EQUINE VETERINARY JOURNAL
318
Equine ver. J. (1992) 24 (4) 3 18-320
Ultrasonographical and pathological studies of equine superficial digital flexor tendons; initial observations, including tissue characterisation by analysis of image grey scale, in a Thoroughbred gelding R. G. NICOLLt, A. K. W. WOOD* and T. L. W. ROTHWELL Departments of Veterinary Pathology and 'Veterinary Clinical Sciences, University of Sydney, N. S. W. 2006, Australia.
Introduction
THE value of ultrasonography in determining the location, extent and nature of tendon and ligament injuries in the horse is well established (Genovese and Simpson 1989). Even small, non-palpable lesions can be detected (Rantanen, Hauser and Genovese 1985). Injuries lead to structural changes with resultant alterations in the acoustic properties of tendons and ligaments which can be shown ultrasonographically. Little attention has been given, however, to correlating the ultrasonographical changes in naturally occurring injured tendons with their histological appearance. No previous studies have been found of the use of ultrasonographical tissue characterisation techniques to quantify the increase in echogenicity as an injured tendon or ligament heals. In this report details are given of the correlations that were established between the ultrasonographic images of an injury to a superficial digital flexor tendon (SDFT), that occurred during racing, and its histopathological appearance. Results are also presented of the quantification of early tendon healing by the use of changes in ultrasonographical mean grey scale (MGS). Materials and methods
Twelve months before presentation, a six-year-old Thoroughbred gelding strained the SDFT in its right foreleg. After nine months rest the horse returned to racing but restrained the tendon in its third race. Subsequently, during a period of stall rest, dorsal (Dyce, Sack and Wensing 1987; 5.0 MHz phased array transducer: PSE-SOH, Toshiba Corporation, Japan) and sagittal (7.5 MHz linear array transducer: PLE-705S, Toshiba Corporation, Japan) ultrasonographical images of the flexor tendons and ligaments of both metacarpal regions were made weekly over six weeks, starting two weeks after the reinjury of the tendon. Images were made 10, 15, 20 and 25 cm distal to the mid-length of the palmar border of the accessory carpal bone and also at sites of pathological change. The MGS of each SDFT was recorded at each level in each plane; additional recordings were made in the dorsal plane of the MGS of the injured portion of the tendon alone. The 'track-ball' function of the ultrasonographical machine was used to trace the boundaries of the region of interest from which image MGS was recorded. There were 64 shades in the grey scale of the image, tPresent address: Bathurst Veterinary Clinic, 90 Rankin Street, Bathurst, NSW 2795, Australia.
from 0 (black) to 63 (white). Constant imaging parameters (time gain compensation, gain, contrast, brightness, and dynamic range) were used. An analysis of covariance of MGS using the normal tendon as covariate was performed on the array of data. The variance associated with time was partitioned using standard sets of orthogonal polynomials to investigate the rate of change in the echogenicity of the healing tendon. Following each set of clinical observations, additional images were made with each transducer of an ultrasonographical phantom (Nicoll 1989). The phantom had an MGS similar to that of normal equine tendons and ligaments. An analysis of variance of the phantom MGS recorded over time, using machine sampling variance as the error term, showed no significant variations in MGS (Nicoll 1989). At the completion of the ultrasonographic studies, the horse was killed and the flexor tendons and ligaments of each metacarpal region were examined histopathologically.
Results In the initial dorsal ultrasonographical images, the injured SDFT was grossly thickened over 15 cm of its length and contained an extensive hypoechoic core, which involved more than 50% of its total cross-sectional area (Fig la). In images made in the sagittal plane, thickening of the SDFT was also evident and the injured region of the tendon showed a predominantly granular, hypoechoic pattern with occasional, localised, anechoic areas. Over time, in the dorsal images there were increasing numbers of echogenic foci within the core lesion, which gave the damaged area a mottled, variable echogenicity (Fib 1b). In the sagittal plane, the damaged SDFT remained thickened and hypoechoic with a granular sonographic texture. Anechoic foci were present in all but the proximal levels of the injury and there was a return of linear echoes, particularly proximally and distally. No ultrasonographical abnormalities were detected in the other tendons and ligaments of the right and left forelegs. The analysis of covariance showed significant increases over time in the echogenicity of the injured SDFT in both the dorsal (P < 0.001, Fig 2) and sagittal (P < 0.01) planes as well as in the lesion alone in the dorsal plane (P c 0.0003; Fig 2). The echogenicity of the injured SDFT increased progressively during the period of observation (linear component; P < 0.01) but the greatest rate of increase in echogenicity lay between observations made at the fourth and fifth week after injury (cubic component; P < 0.02). Over time, in the dorsal plane, but not the sagittal, there was also a significant increase (P < 0.001)
EQUINE VETERINARY JOURNAL
319
E E20
m
NormalSDFf
+ Injured S D F f - entire tendon * Injured SDFT - lesion only
2
3
4
5
6
7
Weeks post-injury Fig 2: Mean grey scale values (+I- standard error) obtained afier pooling data from recordings made in the dorsal plane in normal and strained superficial digital flexor tendons (SDFT) of a Thoroughbred gelding. The mean grey scale values for the injured tendon have been corrected hy covariance to take account of the temporal variations in the normal tendon. The graphs demonstrate the significant difference in echogenicity hemeen the injured and normal tendons.
Histologically the injured tendon was hypercellular and hypervascular. The endotendon had proliferated and the tendon contained hypercellular tracts with fibroblasts (which had variably staining nuclei that were shorter and rounder than normal), capillary buds, and focal haemorrhages. The other flexor tendons and ligaments were grossly and histologically normal. Discussion
In this study the ultrasonographical observations of the injured
SDFT correlated well with the histopathological findings. The
Fig I : Dorsal ultrasonographicalimages of the palmar aspect of the right metncarpus of a 6-year-old Thoroughhred gelding. The images were made 10 cm distal to the mid-point of the palmar border of the accessory carpal bone. 2 weeks (a) and 7 weeks (h) after the superficial digital flexor tendon (SDFT) was strained. The SDFT is thickened and its medial and central parts contain multiple hypoechoic areas. Using a statistical package provided with the ultrasonographical equipment, regions of interest have heen traced around the entire SDFT and around the core lesion within the tendon. Histograms of the grey scalesfor each region are displayed across the bottom of the figure. Note that there has been an increase in the echogenicity of the lesion in the image made 7 weeks afrer injury; this subjective assessment is supported hy the objective increase in mean grey scale of hoth the entire tendon and its lesion. Key: MED = medial; X = stand-off attachment; S = SDFT; CHI = histogram of grey scale of entire SDFT; CH2 = histogram of grey scale of lesion within SDFT; MAX = % grey scale recordings at maximum value; M = mean grey scale; SD = standard deviation; N = numher of pixels within region of interest; D = deep digital flexor tendon; A = accessory ligament of deep digital flexor muscle; L = suspensory ligament
in the echogenicity of the uninjured tendon. At necropsy, the damaged area of the SDFT had a gelatinous nature, was red-orange in colour and contained fresh haemorrhagic foci among bundles of tendon fibres which frequently deviated from their normal parallel course.
disrupted bundles of tendon fibres, which acted as diffuse rather than specular reflectors, the fibroblast-containing hypercellular tracts, and the occasional fresh haemorrhagic foci, all contributed to the observed hypoechogenic areas in the tendon. During the 6-week period of observation the injured SDFT was at the early maturation phase of tendon healing. The progressive increase in tendon echogenicity was related to (a) a gradual reorientation of the bundle\ of tendon fibres along the lines of stress of the tendon (Strombere 1971: Silver eta1 1983) so that the re-orientated 'bundles ;ow acted as s p e d & reflectors, (b) an increase in the acoustic density of the tendon fibre bundles (due to an increase in the number of intramolecular and intermolecular linkages in the collagen fibres (Silver et a1 1983) and (c) a decrease in the number of fibroblasts (Silver et af 1983). Other ultrasonographic reports of the extent of tendon and ligament injuries have been based on a qualitative assessment of their echogenicity; four types of lesions were described (Genovese, Rantanen, Hauser and Simpson 1986). A more detailed method of determining the severity of a tendon or ligament injury and the prognosis for repair was suggested by Reef, Martin and Elser (1988). They proposed that recordings be made of the percentage cross-sectional area that was damaged in the tendon or ligament, the length of the lesion, and whether the origin or insertion of the tendon or ligament was involved. In a later study, Genovese, Rantanen, Simpson and Simpson (1 990) recorded the percentage cross-sectional area of the damaged part of SDFTs and multiplied them firstly by the qualitative assessment (Genovese et af 1986) and then by a scaling factor of 0.025. The resultant 'severity rating' was used to provide information on the extent of tendon injury and to give a prognosis for satisfactory return to racing. As shown in this study, the accuracy of the ultrasonographical examination could be further increased by including a quantitative, rather
EQUINE VETERINARY JOURNAL
320
than a qualitative measurement of tendon or ligament echogenicity or MGS. In the analysis of covariance the uninjured normal tendon served as a control and the analysis took account of any temporal variations in the uninjured tendon. Thus, although based on a single horse, the MGS findings provided unequivocal evidence of an increase over time in the echogenicity of the injured tendon that was related to healing of the tendon and not to simple day-to-day variations in the amount of tissue fluid in the tendon or paratendonous tissues. Should uninterrupted healing occur, it would be expected that the echogenicity of the injured tendon would progressively increase until it is of the same order as that of the uninjured tendon. Such tissue characterization by MGS recordings could thus be used to assess tendon or ligament healing objectively and to provide information about the efficacy of different treatment regimens.
Acknowlegements We thank the Selby Scientific Foundation for financial support; Dr Michael Robinson, Dr Dean Hendrickson, Dr Peter Knight, Beverley Horsburgh, Karen Wadwell, Peter Stevens and Roman Vekselstein for assistance and Dr Ian Martin for the analysis of covariance.
References Dyce. K.M.. Sack, W.O. and Wensing. C.J.G. (1987) Textbook of Veterinary Anatomy, W. B. Saunders. Philadelphia, p 3. Genovese. R.L., Rantanen. N.W.. Hauser. M.L. and Simpson, B.S. (1986) Diagnostic ultrasonopphy of equine limbs. Ver. Clinics N.Am.: Equine Pracr. 2. 145-226. Genovese. R.L.. Rantanen. N.W.. Simpson. B.S. and Simpson. D M. (1990) Clinical experience with quantitative analysis of superficial digital flexor tendon injuries in thoroughbred and standardbred racehorses. Raceback Practice. Ver. Clinics N.Am.: Equine Pracr. 6. 129-145. Genovese. R.L. and Simpson, B.S. (1989) Diagnostic ultrasound. In: Equine Sporrs Medicine. Ed. W. E.Jones. Lea and Febiger, Philadelphia. pp 231-241. Nicoll. R.G. (1989) Ultrasonographic studies of the equine memarpus. Bachelor of Science (Veterinary)thesis, University of Sydney. NSW, Australia. Rantanen, N.W.. Hauser, M.L. and Genovese. R.L. (1985) Superficial digital flexor tendinitis: diagnosis using real-time ultrasound imaging. J. equine ver. Sci. 5. 115-119. Reef, V.B., Martin, B.B. and Elser. A. (1988) Types of tendon and ligament injuries detected with diagnostic ultrasound: description and follow-up. Prm. Am. Ass. Equine Pracnoners34. pp 245-248. Silver. LA., Brown. P.N.. Goodship, A.E., Lanyon. L.E..McCullagh, K.G..Perry, G.C. and Williams. I.F. (1983) A clinical and experimental study of tendon injury. healing and treatment in the horse. Equine vet. J., Suppl. 1. 1-43, Smmberx. B. (1971) The normal and diseased suoerficial flexor tendon in race6m.s. A mobhologic and physiologic investigation. Acta radio/.. Suppl. Jo5. 1-94.
Receivedfor publication: 8.1.91 Accepted: 8.11.91
THE THIRD INTERNATIONAL FARRIERY AND LAMENESS SEMINAR
-
ROBINSON COLLEGE CAMBRIDGE ENGLAFID ~ T H 9m AUGUST 1992 Sponsored by Newmarket Farriers' Association In 1990 the Second International Farriery and Lameness Seminar attracted 150 Faniers and Vets from 1 0 countries around the world. This year we have decided to move to Robinson College, Cambridge. Robinson College has state of the art facilities set in tranquil gardens. The format for the seminar will follow previous years; two days of lectures with published papers, discussion periods, trade stands and social events. Topics to be covered: 0 The use o f wedge heels in cases o f FTD 0 The use of lateral extension shoes on mature horses 0 Bone scanning in lameness diagnosis 0 Significant prognostic parameters in equine laminitis 0 Hoofcracks - causes and repair 0 Shoeing for gait and conformation. What are our limitations? 0 Effects upon hoofgrowth 0 Pathological anatomical changes in acute and chronic founder/clinical management of
resected cases 0 Repairing coronary band lesions and hoofwall avulsions Our speakem include:
T. F. M. Head, WCP J. Ferrie, FWCP R. Eustace, MRCVS
Dr. K. D. Butler, FWCP R. F. Redden, DVM
T. Ryan, FWCP Dr. C. M. McQregor, R. Pilswotth, MRCVS
MRCVS
For more infbmationcontact: Beverley C W s , 6 ZUmpike Rd., Red Lodge, Bury St. Edmunds, SukTolk, England lP28 8JZ. Telephone: 0638 750522
318
Equine ver. J. (1992) 24 (4) 3 18-320
Ultrasonographical and pathological studies of equine superficial digital flexor tendons; initial observations, including tissue characterisation by analysis of image grey scale, in a Thoroughbred gelding R. G. NICOLLt, A. K. W. WOOD* and T. L. W. ROTHWELL Departments of Veterinary Pathology and 'Veterinary Clinical Sciences, University of Sydney, N. S. W. 2006, Australia.
Introduction
THE value of ultrasonography in determining the location, extent and nature of tendon and ligament injuries in the horse is well established (Genovese and Simpson 1989). Even small, non-palpable lesions can be detected (Rantanen, Hauser and Genovese 1985). Injuries lead to structural changes with resultant alterations in the acoustic properties of tendons and ligaments which can be shown ultrasonographically. Little attention has been given, however, to correlating the ultrasonographical changes in naturally occurring injured tendons with their histological appearance. No previous studies have been found of the use of ultrasonographical tissue characterisation techniques to quantify the increase in echogenicity as an injured tendon or ligament heals. In this report details are given of the correlations that were established between the ultrasonographic images of an injury to a superficial digital flexor tendon (SDFT), that occurred during racing, and its histopathological appearance. Results are also presented of the quantification of early tendon healing by the use of changes in ultrasonographical mean grey scale (MGS). Materials and methods
Twelve months before presentation, a six-year-old Thoroughbred gelding strained the SDFT in its right foreleg. After nine months rest the horse returned to racing but restrained the tendon in its third race. Subsequently, during a period of stall rest, dorsal (Dyce, Sack and Wensing 1987; 5.0 MHz phased array transducer: PSE-SOH, Toshiba Corporation, Japan) and sagittal (7.5 MHz linear array transducer: PLE-705S, Toshiba Corporation, Japan) ultrasonographical images of the flexor tendons and ligaments of both metacarpal regions were made weekly over six weeks, starting two weeks after the reinjury of the tendon. Images were made 10, 15, 20 and 25 cm distal to the mid-length of the palmar border of the accessory carpal bone and also at sites of pathological change. The MGS of each SDFT was recorded at each level in each plane; additional recordings were made in the dorsal plane of the MGS of the injured portion of the tendon alone. The 'track-ball' function of the ultrasonographical machine was used to trace the boundaries of the region of interest from which image MGS was recorded. There were 64 shades in the grey scale of the image, tPresent address: Bathurst Veterinary Clinic, 90 Rankin Street, Bathurst, NSW 2795, Australia.
from 0 (black) to 63 (white). Constant imaging parameters (time gain compensation, gain, contrast, brightness, and dynamic range) were used. An analysis of covariance of MGS using the normal tendon as covariate was performed on the array of data. The variance associated with time was partitioned using standard sets of orthogonal polynomials to investigate the rate of change in the echogenicity of the healing tendon. Following each set of clinical observations, additional images were made with each transducer of an ultrasonographical phantom (Nicoll 1989). The phantom had an MGS similar to that of normal equine tendons and ligaments. An analysis of variance of the phantom MGS recorded over time, using machine sampling variance as the error term, showed no significant variations in MGS (Nicoll 1989). At the completion of the ultrasonographic studies, the horse was killed and the flexor tendons and ligaments of each metacarpal region were examined histopathologically.
Results In the initial dorsal ultrasonographical images, the injured SDFT was grossly thickened over 15 cm of its length and contained an extensive hypoechoic core, which involved more than 50% of its total cross-sectional area (Fig la). In images made in the sagittal plane, thickening of the SDFT was also evident and the injured region of the tendon showed a predominantly granular, hypoechoic pattern with occasional, localised, anechoic areas. Over time, in the dorsal images there were increasing numbers of echogenic foci within the core lesion, which gave the damaged area a mottled, variable echogenicity (Fib 1b). In the sagittal plane, the damaged SDFT remained thickened and hypoechoic with a granular sonographic texture. Anechoic foci were present in all but the proximal levels of the injury and there was a return of linear echoes, particularly proximally and distally. No ultrasonographical abnormalities were detected in the other tendons and ligaments of the right and left forelegs. The analysis of covariance showed significant increases over time in the echogenicity of the injured SDFT in both the dorsal (P < 0.001, Fig 2) and sagittal (P < 0.01) planes as well as in the lesion alone in the dorsal plane (P c 0.0003; Fig 2). The echogenicity of the injured SDFT increased progressively during the period of observation (linear component; P < 0.01) but the greatest rate of increase in echogenicity lay between observations made at the fourth and fifth week after injury (cubic component; P < 0.02). Over time, in the dorsal plane, but not the sagittal, there was also a significant increase (P < 0.001)
EQUINE VETERINARY JOURNAL
319
E E20
m
NormalSDFf
+ Injured S D F f - entire tendon * Injured SDFT - lesion only
2
3
4
5
6
7
Weeks post-injury Fig 2: Mean grey scale values (+I- standard error) obtained afier pooling data from recordings made in the dorsal plane in normal and strained superficial digital flexor tendons (SDFT) of a Thoroughbred gelding. The mean grey scale values for the injured tendon have been corrected hy covariance to take account of the temporal variations in the normal tendon. The graphs demonstrate the significant difference in echogenicity hemeen the injured and normal tendons.
Histologically the injured tendon was hypercellular and hypervascular. The endotendon had proliferated and the tendon contained hypercellular tracts with fibroblasts (which had variably staining nuclei that were shorter and rounder than normal), capillary buds, and focal haemorrhages. The other flexor tendons and ligaments were grossly and histologically normal. Discussion
In this study the ultrasonographical observations of the injured
SDFT correlated well with the histopathological findings. The
Fig I : Dorsal ultrasonographicalimages of the palmar aspect of the right metncarpus of a 6-year-old Thoroughhred gelding. The images were made 10 cm distal to the mid-point of the palmar border of the accessory carpal bone. 2 weeks (a) and 7 weeks (h) after the superficial digital flexor tendon (SDFT) was strained. The SDFT is thickened and its medial and central parts contain multiple hypoechoic areas. Using a statistical package provided with the ultrasonographical equipment, regions of interest have heen traced around the entire SDFT and around the core lesion within the tendon. Histograms of the grey scalesfor each region are displayed across the bottom of the figure. Note that there has been an increase in the echogenicity of the lesion in the image made 7 weeks afrer injury; this subjective assessment is supported hy the objective increase in mean grey scale of hoth the entire tendon and its lesion. Key: MED = medial; X = stand-off attachment; S = SDFT; CHI = histogram of grey scale of entire SDFT; CH2 = histogram of grey scale of lesion within SDFT; MAX = % grey scale recordings at maximum value; M = mean grey scale; SD = standard deviation; N = numher of pixels within region of interest; D = deep digital flexor tendon; A = accessory ligament of deep digital flexor muscle; L = suspensory ligament
in the echogenicity of the uninjured tendon. At necropsy, the damaged area of the SDFT had a gelatinous nature, was red-orange in colour and contained fresh haemorrhagic foci among bundles of tendon fibres which frequently deviated from their normal parallel course.
disrupted bundles of tendon fibres, which acted as diffuse rather than specular reflectors, the fibroblast-containing hypercellular tracts, and the occasional fresh haemorrhagic foci, all contributed to the observed hypoechogenic areas in the tendon. During the 6-week period of observation the injured SDFT was at the early maturation phase of tendon healing. The progressive increase in tendon echogenicity was related to (a) a gradual reorientation of the bundle\ of tendon fibres along the lines of stress of the tendon (Strombere 1971: Silver eta1 1983) so that the re-orientated 'bundles ;ow acted as s p e d & reflectors, (b) an increase in the acoustic density of the tendon fibre bundles (due to an increase in the number of intramolecular and intermolecular linkages in the collagen fibres (Silver et a1 1983) and (c) a decrease in the number of fibroblasts (Silver et af 1983). Other ultrasonographic reports of the extent of tendon and ligament injuries have been based on a qualitative assessment of their echogenicity; four types of lesions were described (Genovese, Rantanen, Hauser and Simpson 1986). A more detailed method of determining the severity of a tendon or ligament injury and the prognosis for repair was suggested by Reef, Martin and Elser (1988). They proposed that recordings be made of the percentage cross-sectional area that was damaged in the tendon or ligament, the length of the lesion, and whether the origin or insertion of the tendon or ligament was involved. In a later study, Genovese, Rantanen, Simpson and Simpson (1 990) recorded the percentage cross-sectional area of the damaged part of SDFTs and multiplied them firstly by the qualitative assessment (Genovese et af 1986) and then by a scaling factor of 0.025. The resultant 'severity rating' was used to provide information on the extent of tendon injury and to give a prognosis for satisfactory return to racing. As shown in this study, the accuracy of the ultrasonographical examination could be further increased by including a quantitative, rather
EQUINE VETERINARY JOURNAL
320
than a qualitative measurement of tendon or ligament echogenicity or MGS. In the analysis of covariance the uninjured normal tendon served as a control and the analysis took account of any temporal variations in the uninjured tendon. Thus, although based on a single horse, the MGS findings provided unequivocal evidence of an increase over time in the echogenicity of the injured tendon that was related to healing of the tendon and not to simple day-to-day variations in the amount of tissue fluid in the tendon or paratendonous tissues. Should uninterrupted healing occur, it would be expected that the echogenicity of the injured tendon would progressively increase until it is of the same order as that of the uninjured tendon. Such tissue characterization by MGS recordings could thus be used to assess tendon or ligament healing objectively and to provide information about the efficacy of different treatment regimens.
Acknowlegements We thank the Selby Scientific Foundation for financial support; Dr Michael Robinson, Dr Dean Hendrickson, Dr Peter Knight, Beverley Horsburgh, Karen Wadwell, Peter Stevens and Roman Vekselstein for assistance and Dr Ian Martin for the analysis of covariance.
References Dyce. K.M.. Sack, W.O. and Wensing. C.J.G. (1987) Textbook of Veterinary Anatomy, W. B. Saunders. Philadelphia, p 3. Genovese. R.L., Rantanen. N.W.. Hauser. M.L. and Simpson, B.S. (1986) Diagnostic ultrasonopphy of equine limbs. Ver. Clinics N.Am.: Equine Pracr. 2. 145-226. Genovese. R.L.. Rantanen. N.W.. Simpson. B.S. and Simpson. D M. (1990) Clinical experience with quantitative analysis of superficial digital flexor tendon injuries in thoroughbred and standardbred racehorses. Raceback Practice. Ver. Clinics N.Am.: Equine Pracr. 6. 129-145. Genovese. R.L. and Simpson, B.S. (1989) Diagnostic ultrasound. In: Equine Sporrs Medicine. Ed. W. E.Jones. Lea and Febiger, Philadelphia. pp 231-241. Nicoll. R.G. (1989) Ultrasonographic studies of the equine memarpus. Bachelor of Science (Veterinary)thesis, University of Sydney. NSW, Australia. Rantanen, N.W.. Hauser, M.L. and Genovese. R.L. (1985) Superficial digital flexor tendinitis: diagnosis using real-time ultrasound imaging. J. equine ver. Sci. 5. 115-119. Reef, V.B., Martin, B.B. and Elser. A. (1988) Types of tendon and ligament injuries detected with diagnostic ultrasound: description and follow-up. Prm. Am. Ass. Equine Pracnoners34. pp 245-248. Silver. LA., Brown. P.N.. Goodship, A.E., Lanyon. L.E..McCullagh, K.G..Perry, G.C. and Williams. I.F. (1983) A clinical and experimental study of tendon injury. healing and treatment in the horse. Equine vet. J., Suppl. 1. 1-43, Smmberx. B. (1971) The normal and diseased suoerficial flexor tendon in race6m.s. A mobhologic and physiologic investigation. Acta radio/.. Suppl. Jo5. 1-94.
Receivedfor publication: 8.1.91 Accepted: 8.11.91
THE THIRD INTERNATIONAL FARRIERY AND LAMENESS SEMINAR
-
ROBINSON COLLEGE CAMBRIDGE ENGLAFID ~ T H 9m AUGUST 1992 Sponsored by Newmarket Farriers' Association In 1990 the Second International Farriery and Lameness Seminar attracted 150 Faniers and Vets from 1 0 countries around the world. This year we have decided to move to Robinson College, Cambridge. Robinson College has state of the art facilities set in tranquil gardens. The format for the seminar will follow previous years; two days of lectures with published papers, discussion periods, trade stands and social events. Topics to be covered: 0 The use o f wedge heels in cases o f FTD 0 The use of lateral extension shoes on mature horses 0 Bone scanning in lameness diagnosis 0 Significant prognostic parameters in equine laminitis 0 Hoofcracks - causes and repair 0 Shoeing for gait and conformation. What are our limitations? 0 Effects upon hoofgrowth 0 Pathological anatomical changes in acute and chronic founder/clinical management of
resected cases 0 Repairing coronary band lesions and hoofwall avulsions Our speakem include:
T. F. M. Head, WCP J. Ferrie, FWCP R. Eustace, MRCVS
Dr. K. D. Butler, FWCP R. F. Redden, DVM
T. Ryan, FWCP Dr. C. M. McQregor, R. Pilswotth, MRCVS
MRCVS
For more infbmationcontact: Beverley C W s , 6 ZUmpike Rd., Red Lodge, Bury St. Edmunds, SukTolk, England lP28 8JZ. Telephone: 0638 750522
