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The California Postmortem Program: Leading the Way
Vet Clin Equine 24 (2008) 21–36
The California Postmortem Program: Leading the Way Susan M. Stover, DVM, PhD*, Amanda Murray, DVM, MPVM Department of Veterinary Medicine:Anatomy, Physiology, Cell Biology, J.D. Wheat Veterinary Orthopedic Research Laboratory, School of Veterinary Medicine, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA
The California Postmortem Program (PMP) was initiated in1990 by the California Horse Racing Board (CHRB), a subcommittee of the California State Legislature. The program statute mandates that every horse that dies at a racetrack under the jurisdiction of the CHRB be necropsied. Necropsy is performed by veterinary pathologists at one of the laboratories of the California Animal Health and Food Safety (CAHFS) Laboratory System (formally called the California Veterinary Diagnostic Laboratory System). The huge success of the PMP is the result of the partnership between the CHRB, racetracks, CAHFS, School of Veterinary Medicine of the University of California at Davis (SVM-UCD), racetrack personnel, and equine research funding agencies. The CHRB designates funds toward the necropsy examinations, and state veterinarians ensure transfer of racehorse cadavers to CAHFS diagnostic laboratories. The racetracks provide funds for transporting racehorse cadavers to CAHFS laboratories. The CAHFS laboratory system is operated by the SVM-UCD. Veterinary pathologists at the CAHFS perform the standardized necropsy examinations. An Equine Medical Director serves as the liaison between the CHRB, CAHFS, and racetrack industry. Racehorse trainers, owners, veterinarians, grooms, and management personnel facilitate information gathering for the program. Faculty researchers at the SVM-UCD investigate specific problems identified through the PMP. In-depth research projects have been supported by the (1) Center for Equine Health with funds provided by Oak Tree Racing Association, the State of California parimutuel fund, and contributions by private donors; (2) Grayson Jockey Club Research Foundation; (3) Dolly * Corresponding author. E-mail address: [email protected] (S.M. Stover). 0749-0739/08/$ - see front matter Ó 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.cveq.2007.11.009 vetequine.theclinics.com
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Green Endowment; (4) US Department of Agriculture; (5) Niarchos Foundation; and (6) J.D. Wheat. Overview The primary objectives of the PMP are to (1) determine the nature of fatal injuries in racehorses, (2) determine the reasons for these injuries, and (3) develop injury prevention strategies. Surveillance of fatal injuries and diseases is accomplished through necropsy examination of all horses that die at racetracks sanctioned by the CHRB. All horses (racehorses and nonracehorses) that die from injuries incurred during racing or training, or from any other disorder at any location on the racetrack grounds, are necropsied. This complete sample has proved valuable, because, for example, the causes of death for horses that die from injuries incurred during a race are different from the causes of death for horses that die from injuries incurred during training [1]. Summary statistics A sobering statistic is that necropsy examinations have been performed on more than 4000 horses through the PMP from 1990 through 2006. Although numbers fluctuate from year to year (Fig. 1), the number of horses of all breeds that were necropsied increased by approximately 5 horses per year (P ¼ .002, r2 ¼ 0.50), ranging from, on average, 212 to 291 horses per year. Thoroughbreds represented 84% of submissions, quarter horses represented 10%, and standardbreds represented 2%. Breed statistics likely reflect underlying population demographics. For example, greater numbers of thoroughbred horses race in California than quarter horses. Three-year-old
Fig. 1. Annual numbers of all horses necropsied through the PMP from 1991 through 2006. A best-fit linear regression line demonstrates an overall increase in the number of horses necropsied over time.
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horses had the greatest number of submissions (31%), followed by 4-year-old (21%), 2-year-old (18%), 5-year-old (13%), and 6-year-old (3%) horses. The 3- and 4-year-old horses likely reflect the most common race entrants [2]. Musculoskeletal injuries were the primary cause of death for 79% of horses. Gastrointestinal and respiratory conditions were each the cause of death for 6% of necropsied horses. Central nervous system disorders affected 2% of horses, and skin and known cardiovascular disorders each affected 1% of horses. Remaining disorders (5%) included sudden death of unknown cause and miscellaneous conditions. Discovery, surveillance, and enhanced diagnostics The PMP has created opportunities for discovery of new diseases and the development of advanced disease diagnostics. Sudden death attributable to Taxus (yew) poisoning from ingestion of ornamental plants in the barn area was diagnosed using gas chromatography/mass spectrometry to identify Taxus alkaloids in stomach contents [3]. Endocardial hemorrhages and multifocal necrosis of papillary muscles and ventricles were new pathologic findings associated with Taxus toxicity. Oleander ingestion was the cause of myocardial pathologic findings in another horse. Further study determined that immunohistochemical detection of cardiac Troponin C is useful as a biomarker of myocardial necrosis in horses with Nerium oleander poisoning [4]. Jimson weed in stall bedding was determined to be the source of scopolamine, which clarified the source of a positive drug finding. An extensive study of equine protozoal myeloencephalitis elucidated the low specificity and high sensitivity of Western blot tests of cerebral spinal fluid for disease detection [5]. Subsequent investigation of an indirect fluorescent antibody test demonstrated higher overall accuracy for disease detection than accuracy of Western blot tests [6,7]. New sites for stress fracture disease were discovered through the PMP [8–10]. The recognition that catastrophic humeral and scapular fractures were related to preexisting stress fractures and the identification of sites of predisposition for these conditions enhanced their recognition by veterinary practitioners. The discovery of humeral stress fractures was one factor that led to the installation of a scintigraphy unit at Santa Anita Racetrack. Forelimb bone scans were expanded to include the upper portion of the limb (ie, scapula, humerus) routinely. The recognition that scintigraphic signs of pelvic stress fractures located adjacent to the sacroiliac joint could be obscured by superimposition of tuber sacrale metabolic bone activity led to the use of oblique views to distinguish the two findings [11]. Musculoskeletal injury statistics The number of thoroughbred racehorses necropsied because of a fatal musculoskeletal injury increased by approximately three horses per year (Fig. 2;
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Fig. 2. Annual numbers of thoroughbred (Tb) racehorses that died because of a musculoskeletal injury necropsied through the PMP from 1991 through 2006. A best-fit linear regression line demonstrates an overall increase in the number of these horses necropsied over time. MS, musculoskeletal.
P ¼ .003, r2 ¼ 0.48). The increase in fatal musculoskeletal injuries is largely attributable to an increase in fatal injuries of structures that support the fetlock region (Fig. 3; P!.001, r2 ¼ 0.63), which comprise a large proportion of musculoskeletal fatal injuries (Table 1). These fetlock injuries include uniaxial and biaxial proximal sesamoid bone fractures and suspensory apparatus ruptures. Lateral condylar fracture may accompany these injuries within a horse. On average, injuries incurred during racing resulted in the death of 43% of the horses. Injuries incurred during training resulted in the death of 32%
Fig. 3. Annual numbers of thoroughbred (Tb) racehorses that incurred a fatal injury of the proximal sesamoid bones or suspensory apparatus from 1991 through 2006. A best-fit linear regression line demonstrates an overall increase in the number of these horses necropsied over time.
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Table 1 Proportion of specific fatal musculoskeletal injuries relative to all musculoskeletal fatal injuries within the thoroughbred breed and within the quarter horse breed for California racehorses over the period 1991 through 2006 Musculoskeletal injury
Thoroughbred (%) Quarter horse (%)
Fetlock support injuries: proximal sesamoid bone fractures or suspensory apparatus rupture Carpal fracture Metacarpal fractures: condylar fractures and noncondylar fractures Humeral fracture Vertebral fracture Scapular fracture Pelvic fracture Proximal phalangeal fracture Metatarsal fracture Tibial fracture
34
28
7 19
21 5
9 2 2 3 4 4 2
2 7 6 4 1 1 1
Only sites that incurred more than 2% of fatal musculoskeletal injuries are listed.
of the horses. There was a disparity in the proportion of injuries incurred during racing versus during training between thoroughbred horses and quarter horses. Racing-incurred injuries represented 54% of racing and training injuries for thoroughbred horses but 90% of injuries during both activities for quarter horses. Proximal sesamoid bone and suspensory apparatus (fetlock) injuries were most common in both breeds. Thereafter, metacarpal and humeral fractures were most common in thoroughbred horses, whereas carpal and vertebral fractures were most common in quarter horses (see Table 1). Presumably, these differences relate to different occupational training and racing activities and differences in limb loading conditions between distance races and sprints. Scapular and pelvic fractures also occurred with some frequency. Most injuries affect the forelimbs; however, differences in injury incidence between left and right limbs have been less frequently apparent when large numbers of injuries are evaluated [1,12]. The proportion of thoroughbred fatalities attributable to musculoskeletal injuries incurred during racing and training relative to thoroughbred racehorses that started a race (starters) and the number of thoroughbred race entrants (starts) has gradually risen from 1991 through 2005 (2006 data not available). The proportion of thoroughbred horses with a fatal musculoskeletal injury rose from 3 to 5 horses per 1000 starts (Fig. 4; P!.001, r2 ¼ 0.74). This number is larger than the 1.7 fatal musculoskeletal injuries reported for California thoroughbred horses per 1000 race starts for 1992 [13], because 1.7 fatalities represented only those fatalities that resulted from injuries incurred during racing (and not training). The proportion of thoroughbred horses with a fatal musculoskeletal injury has increased from 17 to 24 horses per 1000 starters (Fig. 5; P!.001, r2 ¼ 0.61).
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Fig. 4. Thoroughbred (Tb) racehorses that had a fatal musculoskeletal (MS) injury as a proportion of Tb race starts for the period from 1991 through 2005. A best-fit linear regression line demonstrates an overall increase in the proportion over time.
Musculoskeletal injuries The two most important concepts recognized through discoveries from the PMP were (1) the recognition that injuries occur at consistent locations and in characteristic configurations for each specific bone [8] and (2) the recognition that preexisting pathologic conditions commonly precede catastrophic injury. The consistent location and characteristic configuration for each injury indicate that the forces causing injury are uniformly similar among horses. If catastrophic injuries were attributable to stepping in a hole in some instances and twisting about the hoof in other instances, fracture sites and configurations would be different. Second, the common
Fig. 5. Thoroughbred (Tb) racehorses that had a fatal musculoskeletal (MS) injury as a proportion of Tb racehorses that started at least one race (starters) each year for the period from 1991 through 2005. A best-fit linear regression line demonstrates an overall increase in the proportion over time.
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Fig. 6. Third metacarpal condylar fractures. (A) Dorsal view of a typical lateral condylar fracture (left image) and the contralateral nonfractured bone. (B) Lateral condylar fracture from a different horse displays the typical subchondral lesion (arrow). A small fragment of bone is missing. A focal area of dark discoloration is surrounded by a rim of dense light-colored bone. (C) Lateral condyle of the contralateral nonfractured bone had been sectioned in the sagittal plane at the same level as the condylar fracture. A dark subchondral crescent (arrow), characteristic of traumatic osteochondrosis of the palmar aspect of the condyle, is apparent.
presence of reactive periosteal new bone tissue at sites of complete fracture indicates that catastrophic fracture is the acute manifestation of a more chronic pathologic process. Consequently, there is time during injury pathogenesis to intervene for prevention of injury. Patterns of injury Clearly, the most common catastrophic injuries involve the structures that support the fetlock joint (see Table 1). These injuries include uniaxial and biaxial (medial and lateral) proximal sesamoid bone fracture and suspensory apparatus rupture [12,14]. Affected horses may also have tears of the deep and superficial digital flexor tendons in regions adjacent to the fetlock, lateral condylar fracture, or severe tearing of the intersesamoidean ligament. Traumatic osteochondrosis of the palmar aspect of the metacarpal condyle is often present bilaterally, but this lesion is also common in necropsied horses that did not have catastrophic pathologic findings of the fetlock region. When lateral condylar fractures are included in this category, the number of fatal injuries involving the fetlock region is even higher.
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Fig. 7. Third metacarpal stress fractures. (A) Lateral view of a completely fractured third metacarpal bone (right) and the contralateral nonfractured bone. The distal end of the proximal fragment of the fractured bone (upper right ellipse) is thickened by periosteal callus. The nonfractured bone has a distorted cortical surface contour (lower left ellipse) characteristic of stress fracture in the distodorsolateral location. (B) Proximal surface of the distal fracture fragment of another horse illustrates a layer of periosteal callus (double-headed arrow) and an intracortical region of discoloration (arrow).
Most other catastrophic fractures are associated with preexisting pathologic conditions. Gross pathologic features are usually consistent with stress remodeling or stress fracture. Many catastrophic fractures occur early in the course of stress remodeling, when periosteal new bone formation is relatively thin (!1 mm thick). Meticulous manual debridement of the soft tissues from bone surfaces, particularly at the origins and insertions of muscle attachments, is necessary to allow visualization or palpation of gross abnormalities. Periosteal bone proliferation can vary from thin, red, flat, rough-surfaced lesions of recent formation to thick, white, nodular, smooth-surfaced lesions of older formation. Bone fragment margins should be thoroughly examined for foci of discoloration, thickening attributable to periosteal new bone production on parent bone surfaces, and change in coloration and bone density associated with the abrupt transition from pale compact parent bone to red woven periosteal bone proliferation. Knowledge of the sites of predisposition for abnormalities enhances the likelihood of disease detection. Metacarpal fractures Catastrophic metacarpal fractures are usually comminuted. Metacarpal fractures are usually associated with one of three preexisting conditions: traumatic osteochondrosis of the palmar aspect of the distal condyle, stress
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Fig. 8. Third metacarpal comminuted diaphyseal fractures. (A) Dorsal oblique view of a comminuted diaphyseal third metacarpal bone fracture. (B) Higher magnification view of the rough porous bone on the dorsal surface of fracture fragments.
fracture, and dorsal metacarpal disease. Lateral and, less commonly, medial condylar fractures course in the sagittal plane. These fractures are often (but not always) associated with subchondral lesions (Fig. 6). A dark focus of chalky subchondral bone is usually surrounded by a crescent of pale dense bone located deep to the focus. A roughly triangular osteochondral fragment may be absent. This fragment corresponds to the triangular-shaped palmar fragment recognized in clinical patients and is associated with a poorer prognosis for return to performance [15–18]. Transverse or slightly oblique (caudoproximal-to-craniodistal plane) fractures of the distal portion of the third metacarpal bone are usually associated with stress fractures on the dorsal or dorsolateral side of the bone (Fig. 7). Periosteal callus is usually visible bridging the fracture line. Occasionally, discoloration within the parent cortical bone underlying periosteal callus can also be visualized. It is not unusual for these fractures to be comminuted, and they may also have a condylar fracture component. Middle diaphyseal third metacarpal fractures are often comminuted. Occasionally, some fracture fragments have evidence of dorsal metacarpal disease (Fig. 8). Comminuted fractures that are confined to the middle of the diaphysis may not have gross evidence of preexisting pathologic conditions. Some of these fractures are extensions of a medial condylar fracture [15,19,20].
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Fig. 9. Humeral fractures in two horses. (A) Lateral view of the caudal aspect of a proximal humeral fragment from a humerus that had a complete oblique fracture. Bone callus (lighter in color than the parent bone surface) covers the periosteal surface adjacent to the complete fracture surface. (B) Caudal aspect of a fresh humerus with a complete fracture. The fracture fragments are reduced to illustrate the thin (!1 mm thick), vascular, periosteal new bone bridging components of the fracture line. This fracture is commonly comminuted at the proximal end of the fracture.
Humeral fractures Humeral fractures are almost always oblique to softly spiraling fractures that extend the length of the diaphysis [8,9]. They originate proximally, just beneath the humeral head, and course distocranially. Periosteal callus can usually be observed bridging the fracture line in one of three locations: caudoproximal, medial, or craniodistomedial (Fig. 9). The caudoproximal location is deep to the origin of the brachialis muscle. The medial location is adjacent to the insertion of the teres major muscle. The craniodistomedial location is in the medial epicondylar region. Careful soft tissue debridement and examination are needed to detect bone callus of recent origin. Scapular fractures Fracture most commonly occurs transversely through the distal end of the scapular spine (Fig. 10) [8]. The fracture may be comminuted. Comminuted fracture lines commonly extend to the glenoid cavity. Occasional incomplete fracture lines course proximally from the transverse fracture component into the body of the scapula. Periosteal new bone production usually bridges the fracture line as it courses through the spine of the
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Fig. 10. Scapular fractures from two horses. (A) Dried bone specimen. Characteristic fracture configuration includes a transverse component through the distal end of the scapular spine. The fracture commonly extends distally to the glenoid cavity and may have some comminution and incomplete fracture lines that extend proximally from the transverse fracture line. (B) Lateral view of the distal end of the scapular spine illustrates periosteal bone production that bridges the fracture site. (C) Caudal view of the distal end of the scapular spine of a fresh specimen from a different horse illustrates the hyperemic and rough-surfaced nature of the periosteal callus.
scapula. Bone production can be less than 1 mm thick. New bone is highly vascular (red) and has a rough surface. More chronic periosteal bone production manifests as focal enlargement of the abaxial aspect of the spine. Pelvic fractures Pelvic fractures are usually comminuted. Evidence of stress remodeling manifested as periosteal bone production is usually present in a focal region that bridges the fracture line [8]. Bone callus occurs in a variety of locations but, most commonly, on the ilium, particularly adjacent to the sacroiliac joint (Fig. 11). Other locations include the pubis, ischium, broad surface of the ilium, and ilial shaft. Not all stress fracture lesions result in catastrophic fracture. In a survey of pelvises from horses that died for any reason, 28% had evidence of stress remodeling [10]. Tibial fractures Complete catastrophic fractures of the tibia are rare relative to the clinical recognition of tibial stress fractures. Perhaps ease of clinical recognition and appropriate management prevent progression to complete fracture [21,22].
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Fig. 11. Pelvic fracture configurations in three horses. (A) Pelvic diagram viewed from the dorsal aspect. (B) Raised callus on the ventral bone surface bridges the two fractures in the symphyseal parts of the pubis and ischium. (C) Bilateral fractures of the ilium emanate from the region of the sacroiliac joints. (D) Unilateral fracture of one ilium is accompanied by incomplete stress fracture of the contralateral ilium.
Focal periosteal new bone production can be found in numerous locations in fatal fractures (Fig. 12) [8]. The two predominant locations are the proximolateral aspect of the tibia just distal to the level of the head of the fibula and the caudal aspect of the distal aspect of the tibial diaphysis, however. Carpal fractures Fatal carpal bone fractures include comminuted fractures of multiple carpal bones (Fig. 13). Several carpal bones often have foci of articular cartilage degeneration of varying severity located near dorsal margins. Some of these articular lesions have subchondral bone changes that could predispose to marginal osteochondral chip fracture or catastrophic bone fracture. Summary The PMP achieves disease surveillance, discovery of new causes of death, and development of new diagnostic methods for disease detection, and it informs directions for research focused on elucidating the etiopathogenesis
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Fig. 12. Bilateral tibial dried bone specimens from one racehorse. (A) Caudal aspect of bilateral tibia from one horse with bilateral tibial stress fractures and unilateral complete fracture. (B) Nonfractured tibia has a large stress fracture callus (left ellipse), whereas the fractured tibia has periosteal new bone less than 1 mm thick adjacent to the fracture line (right ellipse). (C) Periosteal new bone, less than 1 mm thick, is also located across an incomplete fracture line on the caudal aspect of the diaphysis.
of, and risk factors for, catastrophic fractures [23] and other causes of death. Because most fatal injuries seem to be the acute culmination of a more chronic process, intervention and prevention of injuries is possible with enhanced knowledge of the etiopathogenesis of injuries and risk factors for injuries, and development of management strategies for injury prevention is also possible. It is unclear why the apparent incidence of fatal injuries has increased despite knowledge about the causes and sites of injury and access to improved diagnostic methods and facilities. Perhaps education of trainers, owners, and veterinarians about PMP findings has been inadequate or unsuccessful. Perhaps short-term goals and industry economic issues create circumstances that make it difficult to focus on other goals. The mandates to limit toe-grab height on horseshoes and to install synthetic race surface materials at major California racetracks highlight the commitment that horsemen and the state of California have made to enhancing equine welfare, however. Unfortunately, little is known about incidence rates of injury/illness (other than annual descriptive summaries) relative to the populations of live racehorses in the United States. The population of live horses that the deceased horses come from is difficult to determine for several reasons.
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Fig. 13. Bilateral proximal and distal rows of carpal bones from one racehorse. (A) Left carpus: multiple bones of the proximal and distal carpal bone rows are fractured. (B) Right carpus: third carpal bone has a focal partial-thickness articular cartilage lesion near the dorsal margin. The intermediate carpal bone has articular cartilage fibrillation near the dorsal margin. (C) High-detail radiograph of a sagittal section of the left fractured third carpal bone illustrates the bed for a missing osteochondral chip fracture (upper right corner is missing). (D) Highdetail radiograph of a sagittal section of the right intact third carpal bone illustrates focal subchondral osteoporosis. (E) Microradiograph of the intact carpal bone illustrates intensely remodeling subchondral bone. The darker bone tissue beneath the layer of calcified cartilage reflects newer less mineralized bone material. (F) Remodeled tissue contains large resorption bays. (G) Cracks extend from one resorption bay to another.
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At many racetracks, horse inventory is unknown or information is difficult to retrieve from the information database system. The California racehorse population has been estimated using the number of stalls at racetrack facilities [24]. The pool of horses contributing horses that are transported to a racetrack on the day of race has only been estimated. Turnover of horses through barns has been estimated at approximately 20% of horses every 3 months [14]. The proportion of inactive horses that occupy stalls is unknown. Fortunately, incidence rates per number of starts and number of starters have proved useful in epidemiologic studies. Efforts to implant microchips in horses for identification should allow monitoring of horse movement between racetracks, however, and facilitate monitoring of injury and disease incidences relative to the live horse population.
Acknowledgments Some data were provided by the Jockey Club Information Systems.
References [1] Johnson BJ, Stover SM, Daft BM, et al. Causes of death in racehorses over a 2 year period. Equine Vet J 1994;26:327–30. [2] Estberg L, Stover SM, Gardner IA, et al. Fatal musculoskeletal injuries incurred during racing and training in thoroughbreds. J Am Vet Med Assoc 1996;208:92–6. [3] Tiwary AK, Puschner B, Kinde H, et al. Diagnosis of Taxus (yew) poisoning in a horse. J Vet Diagn Invest 2005;17(3):252–5. [4] Mahakian LM. Lack of immunohistochemical detection of cardiac Troponin C as a biomarker of myocardial necrosis in horses with Nerium oleander poisoning. Davis (CA): Comparative Pathology, University of California; 2003. [5] Daft BM, Barr BC, Gardner IA, et al. Sensitivity and specificity of Western blot testing of cerebrospinal fluid and serum for diagnosis of equine protozoal myeloencephalitis in horses with and without neurologic abnormalities. J Am Vet Med Assoc 2002;221(7):1007–13. [6] Duarte PC, Daft BM, Conrad PA, et al. Comparison of a serum indirect fluorescent antibody test with two Western blot tests for the diagnosis of equine protozoal myeloencephalitis. J Vet Diagn Invest 2003;15(1):8–13. [7] Duarte PC, Daft BM, Conrad PA, et al. Evaluation and comparison of an indirect fluorescent antibody test for detection of antibodies to Sarcocystis neurona, using serum and cerebrospinal fluid of naturally and experimentally infected, and vaccinated horses. J Parasitol 2004;90(2):379–86. [8] Stover SM. Stress fractures. In: White NA, Moore JN, editors. Current techniques in equine surgery and lameness. 2nd edition. Philadelphia: W.B. Saunders Company; 1998. p. 451–9. [9] Stover SM, Johnson BJ, Daft BM, et al. An association between complete and incomplete stress fractures of the humerus in racehorses. Equine Vet J 1992;24:260–3. [10] Haussler KK, Stover SM. Stress fractures of the vertebral lamina and pelvis in Thoroughbred racehorses. Equine Vet J 1998;30:374–81. [11] Hornof WJ, Stover SM, Koblik PD, et al. Oblique views of the ilium and the scintigraphic appearance of stress fractures of the ilium. Equine Vet J 1996;28:355–8. [12] Anthenill LA, Stover SM, Gardner IA, et al. Association between findings on palmarodorsal radiographic images and detection of a fracture in the proximal sesamoid bones of forelimbs obtained from cadavers of racing Thoroughbreds. Am J Vet Res 2006;67(5):858–68.
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[13] Estberg L, Stover SM, Gardner IA, et al. Relationship between race start characteristics and risk of catastrophic injury in thoroughbreds: 78 cases (1992). J Am Vet Med Assoc 1998;212: 544–9. [14] Hill AE, Stover SM, Gardner IA, et al. Risk factors for and outcomes of noncatastrophic suspensory apparatus injury in Thoroughbred racehorses. J Am Vet Med Assoc 2001; 218(7):1136–44. [15] Zekas LJ, Bramlage LR, Embertson RM, et al. Characterisation of the type and location of fractures of the third metacarpal/metatarsal condyles in 135 horses in central Kentucky (1986–1994). Equine Vet J 1999;31(4):304–8. [16] Zekas LJ, Bramlage LR, Embertson RM, et al. Results of treatment of 145 fractures of the third metacarpal/metatarsal condyles in 135 horses (1986–1994). Equine Vet J 1999;31: 309–13. [17] Rick MC, O’Brien TR, Pool RR, et al. Condylar fractures of the third metacarpal bone and third metatarsal bone in 75 horses: radiographic features, treatments, and outcome. J Am Vet Med Assoc 1983;183(3):287–96. [18] Schoenborn WC, Rick MC, Hornof WJ. Computed tomographic appearance of osteochondritis dissecans-like lesions of the proximal articular surface of the proximal phalanx in a horse. Vet Radiol Ultrasound 2002;43(6):541–4. [19] Bassage LH II, Richardson DW. Longitudinal fractures of the condyles of the third metacarpal and metatarsal bones in racehorses: 224 cases (1986–1995). J Am Vet Med Assoc 1998; 212:1757–64. [20] Richardson DW. Medial condylar fractures of the third metatarsal bone in horses. J Am Vet Med Assoc 1984;185(7):761–5. [21] O’Sullivan CB, Lumsden JM. Stress fractures of the tibia and humerus in Thoroughbred racehorses: 99 cases (1992–2000). J Am Vet Med Assoc 2003;222:491–8. [22] Ruggles AJ, Moore RM, Bertone AL, et al. Tibial stress fractures in racing standardbreds: 13 cases (1989–1993). J Am Vet Med Assoc 1996;209(3):634–7. [23] Stover SM. The epidemiology of Thoroughbred racehorse injuries. Clinical Techniques in Equine Practice 2003;2(4):312–22. [24] Hill AE, Carpenter TE, Gardner IA, et al. Evaluation of a stochastic Markov-chain model for the development of forelimb injuries in Thoroughbred racehorses. Am J Vet Res 2003; 64(3):328–37.
The California Postmortem Program: Leading the Way Susan M. Stover, DVM, PhD*, Amanda Murray, DVM, MPVM Department of Veterinary Medicine:Anatomy, Physiology, Cell Biology, J.D. Wheat Veterinary Orthopedic Research Laboratory, School of Veterinary Medicine, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA
The California Postmortem Program (PMP) was initiated in1990 by the California Horse Racing Board (CHRB), a subcommittee of the California State Legislature. The program statute mandates that every horse that dies at a racetrack under the jurisdiction of the CHRB be necropsied. Necropsy is performed by veterinary pathologists at one of the laboratories of the California Animal Health and Food Safety (CAHFS) Laboratory System (formally called the California Veterinary Diagnostic Laboratory System). The huge success of the PMP is the result of the partnership between the CHRB, racetracks, CAHFS, School of Veterinary Medicine of the University of California at Davis (SVM-UCD), racetrack personnel, and equine research funding agencies. The CHRB designates funds toward the necropsy examinations, and state veterinarians ensure transfer of racehorse cadavers to CAHFS diagnostic laboratories. The racetracks provide funds for transporting racehorse cadavers to CAHFS laboratories. The CAHFS laboratory system is operated by the SVM-UCD. Veterinary pathologists at the CAHFS perform the standardized necropsy examinations. An Equine Medical Director serves as the liaison between the CHRB, CAHFS, and racetrack industry. Racehorse trainers, owners, veterinarians, grooms, and management personnel facilitate information gathering for the program. Faculty researchers at the SVM-UCD investigate specific problems identified through the PMP. In-depth research projects have been supported by the (1) Center for Equine Health with funds provided by Oak Tree Racing Association, the State of California parimutuel fund, and contributions by private donors; (2) Grayson Jockey Club Research Foundation; (3) Dolly * Corresponding author. E-mail address: [email protected] (S.M. Stover). 0749-0739/08/$ - see front matter Ó 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.cveq.2007.11.009 vetequine.theclinics.com
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Green Endowment; (4) US Department of Agriculture; (5) Niarchos Foundation; and (6) J.D. Wheat. Overview The primary objectives of the PMP are to (1) determine the nature of fatal injuries in racehorses, (2) determine the reasons for these injuries, and (3) develop injury prevention strategies. Surveillance of fatal injuries and diseases is accomplished through necropsy examination of all horses that die at racetracks sanctioned by the CHRB. All horses (racehorses and nonracehorses) that die from injuries incurred during racing or training, or from any other disorder at any location on the racetrack grounds, are necropsied. This complete sample has proved valuable, because, for example, the causes of death for horses that die from injuries incurred during a race are different from the causes of death for horses that die from injuries incurred during training [1]. Summary statistics A sobering statistic is that necropsy examinations have been performed on more than 4000 horses through the PMP from 1990 through 2006. Although numbers fluctuate from year to year (Fig. 1), the number of horses of all breeds that were necropsied increased by approximately 5 horses per year (P ¼ .002, r2 ¼ 0.50), ranging from, on average, 212 to 291 horses per year. Thoroughbreds represented 84% of submissions, quarter horses represented 10%, and standardbreds represented 2%. Breed statistics likely reflect underlying population demographics. For example, greater numbers of thoroughbred horses race in California than quarter horses. Three-year-old
Fig. 1. Annual numbers of all horses necropsied through the PMP from 1991 through 2006. A best-fit linear regression line demonstrates an overall increase in the number of horses necropsied over time.
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horses had the greatest number of submissions (31%), followed by 4-year-old (21%), 2-year-old (18%), 5-year-old (13%), and 6-year-old (3%) horses. The 3- and 4-year-old horses likely reflect the most common race entrants [2]. Musculoskeletal injuries were the primary cause of death for 79% of horses. Gastrointestinal and respiratory conditions were each the cause of death for 6% of necropsied horses. Central nervous system disorders affected 2% of horses, and skin and known cardiovascular disorders each affected 1% of horses. Remaining disorders (5%) included sudden death of unknown cause and miscellaneous conditions. Discovery, surveillance, and enhanced diagnostics The PMP has created opportunities for discovery of new diseases and the development of advanced disease diagnostics. Sudden death attributable to Taxus (yew) poisoning from ingestion of ornamental plants in the barn area was diagnosed using gas chromatography/mass spectrometry to identify Taxus alkaloids in stomach contents [3]. Endocardial hemorrhages and multifocal necrosis of papillary muscles and ventricles were new pathologic findings associated with Taxus toxicity. Oleander ingestion was the cause of myocardial pathologic findings in another horse. Further study determined that immunohistochemical detection of cardiac Troponin C is useful as a biomarker of myocardial necrosis in horses with Nerium oleander poisoning [4]. Jimson weed in stall bedding was determined to be the source of scopolamine, which clarified the source of a positive drug finding. An extensive study of equine protozoal myeloencephalitis elucidated the low specificity and high sensitivity of Western blot tests of cerebral spinal fluid for disease detection [5]. Subsequent investigation of an indirect fluorescent antibody test demonstrated higher overall accuracy for disease detection than accuracy of Western blot tests [6,7]. New sites for stress fracture disease were discovered through the PMP [8–10]. The recognition that catastrophic humeral and scapular fractures were related to preexisting stress fractures and the identification of sites of predisposition for these conditions enhanced their recognition by veterinary practitioners. The discovery of humeral stress fractures was one factor that led to the installation of a scintigraphy unit at Santa Anita Racetrack. Forelimb bone scans were expanded to include the upper portion of the limb (ie, scapula, humerus) routinely. The recognition that scintigraphic signs of pelvic stress fractures located adjacent to the sacroiliac joint could be obscured by superimposition of tuber sacrale metabolic bone activity led to the use of oblique views to distinguish the two findings [11]. Musculoskeletal injury statistics The number of thoroughbred racehorses necropsied because of a fatal musculoskeletal injury increased by approximately three horses per year (Fig. 2;
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Fig. 2. Annual numbers of thoroughbred (Tb) racehorses that died because of a musculoskeletal injury necropsied through the PMP from 1991 through 2006. A best-fit linear regression line demonstrates an overall increase in the number of these horses necropsied over time. MS, musculoskeletal.
P ¼ .003, r2 ¼ 0.48). The increase in fatal musculoskeletal injuries is largely attributable to an increase in fatal injuries of structures that support the fetlock region (Fig. 3; P!.001, r2 ¼ 0.63), which comprise a large proportion of musculoskeletal fatal injuries (Table 1). These fetlock injuries include uniaxial and biaxial proximal sesamoid bone fractures and suspensory apparatus ruptures. Lateral condylar fracture may accompany these injuries within a horse. On average, injuries incurred during racing resulted in the death of 43% of the horses. Injuries incurred during training resulted in the death of 32%
Fig. 3. Annual numbers of thoroughbred (Tb) racehorses that incurred a fatal injury of the proximal sesamoid bones or suspensory apparatus from 1991 through 2006. A best-fit linear regression line demonstrates an overall increase in the number of these horses necropsied over time.
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Table 1 Proportion of specific fatal musculoskeletal injuries relative to all musculoskeletal fatal injuries within the thoroughbred breed and within the quarter horse breed for California racehorses over the period 1991 through 2006 Musculoskeletal injury
Thoroughbred (%) Quarter horse (%)
Fetlock support injuries: proximal sesamoid bone fractures or suspensory apparatus rupture Carpal fracture Metacarpal fractures: condylar fractures and noncondylar fractures Humeral fracture Vertebral fracture Scapular fracture Pelvic fracture Proximal phalangeal fracture Metatarsal fracture Tibial fracture
34
28
7 19
21 5
9 2 2 3 4 4 2
2 7 6 4 1 1 1
Only sites that incurred more than 2% of fatal musculoskeletal injuries are listed.
of the horses. There was a disparity in the proportion of injuries incurred during racing versus during training between thoroughbred horses and quarter horses. Racing-incurred injuries represented 54% of racing and training injuries for thoroughbred horses but 90% of injuries during both activities for quarter horses. Proximal sesamoid bone and suspensory apparatus (fetlock) injuries were most common in both breeds. Thereafter, metacarpal and humeral fractures were most common in thoroughbred horses, whereas carpal and vertebral fractures were most common in quarter horses (see Table 1). Presumably, these differences relate to different occupational training and racing activities and differences in limb loading conditions between distance races and sprints. Scapular and pelvic fractures also occurred with some frequency. Most injuries affect the forelimbs; however, differences in injury incidence between left and right limbs have been less frequently apparent when large numbers of injuries are evaluated [1,12]. The proportion of thoroughbred fatalities attributable to musculoskeletal injuries incurred during racing and training relative to thoroughbred racehorses that started a race (starters) and the number of thoroughbred race entrants (starts) has gradually risen from 1991 through 2005 (2006 data not available). The proportion of thoroughbred horses with a fatal musculoskeletal injury rose from 3 to 5 horses per 1000 starts (Fig. 4; P!.001, r2 ¼ 0.74). This number is larger than the 1.7 fatal musculoskeletal injuries reported for California thoroughbred horses per 1000 race starts for 1992 [13], because 1.7 fatalities represented only those fatalities that resulted from injuries incurred during racing (and not training). The proportion of thoroughbred horses with a fatal musculoskeletal injury has increased from 17 to 24 horses per 1000 starters (Fig. 5; P!.001, r2 ¼ 0.61).
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Fig. 4. Thoroughbred (Tb) racehorses that had a fatal musculoskeletal (MS) injury as a proportion of Tb race starts for the period from 1991 through 2005. A best-fit linear regression line demonstrates an overall increase in the proportion over time.
Musculoskeletal injuries The two most important concepts recognized through discoveries from the PMP were (1) the recognition that injuries occur at consistent locations and in characteristic configurations for each specific bone [8] and (2) the recognition that preexisting pathologic conditions commonly precede catastrophic injury. The consistent location and characteristic configuration for each injury indicate that the forces causing injury are uniformly similar among horses. If catastrophic injuries were attributable to stepping in a hole in some instances and twisting about the hoof in other instances, fracture sites and configurations would be different. Second, the common
Fig. 5. Thoroughbred (Tb) racehorses that had a fatal musculoskeletal (MS) injury as a proportion of Tb racehorses that started at least one race (starters) each year for the period from 1991 through 2005. A best-fit linear regression line demonstrates an overall increase in the proportion over time.
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Fig. 6. Third metacarpal condylar fractures. (A) Dorsal view of a typical lateral condylar fracture (left image) and the contralateral nonfractured bone. (B) Lateral condylar fracture from a different horse displays the typical subchondral lesion (arrow). A small fragment of bone is missing. A focal area of dark discoloration is surrounded by a rim of dense light-colored bone. (C) Lateral condyle of the contralateral nonfractured bone had been sectioned in the sagittal plane at the same level as the condylar fracture. A dark subchondral crescent (arrow), characteristic of traumatic osteochondrosis of the palmar aspect of the condyle, is apparent.
presence of reactive periosteal new bone tissue at sites of complete fracture indicates that catastrophic fracture is the acute manifestation of a more chronic pathologic process. Consequently, there is time during injury pathogenesis to intervene for prevention of injury. Patterns of injury Clearly, the most common catastrophic injuries involve the structures that support the fetlock joint (see Table 1). These injuries include uniaxial and biaxial (medial and lateral) proximal sesamoid bone fracture and suspensory apparatus rupture [12,14]. Affected horses may also have tears of the deep and superficial digital flexor tendons in regions adjacent to the fetlock, lateral condylar fracture, or severe tearing of the intersesamoidean ligament. Traumatic osteochondrosis of the palmar aspect of the metacarpal condyle is often present bilaterally, but this lesion is also common in necropsied horses that did not have catastrophic pathologic findings of the fetlock region. When lateral condylar fractures are included in this category, the number of fatal injuries involving the fetlock region is even higher.
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Fig. 7. Third metacarpal stress fractures. (A) Lateral view of a completely fractured third metacarpal bone (right) and the contralateral nonfractured bone. The distal end of the proximal fragment of the fractured bone (upper right ellipse) is thickened by periosteal callus. The nonfractured bone has a distorted cortical surface contour (lower left ellipse) characteristic of stress fracture in the distodorsolateral location. (B) Proximal surface of the distal fracture fragment of another horse illustrates a layer of periosteal callus (double-headed arrow) and an intracortical region of discoloration (arrow).
Most other catastrophic fractures are associated with preexisting pathologic conditions. Gross pathologic features are usually consistent with stress remodeling or stress fracture. Many catastrophic fractures occur early in the course of stress remodeling, when periosteal new bone formation is relatively thin (!1 mm thick). Meticulous manual debridement of the soft tissues from bone surfaces, particularly at the origins and insertions of muscle attachments, is necessary to allow visualization or palpation of gross abnormalities. Periosteal bone proliferation can vary from thin, red, flat, rough-surfaced lesions of recent formation to thick, white, nodular, smooth-surfaced lesions of older formation. Bone fragment margins should be thoroughly examined for foci of discoloration, thickening attributable to periosteal new bone production on parent bone surfaces, and change in coloration and bone density associated with the abrupt transition from pale compact parent bone to red woven periosteal bone proliferation. Knowledge of the sites of predisposition for abnormalities enhances the likelihood of disease detection. Metacarpal fractures Catastrophic metacarpal fractures are usually comminuted. Metacarpal fractures are usually associated with one of three preexisting conditions: traumatic osteochondrosis of the palmar aspect of the distal condyle, stress
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Fig. 8. Third metacarpal comminuted diaphyseal fractures. (A) Dorsal oblique view of a comminuted diaphyseal third metacarpal bone fracture. (B) Higher magnification view of the rough porous bone on the dorsal surface of fracture fragments.
fracture, and dorsal metacarpal disease. Lateral and, less commonly, medial condylar fractures course in the sagittal plane. These fractures are often (but not always) associated with subchondral lesions (Fig. 6). A dark focus of chalky subchondral bone is usually surrounded by a crescent of pale dense bone located deep to the focus. A roughly triangular osteochondral fragment may be absent. This fragment corresponds to the triangular-shaped palmar fragment recognized in clinical patients and is associated with a poorer prognosis for return to performance [15–18]. Transverse or slightly oblique (caudoproximal-to-craniodistal plane) fractures of the distal portion of the third metacarpal bone are usually associated with stress fractures on the dorsal or dorsolateral side of the bone (Fig. 7). Periosteal callus is usually visible bridging the fracture line. Occasionally, discoloration within the parent cortical bone underlying periosteal callus can also be visualized. It is not unusual for these fractures to be comminuted, and they may also have a condylar fracture component. Middle diaphyseal third metacarpal fractures are often comminuted. Occasionally, some fracture fragments have evidence of dorsal metacarpal disease (Fig. 8). Comminuted fractures that are confined to the middle of the diaphysis may not have gross evidence of preexisting pathologic conditions. Some of these fractures are extensions of a medial condylar fracture [15,19,20].
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Fig. 9. Humeral fractures in two horses. (A) Lateral view of the caudal aspect of a proximal humeral fragment from a humerus that had a complete oblique fracture. Bone callus (lighter in color than the parent bone surface) covers the periosteal surface adjacent to the complete fracture surface. (B) Caudal aspect of a fresh humerus with a complete fracture. The fracture fragments are reduced to illustrate the thin (!1 mm thick), vascular, periosteal new bone bridging components of the fracture line. This fracture is commonly comminuted at the proximal end of the fracture.
Humeral fractures Humeral fractures are almost always oblique to softly spiraling fractures that extend the length of the diaphysis [8,9]. They originate proximally, just beneath the humeral head, and course distocranially. Periosteal callus can usually be observed bridging the fracture line in one of three locations: caudoproximal, medial, or craniodistomedial (Fig. 9). The caudoproximal location is deep to the origin of the brachialis muscle. The medial location is adjacent to the insertion of the teres major muscle. The craniodistomedial location is in the medial epicondylar region. Careful soft tissue debridement and examination are needed to detect bone callus of recent origin. Scapular fractures Fracture most commonly occurs transversely through the distal end of the scapular spine (Fig. 10) [8]. The fracture may be comminuted. Comminuted fracture lines commonly extend to the glenoid cavity. Occasional incomplete fracture lines course proximally from the transverse fracture component into the body of the scapula. Periosteal new bone production usually bridges the fracture line as it courses through the spine of the
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Fig. 10. Scapular fractures from two horses. (A) Dried bone specimen. Characteristic fracture configuration includes a transverse component through the distal end of the scapular spine. The fracture commonly extends distally to the glenoid cavity and may have some comminution and incomplete fracture lines that extend proximally from the transverse fracture line. (B) Lateral view of the distal end of the scapular spine illustrates periosteal bone production that bridges the fracture site. (C) Caudal view of the distal end of the scapular spine of a fresh specimen from a different horse illustrates the hyperemic and rough-surfaced nature of the periosteal callus.
scapula. Bone production can be less than 1 mm thick. New bone is highly vascular (red) and has a rough surface. More chronic periosteal bone production manifests as focal enlargement of the abaxial aspect of the spine. Pelvic fractures Pelvic fractures are usually comminuted. Evidence of stress remodeling manifested as periosteal bone production is usually present in a focal region that bridges the fracture line [8]. Bone callus occurs in a variety of locations but, most commonly, on the ilium, particularly adjacent to the sacroiliac joint (Fig. 11). Other locations include the pubis, ischium, broad surface of the ilium, and ilial shaft. Not all stress fracture lesions result in catastrophic fracture. In a survey of pelvises from horses that died for any reason, 28% had evidence of stress remodeling [10]. Tibial fractures Complete catastrophic fractures of the tibia are rare relative to the clinical recognition of tibial stress fractures. Perhaps ease of clinical recognition and appropriate management prevent progression to complete fracture [21,22].
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Fig. 11. Pelvic fracture configurations in three horses. (A) Pelvic diagram viewed from the dorsal aspect. (B) Raised callus on the ventral bone surface bridges the two fractures in the symphyseal parts of the pubis and ischium. (C) Bilateral fractures of the ilium emanate from the region of the sacroiliac joints. (D) Unilateral fracture of one ilium is accompanied by incomplete stress fracture of the contralateral ilium.
Focal periosteal new bone production can be found in numerous locations in fatal fractures (Fig. 12) [8]. The two predominant locations are the proximolateral aspect of the tibia just distal to the level of the head of the fibula and the caudal aspect of the distal aspect of the tibial diaphysis, however. Carpal fractures Fatal carpal bone fractures include comminuted fractures of multiple carpal bones (Fig. 13). Several carpal bones often have foci of articular cartilage degeneration of varying severity located near dorsal margins. Some of these articular lesions have subchondral bone changes that could predispose to marginal osteochondral chip fracture or catastrophic bone fracture. Summary The PMP achieves disease surveillance, discovery of new causes of death, and development of new diagnostic methods for disease detection, and it informs directions for research focused on elucidating the etiopathogenesis
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Fig. 12. Bilateral tibial dried bone specimens from one racehorse. (A) Caudal aspect of bilateral tibia from one horse with bilateral tibial stress fractures and unilateral complete fracture. (B) Nonfractured tibia has a large stress fracture callus (left ellipse), whereas the fractured tibia has periosteal new bone less than 1 mm thick adjacent to the fracture line (right ellipse). (C) Periosteal new bone, less than 1 mm thick, is also located across an incomplete fracture line on the caudal aspect of the diaphysis.
of, and risk factors for, catastrophic fractures [23] and other causes of death. Because most fatal injuries seem to be the acute culmination of a more chronic process, intervention and prevention of injuries is possible with enhanced knowledge of the etiopathogenesis of injuries and risk factors for injuries, and development of management strategies for injury prevention is also possible. It is unclear why the apparent incidence of fatal injuries has increased despite knowledge about the causes and sites of injury and access to improved diagnostic methods and facilities. Perhaps education of trainers, owners, and veterinarians about PMP findings has been inadequate or unsuccessful. Perhaps short-term goals and industry economic issues create circumstances that make it difficult to focus on other goals. The mandates to limit toe-grab height on horseshoes and to install synthetic race surface materials at major California racetracks highlight the commitment that horsemen and the state of California have made to enhancing equine welfare, however. Unfortunately, little is known about incidence rates of injury/illness (other than annual descriptive summaries) relative to the populations of live racehorses in the United States. The population of live horses that the deceased horses come from is difficult to determine for several reasons.
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Fig. 13. Bilateral proximal and distal rows of carpal bones from one racehorse. (A) Left carpus: multiple bones of the proximal and distal carpal bone rows are fractured. (B) Right carpus: third carpal bone has a focal partial-thickness articular cartilage lesion near the dorsal margin. The intermediate carpal bone has articular cartilage fibrillation near the dorsal margin. (C) High-detail radiograph of a sagittal section of the left fractured third carpal bone illustrates the bed for a missing osteochondral chip fracture (upper right corner is missing). (D) Highdetail radiograph of a sagittal section of the right intact third carpal bone illustrates focal subchondral osteoporosis. (E) Microradiograph of the intact carpal bone illustrates intensely remodeling subchondral bone. The darker bone tissue beneath the layer of calcified cartilage reflects newer less mineralized bone material. (F) Remodeled tissue contains large resorption bays. (G) Cracks extend from one resorption bay to another.
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At many racetracks, horse inventory is unknown or information is difficult to retrieve from the information database system. The California racehorse population has been estimated using the number of stalls at racetrack facilities [24]. The pool of horses contributing horses that are transported to a racetrack on the day of race has only been estimated. Turnover of horses through barns has been estimated at approximately 20% of horses every 3 months [14]. The proportion of inactive horses that occupy stalls is unknown. Fortunately, incidence rates per number of starts and number of starters have proved useful in epidemiologic studies. Efforts to implant microchips in horses for identification should allow monitoring of horse movement between racetracks, however, and facilitate monitoring of injury and disease incidences relative to the live horse population.
Acknowledgments Some data were provided by the Jockey Club Information Systems.
References [1] Johnson BJ, Stover SM, Daft BM, et al. Causes of death in racehorses over a 2 year period. Equine Vet J 1994;26:327–30. [2] Estberg L, Stover SM, Gardner IA, et al. Fatal musculoskeletal injuries incurred during racing and training in thoroughbreds. J Am Vet Med Assoc 1996;208:92–6. [3] Tiwary AK, Puschner B, Kinde H, et al. Diagnosis of Taxus (yew) poisoning in a horse. J Vet Diagn Invest 2005;17(3):252–5. [4] Mahakian LM. Lack of immunohistochemical detection of cardiac Troponin C as a biomarker of myocardial necrosis in horses with Nerium oleander poisoning. Davis (CA): Comparative Pathology, University of California; 2003. [5] Daft BM, Barr BC, Gardner IA, et al. Sensitivity and specificity of Western blot testing of cerebrospinal fluid and serum for diagnosis of equine protozoal myeloencephalitis in horses with and without neurologic abnormalities. J Am Vet Med Assoc 2002;221(7):1007–13. [6] Duarte PC, Daft BM, Conrad PA, et al. Comparison of a serum indirect fluorescent antibody test with two Western blot tests for the diagnosis of equine protozoal myeloencephalitis. J Vet Diagn Invest 2003;15(1):8–13. [7] Duarte PC, Daft BM, Conrad PA, et al. Evaluation and comparison of an indirect fluorescent antibody test for detection of antibodies to Sarcocystis neurona, using serum and cerebrospinal fluid of naturally and experimentally infected, and vaccinated horses. J Parasitol 2004;90(2):379–86. [8] Stover SM. Stress fractures. In: White NA, Moore JN, editors. Current techniques in equine surgery and lameness. 2nd edition. Philadelphia: W.B. Saunders Company; 1998. p. 451–9. [9] Stover SM, Johnson BJ, Daft BM, et al. An association between complete and incomplete stress fractures of the humerus in racehorses. Equine Vet J 1992;24:260–3. [10] Haussler KK, Stover SM. Stress fractures of the vertebral lamina and pelvis in Thoroughbred racehorses. Equine Vet J 1998;30:374–81. [11] Hornof WJ, Stover SM, Koblik PD, et al. Oblique views of the ilium and the scintigraphic appearance of stress fractures of the ilium. Equine Vet J 1996;28:355–8. [12] Anthenill LA, Stover SM, Gardner IA, et al. Association between findings on palmarodorsal radiographic images and detection of a fracture in the proximal sesamoid bones of forelimbs obtained from cadavers of racing Thoroughbreds. Am J Vet Res 2006;67(5):858–68.
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[13] Estberg L, Stover SM, Gardner IA, et al. Relationship between race start characteristics and risk of catastrophic injury in thoroughbreds: 78 cases (1992). J Am Vet Med Assoc 1998;212: 544–9. [14] Hill AE, Stover SM, Gardner IA, et al. Risk factors for and outcomes of noncatastrophic suspensory apparatus injury in Thoroughbred racehorses. J Am Vet Med Assoc 2001; 218(7):1136–44. [15] Zekas LJ, Bramlage LR, Embertson RM, et al. Characterisation of the type and location of fractures of the third metacarpal/metatarsal condyles in 135 horses in central Kentucky (1986–1994). Equine Vet J 1999;31(4):304–8. [16] Zekas LJ, Bramlage LR, Embertson RM, et al. Results of treatment of 145 fractures of the third metacarpal/metatarsal condyles in 135 horses (1986–1994). Equine Vet J 1999;31: 309–13. [17] Rick MC, O’Brien TR, Pool RR, et al. Condylar fractures of the third metacarpal bone and third metatarsal bone in 75 horses: radiographic features, treatments, and outcome. J Am Vet Med Assoc 1983;183(3):287–96. [18] Schoenborn WC, Rick MC, Hornof WJ. Computed tomographic appearance of osteochondritis dissecans-like lesions of the proximal articular surface of the proximal phalanx in a horse. Vet Radiol Ultrasound 2002;43(6):541–4. [19] Bassage LH II, Richardson DW. Longitudinal fractures of the condyles of the third metacarpal and metatarsal bones in racehorses: 224 cases (1986–1995). J Am Vet Med Assoc 1998; 212:1757–64. [20] Richardson DW. Medial condylar fractures of the third metatarsal bone in horses. J Am Vet Med Assoc 1984;185(7):761–5. [21] O’Sullivan CB, Lumsden JM. Stress fractures of the tibia and humerus in Thoroughbred racehorses: 99 cases (1992–2000). J Am Vet Med Assoc 2003;222:491–8. [22] Ruggles AJ, Moore RM, Bertone AL, et al. Tibial stress fractures in racing standardbreds: 13 cases (1989–1993). J Am Vet Med Assoc 1996;209(3):634–7. [23] Stover SM. The epidemiology of Thoroughbred racehorse injuries. Clinical Techniques in Equine Practice 2003;2(4):312–22. [24] Hill AE, Carpenter TE, Gardner IA, et al. Evaluation of a stochastic Markov-chain model for the development of forelimb injuries in Thoroughbred racehorses. Am J Vet Res 2003; 64(3):328–37.