Contemporary Concepts in Soft-Tissue Wound Management

OPBSPathologyMusculoskeletal

Must Know

  • Epidermis is keratinised stratified squamous epithelium, avascular and fed by diffusion from capillaries below the basal lamina.
  • Skin is a water-impermeable barrier against abrasion and microbes.
  • Muscle fibres sit in endomysium, fascicles in perimysium and whole muscles in epimysium.
  • Muscle cells cannot divide. Satellite cells give muscle its regenerative capacity.
  • Most traumatic soft-tissue wounds heal by scar, sometimes with contracture.
  • Healing runs on a spectrum from scarless regeneration through normal scar to hypertrophic scar and keloid.
  • Fetal skin heals without scar up to about 24 weeks.
  • Keloid appears to carry a genetic predisposition. Hypertrophic scar follows burns.

Phases of Wound Healing

PhaseDurationDominant cellsEvents
Inflammation48 to 72 hoursPlatelets, neutrophils, then macrophagesHaematoma, mediator release, phagocytosis
ProliferationAt least 2 to 3 weeksFibroblasts, endothelial cellsGranulation tissue, angiogenesis, contraction, epithelialisation
RemodellingMonthsFibroblasts, many cells apoptoseType III collagen replaced by type I
  • Platelets release PDGF and IL-8. Mast cells raise blood flow and permeability.
  • Neutrophils amplify inflammation with IL-1, IL-6 and TNF-α.
  • Macrophages dominate late inflammation and drive the switch to proliferation.
  • PDGF is the main stimulus for fibroblast migration.
  • Myofibroblasts express smooth muscle actin, via MRTF-A, and contract the wound.
  • Fibroblasts secrete MMPs to clear a path for migration and vessel ingrowth.
  • Angiogenesis is driven by VEGF, FGF, angiopoietin, TGF-β, hypoxia and lactic acid.
  • Fibroblast Neu differentiation factor drives keratinocyte migration from wound edges and hair follicles.
More on mediators
  • TGF-β and MCP-1 attract monocytes and drive their maturation into macrophages.
  • Macrophages release PDGF, VEGF, FGF, NGF, TGF-β, CTGF and Cyr-61 to build granulation tissue.
  • T lymphocytes, fibrocytes and eosinophils also take part in inflammation.
  • Fibroblasts migrate along fibrin, fibronectin, vitronectin and hyaluronic acid through integrin binding.
  • Endothelial cells break down their own basement membrane to form new tubules.

Scar Versus Normal Skin

FeatureNormal skinMature scar
Collagen arrangementBasketweaveParallel bundles
Collagen typeNot stated80 to 90 percent type I, rest type III
Tensile strengthFullAbout 70 percent
Appendages and rete pegsPresentAbsent
ElastinNormalReduced
  • Early scar is disorganised type III collagen.
  • Scar never regains the full strength or flexibility of the original tissue.

Injury Patterns

  • Fracture blisters form at the dermoepidermal junction from shear, often on the foot, ankle, leg, wrist and forearm.
  • Haemorrhagic blisters signal deeper injury and scar more than serous blisters.
  • Both blister types raise the risk of skin breakdown and infection.
  • Morel-Lavallée lesion is shear separation of hypodermis from deep fascia, filling with blood, lymph and necrotic fat.
  • The collection enlarges with time and forms a pseudocapsule.
  • Up to almost 50 percent of Morel-Lavallée lesions are culture positive on aspiration.
  • Aspirated or débrided lesions carry higher infection risk and recur often.
  • Ballistic damage extends beyond the tract, worse with higher velocity, larger or deforming bullets and close range.
Mellado and Bencardino typeMorel-Lavallée appearance
1Simple seroma
2Subacute haematoma
3Mature organised haematoma
4Closed fatty laceration with perifascial dissection
5Perifascial nodular lesion
6Infected, with sinus, septations and capsule

Open Fracture Classification

  • Gustilo and Anderson is the most used but has poor interobserver reliability.
  • OTA Open Fracture Classification grades skin, muscle, bone, arterial injury and contamination, with better reliability.
  • OTA OFC helps predict repeat débridement, NPWT or bead use and amputation.

Host Factors

  • Low albumin and prealbumin prolong healing and raise infection.
  • Poor oxygen delivery from vascular disease, diabetes, smoking or lung disease delays healing.
  • Exogenous steroids impair scar formation and infection resistance.
  • Healing capacity falls with age and with sun or therapeutic radiation.
  • A wound is infected once pathogen load provokes a meaningful immune response. Below that it is colonised.
  • Necrotic tissue cannot receive immune cells or systemic antibiotics, so needs débridement.
  • Infected wounds should not be closed.

Interventions

  • Donati-Allgöwer vertical mattress suture best preserves skin edge perfusion.
  • No consensus exists on drain use.
  • NPWT uses open cell foam at 75 to 125 mmHg, continuous or intermittent.
  • NPWT shifts cytokines to an anti-inflammatory profile. TNF falls while VEGF, FGF-2, TGF-β and PDGF rise.
  • Chronic wounds show raised cytokines and a prolonged, hyperactive neutrophil response.
  • A moist occlusive environment speeds epithelialisation, by up to 40 percent in skin grafts.
  • Bilayer collagen and silastic constructs can grow granulation over small areas of exposed tendon or bone.
Morykwas pig work at 125 mmHgEffect
Blood flowFourfold rise
Granulation tissue63 percent more continuous, 103 percent more intermittent
Bacterial clearanceBetter by day 4
Random flap survivalUp 21 percent
AntisepticPoint to remember
Dakin solutionBuffered sodium hypochlorite, from World War I
Povidone-iodineFibroblast growth slowed at 0.01 percent, stopped at 0.1 percent
Hydrogen peroxide0.5 percent delayed early healing in rats, no difference by day 8 to 10
More on wound adjuncts
  • Dakin solution at 0.00025 percent controlled four mould species with limited cytotoxicity in vitro.
  • NPWT reduced wound complications in pilon, calcaneus and bicondylar plateau fractures.
  • In NPWT, IL-1β fell only in acute wounds.
  • Early flap cover of exposed tendon or bone adds vascularity and lowers infection risk.
  • Morel-Lavallée lesions left alone may persist for months or years and leave thinned skin.

Exam Traps

  • Scar collagen lies in parallel bundles. Normal skin collagen is basketweave.
  • Early scar is type III collagen, mature scar is mostly type I.
  • Gustilo and Anderson is common yet less reliable than OTA OFC.
  • Intermittent NPWT produced more granulation than continuous.

Related pages. Debridement of Open Fractures, Surgical Site Infection, Union / Non-union

Source

Evans AR, Hayda RA. Contemporary Concepts in Soft-Tissue Wound Management. In. Aaron RK, editor. Orthopaedic Basic Science. Foundations of Clinical Practice. 5th ed. Philadelphia, Wolters Kluwer, 2021.

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Reviewed by Professor Phong Tran, Head of Orthopaedic Surgery, Western Health. Last updated 17 October 2026.