INTRODUCTION This chapter is a revision of the chapter by Luis E. Rodriguez, MD, & John E. Gough, MD, 1 .

FACEP IMMEDIATE MANAGEMENT OF LIFE-THREATENING INJURIES All trauma patients presenting to the emergency department should be managed initially in the same manner, with similar guiding principles of trauma care regardless of their underlying injuries. Orthopedic injuries may be dramatic, but they should not draw attention away from more critical elements of initial patient assessment and treatment. In fact, less obvious closed fractures may be associated with significant blood loss. The emergency physician must remain objective and proceed with the primary survey, which consists of evaluating the airway, .)breathing, circulation, disability, and exposure (ABCDEs) (Table 26-1 Table 26-1. Potensi darah yang hilang dalam fraktur tertutup Site Amount (L) Pelvis 1-5+ Femur 1-4 Spine 1-2 Leg 0.5-1 Arm 0.5-0.75

IMMEDIATE MANAGEMENT OF LIMB-THREATENING INJURIES

PENANGANAN LINI PERTAMA PADA SEPTIK ARTRITIS SEPTIK ARTRITIS Adalah infeksi mikroorganisme yang merupakan reaksi invasi pada rongga persendian. Steril arthritis apabila tidak ditemukan kuman pada peradangan sendi. Septik arthritis meningkat pada pria, 45% Pada usia 65 tahun, dan meningkat pada penggunaan prothese. Jenis kuman yang menjadi penyebab septic arthritis adalah: Neisseria Gonorrheae (75% dari kasus, banyak pada dewasa muda), Staphylococcus aureus , Streptococcal sp (Streptococcus viridans, S

pneumoniae,[9,

10]

dan streptococci grup B), dan pseudomonas aeruginosa, selain itu

dapat juga disebabkan oleh virus dan mikobakterial. Septik arthritis juga dapat timbul sebagai komplikasi dari osteomyelitis akut yang terlambat ditangani, bila septic arthritis

tidak ditangani dapat menyebabkan kematian. Invasi kuman ke jaringan tulang dapat menyebar melalui inokulasi langsung, penyebaran lewat jaringan periartikuler, atau per hematogen (yang paling umum terjadi) The major consequence of bacterial invasion is damage to articular cartilage. This may be due to the particular organism's pathologic properties, such as the chondrocyte proteases of S aureus, as

DIAGNOSIS SEPTIK ARTRITIS: PANAS Biasanya subfebril, riwayat panas lama, kadang-kadang disertai selulitis pada lesi yang terkena, dapat disertai gejala penyakit sesuai etiologi kuman, ataupun virusnya SENDI BENGKAK Adakah riwayat trauma atau peyakit persendian, berapa sendi yang terlibat NYERI SENDI Perhatikan onset nyerinya, apakah akut, nyeri pada persendian, gangguan ROM. LEUKOSITOSIS X FOTO RONGGA SENDI MELEBAR Pemeriksaan fisik Lokasi sendi yang terkena: lutut (50%), panggul (20%), pergelangan kaki dan pergelangan tangan, sikut, ruas jari, sternoklavikular, dan sendi sakroiliaka. Pemeriksaan fisik ditemukan eitema, pembengkakan, panas, dan tegang pada kulit, adanya efusi yang jelas, ditandai dengan keterb, atasan pada ROM Aktif maupun pasif, pada pasien imunokompromis dan orang tua, gejala dapat tersamar PENANGANAN LINI PERTAMA SEPTIK ARTRITIS ANTIBIOTIK

Seleksi antibiotik sebaiknya adalah antibiotik bakterisidal dengan efek menghambat pertumbuhan terutama untuk kuman-kuman yang memproduksi biofilm,seperti S aureus koagulase negative, waspadai terutama bila prevalensi MRSA tinggi di daerah tersebut. Pemberian antibiotic harus dievaluasi setelah lewat 5 hari, apakah ada perbaikan gejala bila tidak didapatkan perbaikan, lakukan kultur . Untuk pemilihan jenis antibiotik yang digunakan terutama adalah yang sensitif terhadap kuman gram negative, contoh: Sefalosporin generasi ke 3, ciprofloksasin (diberikan 1-2minggu), untuk bakteri MRSA atau CONS yang dipergunakan adalah anti biotic oxacillin, dan vancomisin

ANALGETIK DAN ANTIPIRETIK

Pemberian AINS dapat membantu, terutama setelah 5 hari pemberian antibiotic, terutama pada kasus sepsis arthritis yang reaktif IMMOBILISASI Sesuai dengan lokasi persendian

SINDROMA KOMPARTEMEN Adalah suatu sindrom yang dirasakan pada ekstrimitas akibat peningkatan tekanan intrakompartemen oleh karena adanya desakan yang timbul akibat odem hebat, dapat terjadi pada non trauma seperti penyakit metabolic, gigitan ular berbisa, namun sering diakibatkan oleh trauma seperti : cedera arteri pada luka, peningkatan permeabilitas yang mengakibatkan larinya cairan ke dalam jaringan akibat cedera dan inflamasi, pemakaian traksi atau gips yang terlalu kencang, luka bakar, dan lain-lain. Apabila terlambat ditangani dapat menyebabkan cedera saraf, dan infark jaringan yang akhirnya menyebabkan nekrosis Gejala yang perlu diperhatikan ada 5P yaitu: 1. PAIN 2. PALE 3. PULSELESSNESS 4. PARAESTHESIA 5. PARALYSIS

PENANGANAN INISIAL 1. IMOBILISASI KEMUDIAN DILETAKKAN LEBIH TINGGI DARI JANTUNG (ELEVASI) 2. BUKA BEBAT 3. BIVALVE GIPS Apabila gips terpasang terlalu kuat, maka kedua sisi lateral gips dibuka sedikit untuk merenggangkan gips, kaki didinginkan, 4. segera rujuk ke ortopedi untuk terapi definitive : Fasciotomi

Pathogenic invasion
Previously damaged joints, especially those damaged by rheumatoid arthritis, are the most susceptible to infection. The synovial membranes of these joints exhibit neovascularization and increased adhesion factors; both conditions increase the chance of bacteremia, resulting in a joint infection. Some microorganisms have properties that promote their tropism to the synovium. S aureus readily binds to articular sialoprotein, fibronectin collage, elastin, hyaluronic acid, and prosthetic material via specific tissue adhesion factors (microbial surface components recognizing adhesive matrix molecules [MSCRAMMs]). In adults, the arteriolar anastomosis between the epiphysis and the synovium permits the spread of osteomyelitis into the joint space. The major consequence of bacterial invasion is damage to articular cartilage. This may be due to the particular organism's pathologic properties, such as the chondrocyte proteases of S aureus, as well as to the host's polymorphonuclear leukocytes response. The cells stimulate synthesis of cytokines and other inflammatory products, resulting in the hydrolysis of essential collagen and proteoglycans. Infection with N gonorrhoeae induces a relatively mild influx of white blood cells (WBCs) into the joint, explaining, in part, the minimal joint destruction observed with infection with this organism relative to destruction associated with S aureus infection. As the destructive process continues, pannus formation begins, and cartilage erosion occurs at the lateral margins of the joint. Large effusions, which can occur in infections of the hip joint, impair the blood supply and result in aseptic necrosis of bone. These destructive processes are well advanced as early as 3 days into the course of untreated infection. Viral infections may cause direct invasion (rubella) or production of antigen/antibody complexes. Such immunologic mechanisms occur in infections with hepatitis B, parvovirus B19, and lymphocytic choriomeningitis viruses.[14]

Reactive/postexposure process
Reactive, or postexposure, arthritis is observed more commonly in patients with human lymphocyte antigen B27 (HLA-B27) histocompatibility antigens. Although various infections can cause reactive arthritis, gastrointestinal processes are by far the most common. Gastrointestinal pathogens associated with reactive arthritis include the following:

Salmonella enteritidis Salmonella typhimurium Yersinia enterocolitica Campylobacter jejuni Clostridium difficile Shigella sonnei Entamoeba histolytica Cryptosporidium

Genitourinary infections, especially those due to Chlamydia trachomatis, are the second most common cause of reactive arthritis. The arthritis of Lyme disease usually results from immunologic mechanisms, with a minority of cases due to direct invasion by an organism. A reactive/postexposure process may occur months after the gastrointestinal or genitourinary process has resolved.

Local infection
Prosthetic joint infections (PJIs) may be a consequence of local infection, such as intraoperative contamination (60-80% of cases), or of bacteremias (20-40% of cases).[2] The bacteremias may be spontaneous (ie, gingival disease) or secondary to various manipulations. Delayed wound healing is a major factor behind early prosthetic joint infection. Until the fascia has healed, the usual tissue barriers to infection of the implant are not present. Eventually, the implanted hardware becomes less susceptible to infection by hematogenous spread, because the pseudocapsule develops around it. The biofilm of coagulase-negative S aureus (CoNS) protects the pathogen from the host's defenses, as well as from various antibiotics. Polymethylmethacrylate cement inhibits WBC and complement function. Overall, the most common organisms of prosthetic joint infections are CoNS (22% of cases) and S aureus (22% of cases). Enteric gram-negative organisms account for 25% of isolates.[16] Streptococci, including S viridans, enterococci, and the beta-hemolytic streptococci, cause 21% of cases. Anaerobes are isolated from 10% of patients. Other distinctive host and/or situation-pathogen associations have been described, including Pasteurella multocida, Capnocytophaga species (dog and cat bites), Eikenella corrodens, anaerobes (especially Fusobacterium nucleatum and streptococcal species [human bites]), Aeromonas hydrophila (myelogenous leukemia), P aeruginosa, Serratia species, Candida species (particularly common in persons who abuse intravenous drugs), Mycobacterium marinum (water exposure), S schenckii (gardening), and S pneumoniae (sickle cell anemia). Unlike osteomyelitis, Salmonella species are not associated with the septic arthritis of sickle cell anemia. Ten to 30% of patients with brucellosis have lumbosacral spine involvement.

Prognosis
The primary morbidity of septic arthritis is significant dysfunction of the joint, even if treated properly. Fifty percent of adults with septic arthritis have significant sequelae of decreased range of motion or chronic pain after infection.[1] Thirty percent of cases of reactive arthritis may become chronic. Complications include dysfunctional joints, osteomyelitis, and sepsis. Predictors of poor outcome in suppurative arthritis include the following:

Age older than 60 years

Infection of the hip or shoulder joints Underlying rheumatoid arthritis Positive findings on synovial fluid cultures after 7 days of appropriate therapy Delay of 7 days or longer in instituting therapy

The mortality rate depends primarily on the causative organism. N gonorrhoeae septic arthritis carries an extremely low mortality rate, whereas that of S aureus can approach 50%.[17] Previous Proceed to Clinical Presentation

History
Because joint infections are uncommon, be especially attentive to features of the patient's history that may indicate an infectious process instead of a primary rheumatologic or orthopedic process.[5] Pay attention to the following symptoms:

Acuteness of onset of the joint pain Whether the pain is superimposed on chronic pain Previous history of joint disease or trauma, whether accidental or iatrogenic (eg, infection complicates 0.4% of arthrocenteses) Whether the process is monoarticular or polyarticular and which joints are involved The presence of extra-articular symptoms Whether the patient has had vascular invasion due to catheterizations or intravenous drug abuse

Obtain a thorough history regarding the possible presence of sexually transmitted diseases (STDs) or exposure to ticks (Lyme disease). The increase of group B streptococcal joint infections is associated with the increased prevalence of diabetes and increasing life expectancy. Numerous conditions that adversely affect the host's defenses (eg, liver disease, diabetes mellitus, lymphoma, solid tumors, complement deficiencies [C7, C8], immunosuppressive drugs, hypogammaglobulinemia) are increasingly observed in patients with septic arthritis. Determine the possible contribution of these diseases to the clinical presentation. The most important historical feature is the existence of underlying joint disease, especially rheumatoid arthritis. In addition, the possibility of recent injury to the joint or penetrating or blunt trauma must be explored. Ask the patient about needle aspiration of the joint or injections of corticosteroids into the joint. Elicit a history of diarrheal disease.

Symptoms

Patients with an infected joint typically present with the triad of fever (40-60% of cases), pain (75% of cases), and impaired range of motion. These symptoms may evolve over a few days to a few weeks. Fever is usually low-grade (< 102F), with rigors present in only 20% of cases. Spiking fevers and chills are much more common with crystalline arthritis. Lyme disease Months after infection onset, 60% of patients with untreated Lyme disease develop swelling and pain, chiefly affecting the large joints. Usually, Lyme disease affects 1-2 joints at a time, with the knee involved most commonly. The distinguishing pattern is attacks extending from a few weeks to months and separated by periods of complete remission. The rate of recurrence lessens by about 15% per year. A small percentage of individuals develop chronic arthritis (ie, inflammation of a joint lasting 1 y). This type of relapsing course almost always precedes the chronic stage of Lyme arthritis. Prosthetic joint infection Compared with patients with infections of native joints, most patients with prosthetic joint infection (PJI) exhibit a prolonged low-grade course with gradually increasing pain. However, with gram-negative infections, especially with enteric organisms, PJI may be far more acute in onset. Usually, no significant fever or swelling occurs (delayed prosthetic joint infection). However, individuals with early prosthetic joint infection present with an acute illness characterized by high-grade fever, focal swelling, and redness. Cellulitis and draining sinus tracts often develop. Because late prosthetic joint infection is usually secondary to bacteremia, the clinical picture is often dominated by the source of the bloodstream infection. The nature of the invading organism, the type of tissue infected, and the route of infection determine presentation. Thus, a high index of suspicion is needed for identification of bacteremic and delayed prosthetic joint infection. Because of its many pathogenic mechanisms, S aureus is usually associated with a fulminant course, as opposed to the indolent course of coagulasenegative S aureus (CoNS) that dominates delayed prosthetic joint infection. Relatively devitalized tissues (eg, wound hematomas) are conducive to rapid bacterial replication and a more acute course. Bacteremic spread allows infection with fewer organisms and leads to a more muted course. Reactive and tuberculous arthritides Reactive arthritis usually begins several weeks after the underlying infection has resolved. Few concurrent systemic symptoms occur. Symptoms of tuberculous arthritis are quite indolent; the diagnosis may be delayed for several years. Usually, the purified protein derivative (PPD) results are negative, and no signs, past or present, of pulmonary tuberculous exist.

Viral septic arthritis Table 1, below, provides a summary of the clinical features of septic arthritis caused by various viral organisms. Table 1. Clinical Features of Viral Septic Arthritis
VirusClinical Features of Viral Septic ArthritisParvovirus B19Occurs in adult women with erythema infectiosum, often an itchy rashHepatitis AMuscle aches and rash in 10% of casesHepatitis BOnset in the preicteric phase; usually resolves as jaundice develops; chronic arthritis possible in patients with chronic hepatitis B infection Hepatitis CHistory similar to hepatitis B joint infectionRubella (natural infection and vaccine related)Onset is possible before, during, or after the appearance of the rash; usually resolves in a few weeks; may recur and, more commonly, may persist Human immunodeficiency virus [HIV] (2 types occur, both with noninflammatory, sterile joint fluid)Develops over several days, and severe knee or ankle pain is characteristic; excellent response to nonsteroidal anti-inflammatory agents (NSAIDS) Sudden onset of severe pain in the shoulders and elbows, closely resembling an acute gouty attack; Opiates often necessary to control pain MumpsOccurs in adult men 2 weeks after the presentation of parotitis

Physical Examination
The most commonly involved joint in septic arthritis is the knee (50% of cases), followed by the hip (20%), shoulder (8%), ankle (7%), and wrists (7%). The elbow, interphalangeal, sternoclavicular, and sacroiliac joints each make up 1-4% of cases. A thorough inspection of all joints for signs of erythema, swelling (90% of cases), warmth, and tenderness is essential for diagnosing infection. Infected joints usually exhibit an obvious effusion, which is associated with marked limitation of both active and passive ranges of motion (ROMs). Frequently, these findings are apparent but may be diminished or poorly localized in cases of infection of the spine, hip, and shoulder joints.[14] Signs and symptoms of infection may be muted in people who are elderly, who are immunocompromised (especially those with rheumatoid arthritis), and who abuse intravenous drugs.

Pattern of joint involvement

Nongonococcal bacterial/suppurative arthritis The pattern of joint involvement is an extremely important diagnostic feature. Of cases of nongonococcal suppurative arthritis, 85-90% are monoarticular. If the disease affects more than one joint, S aureus is most commonly implicated. Polyarticular arthritis is usually observed in gonococcal disease, various viral infections, Lyme disease, reactive arthritis, and various noninfectious processes. Gonococcal arthritis may be part of the gonococcal arthritis/dermatitis syndrome.

Group B streptococci most commonly infect the sacroiliac and sternoclavicular joints. Gonococcal bacterial/suppurative arthritis Gonococcal musculoskeletal involvement may present in 1 of 2 ways, as described below. Fever, arthralgias of multiple joints, and multiple skin lesions (dermatitis-arthritis syndrome) characterize disease that develops soon after the gonococcus disseminates from the cervix, urethra, or pharynx. Usually, this disease exhibits no clinical direct joint findings, but the process is one of tenosynovitis of asymmetric distribution. Typically, hand joints are involved most often, as well as those of the knee, wrist, ankle, and elbow. Skin lesions are multiple but seldom number more than 12, whereas lesions associated with meningococcemia may number more than 100. The lesions evolve over a few days from papular to pustular or vesicular to necrotic. This course may recur for several months. Findings on cultures of blood and mucosal surfaces are often positive; findings on cultures of joint fluid are usually negative. Sixty percent of disseminated gonococcal infections are of this type. Monoarticular arthritis without associated systemic symptoms, tenosynovitis, or skin lesions characterizes disease that begins later after gonococcal dissemination than does dermatitis arthritis syndrome.[7] Dermatitis-arthritis syndrome may or may not precede this phase. In a joint infected by the Lyme organism, swelling may be disproportionate to the level of pain. Baker cysts are a frequent feature of this type of infectious arthritis. Because the pain of an infected hip joint may not be localized directly and swelling of the joint is inconspicuous, perform specific maneuvers, such as the Fabere maneuver. Infection of the sacroiliac joint often presents as buttock, hip, or anterior thigh pain. Direct pressure usually elicits tenderness in the joint. Alternatively, hyperextension of the hip and leg while the patient is lying down (ie, Gaenslen maneuver) elicits pain in a suppurative sacroiliac joint. Septic bursitis most commonly involves the olecranon and prepatellar bursae. Swelling and pain are present. However, an infected bursa does not limit the range of motion of the underlying joint the way an actual joint infection does.[18]

Prosthetic joint infections

Physical findings are usually minimal in an infection of the prosthetic joint, and swelling is usually slight. The most distinctive finding is a draining sinus presumed to originate in the underlying infected prosthetic joint.

Reactive, viral, and tuberculous arthritides

Most cases of reactive arthritis involve a few large joints in an asymmetric fashion, whereas viral arthritis usually exhibits symmetric involvement of the smaller joints, especially the hands, with a concurrent rash. The joints of tuberculous arthritis can appear to be boggy on palpation.

Diagnostic Considerations

When evaluating a patient with suspected septic arthritis, also consider conditions such as primary rheumatologic disorders (eg, vasculitis, crystalline arthritides), drug-induced arthritis, and reactive arthritis (eg, postinfectious diarrhea syndrome, postmeningococcal and postgonococcal arthritis, arthritis of intrinsic bowel disease[14] ). In early disseminated gonococcal infection, an early tenosynovitis predominates without actual joint invasion such as occurs in the later variety of disseminated gonococcal infection. A viral syndrome usually produces polyarticular arthritis. Pustular lesions are consistent (as is almost any type of skin lesion) with staphylococcal bacteremia. Whenever vesicles are present, always consider staphylococcal infection. Unlike salmonella osteomyelitis, the frequency of salmonella septic arthritis is not greatly increased in patients with sickle cell anemia. However, when septic arthritis does occur, Salmonella is more commonly identified. Staphylococcus aureus remains the most common infectious agent in people who abuse intravenous drugs. However, a high rate of infections with gram-negative organisms, especially Pseudomonas aeruginosa and Serratia species, occurs in cases of septic arthritis. In addition, a higher rate of fungal and anaerobic infections occurs. Unusual locations, such as the sternoclavicular joint, are involved.

Approach Considerations
An approach to rapid evaluation of an acutely inflamed joint is to screen the synovial fluid for crystals via polarizing microscopy and for organisms via Gram stain (63-96% sensitive). If crystals are present and the Gram stain findings are negative, treatment for crystal-associated arthritis should be initiated. However, an exception to this would be the presence of significant risk factors for infection (eg, the focus of infection lies somewhere that could lead to bacteremia, such as pneumonia or pyelonephritis). Therapeutic decisions cannot be delayed until results of the synovial fluid culture are available. If microscopy demonstrates no crystals, treat the patient for presumed infection even if the Gram stain findings are negative. The Gram stain is less than 60% sensitive for detection of bacteria in synovial fluid. Always send the fluid for culture, regardless of the result of the screening evaluation. A joint damaged by gout or pseudogout is prone to be infected. Culture of synovial tissue is indicated primarily to detect mycobacteria or fungi. If the patient's condition does not improve significantly after 5 days, the joint must be reaspirated and examined. Most septic joints have a white blood cell (WBC) count that exceeds 50,000/L, with more than 75% polymorphonuclear leukocytes. However, various sterile inflammatory processes may exhibit the same cellular profile.

Other considerations
The fluid of an infected bursa closely resembles that of a bacterial joint infection.[15]

An elevated erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) is useful in following response to therapy, as well as in detecting an acute process in chronically affected joints. Measurement of serum uric acid levels cannot be used to establish or negate the diagnosis of uric acid arthropathy. Values may range widely during an acute attack. Appropriate serologic tests for the diagnosis of various vasculitides or rheumatologic disorders are often indicated.[19] Obtaining a biopsy of the synovium may be necessary to diagnose one of the many causes (ie, mycobacterial, fungal) of granulomatous synovitis. Examining the synovium histologically often establishes a diagnosis of fungal or mycobacterial joint infections.

Approach Considerations
Medical management of infective arthritis focuses on adequate and timely drainage of the infected synovial fluid, administration of appropriate antimicrobial therapy, and immobilization of the joint to control pain. Acute prosthetic joint infection (PJI) (< 3 wk in duration) can be cured medically if it is of the early type or secondary to hematogenous spread without any evidence of periarticular soft-tissue involvement or joint instability.[6] Overall, the mean length of hospitalization for septic arthritis is 11.5 days. However, outpatient antibiotic therapy in stable patients can significantly reduce hospital stays.

Consultations
In general, obtain a consultation with an orthopedic surgeon or rheumatologist. If the initial treatment response is poor or the etiology of the synovitis remains unknown, consult with an infectious disease specialist.

Antibiotic Therapy
In native joint infections, antibiotics usually need to be administered parenterally for at least 2 weeks. However, each case must be evaluated independently. Infection with either methicillinresistant S aureus (MRSA) or methicillin-susceptible S aureus (MSSA) requires at least 4 full weeks of intravenous antibiotic therapy. Orally administered antimicrobial agents are almost never indicated in the treatment of S aureus infections. Gram-negative native joint infections with a pathogen that is sensitive to quinolones can be treated with oral ciprofloxacin for the final 1-2 weeks of treatment. As a rule, a 2-week course of intravenous antibiotics is sufficient to treat gonococcal arthritis.[23]

Antibiotic selection
Initial antibiotic choices must be empirical, based on the sensitivity pattern of the pathogens of the community. Consider the rise of resistance among potential bacteria when choosing an initial antibiotic regimen. If local incidence of MRSA is high (in particular, marked increase in the resistance of the pneumococcus), prescribe alternate antibiotics initially. Because many isolates of group B streptococci have become tolerant of penicillin, use a combination of penicillin and gentamicin or a later-generation cephalosporin. MRSA is becoming established outside of the hospital setting. Enterobacteriaceae and P aeruginosa are becoming more resistant to multiple antibiotics. Knowing the resistance patterns in the community, as well as in the hospital, is most important. Preferably, the antibiotic should be bactericidal with some effect against the slow-growing organisms that are protected within a biofilm (eg, coagulase-negative S aureus [CONS]). Rifampin fulfills these requirements; however, this agent should never be used alone because of the rapid development of bacterial resistance to the drug. If, after 5 days of therapy, the joint shows some degree of improvement, consider an empirical trial of an anti-inflammatory agent. If the joint fails to respond after 5 days of appropriate antibiotic therapy (eg, presence of clinically significant fever, continued synovial purulence, persistently positive findings on culture), reassess the therapeutic approach, as follows:

Reculture the fluid and reexamine for crystals Perform appropriate serologies for diagnosis of Lyme disease; if these are positive, treat per current guidelines If fungal or mycobacterial infection is possible, consider obtaining a synovial biopsy Consider the possibility of reactive arthritis; nonsteroidal inflammatory agents (NSAIDs) are the primary therapeutic agents for reactive arthritis Perform imaging studies, either radiographs or magnetic resonance imaging (MRI), to rule out periarticular osteomyelitis.

Antibiotics have a role in suppressing associated chronic osteomyelitis and chronically infected prosthetic material that cannot be removed for various reasons. The use of fluoroquinolones for an extended period should be considered when the removal of an infected prosthesis is not possible. Cure rates as high as 62% have been documented in relatively small series. Generally, such prolonged therapy is seen as suppressive and not curative.[24] Oral antibiotics are usually used in treating gonococcal joint infections.

Joint Immobilization and Physical Therapy

Usually, immobilization of the infected joint to control pain is not necessary after the first few days. If the patient's condition responds adequately after 5 days of treatment, begin gentle mobilization of the infected joint. Most patients require aggressive physical therapy to allow maximum postinfection functioning of the joint.

Initial physical therapy consists of maintaining the joint in its functional position and providing passive range-of-motion exercises. The joint should bear no weight until the clinical signs and symptoms of synovitis have resolved. Aggressive physical therapy is often required to achieve maximum therapy benefit.

Antibiotics
Class Summary
Antibiotic therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting. The use of linezolid with or without rifampin should be considered for staphylococcal prosthetic joint infection (PJI). Note: After a period of unavailability, oral cefixime is again US Food and Drug Administration (FDA)approved in tablet and suspension formulations.[26, 28] Wyeth Pharmaceuticals (Collegeville, Pa) discontinued manufacturing Suprax in the United States. In October 2002, the company ceased marketing cefixime tablets (200 mg and 400 mg) because of depletion of company inventory. Wyeth's patent for cefixime expired on November 10, 2002. However, cefixime 400-mg tablets became available again in the US in April 2008. Lupin Pharmaceuticals received FDA approval to manufacture and market oral cefixime (table and suspension formulations) in February 2004. View full drug information

Ceftriaxone (Rocephin)

Ceftriaxone is the drug of choice (DOC) against N gonorrhoeae. This agent is effective against gram-negative enteric rods. Monitor sensitivity data. View full drug information

Ciprofloxacin (Cipro)

Ciprofloxacin is an alternative antibiotic to ceftriaxone to treat N gonorrhoeae and gram-negative enteric rods. View full drug information

Cefixime (Suprax)

Cefixime is a third-generation oral cephalosporin with broad activity against gram-negative bacteria. By binding to one or more of the penicillin-binding proteins, this agent arrests bacterial cell wall synthesis and inhibits bacterial growth. Oral cefixime is used as a follow-up to intravenous (IV) ceftriaxone to treat N gonorrhoeae. Note: After a period of unavailability, oral cefixime is again US Food and Drug Administration (FDA)approved in tablet and suspension formulations. Wyeth Pharmaceuticals (Collegeville, Pa) discontinued manufacturing Suprax in the United States. In October 2002, the company ceased marketing cefixime tablets (200 mg and 400 mg) because of depletion of company inventory. Wyeth's patent for cefixime expired on November 10, 2002. However, cefixime 400mg tablets became available again in the US in April 2008. Lupin Pharmaceuticals received FDA approval to manufacture and market oral cefixime (table and suspension formulations) in February 2004. View full drug information

Oxacillin

Oxacillin is useful against methicillin-sensitive S aureus (MSSA). View full drug information

Vancomycin (Vancocin)

Vancomycin is an anti-infective agent used against methicillin-sensitive S aureus (MSSA), methicillin-resistant coagulase-negative S aureus (CONS), and ampicillin-resistant enterococci in patients allergic to penicillin. View full drug information

Linezolid (Zyvox)

Linezolid is an alternative antibiotic that is used in patients allergic to vancomycin and for the treatment of vancomycin-resistant enterococci.