Chapter 63 Severe soft-tissue infections
The skin is the largest organ and acts as an excellent barrier against infection. It consists of the epidermis and dermis and resides on fibrous connective tissue, the superficial and deep fasciae (Figure 63.1). The fascial cleft, with nerves, arteries, veins, lymphatic and adipose tissue, lies between these fascial planes. Normal skin flora includes Corynebacterium spp., coagulase-negative staphylococci, Micrococcus spp., Lactobacillus and, rarely, Staphylococcus aureus. Colonisation by Gram-negative bacteria occurs in hospital patients; once altered, skin flora includes a higher proportion of S. aureus which ultimately becomes pathogenic.
These colonising microorganisms seldom cause skin and soft-tissue infections, but serious infections can occur if: there is a break in the skin because of traumatic lesion or maceration; soft tissues are ischaemic and non-viable; colonising bacteria are particularly virulent; or the patient is immunocompromised (Figure 63.2).1–9 Conditions predisposing to infection include diabetes mellitus, cirrhosis, malnutrition, major trauma, advanced age, renal failure, steroid use, collagen vascular disease and malignancies.1–10 Differentiation between soft-tissue infections can be difficult and one unified management approach to severe forms is appropriate.11–13 Management decisions are further based on likely causative organism, depth of infection and clinical severity.8
Soft-tissue infections are usually caused by bacterial entry through skin lesions or perforation of adjacent intestinal structures. Skin lesions can on occasion be the manifestations of systemic infection; examples of this are bacteraemia by meningococci, staphylococci, Pseudomonas aeruginosa, Candida spp., and bacterial endocarditis.3 These will not be specifically addressed here.
CLASSIFICATION
The bacteriology and subtypes of severe soft-tissue infections have not changed significantly over the last century.8,14–16 Community-acquired meticillin-resistant Staphylococcus aureus (MRSA), however, can be seen as an emerging cause of severe tissue infection with a high prevalence in certain parts of the world.17–19 The classification of soft-tissue infections can be confusing, partly because individual organisms can cause different clinical syndromes. Consequently, there are a wealth of terms often referring to the same diseases (e.g. Meleney’s gangrene, haemolytic streptococcal gangrene and progressive bacterial synergistic gangrene).14 Classification by the anatomical structure involved is more logical, but it has to be borne in mind that some conditions involve several soft-tissue levels and that some cases may evolve froma minor entity to a more severe form with more diffuse anatomical involvement (see Figure 63.1).
IMPETIGO
Impetigo,1–3 more common in children, is a superficial skin infection caused by group A streptococci, Staphylococcus aureus, or both. Mild infections can be managed with topical antibiotics; more serious infections need a first-generation cephalosporin. A penicillinase-resistant penicillin is mostly chosen in severe empirical conditions (e.g. dicloxacillin).20 Increasing resistance in streptococci and staphylococci might prohibit the use of erythromycin, which has been the alternative in the penicillin-allergic patient. For community-acquired MRSA, co-trimoxazole is an alternative.
FOLLICULITIS
This is an infection arising in hair follicles and apocrine glands.2,3 S. aureus is the usual causative organism. Topical antibiotic treatment is usually all that is required. When confluent, folliculitis can evolve to furunculosis and may need surgical drainage as sole effective therapy. If accompanied by cellulitis and/or sepsis, antibiotics are added (see section on cellulitis). Repeated folliculitis raises the possibility of chronic granulomatous disease, an inherited immunodeficiency syndrome based on granulocyte malfunction.21 Affected individuals are at risk for severe soft-tissue infections, sometimes with rare pathogens such as Aspergillus spp.
ERYSIPELAS
This superficial dermal infection is largely caused by group A streptococci and also by other streptococci and Staphylococcus aureus.1–3,8,9 The prominent lymphatic blockade results in a painful bright red patch with a raised sharp border, which clearly demarcates the infection from normal surrounding skin. Fever and chills often precede the skin eruption. Predisposing conditions include ulcers, venous stasis, diabetes, alcoholism and paraparesis. High-dose penicillin is still the drug of choice in the absence of underlying disease and the possibility to observe the evolution of the lesion. Severe infections in diabetic patients require a third-generation cephalosporin, piperacillin-tazobactam or a carbapenem. If mobilisation is premature, signs recur and treatment failure may falsely be suspected. However, recurrent erysipelas does occur with persistent lymphoedema.
CELLULITIS
Cellulitis1,2,3,5–9,22 is an acute spreading infection of the skin extending below the superficial fascia, usually involving only the upper part of the subcutaneous tissue. It can occur at any body site, but is most frequent in the lower extremities and in the face. There is less lymphatic involvement so the borders of the infection are often not well defined and differentiation between cellulitis and erysipelas is sometimes difficult. Fever, malaise and rigors are common. It is more common in patients with tissue oedema. Cellulitis is most commonly due to Streptococcus pyogenes, but other Gram-positive and negative organisms can also cause this condition according to location and exposure history.9
Typically, S. pyogenes cellulitis may appear hours after surgical intervention with fast progression of the erythematic zone over a large surface and can be accompanied by bacteraemia and sepsis. Many of these organisms may produce gas, hence crepitus is sometimes present (Table 63.1).
| Cellulitis | Usually anaerobic organisms, clostridial and non-clostridial |
| Bursitis | Gram-negative organisms |
| Necrotising fasciitis | Usually type I (mixed infections, Gram-negative organisms) |
| Myonecrosis | Clostridial organisms |
| Infected vascular gangrene | Any organism |
A severe and fulminant form of cellulitis with hemorrhagic bullous lesions can be caused by marine bacteria of the Vibrio spp., mostly with a history of contact with sea-water or raw fish.23 After fresh-water exposure of wounds24 or application of medical leeches,25Aeromonas hydrophilia is a possible aetiology.
TREATMENT
Appropriate microbiological tests are undertaken prior to starting antibiotics. Any skin abrasion or sites that drain are swabbed for Gram stain and culture. Needle aspiration, skin biopsy and blood cultures produce only a 25% positive yield.1 Treatment involves site elevation and high-dose oxacillin or a first-generation cephalosporin. If there is a possibility of MRSA, vancomycin is indicated instead. In severe cases, the addition of clindamycin is beneficial because of its antitoxic effect and enhanced intracellular activity.26 If Gram-negative rods are suspected or identified (e.g. an immunocompromised patient or involvement of intestinal tract lesions), a third-generation cephalosporin should be considered. In a patient with prolonged hospitalisation or in penetrating foot infections, a cephalosporin with anti-Pseudomonas activity is preferred. If Vibrio
