C O R E T U T O R I A L S I N D E R M A T O L O G Y F O R P R I M A R Y C A R E

S K I N M A L I G N A N C Y

Number 4 in a ser ies of 8

‘Solar’ of the sun

E X T R E M E U L T R A V I O L E TI M A G I N G T E L E S C O P EI M A G E O F T H E S U N

C O R E T U T O R I A L S I N D E R M A T O L O G Y F O R P R I M A R Y C A R E

A U T H O R : D R B R I A N M A L C O L M , BSc, MBChB, DRCOG, DPD, DCH, MRCGP.GENERAL PRACTITIONER, LITCHDON MEDICAL CENTRE, BARNSTAPLE. HOSPITAL PRACTITIONER, ROYAL DEVON & EXETER HOSPITAL.

R E V I E W E D B Y : D R A N D R E W W A R I N , MB, FRCP.CONSULTANT DERMATOLOGIST, ROYAL DEVON & EXETER HOSPITAL.

P R E F A C E A N D I N T R O D U C T I O N

C H A P T E R O N E : T H E E C Z E M A S

C H A P T E R T W O : P S O R I A S I S

C H A P T E R T H R E E : S K I N I N F E C T I O N A N D I N F E S T A T I O N

C H A P T E R F O U R : S K I N M A L I G N A N C Y

C H A P T E R F I V E : L E G U L C E R S

C H A P T E R S I X : A C N E

C H A P T E R S E V E N : U R T I C A R I A A N D R E L A T E D A L L E R G I C D I S O R D E R S

C H A P T E R E I G H T : R E C E N T D E V E L O P M E N T S

SPONSORED BY DERMAL LABORATORIES, TATMORE PLACE, GOSMORE, HITCHIN, HERTS SG4 7QR, UK. TEL: (01462) 458866.

Front cover image: Extreme Ultraviolet Imaging Telescope (EIT) image of ahuge, handle-shaped prominence taken on September 14th 1999 taken in the304 angstrom wavelength – Prominences are huge clouds of relatively cooldense plasma suspended in the Sun’s hot, thin corona. At times, they can erupt,escaping the Sun’s atmosphere. Emission in this spectral line shows the upperchromosphere at a temperature of about 60,000 degrees K. Every feature in theimages traces magnetic field structure. The hottest areas appear almost white,while the darker red areas indicate cooler temperatures.Courtesy of SOHO/Extreme Ultraviolet Imaging Telescope (EIT) consortium. SOHO is a project of international cooperation between ESA and NASA.

C O N T E N T S

C H A P T E R F O U R : S K I N M A L I G N A N C Y

S K I N C A N C E R 1

A c t i n i c / s o l a r k e r a t o s e s 1

B o w e n ’ s d i s e a s e 3

K e r a t o a c a n t h o m a s 4

B a s a l c e l l c a r c i n o m a 5

S q u a m o u s c e l l c a r c i n o m a 7

M a l i g n a n t m e l a n o m a 8

P r e v e n t i o n o f s k i n c a n c e r 1 3

S K I N S U R G E R Y 1 4

T E A C H I N G P O I N T S 1 6

R E F E R E N C E S 1 6

C H A P T E R 4 S K I N M A L I G N A N C Y

S K I N C A N C E R

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Let us look at the relatively small number of conditions that compose the vast majorityof cutaneous malignancy and pre-malignancy in ascending order of importance:

A C T I N I C / S O L A R K E R A T O S E S – These compriseby far the most common of conditions considered pre-malignant. Their very presence acts as a marker ofsignificant cumulative exposure to ultravioletradiation. The exact individual risk of progressionfrom a solar keratosis to squamous cell carcinoma(SCC) is unknown but is considered to be in the ‘ballpark’ of 1:1000.2 Prevalence in the UK is between6-15% of the population aged over 40, contrastingwith a prevalence in Australia of 40-60% in the sameage group. Males are most commonly affected. Theclinical appearances are classically those of a textured,circumscribed, scaly, keratotic plaque usually less than1 cm in diameter. Colouration is varied from franklyerythematous through to yellow, pigmented or flesh-coloured. They always occur in sun exposed sites andparticularly the scalp, ears, nose, dorsum of hands and forearms.

Progression to squamous cell carcinoma follows a prolonged latent period of a decade ormore, and the resultant SCC’s themselves are generally low grade with low metastaticpotential with the exception of those on the ear and lip which tend to behave moreaggressively. Signs of change to frank SCC can be subtle – a more rapid growth phasemay be noted especially if there are multiple solar keratoses and one appears to bebehaving differently. Also there may be an increased erythema or induration. Even to thepractised eye it can be extremely difficult reliably to differentiate between solar keratosis,Bowen’s disease, early SCC and superficial or morphoeic basal cell carcinoma (BCC).Keratoacanthomas can usually be more reliably differentiated by a classical history of an‘explosive’ growth phase over a number of weeks. The presence of multiple keratoses canbe associated with arsenical exposure. Examples of this would be ingestion of Parrish’sfood, which was previously used as a children’s tonic, or exposure to Fowler’s solutionhistorically used for the treatment of psoriasis. Such keratotic lesions classically appearon the palms and soles which are themselves unusual sites for the development ofactinic keratoses.

M U L T I P L E K E R A T O S E S

As a consequence of the well established and indeed alarming epidemiologicaltrends in the increasing incidence of all skin cancers in the United Kingdom,1

there is an enormous amount of literature available to the primary carephysician. In this article I plan to review the present situation regarding thecommon forms of skin malignancy and pre-malignancy. I also feel that this isa useful forum to discuss the related provision of services for skin surgery. Thediscussion on the latter is very much a personal view, but this has beenformulated after involvement in discussion groups on this subject, both at alocal and national level. There is inevitably a degree of political ‘spin’!

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Indeed, arsenic exposure predisposes to a variety of skin cancer types. Particular mentionalso should be made of actinic cheilitis presenting as whitish or erythematous patches onthe lips which can progress to erosion, ulceration and frank SCC. This is especially trueof the lower lip.

There are various accepted treatments for solar keratoses and each will have itsenthusiastic advocates. It is worth noting, however, that 25% of solar keratoses remitspontaneously over a 12 month period.3 Established treatments include:

a) Topical application of 5-fluorouracil (Efudix) cream – this is a cheap and effectivetreatment but care must be taken with fair-skinned individuals and a well establishedprotocol followed. My preferred regime is:

i) Apply the cream thinly twice a day to all affected areas. Be particularly carefulnot to get the cream near to the eyes. Wash your hands thoroughly after use;

ii) After a few days (usually three to five), the keratoses will go red and may, insome cases, even blister and weep. There may be some soreness;

iii) Once the reaction has started, and provided it is not too sore or severe,continue the application of the cream for a further two weeks. If at any time thereaction is really unpleasant and sore, stop treatment and apply a steroid cream orointment (usual hydrocortisone 1% will be prescribed). If a severe reaction hasoccurred it is likely that the keratoses will have been effectively treated and nofurther application will be required. If in doubt, consult your doctor and he/shewill advise as to whether you should continue treatment;

iv) At the end of treatment (usually after three weeks in all) any reaction stillpresent may be treated with hydrocortisone 1%. It may take four weeks after theend of treatment before all the lesions have healed.

b) Cryotherapy using very short bursts of liquid nitrogen spray of 5-15 seconds.

c) Curettage and cautery.

d) A new topical application for the treatment of solar keratosis has recently becomeavailable, marketed under the name of ‘Solaraze’. The active agent is 3% diclofenacgel. Treatment regimes take 2-3 months and more data are needed on long termoutcomes, both clinical and histological. If this treatment becomes better established,I may well choose to highlight this in my final article ‘Recent developments’.

e) Photodynamic therapy (PDT) – this is a treatment modality that is not, in fact, newbut is undergoing somewhat of a renaissance. It remains available, however, only incertain centres. It combines the application of a topical photosensitiser with exposureto particular wavelengths of light. Capital equipment costs are high and the maindrawback can be the pain induced during treatment and long term outcomesremain uncertain.

f) Excision if the lesion is indurated or clinically suspicious of having undergonetransition to SCC.

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BOWEN ’ S D I S EASE (Intraepithelial carcinoma) – This common condition is ‘in situ’ SCC.The potential for malignant changes is considerably higher than solar keratoses,estimated at 8% of untreated cases with a consequent metastatic potential of 13%.Clinically, it presents as an asymptomatic well defined erythematous, scaly plaque with apattern of centrifugal spread. It can mimic an isolated patch of eczema and psoriasis.Sites of predilection include the face, lower limbs and fingers. A degree of definitionhelps to distinguish it from a solar keratosis while the absence of a finely elevated ‘whipcord’ margin help to distinguish it from a superficial BCC (see page 5). However, suchdifferentiation can be very challenging and the microscope is often the final arbiter.There is occasionally an association with a past history of arsenical exposure andtreatment modalities mirror those of actinic keratoses, as discussed previously.

There are a number of other conditions considered to be potentially pre-malignant stagesof SCC; these include Erythroplasia of Queryat which equates to an in situ SCC of thepenis and presents as a sharply demarcated erythematous plaque. There is a 10% risk ofprogression to invasive carcinoma.

Squamous cell carcinomas are also wellrecognised to arise in areas of prior skin damage,either through radiation or chemical exposure, orin sites of chronic sepsis and inflammation suchas scars, sinuses and leg ulcers (so calledMarjolin’s ulcer).

In addition, 15% of cutaneous horns havehistological changes of SCC in the base and allsuch lesions should be submitted for histologicalexamination.

B O W E N ’ S D I S E A S E O N L E G

C U T A N E O U S H O R N

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K E R A T O A C A N T H O M A S – These are considered by some authorities a ‘form fruste’ offrank squamous cell carcinoma. These tumours characteristically arise de novo and eruptrather like a small volcano over a period of 6-12 weeks. They grow at both an alarmingrate and to quite a large size but on average plateau at between 10-20 mm diameter. Thehistory then is of a spontaneous regression over the next 3 months. Present advice,however, is to treat these tumours either by excision or possibly by curettage and cauteryin experienced hands; this is both to avoid the risk of missing frank squamous cellcarcinoma, but also if keratoacanthomas are left to resolve naturally they may leave amore unsightly scar than would have been obtained by early surgical intervention. Life iscomplicated, however, by the fact that histologically the pathologist can on occasionhave problems differentiating between keratoacanthomas and well differentiatedsquamous cell carcinomas.

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B A S A L C E L L C A R C I N O M A (BCC) aka basal cell epitheliomas or, more colloquially,rodent ulcers – These are extremely common tumours, presenting most frequently on theface and unlike squamous cell carcinoma there is no commonly recognised pre-malignantstage. Worthy of mention, however, is the congenital naevus sebaceous which presents asan indolent, indurated hairless yellow plaque, most commonly on the scalp. This isestimated to have 10% risk of progression to basal cell carcinoma in adulthood, andthere is need for consideration for excision post puberty.

The incidence of BCC has increased 75% in the last decade alone. The risk ofdevelopment appears to relate to intermittent cumulative ultraviolet exposure. This is notthe whole story, however, as the sites most common for BCC do not correspond exactlywith sites of maximal sun exposure. There is a common perception that this is an ‘oldperson’s’ disease but it is really not unusual to diagnose BCC in people in their 20’s and30’s, the youngest I have treated, indeed was 12 years old! Most doctors equate theappearance of a BCC with that of a classical nodular cystic lesion with a ‘rolled’ edge, acentral keratotic or ulcerative core and the presence of telangiectasia. There are,however, a variety of other distinct presentations:

• Superficial BCC – These are common on the trunk and lower limbs presenting as verywell circumscribed patches of erythema with a subtle ‘whip cord’ edge. They are oftendismissed or overlooked and can reach very significant proportions before the diagnosisis reached, thereby narrowing the treatment options.

• Pigmented BCC – These are often classically nodulocystic but the presence ofpigmentation can cause confusion and concern regarding the possibility of amalignant melanoma.

M A L I G N A N T C H A N G E S I N S E B A C E O U S N A E V U S

S U P E R F I C I A L B C C P I G M E N T E D B C C

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• Cystic BCC – These canpresent as well defined smoothdomed lesions.

• Morphoeic/pleomorphoeic –As the name suggests, thesecan be varied in appearance,often presenting as nondescript, ill defined lesionswith chronic scabbing,scarring, infiltration andinduration. The degree ofinvasiveness can be veryadvanced before the diagnosisis reached and often a procedure such as Moh’s micrographic surgery is needed fordisease clearance. Such advanced dermatological surgery is standard practice in the USbut is only available in a relatively small number of specialised units here in the UK.

There are numerous ways to treat BCC’s, all with enthusiastic proponents; these includemany of the modalities already mentioned for actinic keratoses, namely cryotherapy,curettage and cautery, electrosurgery, excision and PDT. Also employed is radiotherapyfor larger lesions, especially superficial BCC’s, and they can also be treated withintralesional 5-fluorouracil. There is no one right way to ‘skin this particular cat’! Theoperative must be confident and experienced in whatever modality they choose, and beprepared to be flexible in approach according to the age and fitness of the patient andthe anatomical site.

Excision is the only method giving histological confirmation of clearance, but even this isan inexact science. Standard histological preparation of a specimen may miss tumourmargins. Not infrequently tumours deemed histologically clear, clinically recur.Conversely, tumours that are reported to reach or involve the incision margin are oftenfollowed up rigorously with no clinical recurrence over a prolonged period. It may be bydebulking the tumour, residual tumour is destroyed by the inflammatory immuneresponse invoked. However, every effort to clear disease at the first time of askingshould be made. Surgical clearance is recommended to be ideally with a macroscopicperilesional margin of 2mm; 1 in 3 tumours that histologically are reported to be at thedeep margin do recur. The figure reduces to 1 in 6 for those tumours reported to at ornear the lateral margin. The operative must be particularly careful to achieve tumourclearance at the deep margins if grafts or flaps are employed for, if not, tumour can bedeeply buried and clinical recurrence only evident when the tumour is well advanced.

There are a number of ‘high risk’ sites where particular skill is needed to obtain adequateclearance and cosmetically acceptable results; these include tumour in the post-auricularor nasolabial folds, tumour near a free margin such as an eyelid or lip, or tumoursclosely approximate to vital structures such as the eye itself. My general preference is toexcise surgically tumours on the head and neck, and also on the body of youngerpatients when possible, and to use other techniques, especially double curettage andcautery for truncal and more peripheral tumours. Excision gives a 95-99% ‘cure’ rate incompetent hands. Curettage and cautery is reported as giving a “cure” rate of 80%. Inthe latter, the option to excise recurrences usually remains.

M O R P H O E I C B C CC Y S T I C B C C

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S Q U A M O U S C E L L C A R C I N O M A – This tumour is regarded as potentially moreserious as it has the ability to metastasise. It is the second most common of the nonmelanoma skin cancers, occurring twice as commonly in men than women, and mostcommonly in patients over the age 70. Incidence has increased by 30% in the last decade in the UK. These tumours arise from the keratinising cells of the epidermis and its appendages, and also from mucous membranes. As previously discussed there area number of pre-malignant conditions at risk of squamous metaplasia. Predeterminedrisk factors are chronic cumulative ultraviolet exposure, arsenicals, ionising radiation orimpaired immune factors, for example secondary to transplantation and/orimmunosuppressive medication. Indeed, transplantation poses particular risks withhundredfold increase in the incidence of SCC, and such tumours may behavemore aggressively.

Clinically, the presentation is of an indurated, inflammatory or ulcerated nodule mostcommonly in the dorsum of the hands or the face. High risk sites for primary lesionsmost prone to metastases include the ear, lips, scalp, eyelids and nose.4

In keeping with other non melanoma skin cancers, there are to date no reliableprospective randomised studies to determine the relative efficacies of the varioustreatment modalities used. Excision is the treatment of choice. Squamous cell carcinomais also sensitive to radiotherapy. Excision for larger tumours is considered best practicewith an optimum margin of 4mm. Cure rates are reported of 95%. Moh’s surgery can beconsidered for tumours arising on high risk sites, for larger tumours over 2cm, and alsofor patients with coexisting immunosuppression, for recurrent tumours and for thosethat appear clinically deeper and more infiltrative.

S C C O N C H E E K

T R E A T M E N TO P T I O N S

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M A L I G N A N T M E L A N O M A – Never truer is the old adage ‘prevention better thancure’ than when applied to malignant melanoma. A close second best is early diagnosisand treatment as this most aggressive and life threatening of tumours is infinitelyamenable to often simple surgical intervention in its early stage, but once metastasised,treatment options remain woefully ineffective! It is a tumour of major and increasingimportance, commoner now in the UK than either cervical cancer or Hodgkin’s disease.There are 5,000 new diagnoses and 1,500 deaths annually. The rate in Australia is astaggering fivefold more. The peak age of incidence is in the fourth decade. There hasbeen a threefold increase in the last two decades which represent the greatestproportional rise of any malignancy, except carcinoma of the lung in females. Thisapplies both to the UK and Western Europe. This increasing trend is likely to be at leastsustained for the next two decades.

A number of risk factors are well established:

• Intermittent sun exposure

• Higher social class

• Positive family history of malignant melanoma or dysplastic naevus syndrome; there is a reported 5% incidence in 1st degree relatives

• Presence of large numbers of benign melanocytic naevi (the average person has approximately 40)

• Dysplastic naevus syndrome defined as the presence of over 100 naevi, many greater than 1cm diameter and of atypical appearance

The evidence regarding the risk of sunbeds remains somewhat equivocal, although logicwould suggest that injudicious use of these is likely to increase risk.

Clinically, the diagnosis depends on a number of factors; these have been defined byProfessor Rona Mackie of Glasgow University.5 The original seven point check list hasnow been refined to three major and four minor factors.

Table 1. Year 2000 Glasgow seven point check list (Mackie 2000 p8 Primary Cutaneous Malignant Melanoma)

Major features1. Recent growth in new or pre-existing pigmented lesion.2. Recent change in shape of new or pre-existing pigmented lesion.3. Recent change in colour pattern of new or pre-existing pigmented lesion.

Minor features4. Symptoms – mild itch is the commonest.5. Oozing or crusting – frank bleeding or ulceration.6. Inflammation in and around the lesion.7. Largest diameter 5mm or greater. Although some melanomas are smaller than

this, the majority are 5mm in largest diameter by the time they are recognised.

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Over 90% of patients presenting with malignant melanoma give a history of a changinglesion over the previous few months. The lesion itself will often have three separatecolours or shades within it; these can vary from black to brown to red or evenoccasionally white, which is due to partial regression. Approximately 50% of melanomasarise de novo and 50% are superimposed on existing melanocytic lesions. The back isthe highest risk area for men, accounting for a third of all melanomas, in contrast towomen where 50% arise on the lower limbs. These sites clearly support the theory ofsun exposure as a risk factor.

On a positive note, however, despite the worrying increase in the incidence of malignantmelanoma, the number of deaths is not rising proportionately, neither unfortunately is itfalling! This is due to a trend towards tumour presenting for diagnosis at an early stageas a result of greater public and physician awareness.

There are a number of distinct patterns of malignant melanoma:

• Superficial spreading melanoma – These constitute 80% of malignant melanomas inthe UK;

• Nodular melanoma – Accounting for 10%;

• Acral melanoma (acral = Greek for extremity) – These occur on the soles and palms,the former more commonly. Diagnosis can be delayed, particularly on the soles, andthese lesions can frequently proceed to ulceration. Subungual melanomas can beconsidered as a variation of acral melanoma. Pigmentation involving the nail fold(Hutchinson’s sign) may demonstrate an advanced lesion with a poor prognosis;

• Amelanotic melanoma – Somewhat of a misnomer as there isvery often some pigment present on close examination;

• Lentigo malignant melanoma (aka Hutchison’s Freckle) – These present as flat, brown stains most commonly in old age.The cheek is the site of predilection. They are histologicallymelanoma in situ. The history is usually of a very gradualextension over a number of years. The tumour can havereached quite a large size by the time of diagnosis, often inexcess of 20mm. Old photographs can be helpful with adiagnosis here. These in situ tumours do have the potential forundergoing vertical growth phase to frank invasive nodularmalignant melanoma.

S U P E R F I C I A L S P R E A D I N GM E L A N O M A

A C R A L M E L A N O M A O N S O L EO F F O O T

L E N T I G OM A L I G N A N TM E L A N O M A

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There are a number of benign conditions that can cause both confusion and concern:

• Pigmented dermatofibroma/histiocytoma – These lesions should, however, remainstatic and unchanging with a textural feel described as feeling ‘like a lentil underneaththe skin’;

• Halo naevus (Sutton’s) – These lesionscommonly occur in adolescents and cause undueconcern because of their changing nature.However, the well circumscribed perilesionaldepigmentation gives the diagnosis. The process isof a benign melanocytic naevus undergoingautoimmune destruction;

• Blue naevus – Their monomorphic blue/greypigmentation due to their positioning deep in theskin, along with a regular outline and a history ofarising in puberty and being unchanging,differentiate these from malignant melanoma;

• Pyogenic granuloma – These sometimes needdifferentiation from amelanotic melanomas, but ahistory of trauma, a characteristic exposed siteespecially in a digit and a complete lack ofpigment, support a benign diagnosis;

• Junctional naevi – These commonly occur on thepalms and soles and often cause anxiety. Theoutline is often irregular but the colour is characteristically uniform;

• Seborrhoeic keratoses aka seborrhoeic warts orbasal cell papillomas (unkindly known in someolder textbooks as ‘senile warts’) – These benignskin growths are almost ubiquitous on elderlyskin, either occurring singularly or multiply, witha predilection for the trunk and face. They have a‘stuck on’ rough, cerebriform appearance usuallywith a clear definition from surrounding skin andthe presence of plugs or pits on the surface.However, particularly when arising in an areaprone to friction such as a bra strap or waistband,they can become irritated and inflamed and take on a ‘worrying’ appearance;

• Angiomas – These particularly can often be reliably distinguished with the use of adermatoscope, discussed later in the article;

• Pigmented BCC’s – As previously discussed, these have a characteristic raised ‘rolled’edge associated with such tumours.

D I F F E R E N T I A LD I A G N O S I S

H A L O N A E V U S

B L U E N A E V U S

S E B O R R H O E I C W A R T

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Studies demonstrate that experienced clinicians can differentiate malignant melanomawith approximately 85% accuracy from other pigmented skin lesions. The results forprimary care physicians were 50%. The ‘gold standard’ for diagnosis of malignantmelanoma has remained the histological assessment. There are two well knownclassifications, the Breslow thickness and the Clarke’s levels. The former relates to asimple measurement of depth of tumour in millimetres; the latter to the anatomical depthreached by the tumour in the dermal/epidermal architecture.

Problems do not end, however, with histological examination! A recent NationalInstitute of Health review of histological diagnosis of early malignant melanomaemploying eight pathologists with a special interest in the disease demonstrated majordisagreement on examining a range of histological specimens. The summary of the studycommented: “The conclusions of the article should be chilling, not only to physicians,but to patients and sobering to lawyers for plaintiffs”.

Table 2. Prognostic indicators in malignant melanoma (Hunter et al. Clinical Dermatology Vol 3 p204)

Indicator Significance

Depth of primary tumour Breslow <1.5mm good>3.5mm bad

Sex Females do better than males.

Age Prognosis worsens after 50 years, especially in males.

Site Poor prognosis with tumours on trunk, upper arms, neck and scalp.

Ulceration Signifies poor prognosis.

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Treatment of established malignant melanoma is surgical. Frequently, by definition, thisrequires a 2mm margin excision for diagnosis and a secondary procedure according tothe staging of the tumour. The present thinking is of an excision margin of 1cm per1mm of depth to a maximum of 3cm. Narrower margin excisions are consideredadequate for in situ tumours. Incisional biopsy, with the exception of lentigo malignantmelanoma, is frowned upon due to a theoretical but unquantified risk of vasculardissemination. A topical issue presently is the concept of sentinel node biopsy whichrequires the use of lymphoscintography to identify lymphatic drainage pathways andsubsequent biopsy of the ‘so called’ sentinel node. This is an expensive, invasive andlabour intensive process which is useful for prognosis and staging, but until effectivesecondary treatments are available could arguably be considered of academic value only.

Metastatic spread is classically to the lymph nodes, liver, lung, brain, bone and skin.Long dormant intervals of up to 20 years can occur before secondary tumour appears.Clearly, patients with malignant melanoma need access to ongoing advice, support andfollow up. Pragmatically, follow up could be carried out either exclusively in primarycare or along shared care guidelines to unburden the secondary care services. Unless themalignant melanoma was to develop de novo during pregnancy, further pregnancy,hormone replacement and the oral contraceptive pill are not risk factors for malignantmelanoma. Secondary treatment of metastatic malignant melanoma remains verydisappointing. The disease is radio, chemo and immunotherapy resistant, althoughradiotherapy can be a useful palliative measure. There were high hopes for interferon butresults are not very encouraging.

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P R E V E N T I O N O F S K I N C A N C E R – Of the 100,000 new cases of skin cancer peryear it is thought that 80-90% are related to sun exposure. Sunscreens have been pushedvery energetically as the solution to this ‘epidemic’. The benefits of sunscreens areestablished for reducing sunburn, photoageing and photocarcinogenesis in animalmodels.6 The benefits in tumour prevention in the population are unclear. Onesignificant episode of sunburn in childhood is an established risk factor for thesubsequent development of malignant melanoma. A WHO working group concluded,however, that although appropriate use of potent sunscreens (SPF = greater than 15)probably reduce the risk of SCC, paradoxically, users of sunscreens had an increased riskof malignant melanoma.7 Sunscreens, theoretically, allow people to have longerexposures to potentially carcinogenic wavelengths of ultraviolet light while negatingnature’s reminder of too much sun exposure – sunburn! This problem was historicallyperpetuated by the fact that until recently the emphasis in sunscreens was UVBprotection, which is what the SPF refers to. This imbalance has been corrected somewhatby rating systems for UVA protection as well to produce more ‘balanced’ sunscreens.The use of sunscreens cannot be relied upon as a single strategy but has to be anintegrated skin protection package along with other photo-protective measures. This hasbeen energetically pursued in Australia with enormous public health campaigns to raiseawareness, such ‘Slip, Slap, Slop’ which reminded people to slip on a shirt, slap on a hatand slop on the sun cream.

Dermatoscope – This instrument previously referred to in this article is a simple andaffordable skin magnification system that resembles a glorified auriscope. It has anumber of enthusiasts but should only be considered as a diagnostic aid and nosubstitute for careful history taking, traditional clinical assessment and experience. At theend of the day, as in most things in life, there is no substitute for the latter. You justhave to see an awful lot of skin lesions before you can reliably separate the pathological‘wheat from the chaff’! The dermatoscope, however, is particularly good atdifferentiating angiomatous lesions and seborrhoeic keratosis from moreworrying pathologies.

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In this article it is not appropriate to provide a comprehensive treatise on all aspects ofskin surgery. Personally, I prefer this term to ‘minor surgery’ as somehow this trivialisesthis type of surgery. Indeed, in many ways surgery carried out under local anaesthetic,with a patient who is awake and aware of what is going on, is much more challengingand often requires excellent communicational and interpersonal skills from the doctorand his support staff. Ultimately, it is rather a medical truism to state that everyphysician must assess his experience and technical expertise when providing any service.Historically, dermatologists were often confident diagnosticians concerning skin lesions,but didn’t necessarily have the technical surgical abilities to treat such problems. On theother hand, surgeons were not confident of diagnosis but did have the necessary skills.This is increasingly a thing of the past as SPR rotations produce good and often excellentdermatological surgeons, in addition to the traditional diagnostic skills. The range ofdifferent skills in primary care is protean. In my locality alone, we have five generalpractitioners fully accredited with FRCS. However, each individual must recognise his orher limitations and if a small voice inside says: “I am not comfortable with undertakingthis procedure”, then never be afraid to refer on. First and foremost, a patient’streatment should never be compromised; their disease must be professionally treated andadequate clearance, particularly in relation to skin malignancy, must not becompromised by a fear of the operator not being able to close the resultant wound. Onthe other hand, as discussed above, there is not a single correct way of treating themajority of non melanoma skin cancers, and if an operator is confident in his techniqueand preferably has the support of a robust outcome audit, then he or she should befacilitated and encouraged in offering the service to patients.

To my mind, however, the present provision for dealing with skin cancers in primarycare is frankly chaotic! The emphasis in vocational training schemes for GP registrars isin the acquisition of minor surgical skills. This is achieved by mandatory attendance at adesignated course. These usually run over one or two days. However, the focus of thesecourses is in learning technical skills to remove ‘lumps and bumps’, but there is rarely inmy experience any input about diagnosing what the ‘lump and bump’ may be in the firstplace! Surely, this is a classic example of putting the ‘cart before the horse’. A pre-requisite for a successful outcome is having a good idea of what you are intending toremove or indeed does this particular lesion need removing in the first place. Suchcourses, as they are presently provided, only serve to compound the already poordiagnostic skills in dermatology in primary care due to the well recognised shortfalls inteaching the subject at all levels of undergraduate and postgraduate medical education.This also manifests in the common practice of biopsying undiagnosed rashes in generalpractice. This has been described by one of my colleagues as ‘the last bastion of thetherapeutically destitute!’ If the clinician fails to make a diagnosis or an accuratedifferential diagnosis when presented with the complete clinical picture, how can heexpect his histopathological colleague to make such a diagnosis on a small piece of tissuemarinated in haematoxin and eosin! However, I digress!

There are a number of conflicting messages coming from Government regarding socalled minor surgical services. The original ‘new’ contract claimed to offer incentives togeneral practitioners to do agreed procedures ‘in house’. However, the rewards are

S K I N S U R G E R Y

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C H A P T E R 4 S K I N M A L I G N A N C Y

derisory and a major disincentive to those GP’s wishing to do any procedures of clinicalsignificance. The fact that the payment is the same for snipping off a skin tag or freezinga wart, as for excising a challenging epidermal cyst, or removing a skin cancer, istransparently iniquitous. Indeed any procedure of significance at the present rate ofremuneration carried out properly to professional high standards actually results in theGP subsidising the NHS! There are no firm guidelines either on whether minor surgicalprocedures carried out for purely cosmetic purposes should be the remit of the NHS.Another disincentive is the firm recommendation from the Royal Colleges regarding thesubmission of specimens for histology. There must be some flexibility and commonsensedemonstrated in interpreting such advice using one’s clinical and diagnostic skills;otherwise we may as well equally x-ray every sprained ankle or CAT scan every headinjury, however minor. If you are removing something for patient convenience, on purelycosmetic grounds, where is the sense in submitting histology, putting further strain onour already overstretched histopathology infrastructure. Various studies have showngood correlation of diagnostic accuracy of benign lesions by GP’s. Clearly, if there is theslightest doubt, of course histology should be obtained and this is especially true ofpigmented lesions. For those who like acronyms, the one that I constantly regurgitate isthat the pathologist will be SAD unless he has three pieces of information on thespecimen form, in addition to patient details.

S = Site

A = Age

D = Duration

This information is often pivotal in order to narrow a differential diagnosis.

It is my firm opinion that the majority of ‘lumps and bumps’ surgery, includinguncomplicated skin cancer, could safely, economically and conveniently be provided inthe community if the skills are properly taught and the financial rewards wereproportionate. Perhaps the advent of national framework of recognised GP’s with aspecial interest (GPSI) may finally address this problem, but I remain pessimistic andsuspect that this exciting concept will be hijacked by a politically driven imperative forshort term ‘results’ because such a framework properly constructed and funded wouldtake many years to truly evolve. We must wait and see!

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T E A C H I N G P O I N T S

1). Solar keratoses have only a low risk of transition to SCC.

2). A quarter of all solar keratoses remit spontaneously in a twelve month period.

3). The incidence of all common forms of skin malignancy continues to rise sharply.

4). There are a number of clinical presentations associated with BCCs.

5). Malignant melanoma is now more common than cervical cancer.

R E F E R E N C E S

1). Holme SA, Malinowsky K, Roberts DL Changing trends in non melanoma skin cancer in S WalesBrit J Dermatol 2000; 143: 1224-1229.2). Frost CA, Green AC Epidemiology of Solar Keratosis Brit J Dermatol 1994; 131: 455-464.3). Marks R, Foley P, Goodman G, Hage BH, Selwood TS Spontaneous remission of solar keratoses:The case for conservative management Brit J Dermatol 1986; 115: 649-655.4). Rowe DE, Carroll RJ, Day CL Prognostic factors for local recurrence, metastasis + survival rates inSCC of skin, ear and lip J Am Dermatol 1992; 26: 976-990.5). Healsmith MF, Bouke JF, Osborne JE, Graham-Brown RG An evaluation of the revised sevenpoint check list for the early diagnosis of cutaneous malignant melanoma Brit J Dermatol 1994; 130:48-50.6). Green A et al. Daily sunscreen application and beta carotene supplements in prevention of BCCand SCC of the skin: A randomised controlled trial Lancet 1999; 354: 723-729.7). Graham-Brown RAC Sun education in the UK Clinics in Dermatology 1998; 16: 523-525.