Plastic Surgery Flashcards
Evaluating size of burn
Wallace’s rule of 9s
Hand = 1.25%
Palm alone = 1%
ONLY COUNT SUPERFICIAL PARTIAL AND DEEPER (don’t include epidermal burns)
Most common causes of burns
60% scald from oil or water 30% explosion and flame 4% contact burn 3% electrical 3% chemical
Zones of Jackson’s burn model
- zone of necrosis (dead)
- zone of stasis (salvageable)
- Zone of hyperaemia - healthy, providing increased circulation to zone of stasis THEREFORE DON”T USE ICE - YOU WILL CONSTRICT THESE VESSELS AN REDUCE BLOOD FLOW
Evaluating depth of burn
Epidermal:
epidermal integrity (Nikolsky sign negative)
SUPERFICIAL DERMAL:
Nikolsky +ve, slippery surface, thin walled blisters, blanches with pressure, very painful, oozing
MID DERMAL:
Nik +ve, slippery, thick walled blisters, some mottling, sluggish blanching, dark, red base, less oozy and less painful than superficial dermal
DEEP DERMAL:
Nik +ve, not slippery, red colour, red sensation, absent or red refilling after blanching, mixed mottling, little or no ooze
FULL THICKNESS:
Not painful, no refilling after blanching, white/brown with visible black vessels, hairs fall out easily, dry
Criteria for review of a burn by burns unit (11)
- Adult burn over 10%
- full thickness burns
- burns of special areas (face, neck, hands, feet, breasts, genitalia, perineum)
- Electrical burns
- Chemical burns
- Circumferential burns
- Extremes of age (children or elderly)
- Comorbid medical illness (Dm, paraplegia)
- Concomitant trauma
- Comorbid psychiatric illness
- Any burn that referring department is not confident to send home
Fluids in burns
If over 15% TBSA
MODIFIED PARKLAND FORMULA
First 24h: Hartmann’s solution 4 x %TBSA x weight
give half in first 8 hours, half in next 16 hours
Aim for 0.5mL/kg/hr urine output - CATHETERISE TO MONITOR
Acute complications of burns
Inhalational injury (airway oedema and obstruction, pneumonia, atelectasis) Acute respiratory distress syndrome Hypothermia Hypovolaemia Renal failure
Subacute complications of burns
Secondary infection
Graft loss
Early hypergranulation
Scar contracture/post-burn deformities
Pathogens most likely in secondary infections of brrns
First 48h: GRAM +VE - appears of loss of wound granulation
- staph aureus (from hair follicles)
- GBS
- VRE
5-7d: GRAM -VE: appears as surface necrosis and patchy black colouring
- pseudomonas aeruginosa
3-4w: COMPLICATED INFECTIONS AND FUNGUS Appears as minimal exudate 30-50% mortality! - Candida - MRSA
Components of acute respiratory distress syndrome (secondary to burns)
Hypoxaemia (due to V/Q mismatch)
Pulmonary HTN (inc. pulmonary oedema)
Bronchoconstriction (systemic inflammatory response)
Reduced lung compliance (secondary to oedema and red. surfactant)
Definition of folliculitis
Acute infection of multiple hair follicles
Pathogens in folliculitis
Staph aureus
“Hot Tub” version = psudomonas aeruginosa
Clinical features of folliculitis
Clusters of multiple lesions
Small, raised, pruritic erythematous lesions +/- central pustule
Each lesion under 5mm (in staph) may be up to 30mm in hot tub version
Frequently observed in areas of repeated shaving (e.g. beard)
Management of folliculitis
Usually self-limiting
Warm compresses can be applied TDS
Avoid shaving area
If lesions persist, topical mupirocin for s. aureus version
definition of furuncle
AKA boil
An acute infection of a single hair follicle
Definition of carbuncle
Multi-loculated furuncle (coalescence of several inflamed follicles into a single inflammatory mass with purulent drainage from multiple follicles)
Pathogen involved in furunculosis/carbuncles
Staph aureus almost always
If use foot baths at nail salons, at risk for myobacterium
Management of furunculosis and carbuncles
Small: warm compresses to promote drainage
Larger/carbuncles: incision and drainage, MCS of material drained
If at risk of endocarditis: antibacterial prophylaxis prior to I/D (vancomycin preferred)
Definition of impetigo
Superficial bacterial infection involving the epidermis proper
Age group impetigo most commonly seen in
2-5y
Pathogens in impetigo
Classic impetigo: strep pyogenes
Bullous impetigo: Staph aureus (exofoliative A toxin - loss of cell adhesion in superficial epidermis - bullae)
Features of non-bullous impetigo
Lesions begin as papules - vesicles surrounded by erythema - become pustules - thick adherent crusts with golden appearance
typically involves face and extremities
Features of bullous impetigo
Vesicles enlarge to form flaccid bullae with clear-yellow fluid - becomes darker and more turbid - ruptures - thin brown crust
Trunk more frequently affected than in non-bullous
Management of impetigo
Soak moist or crusted areas with water/white vinegar
Antiseptic/antibiotic ointment
(Betadine, OH, chlorhexadine, mupirocin etc.)
Oral Fluclox 7d
Cover affected areas, avoid close contact with others, stay home until crusts have dried out, change and wash clothes and linen daily
Definition of erysipelas
Superficial skin infection involving the upper dermis with deeper layers not affected
Pathogen of erysipelas
ALWAYS streptococcus pyogenes
Clinical features of erysipelas
most commonly lower extremities
Lesions raised above level of surrounding skin
Clear line of demarkation
Milians ear sign - involvement of ear (has no deeper tissue therefore must be cellulitis)
Butterfly involvement of face
Acute systemic symptoms (fever, chills)
Management of erysipelas
Non-pharm: elevation, hydration
Parenteral ABx if systemic manifestations (ceftriaxone or cephazolin)
Mild infection - oral amoxicillin
Definition of cellulitis
Bacterial infection of the deep dermis and subcutaneous fat
Pathogens in cellulitis
Staph OR strep pyogenes (less unwell)
Water related:
Fresh water- - aeromonas hydrophilia
Salt water - vibrio species (vulnificus)
Dog/cat bites: pasteurella
Human bite: mixed oral flora
Clinical features of cellulitis
Redness, swelling, warmth, tenderness
More indolent course of disease than erysipelas
+/- purulent drainage/exudate
Management of cellulitis
Oral flucloxacillin (IV if severe) If purulent: clindamycin, bactrim or doxycycline
Definition of necrotising fasciitis
An infection of the deeper tissues that results in progressive destruction of the muscle fascia and overlying subcutaneous fat; muscle tissue frequently spared because of its generous blood supply
Types of necrotising fasciitis
Type I: polymicrobial
Type II: Streptococcal (pyogenes)
Type III: Gas gangrene - clostridium perfringens
Clinical features of necrotising fasciitis
Acute rapid progression over several days (usually appear within 24h of minor injury)
Flu-like sx
Intense thirst (dehydrated)
Erythematous without sharp margins
Swollen, warm, shiny, exquisitely tender
Pain out of proportion to physical exam findings
Red-purple skin - patches of blue-grey
3-4d: large dark marks, skin breakdown with bullae and frank cutaneous gangrene
4-5 days: severely unwell, high fever, v low BP, toxic shock
Gas gangrene has subcutaneous crepitus
Investigations in necrotising fasciitis
Surgical exploration - cultures of deep specimens
Radiographic imaging ?muscle involvement
Management of necrotising fasciitis
Surgical emergency
- aggressive debridement of all necrotic tissue
- Cover with sterile dressing - re-evaluate in 24 hours
Antibiotic:
Empirical - meropenem IV + clindamycin
Type II: BenPen, clindamycin, IVIG +/- amputation
Type III: hyperbaric O2 +/- amputation
Basal cell carcinoma definition
a non-melanoma skin cancer which arises from the cells in the basal epithelium layer of the skin
From which cells to BCCs arise
Pluripotential cells of basaly layer of epithelium OR from hair follicle
Types of BCC
nodular (50-60%) Superficial spreading (10-15%) Infiltrative (7%) Pigmented (6%) Morpeaphorm (sclerosing/fibrosing) (2-3%)
Clinical features of nodular BCC
Well defined borders
Fleshy coloured, pearly nodule
Overlying telangiectasia
May ulcerate - rodent ulcer
On which surfaces do BCCs NOT occur
MUCOSAL
Clinical features of superficial spreading BCC
In epidermis, no dermal invasion
Flat, pink, scaly ulcerations +/- crusting
Usually on trunk
May be misdiagnosed as fungus, psoriasis, eczema etc.
Clinical features of infiltrative BCC
opaque, yellow-white
Blends well with surrounding skin
Clinical features of morephaephorm BCC
“enlarging scar”
indurated, flat/slightly elevated papule
White-yellow scarlike appearance
High i
Investigations for BCCs
Punch biopsy 3-4mm
- scar, but not a problem if excised after histology
Shave biopsy cause minimal scarring, therefore may be good for facial lesions, but may be difficult to localise later
Management options for BCC
Medical: Imiquimod 5% (Aldara) Radiotherapy: - if not fit for surgery - risks: osteitis, skin necrosis Destructive: - curettage and electrodissection - cryosurgery (esp good for nodular) - laser (CO2) ablation Surgical: - +/- flap - Moh's surgery if central face, or recurrent tumours, OR high risk histological type, large or ill defined
Margins for BCC excision
Low risk lesions on face: 2-5mm
High risk/larger tumours: 10mm
Definition of SCC
Squamous cell carcinoma: a non-melanoma tumour of the skin arising in the squamous cells of the epithelium
Genetic mutation associated with high risk of SCCs
MC1R gene
Types of SCC
Verrucous ulcerative Marjolin's ulcer Subungal SCC Metastasis
Clinical features of SCC
predominantly head/neck, dorsum of hands and forearms
tender, painful, hyperkeratotic growing nodule in area of sun damage
Squeezing causes pain
May ulcerate
Histology of SCC
Lobular proliferations of keratinocytes
Intradermal invasion of keratinocytes with prominent keratin production
Prognosis of SC with distant nodal involvement
35% 5 year survival
Management of SCC
Medical
- Retinoic acid (activates tumour suppression genes)
- Fluorouracil (5FU) cream for premalignant lesiosn
- chemotherapy (cisplatin)
Destructive:
- curretage and electrodessication for small superficial lesions
Surgical:
- 4-6mm margins
Margins for SCC
4mm if under 2cm diameter
Definition of melanoma
A skin malignancy arising from the malignant degeneration of melanocytes
How common is melanoma
less than 5% of all skin cancers
but causes most amount of deaths
Risk factors for melanoma
Large number of naevi Atypical mole syndrome Sun exposure Family history transplant recipients Xeroderma pigmentosum
Clinical features of melanoma
ABCDE Asymmetry Border irregularity Colour variation Diameter over 6mm Evolving (enlarging, changing)
Types of melanoma
Superficial spreading (70%)
Nodular (15%)
Lentigo maligna/ melanoma in situ (5-10%)
Acral lentiginous melanoma (5-10%)
Clinical features of superficial spreading melanoma
Peaks 30-50y
Can arise in pre-existing naevus
Pigment varies from black and blue-grey to pink or grey-white
Irregular borders
Nodular melanoma clinical features
Peak in 50s Uniform blue-black, blue-red or red nodule Rapidly growing 5% are amelanotic Mostly on trunk, head, neck
Lentigo maligna clinical features
Irregular tan-brown macule
Slowly expanding on sun-damaged skin of elderly
Acral lentiginous melanoma clinical features
Peak in 60s On palms, soles or under nails 3cm diameter on average at diagnosis tan, brown-to-black, flat macule with colour variation and irregular borders Not linked to sun exposure
Grading of melanoma and margins for excision
Breslow thickness:: Melanoma in situ: 5mm under 1mm: 1cm 1-4mm: 1-2cm Over 4mm: 2cm
Excisional depth in melanoma
Muscle fascia
+ sentinel node biopsy
Definition of actinic/solar keratosis
Abnormal skin cell development due to exposure to UV radiation which are considered to be pre-cancerous
Rates of transformation of solar keratosis to SCC
0.1-2% per year
Percentage of SCCs that arise from pre-existing solar keratoses
60%
Clinical features of solar keratosis
Adjacent skin shows signs of solar damage (yellow or pale, spotty hyperpigmentation, telangiectasias, xerosis)
Classic: erythematous, scaly macule plaque or papule
Hypertrophic: thick adherent scale on erythematous base
Atrophic: scale absent, lesions smooth red macules
With cutaenous horn: keratotic projection of height at least half the largest diameter (spicule or cone)
Management of solar keratosis
Cryotherapy Curettage and cautery Excision biopsy 5-fluorouracil cream (Efudix) - 2 weeks Imiquimod Photodynamic therapy
Hutchinson’s melanotic freckle AKA
Lentigo maligna (melanoma in situ)
Features suspicious of progression of lentigo maligna into invasive melanoma
Thickening of part of the lesion
Increasing number of colours (esp. blue or black)
Ulceration or bleeding
itching or stinging
Management of lentigo maligna
diagnostic biopsy with 5mm margin
Radiotherapy
Cryotherapy
Imiquimod cream
What is Bowen’s disease
AKA SCC in situ
A common type of skin cancer arising from epidermal squamous cells that is confined to the epidermis
Clinical features of bowen’s disease
1+ irregular, flat, red, scaly patches of up to several cm in diameter
May arise on any area of skin
most often diagnosed on sun exposed areas (ears, face, hands, lower legs)
Management of bowen’s disease
cryotherapy superficial skin surgery Fluorouracil cream (Efudix) Imiquimod cream photodynamic therapy
What is a keratoacanthoma
A skin lesion that erupts in skin damaged skin, growing rapidly over a few months, then may shrink and resolve itself. Considered to be a variant of SCC and cannot reliably be distinguished from SCC clinically
Clinical features of keratoacanthoma
May first appear as small pimple/boil but found to have solid core when squeezed
Grows rapidly
May be up to 2cm diameter by time it presents
Diagnose as keratoacanthoma with biopsy or after regression
Management of keratoacanthoma
Obtain pathology (ensure not invasive SCC) Treat as if SCC unless horn has already fallen off
Cryotherapy
Curettage and cautery
Excision
Radiotherapy
Signs of melanoma on dermoscopy
Reticular lines (not crossing, just growing out)
Multiple colours
Pseudopods
Blue-grey veil
Intermittent bleeding on face with incomplete healing
Nodular BCC until proven otherwise
EFG for nodular melanomas
Elevation
Firm to touch
Growing persistently for more than 1 month
investigations if suspect melanoma
Excisional biopsy with 2mm margins
Management of melanoma
Excision with appropriate margins
+/- sentinel node biopsy
regular full skin examination + LN palpation
(6, monthly, annual, 2, yearly)
Counsel to present immediately if worrying spots
Adverse effects of imiquimod/Aldara
Flu-like symptoms for duration of treatment (occur in 5%)
No long-lasting side effects
Congenital spots with high risk of melanoma
LARGE congenital naevi
Giant (over 20mm) 5-10% lifetime risk
higher in lesions that cross the spine!
