Wound Healing, Tissue Repair & Scar

When we get a wound, it takes a few days to heal but it happens quickly enough and on its own. But within that process of healing, there are a lot of processes and entities involved. Even wounds are classified into different types. This is exactly the kind of information that a pro-surgeon would need to have. 

Read the blog post below to enhance your understanding of Surgery and ace the next NEET PG exam.  

Wound Healing

• Mechanism by which body attempts to restore the integrity of injured part 

Phases of wound healing

1. Inflammatory phase

• Begins immediately after wounding 
• Lasts for 2-3 days 

Bleeding

↓

Vasoconstriction & thrombus formation to limit blood loss

↓

Platelets stick to damaged endothelial layer scab formation, recruitment of fibroblasts & macrophages

2. Proliferative phase

• It lasts from 3rd day to 3 rd week
• This phase has

• Fibroblast activity
• Production of collagen, Glycosaminoglycans & Proteoglycans
  Angio-Neogenesis: Growth of new vessels as capillary loops
• ↑Increased Tensile strength of wounds: Due to increased Type III collagen deposition in random fashion which leads to increased tensile strength of wound.
• Wound contraction: ↓decreased surface area of wound

3. Remodelling phase

• Characterized by Maturation of collagen
• Type I collagen is replaced by Type III until a Ratio of 4:1 is achieved
• Hence, Tissue remodelling shows

• Realignment of collagen fibers
• ↓sed wound vascularity
• Wound contraction

• Maturation of collagen leads to ↑sed Tensile strength of wound
• Maximum wound strength is seen at-12th week or 3^rd month   Post-injury
• Maximum wound strength achieved is Approximately 80% of un-injured skin strength

Factors adversely affecting wound healing

Local factors	Systemic factors
Infection Ischemia Foreign body Hematoma Movement Mechanical stress Presence of necrotic tissues	Diabetes mellitus Ionizing radiation (impairs wound healing by causing obliterating end arteritis & decreases vascularity Temperature Advancing age Malnutrition Vitamin A & C deficiency Zinc & Iron deficiency Drugs (e.g. steroids, doxorubicin)Jaundice Uremia Malignancy

Wound

• Breach in continuity of skin or surface epithelium 

Types of wound

Simple wound	Complex wound
Only skin + subcutaneous tissue is involved	Skin + underlying nerves, vessels, tendons with devitalized tissue are involved.

Surgical classification of wound

Class I

• Also known as clean wound 
• It includes 
  • Uninfected operative wounds without inflammation 
  • Respiratory, alimentary, genital or urinary tract are not entered
• These wounds are closed primarily (if necessary drained with closed drainage)
• Examples
  • Inguinal hernia operation
  • Mastectomy
  • Thyroidectomy
  • Joint replacement
  • Abdominal Aortic Aneurysm repair

Class II

• Also known as Clean contaminated wound
• It includes
• Operative wound in which Respiratory tract, GIT, Genito urinary tract is entered under controlled condition without unusual contamination
• Examples

• Cholecystectomy
• CBD exploration
• Elective Gl surgery (Elective colonic Resection, Elective Gastrectomy)

Class III

• Also known as Contaminated wounds
• It includes

• Open, fresh Accidental wounds
• Operations with major break in sterile techniques or gross spillage from GIT
• Incisions in which acute non-purulent inflammation is encountered
• Examples

• Appendicular perforation
• Gastric perforation
• Enterotomy during bowel obstruction
• Human bite
• Open fracture

Class IV

• Also known as Dirty wound
• It includes

• Old traumatic wound with retained devitalized tissue
• Wound with clinical infection or perforated viscera with high degree of contamination
• Organism causing post-operative infection is already present in the wound before operation
• Associated with severe inflammation
• Examples 

• Perforated diverticulitis 
• Fecal peritonitis 
• Presence of frank pus 
• Necrotizing soft tissue infection 

Risk of infection	Antibiotic prophylaxis
Clean wound: 5% risk	Not required (usually)
Clean contaminated wound: 10% risk	Usually required
Contaminated: 20-30% risk	Required
Dirty wound: 30-40% risk	Treatment is required (not the prophylaxis)

How to avoid surgical site infection?

1. Staff should follow hand washing between patients
2. Length of hospital stay-should be kept minimum (to prevent hospital acquired infections)
3. Preoperative shaving-should be avoided if possible
4. Antibiotic skin preparation-should be Standardized
5. Bowel preparation for intra-abdominal surgery should be followed
6. Best time to give Preoperative antibiotics-At the time of induction via IV route or 1 hour before surgery
7. Attention to theatre technique & discipline
8. Avoid hypothermia Pre-operatively
9. Monofilament sutures should be preferred over polyfilament sutures (Increased risk of infection in polyfilament)
10. Proper Apposition of wound during suturing
11. Prevention of dead space & hematoma

Classification of wound closure & healing 

Healing by primary intention 

• Aka healing by first intention 
• Occurs when there is
  • Apposition of wound edges 
  • Minimal surrounding tissue trauma (least inflammation)
• Associated with Best Scar (hair line scar)

Healing by secondary intention 

• It occurs in the wound that is
  • Left open 
  • Allowed to heal by granulation, contraction and epithelization 
• Associated with large scar (cosmetically poor)

Healing by tertiary intention 

• Also known as delayed primary intention healing 
• It occurs when the
  • Wound edges are not opposed 
  • Wound is contaminated 
• Delayed closure is performed when inflammation & proliferative phase is well established 
• Associated with less satisfactory scar 

Chronic wound

• Wound, that does not heal within 3 months 
• Delay in healing can occur in any phase: Most frequently inflammatory phase 
• Examples: Pressure ulcers/Pressure sores 

Treatment 

• Surgical intervention is done only when
  • Non-operative treatment fails & 
  • When patient suffer from intractable pain 

Degloving injury

• In this type of injury
  • Skin & subcutaneous fat are stripped by avulsion from underlying fascia. 
  • Leaves neuromuscular structures, tendons & bone exposed 

Compartment syndrome

• Typically occur in closed lower limb injuries 

Clinical features 

• Severe pain 
• Pain or passive stretching of affected compartment muscle 
• Distal sensory disturbances 
• Absence of distal pulses (late sign)

Investigation

• For diagnosis: compartment pressure is measured 

↓

Pressure monitor & catheter inserted into muscle compartment

• If pressure greater than 30 mm hg then diagnosis of compartment syndrome is made. 

Treatment 

• Fasciotomy 
• Indication for fasciotomy
  • If compartment pressure is > 30 mmHg
  • Clinical signs and symptoms of compartment syndrome 
• Procedure
  • Two longitudinal incision should be given – one on medial and the other on lateral side 
  • Incised layers are
    • Skin 
    • Subcutaneous fat 
    • Fascia 
• After incision, Muscle should be bulging through fascia

Pressure sore 

• Definition: tissue necrosis & ulceration due to prolonged pressure 
• Other names
  • Bed sore 
  • Decubitus ulcer 
  •  Trophic ulcer 
  • Penetrating ulcer 

Pathophysiology 

• External pressure more than capillary occlusive pressure 
• Which is more than 30 min
• There occurs stoppage of perfusion leading to ischaemia 
• Leading to necrosis and ulceration. 
• Other mechanisms
  • Malnutrition 
  • Neurological deficit. 

Incidence of pressure ulcer 

• Generally seen in 5 percent of hospitalised patients 
• Mnemonic: Indira Gandhi Stadium Inaugurated By Home Minister Office.
  • I - Ischium (Most common site)
  • G - Greater trochanter 
  • S - Sacrum 
  • H - Heel 
  • M - Malleolus (lateral> medial)
  • O - Occiput 

Neurological cause of pressure ulcer

• Mnemonic: SPL  DPT

• S - Syringomyelia
• S - Spina bifida
• S - Spinal surgery
• P - Peripheral neuritis
• P - Peripheral nerve injury
• L - Leprosy
• D - Diabetic neuropathy
• P - Paraplegia
• T - Tabes dorsalis

Staging of pressure sore

Stage I

• Non blanchable erythema of skin without breach in epidermis 
• Early superficial ulcer 

Stage II

• Partial thickness less including epidermis + dermis. 
• Late superficial ulcer 

Stage III

• Full thickness skin loss involving subcutaneous tissues but not through underlying fascia. 
• Early deep ulcer 

Stage IV

• Full thickness skin loss involving subcutaneous tissue, muscle bone, joints or tendon. 
• Late deep ulcer 

Management 

• Can be prevented by
  • Good skin care 
  • Use of special pressure dispersion curshions/foams 
  • Use of low air loss & air fluidised beds 
  • Urinary and fecal diversion: if required 
• In cases of bed bound patients: patients should be turned at least every 2 hourly 
• Wheel chair bound patients: patient should lift themselves off their seats for every 10 seconds every 10 minutes. 

Surgical treatment

• Reserved for patients with no improvement after conservative management 
• Surgical options are
  • Adequate debridement 
  • Vacuum assisted closure 
  • Flap closure: large skin flap with muscle & intact sensory innervation 

↓

MC used flap for pressure sores: Extensor fascia lata flap with lateral cutaneous nerve of thigh  

Vacuum assisted closure

• Aka negative pressure wound therapy (NPWT)
• (-125 mmHg) pressure is applied 2-3 times a week 
• Promotes wound healing by applying vacuum through a special sealed dressing.
• Continued vacuum by NPWT.
  • Draws out fluid from wound
  • Increases blood flow to the area.
• Vacuum can be applied continuously or intermittently.

Primary effects of Negative pressure wound therapy

• Cause: Macrodeformation → Draws wound edges together 

↓

Contraction (helps in wound edge approximation)

• Stabilization of wound environment: By protecting the wound from outside microorganisms, provides warm & moist environment to wound
• Reduces edema: by removal of soft tissue exudate 
• Micro deformation leading to cellular proliferation at the wound surface 

Contraindications of NPWT 

• Mnemonic: MUNNA

• M - Malignancy in the wound 
• U - Untreated osteomyelitis 
• N - Non enteric & undrained fistula 
• N - Necrotic tissue with eschar 

Scar formation

• Maturation phase of wound healing leads to formation of
  scar
• Immature scar
  • Pink, hard, raised & itchy

• Mature scar
  • Maturation of collagen
  • Denser collagen
  • Scar becomes acellular (Fibroblasts and blood vessels
    reduce over a period of time)
• Changes in scar from immature state to mature state
  • Pallor
  • Softer
  • Flattens
  • Itching diminishes
• Maximum tensile strength: 12 weeks/3 months post injury 

↓

Approximately 80% of uninjured skin

Types of abnormal scars

1. Atrophic Scar
2. Hypertrophic Scar
3. Keloid

1. Atrophic Scar 

• Pale, flat and stretched in appearance 
• Site: Back (in areas of tension)
• Easily traumatized (due to thin epidermis and dermis)
• Excision & Resuturing rarely improves it 

2. Hypertrophic Scar

• Has excessive scar tissue 
• Scar doesn’t extend beyond the boundary of original wound/incision
• Results from 

• Prolonged inflammatory phase
• Unfavourable scar siting (across tensions lines)
• On histology 

• Excess collagen 
• Hypervascularity 
• Well organized type III collagen 
• Improves spontaneously with time 

• Management 
  • For linear hypertrophic scar: pressure therapy/ silicone gel sheet application 
  • For ongoing hypertrophy in the scar: intralesional steroids (triamcinolone)
  • If scar persists after 1 year: Surgical excision + Primary closure of wound 

3. Keloid 

• Has excessive scar tissue 
• Scar extends beyond the boundaries of original wound or incision 
• Etiology: Unknown 
• Associated with 

• Elevated levels of growth factors 
• Deeply pigmented skin 
• Genetic predisposition
• Areas of body where there is increased risk of keloid formation 
• Sternum is the most common site.
• Above clavicle 

• Upper extremities 
• Face, Ear (ear lobule). 
• Especially seen in the triangular region with boundaries of each shoulder tip and Xiphisternum 

On Histology

• Excess collagen & Hypervascularity
• Contains disorganized Type I & III collagen
• Contains thicker collagen bundles - causes formation of acellular node like structures
• Rarely regresses with time
• Often refractory to Medical & Surgical intervention

Treatment

• First line treatment: Silicones + Pressure therapy + Intralesional injection of triamcinolone
• In Refractory Cases (No improvement after 12 months of treatment): Excision + Post-operative Radiotherapy (External beam radiotherapy/Brachytherapy)

Difference between hypertrophic scar & keloid

	Hypertrophic scar	Keloid
Genetic	Not familial	May be familial
Race	Not race related	More common in blacks > whites
Sex	Females=males	Females > males
Age	Children	10 to 30 years
Border	Remains within the wound	Outgrows wound area
Sites	Flexor surface	Sternum Shoulder Face
Etiology	Related to tension	Unknown
Development	Within 4 weeks	3 months to 1 year
Clinical findings	Raised Some pruritis Respects wound confines	Pain Pruritis Grown beyond the wound margins
Histology	Parallel orientation of type III collagen fibers	Thick wavy type I & III collagen in random orientation

And that is it! That is everything you need to know about wound healing, tissue repair and scars for NEET PG Surgery preparation. For more interesting and informative posts like these, keep reading PrepLadder blogs!