Wound Healing & Surgical Site Infections
A board-focused walk through the three phases of wound healing (key cells, collagen shift, cofactors) and surgical site infections — organism-by-timing, wound classification, prophylaxis, and the next-best-step decisions for early wound infection, dehiscence, and necrotizing fasciitis.
Why this is tested
Wound healing proceeds through three overlapping phases — inflammation → proliferation → remodeling — and anything that stalls a phase (ischemia, infection, malnutrition, glucocorticoids, diabetes) delays closure. The boards test two flavors: basic-science stems on the key cell or collagen type of each phase (Step 1), and management stems on the febrile post-op patient with a wound complication (Step 2 CK). Surgical site infections (SSIs) are among the most common nosocomial infections in surgical patients; the tested skill is matching time since surgery to the likely organism and choosing the correct next step — which is often opening the wound rather than reaching first for antibiotics.
- Inflammatory phase (day 0–3): platelets → clot/hemostasis; neutrophils arrive first (24–48h); the macrophage is the KEY cell (48–72h) — debrides and secretes PDGF/TGF-β to launch proliferation.
- Proliferative phase (day 3–~3 wk): fibroblasts deposit type III collagen; angiogenesis, granulation tissue, epithelialization; myofibroblasts contract the wound.
- Remodeling/maturation (3 wk–1 yr): type III → type I collagen; tensile strength climbs to a maximum of ~80% of original skin (never 100%).
- Tensile strength is only ~10% at 1 week — sutures come out while the wound is still weak.
- Required cofactors: vitamin C (prolyl/lysyl hydroxylation), copper (lysyl oxidase cross-linking), zinc (collagenase/MMPs, remodeling).
- Glucocorticoids impair healing; vitamin A reverses this effect.
The three phases at a glance
| Phase | Timeline | Key cell | Hallmark event |
|---|---|---|---|
| Inflammatory | Day 0–3 | Neutrophil → macrophage | Hemostasis, debris clearance, growth-factor release |
| Proliferative | Day 3–3 wk | Fibroblast (+ myofibroblast) | Type III collagen, granulation, angiogenesis, contraction |
| Remodeling | 3 wk–1 yr | Fibroblast | Type III → I collagen, cross-linking, ~80% tensile strength |
- Healing by intention: primary = clean edges approximated/sutured; secondary = left open, heals by granulation + contraction; tertiary (delayed primary) = left open, then closed later (contaminated wounds).
- Hypertrophic scar: excess collagen staying within the original wound borders; can regress.
- Keloid: collagen (types I & III) extends beyond wound borders; does not regress; familial, more common in darker skin, classic on earlobe/sternum/deltoid.
- Wound dehiscence: fascial separation, classically POD 5–8; salmon-colored/serosanguineous drainage from the incision is the warning sign; evisceration is a surgical emergency.
- Impaired-healing risk factors: diabetes, smoking, low albumin/protein malnutrition, tissue ischemia, infection, steroids, radiation, tension/foreign body.
Stem: On post-op day 1, a patient spikes to 39°C with severe incisional pain and thin, grayish 'dishwater' drainage; the surrounding skin is dusky with crepitus.
Dx / bug: Fever with wound findings in the first 24–72 h points to Group A Streptococcus (S. pyogenes) or Clostridium perfringens — essentially the only organisms fast enough to infect a wound this early.
Next step: With crepitus, necrosis, or systemic toxicity → emergent surgical exploration and debridement plus broad-spectrum antibiotics. Do not simply observe — clostridial myonecrosis / necrotizing infection is a surgical emergency.
Contrast: Routine SSIs (S. aureus, gram-negatives) present later, around POD 5–7.
- SSI depth (CDC): superficial incisional (skin/subcutaneous) < deep incisional (fascia/muscle) < organ/space (e.g., intra-abdominal abscess).
- Most common organism overall = *Staphylococcus aureus* (including MRSA); bowel/colorectal cases add gram-negatives and anaerobes.
- Prophylaxis: cefazolin within 60 min before incision (vancomycin or a fluoroquinolone within 120 min because of their longer infusion); redose for long operations (~every 2 half-lives) or major blood loss.
- A single pre-incision dose suffices for most cases; if continued, stop within 24 h — prolonging prophylaxis does not lower SSI rates and drives resistance / C. difficile.
- Superficial SSI management: open the incision, drain, and pack it (source control); add antibiotics only for surrounding cellulitis or systemic signs.
Surgical wound classification → SSI risk
| Class | Definition | Example | ~SSI risk |
|---|---|---|---|
| I — Clean | No viscus entry, no inflammation | Hernia, breast, thyroid | ~1–2% |
| II — Clean-contaminated | Controlled viscus entry, no spillage | Elective colectomy, cholecystectomy | ~3–11% |
| III — Contaminated | Gross spillage, fresh trauma, break in sterile technique | Enterotomy with spill | ~10–17% |
| IV — Dirty/infected | Established infection/perforation, devitalized tissue | Perforated viscus, drained abscess | >27% |
Stem: A diabetic patient has pain out of proportion to exam over a rapidly spreading, dusky area of erythema with hemorrhagic bullae and crepitus; he is now hypotensive and tachycardic.
Dx: Necrotizing fasciitis — Type II = Group A Strep ± S. aureus; Type I = polymicrobial (diabetics); Fournier gangrene = perineal/genital variant.
Next best step: Immediate surgical debridement — the definitive, diagnostic-therapeutic move. Do not delay for imaging. Add broad-spectrum antibiotics, e.g., piperacillin-tazobactam + vancomycin + clindamycin (clindamycin for toxin/protein-synthesis suppression).
Pitfall: CT gas or an LRINEC score may support the diagnosis but must never delay the OR.
5 Ws — sequenced by classic post-op day:
- Wind — atelectasis / pneumonia (POD 1–2)
- Water — UTI (POD 3–5)
- Walking — DVT / PE (POD 4–6)
- Wound — surgical site infection (POD 5–7)
- Wonder drugs / What did we do — drug fever, IV lines, deep abscess (POD 7+)
Exception that scores points: a dramatic fever on POD 0–1 is not atelectasis — think Group A Strep or Clostridium wound infection and head toward the OR.
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