active bleeding or high bleeding risk
• Necrotic wound base/eschar before debridement
• Untreated osteomyelitis
• Malignancy in the wound
• Unexplored/non-enteric fistula
• Exposed vessels, anastomoses, nerves or organs without protective interface
• Do not place foam directly on bowel/vessels/organs

NPWT in Open Abdomen / Laparostomy

• Open abdomen: Abdomen intentionally left open after surgery
• Indications → Damage control surgery, abdominal compartment syndrome, severe peritonitis/sepsis, bowel edema preventing safe closure
• Goals of NPWT → Protect viscera, remove exudate, control contamination, reduce fluid loss, allow planned re-look, facilitate delayed fascial closure
• Use visceral protective layer over bowel
• Dressing changes typically every 48-72 h or during planned re-look laparotomy
• Definitive goal → Early fascial closure when physiology and abdominal conditions permit

IV. Antibiotic Prophylaxis in Surgery

• Purpose: Prevent SSI by adequate tissue antibiotic level at incision and during contamination risk period
• Prophylaxis is not treatment of established infection
• Wrong concept → Routine 3rd generation cephalosporin for all cases
• Correct concept → Narrowest effective spectrum based on operation site, likely flora, local resistance and allergy

Indications

• Clean surgery involving prosthesis/implant/foreign material
• Clean-contaminated surgery → GI, biliary, respiratory, urologic, gynecologic tract entered in controlled manner
• Contaminated surgery → Fresh trauma, gross spillage, acute non-purulent inflammation
• High-consequence clean surgery depending on local protocol
• High-risk patient/procedure → Diabetes, immunosuppression, obesity, prolonged operation, poor perfusion

Not Routine

• Clean, uncomplicated, non-prosthetic surgery
• Dirty/infected wounds → Need therapeutic antibiotics, not prophylaxis alone

Principles

1. Choose antibiotic according to surgical site flora + local guideline
2. Give IV dose before incision / on starting anesthesia
3. Most agents → 30-60 min before incision
4. Long infusion drugs e.g. vancomycin → Start earlier so infusion finishes before incision
5. Re-dose if operation exceeds antibiotic half-life or there is major blood loss
6. Stop within 24 h post-op in most procedures
7. Do not extend prophylaxis because a drain is present

Common Regimens / Logic

• Cefazolin → Common first-line prophylaxis for skin flora: staphylococci + streptococci
• Cefazolin + metronidazole → Colorectal/GI anaerobic coverage if needed by local protocol
• Amoxicillin-clavulanate / ampicillin-sulbactam → Mixed aerobic-anaerobic coverage in selected procedures
• Vancomycin → MRSA colonization/high MRSA risk or severe beta-lactam allergy depending on protocol
• MRSA decolonization → Consider nasal mupirocin + chlorhexidine wash before procedures where S. aureus SSI is likely

Exam Pitfalls

• Abscess → Drain first; antibiotics alone are insufficient
• Necrotizing infection → Do not wait for imaging/labs if clinically suspicious
• SSI with pus → Open wound, remove sutures if needed, drain, culture, debride
• Dirty wound → Therapeutic antibiotics + source control, not just prophylaxis
• Prophylaxis → Timing and re-dosing matter more than prolonged postoperative courses
• NPWT → Use after debridement/source control; avoid necrotic, bleeding or unprotected exposed vital structures