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Surgery > Plastic Surgery > Flashcards

Plastic Surgery Flashcards

1
Q

Evaluating size of burn

A

Wallace’s rule of 9s
Hand = 1.25%
Palm alone = 1%
ONLY COUNT SUPERFICIAL PARTIAL AND DEEPER (don’t include epidermal burns)

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2
Q

Most common causes of burns

A 
60% scald from oil or water
30% explosion and flame
4% contact burn
3% electrical
3% chemical
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3
Q

Zones of Jackson’s burn model

A
  1. zone of necrosis (dead)
  2. zone of stasis (salvageable)
  3. 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
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4
Q

Evaluating depth of burn

A

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

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5
Q

Criteria for review of a burn by burns unit (11)

A
  • 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
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6
Q

Fluids in burns

A

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

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7
Q

Acute complications of burns

A 
Inhalational injury (airway oedema and obstruction, pneumonia, atelectasis)
Acute respiratory distress syndrome
Hypothermia
Hypovolaemia
Renal failure
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8
Q

Subacute complications of burns

A

Secondary infection
Graft loss
Early hypergranulation
Scar contracture/post-burn deformities

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9
Q

Pathogens most likely in secondary infections of brrns

A

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
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10
Q

Components of acute respiratory distress syndrome (secondary to burns)

A

Hypoxaemia (due to V/Q mismatch)
Pulmonary HTN (inc. pulmonary oedema)
Bronchoconstriction (systemic inflammatory response)
Reduced lung compliance (secondary to oedema and red. surfactant)

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11
Q

Definition of folliculitis

A

Acute infection of multiple hair follicles

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12
Q

Pathogens in folliculitis

A

Staph aureus

“Hot Tub” version = psudomonas aeruginosa

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13
Q

Clinical features of folliculitis

A

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)

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14
Q

Management of folliculitis

A

Usually self-limiting
Warm compresses can be applied TDS
Avoid shaving area
If lesions persist, topical mupirocin for s. aureus version

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15
Q

definition of furuncle

A

AKA boil

An acute infection of a single hair follicle

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16
Q

Definition of carbuncle

A

Multi-loculated furuncle (coalescence of several inflamed follicles into a single inflammatory mass with purulent drainage from multiple follicles)

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17
Q

Pathogen involved in furunculosis/carbuncles

A

Staph aureus almost always

If use foot baths at nail salons, at risk for myobacterium

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18
Q

Management of furunculosis and carbuncles

A

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)

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19
Q

Definition of impetigo

A

Superficial bacterial infection involving the epidermis proper

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20
Q

Age group impetigo most commonly seen in

A

2-5y

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21
Q

Pathogens in impetigo

A

Classic impetigo: strep pyogenes

Bullous impetigo: Staph aureus (exofoliative A toxin - loss of cell adhesion in superficial epidermis - bullae)

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22
Q

Features of non-bullous impetigo

A

Lesions begin as papules - vesicles surrounded by erythema - become pustules - thick adherent crusts with golden appearance
typically involves face and extremities

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23
Q

Features of bullous impetigo

A

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

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24
Q

Management of impetigo

A

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

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25
Q

Definition of erysipelas

A

Superficial skin infection involving the upper dermis with deeper layers not affected

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26
Q

Pathogen of erysipelas

A

ALWAYS streptococcus pyogenes

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27
Q

Clinical features of erysipelas

A

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)

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28
Q

Management of erysipelas

A

Non-pharm: elevation, hydration
Parenteral ABx if systemic manifestations (ceftriaxone or cephazolin)
Mild infection - oral amoxicillin

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29
Q

Definition of cellulitis

A

Bacterial infection of the deep dermis and subcutaneous fat

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30
Q

Pathogens in cellulitis

A

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

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31
Q

Clinical features of cellulitis

A

Redness, swelling, warmth, tenderness
More indolent course of disease than erysipelas
+/- purulent drainage/exudate

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32
Q

Management of cellulitis

A 
Oral flucloxacillin (IV if severe)
If purulent: clindamycin, bactrim or doxycycline
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33
Q

Definition of necrotising fasciitis

A

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

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34
Q

Types of necrotising fasciitis

A

Type I: polymicrobial

Type II: Streptococcal (pyogenes)

Type III: Gas gangrene - clostridium perfringens

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35
Q

Clinical features of necrotising fasciitis

A

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

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36
Q

Investigations in necrotising fasciitis

A

Surgical exploration - cultures of deep specimens

Radiographic imaging ?muscle involvement

37
Q

Management of necrotising fasciitis

A

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

38
Q

Basal cell carcinoma definition

A

a non-melanoma skin cancer which arises from the cells in the basal epithelium layer of the skin

39
Q

From which cells to BCCs arise

A

Pluripotential cells of basaly layer of epithelium OR from hair follicle

40
Q

Types of BCC

A 
nodular (50-60%)
Superficial spreading (10-15%)
Infiltrative (7%)
Pigmented (6%)
Morpeaphorm (sclerosing/fibrosing) (2-3%)
41
Q

Clinical features of nodular BCC

A

Well defined borders
Fleshy coloured, pearly nodule
Overlying telangiectasia
May ulcerate - rodent ulcer

42
Q

On which surfaces do BCCs NOT occur

A

MUCOSAL

43
Q

Clinical features of superficial spreading BCC

A

In epidermis, no dermal invasion
Flat, pink, scaly ulcerations +/- crusting
Usually on trunk
May be misdiagnosed as fungus, psoriasis, eczema etc.

44
Q

Clinical features of infiltrative BCC

A

opaque, yellow-white

Blends well with surrounding skin

45
Q

Clinical features of morephaephorm BCC

A

“enlarging scar”
indurated, flat/slightly elevated papule
White-yellow scarlike appearance
High i

46
Q

Investigations for BCCs

A

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

47
Q

Management options for BCC

A 
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
48
Q

Margins for BCC excision

A

Low risk lesions on face: 2-5mm

High risk/larger tumours: 10mm

49
Q

Definition of SCC

A

Squamous cell carcinoma: a non-melanoma tumour of the skin arising in the squamous cells of the epithelium

50
Q

Genetic mutation associated with high risk of SCCs

A

MC1R gene

51
Q

Types of SCC

A 
Verrucous
ulcerative
Marjolin's ulcer
Subungal SCC
Metastasis
52
Q

Clinical features of SCC

A

predominantly head/neck, dorsum of hands and forearms
tender, painful, hyperkeratotic growing nodule in area of sun damage

Squeezing causes pain
May ulcerate

53
Q

Histology of SCC

A

Lobular proliferations of keratinocytes

Intradermal invasion of keratinocytes with prominent keratin production

54
Q

Prognosis of SC with distant nodal involvement

A

35% 5 year survival

55
Q

Management of SCC

A

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

56
Q

Margins for SCC

A

4mm if under 2cm diameter

57
Q

Definition of melanoma

A

A skin malignancy arising from the malignant degeneration of melanocytes

58
Q

How common is melanoma

A

less than 5% of all skin cancers

but causes most amount of deaths

59
Q

Risk factors for melanoma

A 
Large number of naevi
Atypical mole syndrome
Sun exposure
Family history
transplant recipients
Xeroderma pigmentosum
60
Q

Clinical features of melanoma

A 
ABCDE
Asymmetry
Border irregularity
Colour variation
Diameter over 6mm
Evolving (enlarging, changing)
61
Q

Types of melanoma

A

Superficial spreading (70%)
Nodular (15%)
Lentigo maligna/ melanoma in situ (5-10%)
Acral lentiginous melanoma (5-10%)

62
Q

Clinical features of superficial spreading melanoma

A

Peaks 30-50y
Can arise in pre-existing naevus
Pigment varies from black and blue-grey to pink or grey-white
Irregular borders

63
Q

Nodular melanoma clinical features

A 
Peak in 50s
Uniform blue-black, blue-red or red nodule
Rapidly growing
5% are amelanotic
Mostly on trunk, head, neck
64
Q

Lentigo maligna clinical features

A

Irregular tan-brown macule

Slowly expanding on sun-damaged skin of elderly

65
Q

Acral lentiginous melanoma clinical features

A 
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
66
Q

Grading of melanoma and margins for excision

A 
Breslow thickness::
Melanoma in situ: 5mm
under 1mm: 1cm
1-4mm: 1-2cm
Over 4mm: 2cm
67
Q

Excisional depth in melanoma

A

Muscle fascia

+ sentinel node biopsy

68
Q

Definition of actinic/solar keratosis

A

Abnormal skin cell development due to exposure to UV radiation which are considered to be pre-cancerous

69
Q

Rates of transformation of solar keratosis to SCC

A

0.1-2% per year

70
Q

Percentage of SCCs that arise from pre-existing solar keratoses

A

60%

71
Q

Clinical features of solar keratosis

A

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)

72
Q

Management of solar keratosis

A 
Cryotherapy
Curettage and cautery
Excision biopsy
5-fluorouracil cream (Efudix) - 2 weeks
Imiquimod
Photodynamic therapy
73
Q

Hutchinson’s melanotic freckle AKA

A

Lentigo maligna (melanoma in situ)

74
Q

Features suspicious of progression of lentigo maligna into invasive melanoma

A

Thickening of part of the lesion
Increasing number of colours (esp. blue or black)
Ulceration or bleeding
itching or stinging

75
Q

Management of lentigo maligna

A

diagnostic biopsy with 5mm margin
Radiotherapy
Cryotherapy
Imiquimod cream

76
Q

What is Bowen’s disease

A

AKA SCC in situ

A common type of skin cancer arising from epidermal squamous cells that is confined to the epidermis

77
Q

Clinical features of bowen’s disease

A

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)

78
Q

Management of bowen’s disease

A 
cryotherapy
superficial skin surgery
Fluorouracil cream (Efudix)
Imiquimod cream
photodynamic therapy
79
Q

What is a keratoacanthoma

A

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

80
Q

Clinical features of keratoacanthoma

A

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

81
Q

Management of keratoacanthoma

A 
Obtain pathology (ensure not invasive SCC)
Treat as if SCC unless horn has already fallen off

Cryotherapy
Curettage and cautery
Excision
Radiotherapy

82
Q

Signs of melanoma on dermoscopy

A

Reticular lines (not crossing, just growing out)
Multiple colours
Pseudopods
Blue-grey veil

83
Q

Intermittent bleeding on face with incomplete healing

A

Nodular BCC until proven otherwise

84
Q

EFG for nodular melanomas

A

Elevation
Firm to touch
Growing persistently for more than 1 month

85
Q

investigations if suspect melanoma

A

Excisional biopsy with 2mm margins

86
Q

Management of melanoma

A

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

87
Q

Adverse effects of imiquimod/Aldara

A

Flu-like symptoms for duration of treatment (occur in 5%)

No long-lasting side effects

88
Q

Congenital spots with high risk of melanoma

A

LARGE congenital naevi
Giant (over 20mm) 5-10% lifetime risk
higher in lesions that cross the spine!

Surgery (8 decks)

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