Plastic Surgery Flashcards
Venous Ulcer
• Occur due to sustained Venous Hypertension in
Superficial veins, due to incompetent valves in
Deep or Perforating Veins, or Previous Deep Vein
Thrombosis
• Increased pressure leads to Extravasation of
Fibrinogen through Capillary Walls leading to
Fibrin Deposition, causing poor oxygenation of
surrounding skin
• Common (1% of 70+yrs) in later life; Often
Chronic and Recurrent, and found on LL above ankles and may be associated with Oedema,
Venous Eczema, Haemosiderin Deposition, Varicose Veins, Lipodermatosclerosis (Fibrosing
Panniculitis of Subcutaneous Tissue) and scarring white Atrophy with Telangiectasia
Management of Venous Ulcer
• Underlying Venous disease investigated with Duplex Ultrasound
• Treatment with High-compression Bandaging and Leg Elevation; Doppler studies before
bandaging to check for Arterial disease
• Up to 80% of Venous Ulcers healed within 6 months; Slower if Reduced Mobility, Large
Ulcers, Longstanding Ulcer or Bilateral disease
• Diuretics might be useful for Oedema; Antibiotics only for Overt Infection
• Venous Ulcers can be very painful so adequate Analgesia including Opiates required
• Split-Thickness Skin Grafting (E.g. Thiersch Graft) for resistant cases; Lifelong support
stockings might be required
• Surgery for purely superficial venous disease does not help healing but helps prevent
occurrence; No place in therapy for Therapeutic Ultrasound
Arterial Insufficiency Ulcers
• Arterial Insufficiency leading to Ischaemia of skin leading
to impaired ability to heal
• Present as Painful, Punched-out Ulcers which may occur
higher up the Leg or on Feet
• History of Claudication, Hypertension, Angina or Smoking
• Leg is Cold and Pale; Pulselessness, Arterial Bruits and Loss
of Hair might be present
• Doppler Ultrasound confirms disease; Treatment by ensuring cleanliness of wound and
coverings without Compression Bandaging
• Adequate Analgesia and Vascular Reconstruction if appropriate
Pressure Sores
• Occur in the Elderly, Immobile, Unconscious or
Paralysed Patients; Skin Ischaemia from sustained
pressure over Bony Prominence (Commonly on the
Heel or Sacrum)
• Stage I: Non-blanchable Erythema with intact skin;
Stage II: Partial Thickness Skin Loss of
Epidermis/Dermis; Stage III: Full Thickness to
Subcutaneous; Stage IV: Involvement of
Muscle/Bone/Tendon/Joint
• Risk Factors include Prolonged Immobility (Surgery,
Plaster Casts), Decreased Sensation (Coma, Diabetic Neuropathy), Vascular Disease
(Atherosclerosis, Diabetes) and Poor Nutrition
Management of Pressure Sores
• Prevention – Tissue Viability Nurses identify At-risk patients; Evaluate by Norton Scale or
Waterlow Pressure Sore Risk Assessment etc
• Treatment – Bed rest with pillows/fleeces to keep pressure off bony areas, Air cushions,
Pressure mattresses, Regular turning, Nutrition, Non-irritant Occlusive Moist Dressings (e.g.
Hydrocolloid), Adequate Analgesia, Debridement and Grafting
Skin Grafts
Epidermis is taken with variable amount of dermis (Split vs Full Thickness)
Flaps
Tissue taken with original blood supply; Classified based on blood supply, contents,
donor site and geometry
Split Thickness Skin Grafts
• Donor site heals by Epithelialisation, can be
Reharvested, Larger amounts can be harvested and can
Conform to defects due to thinness; Graft is less
resilient to Trauma, poorly cosmesis and can contract,
leading to secondary deformities
• Donor sites typically heal with scarring, so relatively
hidden area preferably
o Healing takes from 1/52 to few weeks, depending to thickness
o Commonly harvested with Watson or modified Humby knife, or Dermatome; Donor
site is held taut as blade is advanced along
• The skin is placed on a carrier board, and is fenestrated (Meshing); This can increase the
surface area of the graft (expanded typically 1:1.5), allows the graft to conform and fit
irregular surfaces better, and prevent blood or serous fluid collection under the graft
• Meshed graft is then applied onto recipient bed; Anchored by stables or sutures
• Negative Pressure Wound Therapy and other dressing therapies post-operatively
Full Thickness Skin Grafts
• Better cosmetic outcome and less prone to contracture, although less can be harvested;
Donor site has no dermal elements left, and might require suturing
• Pattern of defect taken, and transposed onto donor site; Dissection to skin to level of
Subcutaneous fat; Fat is trimmed
o Donor site might be cut to ellipse to allow closure
• Graft is then sutured onto recipient around edges; Quilting sutures might be placed across
surface to reduce shearing or haematomas
o Dress with a ‘tie-over’ – Suture ends are tied over a piece of gauze or cotton wool to
maximise graft contact with bed; Left in place for 5-7 days
Tissue Flaps
• Flap vascular supply can either be from Random pattern (Not from recognised artery; Limited by local blood flow) or Axial (Blood supply from recognised artery) o Local (Transferred adjacent to defect) or Distant (Incontiguous site); Pedicled (Whilst blood supply is attached) or Free flap (Detached and reattached to recipient vessels) o Flaps can also be described based on their configurations
Advancement Flaps
(Adjacent tissue mobilised and sketched; Wrinkling at base of flap can be
reduced by excising small amounts of tissue (Burrows’ triangle)
o Parallel lines, slightly convergent lines, or V-Y advancement flap
Types of Local Skin Flaps
Rotational Flap, Transposition Flaps, Limberg Flaps (Rhomboid defects), Z-plasty Flaps
(Lengthen contracted scar, or alter scar
orientation)
Free Flaps
• Microsurgery for both vascular and nerves;
Vascular clamps allow accurate matching of
ends and vessel ends are cleanly
transected; Flow checked prior to
Anastomosis to ensure patency
o Microneural surgery – Epineural
repair most common; Perineural
more challenging but theoretically advantageous
• Postoperative Management – Monitoring, should not compress pedicle; Analgesia, Hydration,
Warmth; if patency concerns, re-exploration might be required
Burns
• Burns can be classified as Thermal, Chemical, Electrical or Radiation
• Proteins lose 3D configuration and start breaking down, leading to cellular and tissue damage;
Effects can also be due to loss of normal functioning of skin (E.g. Sensory Loss, Water Loss,
Loss of Thermoregulation, Immune barrier)
o In large burns, significant Inflammatory response (vasodilation, vascular permeability)
causes leakage of fluid from capillaries leading to Tissue Oedema
o Overall blood volume loss, Significant plasma loss leading to higher haematocrit,
potentially causing damage to other end-organs
o Burn depth determines healing time/scarring; Burns can evolve over time, particularly
over first 48hrs
- Partial thickness (Painful, Red, Blistered) vs Full thickness (Insensate, Grey-white)
- BSA calculation based on ‘Rule of nines’ or Lund-Browder Charts
First Aid for Burns
• Stop burning process; Cool area with water or wet dressings for 20 mins, ensuring not
hypothermic; Remove clothing from affected area but do not peel off stuck clothing
• Cover with cling film or similar dressings
Emergency Management of Burns
• Resuscitate and transfer all major burns (>25% partial thickness in adults >20% in children,
>5% full thickness in adults); Assess Site, Size and Depth to calculate fluid requirements
• Airway – Caution for Inhalational Injury; Flexi Laryngo/Bronchoscopy useful; Obstruction can
develop within first 24h
• Breathing – Life threatening Chest Injury (E.g. Tension PTX) or Constricting Burns (consider
Escharotomy); Suspect CO poisoning if Cherry-red skin and Hx, as well as COHb levels (SpO2
unreliable); Consider Hyperbaric O2 if Pregnant, CNS signs or >20% COHb)
• Circulation – IV fluid resuscitation by large bore cannula; Intraosseous alternatively
o Parkland Formula – 4 × Weight (kg) × %Burnt = Hartmann’s (ml) in 24h, half in 8hr
o Replace fluid from time of burn rather than time of admission; Adjust based on
clinical response and urine output (aim for 0.5 – 1ml/kg/h, 50% more in electrical and
inhalational injury)
o Monitor body temperature and Cath to avoid abdominal compartment syndrome
• Do not apply cold water to extensive burns for long periods – Might intensify shock
• Circumferential burns – Compartment syndrome can develop rapidly; Decompress as needed
• Do not burst blisters or apply special creams if transferring to burns unit, as might delay
assessment; Simple gauze or Paraffin gauze suitable; Cling film reduces pain
• Titrate IV Morphine, Ensure Tetanus Immunity, Abx not routine
• Definitive Dressings – Biological (Pigskin, Cadaveric Skin), Synthetic or Silver based creams
Surgical Management of Burns
- Escharotomies, Fasciotomies in the immediate and early setting
- Major full thickness burns benefit from Early Tangential Excision with Split-skin grafts
- Late surgery can be Skin Grafting, Local and Free flaps and Cosmetic procedures
Wound Healing
• Wound Healing is affected by Oxygenation, Perfusion and Temperature
• Cells may be Labile, Stable or Permanent; Complex Cellular Architecture cannot be
reconstructed if destroyed; Complete Restitution if part of labile population is damaged
Granulation Tissue
Capillary loops and Myofibroblasts
Wound Organisation
Process where specialised tissues are repaired by formation of Mature
Connective Tissue; Wound Contraction mediated by Myofibroblasts
Factors affecting healing
include Arterial/Venous Supply, Movement/Distention, Infection,
Malignancy, Smoking, Necrosis, Malnutrition and Deficiency, Immunosuppression,
Antineoplastic Agents and Metabolic (E.g. Diabetes, Jaundice, Uraemia, Age)
Wound Infections
most commonly due to S pyogenes, S aureus and MRSA, P aeruginosa; can
also be Enterococci, E coli, Klebsiella, Proteus, Bacteroides and Clostridium
Phases of Wound Healing
Haemostasis Immediate
Vasoconstriction
Platelet Plug Formation and Coagulation
Fibrinolysis occurs after wound starts to heal
Phases of Wound Healing
Inflammation 0-3 days
Neutrophil Infiltration
Monocyte Infiltration and Differentiation to Macrophages
Fibroblast Migration and Proliferation
Phases of Wound Healing
Proliferation 3 days to 3 weeks
Re-epithelisation and Granulation
Angiogenesis stimulated by Hypoxia and Cytokines
Collagen Synthesis and ECM Formation
Wound Contraction by Myofibroblasts containing Actin
Phases of Wound Healing
Remodelling
3 weeks to 1 year
Collagen Remodelling and Maturation increase wound strength
Vascular Maturation and Regression
Classification of Wounds
- Clean – Non-traumatic with no break in Surgical Technique
- Clean Contaminated – Non-traumatic with Contaminated Entry into Viscus but minimal spill
- Contaminated – Clean, Traumatic or Significant spill from Viscus or Acute Inflammation
- Dirty – Traumatic Wounds from Dirt source, or Bacterial/Purulent contamination
Modes of Healing: Primary Intention
• Close apposition of clean edges • Thrombosis prevents Haematoma formation; Fibrin precipitates weak framework between two edges • Capillaries proliferate to bridge the gap and Fibroblasts secrete collage into Fibrin network • Basal Epidermal Cells bridge the gap and are resorbed • NB: Elastic Dermis network not replaced
Modes of Healing:
Secondary Intention
• Where skin edges cannot be cleanly apposed • Phagocytosis to remove debris and Granulation tissue is laid down to fill in defects in the surface • Epithelial regeneration covers surface • Longer period of healing, Hypopigmentation and Re-Epithelised Scar formation, Contraction of surrounding structures • Delayed Primary Closure = 3o intention
Scarring
• Fibrous tissue that replaces normal skin after injury; Lacks elasticity of normal tissues
• Hypertrophic Scars – Overproduction of Collagen resulting in raising skin, might appear as a
raised, red lump (Although raised skin does not typically go beyond margins of incision)
o Might fade within 12 months spontaneously
Keloid Scars
More common in darker-skinned; Smooth, hard nodules
o Scarring goes beyond boundaries of original wound
o More commonly on shoulders, Upper Back and Chest, Earlobes and Skin
o Persistent, continues to emerge; Treated with Steroid injections, Compression with
Gels, or Surgery (plus Adjuvant injected steroids or Superficial Radiotherapy)
