Wound infection

Section: Skin and soft tissue Sub-section: Skin infections and breakdown Curriculum: Curriculum, page 53

Section: Skin and soft tissue Sub-section: Skin infections and breakdown Curriculum:

Classification Wounds

• Can either be by:
  • Type of wound
  • Mechanism of Injury

Type of Wound

• Type 1 (Clean)
• Type 2 (Clean contaminated)
• Type 3 (Contaminated)
• Type 4 (Dirty)

Type 1 (Clean)

• Made in sterile conditions, with no contaminated tissue being breached
• Elective surgical wounds
• Body wall and non-contaminated deep tissues
• Minimal airborne contamination
• Negligible risk of infection (< 2%)
• Primary wound closure is method of choice

Type 2 (Clean Contaminated)

• Minimally contaminated wounds
• Tidy incisional wounds inflicted by sharp cutting instrument in non-sterile fashion
• Or sterile surgical instruments in a non-infected tract
  • Small bowel, biliary, bronchial tree etc.
• Minimal macroscopic contamination
• Risk of infection still low (1-5%)
• Should still be closed primarily after some form of wound toilet

Type 3 (Contaminated)

• Untidy and contaminated wounds created in a dirty environment
• Wounds in operative procedures where an infected tract or dirty tract is opened
  • Infected bronchial tree or infected urological tract
  • Dirty large bowel or rectum
• Wounds in procedures where gross contamination from a non-infected tract
  • Abscess
• May require wide debridement and copious irrigation before delayed primary, or primary closure
• Significant risk of wound infection (2-25%)

Type 4 (Dirty)

• Infected, contaminated or devitalised wounds
• Open wounds of duration > 12 hours
• Operative wounds in areas of gross septic or faecal contamination
• Severe tissue damage and excessive ischaemic tissue
  • Incl. severe crush injuries
• Should never be closed unless confidently converted to type 1 or 2 wound by wide debridement and irrigation
• Often requires healing by delayed primary closure or secondary intention
• Infection rates high (near 50%)
• Risk of severe synergistic infections (gangrene) or other necrotising infections exists

Surgical Site Infection Classification

• Superficial Incisional SSI
• Deep Incisional SSI
• Organ/Space SSI

Mechanism of Injury

Blunt Injury

• Deceleration with significant transfer of kinetic energy
• Object striking person
  • Injury usually limited to site of impact
  • Skin and soft tissue compressed
    • Burst with stellate laceration
  • Underlying blood vessels may burst with subsequent haemorrhage and contusions
  • Energy transfer through tissue can compress/damage bone, underling blood vessels, or tissue (brain/viscera)
    • Brain can be forced against back of skull (Contra-coup injury)
• Moving person striking object
  • Get deceleration trauma, abnormal deformation of bones and joints
  • Also get deceleration injuries of viscera
    • Thoracic aorta at ligamentum arteriosum
    • Small bowel bucket handle injury
    • Avulsion injuries etc.

Penetrating Injury

• Can be simple or complex
  • Main difference is the kinetic energy of the injury
• Low energy wounds
  • Anything up to a small calibre (.22) bullet
  • Cause injury in the line of penetration
• High velocity injuries
  • Transfer much more energy
  • Cause wide cavitation due to pressure wave created by passage through tissue
  • Damage to, and devascularisation of, nearby tissues

Thermal Injury

• Can be
  • Hot
  • Cold
  • Dry heat causes burn
  • Moist heat causes scold
  • Prolonged cold exposure causes chilblains
  • Freezing of tissue by cold causes frostbite

Heat injury

• Pathology of burns and scalds are Coagulative necrosis of epidermis and dermis to a variable depth
• Classification
  • Superficial - only epidermis
  • Partial - epidermis and portions of dermis
    • Superficial partial - superficial dermis
    • Deep partial - deep dermis
  • Full-thickness - all dermis and down to subcutaneous tissue

Rule of 9’s

Cold Injury

• Final effect very similar to hot injury – tissue necrosis
  • But not coagulative from the start
• Prolonged exposure to cold but not freezing
  • Dry – Chilblains
  • Wet - Trench Foot
• Frostbite – actual freezing of body tissues
  • Extent of damage worse due to rapidity of freezing and duration frozen
  • Injury caused by freezing AND by subsequent thawing
• Pathogenesis: Intracellular ice crystallisation, cellular dehydration (and lysis) and microvascular thrombosis
• Warming can cause further injury, but is essential part of treatment
• Don’t debride until all tissue is warmed and assessment of unviable tissue can be made
• Enables minimization of debridement

Frostbite Grading System

• First Degree
  • Very superficial
  • Hyperaemia, oedema, minimal necrosis
• Second Degree
  • Partial thickness
  • Hyperaemia, rapid oedema, large blisters
  • Necrosis present
  • Sensation intact
• Third Degree
  • Full thickness skin injury
  • Pale with slow onset of oedema
  • Eventual necrosis
  • Sensation lost
• Fourth Degree
  • Full skin thickness and deep tissues
  • Limb infarction
  • Requires amputation

Mechanisms

• Direct cold damage to cells
• Direct cell damage from ice crystals, which includes protein and lipid disruption and electrolyte shifts
• Indirect cell damage from intracellular dehydration caused by the presence of extracellular ice crystals
• Microvascular stasis, thrombus formation, embolic events in the microvasculature, and ischemia
• Reperfusion inflammatory injury with ultimate tissue necrosis

Four phases

1. Prefreeze phase - This phase consists of superficial tissue cooling, which results in the increased blood viscosity, microvascular constriction, ischemia, and endothelial plasma leakage that precede the formation of ice crystals
2. Freeze-thaw phase - This phase consists of ice crystal formation, more in the extracellular space than in the intracellular space. Thawing may induce reperfusion injury with an inflammatory response.
3. Vascular stasis phase - This phase consists of arteriovenous shunting at the margin between injured and noninjured tissue. Vasoconstriction may alternate with vasodilation. This may result in a combination of both progressive microvasculature erythrocyte sludging, stasis, coagulation, and thrombus formation, and leakage of blood from the vessels.
4. Late progressive ischemia phase - This phase consists of thrombus-induced inflammation, hypoxia, and anaerobic metabolism leading to tissue necrosis

Management

• Simultaneous assessment and resuscitation
• ABCDE as per EMST
• Rapid rewarming – submerge is 40 degree water for up to 1 hour. Ensure water circulates
• Will be painful so need analgesia
• Dress with sterile non adherent dressings
• Elevate and splint limb
• Ensure tetanus up to date
• Consider infusion of tpA
• Consider hyperbaric oxygen
• Surgery delayed as long as possible waiting for tissue to demarcate. Early surgery has been shown to have increased rates of amputation
• Only acute indication for surgery is compartment syndrome

Chemical Injury

• Cause damage to living tissue through number of mechanisms
• Heat liberation from exothermic reactions
• Liquefactive necrosis by alkali
• Dilapidation by petrochemicals
• Vesicle formation by gasses
• Severity related to type, concentration, amount, and duration of contact
• Initial treatment is copious and prolonged irrigation with water

Electrical Injury

• Direct tissue injury
  • Conversion to thermal energy at site of entry and along planes of conduction
  • As a consequence of current density
• Deeper tissues cool more slowly than superficial tissues
  • Get deeper injury
• Entry wound usually heavily charred
  • At low voltages this will prevent further current flow
• Major injuries generally occur in limb soft tissue (muscle)
  • Leads to myoglobinuria and renal failure
  • Hyperkalaemia and acute renal failure can also occur
  • Can get Compartment Syndrome
• Can also get
  • Cardiac arrest
  • Central and peripheral nervous injury
  • Visceral injury
  • Spinal compression fractures

Ionizing Radiation Injury

• Uncommon source of acute injury
• Radiation disperses energy as it travels through tissue
• Energy ionises molecules and starts chain of events that leads to damage to
  • DNA
  • RNA
  • Cellular fibres
  • Cellular membranes
• Get cell death, chromosomal rearrangements, point mutations
• Individual cells more susceptible if the divide more frequently
• Radiation endarteritis causes progressive devascularisation and fibrosis
  • Affects wound healing and wound breakdown
  • Late manifestations may include
    • Radiation induced malignancies
    • Radiation osteonecrosis
    • Underlying organ damage
• Very high dose radiation exposure
  • Widespread proliferative cell death
  • Host defence breakdown (gut, immune system) leading to death

Normal Wound Healing

Phases

1. Haemostatsis

• Injury leads to platelet adhesion and activation with clot formation
• Stop bleeding

2. Inflammatory

• Clot stops bleeding
  • But also provides matrix rich in growth factors and chemokines
  • Acts as a scaffold for migrating leukocytes and stromal cells
• Also get inflammatory vascular changes followed by inflammatory cell recruitment
  • Within 24hrs neutrophils appear at the margins
  • Begin process of wound sterilization and debris degradation
• Granulation tissue
  • Within 1-2 days (peak 5-7 days)
  • Fibroblasts and endothelium form this
  • Highly vascularised loose connective tissue and hallmark of early tissue repair
  • Vessels leaky, therefore tissue oedema occurs
• At this stage, wound strength will primarily rely on sutures

3. Proliferative

• Migration and expansion of:
  • Parenchymal cells (re-epithelialisation)
  • Endothelial cells (Angiogenesis)
  • Connective tissue cells (provisional matrix)
• Within 2-4 days, neutrophils largely replaced by macrophages
  • Become main cellular elements in clearing debris and directing subsequent angiogenesis and ECM deposition
• Eventually granulation tissue scaffolding is converted to scar composed of fibroblasts and collagen
  • Fibroblast migration and proliferation driven by macrophages
    • TGF-β most important fibrogenic agent
• After 2 weeks, scar formation (collagen deposition) is the most dominant feature
  • Get regression of the vasculature
  • Granulation tissue all converted to avascular scar, without inflammation, covered by intact epithelium
• Get rapid increase in wound strength to 30-50%

4. Remodeling Phase

• Constant absorption and replacement of collagen along the lines of stress
• Wound contraction accomplished by myofibroblasts
  • Have synthetic function of fibroblasts
  • Also contractile capability of smooth muscle cells
  • Cause decreased surface area of the wound
• Remodelling/change in ECM deposition

Strength of Wound Over Time

• Initially dependent on suturing
• At 1 week (when sutures removed)
  • Typically has 10% strength of normal
• Tensile strength eventually plateaus at 70-80% of normal at 3 months
  • Associated with increased collagen synthesis exceeding collagen degradation
  • Followed by cross-linking and increased fibre size

Factors that Affect Wound Healing

• Local Factors

  • Ischaemia
  • Tension
  • Dead Space
  • Foreign Bodies and contamination
  • Wound infection
  • Haematoma
  • Local Trauma
  • Chronic tissue factors – Lymphoedema, past scarring
  • Sutures – too tight, silk (inflammation)
  • Irradiation

• Systemic Factors

  • Age
  • Medical comorbidities - Obesity, CRF, hepatic failure, diabetes
  • Anaemia or blood loss
  • Shock, hypovolaemia, hypoxia
  • Malnutrition
  • Septicaemia
  • Advanced malignancy
  • Immunosuppression and steroid use
  • Chemotherapy
  • Smoking

• Abnormalities of Wound Healing

  • Deficient Scar
    • Inadequate granulation tissue or collage deposition
    • Leads to wound dehiscence or ulceration
  • Keloid and hypertrophic scar
  • Atrophic Scar
    • Surgery, trauma, acne vulgaris & varicella
    • Responds well to laser
  • Contracture Scar
    • Result of contractile wound healing process in a scar that has already been re-epithelialize and adequately healed
    • Normal, but exaggerated, part of the healing process
    • Typically appear as a fixed, rigid scar
    • Contributes to both cosmetic and functional problems
    • Limits joint mobility