Sarah Wood

Acute Wounds

Wound HealingKeloid scars:(children, young adults, genetics, black skin). No improvement with time. Can continue to enlarge. Overgrowth of dense fibrous tissue. HLA associated. No hair follicles or sweat glands on scar. Overgrows margins of original wound. Starts red, becomes pale or brown. Options for Tx: occlusive dressings, intralesional corticosteroid injections, compressive dressings, cryosurgery, radiation, laser.

Hypertrophic Scars:

Lumpy within the confines of the wound. Elevated, rarely painful, regresses spontaneously.

Acute Wounds - burns

1st degree – extend to epidermis of upper dermal layer only. Very painful, dead skin can peal.

3rd degree – skin = black, brown, yellow, red or white. Burn reaches subcut fat. Pain minimal – nerve endings almost all destroyed. No blistering, but hard, inelastic eschar

2nd degree – extends to deeper dermal layers, can blister, more moderate pain (damage to nerve endings.)

Fourth degree – the most serious. Reaches underlying fascia, can affect bone and tendons.no oedema, lots of eschar. Pain minimal.

Chronic Wounds

Venous Ulcers• Venous Ulcers – indicate severe venous

insufficiency. (valve incompetence, increased hydrostatic pressure and capillary permeability, increased pericapillary fibrin deposition.) 80% of leg ulcers. Think about RFs. Haemosiderin, telangectasia, atrophie blanche, eczema, lipodermatosclerosis, ulceration

Atrophie blanche with haemosiderin deposition

telangectasia

Neuropathic Ulcers• Frequently seen in diabetes, decreased

sensation, loss of autonomic function, anhidrosis, loss of intrinsic muscle function. Ulcers typically wet and deep. Often on pressure points and surrounded by callous. Tx: off-load weight, MDT, patient compliance, glucose control.

Arterial Ulcers• Usually below ankle. Look for signs of

decreased blood flow – cooler, hair loss, thin and shiny skin, dependant rubor, thick nails, reduced or absent pulses. Ulcers are typically small, distal with steep “cliff edge” and a dry bottom. Pain at night when leg elevated. Patient can have intermittent claudication. Tx: restore blood flow! Stop smoking! Control RFs (eg hypertension), NO compression.

Mixed arterial and venous ulcer

Photoaging and Skin Tumours

Photoaging (chronic sun exposure)

• Course, wrinkled, pale-yellow skin

• Telangectasia• Irregular pigmentation• Prone to purpura• Benign and malignant skin

tumours.

Bengin Epidermal Tumours

Actinic (solar) Keratoses

Solar (senile) Lentigos (“age spots”)

Seborrheic Keratoses (“seb warts”)

Skin Tags Epidermal Cyst

Milia

Melanocytic naevi

Benign Dermal Tumours

Dermatofibroma (commoner in females, can be a reaction to trauma

Campbell de Morgan spots (cherry angiomas)

Haemangioma

Pyogenic granuloma Chondrodermatitis nodularis

Intradermal Naevus

Low Grade Malignant TumoursBowen’s Disease (intraepidermal carcinoma, squamous carcinoma in situ). Can look like infection to start with.

Keratocanthoma – benign techincally? but can look like squamous carcinoma, so biopsy! Papular lesion with central umbilicated keratinous core.

Lentigo Maligna (Hutchinson’s melanotic freckle). Light brown with development of darker areas. Can turn into cancer later in life. Flat (macular) and when invades dermal layer, becomes lentigo maligna melanoma.

Malignant Skin Tumours• 1) Basal Cell Carcinoma – commonest. Rarely spreads.

Most are painless, history of sun exposure. Biopsy! Proliferation of atypical basal cells. Often clefts between tumour and dermis. Slow growing. Rolled-in edge, telangectasia, or nodular, or pigmented, pearly appearance.

• 2) Squamous Cell Carcinoma

Malignant tumour of epithelial keratinocytes – skin and mucous membranes. Sun exposure = major RF. Persists and grows. Can be solitary, keratotic or eroded, papular or nodular. Can arise from actinic keratoses. Lymph spread. Old men.

Pigmented Skin Lesions

Benign melanocytic naevus “mole” Seborrheic keratosis

• 3) Cutaneous T-cell lymphoma (mycosis fungoides)

Rare. Uncontrolled t-cell growth in the skin.

4) Malignant Melanoma

Questions:

How long have you had it? Has it changed? Over what period of time? Larger? Changed in colour or shape? Has it become itchy?

Facts:

Incidence = 10/100k/year (increasing 7% each year) F:M = 2:1 (equal in hot countries). Commonest sites = lower leg in women, back in men. Pre-existing naevus in 30%.

RFs: Previous Hx, FHx, Red hair, blue eyes, multiple melanocytic naevi, congential naevus.

Is it worrying? Breslow thickness (depth) and Clarks level (where it is in dermis in relation to other structures).

Prevention: SLIP, SLAP, SLOP! Report changes early.

Skin Manefestations of Systemic Diseases and Drug

Eruptions

Vasculitis!• 1) Henoch-Schonlein Purpura necrotising vasculitis of small vessels. Children. Palpable

purpuric rash, arthritis, haematuria, bowel angina and ischaemia. Post strep throat inf = most common.

• 2) Polyarteritis Nodosa rare, autoimmune, necrotising vasculitis of medium vessels.

Middle aged me. Renal failure, CHS, Cardiac involvement, pulmonary, GI, blood. Subcut nodules. Livedo Reticularis p-ANCA and ANA negative. Tends to follow artery lines. Can ulcerate and become necrotic. Common post HepB

• 3) Wegener’s Granulomatosis granulomatous vasculitis. URT and LRT, renal involvement,

arthritis, c-ANCA +ve. Saddle-shaped deformity. M>F

Tx: find and treat cause and systemic involvement. Pred/immunosupression, dapsone for cutaneous involvement.

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Erythema Nodosum• Inflammation of subcut fat causing

painful red nodules on the legs• Causes: 20% idiopathic, infection

(strep, TB), drugs (OCP), systemic diseases (IBD, Sarcoidosis)

• Tx: rest, analgesia, treat underlying cause

Erythema Multiforme• Reaction of dermal vessels

resulting in changes – papular and vesicobullous eruptions, TARGET-LIKE LESIONS!.

• Palms, soles, mucosal membranes

• If severe, “Stevens-Johnson Syndrome”

• Causes: 50% idiopathic. HSV, Strep, pregnancy, SLE, drugs (sulphonamides, phenytoin, barbituates, penicillin, allopurinol)

• Tx: Treat cause. Symptomatic care (analgesia, IV fluids if unable to drink etc)

Pyoderma Gangrenosum• Rapidly progressing ulcer,

often with erythematous to violaceous undermined edge. Can occur at site of trauma/surgical wound

• Causes: 50% idiopathic.• Associated with: RA, IBD,

Haematological malignancy, trauma

• Tx: Systemic steroids, immunosuppression.

Connective Tissue Diseases

SLE – Cutaneous Manifestations:

• Photosensitvity• Malar Rash• Raynauds

Phenomenon• SLE Vasculitis• Alopecia (typically

scarring)

• * Subacute cutaneous lupus erythematosus *

Positive autoantibodies, widespread rash, well defined, can get everywhere on body, photosensitive. Other body systems can be involved – heart (pericarditis), lungs (pneumonitis), CNS.

• * Discoid Lupus Erythematosus *

autoantibodies usually negative (<20% ANA). Only 5% develop SLE. Discoid lesions on sun-exposed sites. Scarring alopeica.

Systemic Sclerosis• Autoantibodies positive: Scl-

70, centromere antibodies. • F:M = 4:1• Proximal skin sclerosis and

any 2 of: sclerodactyly, digital pitting scars, pulp loss and bi-basal lung fibrosis

• CREST Syndrome has less internal involvment and a better prognosis (Calcinosis, Raynauds, Oesophageal stricture, sclerodactyly, telangectasia)

calcinosis

Morphea• Localised fibrotic plaques, atrophic changes, self-limiting,

no internal involvment. Localised cutaneous sclerosis. Indurated plaques with erythematous edge or brown macules. F:M = 3:1.

Dermatomyositis• Spectrum of disease• Polymyositis: high CK, CRP• Jo-1 Antibodies• 60% ANA positive• Photosensitive rash• Heliotrope (purple) changes

on face• Red papules on dorsa of

hands and fingers (gottron’s papules)

• If >55yrs, associated with malignancy – breast, lung, stomach, uterus, colon

Heliotrope rash

Gottron’s papules

Muscle biopsy: pink muscle cells being attacked by inflammatory cells

Manifestations of Malignancy, Endocrine Conditions, and Drug

Eruptions

Manifestations of MalignancyAcanthosis Nigricans: typically neck and axillae. Papillomatous. Associated with GI malignancy.

Pagets Disease of the Nipple: associated with Breast Ca, suspect if unilateral breast eczema.

Secondary Cutaneous Metastases: various. Present late, represents poor prognosis. Usually scalp, trunk, umbilicus.

Erythema Gyratum Repens: associated with Lung Ca.

Cutaneous Manifestations of Endocrine Disease

HYPERPIGMENTATION: Addisons, pregnancy, Cushings

VITILIGO: Addisons, organ specific autoimmunes, DM, thyroid disease

HIRSUITISM: Cushings, PCOS

GRANULOMA ANNULARE: generalised in IDDM

NECROBIOSIS LIPIODICA: IDDM

PRETIBIAL MYXOEDEMA: Grave’s Disease

Drug Eruptions• Almost all drugs can cause rashes. Certain ones more likely to cause a certain

pattern. 2-3% of hospitalised patients. Ask about drugs started in the last 2-3 weeks, inc. OTCs.

Erythema Mobilliform: eg. amoxicillin

Fixed Drug Eruption: eg. Streptomycin, cephs.

Generalised Fixed Drug Eruption: eg. Anticonvulsants, aspirin, NSAIDS, phenobarbs, doxycycline, metronidazole etc etc.

Hypersensitivty Reactions:• Type I: IgE mediated. Causes Urticaria, angioedema,

anaphylaxis• Type II: cytotoxic leading to haemolysis, purpura.• Type III: immune comples reaction, resulting in

vasculitis, serum sickness, urticaria• Type IV: delayed-type reaction with cell-mediated

hypersensitivity resulting in contact dermatitis, exanthematous reactions, photoallergic reactions.

TEN – Toxic Epidermal Necrolysis• Erythema-multiforme =>

Steven-Johnsons Syndrome => toxic epidermal necrolysis

• Allopurinol, Anticonvulsants, aspirin, isoniazid, sulphonamides, penicillins. (can also be cause by things like infection! herpies especially.)

• Fever, chills, headache, D&V, no pruritis. Can get mouth involvment/GU involvment.

• Macules => papules, vesicules, bullae, uritcarial plaques, erythema.

• TEN: Muco-cutaneous detatchement. Burns unit.

• TEN: up to 30% die

Eczema

Exogenous (contact) Eczema

• 1) Irritant

• 2) Allergic

• 3) Photodermatitis

Endogenous and Mixed Eczema

• 1) Atopic Eczema

• 2) Seborrheic Eczema

• 3) Discoid Eczema

• 4) Pompholyx Eczema

• 5) Gravitational Eczema

• 6) Asteatotic Eczema

• 7) Lichen Simplex Eczema

Psoriasis

Types of Psoriasis

• 1) Chronic Plaque

• 2) Guttate

• 3) Flexural

• 4) Scalp Psoriasis

• 5) Palmar-plantar pustulosis

• 6) Generalised Pustular Psoriasis

• 7) Erythroderma

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Nail Changes in Psoriasis

Pitting

Onycholysis

ridging

Nail loss

discolouration