Topic Notes — Wound Healing, Skin & Soft Tissue
Wound Healing, Skin & Soft Tissue
Exam-focused notes on wound healing phases, NPWT, skin grafts, flaps, BCC, melanoma, hidradenitis suppurativa, pressure sores and more for MS and DNB General Surgery.
11 Subtopics
⏱ 16 min read
MS / DNB High-Yield
⚠ Note on diagrams: AI-assisted diagrams have been reviewed for accuracy but may contain errors. Always cross-check with a standard surgical textbook (Bailey & Love, Schwartz).
Phases & Factors Affecting Wound Healing
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Phases of Wound Healing
| Phase | Time | Key Events | Key Cells | Mediators |
| Haemostasis | Minutes–hours | Vasoconstriction, platelet plug, fibrin clot scaffold | Platelets | PDGF, TGF-β, Thromboxane A&sub2; |
| Inflammation | 0–72 hrs | Vasodilation, neutrophil infiltration → phagocytosis; macrophages recruit fibroblasts | Neutrophils → Macrophages | IL-1, TNF-α, IL-6 |
| Proliferation | Day 3–3 weeks | Fibroblast proliferation → collagen III; angiogenesis; granulation tissue; epithelial migration | Fibroblasts, endothelial cells, keratinocytes | FGF, VEGF, EGF |
| Remodelling | Weeks–months | Collagen III → Collagen I; cross-linking → tensile strength (~80% of normal) | Fibroblasts, myofibroblasts | MMPs, TIMPs |
Types of Wound Healing
- Primary intention — clean edges approximated directly (e.g., sutured surgical wound). Minimal granulation. Fastest.
- Secondary intention — large defect heals by granulation, contraction, epithelialisation (e.g., chronic ulcer).
- Tertiary intention (delayed primary closure) — left open initially for infection control, closed surgically after 3–5 days.
Clinical Milestones
- 48 hours: epithelial seal forms over a clean surgical wound
- Day 5–7: peak tensile strength build begins from collagen
- 3 months: ~80% of original tensile strength regained
Factors Affecting Wound Healing
| Local Factors |
| Infection | Prolongs inflammation, increases tissue destruction, delays collagen deposition |
| Poor blood supply / radiation | Reduced O&sub2; delivery → impaired fibroblast function & angiogenesis |
| Excessive tension / foreign bodies | Ischaemia or persistent inflammation |
| Desiccation / maceration | Disrupts optimal moist environment for epithelial migration |
| Systemic Factors |
| Age | Reduced collagen turnover and vascularity |
| Malnutrition | Protein (collagen synthesis); Vit C (proline/lysine hydroxylation); Zinc (DNA synthesis); Copper (collagen cross-linking) |
| Diabetes | Microangiopathy, impaired neutrophil function |
| Steroids / cytotoxics | Steroids inhibit fibroblasts; cytotoxics block cell proliferation |
| Smoking | Nicotine → vasoconstriction; CO → reduced O&sub2; delivery |
| Anaemia / hypoxia | Low oxygen tension delays fibroblast & collagen activity |
Nutritional Role in Healing
| Nutrient | Role |
| Protein | Fibroblast proliferation, collagen formation |
| Vitamin C | Hydroxylation of collagen precursors (proline, lysine) |
| Zinc | DNA & RNA synthesis, epithelialisation |
| Copper | Lysyl oxidase activity for collagen cross-linking |
| Vitamin A | Epithelial repair; counteracts steroid effect on healing |
Exam Tip
The four phases in order: Haemostasis → Inflammation → Proliferation → Remodelling. Tensile strength peaks at 80% of normal — never returns to 100%. Key cell transitions: Neutrophils (day 1) → Macrophages (day 2–3, the “director” of healing) → Fibroblasts (collagen). Vitamin C deficiency = scurvy = poor wound healing.
Negative Pressure Wound Therapy (NPWT / VAC)
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NPWT applies sub-atmospheric pressure (−50 to −125 mmHg) to a wound bed through a sealed dressing to promote healing.
Mechanism of Action
- Macro-deformation — wound edges drawn together by suction, reducing wound size
- Micro-deformation — mechanical stretch at cellular level stimulates fibroblast proliferation and angiogenesis
- Exudate removal — decreases oedema, bacterial load, and proteolytic enzymes
- Improved perfusion — reduces interstitial pressure, improving capillary blood flow
- Moist environment — promotes granulation and epithelialisation
- Barrier function — protects from external contamination
Indications
- Diabetic foot ulcers, pressure ulcers, venous/arterial ulcers
- Traumatic wounds: degloving injuries, open fractures, soft tissue loss
- Post-operative: wound dehiscence, infected surgical wounds
- Burns: as bridge to skin grafting
- Abdominal wound management: open abdomen / laparostomy
- Sternal wound infections post-cardiac surgery
- ciNPWT (closed incision) — prophylactic use over high-risk closed surgical incisions
Contraindications
- Malignancy in wound (promotes tumour growth)
- Untreated osteomyelitis
- Necrotic tissue with eschar (must debride first)
- Exposed vessels, anastomoses, organs without intervening tissue
- Fistulae to body cavities or organs
- Coagulopathies
Exam Tip
VAC = Vacuum Assisted Closure = NPWT — all the same thing. The negative pressure is −125 mmHg for most wounds. ciNPWT (closed incision NPWT) is a Recent Advances topic — used prophylactically over high-risk closed laparotomy wounds to reduce SSI and dehiscence. Contraindication most commonly asked: malignancy in wound.
Wound Dressings — Types & Indications
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| Type | Examples | Indication | Key Property |
| Simple / gauze | Paraffin gauze, tulle gras | Low-exudate clean wounds | Non-adherent, allows drainage |
| Hydrocolloid | DuoDERM | Stage I–II pressure sores, partial thickness burns | Maintains moist environment, autolytic debridement |
| Hydrogel | IntraSite Gel | Dry necrotic wounds, sloughy wounds | Rehydrates eschar, promotes autolytic debridement |
| Foam | Allevyn, Mepilex | Moderate–high exudate wounds | Absorbs exudate, maintains moist environment |
| Alginate | Kaltostat, Sorbsan | High-exudate, bleeding wounds | Haemostatic, forms gel on contact with exudate |
| Silver-containing | Aquacel Ag, Mepilex Ag | Infected / high-risk wounds | Antimicrobial — broad spectrum |
| Biological | Amniotic membrane, collagen sheet | Burns, non-healing ulcers | Growth factor delivery, scaffold for regeneration |
| NPWT | VAC therapy | Complex wounds (see above) | Active negative pressure healing |
Exam Tip
The moist wound healing principle (Winter, 1962) underlies all modern dressing science — wounds heal faster in a moist environment than under a dry scab. Hydrocolloid is the go-to for Stage II pressure sores. Alginate dressings are haemostatic and ideal for cavity wounds. Silver dressings should not be used long-term (fibroblast toxicity with prolonged use).
Keloid vs Hypertrophic Scar
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| Feature | Hypertrophic Scar | Keloid |
| Extent | Stays within wound boundaries | Extends beyond wound boundaries (claw-like) |
| Regression | May regress spontaneously over time | Does not regress; tends to enlarge |
| Recurrence after excision | Low | High (30–100%) |
| Collagen type | Type III (fine, wavy) | Type I (thick, nodular, hyalinised) |
| Predisposing sites | Burns, joints, areas of tension | Sternum, ear lobes, deltoid, jaw line |
| Racial predisposition | None | Dark-skinned individuals (10–15× more common) |
| Symptoms | Pruritus ± pain | Pruritus, pain, cosmetic concern |
Management of Keloid
- First line: Silicone gel sheets (12–24 hrs/day × 3–6 months), pressure garments
- Intralesional steroids: Triamcinolone 10–40 mg/mL, repeated every 4–6 weeks
- Surgical excision + adjuvant: Excision alone has 45–100% recurrence; must combine with steroids or radiotherapy
- Radiotherapy: Postoperative, within 24 hours of excision; reduces recurrence to <10%
- Laser: Pulsed dye laser (PDL) for vascular component; CO&sub2; laser for bulk reduction
- Cryotherapy: Freeze-thaw cycles; useful for small lesions
- Bleomycin / 5-FU intralesional: Emerging options
Exam Tip
The key distinguishing feature: keloid extends beyond wound margins; hypertrophic scar does not. Keloid = thick Type I collagen; hypertrophic = fine Type III. Never excise a keloid without adjuvant treatment — recurrence is almost certain with excision alone. Ear lobe keloids after piercing are the classic example.
Hidradenitis Suppurativa
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A chronic, recurrent, debilitating inflammatory skin condition affecting apocrine gland-bearing areas. Not primarily an infective condition — it is a follicular occlusion disease with secondary superinfection.
Pathophysiology
Follicular occlusion → retention of keratin → follicular rupture → inflammatory response in dermis → sinus tract formation → secondary bacterial colonisation (not primary infection).
Sites
Axilla (most common), groin, perianal area, inframammary folds, buttocks, perineum.
Hurley Staging
| Stage | Description | Treatment |
| I | Abscess formation — single or multiple, no sinus tracts or scarring | Medical: topical clindamycin, doxycycline, intralesional steroids |
| II | Recurrent abscesses with sinus tracts and scarring — single or multiple, widely separated | Medical + surgical: unroofing of sinus tracts |
| III | Diffuse involvement or near-diffuse involvement, multiple interconnected sinus tracts & abscesses across entire area | Wide excision with primary closure or flap/graft reconstruction |
Management
- Medical: Topical clindamycin, systemic tetracyclines, rifampicin + clindamycin combination, adalimumab (anti-TNF-α — FDA approved for Hurley II/III)
- Surgical — Hurley I–II: Incision & drainage (temporary), unroofing of sinus tracts (deroofing)
- Surgical — Hurley III: Wide excision of all involved skin and subcutaneous tissue; reconstruction with split skin graft or local flap
- Laser: Nd:YAG laser hair removal reduces recurrence in Hurley I–II
- Key principle: I&D alone = high recurrence; deroofing or wide excision = definitive
Exam Tip
HS is not primarily infective — it is a follicular occlusion disease. Adalimumab (Humira) is the only biologic approved. Hurley Stage III = wide excision with reconstruction. The triad of follicular occlusion diseases: HS + Acne conglobata + Dissecting cellulitis of scalp + Pilonidal sinus (DAPP syndrome). Long-standing HS can undergo malignant transformation to SCC (Marjolin’s equivalent).
Basal Cell Carcinoma (BCC)
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Most common skin malignancy. Arises from basal cells of epidermis. Locally invasive — metastasis extremely rare (<0.1%). “Rodent ulcer” refers to the classic central ulceration with rolled pearly edges.
Types
- Nodular (most common) — pearly papule with telangiectasia; rolls over on palpation
- Superficial — erythematous plaque, multiple, trunk
- Morphoeaform / sclerosing — scar-like, ill-defined; most aggressive; highest recurrence
- Pigmented — may mimic melanoma
- Basosquamous (metatypical) — hybrid with SCC behaviour; can metastasise
Risk Stratification (NCCN)
| Low Risk | High Risk |
| Nodular or superficial histology | Morphoeaform, infiltrative, basosquamous |
| Tumour <2 cm | Tumour >2 cm |
| Well-defined borders | Poorly defined borders |
| Trunk / extremities | Face, H-zone, ears, genitalia, hands, feet |
| Primary lesion | Recurrent lesion / perineural invasion |
| Immunocompetent | Immunosuppressed |
Management
- Standard excision: Low-risk tumours — 3–5 mm margin
- Mohs micrographic surgery (MMS): High-risk, facial, recurrent — intraoperative margin analysis; lowest recurrence rate (1–2%)
- Curettage & electrodessication: Low-risk nodular on trunk/extremities only
- Topical imiquimod 5%: Superficial BCC <2 cm in non-critical areas
- Radiotherapy: Inoperable, elderly, critical sites
- Hedgehog pathway inhibitors: Vismodegib / Sonidegib — for locally advanced / metastatic BCC (PTCH1/SMO mutation → HH signalling → uncontrolled growth). Side effects: muscle cramps, alopecia, dysgeusia
Exam Tip
Mohs surgery = gold standard for high-risk / facial BCC. Hedgehog pathway inhibitors (Vismodegib/Sonidegib) are the Recent Advances treatment for unresectable BCC — always mention in exams. Basosquamous (metatypical) BCC is the one subtype that can metastasise — behaves like SCC. BCC virtually never metastasises otherwise (<0.1%).
Squamous Cell Carcinoma & Premalignant Lesions
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Premalignant Lesions of Skin
| Lesion | Features | Malignant Potential |
| Actinic (solar) keratosis | Rough, scaly plaque on sun-exposed skin; most common premalignant | ~0.1–0.5% per year; SCC risk |
| Bowen’s disease | SCC in situ; erythematous scaly plaque; full thickness epidermal dysplasia | ~3–5% progress to invasive SCC |
| Erythroplasia of Queyrat | Bowen’s of glans penis; higher malignant potential | Up to 10% |
| Leukoplakia | White patch on mucosa (oral, vulval); cannot be rubbed off | Variable: 5–17% (speckled > homogeneous) |
| Marjolin’s ulcer | SCC arising in chronic scar, burn, or chronic wound (Marjolin 1828) | High — aggressive, metastasises early |
| Xeroderma pigmentosum | AR condition; defective nucleotide excision repair; SCC + BCC + melanoma | Very high; early onset |
Squamous Cell Carcinoma
- Second most common skin malignancy after BCC
- Risk factors: UV exposure, chronic wounds (Marjolin’s), immunosuppression, HPV (16/18 for anogenital SCC), arsenic, industrial carcinogens
- Features: Indurated, ulcerated lesion with everted edges; more likely to metastasise than BCC (2–5% for cutaneous SCC, higher for lip, ear, genitalia)
- Management: Wide excision (1 cm margins for low-risk, 2 cm for high-risk); sentinel lymph node biopsy for high-risk; adjuvant radiotherapy for perineural invasion or nodal disease
- Cetuximab (anti-EGFR): For advanced / metastatic cutaneous SCC not amenable to surgery
Exam Tip
Marjolin’s ulcer = SCC in a chronic scar — classically asked. Features: long latency (10–25 years), painless (no lymphatics in scar), rapid growth, aggressive behaviour. Bowen’s = SCC in situ; Erythroplasia of Queyrat = Bowen’s of the penis. Leukoplakia on the floor of mouth is most dangerous premalignant oral lesion.
Malignant Melanoma
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Subtypes
- Superficial spreading (most common, ~70%) — radial growth phase first; flat, irregular borders; ABCDE features
- Nodular (~15%) — vertical growth phase from outset; most aggressive; no radial phase
- Lentigo maligna — elderly, sun-damaged skin (face); Hutchinson’s freckle; slow growing
- Acral lentiginous — palms, soles, subungual; most common type in dark-skinned patients; Bob Marley’s melanoma
- Desmoplastic — rare; fibrous stroma; high local recurrence; nerve invasion common
Staging — AJCC 8th Edition (Concise)
| T Stage | Breslow thickness | Ulceration |
| Tis | In situ | — |
| T1a | ≤0.8 mm | No ulceration |
| T1b | ≤0.8 mm + ulceration OR 0.8–1.0 mm | — |
| T2 | 1.01–2.0 mm | a = no ulceration, b = ulceration |
| T3 | 2.01–4.0 mm | — |
| T4 | >4.0 mm | — |
Management
Excision margins by Breslow:In situ: 0.5–1 cm; T1 (≤1mm): 1 cm; T2 (1–2mm): 1–2 cm; T3–T4 (>2mm): 2 cm. Wider margins do not improve survival.
Sentinel Lymph Node Biopsy (SLNB):Indicated for T1b and above (≥0.8 mm with ulceration, or ≥1 mm). Uses blue dye + radioisotope. If SLN positive → completion lymph node dissection or observation with surveillance (MSLT-II trial evidence).
Adjuvant therapy (Stage III):Anti-PD-1 checkpoint inhibitors (Nivolumab, Pembrolizumab) or BRAF/MEK inhibitors (Dabrafenib + Trametinib for BRAF V600E-mutant tumours).
Metastatic disease (Stage IV):Ipilimumab (anti-CTLA-4) + Nivolumab (anti-PD-1) combination; BRAF-targeted therapy for BRAF V600E mutants. Median survival has improved from <1 year to >5 years with modern immunotherapy.
Exam Tip
Breslow thickness is the single most important prognostic factor (measured from granular layer to deepest tumour cell). Clark level is of historical interest only. SLNB threshold is T1b/T2 and above. BRAF V600E mutation occurs in ~50% of melanomas — critical for targeted therapy. ICG-guided SLNB is the Recent Advances addition to melanoma management.
Unusual Cutaneous Malignancies
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Dermatofibrosarcoma Protuberans (DFSP)
- Origin: Dermal fibroblasts; associated with COL1A1–PDGFB fusion gene (t(17;22))
- Features: Slowly growing indurated plaque → multinodular protuberant mass. Trunk most common. Locally aggressive, rarely metastasises (<5%).
- Histology: Storiform (cartwheel) pattern of spindle cells; CD34 positive, Factor XIIIa negative
- Management: Wide local excision (2–3 cm margins) or Mohs surgery; imatinib mesylate (tyrosine kinase inhibitor targeting PDGFB) for unresectable/metastatic disease
Merkel Cell Carcinoma
- Rare neuroendocrine carcinoma of skin; sun-exposed areas in elderly immunocompromised
- Aggressive — early nodal metastasis
- Associated with Merkel Cell Polyomavirus (MCPyV)
- Treatment: wide excision + SLNB ± radiotherapy; Avelumab (anti-PD-L1) for metastatic disease
Kaposi’s Sarcoma
- Vascular tumour associated with HHV-8 (Human Herpesvirus 8)
- Types: Classic (Mediterranean elderly), Endemic (African), AIDS-related (most common), Iatrogenic (post-transplant)
- AIDS-related KS: violaceous plaques/nodules; treatment includes HAART (causes regression), liposomal doxorubicin
Exam Tip
DFSP mnemonic: CD34+, storiform, COL1A1-PDGFB, imatinib. The fact that imatinib (a CML drug) works for DFSP is a classic exam question — both driven by PDGFB/ABL kinase pathways. Merkel cell = neuroendocrine + MCPyV + aggressive. Kaposi = HHV-8 + HIV association.
Pressure Sores (Decubitus Ulcers)
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Localised injury to skin and underlying tissue, usually over a bony prominence, caused by prolonged pressure (>capillary closing pressure of 32 mmHg) → ischaemia → necrosis.
Common Sites
- Supine: Sacrum (most common), occiput, heels, elbows, scapula
- Sitting: Ischial tuberosities, greater trochanters
- Lateral: Greater trochanters, malleoli
NPUAP/EPUAP Staging
| Stage | Description | Management |
| I | Non-blanchable erythema of intact skin | Pressure relief, barrier creams, hydrocolloid dressing |
| II | Partial-thickness skin loss (dermis) — shallow ulcer or blister | Moist wound dressings, pressure offloading |
| III | Full-thickness skin loss into subcutaneous fat; no bone/muscle exposure | Debridement, NPWT, surgical closure or graft |
| IV | Full-thickness tissue loss with exposed bone, tendon, or muscle | Debridement + flap reconstruction (musculocutaneous flaps) |
| Unstageable | Covered by slough/eschar obscuring depth | Debride first, then stage and treat |
| Deep Tissue Injury | Purple/maroon intact skin due to underlying damage | Remove pressure, monitor; do not debride prematurely |
Flap Choices for Stage IV Pressure Sores
- Sacral: Gluteus maximus musculocutaneous flap (V–Y or rotation)
- Ischial: Hamstring advancement flap, posterior thigh flap
- Trochanteric: Tensor fascia lata (TFL) flap
Prevention
- Repositioning every 2 hours
- Pressure-relieving mattresses (air-fluidised, alternating pressure)
- Nutrition: protein 1.25–1.5 g/kg/day, Vitamin C, zinc
- Risk scoring: Braden scale / Norton scale / Waterlow scale
Exam Tip
Capillary closing pressure = 32 mmHg — any sustained pressure above this causes ischaemia. Stage III vs IV: III has no exposed bone/tendon; IV does. Long-standing Stage IV can develop SCC transformation (Marjolin’s equivalent). Gluteus maximus flap is the workhorse for sacral pressure sores.
Skin Grafts — STSG vs FTSG
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| Feature | Split-Thickness (STSG) | Full-Thickness (FTSG) |
| Layers | Epidermis + part of dermis | Epidermis + all dermis |
| Donor site | Heals spontaneously (re-epithelialises from adnexae) | Must be sutured or covered (leaves donor scar) |
| Take rate | Better take (thinner, less metabolic demand) | Poorer take (needs better wound bed) |
| Durability | Poor (thin dermis) | Good (full dermis) |
| Cosmetic | Poorer (pigmentation mismatch, texture) | Better (matches donor site) |
| Contraction | More primary contraction; more secondary contraction | Less contraction (better for functional areas) |
| Indications | Large raw areas, burns, chronic ulcers, post-excision cover | Face, hands, eyelids, over joints (where contraction is unacceptable) |
STSG Thickness Classification
- Thin (0.008–0.012″): better take, poor durability
- Intermediate (0.012–0.018″): most commonly used
- Thick (0.018–0.030″): poor take, best durability & cosmesis
Phases of Graft Take
- Plasmatic imbibition (0–48 hrs): Graft absorbs nutrients from wound bed (avascular)
- Inosculation (48–72 hrs): Capillary buds from recipient connect to graft vessels
- Revascularisation (Day 3–5): Blood flow re-established
- Maturation: Graft fully incorporated; adnexal structures may regenerate in FTSG
Causes of Graft Failure
- Haematoma / seroma under graft (most common) — prevents vascular ingrowth
- Infection (especially β-haemolytic Streptococcus — destroys graft at <10&sup5; organisms/gram)
- Movement / shear forces (loss of contact)
- Poor recipient bed (avascular: bone, tendon without periosteum/perichondrium, irradiated tissue)
Exam Tip
Remember: STSG = better take, more contraction, worse cosmesis. FTSG = poorer take, less contraction, better cosmesis. Most common cause of graft failure = haematoma. Meshing a STSG increases surface area coverage (up to 9:1 ratio) but leaves a mesh pattern scar. β-haemolytic Streptococcus is the bacterium that destroys skin grafts even at low counts.
Skin Flaps — Classification & Clinical Use
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Classification by Blood Supply
| Type | Blood Supply | Examples | Advantage |
| Random pattern | Dermal/subdermal plexus only; no named vessel | Rotation, advancement, transposition flaps | Simple, no named vessel needed |
| Axial pattern | Named cutaneous artery (direct or musculocutaneous perforators) | Groin flap (superficial circumflex iliac), deltopectoral flap, DIEP flap | Longer, more reliable |
| Musculocutaneous (myocutaneous) | Vessel to muscle + skin perforators | TRAM, latissimus dorsi, gluteus maximus, pectoralis major | Bring well-vascularised muscle |
| Fasciocutaneous | Vessel in fascial plane | Radial forearm flap (Chinese flap), anterolateral thigh flap | Thin, pliable, sensate possible |
| Perforator flaps | Single perforating vessel from deep source | DIEP (deep inferior epigastric perforator), SIEA, ALT perforator | Spare donor muscle |
| Free flap | Microsurgical anastomosis to recipient vessels | Free TRAM, free ALT, free radial forearm, free fibula | Transfer tissue anywhere in body |
Reconstructive Ladder
Direct closure → Skin graft → Local flap → Regional flap → Distant/pedicled flap → Free flap
Always start with the simplest option that gives adequate reconstruction.
Common Flaps by Indication
| Defect | Flap of Choice |
| Breast reconstruction after mastectomy | DIEP flap (preferred), free TRAM, latissimus dorsi + implant, TRAM |
| Oral cavity / jaw reconstruction | Free fibula flap (bone + skin), free radial forearm |
| Head & neck soft tissue | Pectoralis major (pedicled), free ALT (anterolateral thigh) |
| Sacral pressure sore | Gluteus maximus musculocutaneous (V–Y or rotation) |
| Lip reconstruction | Abbe flap, Karapandzic flap, Estlander flap |
| Hand / forearm | Radial forearm flap (Chinese flap), groin flap |
| Scalp | Rotation flap, free latissimus dorsi for large defects |
Exam Tip
The reconstructive ladder is the conceptual framework for all flap decisions. DIEP flap is the gold standard for breast reconstruction — spares rectus muscle unlike TRAM. Free fibula flap is the gold standard for mandibular reconstruction. Pectoralis major is the workhorse pedicled flap for head & neck. ALT (anterolateral thigh) flap is the most versatile free flap in current practice.
Autologous Fat Graft (Lipofilling) 🆕 Recent Advance
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Transfer of a patient’s own adipose tissue from a donor site (abdomen, thighs, flanks) to a recipient site for volume restoration or contour correction. Also known as fat grafting or lipotransfer.
Reconstructive Indications
- Breast reconstruction — post-lumpectomy contour correction, post-mastectomy volume restoration
- Post-radiation soft tissue fibrosis
- Facial lipoatrophy (trauma, aging, HIV-related)
- Scar revision and skin quality improvement
- Contour deformities (post-traumatic, post-liposuction, congenital)
Technique (Coleman Technique)
- Harvesting: Low-pressure liposuction (hand syringe) to minimise fat cell trauma
- Processing: Centrifugation at 3000 rpm × 3 minutes to separate fat, oil, and blood
- Injection: Small aliquots (<0.1 mL per pass) in multiple planes in a “fan” pattern to maximise surface area contact for revascularisation
Key Points
- Graft survival rate: 40–60% (variable; some volume loss expected)
- Adipose-derived stem cells (ADSCs) in fat graft may enhance regeneration and angiogenesis
- Contraindicated if malignancy at recipient site
- Must not inject in large boluses — central necrosis occurs
Exam Tip
Autologous fat graft (lipofilling) is now standard in oncoplastic breast surgery for contour correction after BCS — major Recent Advance. The key principle is small-volume injection in multiple passes to ensure each fat cell is close to a blood supply. ADSCs are the “bonus” regenerative component. Coleman technique = low-pressure harvest + centrifuge + micro-injection.
Sources & References
- Standard textbook references (Bailey & Love, Sabiston)
- Recent Advances in Surgery