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UNIVERSITAS PEMBANGUNAN NASIONAL VETERAN JAKARTA

JOURNAL READING

SELULITIS

Disusun untuk Memenuhi Syarat Mengikuti Ujian Kepaniteraan Klinik

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 Infirmary, Carlisle, UK

Cellulitis is defined as an acute inflammation 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 financial 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 inflammatory response (Morton and Swartz, 2004). A typical presentation is painful swelling with erythema that is hot and tender to touch, often preceded by flu-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 cellulitisCellulitis 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 identification of streptococci in cellulitis is that the infection is of the dermis, not of the skin surface, so it is difficult to identify. Another possible reason is that treatment has often been initiated at an early stage and may mask symptoms of fever, making microbiological identification more difficult. 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 fluid 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

CellulitisLymphoedemaProphylactic therapyPATCH

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

39Journal 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 significant patient-specific 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 inflammatory 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 confirm 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, confirming 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 cellulitisLocal 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 first 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 specifically linked to leg oedema secondary to lymphoedema and is much less the case with oedema secondary to venous insufficiency. 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 significant 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 findings 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 cellulitisThe 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.



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 flucloxacillin as the first-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 flucloxacillin as first-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 levofloxacin (which is rarely used for cellulitis in the UK) showed that if response to treatment occurs after five days, further treatment may not provide any additional benefit (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 first-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 first-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 first-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 difficult, especially in early localised cellulitis or in cellulitis with a wound as the portal of entry. Flucloxacillin as first-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 flucloxacillin for streptococci, flucoxacillins MIC is sufficiently low that the addition of benzyl penicillin to flucloxacillin in patients who do not respond to the latter is unlikely to produce added beneficial value. This has been proven by a study that showed no difference in outcome when comparing a group of patients treated with flucloxacillin versus a group treated with flucloxacillin and benzyl penicillin (Leman and Mukherjee, 2005).

Treatment of recurrent cellulitisDespite 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 profile as opposed to flucloxacillin 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.

LymphoedemaOedema 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 influence of the sympathetic system as well as the influx 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 filtration oedema which is caused by increased capillary filtration (Mortimer and Levick, 2004).

Primary lymphoedema is the term used for lymphoedema that arises from


41Journal 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 lymphoedemaThe 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 fluid pressure which leads to an increase in both the lymphatic filling and pressure, with a consequential increase in the contractility of the lymphatic ducts. An increase in the flow of the non-contractile lymph ducts is likely to be influenced 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 filtration, 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 filtration. 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 fluid into adjacent areas and its use is therefore limited. The equipment used for this method is designed to inflate and deflate around a swollen limb, exerting a pressure of 3040mmHg. Although it increases the reabsorption of interstitial fluid, 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 flow, and the high pressures can damage the superficial 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-specific 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 cellulitisIt 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 fluid serves as an excellent medium for bacteria to grow, and stagnation of the lymphatic fluid due to impaired lymph drainage with consequent reduction in lymphatic clearance creates a state of local immune deficiency, 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 efficiently by lymphatic drainage (Jeffs, 1998).

Baddour and Bisno (1985) postulated that bacterial toxins which were pooled in insufficiently 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 difficult 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 benefit of agents such as clindamycin and macrolides, as these have immunomodulatory actions as well as



Clinical REVIEW

anti-streptococcal activity, and therefore may have a role in the treatment of patients with recurrent cellulitis that complicates lymphoedema (Ritts, 1990).

ConclusionCellulitis 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 beneficial 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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JL


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.

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