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MANAGEMENT OF OSTEOARTHRITIS IN CATS Elizabeth M. Hardie, DVM, PhD
Osteoarthritis (OA) in cats is not a well-documented disease. Although cats are usually included in reviews of joint disease in small animal patients, dogs are the primary focus of the discussion. 1• 4 When cats are mentioned, it is almost always in reference to one of the polyarthritis syndromes. The lack of attention to feline OA is most likely a combination of the eat's small body stature and its ability to accommodate orthopedic abnormality by redistributing weight-bearing force to other limbs. Furthermore, because the eat's normal behavior frequently prevents critical analysis of gait, many mild-to-moderate lamenesses due to OA may go unnoticed by the owner. As cats continue to live longer lives, however, and because OA is typically a slowly progressive condition, degenerative joint changes are recognized in cats as in other species. This article reviews what little is known about OA in cats and suggests methods of managing animals that suffer debilitating effects. INCIDENCE
The fact that OA is being recognized as a problem in the older cat is illustrated by a recent roundtable discussion on the geriatric cat.23 OA was listed along with hyperthyroidism, diabetes mellitus, renal insufficiency, and oral disease as a treatable chronic disease of the older cat. It is the author's clinical impression that OA occurs most commonly in the shoulders and elbows of older cats. Maine Coon cats appear to be predisposed to hip dysplasia, with the Orthopedic Foundation of From the Department of Companion Animals and Special Species, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina
VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE VOLUME 27 • NUMBER 4 • JULY 1997
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America files indicating an 18% incidence in hip radiographs that were sent for evaluation. 17 In order to more fully quantitate the incidence of OA, radiographs of 68 feline patients over 12 years of age presenting to North Carolina State University for a variety of diseases were examined. Fourteen cats (20%) had radiographic evidence of OA. 1 The elbow was affected in nine cats, the shoulder in three cats, the hip in one cat, and the tarsus in one cat. Eight cats had bilateral disease. Interestingly, spondylosis was present in 39 cats (57%). Clinical Manifestations of OA
The 30-year-old puma at a local zoo slowly limps across her cage, and radiographs demonstrate severe OA in her hip joint. This is the clinical picture that one would expect a domestic cat with OA to display. Unfortunately, many cats with OA do not limp. Cats with OA are presented to the veterinarian for a variety of clinical signs, only one of which is lameness. Change of temperament is common, with the cat becoming depressed, anorectic, or aggressive when handled.4 Loss of weight may occur due to anorexia but can also occur because the cat can no longer access an elevated feeding site on a regular basis. Similarly, accidents may occur outside the litter box because the cat cannot climb to the site where the box is located or cannot climb into the box. The fur may be dull and matted because the cat is not flexible enough to perform a complete grooming routine. Overgrowth of the claws occurs if the cat cannot stand to use the scratching post. Jumping ability is rarely lost completely, but the height of the jump is often low. A cat that used to jump onto the back of the couch in one leap may jump first to the seat, then to the arm, then to the back of the couch. Weight shifting may occur to protect the affected joint, resulting in a stilted, abnormal gait. Observation of the cat going up and down stairs is often revealing: the cat may carefully lift the affected limb onto the higher or lower step rather than freely moving through climbing motions. On physical examination, the cat may resist manipulation of the affected joint. The joint is often thickened due to joint capsule hypertrophyI fibrosis or osteophyte production, or both. If the cat is depressed, it may exhibit little reaction to examination but will crouch in a position that protects the affected joint. DIAGNOSIS OF OA
Following physical examination, the first step in the diagnosis of OA in the cat is to obtain radiographs of the suspected joint.1 Radiographic signs present in OA include new bone formation, subchrondral bone sclerosis, remodeling of bone shape, thickened joint capsule, and soft tissue swelling (Fig. 1). In the more severe forms of OA, loss of
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Figure 1. Radiographic changes characteristic of osteoarthritis in the elbow joint of a cat. Both lateral (A) and cranial/caudal (B) views are shown. There are osteophytes at the articular margins of the medial aspect of the joint, a mineralized osseous body cranial to the joint, and sclerosis of the subchondral bone. These changes were present bilaterally.
bone density may also be present. If radiographic changes are minimal, infective arthritis, nonerosive immune-mediated arthritis (Table 1), or systemic disease may be causing clinical signs.3 • 4• 9• 20 Once bony change associated with one or more joints is confirmed, one must make a decision regarding further diagnostics. Systemic disease, infective arthritis, or erosive immune-mediated arthritis (Fig. 2, see Table 1) should be considered as possible causes of arthritis if more than one joint is affected, if signs of bone loss are present, or if signs of systemic illness (fever, anorexia, depression) are pronounced. If these causes are eliminated, then degenerative joint disease is accepted as the cause of clinical signs.3 • 4• 9• 20 Examination of synovial fluid is a rapid method of distinguishing between inflammatory arthritis and OA (Table 2).4• 7 The amount of synovial fluid in osteoarthritic joints often is similar to that in normal joints, though increased amounts may be present in inflammatory arthritis. It is often helpful to aspirate several joints in order to determine if changes are present only in the obviously affected joint or are more
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Table 1. KNOWN CAUSES OF INFLAMMATORY ARTHRITIS IN THE CAT Syndrome Infective arthritis Bacteria Bacterial L-forms Mycoplasma gatae Mycoplasma felis Borrelia burgdorferi Fungal Calicivirus Feline infectious peritonitis Nonerosive immune-mediated arthritis Systemic lupus erythematosus Idiopathic polyarthritis type 1 Idiopathic polyarthritis type 2 Idiopathic polyarthritis type 3 Idiopathic polyarthritis type 4 Drug induced Erosive immune-mediated arthritis Feline rheumatoid arthritis Chronic progressive polyarthritis
Diagnosis Cytology, joint culture, Pasteurella common SQ abscesses often present. L-form culture, tetracycline trial Cytology, mycoplasmal culture, antibiotic trial (ref 20) Cytology, mycoplasmal culture, antibiotic trial (ref 20) Controversial if exists (see ref 2 for diagnostic criteria) Cytology, fungal culture, usually other sites also infected Kittens, transient arthritis, may be associated with live virus Vaccination, viral culture Arthritis rarely may precede peritoneal effusion Multisystem disease, positive antinuclear antibody, immune complexes or autoantibodies demonstrable No initiating cause demonstrable Secondary to infection elsewhere in body Secondary to gastrointestinal disease Secondary to myeloproliferative disease Trimethoprim-sulfa associated Positive for rheumatoid factor, 7/ 10 rheumatoid criteria present Mostly male cats, often FeSV or FeLV positive, negative for rheumatoid factor, proliferation of periosteal new bone at affected joints
SO = subcutaneous; FeSV = feline synovial virus; FeLV = feline leukemia virus. Data from references 1, 2, 4, 6, 7, 8, 9, 12, 14, 15, 16, 18, 20, 21, and 22.
generalized. In OA, the changes are limited to the affected joint. The fluid is straw colored and viscous. The white cell count is low (< 5000 cells/mm3 ) and neutrophils are rare. Fluid viscosity is good to mildly decreased and the mucin clot test is normal. In inflammatory arthritis, the changes are often present in more than one joint. The fluid may be yellow to red. The white cell count is high (> 5000 cells/ mm3) and neutrophils predominate. Fluid viscosity is decreased and the mucin clot test is fair to poor. If bacterial infection is the cause of inflammation, protein concentration will be increased over normal and glucose concentration will be decreased from normal. The majority of systemic diseases that are associated with joint disease in the cat (see Table 1) cause inflammatory arthritis and can be ruled in or out by synovial fluid analysis. Nevertheless, diabetes mellitus has been associated with a carpal collapse syndrome. 4 Confusion may occur in older cats with multiple diseases that are coexisting with OA. If these diseases are well managed and the cat continues to display signs
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Figure 2. Radiographic changes characteristic of erosive polyarthritis in the elbow (A) and carpus (B) of a cat. There is lysis of bone and joint remodeling.
Table 2. DIFFERENCES BETWEEN OSTEOARTHRITIS AND INFLAMMATORY ARTHRITIS IN CATS Characteristic
Age of onset Clinical signs
Number of joints affected Joints affected Synovial fluid
Osteoarthritis
Any age but most frequently recognized in geriatric cat Insidious onset of clinical signs, decreased movement, decreased grooming, lameness may or may not be present Usually one joint or a symmetrical pair of joints Shoulder and elbow most common Normal-to-moderate white blood cell count (< 5000/mm3 ), mononuclear cells predominate
Inflammatory Arthritis
Any age cat Fever, joint swelling, lameness may or may not be present, relapsing course common Usually multiple joints Carpus, interphalangeal joints often affected Increased white blood cell count (> 5000/mm'), neutrophils predominate
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compatible with pain due to OA, treatment should be pursued. Further confusion may occur if a cat has suffered a previous inflanunatory polyarthritis which spontaneously cured, and then develops OA in the affected joint. Synovial fluid characteristics in these cases should be compatible with OA and not with inflanunatory arthritis. In people, it has been shown that antigens causing inflanunatory arthritis can remain in the joint long after the primary infection has resolved. For example, in people with reactive arthritis after Yersinia infection, bacterial cultures of the joint were negative, but Yersinia antigen could be demonstrated in synovial cells by using immunohistochemical techniques and Western blotting.U Synovial biopsy may thus be helpful in cases in which there is confusion as to the reason for arthritis. MANAGEMENT OF OA
The management of OA in cats is similar to treatment regimens in other species. Environmental modification, treatment of obesity, controlled moderate exercise, pain control, and surgery are all parts of a treatment plan.1 The unique characteristics of the cat must be taken into consideration in designing such a plan in order for it to be successful. In addition, grooming must be performed by the owner if the cat cannot complete its daily routine. Environmental modification begins with placement of food bowls and litter pans in locations that do not require leaping or stair climbing. Small ramps can be built leading to a feeding station or into the litter box. Placement of a ramp or graduated steps leading to a favorite perching site allows the cat to enjoy the site and encourages moderate exercise. Most owners are very inventive if the basic principles are explained: discourage large leaps up or down, encourage controlled spontaneous movement, and do not make the eat's daily routine a difficult obstacle course. Treatment of obesity can be a challenge if a house cat, whose caloric needs are small, further decreases those needs by decreasing its daily movements. Even when "light" formulas are fed, the total daily amount needed can be one third of a cup of dry food or less. Splitting the meal into two feedings can help to decrease begging. Free-choice feeding should be strongly discouraged. The importance of weight control as part of the treatment plan needs to be stressed. Some older cats have the opposite problem: maintaining weight is a struggle and arthritis can worsen if they stop moving as energy levels decrease. 23 These cats should be fed a high-quality, calorie-rich food. Multiple feedings may encourage increased food intake, and rotating flavors may spark interest. If the cat is addicted to one flavor or type of food, supplements may be added to ensure proper nutrition. Controlled exercise is hard to accomplish with cats: few are leash trained and swimming is not their favorite activity. The major method used to encourage movement is to create an environment that allows
Table 3. DRUGS AND NUTRITIONAL SUPPLEMENTS USED TO TREAT OSTEOARTHRITIS IN CATS Drug
Dosage
Aspirin
10-20 mg/kg PO every 48 h
PO
Phenylbutazone Meloxicam
6-8 mglkg twice a day 0.1 mg/kg once daily 0.3 mg/kg once 4 mg/kg once daily 4 mg/kg once 1 mg/kg once daily 1 mg/kg once daily 2 mg/kg once daily 5-15% solution 0.4-1.5 mg/kg every 4-8 h 2 mg/kg every 12-24 h 1 small animal capsule
IV, IM, PO PO IV, SC PO,SC PO,SC PO, IV, IM PO
Tolfenamic acid Carprofen Flunixin meglumine Ketoprofen Dimethylsulfoxide Butorphanol Prednisolone Coseqin
daily, sprinkled on food
PO = oral; IV = intravenous; IM = intramuscular; SC = subcutaneous. Data from references 4, 10, 13, and 19.
\0
01
......
Route
sc
Topical PO IV, IM, PO PO
Comments
May cause gastrointestinal side effects Use on alternate weeks only Limit: 4 days' use One time use Limit: 3-5 days' use One time use Limit: 3-5 days' use Limit: 5 days' use Limit: 3 days' use Causes c-fiber blockade Sedative side effects Taper to every 48 h May taper to one-half capsule after 4 wk
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easy movement within a daily routine. Owners can encourage movement with food, but this may lead to increased begging behavior. Pain control in cats is a problem because drug regimens that are safe in other species are not necessarily safe in cats. Enzyme systems responsible}or metabolizing drugs, particularly those requiring glucuronide conjugation, are limited in cats. 5 These systems are easily saturated, and toxic quantities of drug may accumulate if alternative metabolic pathways are not available. Short-term pain control regimens, designed primarily for use in the postoperative patient, can be used to treat acute flare-ups of OA pain. Most of these drugs cannot be used on a chronic basis due to toxicity problems. In particular, nonsteroidal antiinflammatory drugs (NSAIDs) require hepatic metabolism for either activation or elimination. Currently, aspirin is the only NSAID for which a safe chronic dose has been established in the cat (Table 3).4• 13• 19 Other oral drugs that may be used on a chronic basis include butorphanol and corticosteroids.•· 13 Butorphanol may cause sedation, and corticosteroids may cause progression of OA. In many cases, the quality of the eat's life is of primary importance to the owner, who may be willing to accept these side effects if quality can be improved. The use of an oral nutritional supplement, Cosequin (Nutramax Laboratories, Inc, Veterinary Science Division, Baltimore, MD), may have some benefits in the treatment of cats with chronic pain due to OA. 4 Some feline practitioners indicate that oral nutritional supplements are their first choice for treatment of OA. 23 The efficacy of these agents in the treatment of established OA is controversial, however. A blinded medication trial may be useful in determining whether or not these agents help in the treatment of an individual patient (see Table 3). The ability of the cat to perform a daily grooming routine is a good method of assessing drug efficacy. Surgery is rarely used to treat OA in cats, and prosthetics are not available in sizes that are appropriate for cats. Femoral head and neck excision may be useful for treatment of severe coxofemoral joint arthritis. SUMMARY
OA is a disease of the geriatric cat. Clinical signs include weight loss, anorexia, depression, urinating outside the litter box, poor grooming, and lameness. Radiographs, synovial fluid analysis, and synovial biopsy are used to distinguish this disease from the various forms of inflammatory arthritis that affect the cat. Management consists mainly of environmental manipulation. Aspirin, butorphanol, corticosteroids, and nutritional supplements are used for chronic treatment of painful OA in cats.
References 1. Bennett D: Osteoarthritis-its classification, pathogenesis and clinical relevance. Voor Diergeneeskunde 118(suppl):19S, 1993
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2. Bennett D: Joints and joint disorders. In Whittick WG (ed): Canine Orthopaedics, ed 2. Philadelphia, Lea & Febiger, 1990, p 761 3. Bennett D, Nash AS: Feline immune-based polyarthritis; A study of thirty-one cases. J Small Anim Pract 29:501, 1988 4. Bennett D, May C: Joint diseases of dogs and cats. In Ettinger SJ, Feldman EC (eds): Textbook of Small Animal Medicine, ed 4. Philadelphia, WB Saunders, 1995, pp 2032-2077 5. Boothe DW: Mechanisms and avoidance of adverse drug reactions. J Am Vet Med Assoc 196:1297, 1990 6. Burgess EC: Experimentally induced infection of cats with Borrelia burgdorferi. Am J Vet Res 53:1507, 1992 7. CarroT: Polyarthritis in cats. Compendium on Continuing Education for the Practicing Veterinarian 16:57, 1994 8. Carro T, Pederson NC, Beaman BL, et al: Subcutaneous abscesses and arthritis caused by a probable bacterial L-form in cats. JAm Vet Med Assoc 194:1583, 1989 9. Dawson S, Bennett D, Carter SD, et al: Acute arthritis of cats associated with feline calicivirus infection. Res Vet Sci 56:133, 1994 10. Evans MS, Reid KH, Sharp JB, Jr: Dimethylsulfoxide (DMSO) blocks conduction in peripheral nerve C fibers: A possible mechanism of analgesia. Neurosci Lett 150:145, 1993 11. Granfors K, Jalkanen S, von Essen R, et al: Yersinia antigens in synovial-fluid cells from patients with reactive arthritis. N Engl J Med 320:216, 1989 12. Gibson MD, Young CR, Oman MT, et al: Borrelia burgdorferi in cats. J Am Vet Med Assoc 202:1786, 1993 13. Hansen B: How to prevent and relieve pain. Veterinary Forum, August, 1996, p 34 14. Hooper PT, Ireland LA, Carter A: Mycoplasma polyarthritis in a cat with probable severe immunodeficiency. Aust Vet J 62:352, 1985 15. Levy JK, Marsh A: Isolation of calicivirus from the joint of a kitten with arthritis. J Am Vet Med Assoc 201:753, 1992 16. Magnarelli LA, Anderson JF, Levine HR, et al: Tick parasitism and antibodies to Borrelia burgdorferi in cats. J Am Vet Med Assoc 197:63, 1990 17. Millis DL: Feline Joint Problems. In Proceedings of the Fifth ACVS Veterinary Symposium, Chicago, 1995, p 533 18. Moise NS, Crissman JW, Fairbrother JF, et al: Mycoplasma gatae arthritis and tenosynovitis in cats: Case report and experimental transmission of disease. Am J Vet Res 44:16, 1983 19. Papich MG: Table of common drugs: Approximate doses. I n Bonagura JD (ed): Kirk's Current Veterinary Therapy XII. Philadelphia, WB Saunders, 1995, pp 1429-1446 . 20. Pederson NC, Pool RR, O' Brien T: Feline chronic progressive polyarthritis. Am J Vet Res 41:522, 1980 21. Pederson NC, Wind A, Morgan JP, et al: Joint diseases of dogs and cats. In Ettinger SJ (ed): Textbook of Veterinary Medicine, ed 3. Philadelphia, WB Saunders, 1989, pp 2329- 2377 22. Rosendal S: Mycoplasmal infections of dogs and cats. In Bonagura JD (ed): Kirk's Current Veterinary Therapy XII. Philadelphia, WB Saunders, 1995, pp 301-302 23. Wolf A, Denoff D, Scherk-Nixon M, et al: Roundtable discussion: The geriatric cat. Feline Practice 24:8 and 24:5, 1996
Address reprint requests to Elizabeth M. Hardie, DVM, PhD College of Veterinary Medicine North Carolina State University 4700 Hillsborough Street Raleigh, NC 27606