Chapter 34 General Principles and Techniques Radiographic Findings of Arthropathies in Dogs and Cats *Detection of these signs depends on stage of the disease, type of disease, and joint(s) affected. Synovial fluid aspirates commonly show no bacterial growth when cultured directly on blood agar plates. More reliable results are obtained if the synovial fluid sample is incubated for 24 hours in a blood culture medium or specific enrichment broth before culturing onto blood agar plates. Select the joint or joints that are swollen for initial taps. Clip the appropriate area over the joint, and prepare the site for an aseptic procedure (Fig. 34-1, A-I). Use a gloved hand to palpate landmarks. Insert a needle attached to a syringe into the joint. Apply gentle suction to the syringe. After the fluid has been collected, release the negative pressure on the syringe and withdraw the needle. If blood appears in the syringe, withdraw the syringe immediately; contamination with blood can alter cell counts. If only a few drops of fluid are obtained (common in small dogs and cats), spray the material directly onto a slide, and examine it cytologically. Estimate viscosity as the fluid drops from the needle to the slide. Normal joint fluid is viscous and forms a long string. Place a drop of fluid on a slide and make a smear for an estimated complete cell count and a differential cell count. Culture fluid for bacterial and mycoplasmal growth: with the same needle and syringe aseptically aspirate an appropriate culture broth (e.g., trypticase soy broth from a blood culture vial). Rinse the barrel of the syringe and hub of the needle with the culture medium, and then inject this culture medium into a blood culture vial with the same medium. Differential diagnoses include all of the noninflammatory and inflammatory arthropathies (see Box 34-1). The definitive diagnosis is made by evaluating the animal’s history, clinical signs, radiographic findings (see Table 34-1), results of other imaging modalities, and joint cytology (see Table 34-2). All patients with joint disease except those with additional medical diseases that require specific dietary management can benefit significantly from proper body weight management. Excessive body weight places increased loads on joints, exacerbating concurrent joint disease. Excessive body weight accelerates degeneration of joints with DJD and has been demonstrated to exacerbate clinical signs of osteoarthritis. Excessive body weight also exacerbates signs of dysplastic diseases (e.g., hip dysplasia). Evidence suggests that proper body weight management can lessen and delay clinical signs of osteoarthritis and decrease the need for anti-inflammatory medication and surgery (Huck et al, 2009; Marshall et al, 2010). Studies in dogs suggest that omega-3 fatty acids can ease the pain of osteoarthritis. Recent studies have demonstrated that the use of omega-3 fatty acids can improve weight bearing (Roush et al, 2010) and decrease the need for nonsteroidal anti-inflammatory drugs (NSAIDs) in dogs with osteoarthritis (Fritsch et al, 2010). Fatty-acid supplements rarely cause gastrointestinal problems, although sometimes dog owners claim that the supplement has given their dog “fishy-smelling breath.” Omega-3 fatty acids appear to be safe. Medical management of DJD often includes therapy with NSAIDs. NSAIDs reduce pro-inflammatory mediators (e.g., thromboxanes, prostaglandins, prostacyclin, and oxygen radicals) by inhibiting cyclooxygenase 1 and 2 (COX-1 and COX-2) pathways. Inhibiting COX-1 inhibits normal physiologic responses in the gastrointestinal and renal systems. Uses of NSAIDs that significantly inhibit COX-1 (e.g., aspirin, ibuprofen, and phenylbutazone) have greater potential to cause gastrointestinal ulceration and/or nephrotoxicity (Fig. 34-2). Most contemporary veterinary NSAIDs (Table 34-4) preferentially inhibit COX-2. It was initially believed that these drugs would provide clinical benefit without the risk of the older NSAIDs; however, the mechanisms of action and adverse effects of these drugs are not as clear as was initially postulated. Numerous studies have reported conflicting results regarding the COX-1:COX-2 ratios of these drugs. However, the method by which an NSAID is determined to affect COX-2 versus COX-1 involves in vitro tests that may or may not accurately reflect what happens in vivo. Presently, it is probably best to say that some drugs appear to be COX-1 sparing instead of COX-2 selective, and it may be more accurate to state that these drugs are “safer” as opposed to saying that they are “safe.” There is a high level of comfort (strong evidence) for the efficacy of NSAIDs in lessening the clinical signs of osteoarthritis in dogs (Sanderson et al, 2009). Finally, some drugs (e.g., tepoxalin) significantly inhibit 5-lipoxygenase, an enzyme that is responsible for leukotriene production (another mediator of inflammation). Side effects of the NSAIDs vary depending on the specific drug and means of reporting adverse events. Owners should be cautioned that anti-inflammatory medication may cause gastrointestinal, liver, or kidney disease (see Table 34-4). Other potential side effects include altered platelet function, extended clotting times, and keratoconjunctivitis sicca (Brainard et al, 2007; Klauss et al, 2007; Luna et al, 2007). Aspirin is commonly used in dogs, but owners should be warned of its propensity to cause gastrointestinal toxicity. Concurrent administration of misoprostol may provide some degree of protection against NSAID-induced gastric lesions (Box 34-3), if needed. Pentosan polysulfate, isolated from beechwood hemicellulose, appears to provide protection against cartilage damage. When given once a week (3 mg/kg SC) it may relieve clinical signs associated with canine chronic osteoarthritis. Although not derived from animal sources, the compound preserves proteoglycan content and stimulates hyaluronic acid synthesis. Pentosan polysulfate may also increase bleeding times. One meta-analysis demonstrated a moderate level of comfort for the efficacy of Pentosan polysulfate in the treatment of osteoarthritis in dogs (Aragon et al, 2007), whereas another demonstrated only weak or no evidence to support efficacy (Sanderson et al, 2009). Hyaluronan is a large glycosaminoglycan found in joint fluid and cartilage. In joint fluid, it is a major contributor to viscoelasticity, whereas in cartilage it forms the backbone that links aggrecan molecules. Hyaluronan has been administered intra-articularly to help restore viscosity of joint fluid in arthritic joints. It also has anti-inflammatory activity by interfering with oxygen-free radicals and inhibition of degradative enzymes. There is conflicting information regarding the value of hyaluronan administration in the management of canine osteoarthritis, although there is evidence that it may aid in pain relief of this condition. Two meta-analyses have shown weak or no evidence for the efficacy of hyaluronan in the treatment of arthritis in dogs (Aragon et al, 2007; Sanderson et al, 2009). Antibiotics should be administered for infectious arthritis (see p. 1229) and prophylactically for specific surgical procedures (see Chapter 9). In general, antibiotics should be selected for treatment of bacterial septic arthritis on the basis of identification of the organism and susceptibility testing. Broad-spectrum bactericidal antibiotics should be administered until culture and susceptibility testing results are obtained and then adjusted as necessary (Table 34-5). Gram-positive bacteria are most commonly cultured from septic joints; therefore, initial treatment with first generation cephalosporins is usually indicated before culture and bacterial susceptibility reports are received. If bacterial L-forms are suspected (primarily in cats), doxycycline is the antibiotic of choice. Chloramphenicol and erythromycin might also be effective. If Borrelia spp., Ehrlichia ewingii, Neorickettsia risticii, Anaplasma phagocytophilum, or Rickettsia rickettsii is suspected, doxycycline is the antibiotic of choice. Antibiotics should be administered for 4 to 6 weeks and at least 2 weeks after the cessation of clinical signs. Antibiotics for Septic Arthritis before Culture Results Antibiotics should be administered prophylactically to prevent surgical infections, especially in joint replacement procedures, but they are not a substitute for aseptic technique (see Chapters 1, 5, and 6). A broad-spectrum, bactericidal antibiotic, such as cefazolin (22 mg/kg given IV), should be administered after an intravenous (IV) line has been placed and anesthesia induced. This dose can be repeated every 90 minutes to 3 hours during surgery. Antibiotics can be discontinued after surgery, or they may be continued until culture results are obtained. If culture results are negative, antibiotics should be discontinued; if results are positive, antibiotics may be continued or changed according to the results of susceptibility testing. Synovial joints permit motion while providing stability for load transfer between bones (Box 34-4). Synovial joint cavities are surrounded by joint capsules made up of an outer layer of fibrous connective tissue lined with a synovial membrane. Nerves, blood vessels, and lymphatic vessels are located between the synovial membranes and the fibrous capsules. Synovial fluid is formed as a dialysate of plasma from the rich vascular supply of synovial membranes. This fluid filters through the vascular endothelium and synovial interstitium to lubricate the joint and provide nutrition for the articular cartilage. The synovial membrane is composed of synovial A and B cells and dendritic cells. Mucoproteins, such as hyaluronic acid, are added to the fluid by synovial B cells; synovial A cells function as phagocytes and secrete interleukin-1 and prostaglandin E. The articulating joint surfaces are covered with 1 to 5 mm of a dense, white connective tissue, usually hyaline cartilage. This articular cartilage facilitates the gliding motion of the joint, distributes mechanical loads, and prevents or minimizes injury to underlying subchondral bone. Some synovial joints (e.g., the stifle joint) also have intra-articular ligaments, menisci, and fat pads that further facilitate joint function and stress reduction during weight bearing (Fig. 34-3). External joint support is provided by surrounding ligaments and tendons. General principles of arthroscopy are discussed in Chapter 13. Loss of proteoglycans from matrix occurs with infection, inflammation, and joint immobilization; when cartilage is exposed during surgery; or as a result of traumatic disruption of synovial membranes. With reversible damage, chondrocytes may replace the lost matrix components after the insult is removed. However, irreversible damage may occur. Lacerations or abrasions of the cartilage surface destroy chondrocytes and disrupt the matrix. A standard inflammatory response does not occur with superficial lacerations (those that do not penetrate to subchondral bone) because inflammatory cells from marrow and blood vessels cannot access the joint (Fig. 34-5, A). Chondrocytes near the injury respond by proliferating and synthesizing new matrix; however, this response usually is inadequate for healing. Although superficial lacerations do not heal, they seldom progress. When a full thickness cartilage defect occurs, marrow cells capable of participating in an inflammatory response gain access to the defect (Fig. 34-5, B). The size of the defect affects healing; small defects (1 mm in diameter) heal more completely than large defects. The defect initially is filled with a fibrin clot, which is replaced within 5 days by fibroblast-like cells and collagen fibers. Metaplasia of these fibroblast-like cells into chondrocytes occurs after 2 weeks. These chondrocytes do not function normally, as is indicated by lower concentrations of proteoglycans in the reparative tissue at 6 months after injury. The reparative tissue (fibrocartilage) is also thinner than articular cartilage and is prone to fibrillation and erosive changes. Aragon, CL, Hofmeister, EH, Budsberg, SC. Systematic review of clinical trials of treatments for osteoarthritis in dogs. J Am Vet Med Assoc. 2007;230:514. Brainard, BM, Meredith, CP, Callan, MB, et al. Changes in platelet function, hemostasis, and prostaglandin expression after treatment with nonsteroidal anti-inflammatory drugs with various cyclooxygenase selectivities in dogs. Am J Vet Res. 2007;68:251. Fritsch, DA, Allen, TA, Dodd, CE, et al. A multicenter study of the effect of dietary supplementation with fish oil omega-3 fatty acids on carprofen dosage in dogs with osteoarthritis. J Am Vet Med Assoc. 2010;236:535. Huck, JL, Biery, DN, Lawler, DF, et al. A longitudinal study of the influence of lifetime food restriction on development of osteoarthritis in the canine elbow. Vet Surg. 2009;38:129. Klauss, G, Giuliano, EA, Moore, CP, et al. Keratoconjunctivitis sicca associated with administration of etodolac in dogs: 211 cases (1992-2002). J Am Vet Med Assoc. 2007;230:541. Luna, SP, Basílio, AC, Steagall, PV, et al. Evaluation of adverse effects of long-term oral administration of carprofen, etodolac, flunixin meglumine, ketoprofen, and meloxicam in dogs. Am J Vet Res. 2007;68:258. Marshall, WG, Hazewinkel, HA, Mullen, D, et al. The effect of weight loss on lameness in obese dogs with osteoarthritis. Vet Res Commun. 2010;34:241. Roush, JK, Cross, AR, Renberg, WC, et al. Evaluation of the effects of dietary supplementation with fish oil omega-3 fatty acids on weight bearing in dogs with osteoarthritis. J Am Vet Med Assoc. 2010;236:67. Sanderson, RO, Beata, C, Flipo, RM, et al. Systematic review of the management of canine osteoarthritis. Vet Rec. 2009;164:418. Beale, BS. Use of nutraceuticals and chondroprotectants in osteoarthritic dogs and cats. Vet Clin North Am Small Anim Pract. 2004;34:271. Borer, LR, Peel, JE, Seewald, W, et al. Effect of carprofen, etodolac, meloxicam, or butorphanol in dogs with induced acute synovitis. Am J Vet Res. 2003;64:1429. MacWilliams, PS, Friedrichs, KR. Laboratory evaluation and interpretation of synovial fluid. Vet Clin North Am Small Anim Pract. 2003;33:153. This article provides an excellent review of the interpretation of joint fluid. Millis, D, Levine, D, Taylor, R. Canine rehabilitation and physical therapy. Philadelphia: Saunders; 2004. This text contains a complete description of physical therapy for osteoarthritis in dogs. Schulz, KS, Beale, B, Holsworth, et al. The pet lover’s guide to canine arthritis and joint problems. Philadelphia: Saunders; 2005.
Diseases of the Joints
Diagnosis of Joint Diseases
Diagnostic Imaging
TABLE 34-1
Laboratory Findings
Synovial fluid collection.
Differential Diagnosis
Medical Management
Principle 1: Weight Management
Principle 2: Nutritional Supplementation
Principle 5: Nonsteroidal Anti-inflammatory Drug Therapy and Other Medical Therapies
Other medical therapies.
Antibiotics.
TABLE 34-5
SUSPECTED TYPE
ANTIBIOTIC
Gram-positive
Cephalexin 22 mg/kg PO, IV q8-12hr
Amoxicillin-clavulanate 12.5-25 mg/kg PO q12hr
Borrelia, rickettsiae, Mycoplasma, bacterial L-forms
Doxycycline 5 mg/kg PO q12hr
Gram-negative
Baytril 5-20 mg/kg PO, IV* q24hr
Anaerobes
Metronidazole 10 mg/kg PO, IV* q12hr
Surgical Anatomy
Surgical Technique
Endoscopically Assisted Joint Surgery
Healing of Cartilage Defects and Response of Cartilage to Treatment
References
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Diseases of the Joints
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