Healing by Second Intention: Open Wounds, Granulation, Contraction, Scar and Complications

Learning outcomes

• Define secondary intention and identify when it is appropriate.
• Explain the roles of granulation tissue, angiogenesis, fibroblasts, myofibroblasts and epithelial migration.
• Describe why contraction and scar are greater than in primary union.
• Recognise complications and principles of open-wound management.
• Distinguish secondary from primary and delayed primary closure.

1. Indications for secondary healing

Situation	Why the wound remains open
Large tissue loss	Edges cannot be brought together without excessive tension.
Contamination or infection	Closure would trap bacteria, pus or necrotic debris.
Necrotic tissue	Viability must be assessed and devitalised tissue removed.
Abscess cavity	Drainage is necessary while the cavity fills from its base.
Pressure ulcer	Underlying pressure, ischaemia and tissue loss require staged healing.
Burn or avulsion	Skin/subcutaneous tissue is missing or unsuitable for immediate closure.
Risky anatomic site	Closure could compromise drainage, perfusion or function.

2. Sequence of secondary healing

2.1 Haemostasis and early inflammation

Fibrin forms a provisional matrix, but the clot is larger than in a small incision. Neutrophils and macrophages must clear more debris and bacteria. Persistent contamination prolongs inflammation and increases protease-mediated tissue destruction.

2.2 Granulation tissue and angiogenesis

Fibroblasts migrate from the wound edges and underlying tissue. Hypoxia stimulates VEGF and capillary growth. The wound base becomes red, moist and granular. Granulation tissue fills depth and creates a scaffold for the epidermis.

2.3 Epithelial migration

Keratinocytes migrate from the edges and skin appendages. The larger the defect, the longer the surface remains fragile and vulnerable to desiccation, shear and infection.

2.4 Contraction

Myofibroblasts attach to collagen and contract the matrix, pulling edges inward. Contraction can close a substantial portion of the wound but can distort nearby joints, eyelids, mouth, fingers and neck.

2.5 Remodelling

Collagen III is replaced by collagen I, vessels regress and the scar becomes paler. The final scar is larger than in primary healing and may remain functionally limiting.

3. Why the scar is larger

• The wound contains more dead tissue and matrix to replace.
• Granulation tissue and angiogenesis are extensive.
• Fibroblasts deposit more collagen and extracellular matrix.
• Contraction produces a broad, irregular scar.
• Inflammation persists longer, stimulating TGF-β and fibrosis.

4. Normal appearance and monitoring

Finding	Usually expected	Concerning
Wound bed	Moist pink/red granulation tissue.	Black eschar, grey slough, pallor or exposed tendon/bone.
Drainage	Small amount of clear or blood-tinged fluid.	Increasing purulence, foul odour or heavy bleeding.
Pain	Gradually improves.	New severe pain or pain out of proportion.
Edges	Slow inward contraction and epithelial growth.	Expanding defect, undermining or rapidly spreading erythema.
Systemic state	Stable, afebrile and improving function.	Fever, confusion, hypotension, oliguria or tachypnoea.

5. Open-wound management principles

1. Assess perfusion and depth: pulses, capillary refill, tendon/nerve function and exposed structures.
2. Control contamination: irrigation, appropriate debridement, foreign-body removal and tetanus prevention.
3. Manage infection: culture deep tissue when indicated, drain collections and use antimicrobials for clinically significant infection.
4. Protect granulation: use a moist, non-adherent dressing and avoid traumatic dressing changes.
5. Offload pressure and shear: reposition, use support surfaces and immobilise when necessary.
6. Optimise systemic factors: glucose, nutrition, oxygenation, anaemia, smoking and vascular supply.
7. Consider advanced closure: negative-pressure therapy, skin graft, flap or delayed primary closure when granulation and source control permit.

6. Complications

Complication	Mechanism	Clinical consequence
Chronic ulcer	Persistent pressure/ischaemia, infection, neuropathy or inflammatory disease.	Long-term drainage, pain, osteomyelitis and cancer risk.
Contracture	Excess myofibroblast contraction across a functional structure.	Reduced movement, deformity and disability.
Hypertrophic scar/keloid	Excess collagen and persistent TGF-β signalling.	Raised, itchy or painful scar.
Exuberant granulation	Granulation tissue rises above the wound edge.	Epithelial migration is blocked.
Infection/abscess	Open defect and retained necrotic tissue provide microbial access.	Cellulitis, sepsis or delayed closure.
Bleeding and desiccation	Fragile capillaries and inadequate protection.	Anaemia, pain and loss of viable tissue.

7. When secondary wounds need urgent escalation

• Pain out of proportion, rapidly spreading redness, bullae, crepitus or skin anaesthesia.
• Exposed vessel, tendon, bone, joint or implanted material.
• Absent pulses, cold limb, worsening numbness or motor loss.
• Fever, hypotension, confusion, oliguria or rising lactate.
• Failure to improve despite offloading, cleaning and infection control.

8. Secondary versus primary and tertiary intention

Feature	Primary	Secondary	Tertiary
Edges	Closely apposed immediately.	Open and fill naturally.	Open initially, closed later.
Granulation	Minimal.	Abundant.	Moderate after control.
Contraction	Limited.	Marked.	Variable.
Scar	Small.	Large, often irregular.	Intermediate.
Best use	Clean, low-tension wound.	Defect, infection or contamination.	Contaminated wound suitable for later closure.

9. Applied cases

Case 1: Pressure ulcer

Pressure, shear and ischaemia produce tissue loss. Relief of pressure, staging, debridement, moisture-balanced dressings, nutrition and infection assessment are essential. A persistently non-healing ulcer needs vascular and systemic evaluation.

Case 2: Drained abscess

The cavity is left open so pus can drain and the base can granulate. Packing or negative-pressure therapy is selected according to size and local protocol; unnecessary traumatic packing can injure new tissue.

Case 3: Burn contracture

Deep burns heal by contraction and scar. Early specialist referral, physiotherapy, splinting and later grafting may preserve movement and prevent deformity.

10. Quick self-test

1. What is secondary intention?
   Answer: Healing of an open, tissue-deficient, contaminated or infected wound by granulation, contraction and epithelialisation.
2. Why is contraction greater?
   Answer: Myofibroblasts must reduce a large wound surface area.
3. What does healthy granulation look like?
   Answer: Moist, pink-red, granular and vascular tissue.
4. Name three reasons to leave a wound open.
   Answer: Infection, contamination, necrosis, abscess, large tissue loss or uncertain viability.
5. What findings suggest necrotising infection?
   Answer: Severe pain out of proportion, rapid spread, bullae, crepitus, skin anaesthesia or systemic toxicity.

11. Take-home summary

Selected references

• NCBI Bookshelf: Wound Healing
• NCBI Bookshelf: Wound Closure Techniques

Educational note: This resource supports learning and clinical reasoning. Current local protocols, senior supervision and national guidelines take precedence in patient care.