Wound Healing & Surgical Infections

Wound healing and surgical site infections (SSI) are a perennial favourite in NEET PG, blending basic surgical principles with postoperative complications. Master the phases of healing, the types of closure, the CDC wound classification, and the anaerobic emergencies (gas gangrene, necrotising fasciitis) — these account for the bulk of the questions.

Phases of wound healing

Wound healing is a continuous, overlapping cascade traditionally divided into four phases. A frequent MCQ asks which cell or mediator dominates each phase.

Phase	Timeline	Dominant cell	Key events
Haemostasis	Seconds–minutes	Platelets	Vasoconstriction, platelet plug, fibrin clot, release of PDGF/TGF-β
Inflammatory	Day 0–3	Neutrophils (24–48 h) → macrophages (48–96 h)	Phagocytosis, debridement; macrophage is the most important cell
Proliferative	Day 3–21	Fibroblasts	Granulation tissue, angiogenesis, collagen (type III) deposition, epithelialisation, wound contraction by myofibroblasts
Remodelling/Maturation	3 weeks–1 year	Fibroblasts	Type III → type I collagen conversion, cross-linking, scar maturation

High-yield: The macrophage is the single most important cell in wound healing — orchestrates debridement, angiogenesis and fibroblast recruitment. Depletion of macrophages most severely impairs healing.

High-yield: Wound strength is never 100% of original — peaks at ~70–80% of unwounded skin. At 1 week ~3–5%, at 3 weeks ~20%, at 3 months ~70–80% (the plateau).

Collagen facts (very high-yield):

• Type III collagen is laid down first (early granulation tissue), later replaced by type I (the predominant collagen of mature scar; normal skin ratio I:III ≈ 4:1).
• Collagen synthesis requires vitamin C, oxygen, alpha-ketoglutarate, ferrous iron for proline/lysine hydroxylation.
• Lysyl oxidase (copper-dependent) cross-links collagen → tensile strength.
• Hypertrophic scars and keloids have excess type III.

Epithelialisation flow: Injury → loss of contact inhibition → keratinocyte mobilisation → migration ("leap-frog" / Winter's principle, faster in moist environment) → proliferation → contact inhibition restores → basement membrane reformed.

Types of wound healing (closure)

Type	Synonym	Mechanism	Example
Primary intention	First intention	Clean, apposed edges, sutured	Surgical incision, clean laceration
Secondary intention	Spontaneous	Open wound heals by granulation + contraction + epithelialisation	Pressure sore, abscess cavity, dehisced wound
Tertiary intention	Delayed primary closure	Wound left open initially (contaminated), closed at day 4–7 once clean	Contaminated traumatic wound, fasciotomy

High-yield: Delayed primary (tertiary) closure is the answer for a contaminated wound where you wait for the contamination/oedema to settle and then suture — closure at 3–7 days before granulation tissue appears.

Wound contraction vs contracture: Contraction is a normal, beneficial reduction of wound size by myofibroblasts (α-smooth muscle actin). Contracture is a pathological, fixed deformity, often across a joint or due to burns — treated by Z-plasty/grafting.

Factors impairing wound healing

A classic "which does NOT delay healing" question. Remember DIDN'T HEAL:

Local factors: infection (the most common cause of delayed healing), poor blood supply/ischaemia, foreign body, tissue tension, haematoma, radiation, mechanical trauma, oedema.

Systemic factors: diabetes mellitus, malnutrition (protein, vitamin C, vitamin A, zinc), advanced age, steroids/immunosuppression, malignancy, uraemia, jaundice, smoking, chemotherapy.

High-yield: Vitamin A (retinoids) reverses the inhibitory effect of corticosteroids on healing (steroids block macrophage migration and the inflammatory phase). Dose-tested fact.

High-yield: Zinc is a cofactor for DNA/RNA polymerase and collagenase; deficiency impairs healing. Vitamin C deficiency (scurvy) → defective hydroxylation of proline → weak collagen, wound dehiscence, perifollicular haemorrhage.

High-yield: Of the local factors, infection is the commonest cause of impaired healing; tissue hypoxia/ischaemia is the most important factor in chronic non-healing ulcers.

Abnormal scarring

Feature	Hypertrophic scar	Keloid
Extent	Confined to wound margin	Extends beyond original wound
Onset	Early (weeks), often regresses	Delayed (months), persists/grows
Site	Flexor surfaces, across joints	Sternum, deltoid, earlobe, jaw
Race	Any	More in dark-skinned individuals
Recurrence after excision	Low	High
Collagen	Type III, parallel	Thick, disorganised type I & III

High-yield: First-line for keloid = intralesional triamcinolone (steroid); excision alone has high recurrence so combine with steroid/radiation/pressure/silicone gel. Never excise a keloid in isolation.

Surgical site infection (SSI) — CDC classification

SSI is defined by the CDC as infection occurring within 30 days of surgery (or 90 days if a prosthetic implant is in place).

Class	Type	Description	Expected infection rate
I	Clean	No viscus entered, no inflammation, no break in asepsis (e.g., hernia, thyroid, breast)	<2%
II	Clean-contaminated	Viscus (GI/GU/respiratory) entered under controlled conditions, minimal spillage (e.g., elective cholecystectomy, hysterectomy)	<10% (3–10%)
III	Contaminated	Major spillage, acute non-purulent inflammation, fresh traumatic wound, major break in sterility	15–20%
IV	Dirty/infected	Pus present, perforated viscus, old traumatic wound with devitalised tissue	>30–40%

Depth-based CDC classification of SSI:

1. Superficial incisional → skin & subcutaneous tissue only.
2. Deep incisional → fascia and muscle layers.
3. Organ/space → any organ or cavity manipulated during surgery (e.g., intra-abdominal abscess).

High-yield: Most common organism causing SSI overall = Staphylococcus aureus. After colorectal surgery, gram-negatives (E. coli) and anaerobes (Bacteroides) predominate.

High-yield: The single most important determinant of SSI is the wound class (degree of bacterial contamination). Other predictors are captured in the NNIS/SENIC risk index (ASA ≥3, contaminated/dirty wound, operation longer than the 75th percentile "T-point").

Timing of presentation (an exam favourite):

• Postoperative fever within first 24–48 h with crepitus / "dishwater" discharge → suspect Clostridium or Streptococcus (the only two organisms causing SSI in the first 48 h).
• Day 5–7 → typical staphylococcal wound infection.

Prevention of SSI — antibiotic prophylaxis

Approach (stepwise): correct anaemia/glycaemia → no hair removal or clip (don't shave) → skin prep with chlorhexidine-alcohol (superior to povidone-iodine) → single dose IV antibiotic within 60 min before incision (120 min for vancomycin/fluoroquinolones) → maintain normothermia and normoglycaemia (keep glucose <180 mg/dL) → **redose** if surgery >2 half-lives or blood loss >1.5 L.

High-yield: Prophylactic antibiotic must be given so peak tissue levels coincide with incision — within 30–60 minutes before skin incision. Cefazolin is the standard agent for most clean/clean-contaminated cases; add metronidazole for colorectal.

High-yield: Hair removal by shaving increases SSI (micro-abrasions); if needed, use clippers immediately before surgery.

Surgical wound infections — clinical entities

Stitch abscess / suture sinus

Localised infection around a non-absorbable suture; treated by removal of the offending stitch.

Wound dehiscence & burst abdomen

• Dehiscence = separation of wound layers. Burst abdomen = complete fascial separation with evisceration.
• Classically presents on day 5–8 post-laparotomy with a serosanguineous ("salmon-pink") discharge — a premonitory sign.
• Risk factors: the 8 P's / RIP — raised intra-abdominal pressure (cough, ileus), Poor technique, infection, malnutrition, steroids, malignancy, diabetes, jaundice.
• Management: cover with saline gauze, resuscitate, return to theatre for resuturing (deep tension sutures).

High-yield: Serosanguineous (salmon/pink) discharge from a laparotomy wound on day 5–7 = impending burst abdomen — the most classic warning sign tested.

Anaerobic & necrotising soft-tissue infections

This is the most heavily weighted clinical sub-topic. Distinguish the three big entities.

Feature	Gas gangrene (clostridial myonecrosis)	Necrotising fasciitis	Cellulitis
Organism	Clostridium perfringens (alpha-toxin/lecithinase)	Type I = polymicrobial; Type II = Group A Streptococcus ± S. aureus	Strep pyogenes, S. aureus
Plane	Muscle	Fascia (spares muscle initially)	Dermis/subcutis
Onset	Rapid (hours), post-trauma/surgery	Rapid, often perineum/limb	Slower
Crepitus/gas	Marked	May be present	Absent
Pain	Severe, out of proportion	Pain out of proportion, later anaesthesia	Proportionate
Skin	Bronze discolouration, haemorrhagic bullae, foul "sickly-sweet" odour	Dusky, bullae, necrosis with skin anaesthesia	Erythema, warmth
Systemic toxicity	Profound, haemolysis, shock	Septic shock	Mild

High-yield: Gas gangrene is caused by Clostridium perfringens; the key virulence factor is alpha-toxin (lecithinase/phospholipase C) → myonecrosis and haemolysis. Treatment = aggressive surgical debridement + high-dose IV penicillin + clindamycin (clindamycin suppresses toxin synthesis) ± hyperbaric oxygen.

High-yield: Necrotising fasciitis — earliest reliable sign is pain out of proportion to clinical findings; later, paradoxical skin anaesthesia (cutaneous nerve infarction). Treatment is emergency surgical debridement (the single most important step) + broad-spectrum antibiotics. Imaging must not delay surgery.

Fournier gangrene = necrotising fasciitis of the perineum/scrotum, polymicrobial, classically in diabetics. Surgical emergency.

LRINEC score (Laboratory Risk Indicator for Necrotising Fasciitis) uses CRP, WBC, haemoglobin, sodium, creatinine, glucose; a score ≥6 suggests, ≥8 strongly predicts necrotising fasciitis. (Clinical judgement still overrides the score.)

Diagnostic approach to suspected nec fasc: Severe pain + systemic toxicity → bedside "finger test" (lack of resistance/dishwater pus on probing fascia) → urgent imaging only if diagnosis uncertain (CT/MRI shows fascial gas/oedema) → immediate operative exploration & debridement → cultures → broad-spectrum antibiotics (piperacillin-tazobactam + clindamycin + vancomycin) → IVIG considered in streptococcal toxic shock.

Tetanus (a clostridial special case)

• Clostridium tetani; toxin tetanospasmin ascends along nerves and blocks inhibitory neurotransmitters (GABA, glycine) at Renshaw cells → spastic paralysis (trismus, risus sardonicus, opisthotonus).
• Tetanus-prone wound: >6 h old, >1 cm deep, devitalised tissue, contamination with soil/faeces, puncture/avulsion.
• Management: wound debridement, human tetanus immunoglobulin (passive) + tetanus toxoid (active) at different sites, metronidazole, supportive care.

Other named anaerobic infection

Meleney's synergistic gangrene = slowly progressive postoperative gangrene caused by synergy of microaerophilic Streptococcus + Staph aureus, typically around a wound/stoma; treated by excision + antibiotics.

Chronic wounds & ulcers (quick contrasts)

Ulcer	Edge	Classic site
Venous	Sloping	Gaiter area (medial malleolus)
Arterial	Punched-out	Toes, pressure points
Neuropathic (diabetic)	Punched-out, callused	Sole, metatarsal heads
Malignant (Marjolin's)	Everted/rolled	Chronic scar/sinus (SCC)
Tuberculous	Undermined	Neck

High-yield: A Marjolin's ulcer is a squamous cell carcinoma arising in a chronic wound/burn scar/sinus; it is painless, slow-growing, lacks lymphatic spread initially (scar is avascular) and has everted edges.

Complications summary

• Local: infection, dehiscence/burst abdomen, sinus/fistula, incisional hernia (late), hypertrophic scar/keloid/contracture, Marjolin's ulcer.
• Systemic: sepsis, septic shock, toxic shock syndrome (Group A strep), multi-organ dysfunction.

Key differentials

• Postoperative crepitant wound: gas gangrene vs nec fasciitis vs subcutaneous emphysema vs benign gas-forming organisms — early surgical exploration settles it.
• Postop fever timeline (5 W's): Wind (atelectasis/pneumonia, POD1–2) → Water (UTI, POD3) → Wound (SSI, POD5–7) → Walking (DVT, POD5+) → Wonder drugs/lines (drug fever, line sepsis).

Recently asked / exam angle

• "Most important cell in wound healing" → macrophage.
• "First collagen deposited" → type III; "predominant in mature scar" → type I.
• "Vitamin reversing steroid effect on healing" → vitamin A.
• "Wound class with infection rate <2%" → clean (Class I).
• "Organism in first 48 h SSI" → Clostridium / Group A Streptococcus.
• "Antibiotic of choice in gas gangrene" → penicillin + clindamycin.
• "Earliest sign of necrotising fasciitis" → pain out of proportion.
• "Salmon-pink discharge POD5 laparotomy" → impending burst abdomen.
• "Scoring system for nec fasc" → LRINEC (≥6 suggestive).
• "Tensile strength of wound at 3 months" → ~70–80%.
• "Closure for contaminated wound" → delayed primary (tertiary).
• Image-based: bronze skin + crepitus + sweet odour → clostridial myonecrosis.

Rapid revision

1. Phase order: haemostasis → inflammation → proliferation → remodelling; macrophage is the master cell.
2. Type III collagen first, replaced by type I (final I:III ratio ≈ 4:1); lysyl oxidase (Cu) cross-links.
3. Wound tensile strength peaks at 70–80%, never reaches 100%.
4. Vitamin C for proline hydroxylation; vitamin A reverses steroid inhibition; zinc is a healing cofactor.
5. Three closures: primary, secondary (granulation), tertiary (delayed primary, day 3–7).
6. Myofibroblasts cause contraction (good); contracture is pathological.
7. Keloid crosses wound margin & recurs; treat with intralesional steroid, never excision alone.
8. CDC wound classes: Clean <2%, Clean-contaminated <10%, Contaminated 15–20%, Dirty >30%.
9. Commonest SSI organism = S. aureus; prophylactic cefazolin within 60 min of incision; clip don't shave.
10. SSI defined within 30 days (90 days with implant); depth — superficial/deep/organ-space.
11. Gas gangrene = C. perfringens alpha-toxin (lecithinase), treat penicillin + clindamycin + debridement ± HBO.
12. Necrotising fasciitis — pain out of proportion, LRINEC ≥6, emergency debridement is life-saving; Fournier = perineal variant.