HomeTopic NotesWound Healing, Skin & Soft Tissue
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

Phases of Wound Healing

PhaseTimeKey EventsKey CellsMediators
HaemostasisMinutes–hoursVasoconstriction, platelet plug, fibrin clot scaffoldPlateletsPDGF, TGF-β, Thromboxane A&sub2;
Inflammation0–72 hrsVasodilation, neutrophil infiltration → phagocytosis; macrophages recruit fibroblastsNeutrophils → MacrophagesIL-1, TNF-α, IL-6
ProliferationDay 3–3 weeksFibroblast proliferation → collagen III; angiogenesis; granulation tissue; epithelial migrationFibroblasts, endothelial cells, keratinocytesFGF, VEGF, EGF
RemodellingWeeks–monthsCollagen III → Collagen I; cross-linking → tensile strength (~80% of normal)Fibroblasts, myofibroblastsMMPs, 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
InfectionProlongs inflammation, increases tissue destruction, delays collagen deposition
Poor blood supply / radiationReduced O&sub2; delivery → impaired fibroblast function & angiogenesis
Excessive tension / foreign bodiesIschaemia or persistent inflammation
Desiccation / macerationDisrupts optimal moist environment for epithelial migration
Systemic Factors
AgeReduced collagen turnover and vascularity
MalnutritionProtein (collagen synthesis); Vit C (proline/lysine hydroxylation); Zinc (DNA synthesis); Copper (collagen cross-linking)
DiabetesMicroangiopathy, impaired neutrophil function
Steroids / cytotoxicsSteroids inhibit fibroblasts; cytotoxics block cell proliferation
SmokingNicotine → vasoconstriction; CO → reduced O&sub2; delivery
Anaemia / hypoxiaLow oxygen tension delays fibroblast & collagen activity

Nutritional Role in Healing

NutrientRole
ProteinFibroblast proliferation, collagen formation
Vitamin CHydroxylation of collagen precursors (proline, lysine)
ZincDNA & RNA synthesis, epithelialisation
CopperLysyl oxidase activity for collagen cross-linking
Vitamin AEpithelial 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)

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

TypeExamplesIndicationKey Property
Simple / gauzeParaffin gauze, tulle grasLow-exudate clean woundsNon-adherent, allows drainage
HydrocolloidDuoDERMStage I–II pressure sores, partial thickness burnsMaintains moist environment, autolytic debridement
HydrogelIntraSite GelDry necrotic wounds, sloughy woundsRehydrates eschar, promotes autolytic debridement
FoamAllevyn, MepilexModerate–high exudate woundsAbsorbs exudate, maintains moist environment
AlginateKaltostat, SorbsanHigh-exudate, bleeding woundsHaemostatic, forms gel on contact with exudate
Silver-containingAquacel Ag, Mepilex AgInfected / high-risk woundsAntimicrobial — broad spectrum
BiologicalAmniotic membrane, collagen sheetBurns, non-healing ulcersGrowth factor delivery, scaffold for regeneration
NPWTVAC therapyComplex 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

FeatureHypertrophic ScarKeloid
ExtentStays within wound boundariesExtends beyond wound boundaries (claw-like)
RegressionMay regress spontaneously over timeDoes not regress; tends to enlarge
Recurrence after excisionLowHigh (30–100%)
Collagen typeType III (fine, wavy)Type I (thick, nodular, hyalinised)
Predisposing sitesBurns, joints, areas of tensionSternum, ear lobes, deltoid, jaw line
Racial predispositionNoneDark-skinned individuals (10–15× more common)
SymptomsPruritus ± painPruritus, 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

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

StageDescriptionTreatment
IAbscess formation — single or multiple, no sinus tracts or scarringMedical: topical clindamycin, doxycycline, intralesional steroids
IIRecurrent abscesses with sinus tracts and scarring — single or multiple, widely separatedMedical + surgical: unroofing of sinus tracts
IIIDiffuse involvement or near-diffuse involvement, multiple interconnected sinus tracts & abscesses across entire areaWide 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)

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 RiskHigh Risk
Nodular or superficial histologyMorphoeaform, infiltrative, basosquamous
Tumour <2 cmTumour >2 cm
Well-defined bordersPoorly defined borders
Trunk / extremitiesFace, H-zone, ears, genitalia, hands, feet
Primary lesionRecurrent lesion / perineural invasion
ImmunocompetentImmunosuppressed

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

Premalignant Lesions of Skin

LesionFeaturesMalignant Potential
Actinic (solar) keratosisRough, scaly plaque on sun-exposed skin; most common premalignant~0.1–0.5% per year; SCC risk
Bowen’s diseaseSCC in situ; erythematous scaly plaque; full thickness epidermal dysplasia~3–5% progress to invasive SCC
Erythroplasia of QueyratBowen’s of glans penis; higher malignant potentialUp to 10%
LeukoplakiaWhite patch on mucosa (oral, vulval); cannot be rubbed offVariable: 5–17% (speckled > homogeneous)
Marjolin’s ulcerSCC arising in chronic scar, burn, or chronic wound (Marjolin 1828)High — aggressive, metastasises early
Xeroderma pigmentosumAR condition; defective nucleotide excision repair; SCC + BCC + melanomaVery 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

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 StageBreslow thicknessUlceration
TisIn situ
T1a≤0.8 mmNo ulceration
T1b≤0.8 mm + ulceration OR 0.8–1.0 mm
T21.01–2.0 mma = no ulceration, b = ulceration
T32.01–4.0 mm
T4>4.0 mm

Management

  1. 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.
  2. 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).
  3. Adjuvant therapy (Stage III):
    Anti-PD-1 checkpoint inhibitors (Nivolumab, Pembrolizumab) or BRAF/MEK inhibitors (Dabrafenib + Trametinib for BRAF V600E-mutant tumours).
  4. 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

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)

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

StageDescriptionManagement
INon-blanchable erythema of intact skinPressure relief, barrier creams, hydrocolloid dressing
IIPartial-thickness skin loss (dermis) — shallow ulcer or blisterMoist wound dressings, pressure offloading
IIIFull-thickness skin loss into subcutaneous fat; no bone/muscle exposureDebridement, NPWT, surgical closure or graft
IVFull-thickness tissue loss with exposed bone, tendon, or muscleDebridement + flap reconstruction (musculocutaneous flaps)
UnstageableCovered by slough/eschar obscuring depthDebride first, then stage and treat
Deep Tissue InjuryPurple/maroon intact skin due to underlying damageRemove 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

FeatureSplit-Thickness (STSG)Full-Thickness (FTSG)
LayersEpidermis + part of dermisEpidermis + all dermis
Donor siteHeals spontaneously (re-epithelialises from adnexae)Must be sutured or covered (leaves donor scar)
Take rateBetter take (thinner, less metabolic demand)Poorer take (needs better wound bed)
DurabilityPoor (thin dermis)Good (full dermis)
CosmeticPoorer (pigmentation mismatch, texture)Better (matches donor site)
ContractionMore primary contraction; more secondary contractionLess contraction (better for functional areas)
IndicationsLarge raw areas, burns, chronic ulcers, post-excision coverFace, 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

  1. Plasmatic imbibition (0–48 hrs): Graft absorbs nutrients from wound bed (avascular)
  2. Inosculation (48–72 hrs): Capillary buds from recipient connect to graft vessels
  3. Revascularisation (Day 3–5): Blood flow re-established
  4. 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

Classification by Blood Supply

TypeBlood SupplyExamplesAdvantage
Random patternDermal/subdermal plexus only; no named vesselRotation, advancement, transposition flapsSimple, no named vessel needed
Axial patternNamed cutaneous artery (direct or musculocutaneous perforators)Groin flap (superficial circumflex iliac), deltopectoral flap, DIEP flapLonger, more reliable
Musculocutaneous (myocutaneous)Vessel to muscle + skin perforatorsTRAM, latissimus dorsi, gluteus maximus, pectoralis majorBring well-vascularised muscle
FasciocutaneousVessel in fascial planeRadial forearm flap (Chinese flap), anterolateral thigh flapThin, pliable, sensate possible
Perforator flapsSingle perforating vessel from deep sourceDIEP (deep inferior epigastric perforator), SIEA, ALT perforatorSpare donor muscle
Free flapMicrosurgical anastomosis to recipient vesselsFree TRAM, free ALT, free radial forearm, free fibulaTransfer 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

DefectFlap of Choice
Breast reconstruction after mastectomyDIEP flap (preferred), free TRAM, latissimus dorsi + implant, TRAM
Oral cavity / jaw reconstructionFree fibula flap (bone + skin), free radial forearm
Head & neck soft tissuePectoralis major (pedicled), free ALT (anterolateral thigh)
Sacral pressure soreGluteus maximus musculocutaneous (V–Y or rotation)
Lip reconstructionAbbe flap, Karapandzic flap, Estlander flap
Hand / forearmRadial forearm flap (Chinese flap), groin flap
ScalpRotation 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

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)

  1. Harvesting: Low-pressure liposuction (hand syringe) to minimise fat cell trauma
  2. Processing: Centrifugation at 3000 rpm × 3 minutes to separate fat, oil, and blood
  3. 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.
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Sources & References

  • Standard textbook references (Bailey & Love, Sabiston)
  • Recent Advances in Surgery
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