Skin and soft tissue Flashcards
What are the common animal bite organisms?
Pasteurella
Staphylococcus
Streptococcus
Capnocytophagia canimorsus
Anaerobes (bacteroides, fusobacterium)
Eikenella corrodens (human)
Definition of necrotising fasciitis.
Soft tissue infection extending through deep fascia below subcutaneous layers
Definition of Fournier’s gangrene.
Necrotising fasciitis of the perineum.
Definition of clostridial myonecrosis.
Extension of soft tissue infection into deep muscle compartments.
Gas gangrene.
Water borne infections organisms.
Vibrio
Aeromonas
Organisms causing necrotising myositis.
Group A Streptococus
i.e. strep pyogenes
Clostridium myonecrosis (gas gangrene)
Clostridium Perfingens - post trauma
Clostridium Septicum - sppntaneous
Pathogenesis of necrotising fasciitis.
• 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
LRINEC score
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
Types of necrotising fasciitis.
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
Pathophysiology of gas gangrene
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
Management of gas gangrene (clostridium myonecrosis)
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
Anatomy of skin
- stratum corneum
- stratum lucidum
- stratum granulosum
- stratum spinosum
- stratum basale
- dermis (papillary and reticular)
- subcutaneous
Principles of wound healing by primary intention.
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
Principles of healing by secondary intention
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
Principles of skin grafting healing.
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
Advantages vs disadvantages of split skin graft vs full thickness skin graft
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)
Risk factors for graft failure.
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
Definition of BCC vs SCC
o BCC – basal cell carcinoma, arising from basal layer of epidermis
o SCC – squamous cell carcinoma, arising from superficial layer of epidermis
Risk factors of skin cancer.
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)
Types of BCC
Nodular
Superficial
Sclerosing/morphoeic (more aggresive)
Bowen’s disease
▪ SCC in situ
▪ Keratinocyte dysplasia / atypia in epidermis only
Keratoacanthoma
▪ 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
Pathology of BCC
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
Pathology of SCC
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
Pathology of keratoacanthoma
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
Investiagtion for metastases
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
Surgical management of BCC and SCC
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
Metastases of BCC.
• 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)
Metastases of SCC
• 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
Indications for radiotherapy in SCC/BCC
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
Management of Superficial BCC or bowen’s
• Surgery
• Imiquimod (Aldara)
o Monday-Friday, break on weekends
o Topical. Induces inflammation
o 4-6 weeks
• Cryotherapy
• Radiotherapy
• Photodynamic therapy
Stages of wound healing
Mnemonic VIPR
Haemostasis (hours)
Inflammatory (days)
Proliferation (weeks)
Remodelling (months)
Risk factors for local recurrence or mets in SCC/BCC
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
