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Skin and Soft-Tissue Infec Tions the Early Clinical Presentation of Soft-Tissue Infections May Be Deceptive

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Skin and Soft-Tissue Infec Tions the Early Clinical Presentation of Soft-Tissue Infections May Be Deceptive Skin and soft-tissue infec tions The early clinical presentation of soft-tissue infections may be deceptive. JAN PRETORIUS, MB ChB, MMed (Surg), FCS (SA) Critical Care Adjunct Professor, Department of Surgery, Medical School, Faculty of Health Sciences, University of Pretoria, and Principal Specialist and Head, Surgical Intensive Care Unit, Steve Biko Academic Hospital, Pretoria Jan Pretorius is chairman of the Multidisciplinary Head and Neck Oncology Unit and of the Critical Care Task Team at the Steve Biko Academic Hospital, Pretoria. Correspondence to: Jan Pretorius ([email protected]) indicating infections extending to the deeper layers of the skin. Definitions and terminology Complicated SSTIs may involve the subcutaneous tissue, deep fascia The skin and its appendages, and the subcutaneous tissue, deep fascia and muscle.1,2 Uncomplicated SSTIs1,2 may be defined as conditions and muscle, can all develop infections under various circumstances. that respond to a course of antibiotics or to simple drainage. These Patients with skin and soft-tissue infections (SSTIs) often initially include minor abscesses, impetigo, folliculitis, furuncles or boils, present to family physicians. The signs and symptoms of SSTIs carbuncles, limited cellulitis, and even minor wound infections. 1,2 may overlap, making a comprehensive diagnosis difficult. Early 1,2 Examples of complicated SSTIs are the following: clinical presentation may be deceptively innocent.3 Furthermore, at presentation it is often difficult to assess the depth, severity • infections involving deep skin structures and specific structures or tissues involved. All SSTIs represent a • infections requiring significant surgical intervention, e.g. continuum of symptoms and should be considered collectively: infected burns, major abscesses, infected ulcers, infections in • Erythema, warmth, oedema, skin discoloration and localised diabetics, and deep-space wound infections pain are common presenting signs in the case of superficial, • otherwise uncomplicated infections occurring at anatomical complicated or deep infections. sites (e.g. the rectal area) where the risk of anaerobes and Gram- • Some or all of the following signs are indicative of a necrotising negative pathogens is increased condition affecting deep structures • infections in the presence of significant underlying disease, • when vesicles become manifest e.g. diabetes mellitus, peripheral vascular disease, ischaemic ulceration and chronic lymphoedema, that may complicate the • when oedema is tense response to therapy • when crepitus is present • where immunosuppression may enable unusual or normally • when pain is extreme non-pathogenic bacteria to cause infections or increase the likelihood of developing fulminant infections. • when infection progresses. SSTIs may also be classified according to the presence or absence of • Failure of an SSTI to respond to antibiotics points to a necrotising necrotic or devitalised tissue. In necrotising soft-tissue infections infection. (NSTIs) the devitalised tissue plays an important role in the • Signs of systemic infection, hypotension, tachycardia and pathophysiology of the disease, providing a growth medium for organ dysfunction may indicate toxic shock (staphylococcal or bacteria and preventing cellular and humoral defence mechanisms streptococcal). from reacting. The acidic pH of such tissue or wounds prevents the antimicrobial agents from being delivered effectively or inactivates It is essential to maintain a high index of suspicion for these these drugs. NSTIs may involve the dermal and subcutaneous infections and be aware of possible presenting features. layers (necrotising cellulitis), fascia (necrotising fasciitis), muscle Recognising the extent of the infection is imperative to ensure (pyomyositis or myonecrosis) or any combination of these.2 2 prompt and comprehensive therapy. SSTIs may vary from less 4 The cardinal principles of controlling SSTIs are: severe conditions to severe and invasive conditions, which may lead to soft-tissue loss or limb amputation and even death if not • adequate drainage of infected fluid collections managed promptly. Therefore, patients with severe infections need • debridement of infected, necrotic or devitalised tissue early hospitalisation, surgery and antibiotics. • removal of devices or foreign bodies Early clinical presentation • early, appropriate antibiotic therapy. may be deceptively innocent. Early aggressive surgery is indicated for both complicated SSTIs and NSTIs after prompt resuscitation, adjuvant antibiotic therapy and systemic support. Wound bed preparation and wound healing Classification should receive particular attention. SSTIs can be described as localised or spreading – this may be useful when considering surgical treatment. Epidemiology SSTIs can be classified as uncomplicated, referring to infections SSTIs are common bacterial infections seen by family practitioners affecting the superficial layers of the skin, and as complicated, and surgeons. They account for a substantial portion of June 2010 Vol.28 No.6 CME 265 Skin and soft-tissue infections emergency department visits and hospital cellular response and lead to abscess admissions. formation or spreading of the infection. These exotoxins may be extremely potent SSTIs led to 29 820 hospital admissions and cause forms of toxic shock syndrome in the UK during 1985, with a mean that may be fatal.1 occupancy of 664 hospital beds each day. A more recent study in the UK indicated that SSTIs account for about 10% of hospital admissions, with a mean length of stay Phy sical examination The following findings are important of 5 days. During 1995, 330 000 hospital 1 1 indicators of severity of infection: admissions for SSTIs were reported. • At the site of infection: Over recent decades physician visits for cellulitis and soft-tissue infections • the type of lesion have increased from 32 to 48 per 1 000 • whether fluctuation (fluid that has to population from 1997 to 2005. Necrotising be drained) is present fasciitis caused by group A streptococci is now endemic in the USA. Of great • whether crepitus is present, indicating concern is that Staphylococcus aureus, a gas-forming infection. the predominant cause of cellulitis, and • The size and site of the lesion may abscesses or wound exudates, are becoming indicate the severity of the infection. increasingly resistant to methicillin. Some sites (face, fingers, toes, genitals) Vancomycin and other newer antibiotics Fig. 1. Impetigo (US Department of Health 5 necessitate admission of the patient and are therefore the drugs of choice. This and Human Services). vigilant observation. is true even for community-acquired methicillin-resistant S. aureus (MRSA), • The degree of pain: demonstrating that MRSA is no longer a • pain not in proportion to the pathogen limited to hospitalised patients. appearance of the lesion may indicate a developing necrotising infection Pathogenesis • loss of skin sensation around a wound The role of the skin as an integral part of may be an indication of dead tissue our host defence mechanisms cannot be • in limbs with peripheral vascular underestimated. Intact skin serves as an disease the pain caused by SSTIs may effective physical barrier to the penetration be masked. of micro-organisms because of the tight junctions between epithelial cells. In • Systemic infection, usually indicated addition, the acidic oily matrix produced by extremes of temperature (<35oC or by the sebaceous glands coats the epithelial >40oC), hypotension, tachycardia and Fig. 2. Facial erysipelas (CDC/Dr Thomas F cells. Commensal and saprophytic micro- changed levels of consciousness. Sellers/Emory University). organisms of the normal skin flora are interspersed in this matrix cell surface.1 1,6 Bacteria involved are coagulase-negative Uncomplicated SSTIs staphylococci, corynebacteria, micrococci, Impetigo (Fig. 1) is a bacterial, diphtheroids and propionibacteria. inflammatory skin disease characterised They augment the defence of the skin by by the appearance of pustules, typically on preventing colonisation and invasion by the face or the extremities. This condition more virulent species. In moist skin areas is common during hot, humid conditions. such as the groin the normal flora may also It is highly communicable and facilitated include Gram-negative enteric bacteria, by overcrowding and poor hygiene. e.g. Escherichia coli. Erysipelas (Fig. 2) is a contagious infection To cause SSTIs invading organisms must of the superficial layers of the skin that Fig. 3. A carbuncle on the buttock of a dia- penetrate the skin barrier through a breach may extend to the subcutaneous tissue and betic patient (Wikimedia commons). caused by direct trauma or an underlying form vesicles or bullae. The predominant process such as ischaemia. The two most clinical features are sharply demarcated Folliculitis is a purulent inflammation of common pathogens in SSTIs are S. aureus red edges and oedematous, indurated hair follicles. and beta-haemolytic streptococci, e.g. elevation of the affected area. A furuncle or boil is a painful skin Streptococcus pyogenes. The ability of all Erysipeloid dermatitis is infective, with nodule associated with circumscribed micro-organisms to cause SSTIs is related an erythematous-oedematous appearance. inflammation of the corium or dermis and to their toxin production and resistance to subcutaneous tissue, enclosing a central 1 It may occur on the hands of fishmongers host inflammatory reponses. or
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