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Cellulitis
Only Skin Deep?
Cellulitis is an inflammatory
condition of the skin and
subcutaneous tissue. The
clinical manifestations include
erythema, swelling, warmth and
pain. Streptococcus pyogenes
and Staphylococcus aureus are
the most common aetiological
agents. Erysipelas may closely
resemble cellulitis; however, it
tends to involve only the superficial
lymphatics and upper dermis
and so, has a distinctive raised
appearance with a clearly visible
demarcation line. Clinically, it is
more common in infants, children
and older adults. Cellulitis involves
the deeper dermis. In practice, it
is often difficult to distinguish and
treatment is usually the same.1
The lower limbs are the most
common site for infection.
Lymphangitis and regional lymph
node involvement may also be seen
in addition to skin erythema.
Identifying the source of
infection may be helpful in
providing clues to the causative
microorganismand to guide further
management.1,2 Examples of these
can be found in Table 1.
Risk Factors for Acute
Lower Limb Cellulitis
Multiple studies have suggested
that risk factors include presence
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of sites of entry, being overweight
and lymphoedema.3 Dermatophytic
toe web intertrigo, although in
itself does not cause cellulitis, is a
risk factor as it causes scaling and
fissuring of the skin resulting in a
portal of entry for bacteria.1-4
Diagnosis
The diagnosis is generally based on
the clinical setting and appearance
of the lesion. Cultures of needle
aspirates or punch biopsies are
not indicated in routine care.1
Previous studies have shown that
the microorganisms implicated
remain primarily gram positive
cocci. Special consideration is
warranted in diabetics, which may
also harbour gram negative aerobes
as well anaerobes. Where bullous
lesions are present, however, gram
stain and culture of fluid from these
lesions may be helpful.
Although bacteraemia is
uncommon in cellulitis, blood
cultures should be drawn in
patients who have superimposed
lymphoedema, buccal or periorbital
cellulitis, salt water or fresh water
exposure, and in patients who have
chills and high fevers of more than
38°C.
Radiological imaging is usually
unwarranted unless necrotising
fasciitis or underlying acute
osteomyelitis is being considered
in which case an MRI would
Table 1. Source of infection and possible causes of infection1,2
Source
Likely bacteria
Skin trauma, underlying lesion Staphylococcus aureus, group A
eg, ulcer, fissured toe webs
streptococcus
Animal or Human bites
Oral flora of biter eg, Pasteurella multocida
from cat bites
Oral anaerobes like Bacteroides species,
Peptostreptococcus; Eikenella corrodens;
viridans streptococci; Staphylococcus
aureus
Exposure to sea water
Vibrio vulnificus
Fresh water
Aeromonas hydrophilia
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MD Singapore April 2011
Table 2. Differential diagnosis for cellulitis1,2
Process
Clinical clues
Infectious
Necrotizing fasciitis
Acute rapidly developing, deep fascia: marked pain,
tenderness and swelling. May have bullae and crepitus of
overlying skin. If caused by group A streptococci, may be
accompanied by toxic shock syndrome.
Anaerobic myonecrosis
Rapidly progressive and toxemic infection from injured
muscle. Marked oedema, crepitus and brown bullae. Gram
stain shows gram positive bacilli.
Gas gangrene commonly from
Clostridium perfringens
Furuncles and carbuncles
Infection of hair follicles, usually with Staphylococcus aureus.
Local erythematous pustular appearing lesions. Coalescing
furuncles form carbuncles
Non infectious
Insect and spider bite
Local pruritis, no fever or toxicity
Acute gout
Foot involvement, joint pain, history of previous attacks
Deep venous thrombophlebitis
Leg involvement, sentinel venous cord and linear extension
Fixed drug reaction
Not as rapidly spreading as cellulitis, low fever, history of
medication use
Pyoderma gangrenosa
Lesions become nodular or bullous and ulcerate. History of
collagen vascular disease or inflammatory bowel disease
Sweet’s syndrome (acute febrile neutrophilic
dematosis)
Acute, tender pseudovesiculated plaques, fever and
neutrophilic leukocytosis. Associated with haematologic
malignancy.
Kawasaki’s disease
Fever, conjunctivitis, acute cervical lymphadenopathy,
oropharyngeal erythema, dermatitis of palms and soles,
mainly in young.
Neoplastic process eg, carcinoma erysipeloides,
Marjolins ulcer
Absence of fever, slower progression than cellulitis.
the imaging of choice. In cases
where gas gangrene or chronic
osteomyelitis is suspected, plain
x-rays may show gas pockets in
tissue or cortical luscencies in bone
respectively.
Differential Diagnosis
There are a number of important
differential diagnoses for cellulitis to
consider. They can be divided into
infectious and non-infectious. These
are summarised in Table 2.
Treatment Strategies
Ancillary measures
Local measures to reduce swelling
such as elevation and immobilisation
of the affected limb can be useful.
Non-stick dressings should be
used on any lesions that are
actively purulent. If interdigital
dermatophytic infections are
detected, then topical antifungal
agents should be used.
Patients who suffer from
peripheral oedema, who are at risk
of recurrent cellulitis, should observe
good skin hygiene and use support
stockings. Tinea paedis should be
promptly treated. In some instances,
expert referral to lymphoedema clinics
may be beneficial.
Antibiotic therapy
Most studies of cellulitis have
involved patients with serious
infections. Studies to determine the
specific criteria for case definitions
of mild cellulitis are lacking. In
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MD Singapore April 2011
general however, for mild early
cellulitis, therapy that will cover
Staphylococcus aureus and
Streptococcus pyogenes such as
cloxacillin may be used.
For patients hypersensitive
to penicillin, cephalexin is a
reasonable alternative. In patients
who have immediate penicillin
hypersensitivity, clindamycin
may be considered. The duration
of therapy is usually seven to
ten days.1,2 We do not routinely
recommend broader spectrum
antibiotics such as Augmentin or
the quinolones. For furunculosis,
consider culture and treatment
with co-trimoxazole, particularly in
patients from the US, as there have
been recent cases of community
acquired methicillin-resistant
Staphylococcus aureus (MRSA) in
Singapore.
Who To Admit to Hospital
Patients who have significant
systemic features of high fever,
chills, rigors and tachycardia
hypotension should be referred
to Accident and Emergency for
consideration of admission for
intravenous antibiotic therapy.
Patients who have failed to respond
to oral therapy after 48 hours, or
have rapid spread of cellulitis with
increasing pain should also be
referred immediately.
Failure of Treatment:
What to Consider
There are several things to consider
if cellulitis fails to improve or
resolve. The first is that patients
may have deeper infections such
as myositis or even osteomyelitis
which typically not only need
intravenous therapy but also a
longer duration of antibiotics.
Further imaging may be useful
in this instance. Underlying
conditions such as chronic venous
Patients who have significant systemic features of high
fever, chills, rigors, tachycardia hypotension should be
referred to Accident and Emergency for consideration
of admission for intravenous antibiotic therapy. Patients
who have failed to respond to oral therapy after 48
hours, or, have rapid spread of cellulitis with increasing
pain, should also be referred immediately.
insufficiency or lymphoedema
may also predispose to failure of
conventional treatment due to poor
drainage of infected tissue and
may require a longer duration of
antibiotics.
The microorganisms involved
may not be susceptible to the
antibiotics used. Diabetics are
more vulnerable to anaerobes
and gram negative rods (including
Burkholderia pseudomallei) as
a cause cellulitis. Communityacquired methicillin-resistant
Staphylococcus aureus is also an
increasing problem globally and
has a predilection for causing skin
and soft tissue infection.2 Noninfectious causes may also result in
treatment failure. Skin biopsy, not
only for gram stain and culture but
histology as well, may be helpful in
this scenario.
Conclusion
Cellulitis is a common condition
seen in the community that is readily
amenable to treatment. Ancillary
measures as well as antibiotic
therapy play an important part in its
management. Failure of treatment or
complete resolution should prompt
further investigation.
References
1Swartz MN. Cellulitis. N Engl J Med 2004;350:902-12.
2Stevens DL, Bisno AL, Chambers HF, Everett ED, Dellinger P,
Goldstein EJC et al. Practice Guidelines for the Diagnosis and
Management of Skin and Soft-Tissue Infections. Clin Infect Dis
2005;41:1373-406.
3Bjornsdottir S, Gottfredsson M, Thorisdottir AS, Gunnarsson
GB, Rikardsdottir H, Kristjansson M et al. Risk Factors for Acute
Cellulitis of the Lower Limb: A Prospective Case-Control Study. Clin
Infect Dis 2005;41:1416-22.
4McNamara DR, Tleyjeh IM, Berbari EF, Lahr BD, Martinez J,
Mirzoyev SA et al. A predictive Model of Recurrent Lower
Extremity Cellulitis in a Population-Based Cohort. Arch Intern Med
2007;167:709-715.
Dr Surinder Pada is an Associate Consultant in the Division of
Infectious Disease at the National University Hospital. She is also the
Chairperson of Infection Control at Alexandra Hospital. Dr Pada graduated
from the University of New South Wales (Sydney) in 2000 and obtained
her Fellowship of the Royal Australasian College of Physicians (FRACP)
in 2009. Her areas of interest include infection control, in particular
methicillin-resistant Staphyloccus aureus, as well as Influenza and general
Infectious Diseases.
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