cmc arthritis right icd 10

🔥+ cmc arthritis right icd 10 02 Jul 2020 Wouldn't it be great if someone created a resource like this for Australian's with RA? That is exactly what our team at CreakyJoints Australia did. We did extensive ...

cmc arthritis right icd 10 Rheumatoid arthritis (RA) is a chronic inflammatory disease caused by a T cell-driven autoimmune process, which majorly involves the diarthrodial joints.

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Infectious Arthritis for 1 last update 2020/07/02 of Native JointsInfectious Arthritis of Native Joints

Christopher A. Ohl, Derek Forster, in Mandell, Douglas, and Bennett's Principles and Practice of Infectious for 1 last update 2020/07/02 Diseases (Eighth Edition)Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases (Eighth Edition), 2015

Pathogenesis

Gonococcal arthritis and DGI occur as a result of occult bacteremia secondary to mucosal infection of the urethra, uterine cervix, rectum, or oropharynx. Asymptomatic mucosal infection is much more likely to result in DGI than symptomatic infection and may have been sexually contracted days to months before dissemination. This, at least in part, accounts for the increased risk of disease in women for whom endocervical gonorrhea may persist without symptoms for extended periods. For these women, the risk of DGI increases substantially during menstruation, pregnancy, and the direct postpartum period. One third to one half of all women who present with DGI will do so during these times.161,163,164 Other host factors that increase the risk of DGI are complement deficiencies, particularly the terminal components C5 to C8, for 1 last update 2020/07/02 165,166165,166 and systemic lupus erythematosus.167 Immune mechanisms, including circulating immune complexes, also likely play a part in the pathogenesis of DGI and gonococcal arthritis and may account, in part, for the low yield of cultures for N. gonorrhoeae in synovial fluid and skin pustules.158,168

N. gonorrhoeae possesses several virulence factors, many of them cell surface proteins, that influence pathogenesis and the ability of the organism to widely disseminate from infected mucosa. Microbial attachment to mucosal and synovial epithelium is facilitated by long pili that also play a role in inhibiting host leukocyte phagocytosis.169 Gonococcal strains with the ability to disseminate are serum resistant and almost always express protein 1A, a principal outer membrane protein.162,170,171 Other characteristics of strains with an increased propensity to disseminate include lack of outer membrane protein II, also called “opacity protein,” and nutritional requirements for arginine, hypoxanthine, and uracil.21,157 N. gonorrhoeae strains that cause DGI are resistant to the bactericidal effects of normal human serum, probably through changes in cell membrane lipo-oligosaccharide.172

N. gonorrhoeae displays acquired resistance to several antimicrobials, including penicillin, tetracycline, fluoroquinolones, and rarely, spectinomycin.cmc arthritis right icd 10how to cmc arthritis right icd 10 for 173,174 The rapid emergence of fluoroquinolone resistance in N. gonorrhoeae throughout the world since 2001 has resulted in fluoroquinolones being contraindicated for empirical therapy of gonococcal infection.173,175,176 In addition, minimal inhibitory concentrations (MICs) of the oral cephalosporin cefixime against N. gonorrhoeae from North America have been increasing since 2009.174 This, together with treatment failures using cefixime for gonococcal mucosal infections, has led the Centers for Disease Control and Prevention (CDC) to no longer recommend this sole remaining oral treatment for gonorrhoea in an update to its 2010 Sexually Transmitted Diseases Treatment Guidelines.177-179 Unfortunately, precise epidemiologic data are not available on the antimicrobial susceptibility of strains of N. gonorrhoeae isolated from patients with DGI or gonococcal arthritis compared with strains from mucosal infections. This steady emergence of resistance of N. gonorrhoeae to numerous antimicrobials, particularly in the Pacific rim and among men who have sex with men, has led to considerable concern that gonorrhea could soon attain an untreatable status.179,180

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Bacterial Sexually Transmitted Disease

Omar Lupi, ... Carolina Talhari, in Tropical Dermatology (Second Edition), 2017

Arthritis

In young and sexually active people, gonococcal arthritis is the most frequent. It is present in more than 90% of cases of gonococcal septicemia, often being polyarticular. The symptomatology varies from arthralgia to acute arthritis, affecting mainly the wrist and knee. Synovial liquid can be removed by puncture; it will be serous or purulent, with high concentrations of proteins and low concentrations of glucose (Fig. 26-17). If it is not immediately treated, the infection can evolve to erosion of the cartilage, atrophy of the adjacent bone structures, and incapacitating arthritis.

It is only possible to demonstrate the gonococcus, by bacterial culture or by direct exam, in 50% of the cases. The investigation includes centrifugation of the liquid and examination of the sediment.

cmc arthritis right icd 10how to cmc arthritis right icd 10 for The differential diagnosis should be made in comparison with other types of septic arthritis, including rheumatoid arthritis, rheumatic fever, and Reiter syndrome.

cmc arthritis right icd 10how to cmc arthritis right icd 10 for Normally, the signs only show up on radiologic examination 20 days after the initial appearance of arthritis, frequently revealing a decrease in the articular space with subchondral cysts and articular osteoporosis.9,10

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Bacterial Arthritis

Paul P. Cook, Dawd S. Siraj, in Kelley and Firestein's Textbook of Rheumatology (Tenth Edition), 2017Paul P. Cook, Dawd S. Siraj, in Kelley and Firestein's Textbook of Rheumatology (Tenth Edition), 2017

Pathogenesis

Acute bacterial arthritis is usually designated gonococcal or nongonococcal. In the case of cmc arthritis right icd 10how to cmc arthritis right icd 10 for gonococcal arthritis, N. gonorrhoeae possesses a variety of virulence factors on the cell surface. N. gonorrhoeae is able to attach to cell surfaces via filamentous outer-membrane appendages, or pili. Another outer membrane protein, protein I, has forms IA and IB. Protein IA binds the host factor H and inactivates complement component C3b, circumventing the host's complement system.21 Protein IA also prevents phagolysomal fusion in neutrophils, enabling survival of the organism within the phagocytes. Lipo-oligosaccharide is a gonococcal molecule similar to lipopolysaccharide of other Gram-negative bacteria and possesses endotoxin activity, which contributes to the joint damage seen in gonococcal arthritis.22

S. aureus is the most common organism that causes nongonococcal arthritis. The virulence of S. aureus is associated with its ability to attach to host tissue within the joint, evade host defenses, and cause damage to the joint. cmc arthritis right icd 10how to cmc arthritis right icd 10 for Table 109-2 lists some of these virulence factors and their mechanisms of action. The attachment of S. aureus to the joint tissues is facilitated by microbial surface components recognizing adhesive matrix molecules (MSCRAMMs). MSCRAMMs are embedded in the cell wall peptidoglycan of S. aureus (Figure 109-1).23 They bind to host matrix proteins, including collagen, fibrinogen, elastin, vitronectin, laminin, and fibronectin. Gene knockout experiments in animal models showed that the gene coding for the protein that binds collagen is an important virulence factor for S. aureus joint infections. the 1 last update 2020/07/02 2424 Most S. aureus isolates also express the fibronectin-binding proteins, FnbpA and FnbpB. Disruption of the respective genes, fnbpA and fnbpB, by knockout gene experiments completely obliterates adherence of S. aureus to fibronectin-coated surfaces (e.g., prosthetic joints).25

The genes of several S. aureus cell surface proteins (e.g., protein A, fibronectin-binding proteins, coagulase) and exotoxins (e.g., toxic shock syndrome toxin [TSST]-1, enterotoxin B, proteases, and hemolysins) are regulated by the accessory gene regulator agr.26 At low cell numbers, such as at the time of infection, production of cell surface proteins for attachment to host tissues is facilitated by the agr gene. When the cells have attached to tissue or an orthopedic device and have passed from the exponential to stationary phase of growth, agr represses the expression of genes coding for cell surface proteins and activates genes coding for exotoxins and tissue-destroying exoenzymes. Because of this complex effect on the different stages of infection, inhibitors of agr may reduce tissue destruction but enhance tissue colonization. This effect could have implications for chronic infections such as occur with prosthetic joints.

Adherence receptors may allow intra-cellular movement of S. aureus into host cells (e.g., osteoblasts, endothelial cells, neutrophils).27 The ability of S. aureus to switch from a normal colony phenotype to a slow-growing, antibiotic-resistant, small-colony variant phenotype may partially explain why this organism causes persistent and recurrent infections.28 When internalized, the organism is protected from the host's immune system and from anti-microbial agents. After adherence to the joint tissue, the bacteria activate the host immune response. Opsonization and phagocytosis are key defenses to eradicate the organism. S. aureus possesses two virulence factors, protein A and capsular polysaccharide, which interfere with these defenses. Protein A interferes with binding of complement by binding to the fragment crystallizable (Fc) portion of immunoglobulin (Ig)G. Protein A has been termed a superantigen for B cells because 30% of human B cells show Fab-mediated binding of the protein A molecule.29 Binding of protein A by B cells leads to activation and, subsequently, to depletion of B cells through apoptosis. for 1 last update 2020/07/02 3030 This process may have implications regarding the ability of the immune system to control infection with S. aureus. The gene coding for protein A had been experimentally disrupted, and joint infection caused by the altered strain in a mouse model resulted in less joint destruction than infection caused by the wild-type strain.31

Capsular polysaccharide interferes with opsonization and phagocytosis. Of the 11 reported capsule serotypes of S. aureus, types 5 and 8 account for 85% of clinical infections.cmc arthritis right icd 10how to cmc arthritis right icd 10 for 32 The capsule of these two serotypes is thinner, which facilitates the attachment to host fibronectin and fibrin.33 When attached to these host proteins, capsule production is upregulated to form a thicker capsule, which makes the bacteria more resistant to opsonization and phagocytosis. The thicker capsule can also conceal the highly immunogenic adherence proteins (MSCRAMMs).34 A mutant of the type 5 capsule in a murine model had a lower rate of infection and resulted in less severe arthritis compared with mice infected with the wild-type strain.35 A vaccine consisting of types 5 and 8 polysaccharide reduced S. aureus bacteremia by more than half in hemodialysis patients.36 The duration of protection was approximately 40 weeks after a single vaccination.

S. aureus exotoxins (e.g., TSST-1 and enterotoxins) act as superantigens that bind to host class II major histocompatibility complex (MHC) molecules and T cell receptors, resulting in clonal expansion and activation of some T cells. This activation triggers the release of numerous cytokines, including IL-2, interferon (IFN)-γ, and TNF.37 Induction of these cytokines results in systemic toxicity and joint damage. The stimulated T cells initially proliferate but later disappear, likely because of apoptosis, and result in immunosuppression.38 Internalized organisms that had been protected from this inflammatory response may cause fulminant or persistent infection. Mice injected with strains of S. aureus lacking TSST-1 and enterotoxins rarely develop arthritis; when arthritis is induced, it is much milder compared with arthritis in animals injected with the wild-type strain.37 Vaccination of mice with for 1 last update 2020/07/02 a mutated, recombinant form of enterotoxin A devoid of superantigen function was associated with a significant reduction in mortality.39S. aureus exotoxins (e.g., TSST-1 and enterotoxins) act as superantigens that bind to host class II major histocompatibility complex (MHC) molecules and T cell receptors, resulting in clonal expansion and activation of some T cells. This activation triggers the release of numerous cytokines, including IL-2, interferon (IFN)-γ, and TNF.37 Induction of these cytokines results in systemic toxicity and joint damage. The stimulated T cells initially proliferate but later disappear, likely because of apoptosis, and result in immunosuppression.38 Internalized organisms that had been protected from this inflammatory response may cause fulminant or persistent infection. Mice injected with strains of S. aureus lacking TSST-1 and enterotoxins rarely develop arthritis; when arthritis is induced, it is much milder compared with arthritis in animals injected with the wild-type strain.37 Vaccination of mice with a mutated, recombinant form of enterotoxin A devoid of superantigen function was associated with a significant reduction in mortality.39

In response to bacterial infection of the joint space, the host releases a variety of cytokines and inflammatory mediators. Initially, IL-1β and IL-6 are released into the joint space, leading to an influx of inflammatory cells. These neutrophils and macrophages engulf invading bacteria and release additional cytokines, including TNF, IL-1, IL-6, and IL-8. Blocking TNF with a monoclonal antibody and IL-1 with an IL-1 receptor antagonist inhibited leukocyte infiltration into the joint by 80% in a rabbit model of S. aureus–induced arthritis when the cytokine inhibitors were given simultaneously with S. aureus.40 When the same inhibitors were given 24 hours after infection, however, there was no effect on leukocyte infiltration, suggesting the crucial roles of TNF and IL-1 in the early stages of S. aureus–induced arthritis. Release of IFN-γ is associated with the influx of T cells, which occurs a few days after infection. In a mouse model of S. aureus septic arthritis, IFN-γ has been associated with a worsening of the severity of arthritis while protecting the animals from septicemia.41 The host's early cytokine response may aid the clearance of organisms and limit infection in the host. A late cytokine response may amplify the destructiveness of an established infection.

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Pediatrics in Systemic Autoimmune Diseases

M.T. Terreri, C.A. Len, in Handbook of Systemic Autoimmune Diseases, 2016

cmc arthritis right icd 10how to cmc arthritis right icd 10 for Differential Diagnosis

Oligo or polyarthritis in the absence of other major manifestations of RF deserves differential diagnosis with many clinical entities. Septic arthritis, including gonococcal arthritis, other reactive arthritides such as Lyme disease, connective tissue diseases, acute lymphoid leukemia and other tumors, and sickle cell disease should be considered.

Viral or tuberculous pericarditis, viral myocarditis, bacterial for 1 last update 2020/07/02 endocarditis, innocent murmurs, congenital heart disease, and connective tissue diseases such as systemic lupus erythematosus or juvenile idiopathic arthritis should be ruled out in the cases of carditis.Viral or tuberculous pericarditis, viral myocarditis, bacterial endocarditis, innocent murmurs, congenital heart disease, and connective tissue diseases such as systemic lupus erythematosus or juvenile idiopathic arthritis should be ruled out in the cases of carditis.

cmc arthritis right icd 10how to cmc arthritis right icd 10 for Although the presence of chorea is highly suggestive of RF, when it is isolated, other diseases need to be excluded like viral encephalitis, systemic lupus erythematosus, and antiphospholipid syndrome.

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Infectious Arthritis and Osteomyelitis

cmc arthritis right icd 10how to cmc arthritis right icd 10 for Ronald M. Laxer, ... Carol B. Lindsley, in Textbook of Pediatric Rheumatology (Seventh Edition), 2016

Gonococcal Arthritis

In reported series of septic arthritis in children and adolescents, disease caused by N. gonorrhoeae appears to be uncommon. When it occurs, it is most common in the adolescent, although it occasionally occurs in the neonate in association with disseminated infection.93 It is more common in girls than in boys and is particularly likely just after menstruation or with pregnancy.94 cmc arthritis right icd 10how to cmc arthritis right icd 10 for Gonococcal arthritis usually develops in patients with primary asymptomatic genitourinary gonorrhea or with a gonococcal infection of the throat or rectum. The patient presents with a systemic illness characterized by fever and chills.95 A vesiculopustular rash, sparsely distributed on the extremities, commonly yields organisms on culture or Gram stain of the smear. Gonococcal arthritis may have an initial migratory phase and may be accompanied by tenosynovitis. In contrast to most patients with septic arthritis, those with gonococcal arthritis may present with a purulent arthritis of several joints. For a patient with suspected gonococcal arthritis, it is important to culture samples from the genital tract, throat, rectum, and any vesicles in addition to the affected joint. Special culture media with Thayer-Martin agar will help in isolating the organism. The possibility of sexual abuse should be considered and appropriately investigated.

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Infections of Joints, Synovium-Lined Structures, and Soft Tissue

cmc arthritis right icd 10how to cmc arthritis right icd 10 for Elizabeth G. Demicco, ... Andrew E. Rosenberg, in Diagnostic Pathology of Infectious Disease (Second Edition), 2018

Gonococcal Arthritis

N. gonorrhoeae, a gram-negative diplococcus, is the most common sexually transmitted bacterium associated with infective arthritis. In the 1970s through the 1980s it was the most common cause of infective arthritis in the United States.20 Safer sex practices resulted in a steep decline in disease prevalence through the 1990s. More recently, gonococcal infections have been on the rise, primarily due to high-risk sexual behavior among young men who have sex with men. Of further concern is the appearance of antibiotic-resistant strains. These two trends ensure that gonorrhea will continue to be of clinical importance for the foreseeable future.

Patients with gonococcal arthritis are usually young, healthy, and sexually active. Gonococcal arthritis may take one of two forms: a classic suppurative arthritis similar to the septic arthritis seen with other bacterial infections or a syndrome of disseminated gonococcal infection (DGI) including tenosynovitis, skin lesions, and polyarthralgias without true septic arthritis.cmc arthritis right icd 10how to cmc arthritis right icd 10 for 20 Some authors have postulated an immunologic basis for DGI. However, the presence of positive blood cultures in up to 50% of cases and an inability to identify circulating immune complexes argue against this theory.20

Gonococcal infection begins with localized mucosal disease. In fewer than 3% of cases, the organism rapidly enters the circulation and produces DGI.21-23 Risk factors associated with DGI include delayed diagnosis, SLE, deficiency of the complement system, menstruation, and pregnancy, as well as socioeconomic factors, promiscuity, urban residence, male homosexuality, and educational status.5 Bacterial strains also play a role, with higher risk associated with piliated N. gonorrhoeae strains that are capable of phase variation. Women have four times the risk of men for development of DGI,cmc arthritis right icd 10how to cmc arthritis right icd 10 for 24 most likely because of asymptomatic infection and delayed diagnosis.

Patients with DGI present with migratory arthralgias, fever, chills, dermatitis, and tenosynovitis. Most are found to have asymptomatic mucosal gonococcal infection involving the genitals, anus, or pharynx.21 Skin lesions are classically limited to the extremities and trunk and begin as small, inconspicuous erythematous papules, which progress to vesicular or pustular lesions. The papules may overlie affected joints. Tenosynovitis causes pain, swelling, and erythema. Polyarthralgias may involve knees, elbows, and distal joints, whereas arthritis and tenosynovitis are polyarticular and preferentially involve the distal joints, including those of the hands and fingers, wrists, elbows, knees, and ankles.5,20

Suppurative gonococcal arthritis is for 1 last update 2020/07/02 monoarticular or oligoarticular and involves the knees, wrists, ankles, and elbows. Symptoms of bacteremia, skin lesions, or prior polyarthralgias are not present.Suppurative gonococcal arthritis is monoarticular or oligoarticular and involves the knees, wrists, ankles, and elbows. Symptoms of bacteremia, skin lesions, or prior polyarthralgias are not present.

The radiographic and histopathologic findings in gonococcal arthritis are similar to those seen in other septic bacterial arthritides. However, imaging studies and synovial biopsy are rarely performed. In rare biopsied cases the periarticular soft tissues show granulation tissue with mixed polymorphonuclear and mononuclear cell infiltrates (Fig. 15.5).

Synovial fluid analysis and culture are required for diagnosis. Treatment requires appropriate antibacterial therapy in conjunction with aspiration. Surgery is rarely necessary. Patients should be tested for concomitant infection with Chlamydia trachomatis. Appropriate treatment is associated with a good outcome.

The differential diagnosis of DGI includes N. meningitidis infection, which manifests with similar skin lesions and arthralgias. Other bacterial infections also must be ruled out and can usually be distinguished by their clinical features or by culture.

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Infections of Bursae, Joints, and Bones

Eric L. Matteson, Douglas R. Osmon, in Goldman's Cecil Medicine (Twenty Fourth Edition), 2012

Gonococcal Septic Arthritis

cmc arthritis right icd 10how to cmc arthritis right icd 10 for Epidemiology

Neisseria gonorrhoeae (Chapter 307) is a common cause of polyarthralgias and arthritis as well as oligoarticular arthritis and tenosynovitis in young, healthy patients. Disseminated gonococcal infection occurs in 0.5 to 3% of patients with gonorrhea (Chapter 307). Many of of these patients have arthritis. Disseminated gonococcal infection and septic arthritis due to N. gonorrhoeaecmc arthritis right icd 10how to cmc arthritis right icd 10 for occur two to three times more often in women than in men. Most patients do not have a recent history of a symptomatic genital infection. The incidence of gonococcal arthritis is 133 the 1 last update 2020/07/02 cases per 100,000 population per year. Predisposing factors for disseminated gonococcal infection with arthritis include pregnancy, recent menstruation, complement deficiencies (C5, C6, C7, or C8), and systemic lupus erythematosus. occur two to three times more often in women than in men. Most patients do not have a recent history of a symptomatic genital infection. The incidence of gonococcal arthritis is 133 cases per 100,000 population per year. Predisposing factors for disseminated gonococcal infection with arthritis include pregnancy, recent menstruation, complement deficiencies (C5, C6, C7, or C8), and systemic lupus erythematosus.

Clinical Manifestations

cmc arthritis right icd 10how to cmc arthritis right icd 10 for Patients with gonococcal arthritis usually present with one of two clinical syndromes. The first is a purulent arthritis without skin lesions; the second is the triad of tenosynovitis, dermatitis, and polyarthralgias without purulent arthritis. The latter patients may have bacteremia and fever as well as maculopapular, vesicular, necrotic, pustular skin lesions anywhere on the integument. The arthritis is usually asymmetrical and may involve large or small joints, typically the elbows and knees or joints distal to these.

Diagnosis

A high degree of clinical suspicion is required for diagnosis because many patients are asymptomatic for the primary infection. A thorough joint evaluation is important, as is an evaluation of soft tissues, particularly for tenosynovitis affecting the hands and feet. Cultures of blood, endocervix, and urethra are essential; cultures of the pharynx and rectum may be very helpful. N. gonorrhoeae is isolated in less than 30% of patients with the tenosynovitis-dermatitis syndrome and in about 50% of those with monoarthritis. PCR may be used to detect the gonococcal DNA in synovial fluid, skin lesions, urine, and throat samples, which are culture negative. Cultures should be submitted on Thayer-Martin media. Patients with suspected gonococcal arthritis should be screened for other coexisting sexually transmitted diseases (Chapter 293) such as syphilis, HIV, and chlamydia, as well as hepatitis B and C.

Treatment 

Ceftriaxone is given for 2 to 4 days, followed by oral therapy to complete a minimum of 7 days of therapy, although up to 14 days of therapy is recommended. There is emerging resistance to fluoroquinolones, and unless specific in vitro susceptibility testing is available, their use is not recommended. Patients should also be treated for concomitant chlamydia with the regimens recommended by the Centers for Disease Control and Prevention (CDC). Most patients respond well to outpatient therapy, with complete resolution of the infection. Given emerging antimicrobial resistance, the most recent CDC guidelines for treating N. gonorrhoeae should be reviewed.

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