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FRACS Gen Surg > Skin and soft tissue > Flashcards

Skin and soft tissue Flashcards

1
Q

What are the common animal bite organisms?

A

Pasteurella
Staphylococcus
Streptococcus
Capnocytophagia canimorsus
Anaerobes (bacteroides, fusobacterium)
Eikenella corrodens (human)

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2
Q

Definition of necrotising fasciitis.

A

Soft tissue infection extending through deep fascia below subcutaneous layers

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3
Q

Definition of Fournier’s gangrene.

A

Necrotising fasciitis of the perineum.

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4
Q

Definition of clostridial myonecrosis.

A

Extension of soft tissue infection into deep muscle compartments.
Gas gangrene.

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5
Q

Water borne infections organisms.

A

Vibrio
Aeromonas

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6
Q

Organisms causing necrotising myositis.

A

Group A Streptococus

i.e. strep pyogenes

Clostridium myonecrosis (gas gangrene)

Clostridium Perfingens - post trauma

Clostridium Septicum - sppntaneous

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7
Q

Pathogenesis of necrotising fasciitis.

A

• Breach -> inoculation
• Exotoxins -> local inflammatory
• Obliterative arteritis
• Anaerobic bacteria proliferates in necrotic tissue - reduced oxygen potential
• Induces progressively worsening inflammation
• Liquefactive necrosis
• Further proliferation
• SIRS -> sepsis -> shock

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8
Q

LRINEC score

A

Laboratory Risk Indicator for Necrotizing Fasciitis

CRP
Hb
WCC
BSL
Creatinine
Na
Score >6 highly suspicious of nec fac Score <6 does not rule out

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9
Q

Types of necrotising fasciitis.

A

Type 1 - polymicrobial(Older adults, multiple comorbidities, PVD)

  • Anaerobic
  • Bacteroides
  • Clostridium
  • Peptostreptococus
  • E Coli
  • Enterobacter
  • Klebsiella
  • Proteus
  • Group A Streptococcus
  • Aerobes
  • Pseudomonas
  • Fungus

Type 2 - monomicrobial(any age group)

  • Clostridium perfinges
  • Group A Strep
  • S Aureus
  • Vibrio vulnificus
  • Aeromonas hydrophilia
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10
Q

Pathophysiology of gas gangrene

A

o Aetiology
▪ Post traumatic, Post procedural
▪ Spontaneous

o Bacteriology – clostridium
▪ Anaerobic, spore forming, gram pos bacteria
▪ Found in soil
▪ Spores are heat resistant, can persist for extended time periods in the environment
▪ Usually requires tissue hypoxia for growth
▪ Toxins – all are exotoxins
• Alpha toxin (phospholipase)
o Gas formed by fermentation of glucose

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11
Q

Management of gas gangrene (clostridium myonecrosis)

A

o Resuscitation
o Antibiotics
▪ Benzylpenicillin 2.4g Q4h IV • + Clindamycin 600mg IV TDS
▪ Add gram negative and MRSA cover until definitive diagnosis confirmed
▪ Penicillin allergy
• Metronidazole + clindamycin
o Tetanus treatment and vaccination
o Surgery
▪ Debride muscle to healthy tissue
▪ May require amputation
o Re-explore after resuscitation of 24-72h
o Reconstruction
▪ After infection well controlled
▪ After nutritional state improved (often require supplemental feeding)
o Hyperbaric oxygen
▪ Has a role in aiding treatment of infection and deactivating toxins

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12
Q

Anatomy of skin

A
  • stratum corneum
  • stratum lucidum
  • stratum granulosum
  • stratum spinosum
  • stratum basale
  • dermis (papillary and reticular)
  • subcutaneous
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13
Q

Principles of wound healing by primary intention.

A

First intention
o Focal disruption of basement membrane only with relatively few epithelial cells dying
▪ Heals by epithelial regeneration
▪ Small scar with minimal wound contraction

o Steps
▪ Incision fills with fibrin-clotted blood
▪ Becomes invaded by granulation tissue (macrophages, fibroblasts, angiogenesis) and covered by new epithelium

o Time-course
▪ 0-24h → neutrophils migrate, basal cells increase mitotic activity, epithelial cells migrate and proliferate on dermis
▪ 24h-3 days→ neutrophils replaced by macrophages, granulation tissue invades with collage deposition in vertical fashion
• Epithelial proliferation continues, creating thickened epithelial covering
▪ 3-5 days → neovascularization peaks, collagen fibrils bridge incision, surface keratinization occurs
▪ 7-14 days → collagen accumulation and fibroblast proliferation, regression of vascular channels
▪ 14 days – 28 days → scar matures, essentially normal epidermis remains. Dermal appendages are lost, however

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14
Q

Principles of healing by secondary intention

A

o Extensive tissue loss with ulceration/ infarction / abscess
▪ Heals using granulation tissue and formation of ECM/ scar
▪ Wound contraction follows facilitated by myofibroblasts

o Steps
▪ Large clot or scab forms on surface of wound – rich in fibrin and fibronectin
▪ Intense inflammation
▪ Large volume of granulation tissue
▪ Re-epithelialisation from skin edges
▪ Wound contraction
• In 6 weeks, wounds reduce to 5-10% of original size

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15
Q

Principles of skin grafting healing.

A

o Plasmatic imbibition (drinking)
▪ Absorption of transudate
o Neurovascularisation with capillary inosculation (kissing)
▪ Up to 36h
▪ Ingrowth of blood vessels
▪ Full circulation restored within 4-7 days
o Collagen linking to create firm attachments (bed)
▪ 4-5 days

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16
Q

Advantages vs disadvantages of split skin graft vs full thickness skin graft

A

o Split
▪ Advantages
• Larger area
• Re-use donor sites

▪ Disadvantages
• Fragile
• Poor colour match
• Texture
• Contracture

o Full thickness
▪ Advantages
• Good texture
• Good cosmetics
• No contraction

▪ Disadvantages
• Unable to regenerate donor
• Impaired graft take (fenestrations)

17
Q

Risk factors for graft failure.

A

o Failure rate 5%

o Local
▪ Lack of adhesion – seroma, haematoma, fenestrations in graft
▪ Inadequate vascularity
• Bone/tendon
▪ High contact area or friction

o Systemic
▪ Poor blood supply
• Smoking
• PVD
• Radiotherapy
▪ Wound healing
• Steroids
• Malnutrition
• Age
• Medical comorbidities

18
Q

Definition of BCC vs SCC

A

o BCC – basal cell carcinoma, arising from basal layer of epidermis
o SCC – squamous cell carcinoma, arising from superficial layer of epidermis

19
Q

Risk factors of skin cancer.

A

o Sunlight exposure
o UV light
o Fair-skinned individuals who burn rather than tan
o Sun exposed areas
▪ Face, scalp, neck
o Radiation exposure
o Precancerous lesions
▪ Actinic keratosis
• 15% develop into in situ or invasive SCC
o Genetics
▪ Basal cell naevus syndrome (Gorlins)
- AD
• PTCH gene mutation (tumour suppressor)
• Ch 9q
• Predisposed to developing hundred of cutaneous BCC

▪ Xeroderma pigmentosa
• AR
• Impaired ability to repair UV-induced sun damage
• 8 different genes identified
o Impaired excision and repair of UV damaged DNA
▪ Oncogenes (RIS, DOS)
▪ Sonic hedgehog signaling pathway (BCC)

o Immunosuppression – after 10-15 years
o HPV (SCC)
o Smoking (SCC)

20
Q

Types of BCC

A

Nodular
Superficial
Sclerosing/morphoeic (more aggresive)

21
Q

Bowen’s disease

A

▪ SCC in situ
▪ Keratinocyte dysplasia / atypia in epidermis only

22
Q

Keratoacanthoma

A

▪ Tender with keratin plug
▪ Form of SCC characterized by spontaneous resolution
• Develop in association with solar keratosis
▪ Resolves in 6-12 weeks
▪ Treatment →
• Excision and likely reconstruction
• OR observation
o Usually located head and neck or shin (difficult to excise completely)
o Large partial /incisional biopsy to exclude amelanotic melanoma
o Then can observe in discussion with patient
▪ Must ensure follows pattern of resolution and completely involutes

23
Q

Pathology of BCC

A

Basaloid tumour cells
▪ Arise from stratum basale
• Small, round, large nuclei, appear like basal keratinocytes
▪ Form dermal nests, cords and islands
▪ Have peripheral palisading with cells aligned radially around periphery of tumour
▪ Indian file cells
▪ Retraction of stroma away from tumour – clefts and separation artefacts

24
Q

Pathology of SCC

A

o Pleomorphic cells with atypical nuclei
▪ Present in all layers of epidermis
• Contained to BM (Bowen’s)
• Extend in to dermis (invasive disease)
▪ Variable differentiation
▪ Intraepithelial keratin (keratin pearls) may be seen
▪ Large nucleoli present
▪ Atypical mitoses
▪ Eosinophilic cytoplasm
o Keratin cysts
o Intercellular bridges seen (desmosomes)
o Stain for cytokeratins, P63

25
Q

Pathology of keratoacanthoma

A

o Well differentiated and circumscribed
o No infiltrative invasion, no areas of poor differentiation, no pleomorphism
o Homogeneous atypical cells
o Cryteraphorm architecture with undermining beneath skin
o Hyperkeratotic
o Glassy-pink cytoplasm within cells
o Surrounding inflammation
o Varying degrees of involution

26
Q

Investiagtion for metastases

A

Risk of mets at diagnosis (SCC)
Marjolin 33%, PNI 35%, T3/4 13%, lip/ear/nose/scalp 10-14%
- Consider if evidence of LN mets
- US guided FNAB of lymph nodes
- CT imaging of LN basin
- CT chest abdo pelvis
- Consider PET

27
Q

Surgical management of BCC and SCC

A

o Margins depends on lesion, location and patient
o Complete local excision with full thickness excision aiming for negative margin
▪ BCC aim for 4-5mm margins (low risk Dr Saw – 2-3mm margins), large lesion 10-20mm
• BCC margins
o Stats
▪ >0.5mm or 1HPF = 1% recurrence
▪ <0.5mm 12%
▪ Involved margin 1/3
o Treatment positive margin
▪ Re-excise
▪ Radiotherapy
▪ Aldara (imiquimod) /cryotherapy

▪ SCC aim for 5-7mm margins
• 10mm for tumours >2cm
• +ve margins = 50% recurrence

o Confirmation of negative margins (margin control)
▪ Frozen section
▪ Delayed reconstruction
▪ Moh’s microsurgery

o Reconstruction
▪ Layered primary closure
▪ Skin graft – partial or full thickness
▪ Flap reconstruction

o Lymph node staging
▪ Consider in high risk lesions
▪ Can use FNAB or excisional biopsy

28
Q

Metastases of BCC.

A

• LN – rare
o Usually in setting of multiple recurrences and uncontrollable primary
o Achieve regional control with lymphadenectomy
o Post op radiotherapy if:
▪ extensive disease
▪ multiple involved nodes
▪ extracapsular extension
▪ close/involved surgical margin

• distant mets o incredibly rare
o specialist referral
o vismodegib (SHH inhibitor)

29
Q

Metastases of SCC

A

• LNs – rare, <1%
• Higher risk of LN metastases if
o Patient factors
▪ SCC at mucosal-squamous junction (lips, anus, vulva)
▪ Immunosuppression
▪ Previous radiotherapy
▪ SCC arising from chronic inflamed tissue

o Tumour factors
▪ SCC >2cm
▪ Ear and lip location
▪ Poorly differentiated SCC
▪ Tumour thickness >4mm
▪ Recurrent SCC
▪ Perineural invasion

o Consider post op radiotherapy if
▪ Multiple nodes involved, large tumour, extracapsular extension, tumour spill at operation

• LN nodal mets
o Stage with ultrasound locally / CT chest abdo pelvis / PET CT (non medicare)
▪ Biopsy FNA
o LN basin dissection for local control
o Adjuvant radiotherapy
▪ Depends on size of nodal mets / LVI / extranodal spread
▪ Halves recurrent disease (20-30%→15-10%)

• Distant mets
o Lung and liver commonest > brain / bone
o Treatment
▪ Radiotherapy for local control of mets
▪ Cisplatin or 5FU based chemotherapy / cetuximab
▪ Nivolumab / pembrolizumab

30
Q

Indications for radiotherapy in SCC/BCC

A

o Adjunctive indications
▪ High risk cancers
• Perineural involvement
• Extracapsular spread beyond lymph nodes
• Poorly differentiated SCC with possible in transit spread
▪ Positive margins
▪ Extracapsular spread of lymph nodes

o Primary treatment
▪ Requires many treatments
▪ Indications
• Older patients
• Cosmetic areas difficult to reconstruct

31
Q

Management of Superficial BCC or bowen’s

A

• Surgery
• Imiquimod (Aldara)
o Monday-Friday, break on weekends
o Topical. Induces inflammation
o 4-6 weeks
• Cryotherapy
• Radiotherapy
• Photodynamic therapy

32
Q

Stages of wound healing

A

Mnemonic VIPR
Haemostasis (hours)
Inflammatory (days)
Proliferation (weeks)
Remodelling (months)

33
Q

Risk factors for local recurrence or mets in SCC/BCC

A

Clinical
- Size >2cm at trunk and extremities
- Size >1cm at the neck/pretibia
- Facial lesions
- Poorly defined borders
- recurrent disease
- immunosuppressed
- site of prev RT or chronic inflammatory process
- rapidly growing tumour
- neurological symptoms

Pathology
- poorly differentiated
- thickness >6mm or invasion beyond subcutaneous fat
- perineural, lymphatic or vascular involvement

FRACS Gen Surg (12 decks)

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