Integument problems

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Chapter 1 Integument problems

Jane Fox, David Speakman

1.1 Introduction

Many lesions of skin or subcutaneous tissue are easily recognised and a diagnosis can be made virtually on inspection alone. Lipomas, ‘sebaceous’ cysts and ganglia are very common and usually have classic diagnostic features. Subcutaneous swellings are thus commonly benign — malignancies are rare but important to recognise. Many focal surface lesions are also benign and easily diagnosed; however, skin cancers are also common and any hint of malignancy requires biopsy for a certain diagnosis.

Dermatological conditions are more extensive secondary skin reactions representing a more general abnormality of the skin and subcutaneous tissues. There are many causes of dermatitis and most are not considered here except for a brief outline of common dermatological terms. Skin lesions are often associated with a secondary skin reaction.

An ability to accurately describe skin changes facilitates clinical communication and record keeping.

Focal skin lesions are divided morphologically into four main types: macules; papules or nodules; vesicles or pustules and wheals (Fig 1.1).

A macule is a localised surface change in skin colour without bulk or substance. It is important to note whether the colour change is permanent or blanches on compression. A lightly pigmented brown or tan macule is called a lentigo or freckle. A papule is a small solid projection above the skin surface; a larger papule is called a nodule. A flattened nodule is described as a plaque. Vesicles are elevated fluid-containing lesions: When large they are called bullae or blisters and when they contain pus, pustules. Acne (Greek — a facial eruption) comprises multiple small pustules, which if embedded are described as comedoform. Milia are tiny embedded cutaneous plaques due to keratinous retention foci; they are most common on the facial skin. Wheals are white, raised lesions of localised dermal oedema without blistering. Widespread wheals are often called urticaria, an atopic (allergic) reaction. If the skin is broken the lesion is an ulcer. Distinct morphological types of ulcer are also described (Fig 1.2).

image

Figure 1.2 Types of epithelial ulceration

Sources: Squamous cell carcinoma: From Rakel 2007; Basal cell carcinoma: From Rakel 2007; Venous ulcer: From Bolognia et al 2007; Neuropathic ulcer: From Bolognia et al 2007; Peptic ulcer: Courtesy of Robin Foss, University of Florida; Anal fissure: Courtesy of Gershon Effron, Sinai Hospital of Baltimore; Keratoacanthoma: From Habif 2003.

Secondary skin reactions result from scratching or from the effects of the primary lesion itself. In a dry lesion the flaky or powdery shedding of the stratum corneum, the horny layer of the skin, is known as a desquamative or psoriatic reaction. In many superficial ulcers, vesicles, pustules or bullae, desquamated epidermal cells form a scab: a crust of dried exudate. An eschar is a patch of necrotic skin, typically caused by a deep burn; slough is the dead or devitalised tissue in the base of an ulcer. Lichenification is leathery thickening of the skin around a lesion, usually due to chronic inflammatory fibrosis, which often also produces subcutaneous induration around an ulcer. Induration can also be due to malignant infiltration. Diffuse skin pigmentation is often seen around ulcers, especially venous ulcers of the lower limb — the pigment is brown haemosiderin.

Haemorrhages into the skin occur in various forms. Purpura is a haemorrhagic disorder in which spontaneous bleeding occurs into the dermis and epidermis of skin or into mucous membranes, causing a red or purple macular lesion. Minute (1 mm or less) punctate spots of epidermal bleeding are called petechiae. Larger, less sharply defined areas, often with subcutaneous swelling, are known as ecchymoses or bruises. Haematomas are focal areas of subcutaneous haemorrhage that elevate the skin. Purpura may follow drug reactions, sepsis or haemopoietic malignancies and occurs spontaneously in the old, particularly on the hands and forearms (senile purpura). Purpura is commonly associated with vascular fragility; petechiae are more characteristic of a coagulation disorder such as thrombocytopenia.

Cutaneous haemangiomas are of various types (congenital, hamartomatous, degenerative and neoplastic). Telangiectasis are small focal collections of dilated blood vessels in the skin or mucous membranes. Spider naevi are bright red arteriolar spots with radiating surrounding capillary vessels, located mainly over the upper trunk and face.

Skin pathologies such as haemangiomas or epithelial neoplasms can vary widely in their morphological appearance, despite a common cause. Basal cell carcinoma may appear as: a nodule or plaque; a comedo-like lesion; a cystic lesion; a small area of scaly psoriatiform skin; a pigmented skin lesion; a healing ulcer; or an area of subcutaneous induration and sclerosis. The burrowing ulceration with extensive tissue destruction of the classic ‘rodent’ ulcer is a further late and too-long neglected manifestation.

Morphological terms also define dermatological conditions. Eczema is a blotchy, ill-defined, red macular rash that can progress to papule and pustule formation. Dermatitis can be either wet (usually because of its site e.g. intertrigo, nappy rash) or dry, where it can be associated with the features of hyperkeratosis (hypertrophy and hyperplasia of the stratum corneum), lichenification and pigmentation. When itch precedes the rash, the condition is called neurodermatitis; itchiness following the rash is more suggestive of contact dermatitis. Acanthosis is a hyperkeratotic reaction of prickle cell overgrowth. Acanthosis in association with pigmentation (acanthosis nigricans) is often secondary to a gastrointestinal or haematological malignancy.

A morbilliform rash is a large, red, blotchy, confluent ill-defined macular rash seen on the face, neck and trunk (measles) or on the limbs (drug sensitivity reactions). Psoriatiform lesions are flat, red papules with silvery scales, which can be associated with dry eczema or basal cell carcinoma; psoriasis is a primary skin condition occurring on the extensor surfaces of the limbs and around the nails. Impetiginous lesions are pustular nodules with crusts seen in eczema, herpes, staphylococcal and yeast infections of the skin. Acneiform lesions are small, pointed pustules that may be a primary condition or occur secondary to drug sensitivity. Acne rosacea with telangiectasis, when marked over the nose and associated with sebaceous gland overgrowth, is called rhinophyma. A pemphigoid lesion is a large bullous eruption of the skin.

Erythema nodosum is a condition in which flat red nodules are found on the lower limbs. They occur in association with tuberculosis, rheumatic fever, some drug reactions, sarcoidosis and inflammatory bowel disease. Vitiligo is a well-defined area of depigmentation found on exposed areas and usually is of little clinical significance and poorly understood but sometimes associated with endocrine abnormalities. Erythema ab igne is an area of mottled pigmentation seen on the front of the knees and shins from longstanding exposure to heat, particularly radiant heat such as from sitting in front of a radiator.

The clinical history of a lump or ulcer

2 Change and progression

The rate of progression helps to distinguish between benign and malignant conditions (Table 1.1). A skin lesion that progresses to a significant lump within a few days suggests infection (e.g. pyogenic granuloma); in a few weeks, hyperplasia (e.g. keratoacanthoma); or over several months, malignancy (e.g. basal and squamous cell carcinoma, melanoma). A pigmented skin lump that has not changed over several years suggests a benign mole. Most subcutaneous lumps are benign and very slowly progressive. ‘Sebaceous’ or epidermoid cysts are prone to infection, partial resolution and recurrence. Sometimes a ganglion may rupture after trauma and disappear, to return later. Abdominal wall hernias may appear suddenly after a strain and slowly progress; they are usually reducible and reappear on standing. Basal cell carcinomas may appear to heal in part of their circumference but are usually inexorably progressive.

Table 1.1 Growth pattern of some common skin nodules

  Length of history Clinical appearance
Basal cell carcinoma Months to years Pearly nodule
Central crusting and ulceration
Rolled or beaded, telangiectatic edge
Any site, especially head and neck
Squamous cell carcinoma Months Indurated, ulcerating, raised nodule, everted friable edge
Contact bleeding
Sun-exposed surfaces
Keratoacanthoma Weeks Rapidly growing
Dome shaped
Volcanic apical ulceration
Sun-exposed surfaces
Pyogenic granuloma Days or weeks Small, soft, cherry red lesions
Contact bleeding
Common on mucocutaneous surfaces

The physical examination of a lump or ulcer

The routine sequence of examination involves inspection, palpation, percussion, auscultation and movement.

An abnormality in a bilateral structure should be compared and contrasted with its normal side. Assessment of a lump traditionally follows a sequential analysis of its characteristics (Box 1.1). Although not all the features are applicable to all lumps, it is essential to follow an ordered sequence when characterising any lump. The most important features are the site (which should be defined anatomically in all dimensions) and the physical characteristics, including relationships of the lump to its surroundings.

1 Situation and depth

If you can accurately describe the anatomical position of a lump and know the range of pathology possible at that site you will more easily make a clinical diagnosis.

Situation is described regionally in relation to the body surface. Depth is assessed in relation to the skin and deeper layers. The region occupied by the lesion is defined. The relationship of the lesion to surface landmarks, including distance of the lump from prominent bony points, is recorded. Many lumps are characteristic of specific regions: ‘sebaceous’ cysts occur in the scalp and scrotum, implantation dermoid cysts occur mainly in the hand. Lipomas are most often found in the subcutaneous tissues of the trunk or limbs. Ganglia, tendon sheath swellings and bursae occur at defined points near joints, bony prominences and tendons. Lymph node swellings occur in defined anatomical areas.

The site of ulcers is often also suggestive of their diagnosis. Ischaemic ulcers are at the tips of digits or over points of pressure necrosis — the latter often suggesting neuropathy. The ulcers of venous insufficiency are usually situated around the ankle and lower leg.

The depth of the lesion in relation to the skin must always be noted. A lump is ‘layered’ in the correct anatomical plane; an ulcer’s floor, base and edge are assessed. A lump in a limb will be arising primarily from or involving skin, subcutaneous tissue, muscle layers or the underlying bone. On the trunk it will be important to determine if a lump is within the body cavity or the parieties. Assessment of depth should be ordered and precise and demands accurate sectional anatomical knowledge of the region. Lumps in the subcutaneous fat plane that are attached to the fascia investing deeper muscles will have their mobility impaired when the muscles are tensed. A lump below the fascial plane will be obscured, as well as becoming less mobile, when the muscles are tense. Bony lumps are fixed and immobile.

The edge of an ulcer may be protuberant and elevated above the skin surface, suggesting malignancy. A healing ulcer has pink healthy granulation tissue in the floor and the edge is made less distinct by a thin overlying layer of regenerating epithelium that may appear bluish. A sloughing floor, with induration extending around the base and sharply outlined edges, suggests chronicity. Deep chronic indolent ulcers with little granulation tissue are often ischaemic.

3 Shape and surroundings

The lump’s shape and physical characteristics are defined in the subsequent steps of examination. Following a practised sequence ensures that no important details, such as the presence of pulsation within the lump, are omitted.

The shape of a lump or ulcer can be regular or irregular. Regular shapes are spheres, circles and ovals.

A smoothly regular spherical lump strongly suggests a cyst. Most solid lumps have slight or prominent irregularities of shape, even when generally spherical or oval. To describe a lump’s shape as spherical implies that it has been assessed totally in three dimensions. This is only possible with very mobile lumps or when an adjunct to examination such as an ultrasound is available. More often only a portion of the circumference of the lump can be felt and its roundness implied from this assessment. Cystic liquid collections are common in skin and subcutaneous tissues and include ‘sebaceous’ cysts and bursae.

Solid lumps such as lipomas, neurofibromas and lymph nodes are usually irregularly round or oval in shape. Lipomas have another very characteristic feature: they are lobular, mirroring their origin from lobulated fat. They thus form mobile soft lobulated subcutaneous lesions with an indistinct ‘slipping’ edge, unlike ‘sebaceous’ cysts that are spherical and firmer, are attached to the skin and have distinct margins. Lymph nodes also have discrete margins and, when multiple, present as lobulated or bosselated swellings with a defined edge.

Lumps arising from the skin may be nodular, flattened, dome-like or polypoidal in shape; polyps may be sessile or pedunculated. Neurofibromas of the skin form soft, domed lumps (molluscum fibrosum). Subcutaneous neurofibromas form firm, fusiform subcutaneous swellings at the site of nerves.

Many anatomical structures have such a characteristic shape and such constancy of position that a swelling of the whole organ can often be identified virtually on sight: thyroid and parotid glands, kidney, liver and spleen. Tubular or dumb-bell-shaped subcutaneous lesions suggest enlargements of tendon sheaths.

Ulcers can be regular or irregular in shape and their edges can also be described as serpiginous, sloping, everted, rolled, overhanging or punched-out (Fig 1.2). Brown pigmentation, a desquamative rash and induration of skin and subcutaneous tissues around an ulcer suggest venous insufficiency. Redness, heat, oedema and cellulitis indicate active spreading infection.

The lump’s relationship to its surroundings is assessed. Impaired mobility, with attachment to surrounding structures, is an important diagnostic sign. Relationships must be assessed in all dimensions. Attachments to overlying skin and deeper layers are noted, as well as any effects on key local structures such as nerves, tendons or tubes such as blood and lymph vessels and viscera. Nerve function proximal and distal to the lesion is noted, as are the effects of tendon and joint movements. Evidence of arterial or venous insufficiency, of lymphatic enlargement or obstruction, or of visceral obstruction or fistulation, is sought.

6 Consistency

The consistency of the lesion is often very helpful in diagnosis. The simplest classification of consistency of lumps is:

Apart from these four grades, familiar analogies can help to describe size and consistency (e.g. golf ball or tennis ball size and feel). A diagnostic description (solid or cystic lump) combines the clinical features of shape, contour, consistency and other aspects.

A cyst is a localised collection of fluid: cysts in body tissues mostly contain liquid, a few contain gas (lung cyst, pneumatosis coli). Cysts usually have an epithelial lining. The term pseudo-cyst is often applied to pancreatic and peripancreatic liquid collections without an epithelial lining.

Associated physical features that should be considered along with consistency are compressibility, cough impulse, reducibility and pulsation.

Compressibility is the sign of emptying on pressure. This sign is found with venous lakes and cavernous haemangiomas (compressible, but not pulsatile, vascular lesions); with hernias (compressible and reducible lesions); and with some bursae and ganglia that communicate freely with adjacent joints. After emptying on pressure, lesions may refill when the pressure is released. Hernias may not recur and refill unless the patient stands or is made to cough.

Vascular blushing on compression is an allied important sign, which occurs when some pigmented vascular lesions are compressed with a transparent slide. Cavernous haemangiomas, telangiectasis and spider naevi show this sign; in the case of spider naevi it occurs when the central arteriole is compressed. Port wine stains (capillary haemangiomas) and senile angiomas, where the colour is not due only to easily displaced intraluminal blood, do not show the sign, nor do purpuric or petechial spots.

Cough impulse: on coughing an expansile impulse is felt over a hernia. Hernias share this sign with venous swellings associated with valvular incompetence and with meningoceles.

Reducibility is a term usually applied to hernias. Venous swellings, pharyngeal diverticula and some ganglia communicating with joints can also be reduced by recumbency and pressure.

Pulsation may be apparent on inspection. It should be confirmed by palpation and checked to be synchronous with the pulse. Venous pulsation is usually visible but impalpable; arterial pulsation is visible and palpable. Pulsation may be truly expansile due to an aneurysm or a very vascular solid lump such as a toxic goitre or vascular neoplasm. Pulsation may, however, be transmitted to the lump by a nearby blood vessel. Differentiation between the two forms of pulsation can be very difficult, particularly with deeply situated lumps such as para-aortic lymphadenopathy versus an abdominal aortic aneurysm. Help can sometimes be given by the two finger test: a finger is placed on either side of the swelling — movement of the fingers in the same direction occurs with transmitted pulsation and centrifugally divergent movement occurs with expansile pulsation. The test is often difficult to interpret.

If pulsation is detected it is essential to also test for a thrill on palpation and a bruit on auscultation. These findings suggest arterial stenosis, aneurysm or arteriovenous shunting.

1.2 Focal skin lesions

Most focal skin lesions will be manifestly benign longstanding lesions of congenital or acquired origin that have caused the patient no problem and require no treatment. Benign skin lesions include a large number of congenital blemishes, moles, malformations and hamartomas. Benign neoplasms, localised infections and miscellaneous causes are also common (Fig 1.4). An important group of lesions are dysplastic and premalignant. Accurate diagnosis of this latter group is extremely important, as early surgical treatment of suspicious skin lesions is curative for most forms of skin malignancy. Screening programs and self-examination in high-risk populations have been employed but vary in effectively diagnosing early lesions. Repeated practice at assessing common skin lesions rapidly improves diagnostic skills. Accurate diagnosis relies first on a careful history and examination.

Focal skin disorders can be assessed on clinical grounds into:

Pigmented lesions (naevi) form a distinct category within each of these two groups.

Clearly benign lesions

Benign skin lesions will usually have been present from birth or for many years without change. In children and adolescents, congenital moles and vascular malformations are common, as are freckles and infective warts; skin malignancies are rarely seen (Box 1.2). In adulthood, degenerative and other specific lesions occur with increasing frequency in patients over the age of 40 years (Box 1.3); differentiation of benign lesions from cancers becomes increasingly important. Lesions are defined as macules or nodules. Common macules are the port wine stain, café au lait spots (neurofibromatosis), some junctional naevi and freckles. Freckles are common in children and adolescents. In older patients senile freckling of the skin is common, as are spider naevi and senile purpura. Common benign nodules include pigmented moles and angiomas. Verrucous lesions are also common in children and adults. Benign skin tags and keratoses are seen with increasing frequency in older patients. Benign traumatised lesions may ulcerate. In adults this always invokes suspicion of malignancy; in children benign ulcerated or infective lesions are relatively common. Skin vesicles occur with herpetic infections, eczema and impetigo.

Clinical features, diagnostic and treatment plans

Diagnosis in most instances can be made on clinical assessment including dermoscopy. Most lesions will need no treatment other than reassurance. Many are specifically age-related.

Children

Intradermal, junctional and compound naevus

Intradermal naevus is the most common benign mole, deriving its name from the fact that the pigment cells lie entirely within the dermis (Fig 1.5). The macroscopic appearance varies considerably: from a soft flattened pale brown or flesh-coloured nodule or macule, to a deep brown warty excrescence. The edge is usually well defined. Many contain hair, which is a helpful diagnostic point — hairy moles are virtually always intradermal and benign. Intradermal naevi occur all over the body skin and are usually present from birth but are rare on the palms or finger-tips. They vary in size from a few millimetres to large lesions several centimetres across. They are biologically conservative, wholly benign lesions, throughout life.

Junctional naevus. As its name implies, this lesion contains pigment cells at the junction of epidermis and dermis. Macroscopically these are flatter, often macular lesions, of varying depth of pigmentation. They vary in size from a few millimetres to several centimetres. They may be present at birth or appear later. The edge is sometimes less well defined than that of an intradermal naevus.

Compound naevus contains both junctional and intradermal components. In almost all moles the radical youthful potential of the immature junctional melanocyte progresses to a maturely conservative intradermal adulthood. Occasionally a junctional or compound naevus develops malignant change in adulthood.

Few pigmented moles in children will need treatment. Malignant change does not occur until puberty but skin malignancy is seen in teenagers, albeit rarely. Surgical removal may be required for cosmetic reasons or because of an inconvenient site.

Adults

‘Suspicious’ Lesions

Malignant and premalignant skin lesions are common in countries such as Australia with a susceptible population and excessive solar exposure. Malignant melanoma is virtually unknown in children but occurs throughout adult life. Its frequency in most countries is increasing. Basal and squamous cell cancers occur in older patients. Multiple lesions are common and an individual who has had one malignant skin lesion is at greater risk of developing both non-melanoma skin cancer and melanoma. Many benign lesions can mimic malignancy; excisional biopsy is the preferred treatment for any suspicious lesion. This biopsy should be performed by the surgeon responsible for continuing treatment.

Skin ulcers may be of vascular or traumatic origin. Common focal lesions that ulcerate include pyogenic granuloma, keratoacanthoma, basal cell carcinoma, squamous cell carcinoma, melanoma and any traumatised benign lesion.

Clinical features and diagnosis

5 Malignant melanoma

This is the most malignant of all skin tumours. It occurs throughout adult life. Melanomas are particularly prevalent in fair-skinned populations in tropical climates. They are more common in females than in males and their geographical frequency varies widely. Melanomas are rare in black races, except in depigmented areas of skin. Any brown or black mole that shows increase in size, irritation, bleeding, nodularity or ulceration should arouse suspicion and should be excised (Fig 1.6).

An important subgroup (amelanotic melanoma) are not pigmented and will be difficult to tell macroscopically from SCC or BCC or infective lesions. Common sites for melanoma are the face, limbs and trunk. Poor prognostic factors relate to increasing depth of the lesion, ulceration, mitotic count, satellite or transit nodules and lymph node spread. Spread to regional nodes is common and considerably worsens prognosis. Blood-borne metastases may occur at any site. Several clinically distinct macroscopic types can be recognised and have progressively worsening prognoses.

Hutchinson’s melanotic freckle (lentigo maligna melanoma). This presents initially as a dark brown macular stain on the face of older patients, particularly elderly women. Histology shows junctional activity without invasion and the lesions can remain stationary for years. Spreading growth continues laterally in an irregular fashion, giving a distinct but irregular edge and a typically variegated pigmented appearance of the surface. The lesion will invariably progress ultimately to malignant change and the edge of the malignancy can be difficult to define.

Superficial spreading melanoma. This is the most common type of melanoma. It has a short pre-invasive stage in which spread is lateral, giving a brownish-black papule with an indistinct macular edge, proceeding to invasive spread.

Nodular melanoma. This type has the worst prognosis and spreads laterally and invasively from an early stage; malignant deep invasion is also seen early.

Treatment plans

Focal lesions that are suspicious of malignancy require surgical excision. An ulcerated lesion automatically induces suspicion. Lesions can usually be sorted clinically into those in which the diagnosis of BCC, SCC, keratoacanthoma or melanoma is fairly clear-cut and those in which the diagnosis is equivocal. Many diagnostic mimics exist (Table 1.2). Surgical excision provides a tissue diagnosis and for most lesions is curative with one procedure. Massive and cosmetically disfiguring excisions should not be performed.

Table 1.2 Malignancies and their mimics

Malignant lesion Common mimics
Basal cell carcinoma ‘Sebaceous’ cysts
Acne
Psoriasis
Dermatofibroma
Other focal infective lesions
Squamous cell carcinoma Solar keratosis
Bowen’s disease
Keratoacanthoma
Infected ‘sebaceous’ cyst
Pilomatrixoma
Pyogenic granuloma
Dermatitis artefacta
Any focal ulcer
Malignant melanoma Benign pigmented naevus
Dermatofibroma
Pigmented BCC
Seborrhoeic keratosis
Amelanotic melanoma Squamous cell carcinoma
Pyogenic granuloma
Kaposi sarcoma Benign haemangioma
Dermatofibrosarcoma protuberans Dermatofibroma
Merkel cell tumour BCC, haemangioma

5 Melanoma

Treatment of all suspicious lesions (Box 1.5) is by surgical excision and confirmation of diagnosis by histology. Excision should be adequate in width and depth. It is difficult to define precisely the requirements for adequate excision; for benign skin lesions 1–2 mm is adequate. Recommended margins relate to the depth of the tumour. Where adequate excision and primary closure is not cosmetically acceptable, plastic and reconstructive options should be considered in surgical planning.

The management of melanoma and the prognosis depends on the thickness of the primary tumour, its size and the extent of local and distant spread. If regional nodes are affected they should be removed. Sentinel node biopsy is an important staging procedure.

Melanomas are relatively resistant to most forms of adjuvant treatment: irradiation, chemotherapy and immune therapy have all been employed and further treatment is best considered within a multidisciplinary clinic.

The most reliable prognostic local indicator after putatively curative excision is the depth of the lesion. This can be staged either by:

Lymph node involvement considerably worsens prognosis at any stage. The natural history of recurrences or metastasis is very variable. Late metastases — 10 years or more after the initial presentation — are quite common, so follow-up should be prolonged and meticulous, looking for locoregional and distant metastatic disease and new primary lesions. Therapy for recurrent melanoma may include excision of metastatic disease (Table 1.3).

7 Other malignant or infective skin lesions

Infected or traumatised benign lesions. Infection and recurrent trauma can mimic malignant change. Infected ‘sebaceous’ cysts (Ch 1.3) can mimic squamous or basal cell carcinoma. Other benign lesions mimicking malignancies include seborrhoeic keratosis, dermatofibroma and pilomatrixoma. Pigmented BCC and benign moles can each mimic malignant melanoma.

Lymphoma of skin. Lymphomatous deposits in skin (mycosis fungoides) are sometimes seen; other stigmata of lymphoma may suggest the possible diagnosis. Focal lesions are treated with excision and radiotherapy.

Cancer. Localised skin deposits of various cancers may be due to blood-borne or lymphatic spread or due to direct skin involvement from the underlying disease as in breast cancer.

Acanthosis nigricans presents as a thickened brown induration of skin with warty excrescences, most commonly in the groins and axillae. It is usually a paraneoplastic skin reaction to a gastrointestinal, lung or haematological malignancy. A congenital benign form also occurs. It is uncommon.

Infective skin lesions usually present as ulcers rather than as nodules, but sometimes amoebic or tuberculous (lupus vulgaris) or other infections are seen presenting as nodules in nonendemic areas. They will usually require excision for diagnosis.

Dermatofibrosarcoma protuberans. This uncommon tumour is a malignant soft tissue neoplasm occurring on the skin of the back or trunk. There is usually a biphasic growth pattern with slow growth of an intracutaneous plaque over months or years, followed by rapid development of nodular lesions that might ulcerate and bleed. The tumour is locally malignant but does not tend to metastasise till very late. Wide local excision is required to prevent recurrence.

Merkel cell tumour. This is a rare but very malignant tumour arising from sensory dermal elements, which can mimic BCC or haemangioma.

Pigmented skin lesions

Pigmented skin macules and nodules form a distinctive group. The most common pigmented skin lesion is the benign common ‘mole’. Other causes in children and adults include lesions of vascular origin and a miscellany of benign and malignant conditions.

Colour can range from bright red through all shades of brown to black. Pigment can be due to blood elements in vascular lesions — often easy to pick at a glance but less easy when the pigment is brownish haemosiderin. Melanocytic naevi are brown or black or variegated; other causes of pigmentation include epidermal and dermal debris and carbon. It is important to differentiate from this heterogeneous group the most dangerous skin malignancy of all — malignant melanoma. Rapid growth, irritation, contact bleeding and ulceration should always be presumed due to malignancy until proven otherwise by histology.

1.3 Subcutaneous lumps

A subcutaneous lump is a very common clinical problem. Most are longstanding and the vast majority are benign lesions.

Clinical features and treatment plan

Distinction on clinical grounds alone can almost always be made between the four most common lesions: lipomas, cysts, ganglia and bursae. Most are painless. In many instances simple reassurance is all that is required. Such reassurance can be given with confidence and without any additional investigations if clinical assessment has been thorough and orderly.

1 Lipoma

The most common of all subcutaneous lumps is a benign tumour of adipocytes: lipoma. Lipomas are usually found on the limbs and trunk but can occur anywhere there is fat. Lipomas in less common sites (e.g. breast, parotid gland, subfascial or intramuscular) can cause diagnostic difficulty with other common lumps at these sites (breast cancer, salivary mixed tumour, muscle sarcoma) and the classic physical signs of lipoma can be distorted by the overlying gland capsule or deep fascia. Subfascial lipomas, for example, have their mobility decreased or might even disappear on contraction of the muscle. Lipomas in subcutaneous fat are virtually always benign. Although they can become very large, they always exhibit simple expansile growth — never invading surrounding tissues, just displacing them. If adequately excised, they will not recur. In contrast, lesions in the retroperitoneum are frequently malignant: liposarcoma. These will invade locally and frequently recur after excision.

Subcutaneous lipomas present as very slow-growing, soft, painless, subcutaneous swellings. The surface contour is classically lobulated. In areas of lax skin they are freely mobile in the subcutaneous layer and consequently tend to slip from beneath the palpating finger (Fig 1.8). Mobility and freedom from attachment to the skin, although classic and helpful signs, are not invariable. In regions such as the back of the neck, where the skin is thick and the underlying subcutaneous fat is closely attached to it, a large lipoma just beneath the skin tends to be firmer and flatter. The lipoma then cannot be moved independently of the surface skin nor can the skin be pinched or pushed away from the lump without skin dimpling. Differentiation from sebaceous cyst becomes more difficult in these circumstances but the irregular shape and lobulated contour of the lipoma, as distinct from the spherical shape and smooth surface of the cyst, usually are unequivocal contrasts. In areas of very lax skin, lipomas can become pedunculated but this more commonly occurs with cutaneous neurofibromas. Lipomas are often fluctuant. Firmer or deeper ones and those beneath thick overlying skin are not fluctuant. Lipomas do not usually transilluminate.

Patients often have more than one lipoma. More striking (and quite common) is the condition of multiple, symmetrical, painless subcutaneous lipomas of limbs and trunk, which is sometimes familial. These patients do not have the cutaneous and other manifestations of Von Recklinghausen’s disease (multiple neurofibromatosis) and differentiation between the two conditions is usually obvious.

Occasionally lipomas may show degenerative fat necrosis, particularly after repetitive trauma, and become painful. A quite different and less common condition is painfully indurated lipomatous thickening of the legs, often with vasomotor symptoms, occurring in middle-aged females — painful adipodystrophy or Dercum’s disease. These patients do not have discrete lesions and local surgery has no place in treatment. Sympathectomy may be helpful.

Treating lipomas often consists of just reassuring the patient of the benign nature of the lump. Removal, if required, is usually simple. Even large ones can be shelled out completely from within their soft capsules through quite small incisions (Fig 1.9). Recurrence does not occur after removal of the whole lesion. Incision is preferably along lines of skin cleavage (Langer’s lines).

2 ‘Sebaceous’ cyst

These are also very common and are usually easy to differentiate from lipomas, though the two are often confused by students. The histories are often similar — slow-growing painless subcutaneous lumps — although a history of recurring infection and discharge will sometimes immediately indicate that the lesion is a cutaneous cyst. Two points should be borne in mind during the examination:

(a) ‘Sebaceous’ cysts arise from the skin and its appendages and are thus primarily cutaneous swellings — they move with and not apart from the skin. They are thus always attached to the skin at their summit, even when very large and with the major part of their bulk expanded into the soft tissues beneath the skin. Even so, they remain ensheathed by a dermal layer (Fig 1.8). The presence of a punctum (not always present) makes their epidermal origin even more obvious — it is usually at the summit but may be eccentric and can be missed unless sought for with care.

(b) Cysts almost always assume a rounded form and a smooth regular contour during growth, which distinguishes them from lipomas.

Cysts are often multiple; most are found on the scalp. Other common sites are face, neck, back and scrotum, but they can occur within any area of hair-bearing skin. Usually they are painless, increasing slowly in size over months or years. Infection can cause more rapid and painful increase in size. Most ‘sebaceous’ cysts will present as dome-shaped or spherical lumps with a classically smooth and rounded contour that is tense and fluctuant. They may have an overlying yellow punctum at the site of major skin attachment. Like all superficial cysts, the ease of eliciting signs of liquid content varies with their size, the nature of the liquid within them and the thickness of the cyst wall. Because their contents are usually like toothpaste and their walls quite thick, most ‘sebaceous’ cysts are fluctuant but not transilluminable. Although commonly called ‘sebaceous’ cysts, a more appropriate term is keratinous or epidermoid cyst for they usually have a flattened squamous epithelial lining and contain desquamated keratinous debris, not sebum. The keratinous contents resemble toothpaste or cream cheese — often erroneously described as pus even when not infected. Two subtypes of cysts can be described from examination of this epithelial lining: epidermoid (the common type) and pilar or trichilemmal cysts (where the epithelium resembles that lining the hair follicle). The common disorder of sebaceous glands is acne, seen mainly in young adults.

Complications of keratinous cysts are common:

Infection and abscess formation have already been mentioned. Infected cysts can be very malodorous. Although spontaneous resolution with destruction of the cyst may occasionally occur, simple incision or spontaneous drainage of pus is more usually followed by recurrence of the lesion. Cure requires excision of the cyst, including its wall. A large infected sebaceous cyst of the scalp is known as Cock’s peculiar tumour. This can mimic a squamous cell carcinoma of skin (Ch 1.2) and highlights the importance of always confirming the diagnosis histologically. Another and more serious error is to mistake an underlying bony tumour of the calvarium for a sebaceous cyst. Cysts lie within the skin of the scalp above the epicranial aponeurosis and are always mobile over the underlying bone; however, the scalp is stretched quite tightly over the skull and this sign can be misinterpreted by the inexperienced or careless observer.

‘Seborrhoeic’ horn. Slow extrusion and accretion of keratin occasionally gives an elongated ‘seborrhoeic’ horn. These can result from any keratinising skin lesion, but most are benign. The most common cause is a benign squamous papilloma.

Plaque formation. Slow attrition of the overlying epidermis accompanied by desiccation of the cyst contents can result in a firm, grey cutaneous plaque beneath an ulcer. Calcification in the plaque and epithelial regrowth leads to the lesion known as ‘benign calcifying epithelioma of Malherbe’ (pilomatrixoma), seen most often on the scalp or forehead as a very hard intracutaneous and subcutaneous plaque. It is quite benign but can mimic a skin neoplasm and is usually best excised.

Treatment. Symptomatic ‘sebaceous’ cysts need to be excised in toto, which can be done under local anaesthesia. The simplest technique is to bisect the cyst cleanly and avulse each half from within using a haemostat (Fig 1.10). Bleeding is usually minimal. Complicated cysts need formal excision. Histological confirmation of the diagnosis is always mandatory.

3 Ganglion

Ganglia present as more deeply placed subcutaneous lumps around joints or tendon sheaths. They are seen very commonly throughout adult life; they may be precipitated by work involving repetitive movement or associated with degenerative arthritis of the underlying joint. Associated arthritis may be the cause of symptoms, and treatment of the more obvious ganglion will not then effect a cure. Common sites for ganglia are wrists, fingers and feet. Their consistency and size are variable and may change with movement of the corresponding joint or tendon.

They present either as small localised swellings or as diffuse tendon sheath enlargements.

Localised swellings. A tense focal lump due to herniation or cystic degeneration of the joint capsule or tendon sheath is the most common form of ganglion. A very common presentation is a small (1–2 cm), tense, firm or hard subcutaneous swelling on the dorsum of the wrist joint towards its radial side and made more prominent by hyperflexion of the joint (Fig 1.11). The lump is immobile, fixed to the deep tissues and not attached to skin. Most will be too firm to elicit fluctuation and are not usually transilluminable. These ganglia may be unilocular or multilocular and contain a clear glairy synovial-like fluid. The natural history varies considerably. Many or most are symptomless in themselves and grow very slowly or remain static. Spontaneous resolution sometimes occurs; this may be accelerated by local pressure causing apparent rupture and dissipation. Recurrence is frequent.

Other common sites are: the volar aspect of the wrist near the flexor carpi radialis tendon; the volar aspect of the metacarpophalangeal or interphalangeal joints; or the dorsal and medial aspects of the ankle or forefoot.

Treatment. Localised ganglia often need no treatment. Associated degenerative joint disease may need attention. Acutely painful symptomatic lumps are treated initially by immobilisation; persistently symptomatic lumps are best excised. Compression (banging with a bible) and sclerosant injections are not recommended. Excision needs a bloodless field and a meticulous technique, avoiding neighbouring vital structures (tendons, radial artery, nerves). The lesion is excised in toto, if possible without rupture and including a local segment of joint capsule or tendon sheath. Surgery is usually curative but recurrences can occur.

Synovial (mucous) cyst of the finger is another common type of localised ganglion. This lesion presents as a subcutaneous cystic nodule over the dorsum of the terminal phalanx just distal to the interphalangeal joint. The tense fluctuant subcutaneous cyst is in close proximity to the nail bed and often causes local deformity of nail growth. Treatment is initially conservative (many resolve spontaneously). Local excision is required for persisting lesions; aspiration and local steroid injection may be tried first.

A mucous cyst that is completely subungual can be confused with melanoma.

Diffuse tendon sheath enlargement. A less common type of ganglion presents as a diffuse and usually less tense enlargement of the complete synovial tendon sheath. Flexor and extensor tendons of the wrist are most frequently involved and repetitive occupational stress may sometimes be a precipitating factor. These present as compound palmar or dorsal ganglia affecting the common flexor or extensor tendon sheaths. A compound ganglion comprises a bilocular hourglass swelling proximal and distal to the flexor or extensor retinaculum, exhibiting fluctuation that can be transmitted from one component to the other, often with accompanying crepitus due to inclusion (‘melon seed’) bodies. These swellings are usually transilluminable.

Treatment is initially conservative and directed against any precipitating factors. Aspiration and local steroid injections are usually followed by recurrence. Surgical treatment is almost always curative and involves removal of the superficial parietal tendon sheath.

4 Bursa

Bursae normally comprise collapsed sacs with a smooth lining of flattened synovial epithelium sited where bones, joints, ligaments, aponeuroses, tendons and skin lie in close proximity. They facilitate smooth friction-free movement between gliding tissue planes in a similar manner to synovial tendon sheaths. They often communicate with or are extensions of nearby joints (subacromial bursa, suprapatellar bursa). They lie between the skin and underlying bony prominences (olecranon bursa, prepatellar bursa) or they separate tendons and ligaments (anserine bursa, semimembranosus bursa). Bursae also can develop de novo at any site of abnormal friction (adventitious bursae). Symptoms follow excessive wear and strain leading to acute or chronic bursitis with an effusion of mucoid synovial-like fluid. Clinical presentations accordingly are most common in adulthood after the prolonged and repetitive strains of occupation or sport and are aggravated by age-related arthritic and soft tissue degeneration. Naturally occurring bursae are symmetrical and at defined anatomical sites. Common presentations are student’s elbow (olecranon bursa), bunion (inflamed bursa over first metatarsal head), housemaid’s knee (prepatellar bursa), clergyman’s knee (infra-patellar bursa) and weaver’s bottom (ischial tuberosity bursa).

Bursae thus present as subcutaneous cystic lumps, often with crepitus on movement. The lining of the bursal sac is usually closely adjacent and relatively fixed to the gliding surfaces it separates so the lump may show attachment to both the underlying bone and to overlying skin and thus have limited mobility. Superficial bursae, such as a bunion or prepatellar bursa, will be fluctuant and usually transilluminable. The skin overlying a superficial bursa is often calloused. Associated joint disease and deformities are common. Pain, tenderness and accompanying signs of inflammation will be particularly severe if bacterial infection supervenes from a skin breach.

Treatment. Treatment comprises rest and, for acute bursitis, immobilisation. Antibiotics are given if signs of local or systemic sepsis exist; aspiration may be required to culture the fluid. Surgical excision is required for chronic symptomatic lumps. The incision must be carefully sited to avoid a contracture across a nearby joint; attachments of the lump to skin and to underlying bone or tendon make excision more difficult.

1.4 Cutaneous and subcutaneous infections

Surgical infections of skin and subcutaneous tissues are common. The source or focus of infection is often a wound or skin breach or a lesion such as a sebaceous cyst that has become infected. The focus may be an introduced foreign body or ischaemic tissue. In these latter instances the primary focus acts as a nidus and must be dealt with by local surgical treatment before complete healing will occur. Diabetes mellitus must be excluded in all patients presenting with subcutaneous infections. Diabetes increases both susceptibility to infection and virulence of the septic process, and early surgical treatment should be considered.

Pathology

Surgical infection develops in overlapping phases:

Cellulitis. Early spreading subcutaneous infection is the most common manifestation.

Localisation or necrosis. An inflammatory mass localises around the focus or nidus of infection. Whether necrosis occurs depends upon the type of organism, the tissue or organ involved and the physical characteristics and anatomical confines of the site of infection. A predominantly oedematous inflammatory swelling is called a phlegmon; a necrotic process, a slough.

Abscess formation. Subsequent suppuration comprises polymorphs and liquefied necrotic tissue of the host, usually surrounded by an abscess wall of fibrous tissue. Local suppuration is less likely to be lethal than spreading infection; pus formation is usually a measure of developing host resistance. Nevertheless, unless properly treated by drainage, an abscess will be a significant cause of morbidity and later disability or of mortality.

Systemically invasive infection with accompanying tissue necrosis is the most life-threatening phase of infection.

Antibiotics are essential for the control of invasive infection, manifest clinically by spreading cellulitis and by systemic toxicity. Antibiotics often can stop the process of infection at the cellulitic stage and facilitate resolution. Antibiotics will not control a developed abscess, nor the lethal toxicity associated with tissue necrosis. Antibiotics cannot replace surgical drainage of pus or surgical excision of a focus of dead and foreign tissue. Antibiotics may delay the formation of pus, prolonging the time between the phlegmonous phase of infection and the formation of an abscess. Antibiotics thus tend to delay the spontaneous drainage of abscesses, leading sometimes to the production of a chronic inflammatory swelling (antibioma).

Diagnosis and treatment plans

General principles

Physical examination is the most reliable means of detecting the site of surgical infection. Some deep subcutaneous infections are difficult to localise; the presence of fever, tachycardia and leucocytosis emphasises the need for a continued search for a deep abscess or necrotic focus. Blood culture is an essential step in diagnosis of severe infections, especially when no pus is available for culture, but should not delay treatment with antibiotics, surgical excision or drainage. If pus is available for culture, the method of collection should ensure that both aerobic and anaerobic organisms will be detected. A general history and examination is essential, both to evaluate the severity of the systemic effects of infection and to detect concurrent illness in need of attention. Urinalysis to detect diabetes is part of the clinical examination.

General principles of treatment (Box 1.7) are determined by the three main aetiological factors:

1 The primary site of infection

A minor wound is a common initiating source of infection. Risks of wound infection are increased by poor initial wound management. Prevention of wound infection depends on sound surgical technique: major risk factors are inadequate debridement, clumsy tissue handling, undue tension, ischaemic and foreign tissue and haematoma formation. In the carelessly sutured wound, bacterial defences are impaired and infective organisms can multiply under protected conditions, particularly if the wound remains contaminated by bacteria in the presence of foreign bodies and dead or devitalised tissue. Polymorphs require oxygen to kill bacteria. The PO2 of the dead space within unduly tense skin sutures is markedly reduced. Foreign bodies in tissues form a nidus for infection and bacteria are frequently carried in with the foreign body. Wounds of the lower limbs are often more susceptible to infection, particularly in older patients because of established peripheral vascular disease (arterial or venous) and chronic oedema.

The presence of tension and impending tissue necrosis is suggested by persistent throbbing pain and systemic toxicity, and is an indication for urgent surgical decompression — even in the absence of signs of pus. Fluctuation is frequently a late sign of abscess formation and drainage should not be delayed until this sign is present (Fig 1.12). Superficial infected ulcers or infected wounds are best dressed by adequate drainage and by moist porous dressings. After drainage, later secondary closure by suture or by skin grafting may be required to reduce the length of convalescence. The local region should initially be rested, immobilised and elevated to minimise oedema. Physiotherapy is commenced once there is evidence of resolution of the infection and is an important component in final rehabilitation.

Specific infections of skin and subcutaneous tissues

Clinical features and treatment plan

2 Folliculitis, furuncle, carbuncle, hydradenitis

Folliculitis. This common skin infection is usually quick to resolve but may be troublesome because of a tendency to chronicity (sycosis barbae) or because of its cosmetic significance. The infecting organism is usually Staphylococcus aureus. The lesion can progress to a local pustule around the hair follicle, with surrounding cellulitis. Removal of the hair usually removes the nidus and facilitates drainage and healing. Washing with a detergent soap or with aqueous chlorhexidine helps prevent recurrence; nylon underclothing should be avoided. Perineal and axillary folliculitis tends to persist and may present as chronic recurring nonsuppurative hydradenitis. Hydradenitis may require excision of residual apocrine glands and skin during a quiescent phase.

Furuncles (boils) and carbuncles. These are more florid forms of folliculitis. Boils are staphylococcal abscesses of hair follicles. Abscess formation involves the entire hair follicle and adjacent subcutaneous tissue. The condition is contagious and multiple furuncles are common (furunculosis). Furunculosis normally occurs in young adults with acne and abnormal skin function related to hormonal changes or seborrhoeic dermatitis. Boils may be the presenting symptom of diabetes mellitus. The follicular abscess becomes fluctuant and spontaneously discharges a soft core of necrotic pus after several days. The treatment of a furuncle is minimal incision and drainage, with removal of the hair. Antibiotics are not indicated unless the boil is in an area such as the upper lip, nose or eye, where septic phlebitis and cavernous sinus thrombosis are real risks of spreading infection. Washing with an antiseptic to reduce the skin burden of staphylococci is advisable for recurrent furunculosis. When furunculosis is associated with severe acne vulgaris, long-term tetracycline may be of value.

Furuncles can be confused with similar appearing lesions at specific sites. The site and associated systemic illness will often establish the diagnosis in conditions such as rheumatoid nodules, gout, bursitis, synovitis, erythema nodosum, fungal infections, benign or malignant skin tumours and infected ‘sebaceous’ cysts. Whatever the cause of bacterial suppuration, the general principles of management of infection and drainage of pus must be applied. Biopsy is a prudent addition to bacteriological culture in atypical and resistant infections.

Carbuncles. These are more serious and less common lesions. Diabetes is very likely to be an associated problem. The lesion usually starts as multiple furuncles in adjoining hair follicles that coalesce in the subcutaneous tissue. Further skin sinuses develop from burrowing subcutaneous abscesses. Eventually overlying skin necrosis occurs. Incision alone will be inadequate unless the sinus tracts are widely laid open.

Hydradenitis. This is a more serious form of chronic folliculitis. The condition arises in the apocrine sweat glands of the axillae and groin and usually leads to recurrent abscess formation or chronic nonsuppurative infection. It is common in Europeans living in the tropics and as a complication of diabetes. Treatment of hydradenitis involves drainage of individual abscesses and attention to personal hygiene, avoidance of nylon underclothing, irritant antiperspirants and deodorants, and reduction of the bacterial skin load by chlorhexidine washing. Fungal superinfection should be excluded by examining scrapings and treated if isolated. Excision of hair-bearing skin is sometimes necessary to eradicate the infection.

Anthrax causes a potentially mortal infection that may be confused initially with a boil or carbuncle. The systemic effects, however, are usually out of proportion to the local lesion. Anthrax is due to Bacillus anthracis, usually acquired from domestic and farm animals. The bacillus enters through an area of skin abrasion, generally on the arms or neck. An acute local reaction follows with very severe systemic effects. Local haemorrhagic necrosis develops producing a black lesion (the malignant pustule). The condition, if treated early, responds to penicillin.

3 Erysipelas, cellulitis, impetigo

Erysipelas is a skin infection caused usually by a pathogenic streptococcus and complicated by lymphatic involvement. The infection often involves the face and cheek, is characteristically bright red in appearance and, because of dermal oedema, has a raised sharp edge. Vesicles or bullae may be present in severe disease. Entry is usually from a minor skin abrasion. Prompt treatment with penicillin is usually curative. Culture of the leading edge may yield the infecting streptococcus.

Cellulitis is much more common than erysipelas; it is the most common surgical infection requiring hospital admission. It is a less well demarcated and deeper seated infection than erysipelas and is an invasive, nonsuppurative, streptococcal or staphylococcal infection of connective tissue. The infection may originate from an infected focus such as a minor abrasion, drug injection site, venous eczema or ulcer, diabetic ulcer or tinea pedis. The clinical picture is of severe spreading inflammation of the subcutaneous tissues. The portal of entry is sometimes hard to find.

Cellulitis usually affects the extremities as an area of brawny, hot, oedematous skin without a clear border. Blistering, necrosis and ulceration can develop quite rapidly and may involve the fascia and muscles. Cellulitis is seen frequently in the legs of susceptible patients (e.g. drug addicts and alcoholics) and in patients with oedema from chronic lymphoedema, venous insufficiency or heart failure. Sometimes cellulitis is secondary to arterial insufficiency. Patients with chronic lymphatic oedema are particularly prone to recurrent skin infections. A foreign body from previous injury or underlying osteomyelitis are other important precipitating lesions. Radiological imaging is essential to detect these two predisposing causes. Bacteria may be difficult to obtain for culture but blood culture may be positive. Therapy entails rest, elevation and penicillins — with drainage of any focus of pus, if detected. Failure to respond within 24 hours suggests the need to change antibiotics and that a further search for a hidden abscess should be made and more radical debridement considered.

As cellulitis resolves, the oedema and swelling of the skin and subcutaneous tissues subside. The crinkled appearance of the collapsed skin after its earlier distension (often in longitudinal ridges) is a classic sign of resolving infection — the sign of the ebbing tide.

Phlebitis of the superficial leg veins may be difficult to differentiate from cellulitis; however, the local swelling is usually more discrete with phlebitis and tenderness is localised to the involved vein. At times it may be difficult to distinguish cellulitis from contact allergy or drug-sensitivity reactions. Erysipeloid is another lesion that can mimic cellulitis and is usually a benign infection found on the hands of fishermen or meat handlers due to the organism Erysipelothrix.

Impetigo. Rather than remaining localised, staphylococcal infection of the skin in children may spread in the skin as impetigo, especially when originating from an insect bite, from the pustules of scabies or the excoriation of pediculosis. The lesions consist of macules, vesicles and pustules. Removal of the crusts leaves denuded red areas. Impetigo is contagious and is the most superficial skin infection. If progressive, especially in infants, impetigo requires treatment with an antistaphylococcal penicillin such as flucloxacillin or erythromycin in those allergic to penicillin. Impetigo must be distinguished from contact dermatitis, herpes simplex and varicella.

4 Necrotising soft tissue infections

Fournier’s gangrene. This is a necrotising skin infection commonly affecting the scrotum and perineum in debilitated patients. A mixture of organisms is found and skin necrosis can be extensive. It responds rapidly to wide surgical excision and drainage. The underlying testis is rarely involved.

Necrotising fasciitis. This is a much more serious infection and usually affects susceptible hosts. The major risk factors are intravenous drug abuse, alcoholism, diabetes mellitus, malnutrition and obesity. Extensive necrosis of the superficial and deep fascia occurs, with thrombosis of the cutaneous microcirculation leading to later secondary skin changes of blistering, necrosis and ulceration. There is no common microbiological factor. Polymicrobial infections usually have a longer clinical incubation period than single-organism infections, making the former more difficult to detect at an early stage. The most common organism isolated is Beta-haemolytic streptococcus. The dominant symptom is severe pain in the affected region, out of proportion to the early local physical findings. Persistent pain and progressive cellulitis despite treatment with appropriate antibiotics strongly suggest the diagnosis. The pain is frequently associated with marked systemic toxicity. High fever can occur, as can hypothermia and acidosis. Crepitus due to subcutaneous gas is a late and inconstant sign. Necrotic fasciitis is often triggered by minor trauma, skin infections, drug injection sites, bed sores and perianal sepsis. Early exploration is indicated in all high-risk patients who present with persisting severe pain, particularly when accompanied by cellulitis and skin necrosis or subcutaneous crepitus. The principles of treatment are:

Clostridial necrotising myositis (gas gangrene). This is an acute and rapidly spreading anaerobic infection of muscle with a short incubation period of two to three days. The disease is caused by a mixture of gas-producing clostridial organisms, predominantly Clostridium welchii. These organisms are Gram-positive anaerobes that are inhabitants of the soil and the bowel of humans and other animals. In contrast to tetanus, the exotoxins produced by these organisms cause serious local effects at the site of wounding. Severe systemic toxicity and hypotension also occur, secondary to tissue necrosis and to intravascular haemolysis. Because of the organisms’ fermenting and proteolytic action, gas formation is characteristic. Gas gangrene is often a consequence of neglected or inadequate primary wound treatment — particularly the failure to treat war and other high-risk wounds, such as compound fractures, by delayed primary closure. It can also follow operation in debilitated patients with peripheral vascular disease, diabetes, carcinoma or alcoholism.

The wound is painful, crepitant and discoloured. The brownish discharge has a characteristic sickly sweet, ‘mousy’ odour. Shock, haemolysis, jaundice and renal injury follow unless surgical treatment is prompt. The most important consideration is prevention — by early and adequate primary care of all contaminated wounds, with delayed closure of high-risk wounds. The treatment of established myositis demands prompt radical surgery — sometimes amputation — to remove all dead or dubiously viable tissue and to establish free drainage. Penicillin is given in high doses. Gas gangrene antiserum has little or no place in management. Hyperbaric oxygenation may be of value in treatment but must not delay necessary surgical debridement.

Tetanus is caused by Clostridium tetani, a Gram-negative sporing bacillus. This organism is found particularly in agricultural areas and in faeces. Clostridium tetani is not an invasive organism and does not cause a severe local acute inflammatory reaction. Its clinical effects are the result of a powerful exotoxin that travels in the bloodstream and along nerve sheaths to become firmly bound to anterior horn cells and neuromuscular junctions. Once there, the toxin is unaffected by antitoxin treatment. The bacillus will produce toxins only under anaerobic conditions. As a consequence, the wounds most likely to be infected are deep contaminated wounds and those associated with tissue necrosis. The incubation period of the established disease usually spans about 14 days from inoculation but, in the most severe cases, tetanus may develop within a few days of injury. Persisting hypertonicity develops. The patient complains of stiffness or cramps of the jaws and facial muscles, neck, limbs, back and abdomen. This proceeds to clonic spasms. Treatment requires antibiotics and wound debridement, human antiglobulin, sedation, muscular paralysis and controlled ventilation and the maintenance of nutrition and physiotherapy. Adequate primary wound debridement in high-risk cases, even if the surface wound seems trivial, is the best means of prevention. Universal vaccination with tetanus toxoid is an essential prophylactic public health measure.

5 Specific sites

Subcutaneous infections at specific sites often originate in a focus of established pathology and require special management. Under this heading may be included hand infections (Ch 6.8), perianal abscess (Ch 7.22), bursitis (Ch 6.11), fungal infections, cervical tuberculosis, infected rheumatoid nodules and Ludwig’s angina. Gout and occupational tenosynovitis are aseptic inflammatory lesions that can mimic cellulitis.

Pilonidal abscess is a subcutaneous infection in the natal cleft. Infection will recur unless the nidus of hairs and surrounding granuloma is dealt with. Patients present in an acute attack with severe pain and swelling between the buttocks associated with fever and malaise. The abscess can arise de novo or there may be a past history of abscesses or of a discharging pilonidal sinus. The initial treatment of pilonidal abscess is prompt and adequate drainage, preferably under general anaesthesia. Laying open of all sinus tracts and removal of all hair should be done in this operation. Antibiotics are given to complement surgical drainage only if surrounding cellulitis is extreme. Careful dressing after wide incision can reduce the incidence of subsequent chronic sinus formation. A polymer stent is helpful once the open wound edges are stiffened by granulation.

Chronic pilonidal sinus. For a chronic sinus, the aims of treatment are excising the sinus and contained hair, removing the midline sinus or pits and obliterating the natal cleft to prevent the entry of hair at new sites. Excision of the lesion in toto, with primary suture, is often performed as an elective procedure (Fig 1.13).

1.5 Lymph node swellings

An understanding of the anatomy and function of the lymphoreticular system is essential to informing clinical assessment of both superficial and deep lesions. While lymph node swellings are not cutaneous or subcutaneous, they are readily palpable under the fascia of the relevant region and may present as a lump.

Lymph node swellings may be focal or generalised. Normal lymph nodes may be palpable, particularly in thin individuals, as discrete ovoid or bean-shaped masses up to a centimetre in diameter. The most common cause of palpable regional lymph nodes is reactive lymph node enlargement in response to local infection. The common sites are the cervical node groups and the axillary and inguinal nodes, given that the face and throat and upper and lower limbs and external genitalia are areas of significant environmental exposure. Systemic infection may give rise to generalised lymphadenopathy. The main node groups are deep to the deep fascia but may feel quite superficial when enlarged.

Primary tumours of the reticuloendothelium may present as regional or generalised lymphadenopathy, which is classically nontender and usually mats the individual nodes together.

Enlarged lymph nodes present a very common diagnostic problem. The first question is: Are the palpable nodes really enlarged or otherwise abnormal? Lymph node swellings at any site are usually pathological if the palpable node is 2 cm or more in diameter, firm or rubbery in consistency or painful and tender to palpation. Multiple lymph node groups may be affected.

Lymphadenopathies are conveniently classified into those confined to one group of nodes (usually due to local diseases) and those involving multiple areas (usually due to a systemic disease).

Clinical assessment

Diagnostic and treatment plans

Usually the cause of lymphadenopathy will be obvious or suspected after a thorough clinical assessment. The following investigations are the most likely to be of diagnostic help in generalised lymphadenopathy.

Figures 1.141.16 show lymph nodes in the neck, axilla and groin respectively.

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