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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5230_Библиотеки_им_академика_М_И_Перельмана.pdf
Melanocytic naevi (moles) $ Benign proliferation of melanocytes.
2
Worrying signs isize, change in pigmentation, irregular outline, bleeding,
itching, inammation (may suggest transformation to melanoma Ep. 444).
Symptoms and signsMost common are acquired naevi that develop during
childhood as small, at pigmented areas and may progress to pale, raised,
eshy naevi with age; congenital melanocytic naevi are larger, present from
birth, and carry a higher risk of transformation to melanoma.
ManagementRefer to specialist if worrying signs are present.
Lymphadenopathy
2Worrying signs Non- tender, >3wk, >cm, hard, irregular surface, teth-
ering, weight loss, night sweats, fatigue, absence of infection.
Causes IsolatedLocal/ regional infection; Multiple Ep. 48.
SymptomsLump usually in the neck, axilla, orgroin.
SignsFirm, subcutaneous; usually mobile, well- dened, smooth surface.
Management Enlarged lymph nodes can often be treated by ‘watchful
waiting’; however, biopsy or image if worrying signs are present.
Abscess $ Accumulation of pus within cavity due to infection or foreign
body.
Symptoms Typically single, painful, onset over days, may be febrile.
SignsFluctuant, well dened, under the skin; tender, inamed (red, hot);
may spontaneously discharge; common on neck, axilla, groin, perineum.
ManagementIncision and drainage ±antibiotics eg ucloxacillin g/ 6hPO.
Boil (furuncle) $ Abscess forming in inamed hair follicle, typically
with S.aureus infection.
SymptomsSingle, painful, common on neck, axilla, groin, perineum.
SignsRed, tender, hot, central punctum, may dischargepus.
ManagementOften discharges spontaneously, otherwise treat as abscess;
multiple furuncles may coalesce into a carbuncle which requires drainage
and extended antibiotic therapy.
War ts $ Benign proliferation of epidermis associated with infection
with human papillomavirus (HPV); can occur in varioussites.
Common warts These are papular lesions with a rough surface with black
dots within them, often on hands and feet. Spread is by direct contact.
Plantar warts (verrucas) These are usually at or inward growing with black
dots (‘heads’). Often painful if over pressureareas.
Plane warts These are small, esh- coloured, at- topped lesions usually on
the face or backs of the hands without blackdots.
Anogenital warts These are transmitted sexually and associated with dif-
ferent HPV subtypes from non- genital warts; subtypes 6 and 8 are
strongly associated with cervical carcinoma, so ensure recent cervical
smear in any ♀ with genital warts (or in ♀ partner, of any aected individual); subtype 6 is strongly associated with anal cancer.
Treating warts This is often dicult. Topical keratolytic agents (such as salicylic
acid or trichloroacetic acid) is usually st- line treatment, and cryotherapy
(freezing) is undertaken by many general practitioners as well as in dermatology clinics. Non- genital warts often resolve spontaneously over72– 3yr.
Actinic keratosis $ Scaly lesions seen on sun- exposed skin (fair
skinned). Can progress to skin cancer; usually treated topically.
443SKIN LUMPS
444 CHAPTER6 Skin andeyes
Skin cancers
Basal cell carcinoma(BCC)
$ Commonest form of skin cancer, accounting for 775% of diagnoses.
Risk factors Exposure to UV light (sunlight and sunbeds), PMH or FH of
BCC, exposure to arsenic.
Appearance Slow-growing lesion on sun- exposed skin; most are nodular
(waxy appearance, rolled pearly edges, and central ulceration— ‘rodent
ulcer’ typically found on face); other variants include
scaly patches— found on trunk) and
Investigation Biopsy and histology if large, followed by surgical excision;
pigmented.
usually fully excised initially if small and sent for histological analysis.
Treatment Excision (including Mohs’ surgery), topical chemotherapy,
radiotherapy, cryosurgery. See Box 6.3.
PrognosisBCC very rarely metastasize but can cause local tissue destruc-
tion (eg ear, lip) and very infrequently causedeath.
K Box 6.3 Mohs micrographic surgery
This involves surgical removal of the obvious tumour and a thin layer
of tissue from the site. This layer is frozen and stained then examined under a microscope. If there are tumour cells present, a further
(deeper) layer of tissue is removed, and the process is repeated until
the area is tumour- free. This procedure minimizes the need for large
skin excisions, while ensuring the entire tumour is removed.
Squamous cell carcinoma(SCC)
$ This accounts for 720% of cutaneous malignancies.
Risk factors Exposure to UV light (sunlight and sunbeds) or to industrial
carcinogens (eg arsenic, tar), chronic ulcer inammation, immunosuppression, premalignant conditions (eg Bowen’s disease, actinic keratosis).
Appearance Variable; typically eshy plaque or papule arising on sun-
exposed skin (770% on head and neck), often with bleeding, scaling, or
ulceration; other forms include
edge of legulcer;
Keratoacanthoma A rapidly growing nodule with cen-
Marjolin ulcerNew area of induration at
tral ulceration that usually spontaneously regresses and is considered by
most as a variant ofSCC.
InvestigationUsually none, may be biopsied.
TreatmentSurgical excision; topical chemotherapy, photo dynamic therapy
and immunomodulators used if unsuitable for surgery.
Prognosis If localized disease, excision gives 95% cure rate but SCC can
metastasize rapidly via local lymph nodes with poor outcome.
supercial (at, red,
4
4
Named after Dr Frederic E. Mohs who developed the original technique at the University of
Wisconsin and enthusiastically taught it to many others.
Malignant melanoma
$ Accounts for 74% of all skin cancers, but majority of skin cancer deaths.
Risk factors Pale skin, sun exposure, sunburn, tanning beds, multiple/
congenitalnaevi.
Symptoms/ signs A new, or changing mole, as assessed by ABCDE criteria:
Asymmetry, Border irregularity, Colour variation, Diameter increasing or
>6mm, Evolving over time. The Weighted 7-point checklist can also be
used:
Major features (2 points each) Change in size, irregular shape or
border, irregular colour;
Minor features ( point each) Largest diameter
≥7mm, inammation, oozing or crusting, change in sensation/itch. A
score of ≥3 indicates a more suspicious lesion but any concerning lesion
should be referred to dermatology. A lesion which stands out from those
around it is concerning—the ‘Ugly Duckling sign’.
ManagementSurgical excision, ±lymph node removal, ±chemotherapy, ±
immunotherapy (Box6.4).
Prognosis This depends upon completeness of excision, lymph node involve-
ment, presence of ulceration, and tumour thickness; these are combined to
give a stage (stage I:5yr survival almost 00%; stage IV:30%).
K Box 6.4 Immunotherapy in malignant melanoma
The development of immunotherapies (such as ipilimumab, nivolumab,
and pembrolizumab) and their application in malignant melanoma represent a paradigm shift in the treatment of this condition with even
metastatic disease now being amenable to treatment.
445SKIN CANCERS
5
5
Abbasi NR, etal. JAMA 2004;292:277 available free at Mjama.ama- assn.org
446 CHAPTER6 Skin andeyes
Legulcers
$ Loss of epithelial integrity with failure toheal.
Think about Venous insuciency, peripheral vascular disease,
neuropathic (eg DM), pressure ulcers, trauma, infection, pyoderma
gangrenosum (E p. 440), vasculitides, skin cancer, steroids.
Ask aboutOnset, duration, pain, trauma, claudication; PMH Peripheral
vascular disease, iBP, CVA, MI, angina, varicose veins, DVT, DM;
DHSteroids; SHSmoking, alcohol.
Look forNumber, site, size, base, edge, depth, shape, colour, oedema,
eczema, vascular disease (peripheral pulses, hair loss, cold), neuropathy
(sensation), infection (discharge, lymphadenopathy).
Investigations blds FBC, CRP, HbA
RhF, ANA,ANCA;
plex
USSor CT angiogram If ABPI abnormal; Wound swab(±X- ray/ MRI
if osteomyelitis suspected);
Ankle– brachial pressure index(ABPI E p. 506) ±du-
BiopsyAtypical areas. See Table6.4.
Table6.4 Clinical assessment oflegulcers
Venous (~80%) Arterial (~0%) Neuropathic (~0%)
History Obesity, immobility,
Leg Pigmented, varicose
Site Medial aspect of
Size Can be very large Usually small Usually small
Base Usually supercial
Edge Irregular, areas of
Sensation Painful Painful Relatively painless
varicose veins, DVT
veins, swollen, hot
legs
with sloughy
exudate
repeated healing
and exacerbation
Intermittent
claudication, HTN,
DM, IHD, smoker
Shiny, hairless, cold Joint destruction
Lateral malleolus,
toes, dorsum of
foot
Deep with a dark,
dry base, few signs
of healing
Well dened, often
circular
; consider ESR, complement,
c
Numbness, DM,
family history
Heel, metatarsal
head, pressure
points
Can be very deep
(extend to bone)
Surrounded by
thickened skin
Management Ensure good nutrition and treat the cause, where pos-
sible. Healing often takes weeks to months and is commonly managed by
community nurses, with ulcer clinic visits where appropriate:
• Venous Provided ABPI is >0.8 apply compression bandaging with
absorbable dressings to dry out the slough. Emollients and steroid
creams also help; may need debridement/ grafting
• Arterial Avoid compression bandages (unless under expert guidance);
address vascular risk factors and refer to a vascular surgeon for
consideration for bypass or angioplasty
• Neuropathic Careful footcare to avoid repeated injury, often needs surgical
debridement and antibiotics; osteomyelitis is common; assess for and treat
coexistent vascular disease; specialist diabetic foot teamifDM
• Infection Ulcers usually have bacteria present; infection or cellulitis
should be suspected if there is pus, excessive pain, surrounding
erythema, or pyrexia. Swab the ulcer and treat as for cellulitis,
if clinical signs of infection (Epp. 434–5). Organisms may be
colonizing the wound but not causing infection; be guided by the
clinical picture rather than the swab results.
No improvement Consider other diagnoses (including TB and cancer)
or dermatitis from therapeutic agents. Ensure swabs sent; discuss with
dermatology and consider biopsy. May need curettage or skin grafting.
K Box 6.5 Post- cannula swelling; ‘a tissued cannula’
This occurs when an IV cannula has not been inserted correctly and is sited
only partially in the vein or outside the vein altogether, meaning that uid
or drugs cannot be infused/ injected. Remove the cannula and re- site if
required, elevate the aected limb and give simple analgesia forpain. If no
improvement over next –2d consider possibility of infection of cannula
site (Ep.434); assess swelling for collection— if in doubt request USS— if
present, start IV ABx (eg co- amoxiclav .2g/ 8h IV) and discuss drainage
with surgeons.
447LEG ULCERS
448 CHAPTER6 Skin andeyes
2Acute red eye emergency
3Call for senior help or speak to on- call ophthalmologist urgently if
patient has new- onset dvisual acuity (VA) in aected eye. See Fig.6.3.
Pain?
No
Yes
Yes
Large
(dilated)
Yes
FOREIGN
No
Engorged
No
(constricted)
Foreign body
sensation?
Altered or
blurred vision?
Pupil size?
ACUTE ANGLE
CLOSURE
GLAUCOMA
Fig.6.3 Determining the likely cause of the acute redeye. (Red arrows indicate
topics that are discussed in more detail in the text.)
Sudden
onset?
Yes
BODY
vessels?
Yes
EPISCLERITIS/
SCLERITIS
Small
No
Photophobia?
CONJUNCTIVITIS
No
SUBCONJUNCTIVAL
HAEMORRHAGE
ACUTE ANTERIOR
UVEITIS
No
Yes
KERATITIS
3Keratitis (E OHCS1p. 334.)
$ Corneal infection or inammation; may ulcerate.
Symptoms Pain, photophobia, reduced vision, and foreign body sensation,
commonly in contact lens wearer or patients with dry eyes, blepharitis, or
autoimmune disorders.
Signs Conjunctival redness (can be sectoral rather than diuse as is often
the case in conjunctivitis). Fluorescein with a blue light may show punctate
epithelial erosions, a white patch (corneal inltrate/ ulcer), epithelial defect,
corneal haze (oedema), or hypopyon (pus in the anterior chamber).
ManagementRefer urgently for ophthalmologist, if ulceration present or sus-
pected. They may undertake corneal swabs/ scrapes to establish the cause.
Antibiotic eyedrops or systemic immunosuppression may beused.
3
Episcleritis and scleritis (E OHCS1p. 333.)
$ Inammation of white outer coating; often underlying autoimmune
disorder.
Symptoms Pain and tenderness— often mild in episcleritis but severe in
scleritis (wakes patient from sleep), occasionally with photophobia and
reduced vision.
Signs Mild localized redness (often involving just one sector, but occa-
sionally diuse); normal visual acuity; otherwise normal examination in
episcleritis. In scleritis the globe may be tender to touch and there may
be dvisual acuity.
ManagementUrgent ophthalmology review to consider scleritis.
Likely ophthalmic management Topical steroids or non- steroidal agents for
episcleritis, potentially oral immunosuppressants for scleritis.
3
Acute anterior uveitis (iritis) (E OHCS1p. 332.)
$ Inammation of pigmented parts of eye; associated with systemic
disease (eg IBD, arthropathies, sarcoid); pain on pupil constriction.
SymptomsBlurred vision, photophobia, andpain.
SignsRed eye, dvisual acuity, cornea usually clear, pupil may be irregular
and small, ±hypopyon (pus in the anterior chamber).
ManagementRefer urgently to ophthalmologist.
Likely ophthalmic managementIntensive topical steroids, dilating agents.
3Acute angle closure glaucoma (E OHCS1p. 331.)
K iintraocular pressure due to blockage of anterior chamber drainage.
Symptoms Aching eye pain (usually unilateral and severe), often associ-
ated with N+V; blurred vision and haloes around lights are common.
Signs Red eye, dvisual acuity, hazy cornea (if severe); pupil often mid-
dilated, can be unreactive to light and oval shaped (rugby ball- like); globe
tender and rm to touch. iintraocular pressure; usually >40mmHg.
Management Emergency referral to ophthalmologist; antiemetics and IV
opioids may be needed for symptoms but should not delay referral.
Likely ophthalmic management Constrict the pupil (miosis) with pilocar-
pine drops, and reduce aqueous formation with acetazolamide PO/
IV. Mannitol IV is also sometimes used to reduce intraocular pressure.
Denitive care achieved with peripheral iridectomy to allow constant
drainage of aqueous even when pupil dilated.
449ACUTE RED EYE EMERGENCY
450 CHAPTER6 Skin andeyes
Supercial foreign body (FB) and corneal abrasions
Symptoms Sudden- onset discomfort/ FB sensation; lacrimation and red-
ness; occurs, eg while hammering or chiselling without eye protection or
following minor trauma to the eye. Acontact lens may sometimes have
been ‘lost’ and cause FB sensation.
Signs Red, watering eye; FB may be visible. Always evert both top and
bottom lids to check for FBs here as well; visual acuity is usually reduced.
Fluorescein with a blue light may show corneal ulceration/ abrasion(s).
Treatment Often the eye needs anaesthetizing with topical local anaesthetic
(proxymetacaine, tetracaine, or oxybuprocaine) to allow examination and treatment. Gently pick up FB with cotton bud, or irrigate lavishly with sterile
0.9% saline. Re- examine eye afterwards to ensure all FBs have gone.
Protect the eye with an eye shield until local anaesthetic has worn o
and give chloramphenicol eye drops 0.5% 4h topical or ointment % 6h
topical for 3d.
speak to senior, or on- call ophthalmologist
If unable to remove FB or evidence of corneal abrasion,
.
Conjunctivitis
Symptoms Eye discharge, ±FB sensation, itch, concurrent cold, hayfever.
Signs Red eye, discharge, normal visual acuity, clear cornea. See
Table6.5 for causes.
Treatment Conjunctivitis can be highly contagious so care should be taken
with hand- washing;
Bacterial Topical antibiotics (eg chloramphenicol
drops 0.5%) to both eyes every 2h while awake for 2d, then 6h forwk;
Viral May need topical antibiotics to prevent secondary infections, but
usually self- limiting;
Allergic Identify allergen if possible and encourage
avoidance; topical antihistamine, (eg azelastine), or mast cell inhibitors
(cromoglicate) may oer relief; articial tears (eg Viscotears
if dry eyes are a problem.
Table6.5 Determining thecause ofa conjunctivitis
Bacterial Viral Allergic
Discharge Sticky, pus- like Watery Watery
Itch +/ – +/ – ++++
Recurrent +/ – +/ – Often seasonal
Contagious Yes Yes No
Uni- or bilateral One, then both One, then both Both
Other symptoms Often none Common cold Hay fever
®
) may help
Subconjunctival haemorrhage
Symptoms Often an incidental nding by the patient and usually benign;
can sometimes initially cause mild FB sensation. There should be no pain,
photophobia, or altered vision.
SignsDiuse area of bright red blood under conjunctiva, very dierent to
inamed blood vessels seen in other causes of red eye; normalVA.
TreatmentCheck BP, and if recurrent check FBC and clotting; may need
eye protection (eg tape at night) if swollen and unable to close readily;
discuss with ophthalmologist only if recurrent or severe.
Sudden visualloss
2Worrying features Severe decit, additional neurology, scalppain.
Think aboutRetinal vein occlusion, retinal artery occlusion, giant cell
arteritis, retinal detachment, arteriosclerotic ischaemic optic neuropathy,
vitreous haemorrhage, angle closure glaucoma.
Ask aboutLoss of vision; often painless.
Look for dvisual acuity or no vision in aected eye, RAPD (suggests optic
nerve dysfunction); abnormal fundoscopy. Check for other neurological
signs, for scalp pain/ tenderness, and ECG forAF.
ManagementImmediate referral to on- call ophthalmologist.
3
Giant cell (temporal) arteritis (E p. 373); dvisual acuity in
aected eye, typically with temporal headache/ pain, high ESR. May be
optic neuropathy, retinal artery occlusion, or extra- ocular musclepalsy.
3
Retinal artery occlusion (E OHCS1p. 345.)
SymptomsSudden, painless, and severe loss of vision.
SignsRAPD; pale retina with ‘cherry spot’ macula.
Risk factorsFor vascular disease (DM, smoker, ilipids,IHD).
Treatment If seen within h of onset, you may attempt to dislodge the
embolus by pressing hard on the globe, then suddenly releasing; most
damage will be irreversible.
3
Retinal vein occlusion (E OHCS1p. 346.)
SymptomsSudden, painless, and severe loss of vision; may be segmental.
SignsRAPD; engorged, red retina in aectedarea.
Risk factors These include age, chronic glaucoma, HTN, polycythaemia.
Treatment Supportive; laser photocoagulation and intravitreal steroids/
anti- VEGF can prevent neovascularization and treat macular oedema.
3
Vitreous haemorrhage (E OHCS1p. 347.)
SymptomsSudden painless loss of vision; oaters.
SignsRAPD; loss of red reex; unable to see retina.
Risk factorsDM (proliferative retinopathy), coagulopathy, trauma.
Treatment Haemorrhage should resolve spontaneously; prevent further
episodes by laser photocoagulation of peripheral retina; vitrectomy if
persistent.
3
Retinal detachment
SymptomsFloaters, ashing lights, shadow across vision, loss of vision.
SignsRAPD; loss of red reex, detachment on fundoscopy.
Risk factorsMyopia, iage, intraocular surgery, Marfan’s.
TreatmentUrgent ophthalmology review for vitrectomy or closure.
Optic neuritis This is often associated with a subacute, unilateral loss
of vision, with aching, pain on eye movements, and loss of colour vision.
Relative aerent pupillary defect; optic nerve usually appears normal
when inammation is retrobulbar;
disease (may be a rst presentation of MS);
resolution occurring over a fewweeks.
Causes These include demyelinating
Treatment Supportive, with
451SUDDEN VISUAL LOSS
452 CHAPTER6 Skin andeyes
Gradual visualloss
Think about Refractive error, cataracts, macular degeneration,
chronic glaucoma, diabetic retinopathy, optic atrophy, drug toxicity,
optic neuroma; inherited disease.
Ask about Painless loss of vision, symptoms of underlying disease.
Look for dvisual acuity or no vision in aected eye, pupil unresponsive
to light or RAPD (suggest optic nerve disorder), abnormal cornea, lens,
retina, or optic disc on fundoscopy.
Management This needs full ophthalmic assessment. If in- patient, try
and arrange for review before discharge, or refer as an out- patient. See
also Box6.6.
Cataracts(E OHCS1p. 350.)
Causes Age- related, DM, steroids, trauma, eye surgery; congenital.
SymptomsBlurred vision (bilateral), poor distance judgement (unilateral).
Signs dvisual acuity, cataract visible in lens; retina and red reex visible
unless cataract isdense.
TreatmentCataract surgery is performed on a single eye at a time if the
cataract(s) are interfering with lifestyle (eg reading or driving). They are
usually done as a day- case procedure under local anaesthetic; the lens is
removed (phaecoemulsion) and an articial lens implanted.
Age- related macular degeneration(E OHCS1p. 352.)
CausesAgeing, smoking.
SymptomsDeterioration of central vision.
Signs dvisual acuity, but normal visual elds; normal disc, but macula
often pigmented or bleeding upon fundoscopy.
Treatment This is aimed at reducing further visual loss; ‘wet’ (neovascular)
forms can be treated with intravitreal anti- VEGF injections.
Chronic (open-angle) glaucoma This results in peripheral visual eld
loss in those with iintraocular pressure(IOP);
the opticdisc;
β- blockers, eg timolol, or carbonic anhydrase inhibitors, eg dorzolamide)
or ireabsorption (prostaglandin drops, eg latanoprost); surgery involves
trabeculectomy (allows aqueous drainage into subconjunctiva).
Treatment This aims to dIOP by daqueous formation (topical
K Box 6.6 Registration ofvisual impairment
A consultant ophthalmologist can apply on behalf of a patient to register as
blind or partially sighted; this is a voluntary not a statutory process. Registration
entitles the individual to some tax allowances, benets, and some concessions
for public transport and other public facilities. Generally acuity <3/ 60 (after
correction) qualies as ‘blind’, while corrected vision <6/ 60 qualies as ‘partially sighted’; restriction of visual elds or loss of central vision may also qualify.
The Royal National Institute of Blind People advises on benet entitlements,
aids for the house, and independent living, and for guidedogs:
Royal National Institute of BlindPeople
05 Judd Street, London, WCH9NE
0303 23 9999 Mwww.rnib.org.uk
SignsCupping and atrophy of