Chapter 47The Thigh
Pain that can be demonstrated with digital pressure along a line between the wing of the ilium and the greater trochanter of the femur was first recognized as a cause of lameness more than 50 years ago.1-3 Various aspects of the origin, diagnosis, and management of the syndrome have been appreciated since its initial recognition by Dr. Churchill and myself.1-5 The condition has also been referred to as sacrosciatic lameness or pelvic myositis. We prefer to use the term gluteal syndrome because we believe that there may be more than one abnormality that will result in this type of pain.
Gluteal syndrome has been diagnosed in most breeds and uses of horses. Standardbred (STB) racehorses seem to have the highest incidence, but it is not uncommonly seen in Thoroughbred (TB) and endurance racehorses. One risk factor for STBs is related to the more recent harness and race bike designs that tend to decrease the weight borne by the forelimbs while transferring weight to the hindlimbs. Gluteal syndrome has been diagnosed in horses that are used for hunting, jumping, and eventing.
Based on dissections of cadavers, the accessory head of the middle gluteal muscle was identified as the deep structure that best corresponds anatomically to the characteristic pattern of pain. This muscle originates on the concave surface of the wing of the ilium near a tuber coxae. At its caudal extent, the accessory head of the middle gluteal muscle forms a flat tendon that passes over the cranial aspect of the greater trochanter of the femur and inserts on the crest below it. The accessory head is directly related to other aspects of the middle gluteal and superficial gluteal muscles superficially and is important in propulsion of the hindlimbs6 (Figure 47-1).
Fig. 47-1 Drawing of the anatomy of the lateral pelvic and proximal thigh regions showing the accessory head of the middle gluteal muscle, the most likely source of pain associated with gluteal syndrome. The tendon of the accessory head of the middle gluteal passes over the cranial portion of the greater trochanter, where there is a bursa. Inflammation in this region causes trochanteric bursitis.
The pathological process associated with the accessory head of the middle gluteal muscle is uncertain. It is known that in horses with some acute injuries a hematoma may form in the area between the ilium and the greater trochanter of the femur. Small, hypoechogenic areas may be demonstrated ultrasonographically in muscle tissue in the same area. In other horses, the muscle may become partially detached from the ilium. Horses with the latter condition develop a depression in the musculature caudal to a tuber coxae after the acute stage. In horses with chronic pain, the affected muscle mass may become very firm, presumably as a result of fibrosis. Post mortem evaluation of two horses with chronic refractory gluteal syndrome did not provide any conclusive information. Other potential changes such as fasciitis, gluteal tendonitis, or injury to one or more adjacent muscles have been considered. Whatever the cause, the source of pain is consistently confined to the area described.
To date, the most reliable, practical method of diagnosis is by careful, systematic physical examination of the area between the wing of the ilium and the greater trochanter of the femur with the horse standing on the limb. More specifically, the musculature should be palpated and examined for changes in resilience, swelling, or fibrosis. The position and outline of the tuber coxae should be evaluated. Next, gentle, deep pressure should be applied along the entire area described with the tips of eight digits (Figure 47-2). Initially, light digital pressure should be applied, but then the pressure is gradually increased to firm, deep pressure. The pressure is maintained briefly to evaluate the horse’s response. Finally the area caudal to the ilium, the central portion, and the caudal part of the accessory head of the middle gluteal muscle should be examined similarly. Each third of the area should be considered separately to determine whether the area is affected generally or whether the injury is confined to one or more sections. An unaffected horse will not respond to the examination of any of the areas. An affected horse leans away from the pressure while showing a reluctance to voluntarily bear full weight on the limb as long as the pressure is maintained. A positive response for this syndrome as described is specific and should not be confused with that for trochanteric bursitis (see Trochanteric Bursitis section).
Most horses with acute gluteal syndrome tend to drag the toe of the affected limb on the ground at a walk. Horses with chronic gluteal syndrome do not drag the toe at a walk, but at a slow trot they break over on the inside of the toe and swing the leg medially and then laterally, finally landing on the outside branch or toe of the shoe. At this gait the lameness produced appears identical to that caused by trochanteric bursitis or tarsitis. When the horse trots, paces, or runs at high speed, the abnormality starts off as described, then the limb appears to tire and is carried more in abduction the further in the race or competition the horse proceeds. It appears that early in the race the horse is able to tolerate the gluteal pain and continue to use the limb for propulsion. However, with sustained speed or intensity of effort over distance, compensatory mechanisms within the limb fatigue as pain from the gluteal injury becomes overwhelming. At this point, a STB may make a break or freeze on a line; a TB may bolt or stop trying in the race; and a show horse may refuse to jump or crash when it tries. Many of these horses are believed to have a stifle problem because the quadriceps muscles fasciculate when they pull up. Others are believed to have exercise-induced pulmonary hemorrhage because they stopped like a bleeder, but no blood is seen endoscopically. Regardless, speed, intensity of work, and distance are key factors in how this problem affects an athletic horse. Some horses that accommodate to the injury or are treated and do not recover to total soundness can perform reasonably well at slower speeds or less intense work.
There is not a specific cause for gluteal syndrome. The onset is frequently directly associated with being cast in a stall, slipping or falling while playing in a paddock, or going down in a trailer or van and struggling to get up while the head is tied. Gluteal syndrome also develops when there is a chronic, preexisting problem in the distal aspect of the same limb, such as hock lameness, suspensory desmitis, or other problem that causes the horse to carry its weight on the toe at high speed. Slipping or losing footing on a soft racetrack or other muddy surface is also associated with development of the clinical signs.
Horses with this injury are best treated while in moderate, controlled exercise, regardless of the treatment approach. Rest alone, even for extended periods, has not been successful as a treatment. Several weeks of careful exercise management with repeated evaluations provide the best chance for a favorable response to treatment. Horses with acute injury, hemorrhage, and severe lameness should be rested until they are walking well and the seroma has resorbed before resuming exercise and treatment. Intramuscular injections of a counterirritant, acupuncture, and extracorporeal shock wave therapy are the best treatment options. At present, I still believe that injections of a counterirritant into the area of sensitivity yield the best results in the shortest time. The injection site is prepared with a surgical scrub followed by rinsing with 70% isopropyl alcohol. An injection grid is marked on the horse by drawing three lines in the wet hair over the accessory head of the middle gluteal muscle (Figure 47-3). One hundred milliliters of 2% iodine diluted in sesame oil solution is injected intramuscularly into 20 sites (5 mL/site) on and between the grid lines with a 4-cm, 19-gauge needle. If the pain is concentrated in the cranial or caudal third of the area between a tuber coxae and the ipsilateral greater trochanter of the femur, the injection sites can be limited to the cranial or caudal half of the area, respectively. After injection, daily moderate, controlled exercise is recommended beginning the day after injection for all horses. After injection, horses with acute or recent gluteal syndrome are walked and jogged for 3 weeks and then reexamined. If the lameness is improved but the area is still sensitive or if there has been no improvement, the injection is repeated in the same manner. Horses with chronic gluteal syndrome are walked and jogged for only 1 week before light training is resumed. Some horses respond dramatically to the treatment and appear to be pain-free within less than a week. The injury cannot heal within that time frame; therefore the temptation to resume full training too quickly must be resisted. When the treatment is successful and horses return to full work and racing, 10% to 20% may experience a recurrence of the problem. These horses generally respond well to an additional treatment as they did previously.