CHAPTER 07 : SKIN Flashcards
What is a neoplasm?
What is a malignant neoplasm?
What is a harmartoma?
A neoplasm is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissues and which persists in the same excessive manner after cessation of the stimulus which evoked the change.
A malignant neoplasm is one that invades surrounding tissues and has a propensity to metastasise.
Hamartoma = a developmental anomaly resulting in the formation of a mass composed of tissues normally present in the locality of the mass, but of improper proportion and distribution with dominance of one type of tissue
What is the aetiology of neoplasms?
Initiation = change in the genome of the cell Promotion = change made permanent by cellular division (initiators and promoters include UV and ionising radiation, chemical carcinogens, viruses) Progression = further cell division to form an invasive tumour.
Inappropriate activation of proto-oncogenes to become oncogenes – these proto-oncogenes encode growth factors, growth factor receptors or transcription factors
Inactivation of other cellular genes – tumour suppresser gene mutation:
o P53 tumour suppressor gene is mutated in the majority of human cancers
What is a BCC?
BCC is a malignant tumour of cells derived from the basal layer of epidermis
A malignant tumour of cells derived from pluripotential cells of the epidermis or outer root sheath of hair follicles
most common skin tumour in Caucasians (lifetime risk 23-39% of Whites in US)
What are the risk factors for BCC?
HOST FACTORS
Genetic, skin type, precursors, immunological
ENVIRONMENT
UV, radiation, chemicals
Name the Fitzpatrick skin types
Type 1 → White skin never tans – always burns
Type 2 → Pale skin - burns on exposure – usually burns
Type 3 → Light skin which will tan – may burn
Type 4 → Mediterranean complexion – rarely burns
Type 5 → Indian Complexion – rarely burns
Type 6 → Black skin – rarely (?never) burns
What aetiological factors are associated with BCC?
UVB actinic damage chronic wounds (Marjolin's ulcer) Chemicals - polycyclic aromatic hydrocarbons, arsenicals, nitrogen mustard Immunosuppression - 50-100x risk Malignant transformation of Sebaceous naevus of Jadassohn 10-15% transform into BCC, trichoblastoma and adnexal hamartomas Rhinophyma - 10% have underlying BCC
What genetic diseases are associated with BCC?
Gorlin’s syndrome (basal cell naevus syn)
- AD
- assocd with palmar pits frontoparietal bossing, overdeveloped supraorbital ridges, odontogenic keratocysts of jaw, sebaceous cyst, abnormal ribs and vertebrae, dural calcification (falx cerebra), high arched palate, learning difficulties
Xeroderma pigmentosum
- AR
- primary deficiency of endonuclease enzyme
- unable to repair UV damaged DNA
Albinism
What is a high risk BCC?
- Poorly defined margin
- Recurrent disease
- > 6mm diameter mask area
- > 10mm diameter cheeks, forehead, scalp, neck
- > 20 mm diameter trunk and extremities
- Morphoeic, sclerosing, infiltrative, micronodular
- Immunosuppressed
- Perineural involvement
What are the histological types of BCC?
1. Localised Nodular 50% Nodulocystic Micronodular Pigmented 2. Superficial / Multifocal 10% 3. Infiltrative Morpheaform (=sclerosing/fibrosing) 2% undefined (10%) Basosquamous
What are the clinical features of BCC?
85% H&N danger areas - periorbital, ear, nl fold pinkish pearly nodules, rolled edges, telangectasia, central ulcer, may be pigmented longstanding tumours invade deep 200+ recorded cases of mets
Histology - atypical cells arranged in palisades and well organised surrounding stroma
What is the treatment for BCC?
Telfer's paper 2008? SURGICAL EXCISION excision margins 2-5mm 3mm = 85% clearance 4mm = 95% Morphoiec 15mm = 95% clearance
30-40% incomplete margins recur
residual tumour found in 45-54% re-excision of incompletely excised lesions
embryonic fusion line areas more prone to deep invasion - medial canthus, EAM, alar base
Recurrence rates 4.5%
Other Rx (cure rate)
EFUDIX
DXT 92%
CRYOTHERAPY
CURETTAGE AND CAUTERY 75%, up to 95% for selected small tumours
PDT - aminolevulinic acid cream = sensitiser
tumour cells convert this to photoactive porphyrins
6hrs later - laser / red light - destroys tumour cells
painful, only Rx tumours
MOHS MICROGRAPHIC 99%
(INTRALESIONAL INTERFERON / BCG)
When is Moh’s micrographic surgery indicated? (US)
areas with high recurrence rate poorly delineated / arising within scar tissue >2cm / aggressive malignant features morphoeic / sclerosing BCC impt areas to preserve uninvolved tissue eg eyelid SCC w perineural invasion microcystic adnexal ca DFSP desmoplastic MM recurrent BCC
How is Moh’s surgery performed?
- debulk tumour
- saucer shaped disk of tissue is excised, oriented, mapped, sectioned and placed on slides for microscopic examination (H&E stain)
- remaining tumour is removed only from the mapped site
What topical therapies are there for non-melanoma skin cancers?
Imiquimod (Aldara)
Imiquimod - Aldara (3x/wk for 4 wks)
- activates host immunity against tumour cells, leading to anti-tumour cytotoxic T cell response
- immuno-enhancing drug
- toll-like receptors on macrophages, Langerhans cells and dendritic cells are activated and upregulates Th1 lymphocyte mediated immune response, releasing cytokines that are tumorcidal
- 5% licensed for biopsy-confirmed superficial BCC >2cm diameter
- curettage then imiquimod may improve its efficacy
- metanalysis showed higher efficacy for Rx of AK and BCC (89-93% treated)
Side effects - local
erythema, erosion, ulceration, dyschromia (hyper hypopigmentation). (systemic - rare flu-like symptoms)
AK - 5 days/wks 4wks
BCC - 5 days/wks 6wks
5 - Fluoruracil (Efudix)
Diclofenac (Solaraze)
5-FU (BCC bd for 3wks, Bowen’s 5 days/wk for 3wks)
incorporated into RNA and inhibits DNA formation by covalent bonding
This blocks thymidylate synthase, DNA and protein synthesis is halted leading to necrosis
Side effects - erythema, erosion, ulceration, delayed wound healing esp lower limbs elderly
Diclofenac - Solaraze
3% diclofenac with hyaluronic acid
inhibit COX2, may inhibit neoplastic cell proliferation by inducing apoptosis
What other treatments are there for NMSCs?
5FU and Imiquimod 75-80% for superficial BCCs
Radiotherapy 96%
- Fractionated, 10 sessions over 2wks
- Very good results esp lower eyelids (globe protected with lead shield)
Photodynamic therapy 82%
- involves use of light source to activate a compound (photosensitizer) within malignant cells.
- Compound then transfers energy to molecular oxygen and destroys tumour cells.
ALA - aminolevulinate
MAL - methyl-ALA
Electrodessication and Curettage 70% (80-90% in appropriately selected pts)
Cryotherapy
- reported up to 96% efficacy
Laser
Moh’s micrographic surgery 99%
Chemical Peels - for precancerous conditions
- iatrogenic creation of cutaneous wound, chemical escharotic that damages the epidermal and dermal layers for therapeutic purposes and allow collagen remodelling and reepithelialisation
Intralesional methotrexate, interferon, 5FU, bleomycin
How does radiotherapy for NMSCs work?
Indications
Elderly pt not fit for surgery
Cosmetically sensitive areas eyelids, canthi nose, ears, lips
Young pts more likely to suffer effects of radiotherapy induced skin cancers later in Iife
Relatively painless,
superficial XR or electrons fractionated over 10 sessions in 2wks
Side effects - erythema, soreness, ulcerate, crust, pale atrophic, patchy, telangectasia on skin in longterm
How is PDT administered?
5 aminolaevulinate cream
Methyl-aminolaevulinate cream
Applied to lesions and cover with occlusive dressing for 4hrs
Dysplastic cells preferentially take this up and an excess of intracellular protoporphyrins result, which is an endogenous photosensitiser
Red light is shone and this activates the protoporphyrins
Highly reactive free radicals are produced and this leads to cell death
What is SCC?
Malignant tumours of cells originating from stratum spinosum of epidermis
occurs in skin w
- AK, keratin horn, leukoplakia, Bowen’s, chronic wound
Histo - dysplstic epidermal keratinocytes extend down through bm into dermis (invasion)
well, mod, poorly differentiated
Poor prognosis if
- depth of invasion
- vascular invasion
- perineural invasion
- lymphocytic infiltration
What are the different types of SCC?
Verrucous
ulcerative
variants
spindle cell
verrucous ca
keratoacanthoma
little prospective evidence of excision margins
usu b/t 5mm - 1cm depending on site
What is the commonly quoted paper for SCC and what are the recommended excision margins?
Multiprofessional guidelines for the management of the patient with primary cutaneous squamous cell carcinoma. Brit J Dermatol 2002
High risk
Location - ear, lip, nose, eyelids, scalp
Diameter - 2cm+ are twice as likely to recur locally and 3x more likely to metastasise than smaller tumours
Depth of invasion - 4mm+ (45% incidence of mets)
Histological differentiation - poorly differentiated and perineural involvement
Host immunosuppression
Low risk = 4mm
High risk = 6mm
What is malignant melanoma?
malignant tumour of epidermal melanocytes
with invasion into dermis
How is MM classified?
SNALAD
Superficial spreading (60%)
Nodular (30%)
Lentigo maligna melanoma (7%)
Acral lentiginous (2-8%) (Subungal - Hutchinson’s sign)
Amelanotic (1-3%)
Desmoplastic (spindle cell, neurotropic) (<1%)
What is Spitz naevus?
juvenile melanoma
histologically looks like melanoma
but clinically looks benign, treated as benign
What is the epidemiology of melanoma?
<5% of skin cancer cases 75%-90% of all skin cancer mortalities UK 6/100,000 Commonest cancer of young adults Lifetime risk 0.5% F:M 2:1
Tell me about the mutation of BRAF oncogene.
- Mutations in the BRAF gene allow for BRAF to signal independently of upstream cues,
and results in overactive downstream signaling. - This leads to excessive cell proliferation and survival, independent of growth factors
Oncogenic BRAF has been implicated in: ~50% of melanoma tumors ~40% of papillary thyroid tumors ~30% of serous ovarian tumors ~10% of colorectal tumors ~10% of prostate tumors
Vemurafenib is an orally available, selective BRAF (V-raf murine sarcoma viral oncogene homolog B1) inhibitor for patients with unresectable or metastatic melanoma that tests positive for the BRAF V600E mutation
What is the aetiology of melanoma?
Risk factors PPARENTS Premalignant lesions (giant CMN, acquired MN, dysplastic naevi, lentigo maligna) Previous melanoma (3-5% of 2nd) Age Race Economic status (higher 3x risk) atypical Naevus syndrome (>100 atypicals) Fitzpatrick Type skin 1&2 Sunburn
What genetic factors predispose to MM?
FHx (5-12% have +ve FHx)
1st degree relative 1.8 RR
BRAF proto-oncogene mutation (assoc w papillary thyroid ca, colorectal ca, non-small cell lung ca, leukaemia
tumour suppressor genes, oncogenes CDKN2A gene mutation (regulates cell cycle during G1 checkpoint)
dysplastic naevus syndrome (Familial atypical multiple mole melanoma FAMMM
xeroderma pigmentosum
Pigmented lesion: ?melanoma, what are the differential diagnoses?
Acquired melanocytic naevus, dysplastic
dermal melanocytoses
pigmented BCC, basal cell papilloma, blue naevus, AK
pyogenic granuloma (amelanotic), SCC
How is MM diagnosed?
Glasgow 7-point checklist (Mackie)
Major (SSC - Size, Shape, Colour)
1 Change in size
2 Irregular shape (esp. SSM and LMM not nodular)
3 Irregular colour
Minor (DISC diameter, Inflammation, sensory, crusting /bleeding)
4 Over 7mm
5 Inflammation
6 Oozing
7 Altered sensation/itch
Any major or any 3 minor = suspicious - biopsy whole lesion with 2mm margin
American ABCD System: A = asymmetry B = border irregular C = colour more than 1 D = diameter over 6mm E = elevation (late feature) Plaster on mole = bad sign
WHAT IS THE MINIMUM DATASET FOR MM REPORTING?
Specimen (site)
Specimen type (excision, incisional (etc)
Gross description (size, max diameter, nodule, border, pigmentation)
Histology (LM, SS, nod, AL, desmoplastic, neurotropic, other)
Growth phase (insitu, invasive, radial, vertical)
Breslow thickness mm Clark level ulceration lymphatic / blood vessel invasion perineural invasion regression microsatellites co-existent naevus mitotic rate tumour infiltrating lymphocytes
Excision margins
deep and peripheral
Pathological staging TNM
What tumour markers are there for MM?
check
H&E staining - older, more crude
newer
FISH - fluorescent in situ hybridisation
genomic hybridisation
Tyrosinase (PCR)
S-100 – detects progression
TA-90 – risk of mets
HLA-DQB1*0301 – experimental, identifies metastasis prone pts
How is Breslow depth measured?
How is Clarks level measured?
from granular layer to deepest melanoma cell Clark 1969 I epidermis II into papillary III all papillary IV invasion of reticular V invasion of sc fat
what is the 5 year survival rate according to stage?
Stage Ia: 95%, Ib: 90%
Stage IIa: 80%, IIb: 65%, IIc: 45%
Stage IIIa: 65%, IIIb: 50%, IIIc: 25%
Stage IV: 8%
How is tumour thickness classified?
TX - Primary tumor cannot be assessed (shave biopsy, regressed primary)
Tis - Melanoma in situ
T1 - ≤1.0 mm (a: without ulceration, b: with ulceration)
T2 - 1.01-2.0 mm (a: without ulceration, b: with ulceration)
T3 - 2.01-4.0 mm (a: without ulceration, b: with ulceration)
T4 - < 4.0 mm (a: without ulceration, b: with ulceration)
What is the N and M classification of melanoma?
N classification is as follows:
N1 - 1 lymph node; a: micrometastasis (clinically occult), b: macrometastasis (clinically apparent)
N2 - 2-3 lymph nodes; a: micrometastasis, b: macrometastasis, c: in transit met(s), satellite(s), without metastatic lymph nodes (N2a: 2-3 nodes positive for micrometastasis; N2b: 2-3 nodes positive for macrometastasis; N2c: In transit met(s) or satellite(s) without metastatic nodes)
N3 - 4 or more metastatic nodes or matted nodes or in-transit metastases or satellite(s) with metastatic node(s)
Note that micrometastases are diagnosed after elective or sentinel lymphadenectomy. Macrometastases are defined as clinically detectable nodal metastases confirmed by therapeutic lymphadenectomy or when nodal metastasis exhibits gross extracapsular extension.
M classification is as follows:
M1a - Distant skin, subcutaneous, or nodal metastases, normal lactate dehydrogenase (LDH) level
M1b - Lung metastases, normal LDH level
M1c - All other visceral metastases or any distant metastases with an elevated LDH level
How is MM staged?
Stage 0 - Tis, N0, M0
Stage IA - T1a, N0, M0
Stage IB - T1b, N0, M0; T2b, N0, M0
Stage IIA - T2b, N0, M0; T3a, N0, M0
Stage IIB - T3b, N0, M0; T4a, N0, M0
Stage IIC - T4b, N0, M0
Stage III - Any T, N 1-3, M0
Stage IIIA - pT1-4a, N1a, M0; pT1-4a, N2a, M0
Stage IIIB - pT1-4b, N1a, M0; pT1-4b, N2a, M0; pT1-4a, N1b, M0; pT1-4a, N2b, M0; pT1-4a/b, N2c, M0
Stage IIIC - pT1-4b, N1b, M0; pT1-4b, N2b, M0; any T, N3, M0
Stage IV - Any T, Any N, Any M
What is the evidence of excision margins for primary melanoma excision?
*1.0-cm margin for primary melanomas less than 1.0 mm in thickness.
(Diagnosis and treatment of early melanoma. NIH Con- sensus Development Conference. January 27–29, 1992. Consensus statement/NIH Consensus Development Conference 1992)
*1.0-cm margin may also be effective for lesions up to 2 mm in thickness.
Veronesi U, Cascinelli N, Adamus J, et al. Thin stage I primary cutaneous malignant melanoma: comparison of excision with margins of 1 or 3 cm. N Engl J Med. 1988
*1.0 - 2.0 cm margins are commonly used for lesions between 2 and 4 mm in thickness.
*2.0-cm margin may be most appropriate for melanomas 4 mm or more in thickness.
Balch CM, Urist MM, Karakousis CP, et al. Efficacy of 2cm surgical margins for intermediate-thickness melanomas (1–4 mm): Results of a multi-institutional randomized surgical trial. Ann Surg. 1993
Heaton KM, Sussman JJ, Gershenwald JE, et al. Surgical margins and prognostic factors in patients with thick (>4 mm) primary melanoma. Ann Surg Oncol. 1998
*Margins greater than 2.0 cm do not appear to contribute significantly either to survival or local control
Heaton (as above)
McKinnon JG, Starritt EC, Scolyer RA, et al. Histopathologic excision margin affects local recurrence rate: analysis of 2681 patients with melanomas < or =2 mm thick. Ann Surg. 2005
Evidence for melanoma excision margins
WHO Trial - Veronesi et al (NEJM 1988) - Thin MM
For melanomas less than 2 mm there was no difference in survival between 1 and 3 cm excision however 3 patients with 1cm excisions had local recurrence vs. none with wider excision.
Balch et al (Ann Surg 1993) - Intermediate to Thick
For intermediate thickness melanomas 1-4 mm there was no difference between 2 and 4 cm excision margins.
Karakousis (Ann Surg Oncol) also found that 2 cm margins were as effective as 4 cm in local
control of intermediate thickness (1-4 mm) melanoma
UK melanoma study group/BAPS trial (Meiron Thomas 2004) - Thick MM
1cm v 3 cm in 2mm or thicker MM
1 cm margin is assoc with greater risk of local recurrent but NO different in overall survival at 60 months.
Heaton et al. (Ann Surg oncol 1998) found that there was no difference between excisional margins of < 2 cm and > 2 cm in thick lesions but this was a retrospective study.
What is the evidence for excision margins?
WHO trial (Veronesi 1988)
- thin MM 2mm
- 1cm vs 3cm excision margins
- 1cm: greater risk of local recurrence
- no survival benefit at 60mths
Heaton (1998) retrospective
- thick lesions
- no diff b/t 2cm excision margins
Gillgren Scandinavian study 2011 Lancet
- 936pts
- > 2mm (Clinical stage IIA-C)
- 2 cm vs 4cm excision margins
- There was no significant difference in overall survival (65% in both groups; P = .69) or recurrence-free survival (56% in both groups; P = .82) between the 2 approaches at 5 years
What evidence is there for ELND for stage II?
Veronesi WHO trials (1998) - no survival benefit
The sentinel node biopsy debate in MM
SNB only investigation that upstages from II-III or clinically palpable nodes MSLT-1 trial (Morton et al 2006) - 1.2 - 3.5mm - SLNB vs watch and wait - provides prognostic indicator - SLNB +ve proceed to CLND - 6% survival benefit
What investigations are there for stage II disease?
SLNB if offered
CXR
CT
liver USS
What is the clinical staging and 5 year survival of MM?
clinical staging
0 Tis
IA T1a 95
IB T1b or T2a 90
IIA T2b or T3a 80
IIB T3b or T4a 65
IIC T4b 45
III Any T, N+, No M (clinical)
IIIA no ulceration N1a or 2a 65
IIIB ulcerated N1a or b 50
no ulceration N1b/2b/2c
IIIC ulcerated N1b/2b/2c 25
ulc / no ulc N3
IV Any M 8%
What is the management of Stage III melanoma?
IIIa - SLNB positive microscopic disease
IIIb - clinically palpable macroscopic disease
IIIc - intransit mets
Pts with clinical stage III and pathological IIIB are given high dose interferon in most units
MSLT 2 trial - looking at +ve SLNB - immediate CLND or watch and wait.
Veronesi WHO - 2 prospective trials showed no benefit
Balch (1996) and Cascinelli (1998) found benefit in immediate CLND
What is the manangement of Stage IV melanoma?
Chemotherapy - 15% response Immunomodulatory agents (high dose interferon, cisplatin, IL2) - marginal effect on survival Radiotherapy (local, cerebral mets) ANTI CTLA4 AB TRIALS Tremelimumab IgG2 & Ipilimumab
What treatment is there for Stage IV MM?
- Immunotherapy
- Ipilimumab
- Interleukin-2 (IL-2) - Signal transduction inhibitors
- Vemurafenib (for patients who test positive for the BRAF V600 mutation). - Chemotherapy
- Palliative local therapy
Merkel cell tumour
tumours of mechanoreceptors of neural crest origin
worst prognosis of all skin lesions
50% H&N, elderly
resembles oat cell ca of lung (CXR to rule out lung primary)
locally aggressive, metastasise
Rx - WLE and DXT
Adenoid cystic carcinoma
Malignant tumour of eccrine glands mainly scalp
ACC usu in salivary, lacrimal and mucous glands of URT
Rx WLE, not DXT sensitive
Sebaceous carcinoma
malignant growth differentiating towards sebaceous epithelium
rare (0.2% of all skin cancers)
3rd most common eyelid tumours
50% periorbital, yellowish nodules, mets uncommon
Rx WLE
Sweat gland carcinoma (incl. eccrine porocarcinoma)
Malignant epithelial tumour of sweat glands
rare, middle age +
painful reddish nodules with dermis, firm/hard, irregular
can met
WLE +/- SLNB
What are the borders of the axilla?
Ant - pec major & minor
Post - LD, teres major & subscapularis
Med - serratus, 1st 4 ribs & intercostals
Lat - humerus, coracobrachialis, biceps
apex - 1st rib, scapula, clavicle, subclavius
Base - axillary fascia, fat, skin
What are the important nerves to preserve? Which nerve is sacrificed?
long thoracic thoracodorsal medial pectoral lateral pectoral Intercostobrachial - usu sacrificed
What are the branches of the axillary artery?
SALSAP 1st - superior thoracic 2nd - thoracoacromial - lateral thoracic 3rd - subscapular - anterior circumflex humeral - posterior circumflex humeral
What are the borders of the femoral triangle?
Femoral Triangle Borders o Medial border of sartorius o Medial border of Adductor Longus o Inguinal Ligament o Floor – Iliopsoas and Pectineus o Roof – Fascia
What types of incisions are there for groin dissection? What are the pros and cons of each?
Longitudinal / lazy S
- good access to femoral triangle
- can be extended superiorly if ilioinguinal dissection needed
Transverse incision
- poor visualisation of apex of triangle
- theoretically increases chances of lymphoedema
How do you locate the lateral femoral cutaneous nerve?
2cm medial to ASIS under fascia overlying sartorius
What nodes are removed in a suprainguinal groin dissection?
external iliac nodes (skeletonise EIA) obturator nodes (in obturator fat pad)
Describe how a groin dissection is performed
o Curvilinear Incision o Thick medial and lateral flaps o Identify apex, medial and lateral borders o Elevate tissue off femoral N, A, V o Ligate long saphenous o mark specimen o Identify lat cut n of thigh o perform sartorius switch o if iliac node dissection performed, no need to divide ligament (send as 2 specimens)
What are the definite indications for suprainguinal dissection?
What are the relative indications?
BAPRAS guidelines
Definite
- macroscopic disease in iliac/obturator nodes
- 2+ inguinal nodes (micro/macro)
- Cloquet +ve
(- +ve SNB above ligament)
Name some benign epithelial tumours
Seborrhoeic Keratosis Digital Fibrokeratoma Keratoacanthoma Actinic Keratosis Bowens Others - Squamous papilloma, viral wart, keratin horn,
Classify the benign dermal tumours
Hair follicles → Trichilemmal cyst, Trichofolliculoma, Tricholemmoma, Tricho-epithelioma, Pilomatrixoma (Benign Calcifying Epithelioma of Malherbe) (ghost cells on histo)
Sebaceous Glands → Sebaceous Adenoma, Sebaceous Hyperplasia, Sebaceous Naevus of Jadassohn
Sweat Gland - Eccrine Gland → Syringoma, Acrospiroma (Eccrine poroma), Cylindroma
Neural Tissue → Neurofibroma
What types of benign pigmented lesions are there?
Naevus cell naevi
Congenital → Giant hairy naevus (GHN) or Non GHN.
Acquired → Junctional, Compound, Intradermal
Special → Spitz, Dysplastic, Halo
Melanocytic naevi
Epidermal → Ephelis, Lentigo, Café-au-lait patch, Becker’s naevus, Albright’s syndrome.
Dermal → blue naevus, Mongolian blue spot, Naevus of Ota, Naevus of Ito
Name some cystic lesions found in the skin
Epidermoid cysts
Pilar cysts
Milia
Xanthelasma
What does LASER stand for?
Light Amplification by Stimulated Emission of Radiation
Explain how LASER works
A device that transforms 1 type of energy (electrical) into optical energy
- Laser medium is energised to excite electrons into a higher energy state.
- As electrons move back into a stable orbit, it emits a photon of light of a particular wavelength.
- These photons hit other excited electrons producing more photons.
- The photons are reflected back and forth by 2 mirrors to put them in phase and parallel to each other.
- One of the mirrors only partly reflects – allowing some photons to escape.
light beam is
- collimated
- monochromatic (single wavelength)
- coherent (in phase)
Q-Switching = Pulsed - ‘giant pulse formation’ – produces a short-pulsed output beam - if full bath = energy, like suddenly taking bottom of bath away - dump of energy
What are the uses of LASER and what is recommended for each?
- Ablation of vascular lesions
(a) haemangioma, capillary malformation - pulsed yellow dye
(b) venous & venolymphatic malformn - KTP / Nd:Yag - Skin resurfacing - CO2, Erbium:Yag (water)
- Benign cutaneous lesions - CO2
- Benign pigmented lesions - IPL, diode, ruby
- Hair removal - Long Pulsed Ruby, Long Pulsed Alexandrite, diode, Nd:YAG, IPL
- Tattoo removal - Q-Switched Nd:Yag, Ruby, Alexandrite
Explain laser safety
Class IV devices Potential fire eye & skin hazard Safety equipment - wavelength specific goggles - warning signs - windows covered - remove / cover all reflective surfaces, incl instruments
wet drapes to protect patient from scatter
be aware of laser use near oxygen source
plume hazards - use special masks, plume evacuator, shave bulk of lesion 1st
lasers operated only by those who have received formal training in laser theory, control techniques, and operation, laser nurse
fire extinguishers
What happens to the laser energy when it hits skin?
STARR
- scattered
- transmitted
- absorbed - light energy transferred to target cells and turned into heat energy, causing coagulation and vaporisation
- reflected
- refracted
What does a laser device consist of?
- Energy source
- electricity (argon)
- flashlamp (PDL)
- another laser (CO2) - Laser medium (solid or gas)
- Laser cavity (resonator)
active medium excitation mechanism feedback mechanism (high reflectance mirror), output coupler (partially transmissive mirror)
Can you summarise the types of skin tumours found in the epidermis and dermis?
- The Epidermis → Epithelial Tumours
Seborrhoeic Keratosis,
Digital Fibrokeratoma,
Keratoacanthoma,
Actinic Keratosis
Others - Squamous papilloma, viral wart, , keratin horn, Bowens - The Dermis
Hair follicles → Trichilemmal cyst, Trichofolliculoma, Tricholemmoma, Tricho-epithelioma, Pilomatrixoma (Benign Calcifying Epithelioma of Malherbe)
Sebaceous Glands → Sebaceous Adenoma, Sebaceous Hyperplasia, Sebaceous Naevus of Jadassohn
Sweat Gland - Eccrine Gland → Syringoma, Acrospiroma (Eccrine poroma), Cylindroma
Neural Tissue → Neurofibroma
Name some benign cystic skin lesions and pigmented lesions
3. Cysts Epidermoid cysts Pilar Cysts Milia Xanthelasma 4. Pigmented Lesions Naevus cell naevi Melanocytic naevi
Epidermal - what is a seborrhoiec keratosis?
SK = Seborrhoeic Wart, Senile Wart, Basal Cell Papilloma
Incidence
- M=F, Over 50, Caucasians
- Stucco Keratosis – non pig SK on limbs
- Dermatosis papulosa nigra – multiple facial SK, dark skin, early onset
Aetiology
- Familial – AD
- Inflammatory dermatosis
- Visceral malignancy manifestation
- Oestrogen administration
Pathology
- Accumulated immature keratinocytes b/n basal and keratinizing layers
- Acanthosis – thickening of epidermis
- Elongated dermal papillae
- Rarely malignant transformation (SCC)
Clinical
- Verrucous plaque
- Face hands and upper trunk
- May be pigmented
- May bleed, get inflamed, itch, shed, reform
Treatment
- Curettage or excision
- Cryotherapy
- Topical TCA
Epidermal - What is a keratoacanthoma?
- Rapidly evolving tumour → resolves
- Keratinizing squamous cells originating in pilosebaceous follicles
Incidence
- Caucasian, 40+, M>F 3:1, 1/3 freq of SCC
Aetiology
- Sun, Coal, Tar, carcinogenic hydrocarbons, Injury and infection inc SSG donors, Assoc with Ca larynx, internal ca, leukaemia, deficient cell-mediated immunity.
Pathology
- Keratin-filled crypt, Rapidly dividing squamous cells from skin appendages, Atypical mitosis and loss of polarity
Clinical
- Globular tumour
- Keratin plug or horn
- Radial symmetry
- Resolution after 6 weeks ~ 3 months, leaves depressed scar
- Face, dorsum hand
- Ferguson-Smith syndrome (single gene mutation on West Scotland) → AD + multiple self healing epitheliomas which look and behave as KA.
- Torre’s syndrome = multiple internal malignancies, KA’s and sebaceous adenomas
- Distinguish from SCC
Treatment
- Excise to get good specimen
- Spontaneous resolution leaves unsightly scar
- 5 FU and radiotherapy shorten time to resolution
Epidermal - What is actinic keratosis?
- Scaly crusted areas in sun exposed areas of elderly pts
- 20-25% develop into SCC
Treatment
- Efudix (5FU) or
- Solaraze (Diclofenac) gel
Benign epithelial tumours - others
Others
Digital fibrokeratoma - papillary / keratotic outgrowth in finger near joint
Squamous papilloma - Skin tag or acrochordons → excise
Viral Warts - HPV → cryotherapy or curettage
Keratin Horn - Hard protruding lump of cornified material, Likely to have an AK or SCC in the base
Bowens - Red scaly lesion on the legs of elderly patients, Histology resembles SCC, limited to epidermis → in situ, can progress to SCC so worth removing
How do you classify benign dermal tumours?
Hair follicle
Sebaceous gland
Sweat gland
Neural tissue
What are the hair follicle tumours are commonly found in adults?
- Trichilemmal cyst
- Sebaceous cyst of hairy skin
- Scalp, F>M, middle age, AD
- Rupture → cell proliferation, occasional malignant change
Treat → excision - Trichofolliculoma
- Multiple malformed hair roots arising from an enlarged follicle canal
- Keratin-filed crater, mainly face
- White Hairs from a central punctum
- Histology like BCC But contain keratin-filled macrocysts - Tricholemmoma
- Hair follicle tumour – clinically like BCC
- Small warty papules
- Cowden’s syndrome → Multiple facial tricholemmomas, Keratoses on palms and soles, Oral polyps, Breast Cancer in 50% of patients
- Plaques of squamous cells containing glycogen
- Face, middle aged → elderly men
What are the hair follicle tumours can be found in children?
- Tricho-epithelioma
- Epithelial tumour differentiating towards hair follicle cells
- Rare, at puberty, AD
- Path – rounded masses of fusiform cells, Keratin filled lacunae
- Malignant change to BCC
- Clinical – pinkish nodules, cheeks and eyelids and NL folds, (around mouth)
- often misdiagnosed as BCC, or MM if pigmented
- Treatment – Excision
Pilomatrixoma (Benign Calcifying Epithelioma of Malherbe)
- Hamartoma of dead calcified cells which resemble hair matrix
- Uncommon, M assoc with myotonia atrophica
- Path – Well circumscribed dermal tumour, cells mature out to inner layers
- Central calcification and ghost cells, no basophilic granules
- Clinical – Dermal, s/c tumour, Head/neck/upper limb.
- Stony Hard lesion on the face of a child.
- Treat by excision
Name some sebaceous gland tumours
- Sebaceous Adenoma (Sebaceous Carcinoma)
- Sebaceous Hyperplasia
- Sebaceous Naevi (of Jadassohn) (Organoid Naevus)
What is sebaceous adenoma?
- Sebaceous Adenoma → smooth papules on scalp of elderly
- Benign tumour of incompletely differentiated sebaceous cells
- Rare, mainly elderly
- Path – multilobular tumour of upper dermis, small basophilic sebaceous matrix cells and larger cells with fat globules
- Clinical Ulcers/plaques/sessile/pedunculated Yellowish, Face/scalp, Sudden ↑ growth
- Treat – Excision, Radiosensitive
What is sebaceous hyperplasia?
- Small yellowish lesions usually found on face → can look clinically like BCC
- Severe seb hyperplasia of nose = rhinophyma
What is sebaceous naevus (of Jadassohn) (Organoid Naevus)?
- Normally present at birth but usually enlarges and becomes raised in puberty, due to hyperplasia of the sebaceous glands.
- Usually removed - 20-30% chance of mailgnant transformation → BCC / mixed appendigeal tumour (rare)
Name 3 sweat gland tumours
- Syringoma
- Acrospiroma
- Cylindroma
What is a syringoma?
aka Papillary Eccrine Adenoma
- Benign tumour of eccrine sweat gland origin
- Uncommon, F>M, adolescence, multiple with Downs
Path
- Convoluted sweat ducts in upper dermis, tail like (tadpole) projections of cells
Clinical
- Small yellow dermal papules ,<3mm, Cystic, release clear fluid on injury,
- Chest face neck, may look like tricho-epithelioma or xanthelasma
Treatment
- Excision, Intralesional desiccation, Laser
What is Eccrine Acrospiroma (Eccrine poroma)?
- Tumour from eccrine sweat duct epithelium
- Epidermal, juxta or dermal
- Eccrine poroma commonest
- M=F, middle age, usually acral
Path
- Sweat gland duct proliferation, cells with glycogen and glycolic enzymes
- Overlying hyperkeratosis. Malignant change (malignant eccrine poroma) reported
Clinical
- Hyperkeratotic plaque on sole or palm, may ulcerate
Treatment – Excision
What is a Dermal Cylindroma (Dermal Eccrine Cylindroma, Turban Tumour, Spiegler’s Tumour)?
- Derived from coiled part of sweat gland (part secretory and part duct)
- Uncommon F>M 2:1, Often AD, Early adult
Path
- columns of cells with hyaline between large and small (peripheral) cell types
Clinical
- Scalp and adjacent skin. Pinkish fleshy tumours, Hairless and multiple, maybe painful
- Large or multiple = Turban tumour
- Malignant change very rare
- Distinguish from trichilemmal cyst
Treat – excision
What benign tumours of neural tissue are there?
Neurofibroma
- Skin coloured nodules composed of neural tissue and keratin
- Neurofibromatosis (von Recklinghausen’s disease) = Multiple cutaneous NF, 6 or more café-au-lait patches >1.5 cm, axillary freckling, Lisch nodules on the iris (ocular neurofibromatosis)
How is neurofibromatosis classified?
NF Classification
o Type 1 → most common with features above
o Type 2 → assoc with CNS NF’s – very rare
o 3rd Type – Schwannomatosis – very painful, very rare
o Plexiform neurofibromas
- large infiltrative lesions found in the head or neck region
- more diffuse, may cause neurological deficit, risk of malignancy transformation- pain, rapid growth, go hard, neuro compression, rapid met spread
- wound complications common following their excision
- chromosome 17q
- 1/3500 prevalence
- 1/2500 births
2 or more of- o Axillary Freckling o 6 or > Cafe au lait patches o Iris Lisch nodules o Thickening (glioma) of optic n. o Bony abnormality
What are congenital dermoids?
Congenital dermoids
- Entrapment of epidermis during facial development.
(a) Angular dermoid
- most common
- Usually located in submuscular plane towards outer corner of the eye
(b) Midline dermoid
- anywhere between forehead and nasal tip
- May have deep intracranial extension → preop scan needed.
What is a sebaceous cyst?
= Epidermoid Cyst
- Young and middle aged
- Inflammation and obstruction of pilosebaceous follicles
Path
- Epidermal lining, keratin and break down products + sebum secreted by sebaceous glands
Clinical
- Dermal spherical cyst, Tethered epidermis, Enlarge, Suppurate via punctum
- Gardener’s syndrome → multiple cysts + osteomas of jaw + polyposis coli
Treat – complete excision
What other cysts do you know of?
Implantation dermoids
- After trauma → trapping of segment of epidermis in dermis
Pilar cysts
- Similar to epidermoid cysts but occur on scalp
Milia
- Small intra-epidermal cysts usually on cheeks
- Treat by needle enucleation
Xanthelasma
- Accumulation of lipid within the skin
- Usually around eyes
- Treat by excision → vertical to avoid ectropion
What is a naevus?
Cutaneous hamartomas usually incorporating a proliferation of
Sebaceous glands = sebaceous naevus
Melanocytes = melanocytic naevus
Vascular tissue = vascular naevus
What epidermal naevi syndromes are there?
Association of EN with developmental anomalies of other organ systems
Proteus syndrome - overgrowth syndrome, multiple sites
Sebaceous naevus syndrome - with neurological features (seizures, developmental delay, palsied, structural abnormalities of the brain)
Becker’s naevus syndrome - Beckers naevus with unilateral pectoral hypoplasia and skeletal abnormalities
Structure and function of melanocytes
- derived from neural crest
- Spindle shaped clear cells, contain a dark nucleus + dendritic processes
Melanin is synthesized within melanocytes from dihydroxyphenylalanine (DOPA) → tyrosine - Melanin accumulates in vesicles within melanocytes called melanosomes
- Melanosomes are distributed to surrounding cells via long dendritic processes
- number of melanocytes does NOT vary bn races
- ↑ pigmentation is due to ↑ production
- Melanin production is stimulated by sunlight and (MSH) melanocyte-stimulating hormone (pituitary)
Naevus Cells
- Melanocyte leaves epidermis and enters dermis = Naevus cell
- They are round rather than spindle shaped
- DO NOT have dendritic processes
- Tend to congregate in nests
Summarise the types of melanocytic lesions
Malignant melanocytic lesion = malignant melanoma
Benign → melanocyte or naevus cell
o Naevus cell lesion = congenital or acquired
o Melanocytic lesions arise in = epidermis or dermis
Naevus Cell Naevi
Congenital → Giant hairy naevus (GHN) or Non GHN.
Acquired → Junctional, Compound, Intradermal
Special → Spitz, Dysplastic, Halo
Melanocytic Naevi
Epidermal → Ephelis, Lentigo, Café-au-lait patch, Becker’s naevus, Albright’s syndrome.
Dermal → blue naevus, Mongolian blue spot, Naevus of Ota, Naevus of Ito
CMN MANAGEMENT
- > 20cm in adult or > 5% BSA
- Malignant transformation of any CMN = 0.7-2.4% (prev 2-4% or up to 40% in some series)
- MM in CMN 4-14% (5%) Risk highest in 1st 10yrs of life - worse prognosis than other MM
- Leptomeningeal melanosis assoc with GHN = very poor prognosis
- Rarely can get tumours of neural or mesenchymal origin e.g. rhabdomyosarcoma or liposarcoma
- Treatment → controversial
- Pigment more superficial in early neonatal period then goes deeper? → excise, dermabrade, laser, curette may work BUT ↑↑ blood loss for neonate. Superficial excision can develop residual black areas later → leopard skin type appearance.
- Debatable if superficial excision prevents malignant change.
- Can excise later during childhood → wide undermining and direct closure, tissue expansion, skin grafting, integra resurfacing.
- Some advise just to watch and excise any changing areas.
- Little prospective data on incidence of malignant change or impact of Rx.
CMN guidelines 2008 Kinsler Bulstrode GOSH
1) untreated CMNs can lighten spontaneously, sometimes dramatically;
2) routine surgery with current techniques has not been shown to reduce the risk of malignancy in CMNs and is therefore for cosmetic reasons only;
3) early surgery has not been shown to be advantageous and carries increased anaesthetic risk;
4) there is some evidence that surgical intervention may adversely affect the behaviour of the CMN cells.
As a result, our current practice is based on the following guidelines:
1) patients are treated in a MDT setting
which includes paediatric dermatology, plastic surgery and neuroradiology, with access to neurology, neurosurgery and oncology;
2) serial photographs are taken at yearly intervals to assess spontaneous lightening;
3) all routine surgery is delayed for at least the first year;
4) patients with facial CMNs (either the principal lesion or large satellites) are offered surgery for cosmetic reasons;
5) patients with a single, easily excisable CMN are offered surgery for cosmetic reasons;
6) All families are made aware of the possibility of spontaneous lightening and the possibility that surgery may have effects on the behaviour of naevus cells
What is the quoted rate of malignant transformation of a CMN?
Risk of melanoma proportional to size of nevus.
Large CMN: 6.3-12.2%. (40% of the malignant melanomas observed in children)
Giant CMN: 2-42% (Lifetime expert monitoring
50% of the malignancies develop by 3 years of age, 60% by childhood, and 70% by puberty
GOSH paper - more likely to be lower
What are the types of acquired naevus cell naevi?
Rare in infancy, appear in childhood and adolescence, less appear in early adulthood, stable numbers in middle age.
- Junctional Naevi
- Flat Smooth and irregularly pigmented, usually in the young
- Nests of naevus cells clustered around the epidermal/dermal junction - Compound Naevi
- Round well-circumscribed slightly raised lesions
- Nests of naevus cells clustered at epidermal/dermal junction extending into dermis - Intradermal Naevi
- Dome shaped lesions, non-pigmented or hairy
- Usu adults, composed of nests of naevus cells clustered within dermis
What are the special naevus cell naevi?
- Spitz Naevus (juvenile melanoma)
- See 7.4 Melanoma - Dysplastic Naevi
- Irregular outline, Patchy pigmentation
- >5mm
- Atypical naevus (atypical mole) syndrome = >100 dysplastic naevi in 1 pt – associated with ↑ risk MM (risk also related to FHx) - Halo Naevus
- Naevus surrounded with depigmented area of skin
- Relatively common in older children and teenagers
- Tend to regress leaving a small scar
- Antimelanoma antibodies have been detected in some pts with halo naevi
- Treatment → expectant
Melanocytic naevi - epidermal
- Ephelis → freckle
- Normal number of melanocytes but ↑ production
- Disappear in the absence of sunlight - Lentigo
- ↑ number of melanocytes
- Persist without sunlight
- 3 types
a) lentigo simplex → young and middle aged
b) lentigo senilis → elderly
c) solar lentigo → after sun exposure - Café-au-lait patch
- Pale brown patch
- >6 lesions > 1.5cm = neurofibromatosis.
Becker’s Naevus
- Dark patch on the shoulder, normally appears during adolescence and may become hairy
Albright’s syndrome (see 5.4 Cleft)
- Pigmented skin lesions, Fibrous dysplasia, Precocious puberty.
Melanocytic naevi - dermal
- Blue naevus
- Round areas of blue/black colouration
- Arrested migration of melanocytes bound for dermal/epidermal junction
- Differential diagnosis - melanoma - Mongolian blue spot
- Bluish grey pigmentation over the sacrum
- Present in 90% of Mongolian infants - Naevus of Ota
- Bluish pigment of the sclera and adjacent periorbital skin
- Caused by intradermal melanocytes, prevalent among Japanese - Naevus of Ito
- Blue-grey discolouration around the shoulder
- Intradermal melanocytes
- Rare in Caucasians but common in Japanese
What is atypical mole syndrome?
> 100 melanocytic naevi measuring 6-15mm
Present at birth
Increase in number around puberty
10% risk of melanoma
What is xeroderma pigmentosum?
1882 Kaposi “Xeroderma pigmentosum” Rare, AD Photosensitivity, pigmentary changes, premature skin aging, and malignant tumor development Defect in nucleotide excision repair Deficiency in thiamine dimerase M=F, all races Identified by age 2 <20 yrs: 1000-fold increase in the incidence of NMSC and melanoma Mean patient age of skin cancer is 8 yrs Actinic damage between 1-2 yrs of age
What are the Fitzpatrick skin types?
Skin colour Burns
I very white / freckled always
II white usually
III white - olive sometimes
IV brown rarely
V dark brown v rarely
VI black never
What are the contraindications to chemical peels (med depth)?
Absolute
- unrealistic expectations
- poor general health and nutritional status
isotretinoin therapy last 6mths
complete absence of intact pilosebaceous units on face
active infections / open wounds
Relative
resurfacing procedure last 3-12mths
recent facial surgery w excess undermining e.g. facelift
hx of abnormal scarring / delayed wound healing
hx of DXT
hx of rosacea, web dermatitis, atopic dermatitis, psoriasis, vitiligo)
What are the predisposing factors for MM?
Moderate increase in risk (8-10x popn)
- Previous Melanoma: 3-5% chance 2nd primary
- Organ transplant patients
Greatly increased risk (>10x popn)
- Atypical mole syndrome
- Giant congenital pigmented hairy naevus
- Strong FH (>3 cases pancreatic ca. / melanoma)
- Dysplastic naevus
- Xeroderma pigmentosum
- Lentigo maligna
What are the MM excision margin trials?
Trial, Excision plan, N, F/U, Local Control, Survival
Veronesi (WHO) New Eng J Med 1988
1 vs 3cm MM0.8-2.0mm trunk or extremities
989
11
No diff
No diff
Balch (Intergroup Melanoma Surgical Trial) Ann Surg Oncol 2001 2 vs 4cm MM 1-4mm trunk/UL 468 10 No diff No diff
Khayat (French Co-operative Study) Cancer 2003 2 vs 5cm MM2cm 900 5 Inc. local rec with 1cm margin No diff
What are the indications for LN surgery in MM?
If Clinically node –ve:-
- SLNB – “can be considered” in stage >IB
- No proven therapeutic value
- Only assists in prognosis
- Significant risks, false –ve etc.
If Node +ve:-
FNAC (+/- repeat or open biopsy)
Radical LND (SSMDT member >15/yr), CT and LDH
What is SLNB?
1st node draining area of lesion
NICE Guideline (2006)
- Centres with experience of SLNB
- ONLY in context of trials
More accurate staging
No survival benefit
Small decrease in disease-free survival
Delineation of populations for trials
SLNB positivity depends on stage of primary
SLNB negative pts have better D-F Survival
What are the indications for lymphadenectomy?
Superficial inguinal LND
- Single clinically involved ing. / fem. triangle node
- Single +ve superficial ing. SLN
Pelvic LND
- > 1 palpable ing. +⁄or fem. triangle node
- CT / USS evidence: >1 ing. +⁄or fem. triangle node or pelvic node involvement
- > 1 microscopically involved node at SLNB
- Conglomerate of ing. / fem. triangle LNs
- Microscopic /macroscopic involvement of Cloquet’s node
How is local recurrence managed?
Excision / Laser ablation
Progressive disease: ILI (5cm)
Radiotherapy
Electrochemotherapy using bleomycin under evaluation
What adjuvant treatment is available for MM?
Interferon:
- Significantly increase relapse-free survival
- Inc overall survival
- Greatest benefit if Stage IIB/III-n1
Decarbazine: alkylating agent
Melanoma vaccines: unsuccessful so far
DXT: 48Gy in 20 fractions
What new treatments are there for stage IV disease?
Selective BRAF inhibitors
- Vemurafenib: 6-10/12 increase in median survival
- S/E: SCC (KA type)
CTLA-4 monoclonal antibodies
- Ipilimumab (human IgG1), for advanced metastatic melanoma
- Dose: 3mg/kg every 3/52 for 3/12
- block cytotoxic T- lymphocyte- associated antigen 4 (CTLA-4), a negative regulator of T cells, and thereby augment T-cell activation and proliferation
Tell me about the MSLT 1 Trial
- 1269 pts: 60% SLNB, 40% observed
- Median follow up 5 yrs
- No overall survival benefit to early vs. delayed CLND
- Prognostic indicator: significant decrease in overall 5yr survival with positive SLN (90.2% vs. 72.3%)
~20% of SLND +ve pts will have +ve nodes on CLND, of which 65% will have only 1 node
Tell me about the MSLT 2 Trial
Pts stratified according to BT, ulceration and size of SLN mets
Pts then randomised to
CLND + observation or
Serial USS of SNB basin and CLND if node recurrence
What are the excision margins?
in situ (5-10mm) less than 1mm (1cm) 1 to 2mm (1-2cm) 2 to 4mm (2cm) greater than 4mm (2-3cm)
Excise down to fascia
No diff in local recurrence rates whether fascia is excised or not
How do you biopsy a suspected MM?
Excision biopsy 2mm margins
Incision biopsy if greater than 1.5cm (MDT)
Shave incision if subungal melanoma (only by SSMDT member)
What other investigations are there for MM?
Stage I,II +IIIA: No further investigation
Stage IIIB or C: CT head, chest, abdo + pelvis
Stage IV: According to clinical need + LDH
What is sentinel lymph node biopsy?
SLN = first node in the lymphatic basin that drains the lesion and is the node at greatest risk for the development of metastasis
Standard for SLNB is a triple diagnostic approach
(a) lymphoscintography
(b) blue dye dermal infiltration and
(c) localisation with gamma probe
- requires appropriate surgical expertise
- specialist nuclear medicine services
- serial sectioning and immunohistochemistry techniques
Indicated in >1mm / Clark level 4 / >4mm (subset of node -ve pts with good prognosis)
How do you perform a suprainguinal groin dissection?
- continuation of inguinal incision, lateral to femoral vessels
- incise through external and internal oblique, retract peritoneum medially to reveal retroperitoneal space
- identify ureter and preserve
- excise all obturator and ext iliac nodes
- mark specimen (excise as 2 specimens, as inguinal ligament division is associated with greater morbidity)
What is the evidence for suprainguinal dissection?
Ilioinguinal dissection offers a survival benefit in patients with palpable positive inguinal nodes compared with inguinal block dissection of the femoral triangle nodes
Sterne Br J Surg (1995) Ilioinguinal block dissection for malignant melanoma.
Karakousis Br J Surg (1994) Groin dissection in malignant melanoma.
