Skin and soft tissue Flashcards
What are the stages of skin graft taking?
- Adherence
- fibrin bonds form
- fibroblasts replace fibrin with collagen - Imbibition
- graft absorbs fluid 48-72 hrs
- fluid contains nutrition to keep graft viable - Inosculation & revascularisation
- capillaries begin to extend into the graft
- begins after 72hrs - Remodelling
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What is this and how is it treated?
Felons are subcutaneous abscesses of the fingertip pulp.
Diagnosis is made clinically by assessing for tenderness, erythema and fluctuance of the fingertip pulp.
Treatment is usually I&D and IV antibiotics.
*I&D incision doesn’t cross DIPJ crease. mid lateral approach is ulnar side in digits 2-4 and radial in thumb and digit 5.
What are the common pathogens in necrotising skin and soft tissue infections?
There are clostridial (gas gangrene) and non clostridial organisms.
Of the non clostridial infections there are 4 types:
Type 1= polymicrobial (75%)
Type 2= Group A strep (most common monomicrobial)
Type 3= marine bacteria e.g. vibrio (3 in the sea)
Type 4= fungal e.g. mucormycedes
How do necrotising soft tissue infections usually present?
These patients are usually systemically unwell with fever and sepsis
-the affected area has pain out of proportion to visual changes seen.
- Ecchymoses,
- bullae,
- cellulitis with ill defined margins,
- crepitus (from anaerobic production of nitrogen and hydrogen not readily absorbed),
- skin necrosis and
- hypoaesthesia (from small blood vessel thrombosis and superficial nerve destruction) is late sign.
During operation:
- murky grey ‘dishwater fluid’ on incising tissue.
- tissue planes fall apart as running fingers through it.
- fat dull and grey, muscle doesn’t twitch and dulled, and skin doesn’t bleed much.
Sarcoma
Overview
Soft tissue sarcomas are malignant tumors of mesenchymal origin, affecting soft tissues such as muscles, fat, and connective tissues.
Classification
The WHO classifies soft tissue sarcomas into over 70 subtypes based on tissue origin, using immunohistochemical markers to guide treatment and predict outcomes.
Risk Factors
Risk factors for soft tissue sarcomas include environmental and chemical exposures, radiation, genetic predispositions like Li-Fraumeni syndrome, and chronic lymphedema leading to angiosarcoma.
Clinical Features
Slow-growing, painless mass; physical examination shows a palpable, encapsulated mass, with the assessment of fascial involvement and lymph nodes being critical for prognosis.
Diagnosis
The evaluation of suspected soft tissue sarcomas involves specialised imaging, biopsy techniques, rigorous pathological assessment per 2020 WHO guidelines, and staging via the AJCC system.
Management
Management of soft tissue sarcomas involves surgical excision, radiotherapy to reduce recurrence, and selective use of chemotherapy for high-grade or aggressive tumours.
Specific Soft Tissue Sarcomas
Undifferentiated pleomorphic sarcoma, rhabdomyosarcoma, and Dermatofibrosarcoma protuberans are among the commonest soft tissue sarcomas seen in clinical practice.
Desmoid
What are the stages of wound healing?
- Haemostasis (immediate - hrs)
- clot formation
- vasoconstriction
- platelet aggregation
- release of growth factors e.g. PDGF and TGFbeta
- release of cytokines and chemokines
- fibrin matrix to act as a scaffold and stabilises wound - Inflammation (days to weeks)
- vasodilation
- vascular permeability
- cellular recruitment of neutrophils, macrophages then lymphocytes
- growth factor elaboration
- seen as oedema - Proliferation (days to weeks)
- Phases (AGE)- Angiogenesis
- Granulation
- Epithelialisation (barrier to bacteria but thin, vulnerable)
- fibroblast proliferation
- contractile proteins and myofibroblasts
- ground substance and collagen deposition
- Remodelling (weeks to months)
- wound contraction
- cross linking of collagen and change from type III to type I
- apoptosis of cells no longer required
- repigmentation
- 80% of tensile strength by 6 weeks
What are factors that impede wound healing?
Patient factors:
- prev radiation site
- medications steroids (systemic), NSAIDs
- diabetes
- peripheral artery disease
- chronic venous insufficiency
- immunosuppression
- smoker
- age
- malnutrition & vitamin deficiencies
- chemo or radiotherapy
Disease factors:
- foreign bodies
- infection
- neoplasm
- dirty wound
- ischaemia
- location e.g. lower legs
Surgical factors:
- secondary intention
How do you classify wound contamination?
I use the National Healthcare Safety Network (NHSN) classification: (% risk of infection)
Clean = uninfected (1-5%)
Clean-contaminated = entry into the respiratory, GIT, urinary or genital tracts. (3-11%)
Contaminated = traumatic wounds, break in sterile technique (10-17%)
Dirty = infected (>27%)
What is a surgical site infection
Defined by the United States Centres for Disease Control and Prevention as an infection related to an operative procedure that occurs near the surgical site within 30 days of the procedure or within 90 days of implanted prosthetic material at time of surgery.
Superficial: Limited to Skin or Subcutaneous Tissue
Deep: Involves Muscle or Fascia
Organ/Space: Involves Body Cavity or Organ
What is an ulcer?
Destruction of the epidermal surface down to underlying subcutaneous fat or deeper tissues.
How does negative pressure wound therapy work?
- reduces excess exudate
- pulls wound edges together/helps with contraction of wound
- barrier to bacteria
- reduces number of dressing changes and therefore disruption of new fragile epithelisation with daily dressing changes.
- stimulates growth factors, promotes angiogenesis and granulation tissue formation, proliferation of fibroblasts, increases collagen formation.
What are some known defects in collagen and their associated sequelae?
Genetic Defects in Collagen
I-I: Type I in Imperfecta (bone deformities, grey sclera)
Al-Four-t: Type IV in Alport (GN, may need renal transplant)
“ED Happens to All Men”: All Types in ED (joint laxity, dislocations, stretchy skin)
Fib-Fan: Fibrillin in Marfan’s (aortic dissection, tall etc)
What are the most common organisms in surgical site infections?
Majority are From Native Flora (Skin, Mucous Membranes or Hollow Viscera)
Most Common Organism: Staphylococcus aureus
Most Common GNR: Escherichia coli
Most Common Anaerobe: Bacillus fragilis
What is the pathogenesis of keloid and hypertrophic scars?
Both are an excess of collagen deposition in the healing process excess is laid down in proliferation and remodelling phases.
Hypertrophic = tissue stays within the margin of the wound edges. Usually regresses with time. No genetic predisposition. Composed of organised type III collagen.
Keloid = tissue extends beyond the original scar and usually does not regress with time. Composed of disorganised Type III & Type I collagen. Genetic predisposition autosomal dominant.
