Plastic Surgery Flashcards

1
Q

Venous Ulcer

A

• 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

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2
Q

Management of Venous Ulcer

A

• 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

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3
Q

Arterial Insufficiency Ulcers

A

• 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

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4
Q

Pressure Sores

A

• 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

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5
Q

Management of Pressure Sores

A

• 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

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6
Q

Skin Grafts

A

Epidermis is taken with variable amount of dermis (Split vs Full Thickness)

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7
Q

Flaps

A

Tissue taken with original blood supply; Classified based on blood supply, contents,
donor site and geometry

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8
Q

Split Thickness Skin Grafts

A

• 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

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9
Q

Full Thickness Skin Grafts

A

• 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

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10
Q

Tissue Flaps

A
• 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
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11
Q

Advancement Flaps

A

(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

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12
Q

Types of Local Skin Flaps

A

Rotational Flap, Transposition Flaps, Limberg Flaps (Rhomboid defects), Z-plasty Flaps
(Lengthen contracted scar, or alter scar
orientation)

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13
Q

Free Flaps

A

• 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

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14
Q

Burns

A

• 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
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15
Q

First Aid for Burns

A

• 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

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16
Q

Emergency Management of Burns

A

• 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

17
Q

Surgical Management of Burns

A
  • 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
18
Q

Wound Healing

A

• 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

19
Q

Granulation Tissue

A

Capillary loops and Myofibroblasts

20
Q

Wound Organisation

A

Process where specialised tissues are repaired by formation of Mature
Connective Tissue; Wound Contraction mediated by Myofibroblasts

21
Q

Factors affecting healing

A

include Arterial/Venous Supply, Movement/Distention, Infection,
Malignancy, Smoking, Necrosis, Malnutrition and Deficiency, Immunosuppression,
Antineoplastic Agents and Metabolic (E.g. Diabetes, Jaundice, Uraemia, Age)

22
Q

Wound Infections

A

most commonly due to S pyogenes, S aureus and MRSA, P aeruginosa; can
also be Enterococci, E coli, Klebsiella, Proteus, Bacteroides and Clostridium

23
Q

Phases of Wound Healing

Haemostasis Immediate

A

Vasoconstriction
Platelet Plug Formation and Coagulation
Fibrinolysis occurs after wound starts to heal

24
Q

Phases of Wound Healing

Inflammation 0-3 days

A

Neutrophil Infiltration
Monocyte Infiltration and Differentiation to Macrophages
Fibroblast Migration and Proliferation

25
Q

Phases of Wound Healing

Proliferation 3 days to 3 weeks

A

Re-epithelisation and Granulation
Angiogenesis stimulated by Hypoxia and Cytokines
Collagen Synthesis and ECM Formation
Wound Contraction by Myofibroblasts containing Actin

26
Q

Phases of Wound Healing
Remodelling
3 weeks to 1 year

A

Collagen Remodelling and Maturation increase wound strength

Vascular Maturation and Regression

27
Q

Classification of Wounds

A
  • 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
28
Q

Modes of Healing: Primary Intention

A
• 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
29
Q

Modes of Healing:

Secondary Intention

A
• 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
30
Q

Scarring

A

• 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

31
Q

Keloid Scars

A

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)