Page 920 - Adams and Stashak's Lameness in Horses, 7th Edition
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886   Chapter 8

            INTRASYNOVIAL

  VetBooks.ir                                                  Lauren e. SmaniK anD Laurie r. GooDrich





              Intrasynovial therapies are used to diminish the   (GAGs) and decreased GAG synthesis, inhibition of pro-
            inflammatory response in synovium, cartilage, tendon   teoglycan synthesis, chondrocyte necrosis, and hypocel-
            (or tendon sheath), or meniscus. An effective  therapy   lularity. 14,25,61,103  Particularly at high concentrations, CS
            should halt progression of degradation of these struc-  inhibit production of important components of cartilage
            tures and restore the normal intrasynovial environment,   such  as  proteoglycans, collagen, and  hyaluronic  acid,
            which should alleviate pain. Equine practitioners cur-  and furthermore result in chondrocyte necrosis. 25,111  It is
            rently have several options available to treat intrasyno-  believed the high concentration and extended exposure
            vial inflammation. Intrasynovial therapies, specifically   used in earlier studies resulted in the detrimental effects
            corticosteroids, are used frequently  in horses to  mini-  of CS on cartilage. As more realistic clinical models have
            mize or control pain associated with synovitis and oste-  emerged, such detrimental effects are less noted, and
            oarthritis (OA).  New therapies are also beginning to be   more cartilage‐sparing effects have been observed with
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            used intrasynovially as potential disease‐modifying   use of low‐dose CS. 66,89  The emerging stand by many
            agents of osteoarthritis (DMOAD); their reputed prop-  clinicians seems to be that intra‐articular (IA) steroids
            erties are prevention, retardation, or reversal of mor-  can be extremely beneficial when used judiciously. This
            phologic cartilaginous lesions of OA. While claims of   has been supported in the human literature as well,
            these properties exist, evidence‐based clinical studies   which has shown that CS have a time‐ and dose‐depend-
            about their true abilities to reverse OA are still in their   ent effect on articular cartilage, with beneficial effects
            infancy. The intrasynovial therapies covered in this sec-  occurring  at  low  doses  (<2–3 mg/dose  or  8–12 mg/
            tion are the most commonly used treatments currently   cumulative  total  dose)  and  durations  and  detrimental
            available for equine practitioners.                effects at high doses (>3 mg/dose or 18–24 mg/cumulative
                                                               total dose) and durations. 117
                                                                  Postinjection flare associated with CS use in the horse
            CORTICOSTEROIDS                                    is rare and usually self‐limiting but associated with some
              Corticosteroids (CS) are the most potent anti‐inflam-  discomfort, necessitating nonsteroidal anti‐inflamma-
            matory drugs available that decrease the catabolic   tory drug (NSAID) therapy. The inflammation is believed
            effects of joint disease. Historically, their use has been   to be caused by the microcrystalline characteristics of
            highly controversial due to the negative effects associ-  CS preparations, as well as the dose and particular ester
            ated with overuse and high dosages utilized in the past.    that is injected; however, the incidence of postinjection
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            Current clinical studies suggest judicious use of CS may   flare has decreased with the advent of branched‐chain
                                                                     113
            be extremely beneficial and can result in long‐lasting   esters.  More concerning is the potential for infection
            pain relief and control of inflammation. 36,66     following  CS  injections,  and  a  reaction  to  medication
                                                               should be treated as a septic process until proven oth-
                                                               erwise.  While the incidence is low, 1 case per 1,279
            Mechanism of Action                                joints injected in one study,  the occurrence of infec-
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              CS have powerful inhibitory effects on inflammation   tion can be devastating and expensive to treat; therefore,
            through stabilization of cellular lysosomal membranes,   strict adherence to aseptic technique is mandatory, and
            reduction of vascular permeability and leukocyte adher-  the combination with an antimicrobial is commonly
            ence to vessel walls (margination), inhibition of platelet   practiced.
            aggregation, and leukocyte diapedesis. Furthermore,   It is important for practitioners to be aware that
            they inhibit prostanoids and nitric oxide, mediators   CS injections associated with sepsis may take up to 10
            integral to the progression of osteoarthritic lesions. 9,56    days to become apparent due to their powerful anti-
            CS are considered to be disease modifying through their   inflammatory properties. When faced with determining
            actions on the abrogation of important mediators of   between a CS flare and joint sepsis, a synovial aspirate
            inflammation, interleukin‐1 (IL‐1), and tumor necrosis   should be performed to determine a leukocyte count
            factor‐α (TNF‐α). Degradative enzymes such as matrix   and differential consistent with bacterial infection.
            metalloproteinases (MMPs) and other related protein-  Clinicians should bear in mind that CS can falsely lower
            ases are also decreased through the actions of CSs which   white blood cell count post‐CS injection.
            alters the progression of an inflamed joint toward osteo-  Laminitis has been associated with CS administra-
            arthritic conditions. 27,60                        tion, and although rare, its occurrence subsequent to IA
                                                               steroids can be devastating. In a study in which 205
            Detrimental Effects and Concerns Regarding         horses were injected with triamcinolone at a dosage
                                                               between 10 and 80  mg/treatment, only 2 of 205 horses
            Intra‐Articular Corticosteroids                    developed laminitis, and 1 of those cases was considered
              The literature is replete with reports describing the   unrelated to the treatment because the laminitic event
            deleterious effects of CS on cartilage.  They include   occurred several months following the treatment. This
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            decreased chondrocyte size, loss of glycosaminoglycans   study reveals the low incidence of this complication,
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