Tuesday, December 20, 2005

Managing cellulitis in primary care

The skin normally provides an excellent barrier to infection, both due to providing an impenetrable layer for pathogenic bacteria, and by harbouring non-pathogenic bacteria which prevent the harmful ones from taking over [1],[2]. Yet this barrier can break down, and when this happens, there are plenty of bacteria waiting to take advantage of the opportunity. In many countries, around one-third of the population are asymptomatic carriers of Staph aureus, either constantly or intermittently [3]. It has been estimated that disrupting the skin merely by inserting one silk suture can increase the infectiousness of Staph aureus by a factor of 10,000 [4] .

However, possibly due to enthusiastic management of skin diseases with antibiotics, most patients with atopic dermatitis have been found to harbour Staph aureus on their skin, with higher infection rates than in non-atopic controls [3], and for antibiotic resistance to be high in these bacteria [2] .

The commonest pathogens for skin and soft tissue infections are Staph aureus and beta-haemolytic streptococci, although many other bacteria can cause infections once the skin defences are weakened
[2],[3],[5],[6]. The mechanisms of attack are varied; in addition to the direct effects of colonisation of the body's tissues, they also can produce toxins which may be able to breach the skin's defences and enable the bacteria to penetrate the deeper tissues [2] .

Beta-haemolytic streptococci tend to cause cellulitis which spreads rapidly through the subcutaneous tissues thanks to the action of enzymes such as hyaluronidases produced by the bacteria, whereas staphylococcal infections tend to be more demarcated [3] .

More recently, they have also been shown to produce proteins which can act as 'superantigens'.

These bind directly to antigen-presenting cells and so cause polyclonal T cell activation, which has been implicated in the aggravation of atopic dermatitis, psoriasis and contact dermatitis, as well as the more rare but serious toxic shock syndrome and Kawasaki's syndrome [3] .

What is cellulitis?

Cellulitis is a diffuse suppurative inflammation of subcutaneous tissues [1]. In older people the leg is the usual site, whereas younger people tend to develop the condition in the upper body [7]. Patients admitted to hospital have an average stay of 10 days and 10% of patients suffer long term morbidity afterwards from persistent oedema, recurrent cellulitis and leg ulceration [8]. Of these patients, a portal of entry was found in just 55%. There is also a small risk of more serious complications in young children and immunocompromised adults such as gangrene, metastatic abscesses and sepsis [1].

Risk factors for cellulitis

As we have seen, cellulitis is more likely to follow some damage to the skin. One study found the following conditions in patients with cellulitis [9]:

Diabetes (50% of patients)
Previous cellulitis (50%)
Oedema (45%)
Peripheral vascular disease (40%)

Tinea pedis (32%) Another study showed that about 55% of patients with cellulitis of the leg had a previous minor injury or tinea pedis infection

Periorbital cellulitis

Periorbital cellulitis is usually associated with paranasal sinusitis (43% in one study), trauma (25%) or dental infection (6%) . While the majority of infections are due to Staph aureus [10],[11], some cases in children have been associated with Haemophilus influenzae [12]. Both the number of cases specifically due to this bacterium, and the total number of cases have dropped since the Hib immunisation campaign began [13].

Diagnosing cellulitis

Clinical signsThe diagnosis of cellulitis is based on the clinical signs and symptoms


Localised redness, warmth and tenderness

Less common:

Mild fever and chills


Investigations are rarely helpful in cellulitis. White cell counts are mildly raised if at all [7] . Needle aspiration, Gram stains and blood cultures are usually negative [7],[12],[14],[15],[16], as are lumbar punctures for periorbital cellulitis in children [12]. On average, even culture of swabs grows pathogens in only about half of samples [11]. This means that diagnosis and treatment will always be empirical [15].

Necrotising facsciitis

Necrotising fasciitits is a very rare but serious infection which presents like cellulitis but causes fulminant tissue destruction [17]. It usually follows trauma to the skin, but this may be merely a contusion, burn or insect bite [18]. The infection spreads extremely rapidly and can cause multiorgan failure, adult respiratory distress syndrome [[18], with a 40% mortality rate [[19]. Most infections are polymicrobial with Gram positive and negative, aerobic and anaerobic bacteria, although Group A streptococci are the most common pathogens [18].

It can be difficult to distinguish between necrotising fasciitis and cellulitis. The main features of necrotising fasciitis are:

Oedema of the area with peau d'orange appearance

Blistering and necrosis

Crepitus of the tissues

Pain out of proportion to the clinical findings

Signs of systemic infection may be present
[19], [20] Treatment should be started as soon as possible, and requires surgical debridement of the area and high dose intravenous antibiotics [19],[20],[21].

Management of cellulitis

Management of cellulitis is essentially with oral antibiotics, although rest and elevation of the affected part, moist heat and analgesia may be helpful [1],[7].

Recommended antibiotics are [22],[23]:

Penicillin V 500 mg QDS and Flucloxacillin 500 mg QDS for 7-14 days Cost: £6.60-£13.21

If allergic to penicillin:

Erythromycin 500 mg QDS for 7-14 days Cost :£6.16-£12.32

Co-amoxyclav 500/125 mg TDS for 7-14 days Cost: £15.73-£31.46 Other antibiotics may be of use if local sensitivities mean penicillins and erythromycin are less effective.

Fusidic acid 500 mg daily for 5-10 days was equally effective as flucloxacillin 500 mg TDS with cure rates of over 92%
[3] Cost of fusidic acid: £6.47-£12.94

Azithromycin 500 mg on day 1 and 250 mg daily for days 2-5 was as effective as cephalexin 500 mg BD for 10 days
[24] Cost of azithromycin: £13.43

Azithromycin 1.5 g in divided doses over 5 days was as effective as erythromycin 500 mg QDS for 7 days a
[25] Cost of azithromycin: £13.43

Clindamycin, as an inhibitor of protein synthesis, should be used additionally for severe infections as it will inhibit toxin production
[3] Cost of 300 mg QDS for 7-14 days: £25.48-£50.96

Antibiotic prophylaxis While recurrent attacks are common, there is little evidence that the use of prophylactic antibiotics can reduce recurrence. A study in China found that monthly injections of penicillin made no overall impact on the recurrence rate of cellulitis
[26]. Eradicating Staph aureus in asymptomatic nasal carriers with monthly mupirocin ointment has been shown to reduce the number of skin infections as long as the treatment is continued [3], but the long-term use of prophylactic antibiotics carries a risk of encouraging the development of antibiotic resistance [3].

Chronic leg ulcers While chronic leg ulcers are always contaminated with bacteria, antibiotics should only be given if there are signs of cellulitis in the surrounding tissues


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JB Medical


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