Skin and hernia Flashcards
Extramammary Paget’s disease
- Rare
- Intraepithelial adenocarcinoma
- Underlying invasive adenocarcinoma of apocrine glands in 30-45%.
- Most common in apocrine dense skin- groins, axillae, natal cleft
- Pruritus is most common symptom
- Appearance is of well demarcated eczema
- Treatment is with WLE
- if surgery prohibited 5-FU, imiquimod, cryotherapy are options
Lymphodema stages
Stage 1
- protein rich fluid acculumlation
- Soft pitting oedema
Stage 2
- infiltration on macrophages, fibroblasts and adipocytes
- Local inflamatory response
- non pitting oedema
Stage 3
- Elephantiasis
- local inflamatory response and recurrent infection
- subcutaneous fibrosis and skin change
Primary and secondary classification of lymphoedema and causes
Primary
- No identified cause
- <1y- Congenital
- Milroy disease
- 1-35- Lymphoedema praecox
- Meige Disease
- >35- Lymphoedaema tarda
- <1y- Congenital
Secondary
- Filariasis (Wucheria bancrofti)
- Trauma
- Surgery
- Lymph node dissection
- Venous
- Radiation
- Tumour impingement or invasion
Lymphoedema treatment
Education
- Skin care and avoidance or trauma
- Weight loss
- Eczema management
Elevation and compression
- 30-60mmHg is ideal
Physiotherapy
- decongestive massage
Pneumatic compression
Operative management
- Lymphaticolymphatic or lymphaticovenous bypass (if dilated lymphatics present)
- Liposuction
- Kontolein subcutaneous excision
- Charles excisional operation
What malignancy is associated with long term >10 year lymphoedema
Lymphangiosarcoma
Very poor prognosis
Pressure injury risk factors
Intrinsic
- Age
- Diabetes
- Malnutrition
- Edema
- Obesity
Extrinsic
- Pressure sites
- Tissue shearing during rolls and movement
- Moisture
- Incontinence
Name a scoring tool used to assist in preventing pressure sores
Braden score
- Routine nursing practice
- Subscales in:
- Sensation
- Moisture
- Activity
- Mobility
- Nutrition
- Friction/Shearing
- Subscales in:
Staging of pressure injury
Stage I
- Skin reddened for longer than 1 hour after pressure relief
Stage II
- Blister or superficial break in dermis
Stage III
- Full thickness dermal injury with visible fat but not muscle, tendon or bone
Stage IV
- Exposed bone, muscle or tendon
- Often extensive undermining and tunnelling
Melanoma subtypes
Common
- Superficial spreading (70%)
- Nodular (15-30%)
- Lentigo Maligna melanoma (10-15%)
- Acral lentiginous
Rare
- Amelanotic (most commonly nodular or desmoplastic)
- Spitzoid melanoma
- Desmoplastic
- Animal type
major prognostic variables in primary melanoma
Depth of invasion
- Continuous variable, subdivided by T staging for convenience
Ulceration
Mitotic rate
- <1 mitosis/mm squared vs > or equal to 1
Age at diagnosis
- Counterintuitively, young people do well
SLNB positive/ nodal staging
Presence of intransit metastasis (included in N staging)
Regression
LVI
Gender
- Men do badly (again)
T Staging in melanoma
Always to the nearest 0.1mm (rounded)
Tis
- Insitu (above the superficial aspect of the granular cell layer of the epidermis)
T1
- <1mm (below the superficial aspect of the granular cell layer)
T2
- 1-2mm
T3
- 2-4mm
T4
- >4mm
Discuss indications for SLNB in melanoma and the rate of LN positive disease in T1 melanomas
Australian cancer council guidelines state SLNB indicated in:
- T2 disease (>1mm) or greater
- T1b (0.8-1mm) with high risk features:
- Mitotic rate >1/mm2
- Ulceration
- Maybe LVI
Likelyhood of positive SLNB
- <5% for T1a disease
- T1b 5-12%
N staging of melanoma
Principles
- Number of positive nodes
- Clinically detectible nodes
- Presence of in-transit or satellite metastasis
N1
- 1 node either detection
- N1c- no nodes, but intransit/satellite met
N2
- 2-3 nodes
- N2c- 1 nodes with in- transit/ satellite met
N3
- 4 or more
- 2 nodes and intransit/satellite met
Clinical features useful in assessment of suspected melanoma
Ugly duckling sign
- used in people with multiple naevi
ABCDE
- Assymetry
- Border
- Colour variegation
- Diameter >6mm
- Evolution
Intransit and nodal examination
Hutchinsons sign
Hyperpigmentation of the proximal nail fold in subungual acral melanoma
MSLT-I
Multicentre Selective Lymphadenectomy Trial-I which confirmed the accuracy of SLNB in prognostication
- Randomised trial, clinically node negative at diagnosis
- Excision of primary and SLNB with selective lymphadenectomy if positive.
- vs
- Excision of primary and observation lymphadenectomy if clinical nodal recurrence
- Excision of primary and SLNB with selective lymphadenectomy if positive.
- Intermediate thickness (1.2mm in this study) no difference in overall survival between groups but:
- In those with nodal involvement and index lymphadenectomy vs only when clinically apparent there was a signficant survival advantage
- Thick melanomas (>3.5mm in this study)
- No difference in survival
MSLT-II
Patients with positive SLNB and
- Breslow >1.2mm and/or
- Clark level III, IV, V and/or
- Ulceration
Randomised to immediate LND vs observation (including USS of nodes)
- Slight improvement in disease free survival in immediate LND group but:
- No improvement in melanoma specific survival
- Higher rate of lymphoedema (8 vs 23%)
Breslow thickness
Depth in mm of melanoma
Measured from superficial aspect of the granular cell layer of the epidermis
Clark’s level
Level I: epidermis
Level II: Papillary dermis
Level III: to the junction of papillary and reticular dermis
Level IV: into reticular dermis
Level V: into subcutaneous fat
Who should be offered SLNB in melanoma
Clinically node negative disease and:
- Breslow 1 mm or greater, or;
- Breslow 0.8-1mm with high risk features
- Ulceration
- High mitotic rate
The risk of SLNB positive disease with breslow <1mm is <5%
- in the 0.8-1mm group this is 7-12%
Genetic markers in melanoma
BRAF
- BRAF inhibitors
Radiotherapy in Melanoma
TROG trial, radiotherapy after clearance
- Presence of extranodal spread
- >3 nodes involved
Excision margins in melanoma
FAMMM
Familial Atypical Mole and Melanoma syndrome
- AKA dysplastic naevis syndrome
- CDKN2A gene
- Chromosome 9p21
- encodes p16, loss of function leads to inappropriate progression through S phase
- Chromosome 9p21
- Autosomal dominant inheritance
- Life time risk of melanoma approaches 100%
- Associated risk of pancreatic, lung and breast cancers
- also brain and leukemia
Gorlin syndrome
Rare
Autosomal dominant
PTCH1 gene
syndrome of:
- multiple BCCs
- odontogenic keratocysts of the jaw
- developmental delay
BCC epidemiology
Common, lifetime risk ~30% in fair skinned people
Risk increases with age
closer to the equator increases risk
men 1.3:1 women
BCC risk factors
UV exposure
- probably more UVA than UVB
Tanning beds
Arsenic exposure
Radiation exposure
Fair skin, red hair
Family history of skin cancer
Pigment disorders
- xeroderma pigmentosum, albinism
Immunosuppression
- HIV, transplant, CRF
BCC origin cell
Basal layer of epidermis
BCC subtypes
More indolent
- Nodular (most common, ~80%)
- Superficial
- Pigmented BCC (6%)
- Fibroepithelial (most indolent)
More aggressive
- Infiltrative/mopheaform
- Micronodular
- Basosqumaous (part BCC part SCC)
Macroscopic features of BCC
Pearly rolled edge, depressed centre
Ulceration common
Teleangiectasia centrally is common
Locally invasive, extremely rarely metastatic
80% are found on the face and neck
BCC excision margins
4-5mm
Although those with 2mm margins only recur 4%
Imiquimod
5% cream
Immune response modifier
- Promotes innate immune response
- Activation of Toll-like receptor 7 incites cells to produce cytokines
- IFN-a, IL-6, TNF-a
Dosing regimens vary per indication
- Warts 3x weekly until clearance max 8/52
- BCC 5x weekly for 6/52
Topical fluorouracil
5% cream
Antimetabolite
- Thymidylate synthase
- inhibits DNA synthesis
Apply 1-2x per day for 2-4 weeks, avoid contact with, or decontaminate, non diseased skin (esp the applying fingertip)
Clinical features of pyoderma gangrenosum
- Rapid course of lesion development
- Initial lesion consistent with papule, pustule, or vesicle
- Pain out of proportion to lesion
- History of preceding trauma (pathergy)
- History of disorders associated with PG
- Ulcerated lesion with violaceous margin and undermining
Pathophysiology of pyoderma gangrenosum
Neutrophilic dermatosis
Neutrophil infiltration, dysfunction and inapproprate action
Often associated with systemic inflamation
- IBD, Arthritis
Progressive dermatitis and erosion of skin and soft tissue, neutrophil mediated
- TNFa implicated
- Responds to antiTNFa treatment (infliximab)
Treatment of pyoderma gangrenosum
Key is diagnosis with biopsy
If associated with IBD surgery for that disease may lead to resolution
Treatment is immunosuppression
- Systemic glucocorticoids
- Topical tacrolimus
- Single small RCT using infliximab shows good resolution
Analgesia
Wound cares
Avoidance of trauma
Surgery is reserved for infection/necrosum
Hidradenitis supparativa pathophysiology
Follicular epithelial hyperplasia
- hyperkeratosis
- follicular plugging and distension
- Mechnical stress forces esp. in intertrigonous areas
- duct rupture, leakage of keratin fragments, sebum and bacteria into tissue
- foreign body granulomatous response
- duct rupture, leakage of keratin fragments, sebum and bacteria into tissue
- Mechnical stress forces esp. in intertrigonous areas
- follicular plugging and distension
NB: Likely not from sweat glands as the name suggests
Hidradenitis treatment
Education and wound care
- Avoid Trauma
- Avoid tape
- Smoking cessation (and nicotine)
- Weight loss
Hurley I
- Topical clindamycin
- Punch debridement
Hurley II-III
- Doxycycline 100mg OD-BD
- OCP, spironolactone may help
- Surgery
- Simple excisions
- Excision and grafting
Staging of Hidradenitis supparativa
Hurley Classification
- Stage I – Simple abscess
- Abscess formation (single or multiple) without sinus tracts and cicatrization/scarring
- Stage II – Sinus/fibrosis without confluence
- Recurrent abscesses with sinus tracts and scarring, single or multiple widely separated lesions
- Stage III – Confluence
- Diffuse or almost diffuse involvement, or multiple interconnected sinus tracts and abscesses across the entire area
Cutaneous SCC clinical features
The clinical appearance of invasive cSCC often correlates with the level of tumor differentiation.
- Well-differentiated lesions usually appear as indurated or firm, hyperkeratotic papules, plaques, or nodules.
- Lesions are usually 0.5 to 1.5 cm in diameter but may be much larger.
- Ulceration may or may not be present.
- In contrast, poorly differentiated lesions are usually fleshy, granulomatous papules or nodules that lack the hyperkeratosis that is often seen in well-differentiated lesions.
- Poorly differentiated tumors may have ulceration, hemorrhage, or areas of necrosis.
Staging for cutaneous SCC
Clinical nodal assessment
- FNA
CT CAP if high risk features
- Bone, muscle, fascia involvement
- Large size (>2cm)
- Breslow >2mm
- Nodal involvement
- Near or invading major nerves
- In transit mets
PET- no evidence
No evidence for (or against) SLNB
Merkel cell cancer cell theories of cell origin
Two theories
- Traditional (and still valid) view is origin in Merkel cells
- Neural mechanoreceptor cell of the basal layer of the dermis
- Alternative view is origin in dermal totipotential cell
- Acquires neuroendocrine features during malignant transformation
Virus implicated in Merkel cell cancers
Merkel Cell Polyomavirus
(present on PCR in 80% of tumours)
AEIOU of Merkel cell cancers
- Asymptomatic
- 88 percent
- Expanding rapidly
- (significant growth in ≤3 months)
- Immune suppression
- HIV infection, solid organ transplant recipient, chronic lymphocytic leukemia
- Older than 50 years age
- Most common >80
- Ultraviolet (UV)-exposed area in a fair-skinned individual
Lumbar herniae and their boundaries
Inferior (Petit)
- between
- external oblique
- iliac crest
- latissimus dorsi
Superior (Grynfeltd)
- between
- quadratus lumborum
- internal oblique
- 12th rib
What are the recommended biopsy types for melanoma
Excision biopsy to 2mm margin is the recommended by the australian cancer council.
Of the incomplete biopsy methods incisional biopsy has the lowest false negative rate (1.4%)
Should prophylactic parastomal mesh be used
STOMAMESH trial shows no reduction in the incidence of parastomal hernia at 1 year
How can necrotizing fasciitis be subtyped
Type I
- polymicrobial
- both anaerobic and aerobic
Type II
- Lancefield group A streptococci
- pyogenes
- or other beta haemolytic strep
Type III
- gas gangrene, or clostridial myonecrosis
Bacteriology of type 1 necrotizing soft tissue infection
Polymicrobial with anaerobic and aerobic bacteria
- Typically at least one each of:
- Anaerobe
- Bacteroides
- Clostridium
- Peptostreptococcus
- Enterobacteriaceae (gram neg family)
- E.coli
- Enterobacter
- Klebsiella
- Proteus
- Facultative anaerobic Streptococci (other than GAS)
- Enterococci
- Strep. agalactiae
- Anaerobe
- Fungi occasionally implicated
Bacteriology of type II necrotizing soft tissue infection
Monomicrobial
- Beta haemolytic streptococcal infection
- Group A Strep, almost always pyogenes
- M protein is the important virulence factor
- bacterial strains can produce pyrogenic exotoxins
- important mediator of toxic shock syndrome
- M protein is the important virulence factor
- Group A Strep, almost always pyogenes
- Staph aureaus
- Uncommon
- Vibrio vulnificus
- Salt water injuries
- Aeromonas hydrophila
- Fresh water injuries
Risk factors for necrotizing soft tissue infection
- Major penetrating trauma
- Minor laceration or blunt trauma
- Skin breach (esp IVDU)
- Recent surgery
- Mucosal breach
- hemorrhoids, rectal fissures, episiotomy
- Immunosuppression
- (diabetes, cirrhosis, neutropenia, HIV infection)
- Malignancy
- Obesity
- Alcoholism
- In women: pregnancy, childbirth, pregnancy loss, gynecologic procedures
Clinical findings in necrotizing soft tissue infection
How frequently are they found
- Erythema
- (without sharp margins; 72 percent)
- Oedema that extends beyond the visible erythema
- (75 percent)
- Severe pain
- (out of proportion to exam findings in some cases; 72 percent)
- Fever
- (60 percent)
- Crepitus
- (50 percent)
- Skin bullae, necrosis, or ecchymosis
- (38 percent)
Fournier Gangrene
Type I (polymicrobial) necrotizing soft tissue infection of the perineum
- More common in men
- often involves penis and scrotum
- Diabets and obesity are major risk factors
Vibrio vulnificus
Gram negative aquatic organism
often implicated in salt water soft tissue infections
treatment with fluoroquinolones or tetracyclines
- In severe infection a 3rd generation cephalosporin may be helpful (ceftriaxone, cefotaxime)
Antibiotic management of necrotizing fasciitis
My choice
- Meropenem, and
- Vancomycin, and
- Clindamycin
General principles are:
- Broad spectrum coverage against gram negatives, gram positives and anaerobes
- Tazosin is a reasonable alternative to a carbapenem
- Cover MRSA
- Vancomycin
- Clindamycin
- Suppresses bacterial toxin production
- Decreases penicillin binding protein production (synergistic beta lactam effect)
How does thermal injury cause tissue loss
By coagulative necrosis
how can burns be classified by cause
Flame
Scald
Hot (or cold) surface contact
Chemical
Electricity
How do chemical and electrical injuries cause tissue loss
Direct cellular membrane injury and thermal injury.
- induces both colliquation and coagulative necrosis
What are the three zones of burn injury
What is their significance
Zone of coagulative necrosis
- Irreversible cellular injury at time of insult
Zone of stasis
- Vascular damage and leaky endothelium
- poor tissue perfusion
- Thromboxane A2 is an important mediator of burn induced vasoconstriction in the zone of stasis
- May be reversible or progress to coagulative necrosis
Zone of hyperaemia
- Vasodilation and inflammation
- Usually not at risk for further necrosis
How should burns be classified by depth
Superficial
Partial
- Superficial partial
- Deep partial
Full thickness
4th degree
Superficial burns
- Involve only the epidermal layer of skin.
- Do not blister but are painful, dry, red, and blanch with pressure.
- Over two to three days the pain and erythema subside, and by approximately day 4, the injured epithelium peels away from the newly healed epidermis.
- Such injuries are generally healed in six days without scarring.
- This process is commonly seen with sunburns.
Superficial-partial burns
- Characteristically form blisters within 24 hours between the epidermis and dermis.
- Painful, red, and weeping and blanch with pressure.
- Burns that initially appear to be only epidermal in depth may be determined to be partial thickness 12 to 24 hours later.
- Generally heal in 7 to 21 days
- A layer of fibrinous exudates and necrotic debris may accumulate on the surface, which may predispose the burn wound to heavy bacterial colonization and delayed healing.
- These burns typically heal without functional impairment or hypertrophic scarring
- pigment changes may occur.
Deep-partial thickness burns
- Extend into the deeper dermis
- Deep burns damage hair follicles and glandular tissue.
- Painful to pressure only
- Almost always blister (easily unroofed), are wet or waxy dry, and have variable mottled colorization from patchy cheesy white to red
- Do not blanch with pressure.
- If infection is prevented and wounds are allowed to heal spontaneously without grafting, they will heal in two to nine weeks.
- These burns invariably cause hypertrophic scarring. If they involve a joint, joint dysfunction is expected even with aggressive physical therapy.
- A deep partial-thickness burn that fails to heal in two weeks is functionally and cosmetically equivalent to a full-thickness burn.
- Differentiation from full-thickness burns is often difficult.
Full thickness burns
- Extend through and destroy all layers of the dermis and often injure the underlying subcutaneous tissue.
- Burn eschar, the dead and denatured dermis, is usually intact.
- can compromise the viability of a limb or torso if circumferential.
- Usually anesthetic or hypo-aesthetic.
- Skin appearance can vary from waxy white to leathery gray to charred and black.
- Skin is dry and inelastic and does not blanch with pressure
- Hairs can easily be pulled from hair follicles.
- Vesicles and blisters do not develop.
- Pale full-thickness burns may simulate normal skin except that the skin does not blanch with pressure.
- Eschar eventually separates from the underlying tissue and reveals an unhealed bed of granulation tissue.
- Without surgery, these wounds heal by wound contracture with epithelialization around the wound edges.
- Scarring is severe with contractures; complete spontaneous healing is not possible.
Fourth degree burns
Fourth-degree burns are deep and potentially life-threatening injuries that extend through the skin into underlying soft tissue and can involve muscle and/or bone.
Name 3 methods of burn area estimation
Lund browder chart (most accurate, especially in children)
Rule of 9’s
Palm method
what depths of burn are included in burn area estimations
All except superficial burns are included
Modified Lund Browder chart
The most accurate method of burn area prediction
Rule of Nines
For adult assessment, the most expeditious method to estimate TBSA in adults is the “Rule of Nines”
- Head represents 9 percent TBSA
- Each arm represents 9 percent TBSA
- Each leg represents 18 percent TBSA
- The anterior and posterior trunk each represent 18 percent TBSA
Palm method of burns area estimation
Small or patchy burns can be approximated by using the surface area of the patient’s palm.
- The palm of the patient’s hand, excluding the fingers, is approximately 0.5 percent of total body surface area
- The entire palmar surface including fingers is 1 percent in children and adults
Signs of airway injury in burns
- Persistent cough, stridor, or wheezing
- Hoarseness
- Deep facial or circumferential neck burns
- Nares with inflammation or singed hair
- Carbonaceous sputum or burnt matter in the mouth or nose
- Blistering or edema of the oropharynx
- Depressed mental status, including evidence of drug or alcohol use
- Respiratory distress
- Hypoxia or hypercapnia
- Elevated carbon monoxide and/or cyanide levels
Who should receive formal fluid resuscitation in burns
>15% TBSA
- Calculated as any burn greater than superficial
Choice of crystalloid in burns resus
Hartmanns or Lactated Ringers
How are burns resuscitaion fluids managed
The Parklands formula
- The traditional formula is
- 4ml x (patient body weight in kg) x (TBSA in %)
- Half is given over the first 8 hours
- Half over the subsequent 16 hours
- This is likely to overestimate fluid requirements
- 4ml x (patient body weight in kg) x (TBSA in %)
- In our local unit a modified Parklands of 3ml/kg/TBSA% is used for initial resus
An early switch to goal directed therapy and urine output monitored resuscitation is recommended with a goal of 0.5ml/kg/hour
- there is evidence that this improves outcomes
FAMMM diagnostic criteria
Recommendations on surveillance
Diagnostic criteria debated but:
- Large number of naevi at an early age
- Multiple atypical naevi (at least 2)
- Classical description is >100 naevi
- At least one >8mm
- One or more atypical
Screening should begin at 10 years of age, melanoma may develop in teens
- Monthly self exam and specialist dermatologist review recommended
Discuss the anatomical issues associated with IVC obstruction in groin hernia surgery
The inferior epigastric vessels (both superficial and proper) form anastomotic arcades with the superior epigastrics and form the thoracoepigastric veins
- These are a site of large volume shunting from IVC to SVC in IVC obstruction
What are the borders of a femoral hernia neck
Medial
- lacunar ligament
Posterior
- pectineal ligament
Anterior
- inguinal ligament
Lateral
- femoral vein
High risk SCC size
2cm or greater
What are the medical treatment options in metastatic melanoma
BRAF inhibitors
- vemurafenib
PD1 inhibitors
- pembrulizumab
Systemic chemotherapy
- doxirubicin
- not very effective and quite toxic
What are the 5 key characteristics to consider in mesh for hernia repair
how does each effect the repair
Elasticity and tensile strength
- mesh must be able to conform to the abdominal wall in motion or it would cause distorsion, tissue disruption and pain
- tensile strength of 16 N/cm2 is the maximum tensile strength required
Porosity
- large pores permit integration with tissues and most importantly integration of immune competent tissue
- microporous meshes <100µm are associated with chronic infection and fibrosis
Density (weight)
- lower density meshes have lower burden of foreign body per unit area, they therefore are associated with a decreased inflammatory response and better tissue integration.
Constitution
- mesh can be either monofilament or polyfolament weave
- the microporous areas within polyfilament weave are associated with increased bacterial infection
- monofilament is generally more stiff
Absorption
- mesh can be either absorbable or non absorbable
- absorbable mesh relies on scar formation which is never as strong as the initial tissue and may increase the risk of recurrence
- non absorbable mesh may stiffen and contract over time and if there is infection it will persist
What is your prefered mesh choice in a routine Lichtenstein hernia repair
why
Atrium prolite mesh
- good tensile strength (too high at 138 N/m2)
- lightweight (80g/m2)
- polypropylene monofilament construction
- nonabsorbable
- large pore size (0.8mm)
