1. Definition and principles
   Controlled subatmospheric pressure applied to a sealed wound dressing to remove exudate, reduce edema, support granulation tissue, and help contract the wound.
2. Equipment and dressing components
   Pump, collection canister, tubing, adhesive drape, foam or gauze wound filler, and an interface layer when vulnerable structures are exposed.
3. How it works
   Macrodeformation draws wound edges inward; microdeformation at the wound-dressing interface may stimulate granulation. It also manages fluid and helps maintain a protected moist wound environment.
4. Indications
   Acute traumatic wounds, dehisced surgical wounds, pressure injuries, diabetic foot wounds after appropriate assessment and debridement, venous ulcers in selected cases, skin graft bolstering, and closed-incision NPWT for selected high-risk surgical incisions.
5. Contraindications and precautions
   Untreated necrotic tissue or eschar, unprotected exposed vessels or organs, unexplored fistulas, malignancy within the wound in many settings, active uncontrolled bleeding, and untreated osteomyelitis. Particular care is needed with anticoagulation, friable tissue, ischemia, pain, and impaired sensation.
6. Settings and modes
   Continuous, intermittent, and variable pressure modes; typical pressure choices and their adjustment according to wound type, tissue tolerance, exudate, ischemia risk, and pain.
7. Technique
   Patient and wound assessment, debridement where appropriate, wound measurement, protection of periwound skin and exposed structures, filler placement without overpacking, airtight sealing, tubing placement, pressure selection, documentation, and dressing-change planning.
8. Monitoring and complications
   Pain, bleeding, loss of seal, maceration, retained foam, infection progression, device malfunction, and rare major hemorrhage. Monitoring includes drainage quantity and character, pain, skin integrity, wound dimensions, and systemic infection signs.
9. Special applications
   Diabetic foot wounds, pressure injuries, open abdomen, grafts/flaps, pediatric care, and closed-incision prophylactic use.
10. Evidence and practical decision-making
    Which wounds are most likely to benefit, limitations of evidence, when conventional dressings are preferable, and cost/resource considerations.

Mechanisms of negative-pressure wound therapy

1. Macrodeformation: visible wound contraction

• Draws wound edges toward the center.
• Decreases wound surface area and, in compliant tissue, wound volume.
• Helps reduce dead space.
• Supports approximation of soft tissue and may make later closure, grafting, or flap coverage easier.

2. Microdeformation: cellular mechanotransduction

• Mechanical stress is sensed by cells through adhesion complexes and the cytoskeleton.
• This can promote fibroblast migration and proliferation.
• It may increase extracellular matrix deposition.
• It may support endothelial-cell activity and angiogenesis.
• These effects favor granulation-tissue formation.

3. Removal of exudate and reduction of interstitial edema

• Excess water
• Proteases such as matrix metalloproteinases
• Inflammatory mediators
• Necrotic debris
• Bacterial products
• Electrolytes and proteins

• Reduce local edema.
• Reduce tissue pressure.
• Restore a more favorable capillary-to-tissue pressure gradient.
• Improve oxygen and nutrient diffusion.
• Limit periwound maceration.
• Lower frequency of dressing changes compared with highly exudative conventional dressings.

4. Changes in perfusion and microcirculation

• The effect is not simply that more negative pressure always means more blood flow.
• Excessive negative pressure can compress tissue and potentially reduce perfusion, especially in ischemic tissue.
• Perfusion changes differ by pressure setting, dressing material, wound shape, anatomical location, and vascular status.

5. Stabilization and protection of the wound environment

• Maintain a moist but not overly wet wound environment.
• Reduce repeated trauma from frequent dressing removal.
• Protect the wound from external contamination.
• Stabilize skin grafts, dermal substitutes, or flap-adjacent wounds by minimizing shear.
• Improve conformity of a graft to the wound bed and prevent fluid collection beneath it.

6. Effects on bacterial burden and biofilm: variable, not guaranteed

• Removing exudate, debris, and some bacterial products.
• Reducing pooling of fluid.
• Providing a sealed barrier to outside contamination.
• Facilitating serial assessment and staged debridement.

• Does not sterilize a wound.
• Does not replace surgical debridement.
• Does not replace systemic antibiotics when infection requires them.
• Can conceal deteriorating infection if the wound is not examined appropriately.

7. Modulation of inflammation and wound fluid composition

• Granulation
• Angiogenesis
• Matrix formation
• Epithelial migration

Mechanism by clinical use

Mechanisms in one flow diagram

Sealed foam/gauze dressing + controlled negative pressure
                         ↓
       Mechanical deformation + fluid evacuation
                         ↓
 ┌───────────────────────┼────────────────────────┐
 ↓                       ↓                        ↓
Macrodeformation     Microdeformation        Exudate removal
wound-edge pull      cellular microstrain    edema/inflammatory
dead-space reduction fibroblast/endothelial  fluid reduction
                     activity                 less maceration
 └───────────────────────┼────────────────────────┘
                         ↓
More favorable wound bed:
granulation, tissue organization, easier closure or grafting

Practical takeaway

• Debride nonviable tissue when indicated.
• Control infection and drainage source.
• Ensure adequate perfusion.
• Off-load pressure injuries and diabetic plantar wounds.
• Use compression where venous disease is appropriate and arterial status permits.
• Optimize glucose control, nutrition, and systemic illness.