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di Bagian Kulit dan Kelamin
Rumah Sakit Umum Daerah Ambarawa




Diajukan Kepada :
Pembimbing : dr. Hiendarto, Sp.KK

Disusun Oleh :
Putri Minang Mandasari 1220221139


Kepaniteraan Klinik Departemen Kulit dan Kelamin
FAKULTAS KEDOKTERAN UPN VETERAN JAKARTA
Rumah Sakit Umum Daerah Ambarawa
PERIODE 27 Mei 30 Juni 2013



LEMBAR PENGESAHAN KOORDINATOR KEPANITERAAN
KULIT DAN KELAMIN

Journal Reading dengan judul :

SELULITIS


Diajukan untuk Memenuhi Syarat Mengikuti Ujian Kepaniteraan Klinik
di Departemen Kulit dan Kelamin
Rumah Sakit Umum Daerah Ambarawa




Disusun Oleh:

Putri Minang Mandasari 1220221139


Telah disetujui oleh Pembimbing:
Nama pembimbing Tanda Tangan Tanggal


dr. Hiendarto, Sp.KK ............................. .............................



Mengesahkan:
Koordinator Kepaniteraan Kulit dan Kelamin





dr. Hiendarto, Sp.KK
NIP. 197308042009091001

Firas Al-Niaimi is Specialist Registrar in Dermatology, Salford
Royal Hospital, Manchester, UK and Neil Cox is Consultant
Dermatologist, Cumberland Inrmary, Carlisle, UK
C
ellulitis is dened as an acute
inammation of the skin and
subcutaneous tissue which is
commonly caused by Streptococcus
pyogenes or Staphylococcus aureus
(Morton and Swartz, 2004). The lower
leg is the most affected site, accounting
for 7590% of all cases (Tsao and
Johnson, 1997). The true incidence of
cellulitis is hard to estimate but a review
of all hospital admissions in a UK district
general hospital showed that about
3% of all admissions were for cellulitis
(Morris, 2004), thereby constituting a
huge nancial burden on healthcare
resources. The NHS Institute for
Innovation and Improvement noted that
there were 45,522 inpatient admissions
for cellulitis in 20032004, costing the
NHS 87m (Carter et al, 2007).
Symptoms of cellulitis vary depending
on the severity, which can range from
mild to a more severe form with systemic
involvement in the form of tachycardia,
hypotension, and general malaise with a
marked inammatory response (Morton
and Swartz, 2004). A typical presentation
is painful swelling with erythema that is
hot and tender to touch, often preceded
by u-like symptoms. Potential long-
term consequences of cellulitis include
lymphoedema and leg ulceration
(Cox, 2002).
Various risk factors have been shown
to be associated with cellulitis, with
lymphoedema showing the strongest
association (Dupuy et al, 1999). This
is particularly the case in recurrent
cellulitis. Streptococcal cellulitis associated
with lymphoedema can be aggressive
with severe symptoms and morbidity
(Bonnetblanc and Bedane, 2003).
Identifying cellulitis
Cellulitis is often clinically apparent due
to the presence of tender erythematous
swelling of the affected limb and
systemic symptoms of malaise (Morton
and Swartz, 2004). Fever and raised
inflammatory markers may also be
present. Blistering and ulceration occur in
severe forms of cellulitis, often associated
with marked oedema (Cox, 2002).
Various laboratory investigations have
been used for diagnosis of cellulitis by
microbiological culture, but overall these
tests have a relatively low diagnostic yield.
Skin swabs for culture from intact skin
are not helpful, but the yield of positive
results increases if a likely portal of
entry is present or if there is secondary
blistering (Dupuy et al, 1999; Tsao and
Johnson, 1997). Swabs from erosions,
exudate and ulcerations, if present, may
be more helpful (Tsao and Johnson,
1997). However, such lesions may have
secondary staphylococcal colonisation
and may not identify the primary cause,
and swabs from pre-existing ulcers may
reveal several different bacteria.
The main reason for the low rate
of identication of streptococci in
cellulitis is that the infection is of the
dermis, not of the skin surface, so it is
difcult to identify. Another possible
reason is that treatment has often
been initiated at an early stage and
may mask symptoms of fever, making
microbiological identication more
difcult. A review of 50 patients with
cellulitis showed that only 26% had fever
at the time of active cellulitis (Hook et
al, 1986). A study performed by one of
the authors showed that 40% of patients
with cellulitis admitted to hospital were
apyrexial and systemically well (Cox et al,
1998). Hospital clinicians are aware that
some patients are referred because they
are not getting better despite antibiotic
treatment, but this will often refer to
redness or swelling which can persist for
some time after antibiotic treatment.
Cellulitis is a relatively common infection of the skin and subcutaneous tissue associated
with high morbidity and a burden on healthcare resources. Lymphoedema the accumulation
of uid in interstitial spaces can occur as a consequence of cellulitis. Similarly, the presence of
chronic lymphoedema can predispose to recurrent episodes of cellulitis. This article explores the
relationship between lymphoedema and cellulitis, with emphasis on diagnosis, management and
methods of prevention.
Firas Al-Niaimi, Neil Cox
Key words
Cellulitis
Lymphoedema
Prophylactic therapy
PATCH
Cellulitis and lymphoedema:
a vicious cycle
38 Journal of Lymphoedema, 2009, Vol 4, No 2
Clinical REVIEW
Cellulitis and lymph/BM.indd 14 25/9/09 11:46:47
39 Journal of Lymphoedema, 2009, Vol 4, No 2
Clinical REVIEW
Blood cultures have been shown
to give a low yield for diagnosis in the
absence of bacteraemia. A retrospective
study among 757 patients with community-
acquired cellulitis showed that only 2% of
patients had a signicant patient-specic
microbial strain isolated (Perl et al, 1999).
A slightly higher rate of positive blood
cultures in patients with leg lymphoedema
has been demonstrated (Baddour and
Bisno, 1985). The authors believe that
blood cultures have a marginal impact
on clinical management in the absence
of systemic symptoms and raised
inammatory markers, and therefore do
not appear to be cost-effective. This does
not however apply for necrotising fasciitis,
which is a more serious infection affecting
the deeper tissue structures associated
with high mortality and systemic sepsis.
Although less common than cellulitis,
necrotising fasciitis is often confused with
cellulitis, particularly at its early phase of
presentation where blood cultures have a
higher diagnostic yield (Cox, 2002).
Antistreptolysin titre (ASOT) levels
may conrm a streptococcal aetiology
in retrospect, as this blood test result
is often raised as early as 710 days
following a streptococcal infection,
and takes several weeks to subside
(Cox, 2002; Eriksson et al, 1996). This
investigation is particularly useful in
patients who are less likely to have a non-
streptococcal aetiology (e.g. patients with
excoriated eczema, carbuncles, abscesses
or leg ulcers), as a negative test helps to
exclude a streptococcal cause. Conversely,
conrming streptococcal infections can be
useful when choosing antibiotic therapy
for patients with recurrent cellulitis.
Skin biopsy and/or aspirate have
been shown to be of limited value in the
diagnosis of cellulitis, but may have a role
in excluding some differential diagnoses
such as vasculitis or eosinophilic cellulitis
in those with atypical presentations (Tsao
and Johnson, 1997; Morton and Swartz,
2004; Cox, 2002).
Treatment with antibiotics (oral
or intravenous) will be discussed later,
however, elimination and treatment
of potential risk factors such as
onychomycosis, tinea pedis or leg ulcers
and the control of lymphoedema, all
contribute to the reduction in morbidity
as well as future recurrence (Collins et al,
1989; Carter et al, 2007).
Risk factors for cellulitis
Local factors in the affected limb are
strongly associated with a predisposition
for cellulitis. General factors that might be
regarded as risk factors include obesity,
smoking, alcohol misuse and diabetes
mellitus. The association with diabetes,
smoking and alcohol has not been proven
in retrospective studies (Dupuy et al, 1999),
but obesity has been shown to be linked
with an increased risk (Scheinfeld, 2004).
Local factors causing defects in the skin
barrier may increase the risk of developing
cellulitis by acting as a portal of entry for
micro-organisms (Morton and Swartz,
2004; Cox, 2002; Dupuy et al, 1999). Skin
trauma, lacerations, puncture wounds, leg
ulcers, dermatitis, toe web maceration
and tinea pedis fall into this group. In a
study involving 647 patients, 77% had local
barrier defects that may have acted as
portals of entry, 50% of which were fungal
infections (mostly of the toe web) (Morris,
2004). Among the aforementioned factors,
leg ulcers form the strongest risk (Dupuy
et al, 1999).
Previous episodes of cellulitis
are associated with a higher risk for
recurrence, possibly due to local soft
tissue and lymphatic damage (de Godoy
et al, 2000). This risk increases particularly
if other factors are present (Bjoornsdottir
et al, 2005).
A retrospective study among patients
with cellulitis who were followed for up
to three years showed that 47% had a
history of recurrent episodes (Cox, 2006).
Another study (n=233) showed that 29%
of patients had a recurrence within the
rst three years after their initial cellulitis
(Jorup-Ronstrom, 1986).
Lymphoedema has been shown
in several studies to be the strongest
risk factor for cellulitis (Dupuy et al,
1999; Duvanel et al, 1989), particularly
in recurrent cellulitis. This is specically
linked to leg oedema secondary to
lymphoedema and is much less the
case with oedema secondary to venous
insufciency. In an epidemiological study
in London involving 823 patients, 28% of
patients with lymphoedema had had an
episode of cellulitis within the previous 12
months (Moffatt et al, 2003).
Dupuy et al (1999) found that
lymphoedema was present in 18% of
their patients affected with cellulitis
involving 167 patients with 294 controls.
A different study in which patients who
had two or more episodes of leg cellulitis
were investigated with lymphoscintigraphy
(n=15) found signicant lymphatic
abnormalities, suggesting a link with
infective episodes (Soo et al, 2008).
Sixty percent of those patients also
had abnormal lymphoscintigrams in
the leg that had not been affected by
cellulitis, suggesting that pre-existing
lymphatic abnormalities can precede the
occurrence of clinical cellulitis. Stoberl
et al (1987) found similar ndings of
abnormal lymphatic ducts among patients
with cellulitis of the leg, and Damstra
et al (2008) showed that 79% of 33
patients with impaired lymph drainage
in the affected limb also had evidence of
impaired drainage in the unaffected limb.
These studies support the increasingly
accepted concept that previously
undetected lymphatic abnormalities may
be present among patients with cellulitis.
Early detection of lymphatic abnormalities
through lymphoscintigraphy the gold
standard method for detecting lymphatic
abnormalities and lymphoedema,
and treatment of any abnormalities
detected, may therefore reduce future
episodes of cellulitis. However, there are
obvious practical limitations to this, as the
abnormalities demonstrated are often
not easy to treat.
Management of cellulitis
The aim of treatment in cellulitis is
resolution of the symptoms, reducing the
duration of hospital admission and the
avoidance of sequelae such as oedema
and ulceration. General measures such as
bed rest, elevation of the affected leg, skin
and wound care and analgesia are the
first-line treatments for cellulitis (Morton
and Swartz, 2004; Cox, 2002). Antibiotics
are required to eradicate the causative
organism, however, national prescribing
advice on choice and duration of
antibiotic therapy for cellulitis varies.
Cellulitis and lymph/BM.indd 15 25/9/09 11:46:47
40 Journal of Lymphoedema, 2009, Vol 4, No 2
Clinical REVIEW
Generally, oral antibiotics are used for the
milder forms of cellulitis where systemic
involvement is minimal. Currently,
recommendations for antibiotic choice
vary with three different guidelines/
recommendations currently existing
in the UK (Clinical Resource Efficiency
Support Team [CREST], 2005; Clinical
Knowledge Summaries [CKS], 2006;
Mortimer et al, 2006).
The CREST guidance (2005) suggests
ucloxacillin as the rst-line antibiotic
(intravenously in severe cases), with the
macrolide clarithromycin for patients who
are allergic to penicillin. In severe cases,
intravenous clindamycin can be used as
a substitute for clarithromycin in cases of
penicillin allergy.
CKS (2006) guidance recommends
ucloxacillin as rst-line and erythromycin
or clarithromycin in the case of penicillin
allergy. The suggested duration of
treatment is for seven days for mild
infections and 10 days for more severe
forms. There is limited evidence available
for the estimated duration of treatment.
One study with levooxacin (which
is rarely used for cellulitis in the UK)
showed that if response to treatment
occurs after ve days, further treatment
may not provide any additional benet
(Hepburn et al, 2004).
Treatment of cellulitis in patients
with lymphoedema differs slightly as the
causative organism is most likely to be
streptococcal. Based on this, the British
Lymphology Society (BLS) recommends
amoxicillin as rst-line therapy for cellulitis
with lymphoedema. Clindamycin is
recommended as second-line for those
allergic to penicillin (Mortimer et al, 2006).
The review of response after
48 hours is recommended in all the
guidelines (CREST, 2005; CKS, 2006;
Mortimer et al, 2006).
In France, benzyl penicillin is the
rst-line recommended treatment for
uncomplicated cellulitis (Societe Francaise
de Dermatologie, 2001). Benzyl penicillin
or phenoxymethylpenicillin both have
a low minimal inhibitory concentration
(MIC) against streptococci (i.e. low
concentrations of the drug will inhibit
the bacteria). However, penicillin alone is
not recommended as rst-line therapy
in the UK, due to its limited effect against
staphylococci (CREST, 2005; CKS, 2006;
Mortimer et al, 2006). This is potentially
important as clinical diagnosis of the
infective organism may be difcult,
especially in early localised cellulitis or in
cellulitis with a wound as the portal of
entry. Flucloxacillin as rst-line treatment,
as recommended by CREST and CKS,
also has a low MIC for streptococci and
in addition has anti-staphylococcal action.
Although the MIC of penicillin is more
favourable than that of ucloxacillin
for streptococci, ucoxacillins MIC is
sufciently low that the addition of benzyl
penicillin to ucloxacillin in patients who
do not respond to the latter is unlikely to
produce added benecial value. This has
been proven by a study that showed no
difference in outcome when comparing
a group of patients treated with
ucloxacillin versus a group treated with
ucloxacillin and benzyl penicillin (Leman
and Mukherjee, 2005).
Treatment of recurrent cellulitis
Despite the current limited evidence
regarding long-term treatment for
recurrent cellulitis, prophylactic therapy
is widely used. Small studies suggest
that oral antibiotic prophylaxis can be
beneficial and cost-effective (Jorup-
Ronstrom, 1986; Pavlotsky et al, 2004),
and a small study (36 patients in the
study randomised to two groups of 18
patients each) showed that prophylactic
erythromycin for 18 months resulted
in no recurrences in cellulitis compared
with a placebo (Kremer et al, 1991). A
large multi-centre national study, being
coordinated by the UK Dermatology
Clinical Trials Network, has already
enrolled five times as many patients as
the largest of the above studies (170 to
date), and will hopefully provide useful
evidence about the role of penicillin
prophylaxis. Called PATCH (Prophylactic
Antibiotics for the Treatment of Cellulitis
at Home), the study is a randomised
multi-centre clinical trial assessing
whether prophylactic penicillin reduces
episodes of cellulitis in patients who had
recurrent (at least two episodes within
the preceding 36 months) episodes of
cellulitis (UK Dermatology Clinical Trials
Networks PATCH Study Group, 2007).
Current guidance regarding
prophylaxis in cellulitis is suggested by the
BLS if two or more episodes of cellulitis
occur annually. The recommendation
for phenoxmethylpenicillin is partly due
to its long-term safety prole as
opposed to ucloxacillin which carries
the risk of hepatic toxicity if used long
term (Mortimer et al, 2006) and
also because recurrent cellulitis, with or
without a background of lymphoedema, is
most likely to be streptococcal infection.
Lymphoedema
Oedema is defined as excessive
interstitial fluid which develops when
there is a discrepancy between the
microvascular filtration rate (in the
capillaries and venules) and lymph
drainage. Increases in interstitial fluid
pressures and volume stimulate lymph
flow through the collecting lymphatics.
This is the main process responsible for
interstitial fluid drainage. Impairment of
the lymphatic drainage in the face of
normal filtration will result in oedema
(lymphoedema). In healthy lymphatic
ducts the lymph flow increases when
capillary filtration increases, thus
preventing the formation of oedema
(Mortimer and Levick, 2004).
The process of lymph transport in the
leg is mainly an active process achieved
through contraction. This contractile
mechanism of the smooth muscle walls of
the collecting ducts is under the inuence of
the sympathetic system as well as the inux
of calcium ions (Levick, 2004). Oedema
related to calcium channel blockers is,
therefore, likely to be partly through their
effect on lymphatics. Activation of the
calf muscle pump through contraction
is generally believed to contribute to an
increase in lymph transport.
The term lymphoedema covers a
range of pathologies, all of which present
clinically as chronic swelling of one or
more limb(s) arising from a defect in
the lymphatic channels. This implies a
fundamental failure in lymph transport,
as opposed to ltration oedema which
is caused by increased capillary ltration
(Mortimer and Levick, 2004).
Primary lymphoedema is the term
used for lymphoedema that arises from
Cellulitis and lymph/BM.indd 16 25/9/09 11:46:48
41 Journal of Lymphoedema, 2009, Vol 4, No 2
Clinical REVIEW
an abnormality of lymphatic development,
either due to genetic or congenital
malformations in the collecting ducts (such
as Milroy disease and Klippel-Trenaunay
syndrome), or due to acquired abnormalities
such as lymphangio-obliterative
lymphoedemas (Consensus Document of
the International Society of Lymphology
Executive Committee, 2003). This represents
a small percentage of lymphoedemas that
often present after puberty.
Secondary lymphoedema refers
to lymphoedema that is caused by
an extrinsic process such as infection,
malignancy or surgery which damages
a previously well-functioning lymphatic
system (Consensus Document of the
International Society of Lymphology
Executive Committee, 2003).
Generally, if oedema is symmetrical a
systemic cause is likely to be found (e.g.
hypoalbuminaemia, nephrotic syndrome),
whereas unilateral limb oedema is often
the result of local pathology to the
lymphatic system.
Clinical lymphoedema manifests with
swelling, pitting and thickening of the skin,
which leads in time to a characteristic
papillomatous appearance and a warty
(hyperkeratotic) texture.
Treatment of lymphoedema
The main component in the treatment
of lymphoedema is an improvement in
lymph drainage. This can be attempted
through several measures which will be
explained briefly.
Exercise induces changes in interstitial
uid pressure which leads to an increase
in both the lymphatic lling and pressure,
with a consequential increase in the
contractility of the lymphatic ducts. An
increase in the ow of the non-contractile
lymph ducts is likely to be inuenced
by exercise which leads to the passive
movement of lymph.
Compression through bandaging or
stockings aims to generate an increased
interstitial pressure by opposing capillary
ltration, leading to an increased venous
return as well as to an increase in the
contractility of the lymphatic ducts.
Multi-layer bandaging is often used in
combination with exercise in cases of
severe lymphoedema.
Elevation of the affected leg may
contribute by reducing the venous
pressure and subsequently the ltration.
It is often used in conjunction with other
measures, as leg elevation on its own has
little effect on the lymphatic drainage.
Manual lymphatic drainage (MLD) in
the form of massaging the affected limb
may stimulate lymph drainage from the
root of the limb to the draining lymphatic
basins. This is often combined with the
aforementioned techniques.
Pneumatic compression therapy
can be used to soften and reduce the
limb volume but may displace uid into
adjacent areas and its use is therefore
limited. The equipment used for this
method is designed to inate and deate
around a swollen limb, exerting a pressure
of 3040mmHg. Although it increases the
reabsorption of interstitial uid, it has no
effect on the reabsorption of proteins. This
leads to an increase in the concentration
of interstitial protein and results in
hardening of the treated limb (Mortimer
and Levick, 2004). Furthermore, single
chambered pumps have no direct effect
on lymph ow, and the high pressures can
damage the supercial lymphatics.
It is well known that diuretics do
not play a role in the treatment of
lymphoedema and should only be used
in oedema secondary to salt and water
retention (Mortimer and Levick, 2004).
The emergence of lymphoedema
clinics led by nurses, physiotherapists
and doctors from various specialties
has allowed for an integrated service
that is aimed to offer patient-specic
treatment(s) based on the degree of
severity and any associated complications.
In severe forms of lymphoedema, a
combination of an intensive period of
treatment with multilayer bandaging,
exercise and MLD is used to reduce the
swelling which is subsequently maintained
with compression garments and exercise.
Relationship between lymphoedema
and cellulitis
It is widely understood and accepted
that the relationship between cellulitis
and lymphoedema is a vicious cycle
where each episode of cellulitis further
damages the lymphatic system, leading
to a degree of secondary lymphoedema,
which in turn constitutes an increased
risk for cellulitis (Collins et al, 1989; Woo
et al, 2000). In unpublished original data
referred to in a Cochrane review, about
a quarter of patients with lymphoedema
will have at least one episode of cellulitis
or related skin infection in the affected
limb (Badger et al, 2004).
This vicious cycle is independent from
the primary aetiology of the lymphoedema
and is thought to be multifactorial. The
protein-rich lymphatic uid serves as an
excellent medium for bacteria to grow, and
stagnation of the lymphatic uid due to
impaired lymph drainage with consequent
reduction in lymphatic clearance creates a
state of local immune deciency, which, in
turn, can increase the risk of local cellulitis
(Baddour and Bisno, 1985; Mortimer and
Levick, 2004).
In patients without lymphoedema,
bacterial components released from
bacteria are eliminated by phagocytosis
and/or antibiotics and are cleared efciently
by lymphatic drainage (Jeffs, 1998).
Baddour and Bisno (1985) postulated
that bacterial toxins which were pooled
in insufciently drained lymphatic tissue
contribute to the systemic symptoms
found in some patients with cellulitis,
complicating lymphoedema. This is largely
attributable to the release of cytokines
as a host response to the presence of
excessive lymph. It is unclear why there
seems to be a great individual variance in
the manifestation of systemic symptoms,
but it is likely that other host immune
mechanisms play a role.
Mortimer et al (2006) suggested
that once bacteria have gained entry to
oedematous tissue, eradication proves
difcult and there is a risk of reactivation
of cellulitis if the local immune system is
impaired (Mortimer and Levick, 2004).
The involvement of such mechanisms
may provide an additional explanation
for the benet of agents such as
clindamycin and macrolides, as these have
immunomodulatory actions as well as
Cellulitis and lymph/BM.indd 17 25/9/09 11:46:48
42 Journal of Lymphoedema, 2009, Vol 4, No 2
Clinical REVIEW
anti-streptococcal activity, and therefore
may have a role in the treatment of
patients with recurrent cellulitis that
complicates lymphoedema (Ritts, 1990).
Conclusion
Cellulitis is a common and potentially
serious infection associated with a
huge cost to the healthcare system and
morbidity to the patient. Various risk
factors have been found to predispose to
cellulitis, with lymphoedema showing the
strongest link. The relationship between
cellulitis and lymphoedema appears to be
a vicious cycle; a pre-existing lymphatic
defect predisposes to cellulitis, episodes
of cellulitis damage the lymphatic system,
and either the primary or post-cellulitic
lymphoedema predispose to recurrent
episodes of cellulitis. It is therefore
important that both cellulitis and
lymphoedema are treated appropriately
to reduce the risk of worsening
lymphoedema and recurrent cellulitis.
Prophylactic antibiotics do appear to
be benecial in reducing the recurrence
rate of cellulitis and are currently
recommended, although without a strong
evidence base, particularly when cellulitis
is associated with lymphoedema. The
large, ongoing multi-centre trial described
earlier, investigating the use of prophylactic
antibiotics in cellulitis (PATCH study), may
in time provide this evidence.
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Cellulitis and lymph/BM.indd 18 25/9/09 11:46:49
Selulitis dan Lymphoedema: Lingkaran Setan
Selulitis adalah infeksi yang relatif umum pada kulit dan jaringan subkutan yang terkait
dengan morbiditas yang tinggi dan membebani sumber daya kesehatan. Lymphoedema
merupakan akumulasi cairan dalam ruang interstitial - dapat terjadi sebagai akibat dari selulitis.
Limphodema kronis dapat menyebabkan seseorang rentan terhadap episode berulang selulitis.
Artikel ini mengeksplorasi hubungan antara lymphoedema dan selulitis, dengan penekanan pada
diagnosis, penatalaksanaan dan metode pencegahan.
Selulitis didefinisikan sebagai peradangan akut pada kulit dan jaringan subkutan yang
umumnya disebabkan oleh Streptococcus pyogenes atau Staphylococcus aureus. Kaki bagian
bawah adalah bagian yang paling sering terkena, jumlahnya 75-90% dari semua kasus. Kejadian
selulitis yang terjadi dirumah sakit inggris yaitu sekitar 3%. Menurut NHS Lembaga Inovasi dan
Peningkatan mencatat bahwa ada 45.522 penerimaan rawat inap untuk selulitis pada tahun 2003-
2004 dengan biaya NHS sebanyak 87 miliar.
Gejala selulitis bervariasi tergantung pada tingkat keparahan, dapat terjadi gejala yang
ringan sampai bentuk yang lebih parah dengan keterlibatan sistemik berupa takikardia, hipotensi,
dan malaise umum dengan adanya respon inflamasi. Gambaran khas selulitis adalah
pembengkakan yang nyeri dengan kemerahan yang panas dan nyeri tekan, sering didahului oleh
gejala flu. Konsekuensi jangka panjang selulitis bisa menjadi lymphoedema dan ulserasi pada
kaki.
Berbagai faktor risiko telah terbukti berhubungan dengan selulitis, lymphoedema
merupakan faktor risiko tersering. Hal ini terutama terjadi di selulitis berulang. Selulitis
streptokokus dengan lymphoedema dapat menjadi agresif dengan gejala yang berat dan
morbiditas.
Mengidentifikasi selulitis
Gelaja klinis selulitis tersering yaitu adanya kemerahan dan pembengkakan yang nyeri
tekan pada anggota tubuh yang terkena dan gejala sistemik berupa malaise, demam dan adanya
tanda inflamasi. Lepuhan dan ulserasi dapat terjadi pada selulitis yang berat, sering dikaitkan
dengan edema. Berbagai pemeriksaan laboratorium telah digunakan untuk mendiagnosis selulitis
yaitu dengan kultur mikrobiologi, tapi secara keseluruhan tes ini memiliki hasil diagnostik yang
relatif rendah. Hapusan kulit untuk kultur dari kulit utuh tidak membantu, hasil test dapat positif
dan meningkat jika ada port de entry atau jika ada luka sekunder seperti lepuhan. Jika ada erosi,
eksudat dan ulserasi maka hapusannya dapat memudahkan diagnosis. Namun, lesi tersebut
mungkin memiliki kolonisasi Staphylococcus sekunder dan tidak dapat mengidentifikasi
penyebab utama, dan hapusan ulser yang sudah ada dapat mengungkapkan beberapa bakteri yang
berbeda.
Alasan utama tidak adekuat mendiagnosis Streptococcus di selulitis adalah bahwa infeksi
terjadi di dermis, bukan dari permukaan kulit, sehingga sulit untuk diidentifikasi. Alasan lain
yang mungkin adalah bahwa pengobatan sering dimulai pada tahap awal dan mungkin menutupi
gejala demam, hal ini membuat identifikasi mikrobiologi lebih sulit. 50 pasien dengan selulitis
menunjukkan bahwa hanya 26% mengalami demam pada saat selulitis aktif. Beberapa pasien
dirujuk karena tidak ada perbaikan gejala meskipun diberikan antibiotik. Kemerahan atau
pembengkakan yang dapat bertahan selama beberapa waktu setelah pengobatan antibiotik.
Kultur darah telah terbukti memberikan hasil yang rendah untuk diagnosis tanpa adanya
bakteremia. Sebuah studi retrospektif di antara 757 pasien selulitis menunjukkan bahwa hanya
2% dari pasien memiliki strain mikroba spesifik. kultur darah positif pada pasien dengan
lymphoedema kaki. Pemeriksaan dengan kultur darah dapat menentukan penatalaksanaan
meskipun gejala sistemik dan peningkatan tanda inflamasi tidak ditemukan. Namun ini tidak
berlaku untuk nekrosis fasciitis, yang merupakan infeksi yang lebih serius mempengaruhi
struktur jaringan yang lebih dalam terkait dengan mortalitas tinggi dan sepsis sistemik. Meskipun
kurang umum daripada selulitis, nekrosis fasciitis sulit dibedakan dengan selulitis, terutama pada
fase awal presentasi di mana kultur darah memiliki hasil diagnostik yang lebih tinggi.
Antistreptolysin titer (ASOT) dapat mengkonfirmasi etiologi Streptococcus dalam
retrospeksi, karena ini hasil tes darah sering meningkat 7-10 hari setelah infeksi Streptococcus ,
dan membutuhkan waktu beberapa minggu untuk mereda. Penelitian ini tidak berarti pada pasien
yang tidak memiliki etiologi non Streptococcus (misalnya pasien dengan excoriated eksim,
bisul, abses atau borok kaki), Tes negatif membantu untuk menyingkirkan penyebab non-
streptokokus. Pemilihan antibiotik pada pasien dengan selulitis berulang biasanya tidak
membrikan hasil yang maksimal.
Biopsi kulit atau aspirasi kurang memberikan hasil yang maksimal dalam mendiagnosis
selulitis, tetapi mungkin memiliki peran dalam mengeliminasi diagnosis banding selulitis seperti
vaskulitis atau eosinofilik selulitis pada mereka dengan presentasi atipikal.
Faktor Risiko
Faktor-faktor internal berhubungan dengan terjadinya selulitis. Faktor-faktor umum yang
mungkin dianggap sebagai faktor risiko termasuk obesitas, merokok, penyalahgunaan alkohol
dan diabetes mellitus. Hubungan dengan diabetes, merokok dan alkohol belum terbukti dalam
studi retrospektif, namun obesitas telah terbukti dihubungkan dengan peningkatan risiko.
Faktor lokal yang menyebabkan luka pada lapisan kulit dapat meningkatkan risiko infeksi
selulitis dengan adanya portal masuk untuk mikro-organisme. Trauma kulit, luka, luka tusuk,
ulkus pada kaki, dermatitis, dan tinea pedis dapat menyebabkan selulitis. Dalam studi yang
melibatkan 647 pasien, 77% luka pada kulit merupakan pintu masuk untuk mikroorganisme,
50% di antaranya disebabkan oleh infeksi jamur. Diantara faktor-faktor tersebut, ulkus pada kaki
merupakan faktor risiko terkuat.
Episode selulitis yang sebelumnya berhubungan dengan peningkatan risiko untuk
kambuh yang lebih tinggi, hal ini dsebabkan karena adanya kerusakan pada jaringan lunak lokal
dan kerusakan jaringan limfatik.
Sebuah studi retrospektif antara pasien dengan selulitis yang diikuti selama tiga tahun
menunjukkan bahwa 47% memiliki riwayat episode berulang. Studi lain (n = 233) menunjukkan
bahwa 29% pasien mengalami kekambuhan dalam tiga tahun pertama setelah selulitis awal.
Lymphoedema merupakan telah faktor risiko tersering untuk selulitis, khususnya di pada
selulitis berulang yaitu adanya edema sekunder dan insufisiensi vena. Dalam studi
epidemiologidi London yang melibatkan 823 pasien, 28% pasien dengan lymphoedema
mengalami episode berulang dari selulitis dalam 12 bulan sebelumnya.
Pada 294 sampel kontrol, 167 pasien diantaranya atau pada 18% pasien lymphodema
mengalami selulitis. Sebuah studi yang berbeda di mana pasien yang memiliki dua atau lebih
episode selulitis diteliti dengan limfoskintigrafi (n = 15). Hasilnya menunjukkan hubungan
dengan episode infektif. 60% pasien juga memiliki lymphoscintigrams abnormal pada kaki yang
tidak terpengaruh oleh selulitis, menunjukkan bahwa kelainan limfatik yang sudah ada dapat
mendahului terjadinya selulitis klinis. 79% dari 33 pasien dengan gangguan drainase getah
bening di anggota badan yang terkena juga memiliki bukti drainase terganggu di ekstremitas
sehingga dapat menyebabkan terjadinya selulitis.
Deteksi dini kelainan limfatik melalui limfoskintigrafi - metode standar emas untuk
mendeteksi kelainan limfatik - dan limfedema, dan pengobatan kelainan terdeteksi, sehingga
dapat mengurangi episode masa depan selulitis.
Manajemen Selulitis
Tujuan pengobatan pada selulitis adalah mengurangi gejala dan menghindari gejala sisa
seperti edema dan ulserasi. penatalaksanaan umum seperti tirah baring, elevasi kaki yang
terkena, perawatan kulit dan perawatan luka dan pemberian analgesia adalah pengobatan lini
pertama untuk selulitis. Antibiotik diperlukan untuk membunuh organisme penyebab, pemberian
antibiotik bervariasi sesuai dengan organism penyebab dan jenis selulitis. Antibiotik oral
digunakan untuk selulitis ringan dengan gejala sistemik yang minimal.
Pada kasus selulitis berat, antibiotik diberikan secara intravena. Antibiotik lini pertama
yang digunakan adalah flukloksasilin, untuk pasien dengan alergi penisilin dapat digunakan
klaritromisin macrolide. Dalam kasus yang parah, klindamisin intravena dapat digunakan sebagai
pengganti klaritromisin dalam kasus alergi penisilin. Untuk pasien dengan selulitis ringan
pengobatan diberikan selama tujuh hari dan untuk pasien dengan selulitis yang lebih berat
engobatan diberikan selama 10 hari.
Pengobatan selulitis pada pasien dengan lymphoedema sedikit berbeda karena
etiologinya disebabkan oleh Streptococcus. Inggris Lymphology Masyarakat (BLS)
merekomendasikan amoksisilin sebagai terapi lini pertama untuk selulitis lymphoedema.
Klindamisin direkomendasikan sebagai lini kedua untuk pasien yang alergi terhadap penisilin.
Evaluasi respon pemberian obat ditinjau setiap 48 jam.
Pada pasien dengan selulitis tidak komplit pengobatan lini utama yang diberikan adalah
benzil penisilin Benzil penisilin atau fenoksimetilpenisilin keduanya memiliki konsentrasi
hambat minimal rendah (MIC) terhadap streptokokus (yaitu konsentrasi obat yang rendah akan
menghambat bakteri). Namun, penisilin saja tidak dianjurkan sebagai terapi lini pertama karena
efek terbatas terhadap Staphylococcus. Hal ini berpotensi penting karena diagnosis klinis dari
organisme infektif mungkin sulit, terutama di selulitis lokal awal atau selulitis dengan luka
sebagai portal masuk. Flukloksasilin sebagai pengobatan lini pertama, seperti yang dianjurkan
oleh CREST dan CKS, juga memiliki MIC rendah untuk streptokokus dan di samping memiliki
efek anti-staphylococcal. Meskipun MIC penisilin lebih menguntungkan dari pada flukloksasilin
untuk streptokokus, MIC flucoxacillin adalah cukup rendah bahwa penambahan benzil penisilin
untuk flukloksasilin pada pasien yang tidak menanggapi yang terakhir ini tidak mungkin untuk
menghasilkan nilai tambah yang menguntungkan. Hal ini telah dibuktikan oleh sebuah studi
yang menunjukkan tidak ada perbedaan dalam hasil ketika membandingkan sekelompok pasien
yang diobati dengan flukloksasilin versus kelompok diobati dengan flukloksasilin dan benzil
penisilin.
Pengobatan selulitis berulang
Meskipun bukti-bukti terbatas saat ini tentang pengobatan jangka panjang untuk selulitis
berulang, terapi profilaksis secara luas digunakan. Penelitian kecil menunjukkan bahwa
profilaksis antibiotik oral dapat bermanfaat dan menghemat biaya. Sebuah studi kecil (36 pasien
dalam penelitian acak dua kelompok dari 18 setiap pasien) menunjukkan bahwa pemberian
profilaksis eritromisin selama 18 bulan lebih efektif mencegah kekambuhan selulitis
dibandingkan dengan pemberian placebo.
Pada Penisilin profilaksis atau PATCH (Antibiotik profilaksis untuk Pengobatan Selulitis
di Rumah), dapat mengurangi episode selulitis pada pasien yang memiliki berulang (setidaknya
dua episode dalam 36 bulan sebelumnya) episode selulitis. Profilaksis pada selulitis disarankan
oleh BLS jika dua atau lebih episode selulitis terjadi setiap tahun. Rekomendasi untuk
phenoxmethylpenicillin sebagian karena keamanan profil jangka panjang - sebagai lawan
flukloksasilin yang membawa risiko toksisitas hati jika digunakan jangka panjang dan juga
karena selulitis berulang, dengan atau tanpa latar belakang lymphoedema, kemungkinan besar
menjadi infeksi streptococcus.


Lymphodema
Edema didefinisikan sebagai cairan interstitial yang berlebihan yang terjadi ketika ada
perbedaan antara laju filtrasi mikrovaskuler (di kapiler dan venula) dan drainase getah bening.
Peningkatan tekanan cairan interstitial dan volume menstimulasi aliran getah bening melalui
limfatik. Proses utama yang bertanggung jawab untuk drainase cairan interstitial. Penurunan
drainase limfatik dalam menghadapi filtrasi yang normal akan menghasilkan edema (limfedema).
Dalam saluran limfatik sehat aliran getah bening meningkat ketika kapiler meningkat filtrasi,
sehingga mencegah pembentukan edema.
Proses transportasi getah bening di kaki terutama proses aktif dicapai melalui kontraksi.
Mekanisme kontraktil dinding otot polos saluran pengumpul berada di bawah pengaruh dari
sistem simpatik serta masuknya ion kalsium. Edema terkait dengan calcium channel blockers,
oleh karena itu, mungkin sebagian melalui efeknya pada limfatik. Aktivasi dari pompa otot betis
melalui kontraksi umumnya diyakini berkontribusi terhadap peningkatan transportasi getah
bening.
Istilah lymphoedema mencakup berbagai patologi, yang semuanya hadir secara klinis
sebagai pembengkakan kronis dari satu atau lebih ekstremitas yang timbul dari kelainan
disaluran limfatik. Ini berarti kegagalan mendasar dalam transportasi getah bening, sebagai
lawan edema filtrasi yang disebabkan oleh peningkatan filtrasi kapiler.
Primer lymphoedema adalah istilah yang digunakan untuk lymphoedema yang timbul
dari kelainan perkembangan limfatik, baik karena kelainan genetik atau bawaan pada saluran
pengumpul atau karena kelainan diperoleh seperti lymphoedemas lymphangio-obliteratif yang
merupakan persentase kecil dari lymphoedemas yang sering hadir setelah pubertas.
Sekunder lymphoedema mengacu lymphoedema yang disebabkan oleh proses ekstrinsik
seperti infeksi, keganasan atau pembedahan yang merusak yang berfungsi dengan baik sistem
limfatik sebelumnya. Secara umum, jika edema simetris penyebab sistemik mungkin ditemukan
(misalnya hipoalbuminemia, sindrom nefrotik), sedangkan edema tungkai unilateral seringkali
merupakan hasil patologi lokal ke sistem limfatik. Manifestasi Klinis lymphoedema adalah
pembengkakan, pitting dan penebalan kulit.
Pengobatan Lymphoedema
Pengobatan lymphoedema yang utama adalah peningkatan drainase getah bening. Latihan
menginduksi perubahan tekanan cairan interstitial yang menyebabkan peningkatan baik dalam
mengisi limfatik dan tekanan, dengan peningkatan konsekuensial dalam kontraktilitas saluran
limfatik. Peningkatan aliran saluran getah bening non-kontraktil kemungkinan akan dipengaruhi
oleh latihan yang mengarah ke gerakan pasif getah bening.
Kompresi melalui perban atau stoking bertujuan untuk menghasilkan tekanan interstitial
meningkat dengan menentang filtrasi kapiler, menyebabkan peningkatan aliran balik vena serta
peningkatan kontraktilitas saluran limfatik. Multi-lapisan perban sering digunakan dalam
kombinasi dengan latihan dalam kasus lymphoedema parah.
Peningkatan kaki yang terkena dapat berkontribusi dengan mengurangi tekanan vena dan
kemudian filtrasi. Hal ini sering digunakan bersama dengan langkah-langkah lain, seperti elevasi
kaki sendiri memiliki sedikit efek pada drainase limfatik.
Drainase limfatik Manual (MLD) dalam bentuk memijat anggota tubuh yang terkena
dapat merangsang drainase getah bening dari akar anggota badan untuk cekungan limfatik
pengeringan. Hal ini sering dikombinasikan dengan teknik tersebut.
Terapi kompresi pneumatik dapat digunakan untuk melembutkan dan mengurangi
volume tungkai, tetapi dapat menggantikan cairan ke daerah sekitarnya dan penggunaannya
karena itu terbatas. Peralatan yang digunakan untuk metode ini dirancang untuk mengembang
dan mengempis sekitar tungkai bengkak, mengerahkan tekanan 30-40 mmHg. Meskipun
meningkatkan reabsorpsi cairan interstitial, itu tidak berpengaruh pada reabsorpsi protein. Hal ini
menyebabkan peningkatan konsentrasi protein interstitial dan hasil dalam pengerasan ekstremitas
Selanjutnya, pompa bilik tunggal tidak memiliki efek langsung pada aliran getah bening, dan
tekanan tinggi dapat merusak limfatik dangkal. Diuretik tidak berperan dalam pengobatan
lymphoedema dan hanya boleh digunakan dalam edema sekunder untuk retensi garam dan air
Hubungan antara lymphoedema dan selulitis
Hubungan antara selulitis dan lymphoedema adalah lingkaran setan di mana setiap
episode selulitis kerusakan lebih lanjut sistem limfatik, yang mengarah ke tingkat lymphoedema
sekunder, yang pada gilirannya merupakan peningkatan risiko untuk selulitis. Seperempat dari
pasien dengan lymphoedema akan memiliki setidaknya satu episode selulitis atau infeksi kulit
terkait di anggota badan yang terkena.
Penyebab utama dari limfedema dan dianggap multifaktorial. Limfatik berfungsi sebagai
media yang tepat untuk bakteri untuk tumbuh, dan stagnasi dari cairan limfatik karena gangguan
drainase getah bening dengan penurunan konsekuen dalam izin limfatik menciptakan keadaan
defisiensi imun lokal, yang, pada gilirannya, dapat meningkatkan risiko selulitis lokal. Pada
pasien tanpa lymphoedema, komponen bakteri dilepaskan dari bakteri dieliminasi oleh
fagositosis dan atau antibiotik dan dibersihkan secara efisien dengan drainase limfatik.
Kesimpulan
Selulitis adalah infeksi umum dan berpotensi serius yang berhubungan dengan biaya
besar untuk sistem kesehatan dan morbiditas kepada pasien. Berbagai faktor risiko telah
ditemukan untuk mempengaruhi untuk selulitis, lymphoedema menunjukkan hubungan terkuat.
Hubungan antara selulitis dan lymphoedema tampaknya menjadi lingkaran setan, cacat limfatik
yang sudah ada predisposisi selulitis, episode selulitis kerusakan sistem limfatik, dan baik
lymphoedema primer atau pasca-selulitis predisposisi episode berulang selulitis. Oleh karena itu
penting bahwa kedua selulitis dan lymphoedema diperlakukan tepat untuk mengurangi risiko
memburuknya lymphoedema dan selulitis berulang.
Antibiotik profilaksis yang tampaknya bermanfaat dalam mengurangi tingkat
kekambuhan selulitis dan saat ini disarankan, meskipun tanpa dasar bukti yang kuat, terutama
bila dikaitkan dengan selulitis lymphoedema.