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Equine September/October 2007 (Vol 2, No 5)

Making the Rounds: Case Notes and Commentary — Glucocorticoids in the Management of Equine Back Pain

by Christopher R. Byron, DVM, MS, DACVS

    The use of corticosteroids to treat synovial joint pathology in horses is well documented.1 However, the management of other musculoskeletal injuries using corticosteroid treatment has not been as rigorously reviewed. In one of the horses in the case presentation, local injection of triamcinolone acetate had a good short-term effect; however, definitive management required surgical intervention. Although the use of corticosteroids to treat a variety of equine back pathologies can be found in the literature, little objective information is available to guide the use of these drugs by practicing equine clinicians.

    Corticosteroids consist of 21 carbon molecules that have a four-ring structure and are secreted by the adrenal cortex in response to adrenocorticotropic hormone stimulation. They are classified as glucocorticoids or mineralocorticoids, according to whether they primarily regulate carbohydrate metabolism or electrolyte balance, respectively. The primary naturally occurring glucocorticoid is cortisol, and the primary naturally occurring mineralocorticoid is aldosterone.2 Most corticosteroids used in equine medicine are synthetic glucocorticoids, which are modified to enhance antiinflammatory effects while reducing mineralocorticoid effects.

    Corticosteroids are not active in ester form and must be hydrolyzed to the free alcohol form to have biologic activity.3 Circulating corticosteroids are highly protein bound, and only the unbound free fraction can enter cells. Glucocorticoids primarily exert their effects through binding with intracellular glucocorticoid receptors, which subsequently regulate transcription of target genes and regulate the function of other transcription factors, although the existence of membrane-bound corticosteroid receptors has been suggested.3,4 Glucocorticoids have widespread effects because they influence most cells in the body and regulate up to 20% of the expressed genes in each cell.4 Corticosteroids are mainly inactivated by the liver and cleared in the urine.

    While glucocorticoids as a class possess excellent antiinflammatory properties, the rapidity of onset, duration of action, and precise effects depend on several attri­butes of the specific drug administered. The administration route, dose form, specific steroid base, ester form, vehicle, and species all affect the actions of the drug. Steroid bases have been grouped according to duration of action into short-acting (hydrocortisone), intermediate-acting (prednisone, prednisolone, triamcinolone, methylprednisolone), and long-acting (betamethasone, dexamethasone) classifications.2-4 These classes are derived from studies in humans, and it is important to recognize that the precise duration of action is influenced by species variation,3 although, in practice, these classic divisions are observed because of a lack of exhaustive pharmacokinetic data for each species. Recent evidence has suggested that triamcinolone may be better classified as a long-acting steroid, which has important implications for recommended dosing schedules and the likelihood of side effects in horses.5

    The specific ester form of the glucocorticoid preparation influences the absorption rate. Because sodium phosphate and sodium succinate esters are water soluble, they are rapidly absorbed from local sites of administration, resulting in their short biologic half-lives. Acetate, diproprionate, and acetonide esters are poorly water soluble with longer absorption times and subsequently longer terms of action.3 These forms are particularly suitable for depot injections, such as sub­cutaneous and intramuscular administration. Most injectable glucocorticoids used to treat musculoskeletal disease in horses are from the medium- or long-acting group and are in a slowly absorbed acetate, diproprionate, or acetonide ester form. It should also be noted that if oral glucocorticoids are indicated, prednisone is poorly absorbed from the equine gastrointestinal tract, whereas prednisolone has excellent absorption when given orally.6

    Glucocorticoids are used in equine medicine primarily for their antiinflammatory and immunosuppressive effects. These drugs inhibit migration of circulating leukocytes into affected tissues, thereby reducing the number of inflammatory cells at the site of injury. As a by-product of this, the number of circulating neutrophils rises because of their increased release from bone marrow along with reduced extravasation into tissues, which is typical of a stress leukogram. Glucocorticoids also inhibit the production and release of cytokines (interleukin-1, tumor necrosis factor-a) and degradative enzymes (matrix metalloproteinases) by macrophages. In addition, glucocorticoids reduce synthesis of several proinflammatory mediators, such as leukotrienes and prostaglandins, through phospholipase A2 and cyclooxygenase-2 inhibition.4 These attributes endow glucocorticoids with their powerful antiinflammatory and pain-reducing properties in treating musculoskeletal disease.

    Glucocorticoids have been used to treat a variety of musculoskeletal maladies in horses, including os­teo­arthritis, focal myositis, impingement of dorsal spinous processes, sacroiliac joint injury, sacral fractures, caudal vertebral fractures, sacral syndrome, navicular disease, bursitis, splint bone periostitis or exostosis, and vertebral articular facet osteoarthritis.1,7-11 Of particular interest to this discussion is the use of glucocorticoids to treat local back pathologies, and there are several specific indications for the use of these drugs in managing equine back pain.

    Impingement of the dorsal spinous processes is one of the most common causes of back pain in horses and can involve portions of vertebrae from T13 to L2.7,12 The diagnosis may be confirmed by physical examination, radiography, and local anesthesia.7,13 Mild to moderate cases may respond to NSAIDs and muscle relaxants, although some cases may require intralesional injection of corticosteroids.7,13 Injections should be made in the interspinous space or, if this is impossible, lateral to the involved processes. Recommended protocols have included the use of triamcinolone acetonide13 and a combination of methylprednisolone acetate, isoflupredone acetate, and pitcher plant extract (Sarapin, High Chemical Company, Levittown, PA).7 Patients with unresponsive cases are candidates for partial resection of the dorsal spinous processes, either under general anesthesia or as a standing procedure in select circumstances.13,14

    Sacroiliac joint pain is diagnosed through physical examination, nuclear scintigraphy, ultrasonography, radiography, and regional anesthesia.15 Traditional therapeutic protocols using NSAIDs and rest are only partially successful.16 While regional glucocorticoid injection of the sacral area may offer some clinical benefit, a more specific technique has been developed in which the lumbosacral joint may be injected directly.17 Although no specific recommendations have been made regarding glucocorticoid use with this technique, it is reasonable to suggest the use of a medium- to long-acting corticosteroid base as has been recommended in humans with sacroiliac joint spondyloarthropathy.18 The drug should be in acetate, diproprionate, or acetonide ester form to allow slow absorption.

    Osteochondrosis and osteoarthritis of the cervical vertebral facet joints may cause cervical pain, back pain, forelimb lameness, and ataxia.7,19,20 Ultrasonically guided injection of the facet joints from C2 to C7 has been described,21 and treatment with intraarticular triam­cinolone (6 mg/joint) or methylprednisolone (100 mg/joint) has been effective.22

    Temporomandibular joint pain may cause secondary back pain. If the temporomandibular joint pain is due to osteoarthritis rather than sepsis, intraarticular cortico­steroid or hyaluronic acid injection is appropriate.7 A reliable injection technique has been described.23

    Anecdotally, back pain related to focal myositis that is unresponsive to NSAIDs and muscle relaxants may respond to local injection of glucocorticoids alone or in combination with local anesthetics, although no objective data exist regarding the efficacy of this therapy.7 The primary aim in treating focal myositis should be identification and treatment of the primary cause along with concurrent symptomatic treatment of the myositis. If corticosteroids will be used for this purpose, the use of a medium- to long-acting glucocorticoid in slowly absorbed acetate, diproprionate, or acetonide ester form would be most appropriate.

    Epidural glucocorticoid injections have been used for several years in humans to relieve lower back, neck, and radicular pain.24 The use of epidural corticosteroids in horses is not well documented, although beneficial results have been reported with caudal epidural injection of 200 mg of methylprednisolone acetate to treat sacral and coccygeal vertebral injuries.8

    When glucocorticoids are used for any purpose, it is important to remember the potential negative side effects of these drugs on horses. Systemic effects may include iatrogenic Cushing's disease, increased susceptibility to infection, and adrenal-pituitary axis suppression.3 These effects are more likely to occur with long-term systemic use.

    Laminitis is a well-known but poorly documented side effect of glucocorticoid use in horses that can have devastating consequences. The specific drugs and doses likely to induce laminitis are not definitively known, although anecdotal evidence suggests dexamethasone and triamcinolone are the most likely, and there is some experimental evidence to support this assertion.5,25,26 Laminitis may be more likely when long-acting glucocorticoids and higher-than-recommended doses or repeated dosing are used.5

    Two primary theories have emerged as to how glucocorticoids may directly induce laminitis. The first theory suggests that glucocorticoid-mediated lamellar tissue insulin resistance results in decreased tissue glucose use, leading to separation of the dermal and epidermal hoof lamellae.5,27 The second theory suggests that laminitis may be caused by the effects of glucocorticoids on digital vasculature. Glucocorticoids markedly potentiate the vascular constriction caused by epinephrine, norepinephrine, and serotonin in digital arteries and veins,28 which may subsequently decrease laminar blood flow, leading to lamellar separation. The detrimental lamellar tissue effects of glucocorticoids may be worsened by local concentration of circulating glucocorticoids because an increase in a steroid-activating enzyme (11b-hydroxysteroid dehydrogenase-1) has been documented in an experimental model of laminitis.29 This suggests that local concentrations of glucocorticoids may increase at the hoof lamellar interface during laminitic episodes, further compounding the problem.

    Glucocorticoids may increase the risk for tendon and ligament rupture, particularly when they are injected intralesionally. Although specific indications for tendon and ligament injection are rare for equine back pain, the risk has been documented in other musculoskeletal diseases. Rupture may occur if local glucocorticoids are used to treat Achilles tendonitis in humans,30 and repeated injection of the navicular bursa with corticosteroids may increase the risk for deep digital flexor tendon rupture.9

    Glucocorticoids are known to potentiate infection, although examples of treatment leading to infection are rare. Corticosteroid injection of dorsal spinous process impingement has resulted in iatrogenic infection in rare cases.7 Iatrogenic epidural abscessation and meningitis secondary to epidural glucocorticoid administration have been reported in humans.31

    Glucocorticoids may be contraindicated in horses positive for hyperkalemic periodic paralysis because the use of these drugs has induced episodes in humans.32 There are no reports documenting induction of hyperkalemic periodic paralysis secondary to glucocorticoid administration in horses, and this seems to be exceedingly rare in humans, but caution should be exercised when using these agents in affected horses.

    Although the use of local glucocorticoid injection was not definitive in treating back pain in the accompanying case report, it can be a useful adjunct for a variety of back pathologies. It is a logical choice when more conservative treatments have failed and more aggressive treatment is not immediately indicated.

    Downloadable PDF

    1. Caron JP: Intra-articular injections for joint disease in horses. Vet Clin North Am Equine Pract 21(3):559-573, 2005.

    2. Schimmer BP, Parker KL: Adrenocorticotropic hormone; adrenocortical steroids and their synthetic analogues; inhibitors of the synthesis and actions of adrenocortical hormones, in Hardman JG, Limbird LE, Molinoff PB, et al (eds): Goodman and Gilman's The Pharmacological Basis of Therapeutics, ed 9. New York, McGraw-Hill, 1996, pp 1459-1485.

    3. Coppoc GL: Relationship of the dosage form of a corticosteroid to its therapeutic efficacy. JAVMA 185(10):1098-1101, 1984.

    4. Chrousos GP: Adrenocorticosteroids and adrenocortical antagonists, in Katzung BG (ed): Basic and Clinical Pharmacology, ed 9. New York, McGraw-Hill, 2004, pp 641-654.

    5. French K, Pollitt CC, Pass MA: Pharmacokinetics and metabolic effects of triamcinolone acetonide and their possible relationships to glucocorticoid-induced laminitis in horses. J Vet Pharmacol Ther 23(5):287-292, 2000.

    6. Peroni DL, Stanley S, Kollias-Baker, et al: Prednisone per os is likely to have limited efficacy in horses. Equine Vet J 34(3):283-287, 2002.

    7. Marks D: Medical management of back pain. Vet Clin North Am Equine Pract 15(1):179-194, 1999.

    8. Grant BD, Cannon JH, Rantanen NW, et al: Medical and surgical treatment of sacral-coccygeal pathology. Proc AAEP:213-215, 1998.

    9. Dabareiner RM, Carter GK, Honnas CM: Injection of corticosteroids, hyaluronate, and amikacin into the navicular bursa in horses with signs of navicular area pain unresponsive to other treatments: 25 cases (1999-2002). JAVMA 223(10):1469-1474, 2003.

    10. Bertone AL: Metacarpal/metatarsal exostosis (splints), in Stashak TS (ed): Adams' Lameness in Horses, ed 5. Philadelphia, Lippincott Williams & Wilkins, 2002, pp 818-821.

    11. Mattoon JS, Drost WT, Grguric MR, et al: Technique for equine cervical articular process joint injection. Vet Radiol Ultrasound 45(3):238-240, 2004.

    12. Jeffcott LB: Symposium on back problems in the horse. (2) The diagnosis of diseases of the horse's back. Equine Vet J 7(2):69-78, 1975.

    13. Walmsley JP, Pettersson H, Winberg F, et al: Impingement of the dorsal spinous processes in two hundred and fifteen horses: Case selection, surgical technique and results. Equine Vet J 34(1):23-28, 2002.

    14. Perkins JD, Schumacher J, Kelly G, et al: Subtotal ostectomy of dorsal spinous processes performed in nine standing horses. Vet Surg 34(6):625-629, 2005.

    15. Dyson S, Murray R: Pain associated with the sacroiliac joint region: A clinical study of 74 horses. Equine Vet J 35(3):240-245, 2003.

    16. Hendrickson DA: Subluxation of the sacroiliac joint (sacroiliac strain), in Stashak TS (ed): Adams' Lameness in Horses, ed 5. Philadelphia, Lippincott Williams & Wilkins, 2002, pp 1049-1053.

    17. Engeli E, Haussler KK, Erb HN: Development and validation of a periarticular injection technique of the sacroiliac joint in horses. Equine Vet J 36(4):324-330, 2004.

    18. Maugars Y, Mathis C, Berthelot JM, et al: Assessment of the efficacy of sacroiliac corticosteroid injections in spondyloarthropathies: A double-blind study. Br J Rheumatol 35(8):767-770, 1996.

    19. Ricardi G, Dyson SJ: Forelimb lameness associated with radiographic abnormalities of the cervical vertebrae. Equine Vet J 25(5):422-426, 1993.

    20. Stewart RH, Reed SM, Weisbrode SE: Frequency and severity of osteochondrosis in horses with cervical stenotic myelopathy. Am J Vet Res 52(6):873-879, 1991.

    21. Nielsen JV, Berg LC, Thoefnert MB, et al: Accuracy of ultrasound-guided intra-articular injection of cervical facet joints in horses: A cadaveric study. Equine Vet J 35(7):657-661, 2003.

    22. Grisel GR, Grant BD, Rantanen NW: Arthrocentesis of the equine cervical facets. Proc AAEP 42:197-198, 1996.

    23. Rosenstein DS, Bullock MF, Ocello PJ, et al: Arthrocentesis of the temporomandibular joint in adult horses. Am J Vet Res 62(5):729-733, 2001.

    24. Hession WG, Stanczak JD, Davis KW, et al: Epidural steroid injections. Semin Roentgenol 39(1):7-23, 2004.

    25. Slone DE, Purohit RC, Ganjam VK, et al: Sodium retention and cortisol (hydrocortisone) suppression caused by dexamethasone and triamcinolone in equids. Am J Vet Res 44(2):280-283, 1983.

    26. Johnson PJ, Slight SH, Ganjam VK, et al: Glucocorticoids and laminitis in the horse. Vet Clin North Am Equine Pract 18(2):219-236, 2002.

    27. French KR, Pollitt CC: Equine laminitis: Glucose deprivation and MMP activation induce dermo-epidermal separation in vitro. Equine Vet J 36(3):261-266, 2004.

    28. Cornelisse CJ, Robinson NE, Berney CA, et al: Thermographic study of in vivo modulation of vascular responses to phenylephrine and endothelin-1 by dexamethasone in the horse. Equine Vet J 38(2):119-126, 2006.

    29. Johnson PJ, Ganjam VK, Slight SH, et al: Tissue-specific dysregulation of cortisol metabolism in equine laminitis. Equine Vet J 36(1):41-45, 2004.

    30. Genovese MC: Joint and soft-tissue injection: A useful adjuvant to systemic and local treatment. Postgrad Med 103(2):125-134, 1998.

    31. Wooten WM, Kinney MO, Huntoon MA: Epidural abscess and meningitis after epidural corticosteroid injection. Mayo Clin Proc 79(5):682-686, 2004.

    32. Numano F, Kubota A, Kitta T, et al: A case of hyperkalemic periodic paralysis induced by administration of synthetic corticosteroids. Nippon Naika Gakkai Zasshi 56(2):165-171, 1967.

    References »

    NEXT: Making the Rounds: Case Presentation — Lameness Originating from Coccygeal Trauma


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