General Plastics/Other Flashcards
What is the definition of extravasation?
Inadvertent leakage of IV fluids or medication into extravascular tissue from an IV vascular access device.
What questions should be included in the history for extravasation?
Patient: Age, sex, occupation, hand dominance, hobbies, social history, smoking/alcohol status, reason for admission.
Extravasation: Site, volume, rate and contents of infusion
PMHx: FIT: Fitness for surgery, Immunosuppression, Thrombosis: previous VTE/anticoagulation
What specific details about the infusion site are important in the history?
Site of infusion, content (vesicants, irritants, non-vesicants), volume, and rate of infusion.
Initial steps
What are vesicants, and how do they cause damage?
Vesicants are drugs that cause tissue damage.
DNA-binding vesicants: Cause cell death by binding to DNA.
Non-DNA-binding vesicants: Cause cell death via other mechanisms.
Give examples of vesicants
DNA-binding: Doxorubicin
Non-DNA-binding: Paclitaxel
What are irritants, and what effects can they cause?
Irritants cause inflammation, irritation, or pain, and rarely tissue breakdown. Examples include Methotrexate and Cisplatin.
What are non-vesicants, and what effect can they have?
Non-vesicants are inert or neutral compounds that can have significant effects at large volumes, e.g., Bleomycin, Cyclophosphamide.
Describe the examination of an extravasation injury?
Look, feel, move:
Look: Swelling, erythema, skin mottling, blisters, necrotic skin; mark erythema with date and time.
Feel: Distal pulses, sensation, motor function, tension of compartments, and warmth/coldness or oedema
Move: Checking for pain on passive stretch and range of motion (ROM).
What are the differential diagnoses for an extravasation injury?
Local allergic reaction
Superficial thrombophlebitis
Compartment syndrome
What is the first step in managing extravasation?
Stop and disconnect the infusion but leave the cannula in place.
What guidelines should be referred to for extravasation management?
2017 NHS England “Guidelines for Management of Extravasation of Systemic Anti-Cancer Therapy”
2024 NIVAS “Infiltration and Extravasation Toolkit”
What antidotes are used in the management of extravasation?
DMSO
Hyaluronidase (Subcutaneous Injection 1500 units in 1ml water)
Describe a technique for washout of extravasation?
Gault Technique:
Prep: Consent, Chlorhexidine skin prep, Analgesia or sedation, Field block with Lidocaine
Procedure: (Hyaluronidase infiltration), Regular incisions or puncture wounds, then infuse 0.9% NaCl into tissue. Expressing fluid through incisions.
Post-op: elevation, loose simple dressings, 6 hours for the first 24-48 hours
Medicolegal aspects of extravasation
Ensure documentation and duty of candour.
Complications of sternal wounds/dehiscence
Reported in 0.5%–5% of midline sternotomies and is a serious complication which can lead to potentially fatal mediastinitis
Local infection
OM
Mediastinitis
Focused history for sternal dehiscence
PC: Surgical wound
Before: premorbid state, indications
During: What surgery (CABG Vessels used: IMA vs Long Saph vs radial artery)
After: any immediate/delayed complications, post-op care
PMHx FIT
Specific PMHx: Congenital chest wall deformity
DHx: Allergies, Antibiotics, Anti-coagulation
SHx: Occupation, Smoking, Social situation at home
Focused examination for sternal dehiscence
General examination: ITU, invasive monitoring
Chest examination
Poland Syndrome (lack of pectoralis)
Pectus excavatum/carinatum
Wound assessment
Size: length, width, depth
Defect: skin, muscle, bone
Wound bed: slough, eschar, pus, exposed bone/metalwork/other repairs
Surrounding tissue: infected, inflamed, sinuses
Investigations for sternal dehiscence?
Bedside: Wound swab MC&S
Bloods: FBC, CRP, U&Es, Clotting, G&S
Imaging:
CXR
CTPA
MRI/MRA
Classifications for sternal dehiscence?
Pairolero and Arnold
AMSTERDAM classification (Assiduous Mediastinal Sternal Debridement & Aimed Management)
Pairolero classification
Type 1: Early wound separation within first 3 days, negative cultures, no cellulitis or osteomyelitis; instability may or may not be present
Type 2: Purulent mediastinitis occurring within first 3 weeks, positive cultures, and cellulitis and/or osteomyelitis
Type 3: Draining sinus tract from chronic osteomyelitis months to years after procedure
Goals of chest wall/sternum reconstruction
Debride/excise devitalised tissue and hardware to obtain health wound bed
Provide airtight pleural cavity
Restore skeletal stability and structure
Reconstruct ribs if >4 or >5cm
Durable well-vascularised soft tissue coverage
Flap options used for sternal reconstruction
Pectoralis major
Latissimus dorsi
Serratus anterior
Rectus abdominis
Omentum
Components of the evaluation for a complex wound
Location (helps determine underlying causes)
Size: Length, width, depth
Extent of defect (Skin; subcutaneous tissue; muscle, tendon, nerve; bone)
Condition of wound bed: Necrotic material, Granulation tissue, Exposed structures, Fibrin, exudate, eschar.
Condition of surrounding tissue: Satellite lesions, Oedema, Inflammation/infection, Tunneling/sinuses
Factors affecting wound healing
PMHx:
o Diabetes mellitus
o End-stage renal disease
o Cardiac disease
o Peripheral vascular disease
Patient Factors
o Tobacco use
o Malnutrition
Iatrogenic
o Steroid therapy
o Radiation
Pressure Injury definition
Areas of damage to skin and underlying tissues as a result of prolonged pressure, sheer or friction forces
Focused History for pressure injury
Location: Ward, Neurosurgery/ Neurology, ITU, community
PC: Site of injury, onset, duration, development. Any previous medical, surgical management for pressure injuries
PMHx: Cause for immobility: acute/chronic illness. FIT
SHx: Smoking, vaping, alcohol, Home support/care home resident
Focused examination for pressure injury
Systemic examination:
o Nutritional status: body habitus
Wound (same as chronic wound assessment)
o Size: length, width, depth
o Defect: skin, muscle, bone
o Wound bed: slough, eschar, pus, exposed bone/metalwork/other repairs
o Surrounding tissue: infected, inflamed, sinuses
o Classify as per NPIAP
How can you classify pressure injuries
NPIAP (National Pressure Injury Advisory Panel) Classification:
I: non-blanching erythematous changes with skin intact
II: Partial-thickness skin loss that presents clinically as a blister, abrasion, or shallow open ulcer
III: Full-thickness tissue loss down to, but not through, fascia
IV: Full-thickness tissue loss with involvement of underlying muscle, bone, tendon, ligament, cartilage, or joint capsule
Unstageable (due to slough or eschar
What investigations would you perform for someone with a pressure injury
Bedside: Wound swab/tissue samples (MC&S)
Bloods:
FBC (WCC for infection, Hb for optimisation)
CRP, U&Es, LFTs
Albumin (associated with recurrence)
HbA1c (if DM)
B12/Folate/Micronutrients
G&S
Imaging:
CT if collection
MRI if exposed bone/concerns for OM
Management of pressure injuries
General Approach: MDT: Plastics, Ward team/nurses, TV nurses, Dieticians, DM specialist nurses (if appropriate), geriatrics, physios
Non-operative:
Meticulous nursing care
Relieve pressure: Rolling, mattress, cushions
Skin care: regular cleaning and gentle drying
Medical
Treat acute illness
Disease optimisation: DM control, spasticity (e.g. if MS)
Nutrition: calories, protein, vitamins
Surgical
Grade I-II: dressings
Grade III-IV: may require surgical management: (Single stage vs multi-stage)
Common anatomical sites of pressure injuries
- Sacrum (28–36%)
- Heel (23–30%)
- Ischial tuberosity (17–20%)
- Trochanter (20%)12
- Scalp
Scoring systems for risk of pressure injury
Waterlow
o BMI
o Skin condition
o Age and sex
o Continence
o Mobility
o Appetite and nutrition
o Individual risk factors
Braden Scale
o Sensory perception
o Skin moisture
o Activity
o Mobility
o Friction and shear
o Nutritional status
Risk factors for developing pressure injuries
Admission related:
Acute illness/ischemia/sepsis: reduced tissue perfusion (causes decreased tissue perfusion and predisposes to necrosis)
Infection
Patient related:
Increased age: Decreased skin moisture, tensile strength, increased friability
Sensory loss: loss of discomfort from prolonged sitting
Vascular disease: decrease tissue perfusion and predispose to necrosis
Anaemia: Decreased wound healing capabilities
Malnutrition: Diminished ability to heal wounds, weight loss leads to reduced soft tissue padding over bony prominences
Altered level of consciousness
Pathophysiology and forces leading to pressure injuries
Shear: Mechanical stress parallel to plane
o Stretches or compresses muscle perforators to the skin resulting in ischemic necrosis—superficial necrosis
Pressure: Mechanical force per unit area perpendicular to plane
o Leads to tissue deformation, mechanical damage, blockage of vessels—deep necrosis
o Pressures of two times capillary arterial pressure for 2 hours produces irreversible ischemia in animal models
Friction: Resistance to movement between two surfaces
o Outermost skin layer lost, resulting in increased water loss
o Most often incurred during patient transfers
Moisture
o Leads to skin maceration and breakdown
o Most often the result of incontinence
Definition of Necrotising Fasciitis
Severe life and limb threatening soft tissue infection of the subcutaneous tissue and fascia
Examination of Necrotising Fasciitis
Look: Erythema, blisters, haemorrhagic bullae, areas of necrosis. Mark area of erythema with date & time.
Feel: pulses, sensation, pain, crepitus
Move: motor function
Special tests: “Sweep Test” if diagnostic uncertainty
Investigations of Necrotising Fasciitis
Bloods: FBC, U&Es, LFTs, CRP, CK, VBG + Lactate, X-match
Blood cultures
Imaging: Plain X-rays
Scoring systems for necrotising fasciitis
LRINEC Score (not validated and poor specificity)
o Leukocytes: WCC
o Renal function: Creatinine
o Insulin: Glucose
o Na
o Erythrocytes: Hb
o CRP
Initial management plan for necrotising fasciitis
Sepsis 6
O FAATT W
o Oxygen
o Fluids
o Antibiotics
o Analgesia
o Tetanus
o Tubes: IV cannula, catheter
o Wounds
Pre-operative management for necrotising fasciitis
Definite/Operative: NMC TABB
NBM
Mark
Consent: “Necrotising Fasciitis Excision”
Theatre Coordinator
Anaesthetics/ITU
Boss: Call the boss.
Brief: PPPSS
Patient. Procedure. Position: GA, Supine, TQ, Flowtron on contralateral
Sets: General plastics set, 10 blade, monopolar
Specialist equipment: MC&S
Operative plan for necrotising fasciitis
Prep: GA, Supine, TQ, Flowtron on contralateral. Catheter
Incision: “Fire breaker incision” proximal to redness
Findings: Foul smelling, “dishwater” pus from the fascia. Infected, necrotic skin and fascia
Procedure: Aggressive excision/debridement of all non-viable tissues. Release all compartments and drain infection. Thorough washout
Closure: leave open, simple dressings
Post-op: ITU, Abx, Relook 24-48hours
Types of necrotising fasciitis
Type 1: Polymicrobial
Mixed aerobes/anaerobes
Type 2: Monomicrobial
Streptococcus Pyogenes (Group A Beta-haemolytic strep)
MRSA
Clostridium species (gas gangrene)
Type 3: Vibrio vulnificus
Type 4: Fungal (Candida albicans)
History for pre-tibial laceration
PC
o Timing/mechanism of injury
o Systemic review to ensure to other cause for fall/injury e.g. UTI, Chest Infection, ACS, Stroke
o First aid/other treatment
o Functional deficit
PMHx: FIT
o Fitness for surgery (cardiac, respiratory history)
o Immunocompromised (including DM)
o VTE and anticoagulation
SHx:
o Mobility, carers, social support
o Smoking, alcohol
Examination for pre-tibial laceration
Look:
o Deformity of limb suggesting fracture
o Length, shape and depth of wound
o Skin flap: distally/proximally based, viability
o Underlying structures exposed
o Presence of Haematoma
o Skin loss % TBSA
Feel
o NVI: sensation/CRT
o Bony tenderness, able to weight bear
Move
o Structures intact: anterior compartment dorsiflexion
Classification of pre-tibial lacerations
Modified Dunkin (Cubison et al)
I: Linear laceration without skin loss
II: Flap laceration viable
III: Flap laceration non-viable
IV: Skin loss
V: Laceration with haematoma
Management of Type I Pretibial Lacerations
I: Linear laceration without skin loss
AATX: antibiotics, analgesia, tetanus, xray
Manage conservatively.
Steristrips to gently oppose wound edges
Simple non-adhesive dressings (Silflex/Mepitel). Dress from toes to knee.
TV input as inpatient
Discharge to GP nurse for ongoing wound management
Management of Type II Pretibial Lacerations
II: Flap laceration viable
AATX: antibiotics, analgesia, tetanus, xray
Manage conservatively.
Steristrips to gently oppose flap and simple non-adhesive dressings (Silflex/Mepitel). Dress from toes to knee.
TV input as inpatient
Discharge to GP nurse for ongoing wound management
Management of Type III Pretibial Lacerations
III: Flap laceration non-viable
A small non-viable flap may be excised and managed conservatively with dressings.
Larger skin flaps can be primarily excised and skin grafted under local anaesthetic.
Do not defat and replace skin.
Management of Type IV Pretibial Lacerations
IV: Skin loss
Manage conservatively if less than 1% TBSA.
If failure to heal within 2-3 months consider delayed primary skin graft under local anaesthetic.
Alternatively, if local circumstances allow primary skin graft under local anaesthetic.
Management of Type V Pretibial Lacerations
V: Laceration with haematoma
Typically patients on anticoagulants, and will often require surgery.
Evacuate haematoma and graft
Indications for surgical management of pre tibial lacerations
Large necrotic skin flaps
Large area of skin loss (consider if >1%TBSA)
Major haematoma
Failure of conservative management after 2-3 months
Gross contamination/infection – may require debridement/grafting
Surgical plan for pre-tibial laceration
Prep: Field block with LA & adrenaline
Procedure:
o Debride any devitalised tissue
o Evacuate haematoma
o Remove contamination
o Grafting is preferable to defatting flaps
Post-op:
o Immediate mobilisation
o Graft check 5-7 days
Definition of flap
A flap is a unit of tissue that maintains its own blood supply while being transferred from a donor site to a recipient site.
Classification of flaps
“FLAPS Move”
Form/composition:
- Skin
- Fascia
- Skin & Fascia: Fasciocutaneous
- Muscle
- Bone
- Visceral (e.g. omental flap)
Location: local, regional, free
Attachments: free, pedicled
Perfusion: direct, indirect, random pattern
Special features: innervated, tubed, retrograde, supercharged
Movement: advancement, transposition, rotation
Classification of muscle flap pedicles
Mathes Nahai
I: one vascular pedicle (e.g. tensor fascia lata)
II: dominant pedicle and minor pedicle (e.g. gracillis)
III: two dominant pedicles (e.g. gluteus maximus)
IV: segmental vascular pedicles (e.g. sartorius)
V: one dominant pedicle and secondary segmental pedicles (e.g. Lat dorsi)
Definition of graft
A unit of tissue transferred from a donor site that is reliant on the recipient blood supply
Split thickness skin grafts vs full thickness skin grafts
SSG
- Contains epidermis and varying amounts of dermis
- Donor heals by re-epithelisation
- Less primary contraction, greater secondary contraction
- Can be meshed and cover larger areas to heal between meshed areas by re-epithelisation
- Donor prox lateral thigh
FTSG:
- Contains epidermis and dermis
- Donor heals by primary closure
- More primary contraction, less secondary contraction
- Various donor sites and can be matched to recipient to match colour and texture
Causes of graft failure
Infection: classically group A/B strep secretes proteases that prevent fibrin adhesion
Haematoma/seroma: creates space and diffusion gradient between graft and wound bed preventing imbibition
Shearing forces: disrupts adherence
Wound Bed: lack of blood supply and nutrient supply from wound bed
Stages of graft take
AIIRR:
Adherence: fibrin bonding
Serum imbibition: serum absorbed into graft providing cells with nutrients
Inosculation: direct vascular connection between cut vessels of skin graft and underlying capillary bed
Revascularisation: neovascularisation (formation of new blood vessels)
Remodeling
Complications of skin grafting
Scarring: hypertrophic, keloid, secondary contraction
Delayed wound healing
Graft failure
Further procedures (laser, scar release)
What is BTM
“Biodegradable temporizing matrix”
Open cell, non-reticulated matrix with interconnected chambers comprised of an estimated 94.2% open space. This microstructure is stabilized by struts and the chambers are linked by pores, allowing free flow of fluid
Cellular migration into the scaffold/struts.
Polyurethane breaks down by hydrolysis over approximately 18 months
