11.1eptic arthritis s · septic arthritis is diagnosed in 2 to 10 persons per 100,000 people per...

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Anna Conen, Olivier Borens

1 Basics

Acute septic arthritis refers to bacterial, or rarely, fungal infections of a joint. It is a medical and surgical emergency because of the rapid destruction of the joint (Fig 11.1-1). Immediate therapeutic intervention is necessary to decrease the associated morbidity and mortality. A delay between symptom onset and initiation of adequate therapy is the major determinant of poor outcome.

1.1 EtiologyIn native joints, septic arthritis is commonly caused by hematogenous seeding of microorganisms from a distant infection focus [1–4]. Because the synovial membrane is highly vascularized and contains no limiting basement mem-brane, microorganisms can quickly pass from the blood into the joint space resulting in an acute onset of purulent joint inflammation. Patients at high risk for hematogenous seeding are intravenous (IV) drug users, patients with indwelling

vascular catheters, patients with infective endocarditis, im-munocompromised hosts, and elderly people [5,6]. Other pathomechanisms in the emergence of septic arthritis are direct inoculation of microorganisms into the joint as a result of intraarticular injections, surgical interventions, open joint injury, or trauma [7,8]. Rarely, microorganisms enter the joint space by spread from a contiguous focus, such as cellulitis, bursitis, or osteomyelitis.

Microorganisms in the joint space trigger an acute synovial inflammatory response. Within a few hours, activated inflammatory cells fill the closed synovial space. The inflam-matory cells release enzymes and cytokines and the microorganisms produce in addition toxins that can kill eukaryotic cells. The consequences are chemical toxic dam-age of the cartilage and underlying subchondral bone but also pressure damage due to the increased joint pressure due to the large accumulated inflammatory effusion [3,9].

11.1 Septic arthritis AnnaConen,OlivierBorens

Fig 11.1-1a–c Rapid joint destruction in a 21-year-old athlete after mistreated septic arthritis with methicillin-susceptible Staphylococcus aureus (3 months between first and last x-rays).

a b c

Section 2 Special situations

11.1 Septic arthritis

214 Principles of Orthopedic Infection Management Stephen L Kates, Olivier Borens

1.2 IncidenceSeptic arthritis is diagnosed in 2 to 10 persons per 100,000 people per year and in 5 to 10 patients per 10,000 patients hospitalized in an acute care facility per year. The incidence is considerably higher in patients suffering from rheumatoid arthritis, ie, 28 to 38 patients per 100,000 patients with rheumatoid arthritis per year. The incidence is increasing in recent years not only because of the aging population and the increasing use of immunosuppressive treatments and indwelling vascular catheters, but also because of the growing numbers of joint interventions [3]. Overall, the risk of postinterventional septic arthritis is small. For joint infiltrations it relates to 1 case per 22,000 interventions/infiltrations and for arthroscopy to 1 case per 250–1,000 interventions, respectively [4,10].

1.3 Risk factorsMost patients who develop septic arthritis have at least one risk factor. Each factor has a modest impact on the risk of septic arthritis, but in combination they can substantially increase the risk [5,11]. The most important risk factor is preexisting arthropathy, such as degenerative and chronic inflammatory joint diseases [4,8]. Older age (> 80 years), comorbidities including diabetes mellitus, cutaneous ulcers, alcoholism, and immunosuppression are also associated with an increased risk for septic arthritis [12]. Diseases with an increased risk for bacteremia, such as IV drug use and infective endocarditis, are other important risk factors, as is the skin colonization with Staphylococcus aureus. Furthermore, the presence of distant infection foci with the possibility of secondary bacteremia increases the risk for septic arthritis, including skin, urogenital, gastrointestinal, and pulmonary infections. Overall, the risk for septic arthritis after a joint intervention is low as mentioned above, ie, < 0.01% after synovial fluid aspiration and 0.01–0.4% after arthroscopy. Intraarticular steroid injections further increase the risk, especially if associated with arthroscopy, where the risk is 27.4 times higher than without the administration of steroids [13,14].

1.4 Location of involved jointsIn 90% of patients with septic arthritis only one joint is involved (monoarthritis), and 10% suffer from multiple joint involvement (oligoarthritis). Oligoarthritis is mainly found in patients with underlying rheumatoid arthritis [15]. Predominantly weight-bearing joints are affected, such as knee joints in 45–55% and hip joints in 15–25%, followed by shoulder, wrist, ankle, and elbow joints (together in 5–10%) [4,16]. Rarely sacroiliac or sternoclavicular joints and the symphysis pubis are infected and infection is more prevalent in IV drug users (sacroiliac or sternoclavicular joints and symphysis) and after gynecological and urologi-cal interventions (sacroiliac joint and symphysis) [17,18]. In children the hip joint is most commonly affected in 60%, followed by the knee joint in 35%.

1.5 Which microbes cause septic arthritis?Overall, S aureus is the predominant causative microorganism in 40–60%, followed by streptococci in 20–30% [1,2,9,19,

20]. Methicillin-resistant S aureus has to be considered in countries with a high prevalence of methicillin-resistance [21]. Gram-negative bacilli are found in 4–20%, especially in IV drug users, immunocompromised hosts, elderly pa-tients, or after trauma [9]. Culture-negative septic arthritis cases are described in 10–20% as a consequence of antimi-crobial pretreatment or fastidious to grow microorganisms. Polymicrobial infections are rare (maximum of 8%) and often associated with penetrating trauma.

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of the skin flora, including S aureus and coagulase-negative staphylococci, should be considered. In children younger than 2 years of age predominantly Kingella kingae is found. If there is a sexual risk behavior, gonococci have to be considered, especially if there is a concomitant macular exanthema and polyarticular involvement [22]. After gyne-cological interventions (eg, curettage or childbirth) and mainly in patients with impaired humoral immune function Mycoplasma hominis can be found. Brucella spp. should be considered in patients who visited the Mediterranean areas or in case of the consumption of unpasteurized milk prod-ucts. Special culture media and serology are required for diagnosis. If the patient history indicates oligoarthritis in combination with gastrointestinal symptoms and mesenteric lymphadenopathy, one should also be aware of Tropheryma whipplei. Borrelia spp. (ie, Lyme arthritis) should be con-sidered in case of an oligoarticular involvement and after a stay in an endemic area, even if no tick bite was recognized.

Depending on the clinical context and the presence of risk factors, one can anticipate the causative microorganism in septic arthritis. Therefore, the medical history is an essential element in narrowing the microbiological differential diag-nosis (Table 11.1-1). In patients without any risk factor for septic arthritis, or in patients with diabetes mellitus or rheu-matoid arthritis S aureus is the predominant cause. In IV drug users S aureus is the most common microorganism as well, but also Pseudomonas aeruginosa (because of tap water use to wash syringe), group A streptococci (because of a concomitant septic phlebitis) and Candida species (spp.) (because of contaminated lemon juice used for drug solution) have to be considered. Cat or dog bites usually result in infections with Pasteurella multocida and Capnocytophaga canimorsus, rat bites in infections with Streptobacillus monili-formis and human bites in infections with microorganisms of the oral cavity such as the HACEK group (Haemophilus spp., Aggregatibacter actinomycetemcomitans, Cardiobacterium

hominis, Eikenella corrodens, and Kingella kingae) or anaerobes. After joint infiltration or surgical intervention, microorganisms

Microorganism Clinical clues/risk factors

Staphylococcus aureus Healthy adults, presence of risk factors (eg, diabetes mellitus, skin breakdown, cutaneous infection), previously damaged joint (eg, rheumatoid arthritis, IV drug users, infective endocarditis)

Coagulase-negative staphylococci After invasive articular manipulation (ie, synovial fluid aspiration, joint infiltration, arthroscopy)

Streptococcus spp. Healthy adults, splenic dysfunction, cutaneous infection, infective endocarditis

Neisseria gonorrhoeae Sexually active patients, promiscuity, complement deficiency, associated tenosynovitis, and vesicular pustules

Enterobacteriaceae Elderly patients, immunocompromised hosts, urogenital or gastrointestinal infection

Pseudomonas aeruginosa IV drug users, immunocompromised hosts

Mycoplasma hominis Immunocompromised hosts, urogenital manipulations

Candida spp. IV drug users, immunocompromised hosts

Table 11.1-1 Microorganisms causing septic arthritis according to patient’s risk factors.Abbreviation: IV, intravenous.




2 Symptoms

Most patients (ie, 78–85%) present with an acute onset of joint swelling and pain. The pain is present at rest, aggra-vated with weight bearing, and the joint motion is limited. Joint erythema and excess heat are present in most cases. Fever is only found in about 50% of patients, possibly because analgesic and antiinflammatory medications are used [11]. About half of the patients have a distant infection focus and may report dysuria, urinary frequency, flank pain, nausea, vomiting, diarrhea, or a productive cough.

3 Diagnostic procedures

3.1 Clinical examinationThe affected joint is painful on palpation and movement. Erythema, excess heat, and a palpable effusion are present. In hip arthritis the latter signs can be absent and pain during movement and axial compression is the only clue for infec-tion. Generally, a monoarthritis is present, in case of oligo-arthritis one should bear in mind gonococccal arthritis, especially if a coexisting exanthema is found. The skin should always be examined for underlying skin diseases, either as the primary infection focus (eg, abscesses, cellulitis) or as a predisposing factor for the colonization with S aureus (eg, eczema, psoriasis). Furthermore, the patient should be examined for other primary infection foci, including uro-genital, gastrointestinal, or pulmonary infections.

The differential diagnosis of septic arthritis manifesting as acute monoarthritis includes predominantly crystal-induced arthritis such as gout (urate crystals) and pseudogout (calcium-pyrophosphate crystals) (Table 11.1-2) [11,23]. The differentiation between septic and crystal-induced arthritis is most challenging and often impossible both clinically and based on the synovial white blood cell (WBC) count. Other differential diagnoses include inflammatory osteoarthritis, inflammatory joint diseases (eg, rheumatoid arthritis, pso-riatic arthritis, sarcoidosis, Still’s disease) or reactive arthritis after gastrointestinal (eg, Campylobacter spp.) or urogenital infections (eg, Chlamydia spp.) among others [24,25]. Fur-thermore, trauma, hemarthrosis, fracture, meniscus tears, or osteonecrosis (after trauma or in steroid-treated patients) should be considered. Extraarticular diseases can also simulate septic arthritis, such as tenosynovitis, skin infections (eg, cellulitis or erysipelas), bursitis, or erythema nodosum.

3.2 Laboratory testsIf septic arthritis is suspected, blood inflammatory param-eters should be examined, including differential WBC count and C-reactive protein (CRP). The sensitivity of a WBC count > 10,000 cells/µL is 90% and a CRP > 100 mg/L is 77%, but both parameters are nonspecific [11]. As the predominant pathomechanism in septic arthritis is hematogenous seeding, two pairs of blood culture should be drawn for microbio-logical analysis; they are positive in about 50% of patients. Furthermore, urine and sputum cultures should be obtained if urogenital or respiratory tract are suspected to be the primary infection focus.

3.3 ImagingImaging is rarely necessary in the acute management of septic arthritis. Conventional x-ray detects preexisting joint diseases (ie, osteoarthritis, rheumatoid arthritis, osteomyelitis, or chondrocalcinosis). Ultrasound can be useful to guide joint aspiration. Bone scintigraphy is usually positive after 10 days, is not specific but may be helpful in the diagnosis of sacroiliac joint infection. Computed tomography is sensitive for the detection of bone erosions, joint effusion and soft-tissue infections. Magnetic resonance imaging is even more sensitive; however, it is only required for the diagnosis of sternoclavicular or sacroiliac arthritis, symphysitis, or post-operative arthritis following cruciate ligament reconstruction [26,27].

Differential diagnosis Specific diagnosis

Septic arthritis Bacterial, fungal, viral, mycobacterial arthritis

Crystal-induced arthritis Gout, pseudogout

Activated osteoarthritis Degenerative joint disease

Reactive arthritis Underlying urogenital (ie, Chlamydia spp. N gonorrhoeae) or gastrointestinal infections (ie, Campylobacter spp., Salmonella spp., Shigella spp., Yersinia spp.)

Systemic rheumatic diseases Rheumatoid arthritis, psoriatic arthritis, sarcoidosis, systemic lupus erythematosus

Trauma Hemarthrosis, fracture, osteonecrosis, meniscal tear

Tumor Osteosarcoma, chondrosarcoma, metastatic disease

Extraarticular disease Tenosynovitis, bursitis, cellulitis, erysipelas, erythema nodosum, Baker’s cyst

Table 11.1-2 Differential diagnosis of acute monoarthritis.

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of > 20'000 cells/μL should be considered to be highly suspicious for septic arthritis. If the proportion of the poly-morphonuclear leukocytes is > 90%, then sensitivity is 73% and specificity 79% [11]. Other inflammatory joint diseases, eg, rheumatoid arthritis or crystal-induced arthritis, can present with WBC counts of 2,000–50,000 cells/µL as well and especially crystal-induced arthritis mimics septic arthri-tis. The Gram stain is positive in only 50% but microbio-logical culture in up to 90% of patients with septic arthritis [11]. The microbiological diagnostic yield can be increased if the synovial fluid is inoculated into pediatric blood culture bottles [29]. If culture results are negative because patients were pretreated with antimicrobials or because of fastidious to grow or atypical microorganisms, bacterial DNA can be identified by polymerase chain reaction [30]. Crystals, ie, urate and calcium-pyrophosphate crystals, can be detected by polarized light microscopy of the synovial fluid. Note that the presence of crystals does not rule out septic arthritis, as coexistence of crystals and infection has been described [31,32].

3.4 Synovial fluid analysisThe examination of the synovial fluid is the most important diagnostic tool in every patient with suspected septic arthritis. Arthrocentesis should be performed before any antimicro-bial treatment is initiated [11,28]. The synovial fluid should be analyzed for the following parameters (ordered by sig-nificance):

1. Differential WBC count (use EDTA tubes to avoid coagulation)

2. Gram stain and microbiological culture (inoculate preferentially pediatric blood culture bottles to increase culture sensitivity)

3. Presence of crystals (use native tubes) (Table 11.1-3)

In septic arthritis, the synovial fluid macroscopically is turbid or purulent in 80–90% of patients. The differential WBC count helps to narrow the differential diagnosis: a WBC count of > 50,000 cells/µL has a sensitivity of 62% and a specificity of 92% for septic arthritis; but mainly in earlier stages of infection and in immunocompromised pa-tients lower WBC counts can be expected, therefore a limit

Clinical entity/Parameter Normal Degenerative joint disease Inflammatory joint disease Crystal-induced arthritis Septic arthritis

Clarity Transparent Transparent Translucent-turbid Turbid Turbid

Leukocyte count, cells/µL < 200 200–2,000 2,000–20,000 > 20,000 > 20,000

Polymorphonuclear leukocytes, [%] < 25 25–75 70–90 > 90 > 90

Culture Negative Negative Negative Negative Positive

Table 11.1-3 Differential diagnosis of arthritis based on synovial fluid analysis.




4 Treatment principles

The key to successful management of septic arthritis is early recognition of the diagnosis, the rapid initiation of appropriate antimicrobial therapy, and joint drainage. Antimicrobial treatment alone is insufficient to cure septic arthritis [33]. If septic arthritis is suspected, the patient should be managed as such until the diagnosis is definitively ex-cluded (Fig 11.1-2). The main treatment goal is the restoration of a painless full joint function by the eradication of infection with antimicrobial agents and by joint decompression with the removal of inflammatory effusion [3,9,34,35].

Before any antimicrobial treatment is started in a clinically stable patient, microbiological analysis of blood and synovial fluid is essential to identify the causative microorganism. For the mechanical and surgical treatment of septic arthritis, different strategies can be followed:

• Repetitive needle aspirations until there is a significant reduction of inflammation (ie, decreasing WBC counts) and negative microbiological culture results

• Arthroscopy• Arthrotomy(Table 11.1-4)

There are only a few studies comparing different surgical treatment strategies[36,42]. Therefore, the selection of the drainage procedure is dependent on the affected joint (large versus small joints), the soft-tissue condition (presence of abscesses or fistula), the patient’s comorbidities, the time lag between the onset of symptoms and the initiation of treatment (chronic inflammation with compartmentalization), and the Gächter stage (Table 11.1-5) [43–46].

The use of irrigation-suction drainage systems increases the risk of secondary infections and should be avoided. Joint irrigation with antiseptics is contraindicated because most antiseptics (chlorhexidine and polyhexanide) lead to chon-drolysis and destruction of the joint [47]. The administration of intraarticular antimicrobial treatment is also contraindi-cated because a chemical synovitis can be induced [2]. Moreover, systemic antimicrobial therapy achieves excellent drug levels in the infected joint, as the inflamed synovia is well perfused [48].

Joint pain and swelling

No definitive alternative diagnosis

Differential diagnosis: • Inflammatory arthritis • Crystal-induced arthritis • Trauma, hemarthrosis • Bursitis, cellulitis

Synovial fluid aspiration: • Cell count • Presence of crystals • Gram stain and culture

No septic arthritisSeptic arthritis

Antibiotic treatment: • High dose and bactericidal initially

IV therapy • Total treatment duration 4–6 weeks

Surgical treatment: • Repetitive needle aspiration • Arthroscopy • Arthrotomy

Fig 11.1-2 Management algorithm for septic arthritis.Abbreviation: IV, intravenous.

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The diagnostic arthrocentesis can already alleviate pain symp-toms in most patients and is therefore not only a diagnostic but also a first therapeutic intervention. It removes the inflamed synovial fluid with harmful enzymes and toxins that are damaging the cartilage. However, one aspiration is rarely enough and is mainly in large and weight-bearing joints (ie, knee, hip, shoulder, elbow, and ankle) only a provisional treatment and should be followed by rapid and aggressive surgical joint lavage via arthroscopy to avoid persisting joint damage.

4.1 Joint aspirationSmall peripheral joints (eg, finger and toe joints, wrist) can be treated with repetitive needle aspirations, if all necrotic and purulent material can be removed [38,39]. Otherwise, arthroscopic or open surgical drainage must be performed, especially if compartmentalized fluid collections are present. In case of repetitive needle aspirations, daily aspirations are necessary until treatment response is documented not only clinically but also microbiologically (ie, culture results turn negative) and by decreasing WBC counts in synovial fluid analysis.

Repetitive needle aspirations*

Arthroscopy Arthrotomy†

Small joints (eg, finger or toe joints and wrist)

Large, weight-bearing joints (eg, knee, hip, shoulder, elbow, and ankle)

Periarticular infection (eg, abscess and fistula)

Patients with persistent or recurrent (reactive) synovial effusion after repetitive arthroscopic lavages‡

Joints difficult to puncture and drain by needle aspiration (eg, hip and shoulder)

Osteomyelitis, presence of bone sequestra

Patients with high perioperative mortality

Treatment failure of repetitive needle aspirations (eg, compartmentalized joint effusion, adhesions)

Need for emergency decompression

Gächter stages 1, 2, and 3 Gächter stage 4

Prosthetic joint

Stage Criteria

1 Synovitis, cloudy fluid, possible petechiae, no radiological changes

2 Highly inflammatory synovitis, clumps of fibrin, pus, no radiological changes

3 Thickening of the synovial membrane (possibly several centimeters), adhesions with pouch formation, no radiological changes visible

4 Pannus formation, proliferation of aggressive synovitis on and later beneath the cartilage (ie, subchondral erosions), radiological changes visible

Table 11.1-4 Interventional and surgical treatment: when to use repetitive needle aspirations, arthroscopy, and arthrotomy?

* Daily repetition until white blood cell count in synovial fluid is decreasing and culture results turn negative; ineffective in compartmentalized joint effusions; no joint irrigation possible.

† Higher intraoperative and postoperative morbidity than arthroscopy in nonprosthetic joints.

‡ Prior documentation of microbiological response (negative culture results).

Table 11.1-5 Staging of septic arthritis as defined by Gächter.




4.2 ArthroscopyIn large weight-bearing joints (eg, hip, knee, shoulder, elbow, and ankle) repetitive needle aspirations are not enough to rapidly clean the joint and eliminate inflammatory effusion. Therefore, in these joints, if a Gächter stage 1, 2, or 3 is present (Table 11.1-5) and in patients with encapsulated inflammatory fluid collections, arthroscopic joint lavage as soon as possible with high-volume fluid irrigation (about 9 L of either Ringer’s solution or NaCl 0.9% solution) is the therapeutic method of choice [45,46,49–51]. Compared to needle aspiration, arthroscopy allows the visualization of the joint, the removal of collections and adhesions, leading to a rapid decompression and mechanical cleaning of the joint. More severe infections, patients with a history of inflammatory arthropathy and infections caused by S aureus often require repeated arthroscopic interventions [51,52]. The general approach is to repeat arthroscopy every 2–3 days if necessary, dependent on the initial intraoperative presentation and the clinical response to surgical and anti-microbial treatment (Fig 11.1-3). If a recurrent synovial effusion after multiple arthroscopies is present, interim needle aspirations can be performed if adequate response to antimicrobial therapy has been proven before (synovial cultures turn negative). A final arthroscopy might be useful to document the end of treatment results. The outcome is dependent on the initial stage of infection. Cure rates of > 80% have been documented.

4.3 Arthrotomy and possible treatment failuresOpen surgical intervention, ie, arthrotomy, is necessary if the infection is not controlled by repetitive arthroscopy, in Gächter stage 4 disease (Table 11.1-5), if there is underlying osteomyelitis or the presence of bone sequestra or in patients with a contiguous spread of the infection into the surround-ing soft tissue with abscess formation [45]. Furthermore, open surgical debridement is mandatory in patients with implants or prosthetic joints [53]. In earlier studies, arthro-tomy was associated with a worse functional outcome and a prolonged hospitalization when compared with arthro-scopy[40,41]. Compared with repetitive needle aspirations, arthrotomy was associated with a lower mortality rate and a trend for a shorter hospitalization [38,39,42]. However, in all these older, retrospective and single-institution studies, the patient numbers were small and a selection and treat-ment assignment bias cannot be excluded. The selection of the treatment modality, ie, needle aspiration versus arthro-tomy or arthroscopy, might depend on the medical depart-ment initially involved, ie, surgical or medical, and on the general health state of the patient: patients with many comorbidities and therefore a higher surgical intervention risk might be excluded from more invasive procedures and vice versa. Recently, two small studies compared arthrotomy and arthroscopy in the treatment of septic arthritis and confirmed the earlier findings [36,37]. Both studies found high cure rates for both treatment modalities (80–100%), but a higher risk for a relapse of infection and a worse functional outcome in patients treated with arthrotomy.

a b

Fig 11.1-3a–b Arthroscopic view of infected joints.a Gächter stage 1.b Gächter stage 2.

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synovial culture results and susceptibility testings are available, targeted treatment is initiated [3,54]. The targeted antimi-crobial treatment is summarized in Table 11.1-6.

When changing IV to oral antimicrobial therapy, the following points have to be respected. Only antimicrobial agents with a good bioavailability and bone penetration should be used; otherwise insufficient drug levels in the bone are achieved with a consecutive treatment failure. Therefore, the authors do not recommend using oral amoxicillin/clavulanate or oral cephalosporins for staphylococcal septic arthritis [55]. Furthermore, if an infective endocarditis is present, the use of an oral therapy is contraindicated. Infective endocarditis usually is treated with a high-dose IV therapy for 4–6 weeks (2 weeks in streptococcal infective endocarditis if combination therapy is used). The authors also advise against bacterio-static treatment regimens in septic arthritis, including clindamycin for staphylococci or streptococci and linezolid for staphylococci, streptococci, or enterococci. Be aware that oral treatment combinations with rifampin should not be used in patients with staphylococcal septic arthritis if they are scheduled for a prosthetic joint implantation in the near future (within a year). The reason is that rifampin-resistant skin flora emerges which—in case of a later postoperative prosthetic joint infection—increases the probability of an infection with a difficult-to-treat microorganism (ie, rifampin-resistant staphylococci) [53].

The duration of antimicrobial therapy is between 2–4 weeks for septic arthritis caused by streptococci and Haemophilus spp. and between 4–6 weeks for septic arthritis caused by S aureus and gram-negative bacilli [3,56,57]. Intravenous treatment duration usually is 1–2 weeks, dependent on the causing microorganism and its susceptibility pattern, the clinical response to treatment, and the presence of a con-comitant osteomyelitis (Gächter stage 4). An earlier switch to the oral therapy is possible if the microorganisms are susceptible to bactericidal oral treatment regimens with a good bioavailability and bone penetration, such as ri-fampin-containing regimens for staphylococci and fluoro-quinolones for enterobacteriaceae.

4.4 SynovectomyFor Gächter stages 1 and 2 (Table 11.1-5), synovectomy should not be carried out as this reduces the diffusion of antimi-crobial agents into the joint, which is facilitated by the strong perfusion in the inflamed synovial membrane. For Gächter stage 3, arthroscopic shaving may also be considered, while an arthrotomy is preferable if the synovial membrane is thick. For Gächter stage 4, an open synovectomy is recom-mended [45,49,51].

4.5 Antimicrobial treatmentIn addition to the surgical and mechanical treatment, the administration of high-dose and bactericidal systemic anti-microbial therapy is mandatory in the management of septic arthritis. Neither treatment strategy alone is sufficient [33]. The isolation of the causative microorganism is essential for a targeted antimicrobial therapy with a long treatment duration. There are no randomized controlled studies eval-uating the efficacy of different antimicrobial treatments.

Following arthrocentesis, empiric antimicrobial therapy is administered intravenously and guided by the presence of risk factors for septic arthritis (Table 11.1-1) and the results of the synovial Gram stain. In case no microorganisms can be detected in the Gram stain, the most common microor-ganisms causing septic arthritis should be covered, ie, staph-ylococci and streptococci. Intravenous amoxicillin/clavulanate 2.2 g every 8 hours or in penicillin-allergic patients IV cefazolin 2 g every 8 hours or IV cefuroxime 1.5 g every 8 hours are recommended. In countries with a high prevalence of methicillin-resistant S aureus empiric treatment should contain IV vancomycin 15 mg/kg body weight every 12 hours (vancomycin trough levels should be held at 15–20 mg/L). If gram-positive cocci are detected in the Gram stain (suggestive for staphylococci or streptococci) the same treat-ment regimen as for patients with a negative Gram stain result is recommended. If the Gram stain shows gram-neg-ative cocci (suggestive for gonococci or meningococci) IV ceftriaxone 2 g per day is suggested, and if gram-negative bacilli are present IV ceftriaxone 2 g per day or IV cefepime 2 g every 8 hours if P aeruginosa is suspected. As soon as




Table 11.1-6 Targeted antimicrobial treatment in septic arthritis.Note: The results of antimicrobial susceptibility testing are required for targeted treatment. Intravenous treatment duration is 1–2 weeks, and total treatment duration is 2–6 weeks, dependent on the microorganism, the clinical response to treatment, and the presence of a concomitant osteomyelitis.

The indicated dosages are for adult patients with normal body mass index, and normal renal and liver function. Abbreviation: IV, intravenous.

* In patients with a delayed-type hypersensitivity to penicillin, IV cefazolin 3 x 2 g or IV cefuroxime 3 x 1.5 g per day can be used.† In patients with an immediate-type hypersensitivity to penicillin, IV vancomycin 2 x 15 mg/kg body weight per day (vancomycin trough level 15–20 mg/L) or IV daptomycin 1 x 8 mg/kg body weight (and 1 x 10 mg/kg body weight in enterococcal infections) per day should

be used.‡ Rifampin combinations should not be used if a prosthetic joint implantation is planned within the upcoming year. Oral treatment

combinations should not be used if an underlying infective endocarditis is present.§ After a single IV loading dose of 1 x 800 mg.|| Intravenous gentamicin 1 x 3 mg/kg body weight.¶ Two weeks IV treatment recommended.# Vancomycin trough level 15–20 mg/L.** Intravenous gentamicin 1 x 3 (-5) mg/kg body weight or IV tobramycin 1 x 3 (-5) mg/kg body weight.†† After a single oral loading dose of 1 x 800 mg.‡ ‡ After a single IV loading dose of 1 x 200 mg.

Microorganism Antimicrobial agent Daily dose ApplicationStaphylococci: S aureus and coagulase-negative staphylococciMethicillin-susceptible staphylococci Flucloxacillin*† 4 x 2 g IV

Levofloxacin AND Rifampin‡

2 x 500 mg2 x 450 mg

OralOral

ORTrimethoprim/sulfamethoxazol ANDRifampin‡

3 x 160/800 mg2 x 450 mg

OralOral

ORFusidic acid ANDRifampin‡

3 x 500 mg2 x 450 mg

OralOral

ORDoxycycline ANDRifampin‡

2 x 100 mg2 x 450 mg

OralOral

Methicillin-resistant staphylococci Vancomycin#, OR 2 x 15 mg/kg body weight IVTeicoplanin, ORDaptomycin

1 x 400 mg§

1 x 8 mg/kg body weightIVIV

Levofloxacin ANDRifampin‡

2 x 500 mg2 x 450 mg

OralOral

ORTrimethoprim/sulfamethoxazol ANDRifampin‡

3 x 160/800 mg2 x 450 mg

OralOral

ORFusidic acid ANDRifampin‡

3 x 500 mg2 x 450 mg

OralOral

ORDoxycycline ANDRifampin‡

2 x 100 mg2 x 450 mg

OralOral

Streptococcus spp. Penicillin G† 4 x 5 Mio Units IVCeftriaxon 1 x 2 g IVAmoxicillin 3 x 750 mg Oral

Enterococcus spp. Amoxicillin†

With or without aminoglycoside||, OR4 x 2 g IV

IVDaptomycin 1 x 10 mg/kg body weight IVAmoxicillin 3 x 750 mg Oral

Enterobacteriaceae, gonococci, meningococci (quinolone susceptible) Ceftriaxon 1 x 2 g IVCiprofloxacin 2 x 750 mg Oral

Nonfermenters¶ (eg, P aeruginosa) Cefepime, ORCeftazidime, OR

3 x 2 g3 x 2 g

IVIV

Piperacillin/tazobactam, ORMeropenem

3 x 4.5 g3 x 2 g

IVIV

AND consider all with aminoglycoside**

Ciprofloxacin 2 x 750 mg OralCandida spp. Fluconazole 1 x 400 mg†† Oral

CaspofunginAnidulafungin

1 x 70 mg1 x 100 mg‡ ‡

IVIV

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5 Conclusion

A high index of suspicion for septic arthritis especially if risk factors are present allows a rapid initiation of therapy and a reduction of complications. Early signs of infection should prompt synovial fluid aspiration, which is the most im-portant diagnostic workup (Fig 11.1-2). The key to successful management of septic arthritis is the rapid initiation of ap-propriate antimicrobial therapy, and joint drainage. Antimi-crobial treatment alone is insufficient to cure septic arthritis. Joint drainage can be achieved by arthroscopy, repetitive needle aspirations or arthrotomy dependent on the involved joint, the extent and Gächter stage of the infection. High-dose and bactericidal systemic antimicrobial therapy is administered initially intravenously. Thereafter, oral treatments with a high bioavailability and bone penetration are necessary. Although treatment is highly efficient, permanent joint damage is the most important complication if adequate therapy is delayed.

4.6 Physiotherapy Physiotherapy of the infected joint is important and necessary to ensure that the cartilage is supplied with nutrients through diffusion [37,54]. An infected joint should never be immobilized with external fixation or in a splint. Passive range-of-motion and isometric exercises to build up strength accelerate reha-bilitation and reduce the risk of subsequent joint stiffness, furthermore they prevent muscular atrophy. For the knee and hip, a passive motion brace is useful. In the acute phase until drains have been removed the joint should not bear any weight, ie, bed rest or relief through two crutches is recommended, as is the placement in a functionally favorable position to avoid contractures (not fully extended).

4.7 PrognosisThe prognosis of septic arthritis has not improved in recent years despite better antimicrobial drugs and surgical inter-vention strategies. The functional prognosis is directly related to the presence of preexisting joint disease, the virulence of the causing microorganism, and the therapeutic delay between onset of symptoms and start of adequate therapy [2,45,56,58,59]. Despite adequate therapy, 25–50% of patients with septic arthritis experience permanent joint damage with impaired joint function. The mortality rate is dependent on age, the presence of comorbidities, and im-munosuppression and ranges between 5–15% [56,58]. In patients with a polyarticular infection, mortality rate is higher and may reach 30% [15].




6 References

1. Morgan DS, Fisher D, Merianos A, et al. An 18 year clinical review of septic arthritis from tropical Australia. Epidemiol Infect. 1996 Dec;117(3):423–428.

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11.1eptic arthritis s · septic arthritis is diagnosed in 2 to 10 persons per 100,000 people per...

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