Teknik Operasi Cruciate Ligament Pada Hewan - Ilmu Bedah Khusus Veteriner [PDF]

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ILMU BEDAH KHUSUS VETERINER TEKNIK OPERASI CRUCIATE LIGAMENT



Disusun Oleh: KELOMPOK 4 KELAS B 1. KOMANG AYU TRIANA SANJIWANI 1809511049 2. FERDY OLGA SAPUTRA



1809511050



3. M. FARHAN AL MA’ARIF



1809511051



FAKULTAS KEDOKTERAN HEWAN UNIVERSITAS UDAYANA DENPASAR 2021



KATA PENGANTAR Puji syukur kami panjatkan ke hadirat Tuhan Yang Maha Esa, karena atas rahmat dan kasih karunia-Nya, kami dapat menyelesaikan paper yang berjudul “Teknik Operasi Cruciate Ligament” ini dengan baik. Tulisan ini dibuat bertujuan untuk menyelesaikan tugas dari mata kuliah Ilmu Bedah Khusus Veteriner dan menambah ilmu pengetahuan dan wawasan bagi para pembacanya. Tak lupa kami juga mengucapkan banyak terima kasih kepada pihak-pihak yang telah membantu dalam pembuatan tulisan ini, sehingga tulisan ini dapat selesai dengan baik dan tepat pada waktunya. Kami sadar, bahwa tulisan ini masih jauh dari kata sempurna, untuk itu kami sebagai penulis menerima dengan lapang dada segala bentuk kritik dan saran yang bersifat membangun. Nantinya semua kritik dan saran yang diberikan tersebut akan kami gunakan sebagai pedoman dan acuan dalam pembuatan tulisan kedepannya. Kami berharap semoga tulisan ini dapat memberikan manfaat dan dapat menambah wawasan bagi para pembacanya. Sekali lagi, kami ucapkan banyak terima kasih.



Denpasar, 11 November 2021



Penulis



ii



DAFTAR ISI HALAMAN JUDUL .................................................................................................................. i KATA PENGANTAR ............................................................................................................... ii DAFTAR ISI............................................................................................................................. iii DAFTAR GAMBAR ................................................................................................................ iii BAB I PENDAHULUAN .......................................................................................................... 1 1.1 Latar Belakang .................................................................................................................... 1 1.2 Rumusan Masalah ............................................................................................................... 1 1.3 Tujuan Penulisan ................................................................................................................. 1 1.4 Manfaat Penulisan ............................................................................................................... 2 BAB II TINJAUAN PUSTAKA ............................................................................................... 3 2.1 Terminologi......................................................................................................................... 3 2.2 Indikasi ................................................................................................................................ 3 2.3 Anestesi ............................................................................................................................... 3 2.4 Manajemen Praoperasi ........................................................................................................ 4 2.5 Teknik Operasi .................................................................................................................... 5 2.6 Manajemen Pascaoperasi .................................................................................................. 13 BAB III PENUTUP ................................................................................................................. 15 3.1 Kesimpulan ....................................................................................................................... 15 3.2 Saran ................................................................................................................................. 15 DAFTAR PUSTAKA .............................................................................................................. 16



iii



DAFTAR GAMBAR Gambar 1. Arthrotomy dengan pendekatan lateral .................................................................. 5 Gambar 2. Arthrotomy dengan pendekatan medial ................................................................. 6 Gambar 3. Rekonstruksi ekstrakapsular menggunakan benang yang berat dan nonabsorbable .................................................................................................................................................... 7 Gambar 4. Rekonstruksi ekstrakapsular menggunakan benang yang berat dan nonabsorbable yang ditambatkan pada sekrup tulang. ....................................................................................... 7 Gambar 5. Teknik operasi ligamentum crucriate dengan metode Tibial Tuberosity Advancement (TTA). ........................................................................................................................................ 9 Gambar 6. Teknik operasi ligamentum crucriate dengan metode Tightrope CCL (TR). .......... 11 Gambar 7. Pendekatan medial ke tibia proksimal ..................................................................... 12 Gambar 8. Teknik operasi ligamentum crucriate dengan metode Tibial Plateau Leveling Osteotomy (TPLO). ................................................................................................................... 12



iv



BAB I PENDAHULUAN 1.1 Latar Belakang Perkembangan teknologi telah berkembang pesat dalam bidang kedokteran hewan terutama dalam bidang bedah. Salah satu jenis pembedahan yang mengalami perkembangan dilakukan adalah pembedahan sisterm persendian karena menjadi salah satu titik kerawanan untuk terjadinya kelainan pada proses pergerakan hewan seperti anjing ras besar. Salah satu pembedahan pada sistem persendian adalah pembedahan ligamen. Ligamen sendiri merupakan jaringan-jaringan keras yang menghubungkan satu tulang dengan tulang lainnya. Cruciate ligament adalah ligamentum (pengikat) yang terdapat pada persendian lutut (stifle joint). Cruciate ligament terletak di tengah sendi lutut dan menghubungkan femur dengan tibia. Ada 2 jenis cruciate ligament, yaitu cruciate ligament bagian depan (cranial) dan cruciate ligament bagian belakang (caudal). Kedua cruciate ligament tersebut terletak di dalam persendian lutut, diantara tulang paha (femur) dan tulang kering (tibia). Salah satu pembedahan pada sistem persendian adalah Cruciat Ligament. Putusnya cruciate ligament menyebabkan persendian lutut menjadi tidak stabil dan tulang femur maupun tibia bisa bergerak ke depan dan ke belakang (drawer movement), sehingga menimbulkan rasa sakit. Ruptur tersebut dapat berlanjut menjadi pembengkakan persendian (arthritis) dan mengecilnya (atropi) otot quadriceps. 1.2 Rumusan Masalah 1.



Apa yang dimaksud dengan cruciate ligament?



2.



Apa saja indikasi dilakukannya operasi cruciate ligament?



3.



Bagaimana anestesi pada teknik operasi cruciate ligament?



4.



Bagaimana manajemen praoperasi cruciate ligament?



5.



Bagaimana teknik operasi cruciate ligament?



6.



Bagaimana manajemen pascaoperasi cruciate ligament?



1.3 Tujuan Penulisan 1.



Untuk mengetahui apa yang dimaksud dengan cruciate ligament.



2.



Untuk mengetahui indikasi dilakukannya operasi cruciate ligament.



3.



Untuk mengetahui bagaimana anestesi pada teknik operasi cruciate ligament.



4.



Untuk mengetahui bagaimana manajemen praoperasi cruciate ligament.



5.



Untuk mengetahui bagaimana teknik operasi cruciate ligament.



6.



Untuk mengetahui bagaimana manajemen pascaoperasi cruciate ligament. 1



1.4 Manfaat Penulisan Adapun manfaat dari penulisan paper ini ialah agar dapat bermanfaat bagi pembaca khususnya mahasiswa fakultas kedokteran hewan dan dapat memahami mengenai Teknik operasi cruciate ligament, beserta indikasi dilakukannya operasi tersebut. Selain itu diharapkan dapat menjadi referensi untuk penulisan selanjutnya.



2



BAB II TINJAUAN PUSTAKA 2.1 Terminologi Cruciate Ligament adalah ligamentum (pengikat) yang terdapat pada persendian lutut (stifle joint), merupakan jaringan fibrosa kuat yang menghubungkan femur distal ke tibia proximal. Ada 2 buah cruciate ligament, yaitu: cruciate ligament bagian depan (cranial) dan cruciate ligament bagian belakang (caudal). Kedua cruciate ligament tersebut terletak di dalam persendian lutut, diantara tulang paha (femur) dan tulang kering (tibia). Ligamen ini bekerja seperti engsel di lutut dan bertanggung jawab untuk menyediakan kestabilan anterior-posterior sendi lutut. Pecahnya ligamen cruciatum kranial jarang terjadi pada kucing. Ini sering terjadi pada anjing yang kelebihan berat badan, paruh baya dan lebih tua. Trah anjing tertentu tampaknya cenderung mengalami rupture ligament cranialis. Umumnya dialami oleh breed cocker spaniel, rottweiler, miniature, toy poodle, Lhasa apso, bichon frise, golden retriever, labrador retriever, German shepherd, dan mastiff 2.2 Indikasi Beberapa indikator yang memungkinkan untuk dilakukannya operasi setelah hewan mengalami pecahnya ligamen cruciatum yaitu: 1.



Hewan mengalami kesulitan berdiri



2.



Hewan mengalami kesulitan melompat



3.



Penurunan tingkat aktivitas



4.



Kepincangan atau pincang (tingkat keparahan bervariasi)



5.



Atrofi otot (penurunan massa otot di kaki yang terkena)



6.



Penurunan rentang gerak pada sendi lutut



7.



Suara letupan (yang mungkin juga menunjukkan robekan meniscal)



8.



Pembengkakan di bagian dalam tulang kering



2.3



Anestesi Terlebih dahulu dilakukan premedikasi yang digunakan yaitu Atropin sulfat 0,025%



dengan dosis (0,02 - 0,04 ml/kg BB) secara subkutan. Untuk anastesi digunakan kombinasi Xylazine 2% dosis 2 ml/kg BB dengan Ketamin HCL 10% dosis 15 mg/kg BB yang diberikan secara intramuskuler pada hewan kecil. Dan dilakukan maintenance dengan anestesi inhalasi



3



seperti isoflurane atau sevoflurane (2% - 3%) dalam oksigen. Pemberian Cefazolin sodium (20 mg/kg BB, IV) diberikan kepada anjing beberapa menit sebelum operasi. 2.4 Manajemen Praoperasi • Persiapan Alat dan Bahan Sebelum tindakan operasi dilakukan, sangat penting untuk mempersiapkan alat dan bahan yang diperlukan selama proses pembedahan. Meja operasi harus dibersihkan dan disterilkan. Alat-alat operasi dipersiapkan dalam keadaan steril dan diletakkan pada meja yang berdekatan dengan meja operasi. Alat-alat yang disiapkan adalah stetoskop, termometer, alat pencukur rambut, instrument pembedahan standar, jarum, tampon, kain drape, scalpel. Sedangkan bahan-bahan yang hams disiapkan yaitu benang nilon, benang jahit absorbable, alcohol 70%, yodium tincture dan anastesi. • Persiapan Ruang Operasi Persiapan ruang operasi meliputi ruang operasi harus bersih, lantai dan meja operasi hendaknya dibersihkan dan didesinfeksi, ruang operasi barns memiliki penerangan yang cukup baik. • Persiapan Hewan Persiapan hewan/pasien sebelum operasi berlangsung sebaiknya dilakukan terlebih dahulu pengecekan anamnesa dilakukan untuk mengetahui bagian rufturnya cruciate ligament, penyebab, kapan terjadinya sehingga dapat membantu diagnosis. Pemeriksaan fisik hewan juga perlu dilakukan, pemeriksaan fisik secara umum meliputi: frekuensi pulsus, nafas, suhu tubuh, postur dan pemeriksaan darah rutin. Hal ini dilakukan untuk mengetahui apakah anjing memenuhi syarat operasi atau tidak. Sebelum operasi hewan biasanya dipuasakan terlebih dahulu selama 8-12 jam yang bertujuan



untuk



menghindari



dampak



pemberian



anastesi



dan



juga



untuk



membersihkansaluran cerna sehingga memudahkan dalam melakukan pembedahan. Pasien ditimbang untuk menentukan dosis obat, premedikasi dan obat anestesi yang akan diberikan. Setelah hewan dilakukan premedikasi dan anestesi hewan diposisikan lateral atau dorsal recumbency, tergantung pada preferensi dokter hewan dan daerah yang akan dioperasi dibersihkan terlebih dahulu dengan pencukuran rambut serta pemberian yodium tincture kemudian dipasangi kain drape pada site operasi •



Persiapan Hewan Dokter hewan selaku operator dan pembantu operator sebelum dan selama



pelaksanaan operasi harus melakukan serangkaian proses operasi dalam kondisi steril. 4



Operator dan pembantu operator mempersiapkan diri dengan mencuci tangan menggunakan air sabun di bawah air bersih yang mengalir, kemudian didesinfektan. Operator dan asistennya juga harus mengenakan masker, sarung tangan steril, dan pakaian khusus operasi. 2.5 Teknik Operasi 1.



PENDEKATAN BEDAH SENDI LUTUT Sebelum melakukan rekonstruksi ligamen crucriate, arthrotomy dilakukan membuka



atau mengekspos persendian lutut. Arthrotomy dapat dilakukan melalui dua pendekatan, yaitu pendekatan lateral dan pendekatan medial. • Pendekatan Lateral Sayatan kulit kraniolateral dilakukan berpusat di atas patela. Kemudian jaringan subkutan diinsisi di sepanjang garis yang sama untuk memvisualisasikan septum antara daun superfisial fasia latae dan otot bisep femoris di proksimal dan retinakulum lateral di distal. Selanjutnya insisi melalui fascia latae dibuat secara proksimal serta insisi melalui fascia latae dan retinaculum lateral ke distal (Gambar 1A). Kemudian dilakukan insisi pada kapsul sendi, dilanjukan dengan insisi di sebelah proksimal tendon patela (Gambar 1B). Setelah itu sayatan dibuat di sepanjang perbatasan vastus lateralis menuju fabella. Pindahkan patela ke medial untuk mengekspos permukaan kranial sendi (Gambar 1C).



Gambar 1. Arthrotomy dengan pendekatan lateral 5



• Pendekatan Medial Sayatan kraniomedial dibuat berpusat di atas patela. Jaringan subkutan diinsisi di sepanjang garis yang sama untuk mengekspos retinakulum medial parapatellar. Kemudian sayatan dibuat melalui retinakulum medial dan kapsul sendi yang berdekatan dengan punggung medial tendon patela (Gambar 2).



Gambar 2. Arthrotomy dengan pendekatan medial 2.



METODE EXTRACAPSULAR Metode ini digunakan untuk anjing-anjing ras besar. Prinsip dari metode ini adalah



menggantikan CCL yang telah putus dengan benang nilon. Langkah pertama, lakukan artroskopi atau artrotomi seperti yang dijelaskan sebelumnya. Sebelum membuat ikatan dari benang nilon, sisa CCL dan meniskus bagian medial yang telah rusak dibuang terlebih dulu. Kemudian ikatan dibuat menggunakan benang nilon monofilamen dari bagian lateral tulang fabela, selanjutnya benang tersebut dimasukkan ke dalam lubang yang dibuat pada tuberositas tulang tibia, di dekat pangkal dari ligamentum patella. Ikatan yang sama dilakukan pula pada bagian medial tulang fabela, menuju lubang yang sama pada tuberositas tulang tibia (Gambar 3A).



6



Gambar 3. Rekonstruksi ekstrakapsular menggunakan benang yang berat dan nonbsorbable. Jahitan melewati fasia dalam yang mengelilingi tulang fabella dan melalui satu lubang yang telah dibor (A) atau dua lubang (B) di puncak tibia. Sebagai alternatif, dapat juga menggunakan benang ortopedi (ukuran 2 FiberWire untuk anjing hingga 10 kg; ukuran 5 FiberWire untuk anjing dengan berat lebih dari 10 kg). Benang juga dapat ditambatkan pada sekrup tulang yang ditempatkan di kondilus femoralis lateral. Sekrup ditempatkan sejauh mungkin ke kaudal pada kutub distal fabella lateral. Selanjutnya, benang dilewatkan di belakang ligamentum patela tepat di proksimal tuberositas tibialis (Gambar 4).



Gambar 4. Rekonstruksi ekstrakapsular menggunakan benang yang berat dan nonabsorbable yang ditambatkan pada sekrup tulang. Alternatif lain dapat juga dilakukan dengan membuat satu atau dua lubang pada krista tibialis untuk menempatkan sekrup tulang. Kemudian benang diikatkan pada sekrup tersebut untuk menstabilkan sendi (Gambar 3B). 7



3.



METODE TIBIAL TUBEROSITY ADVANCEMENT Lakukan artroskopi atau artrotomi, reseksi sisa CCL, dan periksa meniskus apakah ada



robekan atau kerusakan. Angkat bagian meniskus yang rusak dan tutup portal artrotomi atau artroskopi. Buat incisi kulit medial pada tibia proksimal. Setelah itu, kuakkan tibialis medial dan pisahkan perlekatan otot fasia tibialis kranial. Tepat di sebelah distal ujung tibialis, masukkan spons kasa yang dibasahi. Letakkan pelat dengan ukuran yang sesuai pada ujung tibialis untuk menilai lokasi yang tepat, dan pastikan fork akan pas dengan ujung tibialis; jumlah gigi fork sama dengan jumlah lubang pada pelat (Gambar 5A). Tentukan titik yang tepat untuk lubang fork proksimal di ujung tibialis (proksimal dan caudal ke insersi tendon patela pada tuberositas tibialis). Posisikan bor fork di tibia, dan kencangkan dengan forsep. Kemudian palpasi dengan mata bor untuk memastikan lubang bor terletak di atas tulang di lokasi yang sesuai. Bor lubang proksimal, dan masukkan pin penstabil (Gambar 5B). Bor lubang yang sesuai dengan lubang distal pada pelat dan masukkan pin lainnya. Bor semua lubang yang tersisa dan lepaskan jig. Identifikasi ujung proksmial dan distal dari oseteotomy points. Lakukan osteotomi ujung parsial transversal, biarkan korteks lateral tetap utuh di sepertiga proksimal dari osteotomi (Gambar 5C). Ambil spons kasa basah yang sebelumnya dimasukkan. Buat kontur dan rakit pelat dan fork, dan tempatkan fork di ujung lubang tibialis menggunakan inserter fork dan palu. Selesaikan osteotomi (Gambar 5D). Buka celah osteotomi, dan biarkan tuberositas tibialis bergerak secara proksimal dan masukkan cage sekitar 2 hingga 3 mm distal ke proksimal dari osteotomi (Gambar 5E). Bor lubang melalui caudal ear cage (1,8 mm, diarahkan sedikit ke caudal dan sedikit ke distal), dan pasang sekrup 2,4 mm pertama di caudal ear spacer. Bor, ukur, dan masukkan sekrup pelat selftapping (2,7 mm untuk pelat 3, 4, 5 lubang / fork; 3,5 mm untuk pelat 6, 7, 8 lubang / fork), letakkan sekrup paling distal di pelat terlebih dahulu (Gambar 5F) Periksa kembali posisi dan stabilitas patela untuk memastikannya tidak terlepas. Masukkan sekrup 2,4-mm di ear cage secara kranial melalui ujung tibialis (Gambar 5G). Isi celah dan cage osteotomi dengan cangkok tulang yang diperoleh dari femur distal, tibia proksimal, atau allograft tulang demineral. Jahit fasia dalam dengan absorbable suture menggunakan continuous patterns. Jahit fasia superfisial dan jaringan subkutan dengan absorbable suture menggunakan continuous patterns. Jahit kulit dengan nonabsorbable suture menggunakan simple interrupted patterns atau gunakan staples kulit. 8



Gambar 5. Teknik operasi ligamentum crucriate dengan metode Tibial Tuberosity Advancement (TTA). (A) Posisikan pelat dengan ukuran yang tepat pada ujung tibialis untuk menilai pemilihannya. (B) Tempatkan template fork di atas dan bor lubang dimulai dengan lubang proksimal, lubang paling distal, dan kemudian lubang yang tersisa. (C) Lakukan osteotomi parsial transversal, biarkan korteks lateral tetap utuh. (D) Dudukkan pelat ke dalam puncak tibialis, lalu selesaikan osteotomi. (E) Buka celah osteotomi dan masukkan cage pada tingkat aspek proksimal osteotomi dan kencangkan dengan sekrup melalui caudal ear cage. (F) Masukkan sekrup melalui pelat yang dimulai dengan sekrup paling distal. (G) Masukkan sekrup ear cage, isi celah dengan cangkok tulang, dan tutup tempat operasi. 4.



TIGHTROPE CCL (TR) Lakukan artroskopi atau artrotomi, reseksi sisa CCL, dan periksa meniskus apakah ada



robekan atau kerusakan. Angkat atau hilangkan meniskus yang rusak, jika ada, atau lakukan pelepasan meniskus. Buat incisi melalui retinakulum lateral dan distal fasia lata. Palpasi sambungan dari fabella lateral dan posisikan wire penstabil CCL untuk memasuki femur , kurang lebih 2 mm distal ke sambungan condylus fabella-femoralis lateral dan dalam bagian paling caudal dari condylus femoralis lateral (Gambar A). Majukan wire penstabil menggunakan wire driver atau bor pada sudut proksimal diarahkan sedemikian rupa sehingga wire melewati distal femur dan keluar dari diafisis distal femur di sisi medial. Wire harus keluar setinggi proksimal patella. 9



Dengan menggunakan tightrope CCL 3,5 mm dengan mata bor berkanulasi, bor di atas wire penstabil dari lateral ke medial. Setelah mata bor keluar dari korteks femoralis medial, lepaskan mata bor dan wire penstabil dan letakkan wire atau pin lain ke dalam tunnel femoralis untuk menandai lokasinya untuk penempatan implan tightrope yang selanjutnya. Palpasi tendon long digital extensor (LDE) di dalam alur otot tibia lateral proksimal dan buat incisi 510 mm di fasia dan kapsul sendi segera di caudal dan sejajar dengan LDE. Tarik LDE secara kranial untuk memungkinkan penempatan wire penstabil TR di dalam alur otot sehingga dimulai dari caudal dan proksimal mungkin di dalam tanpa memasuki sendi (Gambar B). Arahkan wire penstabil ke tibia proksimal menggunakan penggerak wire atau bor pada sudut yang diarahkan ke distal sehingga wire melintasi tibia proksimal dan keluar di sisi medial. Dengan menggunakan mata bor kanulasi TR 3,5 mm, bor di atas wire penstabil dari lateral ke medial. Setelah mata bor keluar dari korteks tibialis medial, lepaskan mata bor dan wire penstabil dan letakkan wire atau pin lain. Buka wire atau pin penanda di lubang medial tibialis dengan mngincisi kulit. Lewatkan jarum utama tightrope melalui tibial tunnel dari medial ke lateral. Berikan tegangan secara lateral pada jarum TR dan secara medial pada jahitan tightrope untuk menyelaraskan wire TR di sepanjang sumbu tibial tunnel. Tarik wire TR melalui tibial tunnel dari medial ke lateral sampai keluar dari aspek lateral stifle sementara LDE ditarik secara kranial (Gambar C). Dorong jarum TR melalui tunnel femoralis dari lateral ke medial. Tarik jarum TR melalui orifisium pada aspek medial femur, dan berikan tegangan pada jarum TR secara medial dan pada jahitan fiber tape secara lateral untuk menyelaraskan tombol alih TR di sepanjang sumbu tunnel femoralis. Maju wire TR melalui tunnel femoralis dari lateral ke medial sampai keluar dari aspek medial femur, tetap jauh ke dalam vastus medialis. Balik wire untuk menyelaraskannya tegak lurus dengan tunnel femoralis, dan tarik jahitan tightrope di sisi lateral femur untuk menempatkan wire dengan kuat pada korteks femoralis medial. Tarik tightrope kencang pada aspek lateral stifle, dan lepaskan setiap lilitan sehingga untaiannya tetap rata dan kuat pada kapsul sendi lateral jauh ke fasia. Tarik benang fiber tape dengan kencang pada aspek medial tibia, dan tempatkan tombol strap sepenuhnya pada tulang kortikal tibialis. Ikat ujung bebas jahitan tightrope di atas tombol. Gunakan tensioner untuk mengencangkan tightrope tightrope langsung ke tombol. Setelah jahitan kedua dipretensi, tahan tegangan yang diinginkan pada untaian ini dengan tensioner dan ikat jahitan pertama dengan empat hingga lima lemparan.



10



Gambar 6. Teknik operasi ligamentum crucriate dengan metode Tightrope CCL (TR). (A) Bor kawat pemandu CCL tali tegang yang memasuki femur ~ 2 mm distal ke sambungan kondilus fabella-femoralis lateral dan dalam bagian paling ekor dari kondilus femoralis lateral. (B) Setelah kabel dipasang dengan benar, bor kabel secara berlebihan. (C) Cabut LDE secara kranial dan bor kawat pemandu kedua sedemikian rupa sehingga dimulai sebagai ekor dan proksimal mungkin dalam alur dan keluar dari tibia proksimal di sisi medial. (D) Setelah kabel dipasang dengan benar, bor kabel secara berlebihan. (E) Tempatkan tali mulai dari aspek medial lubang tibialis dan berakhir di aspek medial lubang femoralis. (F) Kencangkan tali pengikat dan kencangkan dengan beberapa lemparan. 5.



TIBIAL PLATEAU LEVELING OSTEOTOMY (TPLO) Prosedur TPLO dilakukan seperti yang dijelaskan di tempat lain, dengan variasi kecil



sesuai dengan preferensi ahli bedah. Singkatnya, dibuat incisi parapatellar medial. Artrotomi medial dilakukan untuk menghilangkan sisa-sisa CCL dan memungkinkan ahli bedah untuk memeriksa menisci. Buat incisi kulit medial pada tibia proksimal (Gambar 7). Mulailah incisi 3 cm proksimal tibialis, dan lanjutkan ke distal 5 cm di bawah ujung tibia. Incisi jaringan subkutan di sepanjang garis untuk memvisualisasikan penyisipan M. sartorius. Insisi M. sartorius, dan kuakkan otot secara kaudal untuk melihat aspek kaudal dari tibia proksimal (Gambar 8B). Incisi M. popliteus dari aspek kaudomedial tibia (Gambar 8C). Setelah diangkat, letakkan spons yang dibasahi di antara otot dan tulang untuk melindungi otot, arteri dan vena selama osteotomi. Lakukan prosedur osteotomi. Pin rotasi digunakan untuk memutar segmen tulang proksimal dalam kaitannya dengan segmen tulang distal untuk mencapai kemiringan 11



tibialis 6° relatif terhadap bidang horizontal. Pin penahan ditempatkan, dan pelat diaplikasikan ke tibia. Jahit penyisipan kranial M. sartorius ke fasia dalam tibia dengan absorbable suture menggunakan simple continuous pattern. Jahit sisa fasia dalam dengan absorbable suture menggunakan simple continuous pattern. Jahit fasia superfisial dan jaringan subkutan dengan absorbable suture menggunakan simple continuous pattern. Jahit kulit dengan non-absorbable suture menggunakan simple interrupted pattern atau gunakan staples kulit.



Gambar 7. Pendekatan medial ke tibia proksimal.



Gambar 8. Teknik operasi ligamentum crucriate dengan metode Tibial Plateau Leveling Osteotomy (TPLO). (A dan B) Posisikan jig tegak lurus dengan sumbu panjang tibia. (C) Lakukan osteotomi hingga kedalaman sepertiga tulang, jaga agar gergaji sejajar dengan jig pin. (D) Tandai tulang untuk rotasi. (E) Putar segmen proksimal untuk menyejajarkan tanda. (F) Kencangkan osteotomi dengan pelat tulang yang berukuran sesuai. 12



2.6 Manajemen Pascaoperasi Prosedur postoperasi cranial cruciate ligament (CCL) terdiri atas dua fase yaitu fase pertama dan kedua. Fase pertama, selama enam bulan pertama postoperasi. Pemasangan Elizabeth collar dapat dilakukan setelah operasi benar – benar selesai dilakukan. Hal ini bertujuan untuk mencegah hewan menjilati luka insisi sehingga tidak terjadi infeksi atau komplikasi postoperasi yang mampu memperlambat penyembujan. Light pressure bandage dapat diberikan pada anjing untuk menutup luka serta mencegah pembengkakan. Pembengkakan luka postoperasi biasa terjadi pada hari ke-2 hingga 3. Penggantian bandage perlu dilakukan setiap hari untuk monitoring adanya discharge, pendarahan atau pembengkakan pada luka insisi. Terkadang pada kasus CCL terjadi pembengkakan yang dikarenakan adanya timbunan cairan dibawah kulit sebagai akibat dari aktivitas anjing yang berlebihan dan hal ini dapat membaik dalam 1 minggu. Sehingga hewan harus menjalani cage rest, kondisi kandang perlu diperhatikan seperti permukaan lantai yang tidak licin dan tidak diberikan furniture yang membahayakan kesembuhan luka operasi. Fisioterapi dan hidroterapi dapat dimulai pada minggu ke dua postoperasi. Hewan dapat dilatih untuk berjalan dengan dibawa keluar tetapi perlu diikat dengan tightrope dan dibatasi jaraknya, seperti halnya hanya untuk pee and poo selama dua minggu pertama postoperasi. Jahitan atau staples kulit dapat dilepaskan pada hari ke-10 hingga 14. Setelah jahitan atau staples dikulit dilepas, maka hewan mulai dapat diajak jalan lebih jauh tetapi tetap harus dibatasi dan dalam pengawasan. Selain itu, hewan juga dapat mulai dilatih berenang setelah jahitan atau staples dilepas. Fase kedua, rehabilitasi. Penting untuk disadari bahwa sampai tulang sembuh sepenuhnya, perbaikan akan rentan terhadap cedera jika stres berlebihan. Oleh karena itu, tingkat aktivitas harus dikontrol dengan cermat. Selama enam minggu postoperasi, aktivitas anjing dapat ditingkatkan secara bertahap untuk membantu pembentukan otot. Jumlah aktivitas harus berkembang secara bertahap. Dimulai dari meningkatkan durasi secara perlahan, bukan intensitas aktivitas. Selama fase pemulihan ini kaki yang tidak dioperasi masih berisiko cedera akibat beban lebih berat sementara kaki yang dioperasi menjadi lebih kuat. Berlari, melompat, dan bermain masih tidak diizinkan. Dalam dua minggu pertama rehabilitasi (minggu ke 7 dan 8 setelah operasi), anjing dapat dilatih berjalan lebih jauh dengan intensitas yang ditambah pula seperti 3 sampai 4 kali sehari. X-ray dapat dilakukan pada minggu ke 8 untuk menilai tingkat kesembuhan tulang. Pada minggu ketiga dan keempat masa rehabilitasi (minggu ke-9 dan ke-10 setelah operasi), jalan13



jalan dapat dilakukan selama anjing merasa nyaman dengan panjang durasi yang masih dapat ditoleransi oleh hewan. Mendorongnya untuk melakukan lebih banyak saat ini tidak akan mempercepat rehabilitasi dan berisiko cedera pada kaki belakang lainnya. Pada minggu kelima dan keenam rehabilitasi (minggu 11 dan 12 setelah operasi), latihan exercise anjing dapat dilakukan tanpa tightrope.



14



BAB III PENUTUP 3.1 Kesimpulan Cruciate Ligament adalah ligamentum (pengikat) yang terdapat pada persendian lutut (stifle joint), merupakan jaringan fibrosa kuat yang menghubungkan femur distal ke tibia proximal. . Ada 2 buah cruciate ligament, yaitu: cruciate ligament bagian depan (cranial) dan cruciate ligament bagian belakang (caudal). Persiapan hewan/pasien sebelum operasi berlangsung sebaiknya dilakukan terlebih dahulu pengecekan anamnesa dilakukan untuk mengetahui bagian rufturnya cruciate ligament, penyebab, kapan terjadinya sehingga dapat membantu diagnosis. Sebelum melakukan rekonstruksi ligamen crucriate, arthrotomy dilakukan membuka atau mengekspos persendian lutut. Arthrotomy dapat dilakukan melalui dua pendekatan, yaitu pendekatan lateral dan pendekatan medial. Prosedur postoperasi cranial cruciate ligament (CCL) terdiri atas dua fase yaitu fase pertama dan kedua. 3.2 Saran Semoga paper ini dapat menjadi bahan acuan dan referensi bagi para pembaca, khususnya mahasiswa Kedokteran Hewan Universitas Udayana. Semoga kedepannya dapat dibuat lebih banyak informasi mengenai teknik operasi trepanasio yang diperlukan oleh mahasiswa kedokteran hewan dan seorang dokter hewan ataupun masyarakat secara umum.



15



DAFTAR PUSTAKA Christopher, S. A., Beetem, J., & Cook, J. L. 2013. Comparison of Long-Term Outcomes Associated With Three Surgical Techniques for Treatment of Cranial Cruciate Ligament Disease in Dogs. Veterinary Surgery, 42(3), 329–334. Ferguson, J. 2017. Cruciate Ligament Rupture in Dog. East Neuk Veterinary Clinic St Monans Fife Scotland. Fossum TW, dkk. 2019. Small Animal Surgery 5th Edition. Philadelphia: Elsevier. Gordon-Evans, W. J., Griffon, D. J., Bubb, C., Knap, K. M., Sullivan, M., & Evans, R. B. 2013. Comparison of lateral fabellar suture and tibial plateau leveling osteotomy techniques for treatment of dogs with cranial cruciate ligament disease. Journal of the American Veterinary Medical Association, 243(5), 675–680. Igna, Cornel. 2018. Treatment Options for Cranial Cruciate Ligament Rupture In Dog – A Literature Review. Banat’s University of Agricultural Science and Veterinary Medicine Timisoara, Faculty of Veterinary Medicine, Romania. Innes, J. F. 2017. Management of Cruciate Ligament Rupture: What is ‘Best Practice?’. Veterinary



Ireland Journal 2(1):36-41.



Janna M. Johnson,Ann L. Johnso,: July 1993,Cranial Cruciate Ligament Rupture Pathogenesis, Diagnosis, and Postoperative Rehabilitation.Veterinary Clinics of North America: Small Animal Practice: Elsevier. Koch L, Brockstahler L, Tichy A, Peham C, dan Schnabl-Feichter E. 2021. Comparison of Extracapsular Stabilization Techniques Using an Ultrasonically Implanted Absorbable Bone Anchor (Weldix) after Cranial Cruciate Ligament Rupture in Cats—An In Vitro Study. Animal. 11, 1695. Lafaver, S., Miller, N. A., Stubbs, W. P., Taylor, R. A., Boudrieau, R. J. 2007. Tibial Tuberosity Advancement for Stabilization of the Canine Cranial Cruciate Ligament-Deficient Stifle



Joint: Surgical Technique, Early Resulst, and Complication in 101 Dogs.



Veterinary



Surgery 36:573 – 586.



Mattila, J. 2012. Surgical Treatment of Canine Cranial Cruciate Ligament Deficiency (Thesis). University of Helsinki, Faculty of Veterinary Medicine.



16



Puotinen, C. J. 2010. Saying “No” to surgery “Conservative management” is an often overlooked



but frequently effective – option for ligament injuries. whole-dog-



journal. P14-17. Rooster, H. D. 2001. Cranial Cruciate Ligament Disease in The Dog : Contributions To Etiology,



Diagnosis and Treatment . Faculteit Diergeneeskunde Universiteit Gent.



Spinella G, Arcamone G, dan Valentini S. Ligament Rupture in Dogs: Review on Biomechanics, Etiopathogenetic Factors and Rehabilitation. Vet. Sci. 8, 186. Thompson, Elizabeth. 2019. When A Dog Needs ACL Surgery.



17



TEKNIK OPERASI CRUCIATE LIGAMENT Kelompok 4: KOMANG AYU TRIANA SANJIWANI FERDY OLGA SAPUTRA M. FARHAN AL MA’ARIF Kelas B



1809511049 1809511050 1809511051



Terminologi Cruciate Ligament adalah ligamentum (pengikat) yang terdapat pada persendian lutut (stifle joint), suatu jaringan fibrosa kuat yang menghubungkan femur distal ke tibia proximal. Ligamen ini bekerja seperti engsel di lutut dan bertanggung jawab untuk menyediakan kestabilan anterior-posterior sendi lutut. Pecahnya ligamen cruciatum kranial jarang terjadi pada kucing. Ini sering terjadi pada anjing yang kelebihan berat badan, paruh baya dan lebih tua. Trah anjing yang cenderung mengalami gangguan ini umumnya ialah breed cocker spaniel, rottweiler, miniature, toy poodle, Lhasa apso, bichon frise, golden retriever, labrador retriever, German shepherd, dan mastiff



Indikasi • • • • •



• • •



Hewan mengalami kesulitan berdiri Hewan mengalami kesulitan melompat Penurunan tingkat aktivitas Kepincangan atau pincang (tingkat keparahan bervariasi) Atrofi otot (penurunan massa otot di kaki yang terkena) Penurunan rentang gerak pada sendi lutut Suara letupan (yang mungkin juga menunjukkan robekan meniscal) Pembengkakan di bagian dalam tulang kering



Anestesi Premedikasi Atropin sulfat 0.025% dosis 0.02 - 0.04 mg/kg BB secara SC



Anestesi Umum Xylazine 2% dosis 2 ml/kg BB dan ketamin HCL 10% dosis 15 mg/kg BB secara IM Maintenance dengan anestesi inhalasi isoflurane atau sevoflurane (2% - 3%) dalam oksigen. Pemberian Cefazolin sodium (20 mg/kg BB, IV) diberikan kepada anjing beberapa menit sebelum operasi.



Persiapan alat dan bahan



Preoperasi Sebelum melakukan tindakan operasi terlebih dahulu dilakukan persiapan operasi. Adapun persiapan yang dilakukan adalah:



Persiapan ruang operasi



Persiapan pasien



Persiapan operator



Operasi PENDEKATAN LATERAL



PENDEKATAN MEDIAL



Metode Extracapsular 1. 2.



3.



4.



lakukan artroskopi atau artrotomi sisa cranial crucriate ligament (CCL) dan meniskus bagian medial yang telah rusak dibuang terlebih dulu Ikatan dibuat menggunakan benang nilon monofilamen dari bagian lateral tulang fabela, selanjutnya benang tersebut dimasukkan ke dalam lubang yang dibuat pada tuberositas tulang tibia, di dekat pangkal dari ligamentum patella Ikatan yang sama dilakukan pula pada bagian medial tulang fabela, menuju lubang yang sama pada tuberositas tulang tibia



Metode Extracapsular 1.



2.



3. 4.



Sebagai alternatif, dapat juga menggunakan benang ortopedi (ukuran 2 FiberWire untuk anjing hingga 10 kg; ukuran 5 FiberWire untuk anjing dengan berat lebih dari 10 kg). Benang dapat ditambatkan pada sekrup tulang yang ditempatkan di kondilus femoralis lateral Sekrup ditempatkan sejauh mungkin ke kaudal pada kutub distal fabella lateral. Selanjutnya, benang dilewatkan di belakang ligamentum patela tepat di proksimal tuberositas tibialis



Metode Tibial Tuberosity Advancement (TTA) 1.



2. 3. 4. 5. 6. 7.



Posisikan pelat dengan ukuran yang tepat pada ujung tibialis untuk menilai pemilihannya. Tempatkan template fork di atas dan bor lubang dimulai dengan lubang proksimal, lubang paling distal, dan kemudian lubang yang tersisa. Lakukan osteotomi parsial transversal, biarkan korteks lateral tetap utuh. Dudukkan pelat ke dalam puncak tibialis, lalu selesaikan osteotomi. Buka celah osteotomi dan masukkan cage pada tingkat aspek proksimal osteotomi dan kencangkan dengan sekrup melalui caudal ear cage. Masukkan sekrup melalui pelat yang dimulai dengan sekrup paling distal. Masukkan sekrup ear cage, isi celah dengan cangkok tulang, dan tutup tempat operasi



Metode Tibial Tuberosity Advancement (TTA)



Metode Tightrope CCL (TR) 1. 2.



3. 4. 5. 6.



7.



Buat incisi melalui retinakulum lateral dan distal fasia lata. Palpasi sambungan dari fabella lateral dan posisikan wire penstabil CCL untuk memasuki femur. Bor kawat penstabil tightrope CCL yang memasuki femur kurang lebih 2 mm distal ke sambungan condylus fabellafemoralis lateral dan dalam bagian paling caudal dari condylus femoralis lateral. Setelah wire dipasang dengan benar, bor wire. Cabut LDE secara kranial dan bor wire penstabi; kedua sedemikian rupa sehingga dimulai sebagai caudal dan proksimal dan keluar dari tibia proksimal di sisi medial. Setelah wire dipasang dengan benar, bor wire. Tempatkan tightrope mulai dari aspek medial lubang tibialis dan berakhir di aspek medial lubang femoralis. Kencangkan tali pengikat dan kencangkan dengan beberapa lemparan



Metode Tightrope CCL (TR)



Metode Tibial Plateau Leveling Osteotomy (TPLO)



1. 2. 3. 4. 5. 6. 7. 8.



Mulailah incisi 3 cm proksimal tibialis, dan lanjutkan ke distal 5 cm di bawah ujung Incisi jaringan subkutan di sepanjang garis untuk memvisualisasikan penyisipan M sartorius, dan kuakkan otot secara kaudal untuk melihat aspek kaudal dari tibia pr Setelah diangkat, letakkan spons yang dibasahi di antara otot dan tulang untuk me dan vena selama osteotomy Posisikan jig tegak lurus dengan sumbu panjang tibia. Lakukan osteotomi hingga kedalaman sepertiga tulang, jaga agar gergaji sejajar de Tandai tulang untuk rotasi. Putar segmen proksimal untuk menyejajarkan tanda. Kencangkan osteotomi dengan pelat tulang yang berukuran sesuai.



Metode Tibial Plateau Leveling Osteotomy (TPLO)



MANAJEMEN PASCAOPERASI Fase Pertama (1-6 minggu) 1. Pemasangan bandage 2. Pemasangan Elizabeth collar 3. Cage rest 4. Fisioterapi dan hidroterapi (mulai minggu ke-2) Fase Kedua (7-12 minggu) 1. Rehabilitasi bertahap 2. Pemeriksaan X-ray ulang (minggu ke-8)



Terima kasih



Cruciate ligament rupture in Dogs John Ferguson BVM&S CertSAO MRCVS East Neuk Veterinary Clinic St Monans Fife Scotland KY10 2PZ



_____________________________________________________________ Introduction



Cranial cruciate ligament rupture (CCLR is the most common cause of hindlimb lameness in dogs and is particularly common in certain breeds. The cruicate ligament is one of many ligaments that make up the knee (stifle) joint and maintain the stability of the joint. In people, the same ligament is called the anterior cruciate ligament. In both species the ligament may stretch or tear, leading to pain and osteoarthritis. CCLR can also lead to damage to the menisci in the knee. The menisci are two small cushions of fibrocartilage that sit between the bones of the knee. CCLR can make the menisci vulnerable to tearing, which is



painful.



see this so called degenerative “cruciate disease” in some dogs as young as 12 months old and in most cases both stifles are affected (bilateral disease). This common occurrence in certain breeds strongly suggests an underlying genetic breed-related influence which could be hereditary, although this has not been absolutely proven. Underlying causes such as an inflammatory or vascular disease could be implicated.



What are the signs of cruciate ligament rupture?



What causes the cruciate ligament to rupture?



The cause of CCLR and why it occurs so commonly in certain breeds is not fully understood. Certainly, traumatic rupture of the CCL can occur during traumatic injuries such as these sustained during a fall, twisting of the limb or catching the hindlimb in a gate or fence. However, it is known that the fibres that make up the CCL can degenerate and weaken leading to gradual tearing of the ligament over time. This leads to partial CCLR and once sufficient mechanical weakness occurs, the ligament can suddenly rupture completely. We can



Stiffness rising after resting specifically after exercise is the most common sign of early CCL degeneration and partial rupture. This will often progress to lameness for the first few steps after rising. Chronic progressive lameness occurs and often the dog will become non-weight bearing frequently. If early bilateral cruciate disease is present then difficulty rising, problems negotiating stair and reluctance to jump into the car are evident. Sprain injuries to the knee can aggravate lameness and result in significant deterioration of limb function. Dogs suffering from CCL disease/rupture will rarely cry or vocalise suggesting to owners that the dog is not suffering pain. Certainly, people with cruciate ligament ruptures report the condition to be extremely uncomfortable and frequently painful.



There is no reason to think dogs are any different! Generally, the degree of lameness present equates to the degree of pain the dog is experiencing.



meniscal injuries with a smaller incision than would be necessary with traditional surgery. However, sole arthroscopic treatments of CCLR are not in widespread use mainly because they are technically challenging to perform and because of concerns about effectiveness. Currently, therefore, the treatment of CCLR in dogs differs dramatically from that in people.



Treatment of CCLR



Demonstrating “cranial drawer” sign of instability



How is CCLR diagnosed?



CCLR is first diagnosed by palpation (examination and manipulation by hand – see image above). In a dog with a complete rupture, the clinician will be able to feel the instability present – so called “cranial drawer forward” sign. In dogs with a stretched or partially torn CCL there may be no instability present but a firm swelling on the inside of the knee may be evident and pain may be elicited on manipulation of the knee joint.



Many surgical options for CCLR are available and there is widespread debate and disagreement about the usefulness of these treatments. In a very small number of dogs it is possible for the knee to improve in stability without surgery as the body lays down scar tissue. In most cases this is best achieved with several weeks to 2 months of strict rest, which helps the body to lay down fibrous (scar) tissue around the joint without the forces of vigorous activity. Treatment by rest alone may be attempted in any size dog but in most breeds, particularly large and active dogs, adequate stabilization of the knee will usually not be achieved, and the pain and lameness will continue and therefore surgery is recommended for most dogs.



Radiographs (X-rays) of the joint will usually show early osteoarthritis with an increased volume of fluid (effusion). The actual CCL does not show on X-rays because it is soft tissue. The changes seen on Xrays are therefore not specific and other disease processes need to be considered. However, X-rays will rule out certain conditions such as fractures within the knee, infection and cancer. Aspiration and analysis of joint fluid can rule out other conditions such as infection or inflammatory diseases.



Model showing folded and crushed meniscus



Damage to the meniscus



LEFT: Normal CCL



RIGHT: torn CCL



(as seen by arthroscopy)



CCLR may be diagnosed by arthroscopy (small camera inserted into joint) before surgical treatment of the ligament rupture. Arthroscopy may also be used to “clean out the joint” and treat



The meniscus or menisci (plural) are two small cushions made of fibrocartilage that sit between the bones of the knee. These can be regarded as the “shock-absorbers” within the joint. In approximately one third of dogs they may be found to be crushed or damaged at the time of surgery. In addition to the CCLR, this causes significant pain that can only be resolved by removing the torn and damaged portion. Damage to the meniscus can sometimes also happen after surgery (so called late meniscal injury or LMI) although the incidence is usually low, particularly after procedures such as TPLO. There are certain techniques designed to prevent future damage to the menisci although the value of these techniques is still not clear. Carefully examination of the menisci are necessary in every surgical case.



Extracapsular suture or Imbrication suture



How the TPLO Works When CCLR occurs there is nothing to prevent the upper bone of the knee (femur/thigh bone) from sliding down the slope of the tibia (shin bone). Black arrows on the X-rays below illustrate this sliding force. This slope is termed the tibial plateau angle (TPA). Some dogs have an increased TPA which magnifies this sliding force. This constant sliding places strain on the joint causing pain and discomfort. Patients with an increased TPA may explain why the suture or other material used in “standard” techniques to fail prematurely. The TPLO procedure levels the tibial plateau angle to eliminate the sliding and the instability of the knee and in turn resolves the accompanying pain.



More traditional surgical treatments of CCLR involve replacing of the ligament with either a natural or synthetic material. In these procedures the patients own natural fibrous tissue (graft), a nylon prosthetic suture, or even wire is used to stabilize the knee. These procedures have been used for more than half a century, and the results can be good in many cases. The main concern with these techniques is that the stabilizing material can stretch or break, after which the knee is stabilized by scar tissue. This may lead to a decrease in the range of motion of the joint and persistent lameness. We recommend extracapsular suture surgery for smaller dogs (less than 7-8kg) or when medical or financial limitations contradict or prohibit TPLO from being performed. Extracapsular suture may also be sufficient for less active large dogs living a more sedentary lifestyle – generally this does not apply to certain breeds! So called “standard” surgery can lead to unpredictable results and a less than optimal outcomes with a higher chance of the patient requiring a second operation.



TPA



X-ray of normal knee: note small TPA



TPA



X-ray of abnormal knee with very sloped tibial plateau and large TPA



Tibial Plateau Levelling Osteotomy



The most widely used technique by referral orthopaedic veterinary surgeons in treatment of CCLR is the Tibial Plateau Levelling Osteotomy (TPLO). In this technique, the shin bone (tibia) that lies below the knee is cut and rotated to eliminate the abnormal motion of the knee during normal activity. The advantage of this procedure is that it does not rely on materials to stabilize the knee which can potentially stretch or break. TPLO may give superior outcomes in larger dogs that place more force through the knee and are more likely to stretch traditional repair methods. This technique has gained widespread acceptance because of reports of improved clinical results, especially in larger, active dogs. We recommend TPLO in most of our patients with CCLR and particularly in dogs that are more active, naturally athletic and with exuberant characters.



Post-operative x-ray after TLPO in a Boxer Note: The TPA has been reduced and the sliding force neutralised.



Post-operative care



Aftercare following TPLO surgery is very important with rehabilitation taking around 3-4 months. Painkillers and a short course of antibiotics are prescribed at discharge. If the dog tends to excessively lick the wound it may be necessary to use a plastic Elizabethan collar. Visits to your own veterinary surgeon are necessary within the first two weeks to check the wound and remove sutures. Exercise must be very restricted for the first few weeks until the soft tissues and cut bone heal. Exercise is primarily for toileting purposes. It must be on a lead or harness to prevent strenuous activity, such as chasing a cat or squirrel. At other times confinement to a pen or a small room in the house is necessary with avoidance of jumping and climbing. After a few weeks, exercise may be gradually increased.



Cruciate disease and osteoarthritis



It has been stated that TPLO slows the progression of the pre-existing osteoarthritis within the knee but “standard” surgery does not.



Although this may be true in some cases, this has not been clinically proven. However, the canine knee can cope with moderate amounts of arthritis without causing actual lameness. Medical management of the pre-existing osteoarthritis after surgery is usually unnecessary, but in more severely affected patients medical management may be combined with surgical treatment to eliminate lameness and improve limb function.



Prognosis



The outlook with conservative management for most dogs with CCLR is usually guarded and the lameness usually persists particularly after exercise. Ultimately, hindlimb function deteriorates over time resulting often in a non-weight bearing lameness. The prognosis is usually fair to good after “standard” extra-articular surgery and good to excellent after TPLO surgery, the latter technique restoring painfree limb function in the short and longer term.



Volume 3- Issue 1: 2018



DOI: 10.26717/BJSTR.2018.03.000874 Cornel Igna. Biomed J Sci & Tech Res



ISSN: 2574-1241



Research Article



Open Access



Treatment Options for Cranial Cruciate Ligament Rupture In Dog - A Literature Review Cornel Igna* and Larisa Schuszler Banat’s University of Agricultural Science and Veterinary Medicine Timisoara, Faculty of Veterinary Medicine, Romania Received: March 06, 2018; Published: March 20, 2018



*Corresponding author: Cornel Igna, Banat’s University of Agricultural Science and Veterinary Medicine Timisoara, Faculty of Veterinary Medicine, 119 Calea Aradului, 300645, Timisoara, Romania, Tel: ; Email:



Abstract Cranial cruciate ligament (CrCL) breaks in dogs can be treated by surgical and non-surgical methods. Choice of the treatment method of cranial cruciate ligament rupture in dog continues to be a real problem for veterinarian clinicians. This topic has been the subject of many studies. Investigation of the speciality literature data concerning the surgical treatment options in the management of cranial cruciate ligament injuries) in dogs, remains, in the conditions of an informational avalanche, a present concern, The purpose of this study was to analyze additional evidence which have appeared in the literature in the period of 2006 - January 2017 and which advocate with concrete evidences in the favour or disfavour of a particular method of dogs’ cranial cruciate ligament injuries treatment. Analysis of online searches using PubMed engine in 403 articles suggest that the data analyzed do not allow accurate comparisons between different treatment procedures of cranial cruciate ligament deficiency in dogs and did not show significant differences nor major changes when compared to previous reports (from 1963 to 2005). New long-term clinical studies must be designed and further biomechanical and kinematic analyses are required to determine the optimal technique, and whether these procedures are superior to other stabilization methods. Keywords: Cranial Cruciate ligament deficiency; Dog; Treatment procedures; Trend



Introduction Choice of the treatment method of cranial cruciate ligament (CrCL) rupture in dogs continues to be a real problem for veterinarian clinicians. This topic has been, since 1963 [1], the subject of many concerns and studies. CrCL breaks in dogs can be treated by surgical and non-surgical methods. The latest study investigating the speciality literature on surgical treatment options in the management of CrCL ruptures in dogs was published in 2005 [2] after an online bibliographic search through Medline, PubMed, Veterinary Information Network, and Commonwealth Agricultural Bureau Abstracts, with 240 sources being found and analyzed, and it ends with the conclusion „At this time, the application of evidence-based medicine in analyzing the current available evidence suggests that there is not a single surgical procedure that has enough data to recommend that it can consistently return dogs to normal function after CCL injury”.



Referring only to the surgical procedures used to treat dogs’ CrCL ruptures, a review from 2011 [3] was focused only on extracapsular procedures and shows that there is no data to allow recommendation of a specific technique being necessary „future studies should be directed toward outlining the virtues



and inadequacies of the current techniques” and another study investigating the literature (444 paper works) with constant referring only on surgical procedures occurred in 2014 [4] conclude that tibial plateau levelling osteotomy (TPLO) is superior to the extra capsular lateral side suturing procedures, but there are insufficient data to properly assess other surgical methods. There are also several studies comparing the effectiveness of surgical and non-surgical therapeutic methods, the latest being dated in 2013 [5-7]. The purpose of this study was to analyze additional proof which have appeared lately in the speciality literature in the favour / disfavor of a particular method of CrCL breaks treatment in dog.



Materials and Methods



In January 2017, an online search was conducted, using three search engines: Google scholar (https://scholar.google.ro), PubMed - US National Library of Medicine National Institutes of Health (https://www.ncbi.nlm.nih.gov/pubmed) and Taylor & Francis Online (http://www.tandfonline.com). There have been used as basic search term “cranial cruciate ligament rupture in dog” preceded into three main additional insights by the terms „treatment”, nonsurgical treatment”, surgery treatment”, last with



Cite this article: Cornel I, Larisa S. Treatment Options for Cranial Cruciate Ligament Rupture In Dog - A Literature Review. Biomed J Sci &Tech Res 3(2)- 2018. BJSTR.MS.ID.000874. DOI: 10.26717/BJSTR.2018.03.000874



3131



Cornel Igna. Biomed J Sci & Tech Res



Volume 3- Issue 1: 2018



the following secondary insights „lateral extracapsular stabilization treatment”, “tibial plateau levelling osteotomy - TPLO”, “tibial tuberosity advancement - TTA”, “triple tibial osteotomy - TTO” and “Maquet”. Filtering of the results was done using „most recent” and „best match” for PubMed engine, „article” for Google scholar and subject” and publication date” for Taylor & Francis Online. The results obtained by investigating PubMed were analyzed Table 1: Number of scientific papers identified online.



and classified according to the method proposed by Aragon and Budsberg, 2005 [2], after the evaluation method used: a)



Force plate analysis,



b) Subjective and objective evaluation by the clinician and 3 - subjective evaluation by the pet owner, being considered relevant in this order (1 - maximum and 3 - minimum). Search Engines



Descriptors cranial cruciate ligament rupture in dog



Google scholar (https://scholar. google.ro)



treatment cranial cruciate ligament rupture in dog surgery treatment cranial cruciate ligament rupture in dog lateral extracapsular stabilization treatment in cranial cruciate ligament rupture in dog tplo treatment in cranial cruciate ligament rupture in dog tta treatment in cranial cruciate ligament rupture in dog



tto treatment in cranial cruciate ligament rupture in dog tightrope in cranial cruciate ligament rupture in dog



maquet procedure in cranial cruciate ligament rupture in dog bone anchor in cranial cruciate ligament rupture in dog



nonsurgical treatment in cranial cruciate ligament rupture in dog



Results and Discussion



10.600 9550 8530



Taylor & Francis Online (http:// www.tandfonline.com)



267



51



403



62



251



41



735



5



2



983



33



4



384



3



1



465



140 162



1340 1120



Results of the bibliographic online introspection are shown in Table 1. The analysis of search results with PubMed engine reveals 403 articles (for the period 1963 - January 2017), respectively 391 after manual excluding of those in whose abstract no connection to CrCL was found. In the period 2006 - January 2017, 216 articles were found regarding CrCL in dog, data that reveals a near doubling of number of articles reviewed by Aragon and Budsberg until August 2004 [2]. Instead, between 2006 and January 2017, only 115 articles have appeared regarding therapeutic results evaluation of dogs’ CrCL ruptures from which only 23 were relevant articles of level 1, according to the criterion (evaluation by force plate analysis), 86 articles of level 2 (subjective and objective evaluation by the clinician) and 6 articles of level 3 (subjective evaluation by the pet owner). Of the 23 articles of level 1, six articles promotes kinematics and force plate analysis methods for the diagnosis of dogs’ CrCL ruptures [8-13]; articles describe or compare the results obtained Biomedical Journal of Scientific & Technical Research (BJSTR)



PubMed – US National Library of Medicine National Institutes of Health (https://www.ncbi.nlm.nih. gov/pubmed)



21



4 3 3 3



1



0 0



20 1



with different techniques of surgical treatment [14-24]; Nelson et al. [11]; Mols et al. [25-27] and two articles describe and compare the results obtained with different nonsurgical treatment techniques versus surgical [28]; Wuchereria et al. [7].



If in 2005 there is the opinion that a correct assessment of effectiveness of dogs’ CrCL rupture treatment method only the investigations of level 1 can be considered as reliable [2,29], reaffirmed subsequently [8,14] there are some studies appeared quite recently [25] which conclude that ground reaction forces may be inadequate as a sole method for assessing functional outcome after cranial cruciate ligament repair”. Articles of level 2, for the most part, make the inventory of postoperative complications of different treatment types [30-43] or show mixed results of level 2 with 3 [44-46]. The estimated costs of surgical treatment for cranial cruciate ligament ruptures in dogs in USA in 2003 were 1.32 billion dollars [47]. Surgical techniques for the repair of cranial cruciate ligament deficiency can be classified into three categories: intraarticular grafts, extracapsular suture stabilization and proximal tibial osteotomy (Hulton, 2013 3132



Cornel Igna. Biomed J Sci & Tech Res Intra-Articular Stabilization Techniques: Includes, Use autografts, allografts, xenografts, and synthetic materials to replace the affected CrCL Paatsama et al. [48-61] makes the inventory of the main reasons of intra-articular procedures low use: - auto grafts have inferior stiffness and strength compared with normal ligament; - allografts have the inconvenience of collection and storage; - synthetic materials caused intra-articular fibrosis, bone abrasion and chronic inflammatory response; which has limited their use in veterinary medicine.



Extra-Articular Stabilization Techniques: Includes Lateral fabellar suture (LFS), percutaneous placement of the lateral fabellar suture (pLFS), Tightrope (TR) [62], transcondylar toggle system [63], modified lateral extra-capsular technique with bone anchor. The treatment using lateral flabella suture (LFS) remains at this moment the most practiced method, applied particularly in small dogs. The major shortcoming of the method (overloading of suture anchor points) [64] has benefited from the contribution of several studies [65-68] which introduced the concept of anchoring in isometric position (relatively isometric) but also the anchor through bone anchors [69-79]. Efforts to identify the ideal material for suture when lateral fabellar suture is applied were materialized by the dethronement of nylon wires as the main option [74-79] and by promoting polyethylene wires which are stronger, stiffer and elongate less than nylon leader [60,71,80] promising options offers the poly blend wires [81] and braided polyester [69]. Securing of the suture reveals the existence of three systems: a square knot (SQ), a slip knot (SL) and a crimp clamp (CR). Existing data show no new information being maintained the recommendation [82] “that 27-kgt nylon leader line be secured with a SL, and 27-kgt nylon fishing line be secured with a SQ” as the “clamping the first throw of a square knot in monofilament nylon leader material who increases failure load by two percent and stiffness by 16%, and decreases elongation by 12%” [74] although there are studies showing that “crimping suture alters the biomechanical properties of the loop” [80]. Securing the suture through CR remains a superior method of knotting techniques [83,84] and the wave pattern crimp system is more efficient then the single crimp system [85]. Using tensioning sutures systems before applying a crimp clamp does not bring significant advantages over manual tightening [86].



Difficulties in various procedures’ execution are reported to be the bone tunnels creation in TR and anchoring around the fabella in LSF and pLSF [87]. Evaluation of extra capsular therapeutic methods efficiency, although it is the subject of several studies [74,86,88]; Anderson et al. [83]; [89,90]; Guenego et al. [70]; [62,63,70]; Havig et al. [16,17] with mostly positive reports, show that many of these studies are subjective (level 2 and 3). Studies based on analysis of data obtained through force plate measurements show that peak vertical force was 93% and vertical impulse was 96% of normal values in the limbs of dogs that had extra-articular stabilization at six months following surgery [90], recorded differences being insignificant when compared to normal preoperative values in all studies which appeared before 2006 [88,89] and after [16,17]. Biomedical Journal of Scientific & Technical Research (BJSTR)



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Postoperative complications reported after the application of extraarticular stabilization techniques are between 4.2 and 17.4% [91]; Frey et al. [33] and a 7.2% of them required reintervention [91].



Proximal Tibial Osteotomy Techniques: Includes, tibial plateau levelling osteotomy-TPLO, combined tibial plateau levelling osteotomy and tibial tuberosity transposition (TPLO-TTT), tibial tuberosity advancement-TTA with the variants TTA-1, TTA-2 and TTA-rapid, triple tibial osteotomy -TTO and modified Maquet procedure-MMP. All procedures impart primarily change the biomechanics of the stifle and required specialized and custom equipments. The choice of source of this equipment depend on surgeons’ preferences or/and their affiliation to certain product companies [92]. Recent assessments of the effectiveness of therapeutic methods of tibial osteotomy reveals unanimously that locomotor function of the limb with CrCL insufficiency can be improved using the techniques of tibial osteotomy [93]; Dymond et al. [31,17]; Christopher et al. [44]; described so far Slocum and Devine [94-100].



More prospective and retrospective studies [101-104]; Bruce et al. [93]; Haaland & Sjöström [34]; Lafavere et al. [105] ; Stein et al. [45]; Voss et al. [18]; Duerr et al. [106]; Proot & Cooke [39]; Moles et al. [43]; Dymond et al. [31,33]; Conkling et al. [107] ; Imholt et al. [36]; Taylor et al. [40,41]; Gatineau et al. [108,109]; Steinberg et al. [46]; Etchepareborde [110]; Hishenson et al. [35]; Rotherford et al. [37, 42, 44]; Etchepareborde [111]; Butterworth and Kydd [30] report one or more complications (osteomyelitis, incisional infections, fractures of the tibia or fibula, broken drill bits, hemorrhage, intra-articular implant displacement, intra-osteotomy screw displacement, retained surgical sponges, broken holding pins or screws, septic arthritis, loose implants, draining tracts, ring sequestrum, incisional inflammation, dehiscence and swelling, oedema and seroma formation, bruising, premature staple removal, patellar tendon swelling, and late meniscal injury) after proximal tibial osteotomy procedures.



In TPLO postoperative complication rates, until 2006, ranged between 45.7 and 28% [102,104,107]; compared to 22.2-8.4% after 2006 Duerr et al. [106]; Frey et al. [33,36]; Conkling et al. [107,109] and 4.8% of the cases requiring implant removal [41]. In TTA, the method introduced in practice in 2002 [103], showed postoperative complication rates between 35.5% and 11% [105]; Voss et al. [18]; Dymond et al. [31], with 5.2% reinterventions [42]. In TTO, postoperative complication rate was between 18% and 23% [43]. For MMP, two complications were documented (subsequent meniscal injury) from a series of 12 cases and 10.8% postoperative complications with 3.1% reintervention in a series of 65 cases [93]. Comparative analysis of the obtained data (2006-2007) which assess the therapeutic efficiency by force plate measurements or kinematic data between extra-articular stabilization methods and tibial osteotomy methods [17,11,25,27] as well as between different methods of tibial osteotomy [26] does not show significant differences between methods and no major changes when compared to previous reports.



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Cornel Igna. Biomed J Sci & Tech Res Non-Surgical Treatment Methods: Includes, administration of non-steroidal anti-inflammatory drugs, weight control, restriction of spontaneous locomotion, physiotherapy including hydrotherapy Baker and Bake; Comerford et al. [6,7]. These methods are usually applicable to small dogs with a body weight below 15 kgs [6]. In the treatment of obese dogs with ruptured CrCL, surgical methods had a success rate (was defined as an affected limb net ground reaction force > 85% of the value for healthy dogs and a ≥ 10% improvement of the initial values) at 52 weeks after surgery of 75% compared to 63.6% in those treated by non-surgical methods [7]. The data presented are similar to those of previous studies, based only on clinical examination and with a success rate of 85.7% reported for small dogs with body weight below 15 kgs (Vasseur). Latest data concerning non-surgical methods of treatment (Baker and Bake, 2013; Comerford et al., 2013 [6,7] and veterinarians options for these therapeutic modalities [5] did not show a change in trend compared to previous reports [112], the majority of doctors preferring surgical approaches [113-116].



Conclusion



Currently available data does not allow accurate comparisons between different treatment procedures of cruciate cranial deficiency in dogs. New long-term clinical studies must design and further biomechanical and kinematic analyses are required to determine the optimal technique, and whether these procedures are superior to other stabilization methods.



Acknowledgement



This research work was carried out with the support of the project Dezvoltarea infrastructurii de cercetare, educaţie şi servicii în domeniile medicinei veterinare şi tehnologiilor inovative pentru RO 05, cod SMIS-CSNR 2669. This paper was presented in poster format in The International Conference of the University of Agronom Sciences and Veterinary Medicine of Bucharest “Agriculture for life, life for agriculture”, June 8-10, 2017, Bucharest, Romania.



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91. Casale SA, McCarthy RJ (2009) Complications associated with lateral fabellotibial suture surgery for cranial cruciate ligament injury in dogs: 363 cases (1997-2005). Journal of the American Veterinary Medical Association 234(2): 229-235. 92. Igna C, Bumb D, Tascau M, Rusu L, Dascalu R, et al. (2014) In vitro mechanical testing of monofilament nylon fishing line, for the extracapsular stabilisation of canine stifle joint. Bulletin of University of



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93. Bruce WJ, Rose A, Tuke J, Robins GM (2007) Evaluation of the triple tibial osteotomy. A new technique for the management of the canine cruciatedeficient stifle. Vet Comp Orthop Traumatol 20(3): 159-168.



94. Slocum B, Devine T (1984) Cranial tibial wedge osteotomy: a technique for eliminating cranial tibial thrust in cranial cruciate ligament repair. J Am Vet Med Assoc 184(5): 564-569.



95. Slocum DB (1996) Jig for use in osteotomies. United States patent, USA, pp. 578.



96. Leonard KC, Kowaleski MP, Saunders WB, McCarthy RJ, Boudrieau RJ (2016) Combined tibial plateau levelling osteotomy and tibial tuberosity transposition for treatment of cranial cruciate ligament insufficiency with concomitant medial patellar luxation. Veterinary and Comparative Orthopaedics and Traumatology (VCOT) 29(6): 536-540. 97. Montavon PM, Damur DM (2002) Advancement of the tibial tuberosity for the treatment of cranial cruciate deficient canine stifle, 1st World Orthopeadic Veterinary Congress, Munich, Germany, 152. 98. Maquet P (1976) Advancement of the tibial tuberosity. Clin Orthop Relat Res 115: 225-230.



99. Samoy Y, Verhoeven G, Bosmans T, Van der Vekens E, de Bakker E, et al. (2015) TTA rapid: description of the technique and short term clinical trial results of the first 50 cases. Veterinary Surgery 44(4): 474-484.



100. Damur DM, Tepic S, Montavon PM (2003) Proximal tibial osteotomy for the repair of cranial cruciate-deficient stifle joints in dogs. VCOT Archive 16(4): 211.



101. Pacchiana PD, Morris E, Gillings SL, Jessen CR, Lipowitz AJ (2003) Surgical and postoperative complications associated with tibial plateau leveling osteotomy in dogs with cranial cruciate ligament rupture: 397 cases (1998-2001). Journal of the American Veterinary Medical Association 222(2): 184-193. 102. McCarthy JR (2002) Tibial Plateau Leveling Osteotomy, WSAVA Congress.



103. Priddy NH, Tomlinson JL, Dodam JR, Hornbostel JE (2003) Complications with and owner assessment of the outcome of tibial plateau leveling osteotomy for treatment of cranial cruciate ligament rupture in dogs: 193 cases (1997-2001). Journal of the American Veterinary Medical Association 222(12): 1726-1732.



104. Carey K, Aiken SW, DiResta GR, Herr LG, Monette S (2005) Radiographic and clinical changes of the patellar tendon after tibial plateau leveling osteotomy 94 cases (2001-2003). VCOT Archive 18(4): 235-242. This work is licensed under Creative Commons Attribution 4.0 License



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105. Lafaver S, Miller NA, Stubbs WP, Taylor RA, Boudrieau RJ (2007) Tibial tuberosity advancement for stabilization of the canine cranial cruciate ligament‐deficient stifle joint: surgical technique, early results, and complications in 101 dogs. Veterinary Surgery 36(6): 573-586.



106. Duerr FM, Duncan CG, Savicky RS, Park RD, Egger EL, et al. (2008) Comparison of surgical treatment options for cranial cruciate ligament disease in large‐breed dogs with excessive tibial plateau angle. Veterinary Surgery 37(1): 49-62. 107. Conkling AL, Fagin B, Daye RM (2010) Comparison of tibial plateau angle changes after tibial plateau leveling osteotomy fixation with conventional or locking screw technology. Veterinary Surgery 39(4): 475-481. 108. Gatineau M, Dupuis J, Planté J, Moreau M (2011) Retrospective study of 476 tibial plateau levelling osteotomy procedures. Vet Comp Orthop Traumatol 24(5): 333-341. 109. Coletti T, Anderson M, Gorse MJ, Madsen R (2014) Complications and Biostatistics Associated with Tibial Plateau Leveling Osteotomy 1,519 Cases. Veterinary Surgery 55(3): 249-254. 110. Etchepareborde S, Brunel L, Bollen G, Balligand M (2011) Preliminary experience of a modified Maquet technique for repair of cranial cruciate ligament rupture in dogs. Vet Comp Orthop Traumatol 24(3): 223-227.



111. Etchepareborde S (2014) Adaptation de la procedure de maquet pour le traitement chirurgical de la rupture du ligament croise cranial chez le chien. Universite de Liege PhD thesis.



112. Korvick DL, Johnson AL, Schaeffer DJ (1994) Surgeons’ preferences in treating cranial cruciate ligament ruptures in dogs. Journal of the American Veterinary Medical Association 205(9): 1318-1324. 113. Slocum B, Devine T (1993) Tibial plateau leveling osteotomy for repair of cranial cruciate ligament rupture in the canine. Vet Clin North Am Small Anim Pract 23(4): 777-795.



114. Vasseur PB, Stevenson S, Gregory CR, Rodrigo JJ, Pauli S, et al. (1991) Anterior cruciate ligament allograft transplantation in dogs. Clinical orthopaedics and related research 269: 295-304. 115. Wustefeld-Janssens BG, Pettitt RA, Cowderoy EC, Walton MB, Comerford EJ, et al. (2016) Peak Vertical Force and Vertical Impulse in Dogs With Cranial Cruciate Ligament Rupture and Meniscal Injury. Vet Surg 45(1): 60-65. 116. (2012) Kyon Pharma I: TTA-2. Zurich, KYON Pharma.



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Veterinary Surgery 36:573–586, 2007



Tibial Tuberosity Advancement for Stabilization of the Canine Cranial Cruciate Ligament-Deficient Stifle Joint: Surgical Technique, Early Results, and Complications in 101 Dogs SARAH LAFAVER, DVM, NATHAN A. MILLER, DVM, Diplomate ACVS, W. PRESTON STUBBS, DVM, Diplomate ACVS, ROBERT A. TAYLOR, DVM, Diplomate ACVS, and RANDY J. BOUDRIEAU, DVM, Diplomate ACVS & ECVS



Objective—To describe the surgical technique, early results and complications of tibial tuberosity advancement (TTA) for treatment for cranial cruciate ligament (CrCL)-deficient stifle joints in dogs. Study Design—Retrospective clinical study. Animals—Dogs (n ¼ 101) with CrCL-deficient stifles (114). Methods—Medical records of 101 dogs that had TTA were reviewed. Complications were recorded and separated into either major or minor complications based on the need for additional surgery. In-hospital re-evaluation of limb function and time to radiographic healing were reviewed. Further follow-up was obtained by telephone interview of owners. Results—Complications occurred in 31.5% of the dogs (12.3% major, 19.3% minor). Major complications included subsequent meniscal tear, tibial fracture, implant failure, infection, lick granuloma, incisional trauma, and medial patellar luxation; all major complications were treated with successful outcomes. All but 2 minor complications resolved. The mean time to documented radiographic healing was 11.3 weeks. Final in-hospital re-evaluation of limb function (mean, 13.5 weeks), was recorded for 93 dogs with lameness categorized as none (74.5%), mild (23.5%), moderate (2%), and severe (1%). All but 2 owners interviewed were satisfied with outcome and 83.1% reported a marked improvement or a return to pre-injury status. Conclusions—TTA is a procedure comparable with alternate methods of CrCL repair with expected good to excellent functional outcome. Clinical Relevance—TTA procedure can be successfully used to obtain the dynamic stability of a CrCL-deficient stifle joint in dogs. r Copyright 2007 by The American College of Veterinary Surgeons



during weight-bearing by neutralizing the cranial tibial thrust (CrTT).4,5 This is achieved by radial osteotomy of the proximal tibia, allowing rotation of the tibial plateau along this arc to obtain reduction of the tibial plateau angle (TPA).5–8 Recently, a new technique, tibial tuberosity advancement (TTA), has been proposed to similarly stabilize the stifle joint during weight-bearing by neutralizing the CrTT.9–11 This is achieved by frontal plane osteotomy of the tibial crest to advance the patellar tendon perpendic-



INTRODUCTION



R



UPTURE OF the cranial cruciate ligament (CrCL) leads to abnormal craniocaudal motion of the tibia and excessive internal rotation of the stifle joint, which leads to progressive osteoarthritis.1–3 Restoration of function is obtained surgically by neutralizing the tibiofemoral shear forces in a CrCL-deficient stifle either statically or dynamically. Tibial plateau leveling osteotomy (TPLO) is reported to stabilize the stifle joint functionally



From the Alameda East Veterinary Hospital, Denver, CO and Cummings School of Veterinary Medicine at Tufts University, North Grafton, MA. Address reprint requests to Randy J. Boudrieau, DVM, Diplomate ACVS & ECVS, Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University, 200 Westboro Road, N. Grafton, MA 01536. E-mail: [email protected]. Submitted December 2006; Accepted April 2007 r Copyright 2007 by The American College of Veterinary Surgeons 0161-3499/07 doi:10.1111/j.1532-950X.2007.00307.x



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Fig 1. Transparency Guide (Kyon). Top: Plate sizes from 2-hole to 8-hole, which correspond to the size of the tibial crest (and forks of the identical number to match the plate). Bottom: Measuring guide to determine cage width; horizontal line aligns with the tibial plateau slope (arrow), vertical line aligns with the cranial margin of the patellar tendon (arrowhead), and distance determined by the overlay from the vertical line to the tibial tuberosity (curved arrow; compare with Fig 2). Cage widths correspond to the 3, 6, 9, and 12 mm vertical lines present.



ular to the tibial plateau.9 TTA is also reported to functionally stabilize the stifle joint during weight-bearing by neutralizing CrTT.12 Our purpose was (1) to describe the surgical technique for TTA using a specially designed tension-band plate (Kyon; Zu¨rich, Switzerland) and (2) to describe early results and complications in an initial series of 101 dogs.



MATERIALS AND METHODS Inclusion Criteria Medical records of 101 dogs with CrCL injuries that had the TTA procedure were reviewed. Dogs were admitted to Alameda East Veterinary Hospital (July 2003 to September 2004) and Cummings School of Veterinary Medicine at Tufts



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Fig 2. Pre-operative, true lateral radiographic projection; the stifle joint is at 1351 extension (the femoral and tibial axes are determined by the diaphyses). For simplicity, only 2 lines are drawn (identical to the transparency guide; compare with Fig 1): horizontal line along the tibial plateau slope, and vertical line along the cranial margin of the patellar tendon. The distance to advance the cage in this example is 9 mm.



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University (January 2004 to September 2004) and represent the first series of cases operated using TTA at each institution. Age, gender, weight, and breed were recorded. Complications (intra- and post-operative), treatment, and outcome were recorded. Post-operative complications were defined as any unexpected developments that occurred after surgery. Major complications were defined as those complications requiring subsequent surgical intervention; minor complications were defined as those not requiring additional surgical treatment. Surgical Planning (Guerrero TG, Tepic S, Baviera B, et al: Advancement of the tibial tuberosity for the treatment of cranial cruciate deficient canine stifle [video]. The First Instructional Course for Tibial Tuberosity Advancement (TTA) for Cranial Cruciate Deficient Stifle in Dogs. Denver, CO, 2004). Standard craniocaudal and lateral radiographic projections of the affected stifle joint were obtained pre-operatively to assess the joint. The lateral projection was centered on the stifle joint (perfect positioning confirmed by superimposition of both femoral condyles) at a stifle joint angle of 1351, using the long axes of the femur and tibia (the entire femur was included to determine the appropriate femoral long axis). The joint was positioned so that there was no cranial tibial translocation. A standardized TTA transparency (Kyon) was used to determine the amount of TTA required to position the patellar tendon perpendicular to the tibial plateau in a standing position (1351 stifle joint extension) and the size of the plate to cover the entire extent of the tibial crest (Fig 1). These measurements were obtained from the lateral radiographic projection (Fig 2). Alignment of the plate guide helped to determine holes (for the fork) and the final plate position along the tibial crest; in some cases it was necessary to align the proximal end of the plate slightly caudally (Fig 3).



Fig 3. (A) In most dogs, the plate can be aligned parallel to the rostral border of the tibial crest (arrowheads), which results in a slightly cranial location of the distal end of the plate (arrows); (B) In some dogs, the tibial crest is not as prominent distally; therefore, aligning the template (and plate) parallel to the tibial crest (arrowheads) will result in the distal plate aligning with the central tibial axis before the advancement (arrows); (C) Aligning the template (and plate) so that the proximal aspect is more caudally positioned (short arrow) will result in the distal plate aligning slightly cranial to the tibial long axis (arrows); this is the desired position; (D) Post-operative radiograph showing the plate position (compare with C; short arrow); after advancement of the tibial tuberosity, the distal plate position moves caudally (arrows) and now rests once again along the tibial long axis.



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Fig 4. Sequential intra-operative photographs demonstrating key points in the surgical technique (7-hole plate, 12 mm cage); the dog is in dorsal recumbency, and the right hind limb is rotated onto the surface of a Mayo stand to align the tibia parallel to the floor (for orientation all photographs show the outline of the medial tibial surface). (A) Approach to the medial tibial surface; the caudal belly of the sartorius muscle and the aponeurosis of the gracilis, semi-membranosus, and semi-tendinosus muscle insertions have been incised and elevated (thumb forceps). The incision originates a few millimeters caudal and parallel to the tibial crest and is extended distally to the tibial diaphysis; rostrally, the periosteum is reflected to expose the cranial bone margin along the entire tibial crest; the elevated periosteum allows a point of attachment for re-suturing the aponeurosis of the elevated musculature with wound closure. (B) An 8-hole drill guide (Kyon) is placed parallel to the cranial margin of the tibial crest, with the first hole positioned at the level of the patellar tendon insertion into the tibial tuberosity; in this example, a 7-hole plate is to be applied (the most proximal and distal holes, #1 and #7, are drilled and alignment pins are placed to maintain the guide position before drilling all remaining holes, #3–6). (C) An osteotomy is performed parallel to the frontal plane extending from the distal extent of the tibial crest to a point immediately cranial to the medial meniscus (and cranial to the long digital extensor tendon). A bicortical osteotomy is performed distally, and extended only through the medial cortex proximally. (D) The appropriate size plate and fork are assembled. Note that the central peg of the fork has a notch to match the smaller square central hole of the plate to snap both pieces together. A fork inserter (Kyon) is secured to the base of the fork (and plate combination) to facilitate its application into the tibial crest. (E and F) A small mallet is used to seat the plate/fork combination into the tibial crest (note the cranial position of the distal plate in relation to the tibial long axis); after the plate is seated, the bicortical osteotomy in the tibial crest is completed.



Surgical Technique (Guerrero TG, Tepic S, Baviera B, et al: Advancement of the tibial tuberosity for the treatment of cranial cruciate deficient canine stifle [video]. The First Instructional Course for Tibial Tuberosity Advancement (TTA) for Cranial Cruciate Deficient Stifle in Dogs. Denver, CO, 2004).



Surgery was performed with the dog positioned in dorsal recumbency. The affected limb was aseptically prepared and draped to provide full access to the limb from mid thigh to the hock. All dogs were administered perioperative cefazolin (22 mg/kg).



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Fig 5. Sequential intra-operative photographs demonstrating key points in the surgical technique—continued. (A & B) A T-handle with a 12 mm spreader attached distally (Kyon) is inserted into the osteotomy gap and then rotated 901; the spreader assures a gap of sufficient width to place the 12 mm cage. (C) The appropriate length 12 mm cage is prepared for insertion; the ears are bent to match the corresponding contour of the tibia (the bottom right photo shows the most dorsal (wider) cage surface with the caudal ear bent slightly up and rotated slightly counterclockwise, and the cranial ear bent slightly down and also rotated slightly clockwise. (D) The cage has been secured with a 2.4 mm screw in the caudal ear (directed caudodistally) and the distal drill-hole in the plate is about to be placed (to accept a 3.5 mm screw); note that bone contact is obtained at the distal extent of the tibial crest and there is a slight shift proximally; also note the now central position of the plate along the tibial long axis after the tibial tuberosity has been advanced. (E) An allograft, fine corticocancellous bone chips with Demineralized Bone Matrix powder (Fine Mix Osteo-Allograftt, Veterinary Transplant Services) is placed within the osteotomy gap distal to the cage and also into the cage. (F) Completed appearance of the tibial tuberosity advancement. Inset: again notice the slight proximal displacement of the tibial crest so as to ensure a center of rotation of the patellar tendon’s attachment to the tibial tuberosity based at the patella.



Exploration of the stifle joint before surgical stabilization was completed either by arthrotomy or arthroscopy to evaluate the stifle joint (degree of damage to the cruciate ligaments and menisci, and to evaluate the presence of degenerative joint disease). Remnants of the torn CrCL were debrided and any



meniscal tears were treated by partial or complete meniscectomy. Initially, all intact menisci were left in situ; however, in later cases a medial meniscal release was performed, either mid-substance during arthroscopy or by transection of the caudal meniscotibial ligament during arthrotomy.



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Fig 6. Craniocaudal and lateral post-operative radiographs of a completed tibial tuberosity advancement immediately postoperatively. The slight proximal shift of the tibial crest can be seen (small arrows). Notice in this case that the plate has been placed parallel to the cranial tibial margin of the tibial crest. The lateral border of the osteotomized tibial crest can also be seen; notice that the lateral margin of the cage follows the contour of the bone at this level (large arrows). The cage is placed 2–3 mm below the proximal extent of the tibia (arrowhead). Also notice that the caudal extent of the osteotomy at the level of the tibial joint surface: immediately cranial to the medial meniscus (this position is also cranial to the long digital extensor tendon laterally). Exposure of the craniomedial aspect of the tibial crest was performed by incising the insertion of the caudal belly of the sartorius muscle and the aponeurosis of the gracilis, semimembranosus, and semitendinosus muscle insertions (Fig 4A). This incision was made a few millimeters caudal and parallel to the tibial crest and extended distally to the tibial diaphysis. The periosteum of the tibial crest was reflected cranially to expose the cranial bone margin of the entire tibial crest. An 8hole drill guide (Kyon) was positioned parallel to the cranial margin of the tibial crest, with the first hole aligned with the level of the patellar tendon insertion into the tibial tuberosity (Fig 4B). The number of 2.0-mm holes drilled corresponded to the plate size determined during pre-operative planning. Before drilling these holes, plate orientation was checked so that the distal end was slightly forward of the central tibial axis to ensure that after subsequent advancement/rotation of the tibial tuberosity, the distal screw-holes in the plate would overlay



the central tibia. Sometimes, it was necessary to align the proximal end of the plate slightly caudally (Fig 3). The planned osteotomy, perpendicular to the sagittal plane of the tibia, was oriented from a point immediately cranial to the medial meniscus (and cranial to the long digital extensor tendon) to the distal extent of the tibial crest. A bicortical osteotomy was begun distally, and extended only through the medial cortex for approximately one-half of the total distance proximally (Fig 4C). A TTA tension-band plate was contoured to match the shape of the tibial crest and proximal tibia. The plate was bent with a slight caudal rotation and distomedial bend; all bending/twisting was performed in the area between the fork and screw-holes. A fork designed to fit within the tension-band plate, of the corresponding size, was locked into the plate (Fig 4D). The plate/fork combination was then secured into the tibial crest (which required impaction of the fork with a mallet into the pre-drilled holes in the bone; Fig 4E and F). The remainder of the osteotomy was completed. The tibial crest, with attached plate, was moved cranially using a spacer attached to a T-handle (Kyon) that corresponded to the selected cage width (Fig 5A and B). A cage was placed into the osteotomy site at the proximal extent of the osteotomy (  2–3 mm from the proximal tibial bone margin) and secured at its caudal margin to the tibia with a 2.4 mm screw directed caudodistally; the ‘‘ears’’ of the cage (screw-holes) were contoured to match the corresponding tibial surfaces (Fig 5C and D). The plate was then secured distally to the tibia with the appropriately sized screws (2.7 mm or 3.5 mm); the entire tibial crest was allowed to shift a few millimeters proximally to ensure that the patella position was unaltered (arc of rotation of the patellar tendon’s attachment to the tibial tuberosity centered at the patella). Finally, the cranial cage screw was secured into the tibial tuberosity directed cranioproximally. The limb was evaluated to confirm the absence of CrTT. A bone graft was placed into the osteotomy (Fig 5 E and F). Sources of bone graft material included either autograft retrieved from the dog at surgery (proximal tibia or distal femur) or commercially available frozen allograft (Demineralized Bone Matrix [DBM] powder or Fine Mix Osteo-Allograftt [corticocancellous chips sieved to o2.5 mm and DBM]; Veterinary Transplant Services, Kent, WA). The quantity of graft used was sufficient to fill the entire osteotomy gap, including the cage (generally 2–5 mL depending on the size of the dog). Closure of the surgical site was initially achieved by apposition of the aponeurosis of the medial thigh muscles to the periosteum of the tibial crest to cover the implants. This began at the level of the tibial tuberosity with the stifle joint in full flexion. Occasionally, it was necessary to transect the distal crural fascia of the semitendinosus muscle (attachment to the medial surface of the tibia) and/or incise further proximally along the cranial border of the caudal sartorius muscle to further mobilize these structures. The remaining wound was closed in layers. Post-operative radiographs were obtained to evaluate the osteotomy and plate/cage position (Fig 6). A modified Robert Jones bandage was applied for the first 24–48 hours post-operatively in most dogs at the surgeon’s discretion, and removed before hospital discharge.



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Table 1. Major Complications (Defined as Subsequent Surgical Intervention) After Tibial Tuberosity Advancement in 114 Stifle Joints in 101 Dogs Complication



Number



Additional Details



Treatment



Outcome



Subsequent meniscal tear



7



Mean 24.5 weeks post-operative (range, 13–31 weeks)



Stifle joint re-exploration; partial meniscectomy



Resolution of lameness



Implant failure



1



Multiple forks fractured, loss of fixation to tibial crest (3 weeks post-operative)



Implant removal and replacement



Healed within 6 weeks and resolution of lameness



Tibial fracture



2



Stress fracture though either proximal or distal screw of plate (in both cases osteotomy extended to level of screws)



Open reduction internal fixation using a dynamic compression plate



Healed fracture within 8–12 weeks



Lick granuloma



2



Began within 4–7 weeks post-operative; unsuccessful with E-collar



Excised with primary closure



Healed without future problems



Septic arthritis



1



5 weeks post-operative



Open joint flush with joint culture and antibiotic susceptibility testing (Staphylococcus sp); 30 days doxycycline



Infection resolved



Chronic poor performance



1



#1: Lameness at 16 weeks post-operative #2: lameness at 43 weeks post-operative



#1: meniscal tear with debridement #2: medial patella luxation, (hypermobile patella and rotational joint instability); lateral suture stabilization



Resolution of lameness on both occasions



1 dog with a subsequent meniscal tear is included in both complication categories.



Follow-Up In-hospital evaluations were performed post-operatively at the respective institutions, or by the referring veterinarian, until fracture healing was radiographically evident. All dogs were assessed for lameness as well as any other complications. Limb function was categorized as: no lameness, mild lameness (weight-bearing lame), moderate lameness (weight-bearing lame with intermittent non-weight bearing), severe lameness (non-weight-bearing lameness with brief intermittent weight bearing) and non-weight-bearing lameness. All post-operative complications were recorded. Further longer-term follow-up was obtained by telephone interview of owners who were asked to rate their dog’s performance after surgery and to comment on whether or not they would again consider TTA to treat CrCL injuries in their pets.



RESULTS Signalment TTA for CrCL repair was performed in 101 dogs (50 spayed [49.5%] and 3 intact females [3%] and 48 castrated males [47.5%]). The mean age was 5.9 years (range, 1–13 years) and the mean body weight was 36.7 kg (range, 14.5–83.0 kg). There were 33 Labrador Retrievers (32.7%), 17 mixed breeds (16.8%), 11 German Shepherd Dogs (10.9%), 4 Golden Retrievers (3.9%), 4 Boxers (3.9%), 4 Rottweilers (3.9%), 3 Newfoundland Dogs (2.9%), 3 Australian Shepherd Dogs (2.9%), 3 Cocker Spaniels



(2.9%), 2 Border Collies (1.9%), 2 Springer Spaniels (1.9%), 2 Chesapeake Bay Retrievers (1.9%), and 1 each (1.0%) of the following breeds: Alaskan Malamute, Australian Cattle Dog, Bulldog, Chow chow, Collie, Elkhound, Giant Schnauzer, Great Dane, Great Pyrenees, Mastiff, Samoyed, Chinese Shar-Pei, and Siberian Husky.



Surgical Findings TTA was performed in 114 stifle joints (56 [49.1%] right, 58 [50.9%] left). Thirteen dogs (12.8%) had bilateral TTA, with the second procedure performed at varying intervals after the first. Seventy-four joints were evaluated by arthroscopy and 40 by arthrotomy. Fortysix joints (40.3%) had a medial meniscal tear (buckethandle or caudal pole) at initial surgery that was debrided by partial meniscectomy. Initially, intact menisci were left in situ; however, later in the study, meniscal release (either caudal meniscotibial ligament or mid-substance) was performed in 22 stifle joints. Autograft was used in the first 17 dogs (adjacent proximal tibia in 8 dogs and adjacent distal femur in 9 dogs), and the other 97 had an allograft (DMB matrix powder in the first 20 joints, then Fine Mix in the next 77). Use of the Fine Mix graft was made primarily because of convenience compared with additional autograft procurement, and its improved handling characteristics compared with DBM.



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Long-term telephone follow-up of moderate lameness only after heavy activity Healed, ESF removed at 6 weeks post-operative



Healed by second intention



Resolved within an additional 48–72 hours Resolved 3



2



1 1 1



1



Post-operative stifle joint and distal limb swelling



Superficial skin infection



Incisional dehiscence Incisional trauma Chronic poor performance



Intra-operative tibial fracture (non-displaced)



Opening of distal 2 cm Self trauma (removed staples) Severe lameness at first in-hospital re-evaluation 12 weeks post-operative; Full joint range of motion without pain Fracture occurred during distal plate re-positioning



3 Poor mineralization within osteotomy gap



Suture reaction/local skin infection



Robert Jones bandage in 1 for 48 hours; no treatment in 2 Removed exposed subcutaneous sutures; Oral antibiotics Oral antibiotics None Aggressive physiotherapy {Did not return for further in-hospital evaluation} Type Ia (4-pin) SKt ESF applied immediately intra-operatively



None



3 Implant failure



Incidental finding; fracture of 1–2 forks within tibial crest in 2 cases, lucency around cage in 1 case; no clinical signs Incidental finding; no change in appearance followed  6 þ months; no clinical signs All within first 24–72 hours post-operative



None None; no clinical signs in 2 dogs, Unchanged: 2 dogs remained owner declined treatment in 1 dog asymptomatic, 1 dog with persistent lameness None Incidental finding; no clinical signs Audible clicking; lameness in 1 dog 4 3 Non-displaced tibial tuberosity chip fracture Suspect subsequent meniscal tear



Treatment Additional Details Number Complication



Table 2. Minor Complications (Defined as No Further Surgical Intervention) After Tibial Tuberosity Advancement in 114 Stifle Joints in 101 Dogs



Outcome



TIBIAL TUBEROSITY ADVANCEMENT IN 101 DOGS



In-Hospital Re-Evaluation In-hospital evaluation and radiographic assessment of healing occurred in 93 dogs (102 stifle joints) from 3 to 63 weeks post-operatively with the mean time for final inhospital re-evaluation of limb function being 13.5 weeks post-operatively. Outcome was: no lameness, 67 dogs (76 joints, 74.5%); mild lameness, 23 dogs (24 joints, 23.5%); moderate lameness, 2 dogs (2 joints, 2.0%); and severe lameness, 1 dog (1 joint, 1%). The mean time to complete healing was 11.3 weeks (range, 4–63 weeks); 10 healed within 4–6 weeks, 31 in 6–8 weeks, 37 in 8–12 weeks, and 15 had healing at some point 412 weeks. Thus, 44.1% were healed within 8 weeks and 83.9% within 12 weeks; however, in 7 of the remaining cases that healed 412 weeks, the first radiographic follow-up was obtained between 16 and 63 weeks (mean, 34.6 weeks; median, 40 weeks). The mean time to complete radiographic healing, eliminating these latter cases, was 9.4 weeks (range, 4–20 weeks). No difference in healing was observed between autograft or allograft use to fill the osteotomy gap. Complications Post-operative complications were reported for 36 (31.5%) of the 114 stifle joints. Of these, 14 (12.3%) were classified as major complications (Table 1) and 22 (19.3%) as minor complications (Table 2). Major complications (Table 1). There were 7 documented meniscal tears, 2 tibial fractures, 2 lick granulomas, and 1 each of implant failure, septic arthritis, and medial patellar luxation. Meniscal tears were documented further during exploratory surgery and partial meniscectomy was performed. The 2 tibial fractures were stabilized with plate fixation. The 2 lick granulomas were originally treated with Elizabethan collars to prevent licking, but were unsuccessful and the granulomas were surgically excised. The infection was treated by joint exploration and debridement and based on bacterial culture and susceptibility testing antibiotic therapy was administered for 4 weeks. Medial patellar luxation occurred after a second surgical exploration of the joint to address a subsequent meniscal tear. During this third surgical procedure, the joint had excessive rotational instability and a hypermobile patella. Lateral retinacular stabilization was performed to restabilize the joint. All major complications were corrected and resulted in successful outcomes. Minor complications (Table 2). There were 4 nondisplaced tibial tuberosity chip fractures (small nondisplaced avulsion fracture fragments observed at the proximal end of the tibial tuberosity), 3 implant failures (1 or 2 prongs of the forks fractured, but without any displacement in 2 stifle joints; radiolucency around a



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2 dogs, and application of a Robert Jones bandage in 1 dog. The 2 infections and the incisional dehiscence were treated with antibiotics. In the dog with the non-displaced intra-operative tibial fracture, the tibia was supplemented with a 4-pin Type I external skeletal fixator for the first 6 weeks post-operatively. The patient-induced incisional trauma was treated with an Elizabethan collar only. In the dog with the chronic poor performance, the first in-hospital re-evaluation was at 12 weeks, at which time the dog was minimally weight bearing with marked quadriceps muscle atrophy. The stifle joint had full range of motion and no palpable instability present. Aggressive physical therapy was recommended. This dog was lost to further in-hospital follow-up; however, with subsequent long-term telephone follow-up (at 1 year) the dog was reported to be generally sound, but moderately lame only after heavy activity. All minor complications were successfully resolved, except 1 dog with the audible clicking, which had a persistent lameness, and the dog with chronic poor performance, which was not examined again. Telephone (Owner) Follow-Up Fig 7. Lateral radiograph of a tibial fracture 2.5 weeks postoperatively. A number of technical failures are evident: The osteotomy cut is too far cranial and the cage is located too far proximally. The key error, however, is the distal extent of the tibial osteotomy (white arrow), which extends distal to the distal screw attachment of the plate (arrowhead); a stress-riser is created that pre-disposes to a fracture at this location. The plate should be sufficiently large, and the osteotomy cut should end sufficiently proximal, at the distal tibial crest (black arrow), to ensure an intact tibial cortex at the level of screw insertion of the plate.



portion of the cage in 1 stifle joint), 3 with audible clicking with ambulation, 3 with post-operative swelling, 3 with poor graft mineralization, 2 with superficial incisional infections, and 1 each of chronic poor performance, partial incisional dehiscence (o2 cm), non-displaced intra-operative tibial fracture, and self-inflicted incisional trauma (o2 cm). No treatment was performed in the 4 cases of tibial tuberosity chip fractures, the 3 dogs with implant failure, and the 3 dogs with poor graft mineralization (followed for 6 months without any observable change to the area), all of which were incidental findings. No treatment was performed in the 3 dogs with audible clicking because of the absence of any clinical dysfunction in 2 dogs, and was declined in the other dog. We presumed that these were meniscal tears, which occurred after TTA. Post-operative joint swelling resolved in the 3 dogs within 72 hours; this occurred without treatment in



Follow-up for 91 (90.1%) owners was obtained by telephone survey 3–15 months post-operatively (mean, 8.4 months) and revealed that most owners were satisfied with the outcome. All contacted owners indicated that their dog improved after TTA. Seven (6.9%) owners indicated that their dog improved only slightly, 38 (37.6%) indicated marked improvement, whereas 46 (45.5%) stated that their dog returned to the pre-injury status. Of these 91 owners, only 2 (2.2%) indicated that they were displeased with the surgical procedure and would most likely pursue alternative treatment for a cruciate ligament injury should their pet require similar surgery in the future. One owner was displeased because of the poor long-term outcome, although the last in-hospital evaluation at 8 months post-operatively indicated that the dog was not lame. The other owner was unhappy because of complications that occurred postoperatively, which included a subsequent meniscal tear and medial patellar luxation. The remaining 89 owners (97.8%) indicated that they would choose TTA again without hesitation. DISCUSSION TTA is based on a mechanical model analysis of the human knee that characterizes the joint forces acting on the knee in a weight-bearing position.13 Based on this model, there is a resultant joint force approximately parallel to the patellar tendon with either an anterior or posterior tibiofemoral shear force present based upon



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Fig 8. Immediate post-operative lateral radiograph, and 3-week post-operative lateral and craniocaudal radiograph illustrating implant failure. A number of technical failures are evident in the post-operative radiograph; the osteotomy cut is too far cranial and oriented obliquely (arrows outline the medial extent of the cut—aligning with the medial aspect of the cage). The forks of the plate can be observed secured only in the medial tibial cortex. In addition, the cage is too small for this dog (6 mm cage in a dog with an 8hole plate). In the follow-up radiographs, the forks have fractured and the tibial crest is no longer secured; the tibial crest has rotated caudally (and the cranial ear of the cage has fractured).



the knee flexion angle, and a crossover point of neutral tibiofemoral shear that is dependent upon the patellar tendon angle (PTA—angle between the patellar tendon and tibial plateau slope).13 Similar assumptions have been made in the dog.9–11 The point at which there is a crossover, or neutral tibiofemoral shear force, was proposed to be at a PTA of 901 during the fully extended weight-bearing position of the gait.9–11 Therefore, the basis of the TTA is to move the tibial tuberosity sufficiently far cranially to maintain a PTA  901 during weight bearing so as to obtain a neutral or caudally directed tibiofemoral shear force during ambulation, thereby stabilizing the joint.9–11 The effect of advancing the tibial tuberosity has been validated in an in vitro experimental study.12 The TTA surgical technique has been used with success clinically at the University of Zu¨rich, where it was developed.9 Furthermore, this technique is currently being used clinically by 4250 surgeons, 49000 cases, in the United States and Europe (personal communication, 2007—Slobodan Tepic: Kyon); however, there are no current reports that describe the details of the surgical technique, and there is little information available regarding complications.14,15 TTA is a relatively simple method to alter the effective insertion point of the patellar tendon, thus altering stifle joint function. The surgical dissection is limited to the medial tibial surface, with an osteotomy similar to that performed for tibial tuberosity transposition for



correction of patellar luxation, albeit with osteotomy of a much larger bone fragment. This procedure, therefore, does not involve any major circumferential surgical dissection of the tibia (although currently there are some surgeons performing a more limited dissection with, for example, the TPLO). The specially designed tension-band plate is a thin, pure titanium implant. This implant provides adequate neutralization of the distractive forces, similar to a tension-band wire, and as an implant of commercially pure titanium, has excellent biocompatibility.16–18 In-Hospital Re-Evaluation The in-hospital follow-up (93 dogs) revealed generally good results. Most dogs (84%) had radiographic healing within 12 weeks with either no lameness or mild lameness in 97% of the dogs. These results may be overly optimistic based upon retrospective evaluation of medical records where specific criteria to assess lameness were not established at the time of the in-hospital assessment. Furthermore, the mean follow-up time (13.5 weeks) was short. The mean time to complete radiographic healing was  11 weeks. Radiographic follow-up was not available for all dogs, nor was it available at consistent intervals, and so the actual time to final radiographic healing may have been shorter. For those dogs where radiographic follow-up was available, healing was complete in  50%



LAFAVER ET AL



at 6–8 weeks and in 480% at 8–12 weeks. Almost 50% of the remaining cases did not have their first follow-up radiographs until 412 weeks post-operatively (mean, 34 weeks). It may be reasonably assumed that many of these dogs had probably healed before this time frame. If these cases are excluded, the final time to radiographic healing decreases to a mean of 9.4 weeks (range, 4–20 weeks). Complications Complications are frequently reported as either major or minor depending upon their perceived clinical importance. Because this is a subjective assessment, we chose to adopt a more objective measure, namely whether or not further surgery was required. This classification, however, produced some anomalies; some problems would more likely be classified in the opposite area based upon their severity or perceived clinical importance, or lack thereof, regardless of whether or not further surgery was performed. For example, the 2 lick granulomas could be considered minor issues despite ultimate use of surgery for resolution. Similarly, the 3 dogs with audible clicks in the joint most likely represented meniscal tears, and therefore could be considered major complications. Also, the 1 dog with continued poor performance could also be considered a major complication despite their owner’s reluctance to pursue further treatment, although no diagnosis was obtained. Finally, the 1 intra-operative fracture could be considered a major complication even though no further surgery was required. Based upon these further more subjective and perhaps clinically relevant assessments, we believe it reasonable to state that there were 17 (14.9%) ‘‘major’’ complications and 19 (16.7%) ‘‘minor’’ complications. Moreover, some of the listed minor complications were incidental findings: the 4 non-displaced tibial tuberosity chip fractures at the proximal extent of the tibial tuberosity, 3 implant failures, and 3 poor graft mineralization. If the latter were eliminated, then the minor complication rate could be o8%. Overall complications occurred in  31% of the stifle joints operated, which is similar to that reported for TPLO (18.8–28%).19–21 In 1 TPLO study, complications were classified as major and minor complications, yielding 12.6% major and 21.7% minor complications,19 which is similar to our findings with TTA. Review of the other 2 TPLO studies shows a comparable rate of complications that can be similarly grouped.20,21 Like any surgical procedure, there are nuances that must be learned to avoid intra- and post-operative errors that may result in complications. As noted previously, all cases reported represent our first TTA cases. Some of the major complications seemingly resulted from technical mistakes during the initial learning curve associated with



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TTA. The 3 tibial fractures (1 occurred intra-operatively) and 1 implant failure (Figs 7 and 8) resulted from poor pre-operative planning or surgical execution resulting in incorrect size or position of the osteotomy cut and and/or incorrect plate positioning. The result of these errors was fracture of the tibia, or tibial crest, because of the increased stress-risers thus created. Because these complications occurred within the first 10 cases (at the respective institutions), we believe that they were technical failures related to surgeon inexperience. Attention to detail of the surgical technique cannot be over-emphasized and could eliminate these issues. Most of the other major complications were meniscal injuries. The number of meniscal tears identified at the original surgical procedure appears to be consistent with previous reports.22–25 The number of apparent subsequent meniscal injuries, on the other hand, was a concern despite these evidently accounting for o10% of the cases. This frequency of occurrence could be viewed as an acceptable number of subsequent injuries regardless of the surgical procedure. Meniscal tears discovered during convalescence could have been missed lesions at initial surgery. Because the overall number of meniscal tears observed at initial surgery was consistent with that expected from past clinical and reported experience, we did not believe that we had overlooked some; however, this could have occurred. Subsequent meniscal tears from later trauma, secondary to altered forces within the CrCL-deficient stifle joint, could have occurred. The latter possibility has been the rationale for the meniscal release recommended with TPLO (Seminar titled Tibial Plateau Leveling Osteotomy for Cranial Cruciate Ligament Repair; Slocum Enterprises Inc, Eugene, OR).6 It had been proposed that TTA, because of unaltered tibial plateau position, might spare the caudal portion of the joint and obviate the need to perform meniscal release.7,8 Ten subsequent meniscal tears were assumed to occur (7 documented), with an apparent frequency of 8.8% (10/ 114 joints). However, the number of meniscal injuries reported actually under-represents the number of possible subsequent injuries because 46 joints had an existing meniscal tear and partial meniscectomy was performed. Thus, the corrected frequency of subsequent meniscal tears is seemingly 14.7% (10/68). Nevertheless, both institutions were concerned with the apparently high number of subsequent meniscal tears observed and began performing medial meniscal release of the intact meniscus (22 joints). Therefore, a more accurate representation of frequency of subsequent meniscal tears is 21.7% (10/46 joints). Based on this high frequency, an argument can be made to support meniscal release, especially because no further meniscal injuries were identified after this procedure was instituted, either as a result of a lack of initial



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identification (missed lesion) or further (subsequent) trauma. Conjecture that performing a meniscal release in all cases could have eliminated all subsequent meniscal tears is an attractive proposition. If this were the case, the major complication rate could have been  6% (including those cases that were early technical failures). Such data extrapolation, however attractive, cannot be validated without further follow-up, including operating additional cases, but may be a point to contemplate. This question, however, remains open to debate and is controversial because of the inherent function of the meniscus within the joint, and the ensuing argument of the value of eliminating a crucial stabilizer to the joint.26–28 The effect of meniscal release, and its possible detrimental long-term effects in a large population of dogs, needs to be evaluated. The 4 cases of proximal tibial tuberosity chip fractures were unexplained; however, these were only observed in the initial cases. Our assumption is that there could have been some iatrogenic damage to this region during surgical dissection, perhaps some over-zealous exposure to the area of attachment of the patellar tendon when elevating the periosteum to expose the bone. Regardless, this complication was eliminated with additional experience. No clinical signs were associated with this finding, and no treatment was required. The 3 incidental implant failures, which also occurred during the initial cases, were thought to be technical failures resulting from inexperience with TTA. In these 3 cases, there was incorrect plate positioning as the distal end of the plate was secured along the tibial axis without obtaining bone contact at the distal end of the osteotomized tibial tuberosity. In these instances, the initial proximal plate position was secured without recognizing that the distal plate position was already overlaying the tibia (Fig 3). After advancement of the tibial tuberosity, the distal plate position would have been caudal to the tibial shaft with rotation/advancement of the tuberosity. The distal plate was still secured mid-tibia, which resulted in a gap between the bone fragments. We surmise that the fixation was thus somewhat unstable, resulting in implant failure (forks) and resorption observed around the cage. Despite the uncomplicated healing observed, these observations highlight the limits of the fixation device, and the necessity to obtain a second (distal) point of contact (in addition to the proximal contact with the cage) of the bone to ensure load sharing with the implant. Appropriate pre-operative planning will avoid this problem (Fig 3). Another alternative to address this issue, should it be recognized after the fact, would be to contour the plate around the caudal tibial margin. Although this requires increased surgical dissection, it will make certain bone contact is obtained distally, and thus protect the implants.



Three infections were observed, yielding a frequency of 2.6%, which is comparable with that reported for a clean surgical procedure.29,30 Poor mineralization within the osteotomy gap (3 dogs) was not believed to be of clinical importance because there were no associated clinical signs, lameness, or palpable discomfort. Furthermore, the region was palpated as a firm, unyielding texture, which was consistent with bone. Finally, the radiographic appearance did not change upon repeated evaluations up to 6 months postoperatively. In all 3 dogs, a commercially available allograft was used (2 DBM powder, 1 Fine Mix OsteoAllograftt); 2 cases occurred sequentially at 1 institution, and the other at the other institution. Tracking of these allografts, using the transplant records, was performed with the manufacturer; all allografts were from different donors. Furthermore, these allografts are always manufactured from 2 animals, primarily for the economic advantage related to small sample size, and with the further advantage of homogenization of osteoinductive factors (personal communication, 2007—Helen Newman-Gage: VTS, Kent, WA). It is speculated that the poorer mineralization in 2 cases could have been associated with the lesser osteoinductive capacity of the DBM powder used alone compared with the Fine Mix Osteo-Allograftt. Some form of irritation was noted in 3 dogs (lick granuloma, self-trauma). A multiplicity of reasons could explain this occurrence, from surgical irritation to infection to a reaction to the implants themselves, but none were definitively identified. It is our opinion that the reaction was because of the suture material (Polysorbt; United States Surgical Corporation, Norwalk, CT) based upon its superficial association with the original skin incision (as determined at the time of surgical excision and lack of histologic association with any of the deeper tissues), and only partial implant removal of the plate and fork only (the cage was not removed); however, this cannot be definitively stated, and is only speculation. Post-operative swelling was probably related to the dissection required with the surgical approach, and occurred in 3 dogs and resolved within 72 hours; in 1 dog, a bandage was applied. The importance of this problem appears minimal based on the rapid resolution over a short time frame, and the absence of treatment in 2 cases. Post-operative swelling appears to be a greater problem with TPLO.19,21 The observed difference may reflect disparity in the aggressiveness of the surgical dissection (TPLO4TTA) between techniques. In the dog with medial patellar luxation, it could be hypothesized that the position of the tibial tuberosity was altered, thus misaligning the quadriceps mechanism. Patellar luxation did not occur, however, until after a second surgical procedure to perform a meniscectomy. At



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meniscectomy, there was no palpable or radiographic evidence of a patellar luxation. Similarly, at the time of patellar luxation, before the third surgical procedure, there was no radiographic evidence of mediolateral tibial tuberosity transposition. Furthermore, the observation of increased rotational instability in the stifle joint appeared to be the primary abnormality present. Because this problem occurred after the subsequent partial meniscectomy, the absence of a portion of the meniscus, or another possible injury to this or related structures at the time of the second surgery, or shortly thereafter, could have resulted in the instability we observed. Telephone (Owner) Follow-Up TTA resulted in a functional outcome without lameness in a relatively short time based on in-hospital reevaluation. These results appeared to be supported by the longer-term evaluation obtained from owner interview by telephone. Most owners were pleased with their dog’s function with the dog either returning to pre-injury status or showing marked improvement after surgery. Furthermore, a number of owners had previous experience with either another dog, or the current dog, with CrCL injury treated by an alternate method (e.g. lateral suture, fibular head transposition, over-the-top intra-articular graft, TPLO), and offered [unsolicited] that the recovery from the TTA was much faster and easier compared with those techniques. These latter comments obviously are quite subjective interpretations by the owners, which may be affected by bias toward the most recently performed procedure. Regardless, both the in-hospital evaluations (albeit relatively short term) and the owner evaluations appear to indicate that the TTA is at least comparable with alternate methods of CrCL repair relative to an expected good to excellent function and outcome. We did not, however, attempt to make any functional assessments comparing any of the many available surgical techniques, but only to report on the individual efficacy of TTA, and report on the early complications associated with this surgical technique. The limitations of this study include those inherent to a retrospective study as well as the absence of concrete measures of post-operative performance. Despite these limitations, sufficient data for an overall assessment of the dogs’ function could be obtained. The complications were based upon an objective measure, of whether or not additional surgery was necessary, which allowed us to better assess the owner interpretation of their dog’s outcome. No owner reported any surgical procedures other than those we provided. Regardless, the short-term inhospital follow-up we obtained, confined to the point of radiographic healing only, remains an obvious limitation to any further evaluation of long-term function. Longer-



term objective clinical studies are warranted to assess the continued clinical viability of the TTA, e.g., force plate and kinematic gait analysis, stifle joint range of motion, muscle mass, and long-term radiographic and functional evaluation.



ACKNOWLEDGMENTS We thank Slobodan Tepic, Dr. Sci., and Pierre M. Montavon, DVM (Clinic for Small Animal Surgery of the Vetsuisse Faculty, University of Zu¨rich, Switzerland), for their contribution to the development of this surgical technique and their support.



REFERENCES 1. Elkins AD: A retrospective study evaluating the degree of degenerative joint disease in stifle of dogs following surgical repair of anterior cruciate ligament rupture. J Am Anim Hosp Assoc 27:533–539, 1991 2. Vasseur PB, Berry CR: Progression of stifle osteoarthritis following reconstruction of the cranial cruciate ligament in 21 dogs. J Am Anim Hosp Assoc 28:129–136, 1992 3. Arnoczky SP, Marshall JL: The cruciate ligaments of the canine stifle: an anatomical and functional analysis. Am J Vet Res 38:1807–1814, 1977 4. Slocum B, Devine T: Cranial tibial thrust: a primary force in the canine stifle. J Am Vet Med Assoc 183:456–459, 1983 5. Slocum B, Slocum TD: Tibial plateau leveling osteotomy for repair of cranial cruciate ligament rupture in the canine. Vet Clin North Am 23:777–795, 1993 6. Slocum B, Slocum TD: Tibial plateau leveling osteotomy for cranial cruciate ligament, in Bojrab MJ (ed): Current Techniques in Small Animal Surgery (ed 4). Baltimore, MD, Williams & Wilkins, 1998, pp 1209–1121 7. Warzee CC, Dejardin LM, Arnoczky SP, et al: Effect of tibial plateau leveling on cranial and caudal tibial thrusts in canine cranial cruciate-deficient stifles: an in vitro experimental study. Vet Surg 30:278–286, 2001 8. Reif U, Hulse DA, Hauptman JG: Effect of tibial plateau leveling on stability of the canine cranial cruciate ligamentdeficient stifle joint: an in vitro study. Vet Surg 31:147–154, 2002 9. Montavon PM, Damur DM, Tepic S: Advancement of the tibial tuberosity for the treatment of cranial cruciate deficient canine stifle. Proceedings of the 1st World Orthopaedic Veterinary Congress; Munich Germany, September 2002, p. 152 10. Tepic S, Damur DM, Montavon PM: Biomechanics of the stifle joint. Proceedings of the 1st Word Orthopaedic Veterinary Congress, Munich Germany, September 2002, pp 189–190 11. Tepic S, Montavon PM: Is cranial tibial advancement relevant in the cruciate deficient stifle? Proceedings of the 12th ESVOT Congress, Munich Germany, September 2004, pp 132–133



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12. Apelt A, Kowaleski MP, Boudrieau RJ: Effect of tibial tuberosity advancement on cranial tibial subluxation in canine cranial cruciate-deficient stifle joints: an in vitro experimental study. Vet Surg 36:170–177, 2007 13. Nisell R, Ne´meth G, Ohlse´n H: Joint forces in the extension of the knee: analysis of a mechanical model. Acta Orthop Scand 57:41–46, 1986 14. Damur DM: Tibial tuberosity advancement (TTA): Clinical results. Proceedings of the 2005 ACVS Veterinary Symposium. October, 2005, pp 441–442 15. Boudrieau RJ: Tibial tuberosity advancement (TTA): Clinical results. Proceedings of the 2005 ACVS Veterinary Symposium. October, 2005, pp 443–445 16. Imam MA, Fraker AC: Titanium alloys as implant materials, in Brown SA, Lemons JE (eds): Medical Applications of Titanium and its Alloys: The Material and Biological Issues, ASTM STP 1272. West Conshohocken, PA, American Society of Testing Materials, 1996, pp 3–16 17. Schmidt C, Ignatius AA, Claes LE: Proliferation and differentiation parameters of human osteoblasts on titanium and steel surfaces. J Biomed Mater Res 54:209–215, 2001 18. Pennekamp PH, Gessmann J, Diedrich O, et al: Short-term microvascular response of striated muscle to cp-Ti, Ti-6Al4 V, and T-6Al7Nb. J Orthop Res 24:531–540, 2006 19. Pacchiana PD, Morris E, Gillings SL, et al: Surgical and postoperative complications associated with tibial plateau leveling osteotomy in dogs with cranial cruciate ligament rupture: 397 cases (1998–2001). J Am Vet Med Assoc 222:184–193, 2003 20. Priddy NH, Tomlinson JL, Dodam JR, et al: Complications with and owner assessment of the outcome of tibial plateau leveling osteotomy for treatment of cranial cruciate ligament rupture in dogs: 193 cases (1997–2001). J Am Vet Med Assoc 222:1726–1732, 2003



21. Stauffer KD, Tuttle TA, Elkins AD, et al: Complications associated with 696 tibial plateau leveling Osteotomies (2001–2003). J Am Anim Hosp Assoc 42:44–50, 2006 22. Flo GL: Modification of the lateral retinacular imbrication technique for stabilizing cruciate ligament injuries. J Am Anim Hosp Assoc 11:570–576, 1975 23. Gambardella PC, Wallace LJ, Cassidy F: Lateral suture technique for the management of anterior cruciate ligament rupture in dogs: a retrospective study. J Am Anim Hosp Assoc 17:33–38, 1981 24. Scavelli TD, Schraeder SC, Matthiesen DT, et al: Partial rupture of the cranial cruciate ligament of the stifle in dogs: 25 cases (1982–1988). J Am Vet Med Assoc 196:1135–1138, 1990 25. Thieman KM, Tomlinson JL, Fox DB, et al: Effect of meniscal release on rate of subsequent meniscal tears and ownerassessed outcome in dogs with cruciate disease treated with tibial plateau leveling osteotomy. Vet Surg 35:705–710, 2006 26. Johnson KA, Francis DJ, Manley PA: Comparison of the effects of caudal pole hemi-meniscectomy and complete medial meniscectomy in the canine stifle joint. Am J Vet R 65:1053–1060, 2004 27. Pozzi A, Litsky A, Field JR: Meniscal release impairs load transmission and joint stability in the canine stifle. Abstracts of the 12th ESVOT Congress; Munich, Germany, September, 2004, pp 262 28. Pozzi A, Kowaleski MP, Apelt D, et al: Effect of meniscal release on tibial translation after tibial plateau leveling osteotomy. Vet Surg 35:486–494, 2006 29. Rosin E, Dow S, Daly W, et al: Surgical wound infection and use of antibiotics, in Slatter DH (ed): Textbook of Small Animal Surgery (ed 2). Philadelphia, PA, WB Saunders, 1993, pp 84–95 30. Lipowitz AJ: Surgical wounds, in Lipowitz AJ, Caywood DD, Newton CD, et al: (eds): Complications in Small Animal Surgery: Diagnosis, Management, Prevention. Philadelphia, PA, Williams and Wilkins, 1996, pp 1–6



Licentiate’s thesis



Surgical treatment of canine cranial cruciate ligament deficiency A literature review University of Helsinki, Faculty of Veterinary Medicine, 2012 Department of Equine and Small Animal Medicine, Small Animal Surgery



Jan Mattila, MSc Econ, BSc Vet Med



Tiedekunta–Fakultet–Faculty Eläinlääketieteellinen tiedekunta



Osasto–Avdelning–Department Kliinisen hevos- ja pieneläinlääketieteen osasto



Tekijä–Författare–Author Jan Mattila Työn nimi–Arbetets titel–Title Surgical treatment of canine cranial cruciate ligament deficiency – A literature review Oppiaine–Läroämne–Subject Pieneläinkirurgia Työn laji–Arbetets art–Level Aika–Datum–Month and year lisensiaatintutkielma huhtikuu 2012 Tiivistelmä–Referat–Abstract



Sivumäärä–Sidoantal–Number of pages 49



Cranial cruciate ligament (CrCL) deficiency is the leading cause of degenerative joint disease (DJD) in the canine stifle. The anatomy of the canine stifle is complex and the pathogenesis of CrCL rupture is not fully understood. Several competing theories on the pathogenesis and several techniques based on these theories have been presented mostly during the last 40 years. The main categories of techniques are intraarticular, extracapsular and osteotomy, of which techniques of the two latter categories are still widely in use. The uncertainty about the pathogenesis and thus the correct technique of repair may be a reason for the multitude of proposed surgical techniques and the lack of preventive measures. This literature review attempts to cover the main surgical techniques from the three categories of techniques which are currently or have lately been in use and to determine if a preferred method exists. Approximately half of the literature is from 2000–2012 and half from 1926–2000. The literature encompasses both the original publications of each technique as well as studies on the outcomes and complications of follow-up studies using larger populations of patients. The reporting on the research regarding new surgical techniques is varied and the urge to perform surgery and not research is evident in the amount of surgical procedures reported before any peer-reviewed studies have been published. There are no meta-analyses of studies covering different techniques nor are there robust prospective double blinded placebo controlled studies on any of the alternative techniques. Most of the literature is case reports with some retrospective cohort or statistically insignificant prospective studies. Due to the non-uniform reporting, comparisons between techniques are more difficult. The literature does seem to favor TPLO, one of the oldest and the most researched technique, if the surgeon is able to invest the time and resources to acquiring the equipment and mastering the technique. If combined with the cTTA technique, a newer technique which uses some of the same equipment as the TPLO with very promising preliminary results, a surgeon could be well equipped to handle surgical treatment of CrCL deficiency.



Avainsanat–Nyckelord–Keywords cranial cruciate ligament rupture, surgical techniques, canine, eturistisiteen repeämä, kirurginen tekniikka, koira Säilytyspaikka–Förvaringställe–Where deposited Viikin kampuskirjasto Työn johtaja (tiedekunnan professori) ja ohjaaja–Instruktör och ledare–Director and Supervisor(s) Johtaja: Outi Laitinen-Vapaavuori, pieneläinkirurgian professori, ELT, Dipl. ECVS Ohjaaja: Pauli Keränen, kliininen opettaja, ELT, pieneläinsairauksien erikoiseläinlääkäri



1 Introduction!.............................................................................5 2 Anatomy of the stifle joint!......................................................7 3 Pathogenesis of CrCL rupture !...............................................9 4 Surgical techniques!..............................................................11 4.1 Intra-articular techniques!...............................................................12 4.1.1 Paatsama operation!.......................................................................12 4.1.2 Intra-articular repair or over-the-top !...............................................13 4.1.3 Modified intra-articular repair!..........................................................14 4.1.4 Under-and-over!..............................................................................14 4.1.5 Modified under-and-over!................................................................15 4.2 Extracapsular techniques!..............................................................16 4.2.1 Lateral retinacular imbrication or lateral fabellar suture (LFS)!.......16 4.2.2 Modified LFS !..................................................................................17 4.2.3 Fibular head transposition (FHT)!...................................................17 4.2.4 Tightrope cranial cruciate ligament or Tightrope CCL (TR)!............18 4.3 Osteotomy techniques!...................................................................20 4.3.1 Cranial tibial wedge osteotomy (CTWO)!........................................20 4.3.2 Tibial plateau leveling osteotomy (TPLO)!......................................21 4.3.3 Tibial tuberosity advancement (TTA)!..............................................22 4.3.4 Proximal tibial osteotomy (PTIO)!...................................................23 4.3.5 Triple tibial osteotomy (TTO)!..........................................................24 4.3.6 Circular tibial tuberosity advancement (cTTA)!................................25 4.3.7 Modified Maquet technique (MMT)!................................................26



5 Outcomes!..............................................................................28 5.1 Outcomes of intra-articular techniques!........................................28 5.2 Outcomes of extracapsular techniques!........................................29



5.3 Outcomes of osteotomy techniques!.............................................30



6 Complications!.......................................................................33 6.1 Complications associated with intra-articular techniques!.........33 6.2 Complications associated with extracapsular techniques!.........33 6.3 Complications associated with osteotomy techniques!..............34



7 Ancillary procedures !............................................................38 8 Conservative treatment!........................................................39 9 Prevention!..............................................................................40 10 Discussion!...........................................................................41 11 References!...........................................................................45



1 Introduction Cranial cruciate ligament deficiency is the leading cause of degenerative joint disease (DJD) in the canine stifle (Elkins et al. 1991). Since the source of the deficiency, the complete or partial rupture of the cranial cruciate ligament (CrCL), was first described in veterinary literature (Carlin 1926), a plethora of surgical techniques have been described for use in resolving the issue. One reason for the multitude of options may be the old anecdote “to be considered an orthopedic surgeon [one] must develop a new surgical technique or modify an old technique for treatment of cranial cruciate rupture” (Olmstead 1993). A more likely one is that none of the techniques presently available and introduced in the following pages have been shown to be unequivocally superior to all others. Another good reason for the interest in CrCL techniques stems from the fact that the market for canine CrCL treatments has been estimated at $1,32 billion in 2003, in the US (Wilke et al. 2005). At the time this would have represented a little over 15 % of the total expenditure on all veterinary care of in the US, if the relative share of CrCL treatments has stayed stable (APPA 2011 and APPA 2003). If the relative share has indeed stayed stable, this would mean that the current value of the market for CrCL treatments would be over $2 billion annually in the US alone. The first techniques designed for CrCL deficiency, the intra-articular techniques, aimed at replacing the failed CrCL with one of a different origin. These techniques were started by Paatsama in 1952. The next wave of techniques, the extra-articular or extracapsular ones, aimed at stabilizing the joint without replacing the CrCL. These techniques followed approximately 20 years later with DeAngelis & Lau in 1970 proposing the first method. The third and most recent wave of techniques are the osteotomies, aimed at changing the biomechanics of the stifle joint thus rendering the CrCL unnecessary. These were started by Slocum & Devine in 1983 and much of the research seems to have been concentrating on them for the past 20 years. Currently there are advances in the works in all three categories with new synthetic intra-articular ligaments, new extracapsular attachment materials and new osteotomy techniques being developed by several authors and companies. licenciate’s thesis, © Jan Mattila 2012.!



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The aim of this literature review is to wade through the substantial body of literature covering CrCL deficiency, introduce the most important different surgical techniques recently or currently in use and comment on the outcomes and complications of some of these techniques where the literature required for these comments is available. The literature review will concentrate on literature from the 21st century with half of the literature picked from 2000–2012 and attempt to pick only the most relevant either original or important literature from the years 1926–1999. The ultimate objective of the literature review is to determine whether there is a technique which seems to be the most promising based on the literature.



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2 Anatomy of the stifle joint The canine stifle is a complex, condylar, synovial joint composed of three interrelated articulations: the condyloid femorotibial, the femoropatellar, and the proximal tibiofibular articulations (Robins 1990). The primary motion of the joint is flexion and extension of the hind limb. Due to the sliding of the femoral condyles on the tibial plateau, there is also cranial and caudal displacement, compression and distraction, internal and external rotation, varus and valgus angulation, and lateral and medial translation (Arnoczky et al. 1977). All motions of the stifle involve the complex integration of the distal femur, proximal tibia, and proximal fibula, as well as the muscles of the pelvic limb, joint capsule, joint ligaments, and menisci (Robins 1990).



Figure 1. Dorsal view of the canine stifle. Structures identified: 1 Trochlea ossis femoris, 2 lateral ridge of trochlea ossis femoris, 3 tendon of M. extensor digitorum longus, 4 Lig. popliteum obliquum, 5 Lig. collaterale laterale, 6 Meniscus lateralis, 7 Tuberositas tibiae, 8 Lig. patellae, 9 Patella, 10 Fibrocartillagines parapatellares, 11 Lig. transversum genus, 12 Meniscus medialis, 13 Lig. collaterale mediale, 14 Lig. cruciatum craniale, 15 Lig. cruciatum caudale, 16 medial ridge of the Trochlea ossis femoris. From Carpenter, D. H., & Cooper, R. C. (2000). Mini review of canine stifle joint anatomy. Anatomia, histologia, embryologia, 29(6), 321.



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The CrCL lies intra-articularly, but extrasynovially (Slocum 1983). The CrCL is functionally composed of two parts: a smaller craniomedial band (CrMB) and a larger caudolateral band (CLB). The CrMB is under tension in both flexion and extension, whereas the CLB is under tension in extension only. (Arnoczky et al. 1977) The function of the CrCL is to limit the cranial translation of the tibia in relation to the femur as well as the internal rotation of the tibia (Arnoczky et al. 1977). The CrCL is the main stabilizing structure of the stifle joint and thus its rupture results in mild to severe lameness depending on the extent of the damage (Slocum & Devine Slocum 1993).



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3 Pathogenesis of CrCL rupture Cruciate disease is multifactorial (de Rooster et al. 2006). Rupture of a normal CrCL naturally occurs if it is subjected to a force greater than its breaking strength. The breaking strength of the CrCL is approximately equal to four times the body weight of the dog (Gupta et al. 1969). The site of rupture of the CrCL is predominantly its midsubstance at the point where the ligament rotates 90°. Acute rupture of a healthy CrCL probably only accounts for a small percentage of cases. (Paatsama 1952) Traumatic rupture, which accounts for about 20 % of cases, is attributed to sudden hyperextension and excessive internal rotation of a partially flexed stifle (Moore & Read 1996). Traumatic rupture is more common with juvenile patients (Hayashi et al. 2004). However, the most common etiology for CrCL deficiency is associated with chronic progressive lameness consistent with a non-traumatic degenerative process. This progressive degeneration of the CrCL has been linked to a variety of factors: genetic, conformational, environmental, immune-mediated, and inflammatory. (Griffon 2010) Previously the primary pathogenesis of CrCL rupture was thought to originate with changes in the composition of the ligament caused by aging and lack of use (Vasseur et al. 1985). The rationale behind a genetic component is based on findings of a predisposition to CrCL deficiency with some breeds, e.g. Labrador retrievers, Rottweilers and Newfoundlands, (Duval et al. 1999, Whitehair et al. 1993). Poor conformation may lead to misalignment of the stifle, which may exacerbate the degenerative processes predisposing to CrCL rupture (Johnson & Johnson 1993). Also stifles with medial patellar luxation are predisposed to CrCL rupture because cranial tibial thrust (CTT) is no longer restrained by the patellar tendon (Kaiser et al. 2001). The mechanism of CrCL rupture is currently unknown. There are several theories for the mechanism and the currently dominant one of these is probably the active model theory (Slocum & Devine Slovum 1993). The traditional passive model claims that correction of CrCL rupture can be accomplished with replacement of the deficient structure (Arnoczky et al. 1977). The active model argues that the traditional model fails to explain partial or complete rupture of the CrCL in the absence of trauma, and offers no licenciate’s thesis, © Jan Mattila 2012.!



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explanation for the mechanism of rupture of caudal horn of the medial meniscus (Slocum & Devine Slocum 1993). A later tibiofemoral shear force model (Montavon et al. 2002) argues that total joint force is parallel to the patellar ligament, not the functional axis of the tibia as claimed by the active model (Montavon et al. 2006). Slocum & Devine Slocum (1993) argue that a better alternative than replacing the deficient CrCL is to alter the direction of the forces acting on the stifle joint under dynamic loading by changing the tibial plateau angle (TPA). Montavon et al. (2006) argue that turning the patellar ligament would be more beneficial than turning the tibial plateau.



Figure 2. Schematic representation of forces acting on the stifle joint. From Griffon, D. J. (2010). A review of the pathogenesis of canine cranial cruciate ligament disease as a basis for future preventive strategies. Veterinary surgery, 39(4), 400.



Regardless of the mechanism, rupture of the CrCL causes instability which in turn causes inflammation of the stifle joint. The inflammation and resulting release of inflammatory mediators such as interleukins and collagenases cause degradation of the cartilaginous matrix, which commonly progresses to DJD (Johnson & Johnson 1993). Unilateral rupture of the CrCL also leads to rupture of the contralateral CrCL in as many as 50 % of cases (Buote et al. 2009). This is partly due to the same pathology affecting the contralateral limb and partly by the added stress of weight bearing caused by not being able to use the ruptured limb.



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4 Surgical techniques Surgical techniques for the repair of CrCL deficiency can be classified into three categories: intra-articular, extracapsular and osteotomy techniques. Intraarticular techniques are no longer commonly used. However, surgery with both extracapsular and osteotomy techniques always includes intra-articular inspection of the stifle to either remove remnants of a partially or completely ruptured CrCL or to perform operations on the menisci when indicated. Several techniques require the use of customized equipment. These include most of the osteotomy and some extracapsular techniques which require items such as custom osteotomy saws, jigs, custom compression plates or special high durability suture material. These serve as both a source of revenue for surgeons and their affiliated companies as well as barriers to entry or use of the techniques to surgeons with less well equipped clinics. The surgical techniques can also be divided into two broad categories based on the attempted result: techniques which aim at replacing the deficient CrCL and techniques which aim at removing the need for a CrCL by changing the biomechanics of the joint. Intra-articular and extracapsular techniques are examples of the former and osteotomy techniques of the latter. The following chapters will introduce all three categories of techniques and their main alternatives. Another perspective is that intra-articular techniques aim at removing the cranial drawer sign and retaining complete range of motion. Extracapsular techniques sacrifice range of motion for complete elimination of the drawer sign. (Slocum & Devine Slocum 1993) As osteotomy techniques primarily change the biomechanics of the stifle, many of them do not remove the cranial drawer motion (e.g. Slocum & Devine Slocum 1993, Montavon et al. 2002, Bruce et al. 2007). Instead these techniques rely on an alternative test of the cranial translation of the tibia called the tibial compression test (Hnderson & Milton 1978) for assessing the success of the operation .



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4.1 Intra-articular techniques Intra-articular techniques aim at replacing the failed CrCL with an autogeneous or allogeneic ligament. These techniques were the first ones to be created for addressing the issue of CrCL deficiency in the dog. The different techniques mainly differ in the origin of the replacing ligament and its attachment within the stifle joint. 4.1.1 Paatsama operation Paatsama called his method the plastic operation on the cruciate ligaments using fascia transplant. The operation is performed from a parapatellar approach. The fascial transplant is created from an approximately 1 cm wide strip of fascia lata, starting from the border of the tibia working along the border of m. biceps femoris. The length of the strip is the length of the surgical incision, which is double the distance from the crista tibiae to the patella. The strip is only dissected from the proximal end, leaving the distal end attached. (Paatsama 1952) A tunnel is then drilled in the femur from the femoral insertion of the lateral collateral ligament through the condyle to the femoral insertion of the CrCL. Another tunnel is then drilled to the tibia from the medial border of the crista tibiae obliquely proximal to the tibial insertion of the CrCL. (Paatsama 1952)



Figure 3. Position of tunnels and placement of transplant. From Paatsama, S. (1952). Ligament injuries in the canine stifle - A clinical and experimental study. Academic dissertation. Helsinki: Kauppakirjapaino Oy. p. 64. licenciate’s thesis, © Jan Mattila 2012.!



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The fascial strip is then threaded into the lateral femoral hole, out the femoral insertion of the CrCL, into the tibial insertion of the CrCL and out the medial tibial hole. The leg is then flexed and the transplant pulled taut to eliminate the subluxation of the tibia, after which the end of the transplant can be sutured on to the insertion of the ligamentum rectum patellae on the tibial tuberosity. (Paatsama 1952) 4.1.2 Intra-articular repair or over-the-top Like other intra-articular techniques, the over-the-top method aims at replacing the CrCL with an autogeneous graft. The graft is created from the patellar tendon and attached to the femur (Arnoczky et al. 1979). The surgery is performed from a craniomedial approach. The patella tendon is revealed with a curvilinear incision from the craniomedial midshaft of the femur to the distal patella and over to the proximal tibia. Once the patella tendon is revealed, a linear incision is made through the fascia lata and the fascia covered craniomedial segment of patella is osteotomized free from the patella without splitting the bone entering the joint. The strip of fascia incorporating the wedge of patella is dissected free down to its attachment to crista tibiae. (Arnoczky et al. 1979)



Figure 4. Path of graft and placement of sutures. From Arnoczky, S. P., Tarvin, G. B., Marshall, J. L., & Saltzman, B. (1979). The over-the-top procedure: a technique for anterior cruciate ligament substitution in the dog. Journal of the American Animal Hospital Association, 15(3), 287. licenciate’s thesis, © Jan Mattila 2012.!



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The patella is then displaced laterally and a small incision is made between the lateral fabella and the femur. The free end of the graft is grasped with a pair of curved mosquito forceps passed through this incision, between the femoral condyles and the graft is pulled through the joint and out laterally through the femorofabellar ligament. Tension is applied to the graft until cranial drawer motion is eliminated and the free end of the graft attached to the lateral femoral condyle with stainless steel sutures. (Arnoczky et al. 1979) 4.1.3 Modified intra-articular repair Hulse et al. (1980) introduced a modified over-the-top method in which they substituted the medial patellar tendon replacement ligament with a graft made of a combination of fascia lata, lateral retinacular tissue and the lateral one-third of the patellar tendon. The rationale was to increase the tensile strength of the CrCL substitute. The modification also displaces the origin of the graft to the proximal tibial tuberosity and crista tibiae. (Hulse et al. 1980)



Figure 5. Connective tissue used for graft. From Hulse, D. A., Michaelson, F., Johnson, C., & Abdelbaki, Y. Z. (1980). A Technique for Reconstruction of the Anterior Cruciate Ligament in the Dog: Preliminary Report. Veterinary Surgery, 9(4), 136.



4.1.4 Under-and-over The under-and-over technique is performed from a lateral parapatellar approach. A graft similar to that in the modified over-the-top method is prepared from a 1 to 2 cm wide section from the cranial edge of m. biceps femoris to the femorotibial joint including the lateral third of the patella. The joint capsule is licenciate’s thesis, © Jan Mattila 2012.!



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then incised parallel to the patella ligament and the patella luxated medially to reveal the joint structures. (Shires et al. 1984)



Figure 6. Path (left) and final positioning (right) of the under-and-over graft. From Shires, P. K., Hulse, D. A., & Liu, W. (1984). The under-and-over fascial replacement technique for anterior cruciate ligament rupture in dogs: A retrospective study. Journal of the American Animal Hospital Association, 20(2), 72–73.



A pair of curved gall bladder forceps is then used to grasp the graft and pull it underneath the intermeniscal ligamentum transversum genus into the joint. A small incision is made in the femorofabellar ligament close to the femur. The forceps are passed craniocaudally under the ligament and the graft pulled through the joint and beneath the ligament. (Shires et al. 1984) A hole is then drilled into the lateral femoral metaphysis and a spiked washer secured with a screw. The graft is then wrapped around the shaft of the screw tightening enough to prevent cranial drawer motion before securing the screw to the femoral condyle. The free end of the graft is then sutured to the fixed portion. (Shires et al. 1984) 4.1.5 Modified under-and-over One modification of the under-and-over technique is to not use a screw and washer fastener (Patterson et al. 1991). Instead the graft is secured to the lateral femoral condyle and the femorofabellar ligament with monofilament sutures (Shires 1993).



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4.2 Extracapsular techniques Extracapsular techniques avoid introducing foreign material into the stifle joint and instead achieve the stabilization of the stifle by creating a CrCL replacing structure on the outside of the joint. These techniques were introduced in the early 1970’s with the first widely used technique being the lateral retinacular imbrication by DeAngelis & Lau (1970) and its later modifications. The latest technique in this category, Tightrope CCL (Cook et al. 2007) was originally developed in 2005 with the advent of high tensile strength suture materials became available. 4.2.1 Lateral retinacular imbrication or lateral fabellar suture (LFS) In 1970 DeAngelis & Lau presented what they called a simplified lateral retinacular imbrication technique for the correction of CrCL rupture. The procedure is performed from a craniolateral parapatellar approach. First a mattress suture of monofilament synthetic material or steel wire is placed in the lateral retinacular tissue. A straight cutting needle is then used to enter the tissue caudal and proximal to the lateral sesamoid bone (fabella), and directed craniodistally to emerge in the straight patellar ligament proximal to its insertion in the tibial tuberosity. The needle is then reinserted a few millimeters from the point of emergence and directed caudoproximally to emerge near the original point of entry next to the fabella. (DeAngelis & Lau 1970)



Figure 7. Placement of the suture. From DeAngelis, M., & Lau, R. E. (1970). A lateral retinacular imbrication technique for the surgical correction of anterior cruciate ligament rupture in the dog. Journal of the American Veterinary Medical Association, 157(1), 81. licenciate’s thesis, © Jan Mattila 2012.!



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In the original technique this first suture removed most of the cranial drawer motion. To remove the rest, another suture was placed parallel and close to the first. To operation includes inspection of the stifle joint for which the patella is retracted medially. If medial patellar luxation is observed, either transplantation of the tibial tuberosity, trochlear arthroplasty or both are performed in addition to a medial desmotomy. (DeAngelis & Lau 1970) 4.2.2 Modified LFS Flo (1975) modified the DeAngelis (1970) technique of lateral retinacular imbrication by using a medial and lateral mattress suture which are passed around each fabella and then to the tibial tuberosity. Another lateral suture is then attached to the fascia lateral to the patella. This acts as the imbrication suture. (Flo 1975) 4.2.3 Fibular head transposition (FHT) Smith & Torg (1985) proposed a method of preventing cranial drawer motion and minimizing rotation of the tibia by a technique called fibular head transposition. The technique was developed as a modification of a similar technique in human orthopedics (Smith & Torg 1985). The realignment and tension of the lateral collateral ligament prevents internal rotation and cranial displacement of the tibia. The FHT is mechanically similar to the lateral retinacular imbrication technique (LFS). (Matthiesen 1993) The surgery is performed from a craniolateral approach with a parapatellar incision made through the lateral retinaculum. The proximal head of the fibula is first revealed from under the overlying structures and then freed from the tibia by incising the syndesmosis between the tibia and the fibula. The surface on the tibia where the fibula is to be attached is then roughened with a rongeur or curette. (Smith & Torg 1985) The original technique involves drilling two holes into the tibial crest and passing a loop of steel wire with both ends exiting on the lateral surface of the tibia (Smith & Torg 1985). An alternative method involves drilling only one hole, at the level of the proposed new position of the tibia with the steel wire passed through the hole and looped around the tibial crest (Matthiesen 1993). In both cases ends of the wire are terminated on the lateral surface of the tibia. licenciate’s thesis, © Jan Mattila 2012.!



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After the wires are in position, a Steinmann pin is placed into the caudal aspect of the head of the fibula and the limb held in position with the hock flexed, stifle externally rotated and cranial displacement of the tibia eliminated (Matthiesen 1993). The fibular head is then fixed by driving the Steinmann pin into the proximal tibia. If cranial drawer motion is not significantly reduced, the pin placement should be altered (Smith & Torg 1985).



Figure 8. Placement of the Steinmann pin. From Matthiesen, D. T. (1993). Fibular head transposition. Veterinary Clinics of North America: Small Animal Practice, 23(4), 758.



Once the fibular head is in place the wires passed through the crista tibiae are tightened around the free end of the Steinmann pin to eliminate rest of the cranial drawer motion and minimize internal tibial rotation (Matthiesen 1993). 4.2.4 Tightrope cranial cruciate ligament or Tightrope CCL (TR) The Tightrope CCL technique (Cook et al. 2007) is based on the LFS technique originally by DeAngelis & Lau (1970). TR is also claimed to be superior to the LFS due to bone fixation at both tibial and femoral attachments, more accurate isometric placement and overall strength (Cook et al. 2007). The invasiveness of the techniques is comparable. For the approach either a minimally invasive approach with three small skin incisions or an approach where the lateral aspect of the stifle is exposed to the level of the joint capsule from the lateral fabella to midway down the tibial tuberosity can be used.



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With either approach, to place the TR, a guidewire is drilled from the midbody of the lateral femoral condyle at approximately a 30° angle proximally to the medial edge of the diaphyseal distal femur between m. vastus medialis and m. sartorius. A tunnel is then drilled with a cannulated drill using a drill guide. With the minimally invasive technique care is taken to prevent the cannulated drill from piercing the musculature on the medial side of the femur. The attachment of m. biceps femoris is then revealed on the tibia. A guidewire is drilled through the lateral side at the site of the sulcus muscularis medially in approximately a 20° angle distally to the lateral side of the tibial tuberosity. Another tunnel is then drilled with a cannulated drill using a drill guide, this time through the musculature.



Figure 9. Open technique placement of the double threaded Tightrope CCL FiberTape. From the Arthrex Vet Systems TightRope CCL Multicenter Clinical Outcomes Study brochure (2010).



With the open technique the FiberTape (Arthrex Vet Systems) is threaded with the help of a leadwire through the medial side of the tibial hole, out the lateral tibial hole in the lateral femoral hole and through the medial femoral hole. After placement the proximal femoral washer plate is turned by pulling on the FiberTape thus preventing it form escaping. Finally the FiberTape is tightened by tying it over the medial femoral washer plate. With the minimally invasive technique the direction of the FiberTape is reversed and the knots tied on the medial side of the tibia. The lateral retinaculum is closed with imbrication sutures and the skin incisions in routine fashion. licenciate’s thesis, © Jan Mattila 2012.!



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4.3 Osteotomy techniques Osteotomy techniques, unlike the previous intra-articular and extracapsular techniques rely on changing the biomechanics of the stifle joint to effectively remove the need for the CrCL thus repairing the problem of CrCL deficiency. The paradigm shift from incremental improvements in CrCL replacement to negating the need for a CrCL by altering the loading of the stifle joint started in the early 1980’s with Slocum & Devine identifying cranial tibial thrust (CCT) as an important cause of rupture of the CrCL. Slocum & Devine Slocum further improved on their method and in 1993 published their seminal paper on the technique called tibial plateau leveling osteotomy, which has become perhaps the most widely used and studied osteotomy technique for CrCL deficiency. After the turn of the century several other osteotomy techniques have been described. Some of these attempt to refine Slocum’s original assumptions (e.g. TTO by Bruce 2007), some contest the assumptions and aim at remodeling the biomechanics of the stifle by altering a different site (e.g. TTA by Montavon et al. 2002). 4.3.1 Cranial tibial wedge osteotomy (CTWO) In 1983 Slocum & Devine identified cranial tibial thrust (CTT) as being an important cause of CrCL rupture and cranial drawer motion in dogs. They claimed that then current methods only aimed at eliminating cranial drawer motion, and a new technique was needed to also combat the CTT. A year later they proposed their first technique aimed at eliminating the CTT, called the CTWO. (Slocum & Devine 1984) The CTWO technique is based on removing a wedge shaped fragment of bone from the proximal tibia to change the position of the proximal head of the tibia in relation to the femur. This also results in a change in the tibial axis, moving it cranially. The technique utilizes a steel jig and an osteotomy guide to direct the osteotomy. The resulting wedge, which was between 18° and 30° wide in the 1984 study, is then closed with a compression plate. The CTWO requires the use of another technique to eliminate the cranial drawer motion. In the 1984 paper the most commonly used technique was advancement of m. biceps femoris laterally and m. gracilis and m. semitendinosus medially. (Slocum & Devine 1984) licenciate’s thesis, © Jan Mattila 2012.!



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Figure 10. Cranial tibial wedge osteotomy. From Hildreth, B. E., Marcellin-Little, D. J., Roe, S. C., & Harrysson, O. L. A. (2006). In vitro evaluation of five canine tibial plateau leveling methods. American journal of veterinary research, 67(4), 695.



Figure 10 shows the angle used in the Hildreth et al. 2006 study for a corrective CTWO wedge osteotomy. The original Slocum & Devine 1983 study used an angle of 22,5° although this was realized afterwards (Slocum & Devine 1984). 4.3.2 Tibial plateau leveling osteotomy (TPLO) In their 1993 paper in the stifle surgery compilation of the Veterinary Clinics of North America Small Animal Practice series, Slocum & Devine Slocum methodically detail the short comings of the then current intra-articular and extracapsular techniques. They propose a new osteotomy based technique, the tibial plateau leveling osteotomy. The TPLO is an evolution from CTWO, proposed nearly a decade prior. Like the CTWO, it aims not at replacing or substituting the failed CrCL, but instead on changing the biomechanics of the stifle joint to neutralize the CTT and thus negate the need for the CrCL. This is achieved by leveling the tibial plateau hence the name for the originally patented technique. The leveling is performed by creating a radial osteotomy, with the help of a custom jig and custom radial saw, into the caudal edge of the proximal tibia. This fragment is then rotated so that the tibial plateau is perpendicular with the functional axis of the tibia. Once the fragment is in optimal position it is secured with a custom TPLO compression plate and the surgical site closed routinely. licenciate’s thesis, © Jan Mattila 2012.!



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Figure 11. Tibial plateau leveling osteotomy. From Hildreth, B. E., Marcellin-Little, D. J., Roe, S. C., & Harrysson, O. L. A. (2006). In vitro evaluation of five canine tibial plateau leveling methods. American journal of veterinary research, 67(4), 695.



4.3.3 Tibial tuberosity advancement (TTA) Advancement of the tibial tuberosity for treatment of CrCL deficiency was first published as a lecture during the 1st World Orthopaedic Veterinary Congress in Munich, 2002, by Montavon, Damur and Tepic. They propose that CrCL injury is due to a tibiofemoral shear force (Montavon et al. 2002). They also contend that the total joint force of the stifle is parallel to the patellar ligament, unlike Slocum, who maintains that it is parallel to the functional axis of the tibia (Montavon & Tepic 2006). The principal concept of the TTA technique is to advance the tibial tuberosity to such an extent that the tibial plateau is perpendicular with the patellar ligament. This would reduce the tibiofemoral shear force to zero.



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Figure 12. 3D-model of tibial tuberosity advancement. From Kim, S. E., Pozzi, A., Kowaleski, M. P., & Lewis, D. D. (2008). Tibial Osteotomies for Cranial Cruciate Ligament Insufficiency in Dogs. Veterinary Surgery, 37(2), 118.



The surgery involves sawing apart the cranial edge of the tibial tuberosity, placing a customized spacer (a cage) of appropriate size between the tibial body and osteotomy piece and then securing the pieces with a custom metallic plate or “tension band” (Montavon et al. 2002). To accelerate healing the open wedge osteotomy can be filled with autogeneous or allogeneic cancellous bone graft before standard closure of the surgical site (Montavon & Tepic 2006). 4.3.4 Proximal tibial osteotomy (PTIO) Damur et al. (2003) suggested an alternative technique to the TPLO called the proximal tibial osteotomy or PTIO. The technique attempted to accomplish the same end result as the TPLO technique, neutralizing CTT by changing the tibial plateau angle (TPA), but with the added benefit of not requiring custom tools. The procedure is performed from a medial parapatellar approach. Two linear osteotomies are made to create a wedge necessary for turning the tibial plateau. The pivot point of the wedge being at the level of the caudodistal end of the medial collateral ligament. A horizontal corticotomy is then made from the distal end of the wedge to the caudal edge of the tibia to enable rotation of the caudoproximal fragment. (Damur et al. 2003) The fragment is attached with two positional screws. The distal screw is placed perpendicular to the fragment and the proximal directed through the osteotomy licenciate’s thesis, © Jan Mattila 2012.!



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plane in a caudolateral direction to the tibial tuberosity. The arthrotomy is then closed and the medial and lateral fasciae around the stifle and the femoral condyles imbricated with horizontal mattress sutures. (Damur et al. 2003)



Figure 13. 3D-model of the proximal tibial osteotomy with a modified attachment of the tibial fragment using a positional screw and a compression plate. From Kim, S. E., Pozzi, A., Kowaleski, M. P., & Lewis, D. D. (2008). Tibial Osteotomies for Cranial Cruciate Ligament Insufficiency in Dogs. Veterinary Surgery, 37(2), 120.



4.3.5 Triple tibial osteotomy (TTO) Bruce et al. proposed in 2007 a technique combining a TTA and a CTWO for the treatment of CrCL deficiency. The technique is called the triple tibial osteotomy due to the three osteotomies performed: a partial tibial crest osteotomy like in the TTA and two osteotomies to create a partial tibial wedge as in the CTWO. The final result is similar to the TTA with the tibial plateau made perpendicular to the patellar ligament. (Bruce et al. 2007) The surgery is performed from a medial parapatellar approach. The osteotomies are made with the help of a custom saw guide and osteometer. The tibial crest osteotomy (TCO) is performed first with the wedge osteotomy, which in some early cases was a complete ostectomy, but refined in later cases to a partial osteotomy, performed second. The osteotomies are performed by first drilling a transverse 2 mm hole on the tibia from which the osteotomies are started and proceeding distally and cranially or proximally as necessary (shown in Figure 12). The wedge osteotomy is reduced with the help of forceps and the site secured with a TPLO compression plate. Autogeneous cancellous bone licenciate’s thesis, © Jan Mattila 2012.!



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graft harvested from the wedge osteotomy is used to fill the TCO gap before routine closure of the surgical site. (Bruce et al. 2007)



Figure 14. Triple tibial osteotomy. From Bruce, W. J., Rose, A., Tuke, J., & Robins, G. M. (2007). Evaluation of the triple tibial osteotomy. A new technique for the management of the canine cruciate-deficient stifle. Veterinary and Comparative Orthopaedics and Traumatology, 20(3), 160.



4.3.6 Circular tibial tuberosity advancement (cTTA) Verdonck & Petazzoni (2009) proposed the cTTA technique as a combination of the TPLO and TTA techniques. The key disadvantage of TTA is the opening osteotomy, which creates a bone defect as well as requiring a predetermined sized spacer (cage) for the correction of the advancement of the tibial tuberosity (Petazzoni 2010). The cTTA combines the radial osteotomy of the TPLO with the TTA by performing the radial osteotomy not on the caudal edge of the distal tibia like in the TPLO, but on the tibial tuberosity. After radial osteotomy, the tibial tuberosity is rotated cranially and proximally until the tuberosity advances to a TTA type position with the tibial plateau slope perpendicular to the patellar ligament. The displaced tuberosity is secured with a custom T-shaped locking plate and the surgery site closed routinely. (Petazzoni 2010).



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Figure 15. Preoperative (left) and postoperative (right) radiographs of cTTA. From Petazzoni, M. (2010). cTTA (circular Tibial Tuberosity Advancement). ESVOT-VOS proceedings 2010, 295.



4.3.7 Modified Maquet technique (MMT) Etchepareborde et al. (2011) proposed the use of a modified Maquet technique previously used in human stifle surgery as a modification of the TTA procedure. The technique involves a tibial crest osteotomy similar to the TTA procedure with a TTA cage used for advancing the crista tibiae. Unlike TTA, no tension band implant is placed to secure the cranially displaced crista tibiae. Instead the distal tibial crest is either secured in place with a wire or as in Figure 16, not secured at all. Also, since the crista tibiae is not detached distally and thus not displaced proximally, the patellar ligament is distended and patella may slide distally in the trochlear groove possibly causing patella baja. (Etchepareborde et al. 2011)



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Figure 16. Perioperative (left) and early postoperative (right) radiographs of MMT. From Etchepareborde, S., Brunel, L., Bollen, G., & Balligand, M. (2011). Preliminary experience of a modified Maquet technique for repair of cranial cruciate ligament rupture in dogs. Veterinary and Comparative Orthopaedics and Traumatology, 24(3), 225.



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5 Outcomes The results of the different techniques presented in the previous chapters are discussed below. Earlier, the proponents of intra-capsular techniques claimed extracapsular techniques to be inferior and biomechanically unsound (Hulse 1980). A later force plate study (Conzemius et al. 2005) found that an intraarticular (over-the-top) technique was inferior to extracapsular (lateral suture) and osteotomy (TPLO) techniques, but could not statistically differentiate the preferred method from the two latter ones. As intra-articular techniques are no longer in widespread use, their results are presented here mostly for completeness and not tabled.



5.1 Outcomes of intra-articular techniques The fascia transplant or Paatsama technique study reports the results of only 5 clinical cases and thus the validity of the technique can not be determined (Paatsama 1952). A later study with a few more patients reported a very good result in 87 % (13/15) of the cases with 13 % (2/15) considered poor (Singleton 1963). The initial paper on the over-the-top technique was based on 28 cases of which 61 % (17/28) were considered excellent, 32 % (9/28) good and 7 % (2/28) fair with no poor results (Arnoczky et al. 1979). A later study including 20 cases of unilateral CrCL rupture repaired with the over-the-top technique found improvement in only 15 % of the cases (Conzemius et al. 2005). The modified over-the-top method study was performed with 16 patients of which 25 % (4/16) were sacrificed at 4 weeks, 50 % (8/16) at 8 weeks and 25 % (4/16) at 24 weeks postoperatively. At four weeks all dogs were lame with 50 % (2/4) of the dogs exhibiting mild lameness without exercise (Grade II lameness) and 50 % (2/4) showing continuous lameness (Grade III lameness). At 8 weeks 63 % (5/8) dogs were clinically normal and of the 37 % (3/8) dogs which were lame, 67 % (2/3) showed mild lameness with exercise (Grade I lameness) and 33 % (1/3) mild lameness without exercise (Grade II lameness). At 24 weeks all dogs were classified as normal. (Hulse et al. 1980) The under-and-over technique was performed on 38 stifles in 35 dogs over two and a half years. Of the treated patients 27 returned for “objective licenciate’s thesis, © Jan Mattila 2012.!



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evaluation” (done by the authors). Of the 27 re-examined patients 93 % were eventually evaluated as sound with the time of re-evaluation being anything between 3 to 27 months postoperatively. (Shires et al. 1984)



5.2 Outcomes of extracapsular techniques Extracapsular techniques are still frequently used, but their results do not translate well into table form due to the great variety in the reporting of the results and the tests conducted to assess clinical improvement. Lateral retinacular imbrication (LFS) has been in constant use for over 40 years and is still being performed frequently around the world. Along with the TPLO it is one of the most studied techniques for surgical repair of CrCL deficiency. The original LFS technique study is based on 57 operations performed on 50 patients during a 15 month period. The results of the paper are however only based on 42 operations performed on 37 patients due to the rest of the cases having been operated too recently to be included. The authors reported the results of the procedure to be satisfactory in 86 % (36/42) cases, but considered mild lameness to be acceptable, with 19 % of cases (8/37 or 22 % of patients) suffering from “occasional episodes of slight lameness”. (DeAngelis & Lau 1970) Another study concluded that the LFS technique was superior to two intraarticular techniques (over-the-top and under-and-over) with respect to laxity and stiffness of joint at the second and third loading to 180 N in a test setting (Patterson et al. 1991). A later study with 39 cases treated with LFS found that it was superior to both the FHT and conservative treatment (Chauvet et al. 1996) A later force plate study including 47 cases of unilateral CrCL rupture repaired with the LFS technique found improvement in 40 % of the cases and a return to normal for 15 % of the cases (Conzemius et al. 2005). The FHT technique was assessed on 4 cadaver stifles, 4 dogs with experimentally excised CrCL and 71 dogs with CrCL rupture during a 6 year period (Smith & Torg 1985). A following study on 80 cases operated over a 5 year period found the results of the FHT operation to be good in 90 % of the cases (Mullen & Matthiesen 1989). Another study found the FHT technique to be superior to both LFS and two intra-articular techniques (over-the-top and licenciate’s thesis, © Jan Mattila 2012.!



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under-and-over) with respect to laxity and stiffness under experimental loading to 180N (Patterson et al. 1991). A later study with 22 cases treated with FHT found that it was statistically significantly inferior to LFS (Chauvet et al. 1996). The 2007 non-peer reviewed whitepaper on the TR technique based on 24 patients found the 6 month postoperative recovery of patients treated with TR was comparable to patients treated with the TPLO technique (Cook et al. 2007). Another non-peer reviewed brochure by Arthrex Vet Systems claimed multicenter clinical outcomes of 2 563 TR cases to have a 94,9 % success rate with 64,6 % of patients returning to full function and 30,3 % to acceptable function. A recent gait analysis study comparing two groups of 14 dogs treated with either TR or TPLO could not statistically differentiate the groups when lameness was measured by peak vertical force (PVF) (Böddeker et al. 2012).



5.3 Outcomes of osteotomy techniques The 1993 paper on the TPLO technique states that surgery with either CTWO or TPLO was performed on 394 cases, but fails to separate the numbers of patients receiving TPLO treatment (Slocum & Devine Slocum 1993). Thus the results, however promising, are hard to attribute to either technique. The authors also confess that the technique does not remove the cranial drawer sign, but claim this to be insignificant as the patients return to normal activity. A comparison study of an intra-articular (over-the-top), extracapsular (LFS) and osteotomy (TPLO) technique found TPLO to be comparable to LFS and superior to the intra-articular method. The force plate study concluded that 11 % of the patients operated with TPLO had normal limb function and improvement from the preoperative state was found in 34 % of the patients. (Conzemius et al. 2005) A recent gait analysis study comparing two groups of 14 dogs treated with either TPLO or TR concluded that TPLO leads to faster recovery and improved limb function at 4 months postoperatively, even though there was no statistical difference in lameness when measured by peak vertical force (PVF) between the TPLO and TR groups (Böddeker et al. 2012). No statistics on the successfulness of the TTA technique are reported in the original proceedings book publication (Montavon et al. 2002). Hoffmann et al. (2006) claim there to be no peer-reviewed literature on the technique prior to their article. This is surprising since the technique been performed on over 9000 licenciate’s thesis, © Jan Mattila 2012.!



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patients (Montavon & Tepic 2006). Another study found mean time to documented radiographic healing to be 11,3 weeks (Lafaver et al. 2007). A later force plate gait analysis study concluded that TTA would return 90 % of full limb function, but could not return the limb to normal function (Voss et al. 2008). A recent study concluded on 67 patients that the gap created by the TTA operation healed equally fast with or without the use of a bone graft (Guerrero et al. 2011). The original study on the PTIO technique is based on the results of 100 operations performed on 87 patients with 86 % (75/87) regaining full function of the operated limb within 4 months of the operation (Damur et al. 2003). A later study found 93 % (53/57) of patients had full radiographic healing at 6 weeks postoperatively (Jerram et al. 2005). The Bruce et al. (2007) study is based on a total of 64 TTO operations performed on 52 patients. The success of the operation was measured objectively by scoring radiographs for osteoarthritis (OA) concluding that the OA score was not significantly increased after the procedure (Bruce et al. 2007). In the original cTTA study (Verdonck & Petazzoni 2009), 18 patients with CrCL tears were treated with cTTA and their mean time to radiographic healing was 8 weeks. A later 2010 study (Petazzoni 2010) with 86 patients treated to 89 cTTA procedures found a similar mean time to radiographic healing of 8 weeks. Table 1 shows the publications which mention times to radiographic healing for the patients. When the cases number is larger than the patient number, some patients have received a bilateral CrCL operation.



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Table 1. Outcomes of studies on different osteotomy techniques.



Outcomes Publication



Technique(s)



Patients / procedures



Radiographic healing



Hoffmann et al. (2006)



TTA



57 / 65



8–10 weeks



Lafaver et al. (2007)



TTA



101/114



11 weeks



Damur et al. (2003)



PTIO



87 / 100



16 weeks



Jerram et al. (2005)



PTIO



52 / 60



93 % @ 6 weeks



Bruce et al. (2007)



TTO



52 / 64



6–12 weeks



Verdonck et al. (2009)



cTTA



18



mean 8 weeks



Petazzoni et al. (2010)



cTTA



86 / 89



mean 8 weeks



Etchepareborde et al. (2011)



MMT



20/20



mean 7 weeks



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6 Complications All categories of techniques are prone to three types of complications: perioperative, early postoperative and late postoperative. All intraoperative and any postoperative complications which arise less than 24 hours after surgery are considered perioperative complications. Early postoperative complications arise in the first two weeks, or between 1 and 14 days after surgery. All other complications are considered late postoperative complications. The reporting on complications is varied on all methods and very brief with the earliest methods.



6.1 Complications associated with intra-articular techniques Singleton (1963) reports 13 % (2/15) poor results with the Paatsama procedure but gives no insight as to the cause. Arnoczky (1979) listed 7 % (2/28) results of the over-the-top technique as fair, but gives no details as to the cause. Smith & Torg (1984) note no complications for their under-and-over technique.



6.2 Complications associated with extracapsular techniques Placing two sutures as in the original LFS technique (DeAngelis & Lau 1970) results in only one of the sutures bearing all of the weight as it is not humanely possible to tighten two sutures to exactly the same tension, a prerequisite for both of the sutures halving the total weight. Placing the second suture is thus not only useless, but increases the duration of the surgery, the amount of foreign material in the patient and, should a surgical error occur, may risk the viability of the primary weight bearing suture. The original study on the LFS technique reported continuous lameness in 12 % of cases (5/37 or 14 % of patients) and total non-weight bearing lameness in 2 % of cases (1/37 or 3 % of patients) (DeAngelis & Lau 1970). A recent study with 496 cases treated with LFS found that infection or inflammation developed in 4,2 % (21/496) of cases which was significantly lower compared to cases treated with TPLO (Frey et al. 2010). FHT is technically complicated and thus prone to several intra and postoperative complications. A common intraoperative complication is inadvertent placement of the scalpel blade too deep while incising the tibiofibular ligaments resulting in substantial hemorrhage. Another common licenciate’s thesis, © Jan Mattila 2012.!



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intraoperative complication is fracture of the fibular head when placing the Steinmann pin or fracture of the fibular neck while tightening the steel wires around the pin after transposition. Common post operative complication include seroma formation on the lateral aspect of the proximal tibia and migration of the Steinmann pin requiring pin removal. (Matthiesen 1993) Mullen & Matthiesen (1989) reported the complications of 85 fibular head transposition surgeries performed on 80 dogs during a 5 year period. No total complication rate was reported, but the most common complications was stated as iatrogenic fracture of the fibular head or neck, which accounted for 12,5 % of the perioperative complications, and seroma formation over the pin location, which accounted for 7,5 % of the post operative complications.



6.3 Complications associated with osteotomy techniques The original publication on the TPLO technique (Slocum & Devine Slocum 1993) does not disclose any complication rates for the surgery. They admit cranial drawer motion is not removed, but claim this has no effect on the use of the limb and is thus not evidence of surgical failure. Pacchiana et al. (2003) reported the complication rates of 397 cases on 346 patients from a 4 year period to be 28 % with perioperative complications accounting for 5 %, shortterm 46 % and long-term 49 % of the complications. These complications are grouped by patient and not by operated limb. A later study of 696 TPLO patients from a 2,5 year period (Stauffer et al. 2006) determined the complication rate to be 19 %. The Stauffer et al. (2006) study had a similar distribution of the occurrence of the complications as the Pacchiana et al. (2003) study with perioperative complications accounting for 5 %, short term 50 %, long term 45 % of the complications. A later study found a small but significant, increase in mean DJD score 8 weeks after surgery, compared with mean preoperative score (Hurley et al. 2007). Another later study comparing extracapsular repair (LFS) with TPLO found that patients with larger OA scores were 5,78 times more likely to have had an LFS than a TPLO (Lazar et al. 2005). A recent study with 406 cases treated with TPLO found that infection or inflammation developed in 8 % (34/406) cases (Frey et al. 2010). A recent extensive study of 1146 TPLO procedures performed on 1000 patients found the overall complication to be 15 % of which licenciate’s thesis, © Jan Mattila 2012.!



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7 % were major (Fitzpatrick et al. 2010). Another very recent comparison gait analysis study of TR and TPLO found the complication rate to be greater with TPLO with 26 % (5/19) dogs excluded from further analysis compared to 13 % (2/16) for TR (Böddeker et al. 2012). The original article for the TTA technique does not list any complications rates. The first published study on the TTA technique comprised of 65 TTA cases on 57 dogs presents numerous complications associated with the procedure with the complications grouped into perioperative, early post operative and late post operative issues. Unfortunately the paper does not differentiate between patients with multiple complications and those with single complications. Thus the frequencies of complications are confounding as the maximum number of complications is stated as the total number of complications (34 cases of edema equaling 60 % of the 57 patients) when the list of perioperative complications contains a total of 6 different complications associated with a total of 57 cases. (Hoffmann et al. 2006) From the results it can be assumed that all cases which had edema also had one or several of the other perioperative complications, some of which are nontechnique related (like diarrhea or inappetence). The same can be said for early post operative complications which has a maximum of 34 cases with edema, with 6 different complications associated with a total of 58 cases. The authors discount the early post operative edema and all of the non-technique related complications and raise as “notable” the 3 cases (5 % of the 57 patients) with incisional dehiscence and superficial infection. (Hoffmann et al. 2006) The major issue with the readability of the statistics comes with the late post operative complications, where the most common complications was periosteal proliferation of the tibial diaphysis (9 cases or 16 % of the 57 patients), but another 15 different complications in a total of 25 additional cases. Of the five most frequent the most frequent periosteal proliferation and the third most frequent lethargy are ignored, with joint pain, medial meniscal tear and crepitus raised as “serious” and claimed to be the most common late post operative complications. (Hoffmann et al. 2006) In addition complications occurred in 33 of 57 dogs, which is not 59 % (57,9 %) and also not the same as in Table 1 in the article (34/57 equaling 59,6 %). The licenciate’s thesis, © Jan Mattila 2012.!



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authors further claim that only 12 of 57 dogs (21 %) had more serious complications, but these 12 more serious complications are not revealed anywhere and do not correspond directly to any of the frequencies presented in Table 1 of the article. (Hoffmann et al. 2006) A later study conducted of 114 cases on 101 patients found a total of 32 % of complications of which the authors categorized 12 % as major and 19 % as minor complications (rounding explains the discrepancy in the numbers). The major complications included e.g. implant failure, tibial fracture and infection and all except two of the minor complications resolved. (Lafaver et al. 2007) A force plate study found complications in 25 % of 30 cases on 40 patients (Voss et al. 2008). The original article on the PTIO technique admitted that due to the high incidence of complications, the technique does not appear to be a valid alternative to TPLO. (Damur et al. 2003). A later study comprised of 60 cases on 52 patients reported a total complication rate of 20 % (Jerram et al. 2005). The original publication on the TTO technique found an overall complication rate of 36 % for the procedure (Bruce 2007). All dogs showed mild lameness and cranial draw motion at 12 weeks with 89 % also having a positive tibial compression test. Lameness subsided at 11 to 26 months long term evaluation, but the cranial draw sign was still present in all cases and 91 % still had a positive tibial compression test. Post operative complication were not grouped into short and long term complications, but two of the patients required repeat surgery due to meniscal damage and these have been classed as long term complications in Table 2. (Bruce et al. 2007) The initial study on cTTA reported 14 % (3/21) intraoperative complications (Verdonck & Petazzoni 2009). A later study with more cases found a lower 10 % (9/89) intraoperative complication rate (Petazzoni 2010). In Table 2, perioperative, early postoperative and late postoperative complications are represented as a percentage of all complications and the total complications column represents the percentage of complications in total out of the cases in the publication.



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Table 2. Complication rates of different osteotomy techniques.



Complications Publication



Technique Peri op



Early Late post op post op



Total % / cases



Pacchiana et al. (2003)



TPLO



5 %



46 %



49 %



28 % / 397



Stauffer et al. (2006)



TPLO



5 %



50 %



45 %



19 % / 696



Frey et al. (2010)



TPLO



8 % / 902



Fitzpatrick et al. (2010)



TPLO



15 % / 1146



Böddeker et al. (2012)



TPLO



26 % / 28



Hoffmann et al. (2006)



TTA



44 %



44 %



12 %



59 % / 57



Lafaver et al. (2007)



TTA



5 %



17 %



78 %



32 % / 114



Damur et al. (2003)



PTIO



61 %



6 %



33 %



31 % / 100



Jerram et al. (2005)



PTIO



67 %



33 %



0



20 % / 60



Bruce et al. (2007)



TTO



70 %



22 %



9 %



36 % / 64



Verdonck et al. (2009)



cTTA



14 % / 21



Petazzoni (2010)



cTTA



10 % / 89



Etchepareborde



MMT



25 % / 12



et al. (2011)



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7 Ancillary procedures Signs of both partial and complete rupture of CrCL require inspection of the stifle joint to identify the state of the CrCL and removal of any remains of the ruptured CrCL. In addition the amount of OA changes as well as the state of the menisci should be checked and menisci operated if necessary. Most of the authors of the different techniques discussed in this review advocate a complete or partial meniscectomy when damage to the menisci is observed (e.g. DeAngelis & Lau 1970, Slocum & Devine 1993, Bruce et al. 2007). For example a study of 397 cases on 346 patients treated with TPLO performed a meniscal release on 67 % (267/397) of the cases. Subtotal or total meniscectomy was performed on 9 % (36/397) of the cases. (Pacchiana et al. 2003). However, a study on the effect of medial meniscal release (MMR) on TPLO operated patients found that since performing a TPLO neutralizes the tibial thrust, the wedge effect created on the medial meniscus is also greatly reduced and thus MMR may no longer be indicated (Pozzi et al. 2006). A later study on the effects of transection of the medial caudal meniscotibial ligament on cadavers treated with TPLO found that transection eliminates the load bearing function of the medial meniscus and thus significantly changes the medial femorotibial contact mechanics. This leads to abnormal cartilage stress, which can accelerate the degenerative changes in the joint. (Pozzi et al. 2010) Partial meniscectomy is indicated for longitudinal, bucket-handle, radial, horizontal, and complex tears for which peripheral circumferential collagen fiber integrity or a “rim” can be preserved after resection. Segmental meniscectomy is indicated for all types of tears in the caudal aspect of the meniscus when an intact rim cannot be preserved. Segmental meniscectomy should be performed in conjunction with complete resection of  any pathologic tissue. Total meniscectomy is indicated for tears extending beyond the caudal aspect of the meniscus and for which an intact rim could not be maintained. The goals in performing the meniscal resection are to remove all grossly damaged, displaced and pathologic tissue while preserving as much functional meniscal tissue as possible. (Cook & Pozzi 2010)



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8 Conservative treatment Non-surgical management has been considered a reasonable alternative for dogs less than 15 kg in weight. The study on non-operative management of CrCL rupture found that 85,7 % of the small patients were either normal or improved after 6 months. (Vasseur 1984) However, left untreated, a ruptured CrCL will cause instability in the stifle joint. The disadvantage of conservative management is that even with small dogs, this instability lasts from 4 to 5 months (Vasseur 1984). The extended period of instability may cause meniscal damage and accelerate the progression of DJD. Vasseur (1984) suggest that non-operative management of dogs less than 15 kg in weight is a valid alternative. However, since unilateral CrCL rupture frequently leads to bilateral rupture and any extended period of instability in the stifle joint accelerates the progression of DJD, early surgical treatment of dogs of all sizes is preferred. Surgical treatment should especially be considered with small breed dogs predisposed to patellar luxation due to the compound instability created by the deficient CrCL and luxated patellar ligament. If conservative treatment of complete or partial CrCL is chosen, it should consist of restricted exercise with optional active range of motion physiotherapy, nonsteroidal anti-inflammatory drug therapy and, if necessary, weight management.



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9 Prevention Despite the relatively high cost and morbidity associated with CrCL deficiency and its treatments, research efforts aimed at developing preventive measures remain in their infancy. The main reason for the discrepancy is the currently limited understanding of the origin of CrCL deficiency. (Griffon 2010) Genetic screening appears promising as a long-term option in selected breeds. For breeds where genetic screening is not applicable and where the CrCL deficiency is unilateral, immunomodulating therapies might soon become available for use in reducing the incidence of contralateral disease. (Griffon 2010)



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10 Discussion The current literature on repair of CrCL deficiency is varied in both content and methodology. There are no meta-analyses of the different methods or double blind prospective studies and only a few robustly designed prospective studies and prospective or retrospective cohort or case control studies. Most of the literature is documented case studies with fairly random numbers of patients, moderately suspect statistics and possibly deliberate bias in the presentation of the results. It is also almost customary to see new techniques presented and adapted well before any peer-reviewed research to support their efficacy has been published. In addition some of these new techniques are visibly backed by the company that manufactures the custom equipment required to perform operations using the new technique. New cross sectional studies comparing the different techniques for resolving CrCL rupture are needed. These studies need to be done with objective methodology, such as by using gait analysis and evaluating sufficient numbers of both treated and untreated patients. Careful planning is needed to minimize the risk of bias in those parts of the assessment of the patients where subjective evaluation is still required. Although double blinding in the way that some dogs receive an operation and some do not is clearly unethical, the blinding could be done by randomly selecting the technique to be used. If the technique information is then kept from the person performing the force plait gait analysis, a double blinding of sorts can be thought to have been made. Although the first techniques to combat CrCL deficiency, intra-articular techniques are no longer in use, at least not widely. Modifications of early 1970s extracapsular techniques as well as the more recent osteotomy techniques, however, are. The most used extracapsular technique requires no special equipment bar perhaps a drill and some suitable suture material (DeAngelis & Lau 1970), although the latest arrivals in this field are based on custom equipment (Cook et al. 2007). Most of the osteotomy techniques on the other hand require custom saw bits (Slocum & Devine Slocum 1993, Montavon et al. 2002, Bruce et al. 2007 and Verdonck & Petazzoni 2009) or compression plates for proper application and the ones which do not seem to be prone to failure (Damur et al. 2003). licenciate’s thesis, © Jan Mattila 2012.!



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Development of techniques not requiring custom or at least not requiring specific patented equipment should be encouraged. On the extracapsular technique side the opposite seems to be happening, as new suture materials have recently been introduced and with them new extracapsular techniques being introduced (Hulse et al. 2011). Similarly all osteotomies developed in the last decade require some amount of specialized equipment to be performed efficiently. Some of the osteotomies can be performed with standard tools, but many preferably require the custom equipment marketed by the inventors of the technique (e.g. radial saw by Slocum enterprises for TPLO and cage and tension band by Kyon veterinary surgical products for TTA). To enable more surgeons to perform corrective CrCL surgery, there is a need for a technique which involves less custom equipment. Since the patent for the TPLO technique has expired, it and the cTTA technique which is based on using the same radial saw are superior in this respect. TTO can also be performed without custom equipment, but has an unfortunately high perioperative complication rate. However, the introduction of new techniques has also created more competition in the field of manufacture of surgical instruments which has dramatically decreased the prices of the instrument for all of the techniques. TTO surgery involves an extensive amount of osteotomies, all of which increase the time required for healing. The technique did not remove the cranial draw motion in any cases post operatively or negate the tibial compression test in a majority of cases. The technique also has a relatively high complication rate of 36 % with the most common complication being the complete fracture of the TCO at its distal end. The 2007 study claims that 100 % of the responders both felt the surgery resulted in a marked improvement in the quality of life of their dogs and that they would have the procedure performed again if they had another dog with the same condition. The paper however fails to validate the questionnaire itself and consequently any and all results of the questionnaire part are worthless. Computer assisted force plate or treadmill gait analysis is considered the gold standard in assessing post operative use of limb by the patients. Gait analysis studies are however rare and most of the techniques described in this literature review have only been studied with palpation (cranial draw motion and tibial



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compression test), radiographic findings and owner questionnaires all of which are subjective to a great extent. The reporting of complications with different techniques is colorful to say the least. The most common current grouping of complications is division into three temporally separate groups: perioperative, short term post operative and long term post operative. In the last 25 years the reporting of complications has improved significantly. Where the 1989 study on fibular head transposition by Mullen et al. only reports the most common perioperative and postoperative complication, studies from the last 5 years account in great detail the different complications encountered. However, even in more recent studies, the reporting of complications is still varied. The Hoffmann et al. (2006) study on TTA attempts to discount minor complications such as tissue swelling or incisional discharge to significantly lower the complication rate from 59 % to 21 %. On the other hand the Hoffmann et al. (2006) study includes non-surgery technique related complications such as diarrhea or inappetence. Another study which includes complications caused by non-technique related mishandling of patients (inappropriate application of bandaging) as part of the total complications is the Pacchiana et al. (2003) study on TPLO. While diarrhea and incorrect application of bandages are obviously complications in themselves, they are clearly not related to the surgical technique in the same way as a tibial fracture or a broken implant are. The Hoffmann et al. (2006) study lists 27 distinct complications, but gives no indication as to which of the patients had multiple complications. They then report in Table 1 that 34 (of 57) dogs equaling 59,6 % had tissue swelling but incorrectly claim this to be 59 % of the cases in the text on page 222. The same mathematical error is repeated for inappetence, where 6 (of 57) or 10,5 % (correct in Table 1) is claimed to be 10 % on page 222. The same mathematical inconsistencies are repeated a few pages later with the total of dogs with any kind of complication claimed to be 33 of 57 dogs, which is both not consistent with Table 1 on page 223 and not 59 % (33/57 = 57,8 %). It also seems that the motives of some of the authors are to either decrease the apparent complications associated with a specific technique (e.g. Hoffmann et al. 2006 with TTA) or to increase them (e.g. Pacchiana et al. 2003 with TPLO). licenciate’s thesis, © Jan Mattila 2012.!



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More than anything the reporting of complications is in desperate need of standardization and after that universal adaption of those standards. Currently it is next to impossible to compare any of the complication rates of different studies. This leads ultimately to the fact that it is not possible to pick the best alternative from the multitude of different surgical techniques. It does seem that TPLO which is one of the oldest osteotomy techniques and has been studied the most has one of the lowest complication rates and appears suitable for most patients. TPLO is by far not the simplest of methods and the learning curve is shallow meaning it takes a long time to master the technique. However, should you put in the effort to master the TPLO technique, you could use the technique on most patients. And if you invested in the equipment necessary for TPLO, you could also attempt surgery with the newer and promising cTTA technique as it uses the same radial saw as that used in TPLO. This combination of techniques and the equipment necessary for performing both might be the best investment currently.



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11 References American Pet Products Association (APPA) (2011). National Pet Owners Survey. Summary retrieved on April 19, 2012 from the APPA website http://www.americanpetproducts.org/press_industrytrends.asp



American Pet Products Association (APPA) (2005). National Pet Owners Survey. Summary retrieved on April 19, 2012 from the APPA website http://www.americanpetproducts.org/press_industrytrends.asp



Arnoczky, S. P., & Marshall, J. L. (1977). The cruciate ligaments of the canine stifle: an anatomical and functional analysis. American journal of veterinary research, 38(11), 1807–1814. Arnoczky, S. P., Tarvin, G. B., Marshall, J. L., & Saltzman, B. (1979). The overthe-top procedure: a technique for anterior cruciate ligament substitution in the dog. Journal of the American Animal Hospital Association, 15(3), 283–290. Arthrex Vet Systems TightRope CCL Multicenter Clinical Outcomes Study brochure (2010). Bruce, W. J., Rose, A., Tuke, J., & Robins, G. M. (2007). Evaluation of the triple tibial osteotomy. A new technique for the management of the canine cruciatedeficient stifle. Veterinary and Comparative Orthopaedics and Traumatology, 20(3), 159–168. Buote, N., Fusco, J., & Radasch, R. (2009). Age, tibial plateau angle, sex, and weight as risk factors for contralateral rupture of the cranial cruciate ligament in Labradors. Veterinary surgery, 38(4), 481–489. Böddeker, J., Drüen, S., Meyer-Lindenberg, A., Fehr, M., Nolte, I., & Wefstaedt, P. (2012). Computer-assisted gait analysis of the dog: comparison of two surgical techniques for the ruptured cranial cruciate ligament. Veterinary and Comparative Orthopaedics and Traumatology, 25(1), 11–21. Carlin, I. (1926). Ruptur des ligamentum cruciatum anterius im Kniegelenk beim Hund. Arch Wiss Prakt Tierheilk, 54, 420–423. Carpenter, D. H., & Cooper, R. C. (2000). Mini review of canine stifle joint anatomy. Anatomia, histologia, embryologia, 29(6), 321–329. Chauvet, A. E., Johnson, A. L., Pijanowski, G. J., Homco, L., & Smith, R. D. (1996). Evaluation of fibular head transposition, lateral fabellar suture, and conservative treatment of cranial cruciate ligament rupture in large dogs: a retrospective study. Journal of the American Animal Hospital Association, 32(3), 247–255. Conzemius, M. G., Evans, R. B., Besancon, M. F., Gordon, W. J., Horstman, C. L., Hoefle, W. D., Nieves, M. A., et al. (2005). Effect of surgical technique on limb function after surgery for rupture of the cranial cruciate ligament in dogs. Journal of the American Veterinary Medical Association, 226(2), 232–236. Cook, J. L., & Pozzi, A. (2010). Surgical Treatment of Concurrent Meniscal Injury. In P. Muir (Ed.), Advances in the Canine Crucial Ligament (1st ed. pp. 217–222). Ames: Wiley-Blackwell. Cook, J. L., Luther, J. K., Beetem, J., & Cook, C. R. (2007). Tightrope CCL for treatment of cranial cruciate deficiency in dogs. Technique and results of a prospective comparison to TPLO using a validated outcome measures. licenciate’s thesis, © Jan Mattila 2012.!



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Whitepaper. University of Missouri, Comparative Orthopaedic Laboratory. Retrieved from the Arthrex Vet Systems Inc. website on April 10th 2012 http://www.arthrexvetsystems.com/int/mediacenter/upload/TR-CCL-WHITEPAPER-2007.pdf Damur, D. M., Tepic, S., & Montavon, P. M. (2003). Proximal tibial osteotomy for the repair of cranial cruciate-deficient stifle joints in dogs. Veterinary and Comparative Orthopaedics and Traumatology, 16(4), 211–216. DeAngelis, M., & Lau, R. E. (1970). A lateral retinacular imbrication technique for the surgical correction of anterior cruciate ligament rupture in the dog. Journal of the American Veterinary Medical Association, 157(1), 79–84. Duval, J., Budsberg, S., & Flo, G. (1999). Breed, sex, and body weight as risk factors for rupture of the cranial cruciate ligament in young dogs. Journal of the American Veterinary Medical Association, 215(6), 811–814. Etchepareborde, S., Brunel, L., Bollen, G., & Balligand, M. (2011). Preliminary experience of a modified Maquet technique for repair of cranial cruciate ligament rupture in dogs. Veterinary and Comparative Orthopaedics and Traumatology, 24(3), 223–227. Elkins, A. D., Pechman, R., Kearney, M. T., & Herron, M. (1991). A retrospective study evaluating the degree of degenerative joint disease in the stifle joint of dogs following surgical repair of anterior cruciate ligament rupture. Journal of the American Animal Hospital Association, 27(5), 533–539. Fitzpatrick, N., & Solano, M. A. (2010). Predictive variables for complications after TPLO with stifle inspection by arthrotomy in 1000 consecutive dogs. Veterinary surgery, 39(4), 460–474. Flo, G. L. (1975). Modification of the lateral retinacular imbrication technique for stabilizing cruciate ligament injuries. Journal of the American Animal Hospital Association, 11(5), 570–576. Frey, T. N., Hoelzler, M. G., Scavelli, T. D., Fulcher, R. P., & Bastian, R. P. (2010). Risk factors for surgical site infection-inflammation in dogs undergoing surgery for rupture of the cranial cruciate ligament: 902 cases (2005-2006). Journal of the American Veterinary Medical Association, 236(1), 88–94. Gupta, B. N., Brinker, W. O., & Subramanian, K. N. (1969). Breaking strength of cruciate ligaments in the dog. Journal of the American Veterinary Medical Association, 155(10), 1586–1588. Griffon, D. J. (2010). A review of the pathogenesis of canine cranial cruciate ligament disease as a basis for future preventive strategies. Veterinary surgery, 39(4), 399–409. Guerrero, T. G., Makara, M. A., Katiofsky, K., Fluckiger, M. A., Morgan, J. P., Haessig, M., & Montavon, P. M. (2011). Comparison of Healing of the Osteotomy Gap after Tibial Tuberosity Advancement with and without Use of an Autogenous Cancellous Bone Graft. Veterinary Surgery, 40(1), 27–33. Hayashi, K., Manley, P. A., & Muir, P. (2004). Cranial Cruciate Ligament Pathophysiology in Dogs With Cruciate Disease: A Review. Journal of the American Animal Hospital Association, 40(5), 385–390.



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Henderson, R. A., & Milton, J. L. (1978). The tibial compression mechanism: a diagnostic aid in stifle injuries. Journal of the American Animal Hospital Association, 14, 474–479. Hildreth, B. E., Marcellin-Little, D. J., Roe, S. C., & Harrysson, O. L. A. (2006). In vitro evaluation of five canine tibial plateau leveling methods. American journal of veterinary research, 67(4), 693–700. Hoffmann, D. E., Miller, J. M., Ober, C. P., Lanz, O. I., Martin, R. A., & Shires, P. K. (2006). Tibial tuberosity advancement in 65 canine stifles. Veterinary and Comparative Orthopaedics and Traumatology, 19(4), 219–227. Hulse, D. A., Michaelson, F., Johnson, C., & Abdelbaki, Y. Z. (1980). A Technique for Reconstruction of the Anterior Cruciate Ligament in the Dog: Preliminary Report. Veterinary Surgery, 9(4), 135–140. Hulse, D., Saunders, B., Beale, B., & Kowaleski, M. (2011). Extra-articular stabilization of the cranial cruciate deficient stifle with anchor systems. Tierärztliche Praxis Kleintiere, (5), 363–367. Hurley, C. R., Hammer, D. L., & Shott, S. (2007). Progression of radiographic evidence of osteoarthritis following tibial plateau leveling osteotomy in dogs with cranial cruciate ligament rupture: 295 cases (2001–2005). Journal of the American Veterinary Medical Association, 230(11), 1674–1679. Jerram, R. M., Walker, A. M., & Warman, C. G. A. (2005). Proximal tibial intraarticular ostectomy for treatment of canine cranial cruciate ligament injury. Veterinary surgery, 34(3), 196–205. Johnson, J. M., & Johnson, A. L. (1993). Cranial cruciate ligament rupture. Pathogenesis, diagnosis, and postoperative rehabilitation. Veterinary Clinics of North America: Small Animal Practice, 23(4), 717–733. Kaiser, S., Cornely, D., Golder, W., Garner, M., Waibl, H., & Brunnberg, L. (2001). Magnetic resonance measurements of the deviation of the angle of force generated by contraction of the quadriceps muscle in dogs with congenital patellar luxation. Veterinary surgery, 30(6), 552–558. Kim, S. E., Pozzi, A., Kowaleski, M. P., & Lewis, D. D. (2008). Tibial Osteotomies for Cranial Cruciate Ligament Insufficiency in Dogs. Veterinary Surgery, 37(2), 111–125. Lafaver, S., Miller, N. A., Stubbs, W. P., Taylor, R. A., & Boudrieau, R. J. (2007). Tibial Tuberosity Advancement for Stabilization of the Canine Cranial Cruciate Ligament-Deficient Stifle Joint: Surgical Technique, Early Results, and Complications in 101 Dogs. Veterinary Surgery, 36(6), 573–586. Lazar, T. P., Berry, C. R., de Haan, J. J., Peck, J. N., & Correa, M. (2005). Longterm radiographic comparison of tibial plateau leveling osteotomy versus extracapsular stabilization for cranial cruciate ligament rupture in the dog. Veterinary surgery : VS, 34(2), 133–141. Matthiesen, D. T. (1993). Fibular head transposition. Veterinary Clinics of North America: Small Animal Practice, 23(4), 755–760. Montavon, P. M., & Tepic, S. (2006). Joint Surgery in Canine Hind Limb–Recent Contributions from the University of Zurich. European Companion Animal Health, 25–28. licenciate’s thesis, © Jan Mattila 2012.!



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Montavon, P. M., Damur, D. M., & Tepic, S. (2002). Advancement of the tibial tuberosity for the treatment of cranial cruciate deficient canine stifle. ESVOTVOT 2002 proceedings, 152. Moore, K. W., & Read, R. A. (1996). Rupture of the cranial cruciate ligament in dogs - Part I. The Compendium on Continuing Education for the Practicing Veterinarian, 18(3), 223–233. Mullen, H. S., & Matthiesen, D. T. (1989). Complications of transposition of the fibular head for stabilization of the cranial cruciate-deficient stifle in dogs: 80 cases (1982-1986). Journal of the American Veterinary Medical Association, 195(9), 1267–1271. Olmstead, M. L. (1993). The use of orthopedic wire as a lateral suture for stifle stabilization. Veterinary Clinics of North America: Small Animal Practice, 23(4), 735–753. Paatsama, S. (1952). Ligament injuries in the canine stifle - A clinical and experimental study. Academic dissertation (p. 82). Helsinki: Kauppakirjapaino Oy. Pacchiana, P. D., Morris, E., Gillings, S. L., Jessen, C. R., & Lipowitz, A. J. (2003). Surgical and postoperative complications associated with tibial plateau leveling osteotomy in dogs with cranial cruciate ligament rupture: 397 cases (1998-2001). Journal of the American Veterinary Medical Association, 222(2), 184–193. Patterson, R. H., Smith, G. K., Gregor, T. P., & Newton, C. D. (1991). Biomechanical stability of four cranial cruciate ligament repair techniques in the dog. Veterinary Surgery, 20(2), 85–90. Petazzoni, M. (2010). cTTA (circular Tibial Tuberosity Advancement). ESVOTVOS proceedings 2010, 295–296. Pozzi, A., Kim, S. E., & Lewis, D. D. (2010). Effect of Transection of the Caudal Menisco‐Tibial Ligament on Medial Femorotibial Contact Mechanics. Veterinary Surgery, 39(4), 489–495. Pozzi, A., Kowaleski, M. P., Apelt, D., Meadows, C., Andrews, C. M., & Johnson, K. A. (2006). Effect of medial meniscal release on tibial translation after tibial plateau leveling osteotomy. Veterinary surgery, 35(5), 486–494. Robins, G. M. (1990). The canine stifle joint. In W. G. Whittick (Ed.), Canine Orthopedics (2nd ed. pp. 693–760). Philadelphia: Lea & Febiger. de Rooster, H., de Bruin, T., & van Bree, H. (2006). Morphologic and Functional Features of the Canine Cruciate Ligaments. Veterinary surgery, 35(8), 769–780. Shires, P. K. (1993). Intra-articular repairs for cranial cruciate ligament ruptures. Veterinary Clinics of North America: Small Animal Practice, 23(4), 761–776. Shires, P. K., Hulse, D. A., & Liu, W. (1984). The under-and-over fascial replacement technique for anterior cruciate ligament rupture in dogs: A retrospective study. Journal of the American Animal Hospital Association, 20(2), 69–77. Singleton, W. B. (1963). Stifle joint surgery in the dog. The Canadian Veterinary Journal, 4(6), 142–150.



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Slocum, B., & Devine Slocum, T. (1993). Tibial plateau leveling osteotomy for repair of cranial cruciate ligament rupture in the canine. Veterinary Clinics of North America: Small Animal Practice, 23(4), 777–795. Slocum, B., & Devine, T. (1983). Cranial tibial thrust: a primary force in the canine stifle. Journal of the American Veterinary Medical Association, 183(4), 456–459. Slocum, B., & Devine, T. (1984). Cranial tibial wedge osteotomy: a technique for eliminating cranial tibial thrust in cranial cruciate ligament repair. Journal of the American Veterinary Medical Association, 184(5), 564–569. Smith, G. K., & Torg, J. S. (1985). Fibular head transposition for repair of cruciate-deficient stifle in the dog. Journal of the American Veterinary Medical Association, 187(4), 375–383. Stauffer, K. D., Tuttle, T. A., Elkins, A. D., Wehrenberg, A. P., & Character, B. J. (2006). Complications associated with 696 tibial plateau leveling osteotomies (2001-2003). Journal of the American Animal Hospital Association, 42(1), 44– 50. Vasseur, P. B. (1984). Clinical results following nonoperative management for rupture of the cranial cruciate ligament in dogs. Veterinary Surgery, 13(4), 243– 246. Vasseur, P. B., Pool, R. R., Arnoczky, S. P., & Lau, R. E. (1985). Correlative biomechanical and histologic study of the cranial cruciate ligament in dogs. American journal of veterinary research, 46(9), 1842–1854. Verdonck, B., & Petazzoni, M. (2009). cTTA: circular tibial tuberosity advancement with FIXIN fixators. European Veterinary Conference Voorjaarsdagen proceedings, 290. Voss, K., Damur, D. M., Guerrero, T., Haessig, M., & Montavon, P. M. (2008). Force plate gait analysis to assess limb function after tibial tuberosity advancement in dogs with cranial cruciate ligament disease. Veterinary and Comparative Orthopaedics and Traumatology, 21(3), 243–249. Wilke, V. L., Robinson, D. A., Evans, R. B., Rothschild, M. F., & Conzemius, M. G. (2005). Estimate of the annual economic impact of treatment of cranial cruciate ligament injury in dogs in the United States. Journal of the American Veterinary Medical Association, 227(10), 1604–1607. Whitehair, J. G., Vasseur, P. B., & Willits, N. H. (1993). Epidemiology of cranial cruciate ligament rupture in dogs. Journal of the American Veterinary Medical Association, 203(7), 1016–1019.



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10



 



HEALTH



Saying “No” to Surgery “Conservative management” is an often overlooked – but frequently effective – option for ligament injuries. BY CJ PUOTINEN ogs go lame for all kinds of reasons. Arthritis, Lyme disease,  paw injuries, muscle sprains, bee stings, interdigital dermatitis, and dislocated kneecaps can make any dog limp. But when an active dog suddenly can’t put weight on a hind leg, the most common diagnosis – for more than a million American dogs every year – is a torn cruciate ligament. In 2003, according to the Journal of the the American American Veterinary Veterinary  Medical Association, the cost of treating



can require as much time and effort as  post-surgical  post-su rgical rehabi rehabilitat litation. ion. At its best, conservative management improves the outcome of whatever treatment is needed for full recovery. “Conservativee management consists of “Conservativ any nonsurgical treatment of injuries,” says Faith Rubenstein, who founded an online forum devoted to the subject in 2004, “including physical therapy, chiropractic adjustments, acupuncture, massage, nutrition, the use of a leg brace, nonsteroidal



those injuries exceeded $1.32 billion, and the price tag keeps rising. The most common prescription for canine knee injuries is surgery. Unfortunately, operations don’t always work and some patients, because of age or other conditions, are not good candidates. In recent years a nonsurgical approach called “conservative management” has helped thousands of dogs recover from ligament injuries, and it is growing in  popularity. At the same time, conservative management is not a cure-all. It doesn’t always prevent the need for surgery, it is not necessarily less expensive, and it



anti-inammatory anti-inam matory drugs, medicinal herbs,  prolotherapy, weight loss for overweight  prolotherapy, dogs, and other noninvasive treatments.” Rubenstein, who now lives in Austin, Texas, rst encountered ligament injuries when her 100-pound Briard, Dakota, then six years old, experienced a partial tear of his cranial (anterior) cruciate ligament. “When our veterinarian recommended that we see an orthopedic surgeon,” she says, “I went looking for answers.” An academic researcher who is now a private investigator, Rubenstein discovered the term “conservative management” in a veterinary textbook.



D



Kimber, Shiloh Shepherd, recovered Debbie fully fromKazsimer’s a torn cruciate ligament with the help of a brace, physical therapy, swimming, massage, supplements – and without surgery.



The orthopedic diagnosed a partialsurgeon tear in  both of Dakota’s Dakota’s knees and recommended immediate TPLO (tibial plateau leveling osteotomy) surgery. In this procedure, the tibia is cut, then rotated and held in place with a metal plate and screws so that after the  broken bone heals, weight bearing exercise stabilizes the knee joint. “I had misgivings about this method,” she says, “es pecially because surgeons at the School of Veterinary Medicine at the University of Pennsylvania don’t use



What you can do . . . ■



If your dog is limping, bring him to your veterinarian to determine the cause.







Keep a dog with a ligament injury quiet and confined.







Understand the risks and benefits of knee surgery so you can make an informed decision about which direction to take.







Explore physical therapy and other treatments that strengthen joints.







No matter the treatment, speed your dog’s recovery with nutrition, physical therapy, and other support.



it. spoke with Gail Smith, the of theI University’s department of head clinical research, and with Amy Kapatkin, a boardcertied orthopedic surgeon who was then at Penn. What Dr. Kapatkin said made perfect sense to me. She asked, ‘Why break a  bone to to x a ligament?’ ligament?’ My whole whole interest in conservative management was triggered  by my fear of the TPLO.” The University referred Rubenstein to an orthopedic surgeon who used other methods. He found Dakota to have so few symptoms that he agreed to write a  prescription for physical therapy in hopes that it might make surgery of any kind unnecessary. “Physical therapy and exercise made all the difference,” she says. “Dakota never needed surgery, and neither did



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Both of Faith Rubenstein’s Briards, Dakota and Aubrey, tore a cruciate ligament at different times – turning Faith into something of an expert on dealing with the injury!



his littermate, Aubrey, who tore his cruciate ligament a few months later. Many veterinarians believe that the only effective treatment for these injuries is surgery – either TPLO or another surgery  – but that simply isn’t true. Conservative C onservative management can help most patients, including those who eventually have surgery surgery, , and then recover and lead active, happy lives.”



The main diagnostic tools for ligament injuries are X-rays, which can rule out bone cancer as a cause of leg pain, and a proceprocedure called the “drawer test,” in which the veterinarian holds the femur with one hand and manipulates the tibia with the t he other. If the tibia can be moved forward, resembling a drawer being opened, the cruciate ligament has been torn or ruptured. The drawer test is not necessarily conclusive because the tense muscles of a



ing (including on and off furniture), and no stairs. Walk your dog on-leash when going outside to potty. The dog doesn’t necessarily have to be crated, which can restrict movement so much that it increases stiffness and limits exibility, but should  be conned to a small room or ex-pen, or kept on-leash while with the owner. Exercise restriction must be continued for at least six to eight weeks.” Second, inflammation needs to be



frightened or apprehensive dog can stabilize the knee temporarily. te mporarily. To To produce more accurate results in such cases, patients may  be sedated before being tested. In the tibial compression test, which is another way to check for ligament damage, the femur is held steady with one hand while the other exes the dog’s ankle. A ruptured ligament allows the tibia to move abnormally forward. “A complete cranial cruciate ligament tear is always a surgical case,” says Stacey Hershman, DVM, of Hastings-on-Hudson,  New York, York, “since otherwise otherwise the knee cannot function as a hinge joint.”



controlled. “I would use nonsteroidal anti-inammatories anti-inamma tories ( NSAIDs),” she says. “Inflammation contributes to cartilage degeneration and accelerates the development of arthritis. Don’t avoid  NSAIDs in the hope that pain will keep your dog from overusing the leg. There are natural antiinammatoriess like bromelain, boswellia, inammatorie quercitin, and turmeric, and I would use those as well, but they may not be strong enough alone. You You could use white willow  bark, which is comparable to aspirin, aspirin, but it should not be combined with other NSAIDs. In addition to anti-inammatories, I would give glucosamine-type supplements to try



Advocates of conservative ment recommend that whenevermanagethe tear is partial, nonsurgical techniques be given an eight-week try. If symptoms improve during that time, they say, the odds favor nonsurgical recovery. If symptoms don’t improve, conservative management techniques can be used as pre- and postoperative conditioning and therapy therapy..



The stie (knee) connects the femur (thigh  bone) and tibia (leg bone) with a patella (kneecap) in front and fabella (a small  bean-shaped bone) behind. Cartilage (the medial meniscus and lateral meniscus) cushions the bones, and ligaments hold everything in position. Two key ligaments, the anterior (front) and posterior (back) cruciate ligaments, cross inside the knee joint. In animals, these ligaments are called cranial and caudal, respectively. The anterior or cranial cruciate ligament prevents the tibia from slipping out of position. Veterinarians see most ligament patients immediately after their injuries, when symptoms are acute, or weeks or months later, after symptoms become chronic. If not immediately treated, most ligament injuries appear to improve but the knee remains swollen and abnormal wear between bones and meniscal cartilage creates degenerative changes that result in osteophytes (bone spurs), chronic  pain, loss of motion, and arthritis. In some  patients, osteophytes appear appear within one to three weeks of a ligament injury. Swelling



If your dog is injured, visit your y our vet as soon as possible, but be an informed consumer. Many veterinarians consider cruciate ligament surgery necessary, routine, fast, easy, highly effective, and the only treatment that will help. For many dogs this has been the case, but some veterinary research (see “Surgical Options,” on page 16) places the ligament surgery success rate at well below 50 percent. If surgery is necessary, your investment in conservative management may pay dividends in faster recovery and  better overall health. Canine health and nutrition researcher Mary Straus recommends simple rst-aid strategies for dogs with knee injuries. Straus learned about the benets of such an approach when her dog, Piglet, had surgery for dysplasia on both elbows before her second birthday, followed by surgery



to protectIt’s thequestionable cartilageble and slow arthritic changes. questiona how much these help with cruciate injuries, but they do no harm and I would include them.” Dr. Hershman prescribes Glycoex, a nutritional supplement that contains freeze-dried  Perna canalicul canaliculus us or New Zealand Green Lipped Mussel. This  product  prod uct is reco recomme mmended nded for joi joint nt and connective tissue support, for geriatric and working dogs, and as a follow-up to orthopedic surgery surgery.. In addition, she gives subcutaneous Adequan® injections or teaches the owners to do so at home. Adequan Canine (polysulfated glycosaminoglycan) is a  prescription, water-based, intramuscular,  polysulfated  polysulfa ted glycosamin glycosaminoglycan oglycan that helps  prevent cartilage in the dog’s joint from wearing away. “I give injections twice a week for two weeks,” says Dr. Hershman, “then once a week for maintenance.” She also recommends Wholistic Canine Complete Joint Mobility, which is a powder containing organic vitamins, minerals, digestive enzymes, hydrolized whitesh, immune-support ingredients, and pharmaceutical-grade glucosamine, chondroitin and MSM   (methyl sulfonyl methane), all of which support healing, speed tissue repair, or help alleviate pain



on the inside of the knee, called a “medial  buttre ss,” indica  buttress,” indicates tes the develop development ment of arthritis in patients with old injuries.



for a ruptured cruciate at age three. “First and most importantly,” she says, “exercise must be restricted. No running, no jump-



and inammation. Standard Process products for im proved ligament health include Ligaplex,



Understanding ligaments



14|FEBRUARY 2010



After an injury



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which contains organic raw bone, herbs, and minerals, and the veterinary product Canine Musculoskeletal Support, which contains anti-inammatory herbs,  Perna canaliculus, and whole-food ingredients that enhance tissue regeneration and im prove joint health. It is important to keep injured dogs from gaining weight, which can easily happen when their exercise routine is interrupted. “Overweight dogs have a harder



she puts patients on a home strengthening program with range-of-motion and stretching exercises. “Every program is different depending on the dog’s condition,” she says. “The owners are involved every day; I show them what to do. It’s  just like working with human injuries; i njuries; if you want the best results, you have to do your homework.” Wasmucky, who has worked with wit h thousands of canine patients over the past 10



day in twice-a-day sessions,” she says, “and this can go on for months. It’s a big investment of time and energy energy,, and it requires a motivated dog as well as a motivated owner, but it can make a world of difference in mobility and overall health.” For more about canine rehabilitation, see “Canine Rehab? Go, Go, Go” (WDJ September 2009).



time recovering from“and a cruciate injury,” says Straus, they areligament more at risk for injuring the other knee. I would feed a high-protein, low-carbohydrate, reduced-fat diet. Fat is high in calories and so should be limited, but too little fat will leave the dog feeling hungry all the time. Protein helps with wound healing and also to create and preserve lean muscle, while carbs are more likely to be stored as fat. For F or those who feed kibble, I would cut back on the amount fed and add fresh, high-protein foods such as eggs, meat, and dairy. For seriously overweight dogs, this is one situation where I might consider using the drug Slentrol to help speed weight loss.”



years, encourages anyone whose has a  partial tear to use physical therapydog therapy to build muscle so that even if surgery has to be  performed, the dog goes in and comes out in better shape. “This means shorter rehab time,” she says, “and a faster recovery.” Swimming is such effective exercise for injured dogs that many veterinary clinics have installed swimming pools. “Dogs who can’t yet do weight-bearing exercises can start in a pool,” she says, “and as they get stronger, they’re able to progress through the exercise program. I check their progress in weekly appointments and make adjustments as needed. It takes time to heal from ligament injuries and I like to be sure that dogs are completely well before they resume agility or other demanding sports.” She requires a major commitment from owners. “It’s usually an hour or so every



Although most veterinary experts agree that there is no way to repair a damaged ligament, one alternative therapy claims to do exactly that. Prolotherapy, also known as proliferative or sclerosing therapy, has been used for over 30 years to treat musculoskeletal pain in humans, including arthritis, sports injuries, and damaged or partially torn ligaments, tendons, and cartilage. T h e te r m “prolo”   is short for  prolif erat eration ion , as this treatment is said to cause the proliferation (growth or formation) of new tissue in weakened areas. Ligaments have a limited blood supply, which slows healing, but in  prolotherapy,, injections of dextrose (sugar  prolotherapy water) or other benign substances cause localized inammation that increases the supply of blood and nutrients, stimulating tissue repair.



Physical therapy Faith Rubenstein’s Dakota received physical therapy from Carol Wasmucky, PT, a licensed physical therapist for humans in Herndon, Virginia, who founded Pet Rehab Inc. and works full-time with animals  by referral from veterinarians throughout  Northern Virginia. Virginia. She began Dakota’s treatment by measuring his hind legs, one of which w hich had atrophied and was smaller than the other. “Our goal,” says Rubenstein, “was to have  both legs measure the same. Dakota and I worked with a holistic veterinarian, who  put him on nutritional and herbal supplements, and we did acupuncture as well. I restricted his activity so he was not allowed to run off-leash for six months, and during that time he had regular physical therapy. Dakota wasn’t a swimming dog  but he became one, for swimming was the  perfect exercise for for him. After six months,  both hind legs were the same same 17 inches in girth. He was in great shape, his drawer test results improved to nearly normal, and he didn’t need surgery.” Dogs who are intermittently lame with a partial tear of the cruciate ligament are ideal physical therapy patients, says Wasmucky. In addition to providing weekly or twice-a-week ultrasound, laser, and electrical stimulation treatments, TO SUBSCRIBE: whole-dog-journal.com



Prolotherapy



Which Dogs Are at Highest Risk? Any dog can injure a cruciate ligament, but large breeds are most susceptible. According to one study, Neapolitan Mastiffs, Newfoundlands, Akitas, Saint Bernards, Rottweilers, Chesapeake Bay Retrievers, and American Staffordshire Terriers lead the list. Most veterinary clinics have seen ligament injuries in Labrador Retrievers, Golden Retrievers, German Shepherd Dogs, and other  popular large breeds. Young, athletic dogs playing hard can turn or step the wrong way and suddenly not be able to walk. Cruciate ligament injuries are unfortunately common in dogs who compete in agility agility,, obedience, eld trials, and other active sports. Some veterinarians report progressive lameness in young Labrador Retrievers, Rottweilers, and other large-breed l arge-breed dogs resulting from a partial rupture of the cranial cruciate ligament. This may not associated with a specic injury but may instead result from poor stie biomechanics combined with a yet-to-be-dene yet-to-be-dened d conformation abnormality. Older large-breed dogs can develop weakened ligaments that eventually tear, especially in dogs who are overweight. When a weakened ligament is stressed, its rupture can be triggered by activities that are otherwise insignicant, like sitting on cue, stepping over a curb, or jumping off a sofa. A small dog’s size may not prevent a ligament injury, but smaller dogs usually recover faster. One study that compared dogs six months after their cruciate ligament ruptures found that 85 percent of those weighing less than 30 pounds had regained near normal or improved function while only 19 percent of those weighing more than 30 pounds had regained near normal function. Dogs in both groups needed at least six months to show maximum improvement.



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THE WHOLE DOG JOURNAL | 15



 



Health columnist Jane E. Brody described prolotherapy as “injections to kick-start tissue repair” in the August 7, 2007,  New York Times, where she wrote that most scientically designed controlled studies of prolotherapy have shown “a signicant improvement in the patients’ level of pain and ability to move the painful  joint.” In studies of human knee injuries, she said, patients with ligament laxity and instability experienced a tightening



ing it act like scar tissue and eventually contract with time. The thickening and contraction of the ligaments and joint capsule increase joint stability and relieve  joint pain.” Most canine patients receive ve sessions at three-week intervals. “Although I tell caregivers not to expect any positive results until at least the third treatment,” he says, “I am occasionally surprised to see improvement after just one. Other



Bracing for recovery



of those ligament. ligaments,Other including theshowed anteriora cruciate studies signicant improvement in the symptoms of arthritis in the knee one to three years after prolotherapy injections. In Royal Oak, Michigan, John Simon, DVM, uses prolotherapy to repair damaged cruciate ligaments in dogs. He explains, “Prolotherapy is a way of tightening up loose, unstable, hyper-mobile joints by injecting a ‘sclerosing’ ‘sclerosing ’ agent in and around the joint. The resulting thickening of the  joint capsule and the ligaments li gaments surround-



modalities often recommend in conjunctionthat withI prolotherapy are soft laser therapy and pulse magnetic therapy. These treatments reduce pain and help the t he  joint recuperate.” According to Dr. Simon, the best candidates for prolotherapy ligament repair are dogs whose injuries do not involve torn meniscal cartilage in the joint. During the  past three years, he has treated 35 dogs for cruciate ligament problems and estimates that 80 percent experienced signicant improvement.



corroded the5.5 proximal portion of the(“Sarcoma tibia in a of dog years after tibial plateau leveling l eveling osteotomy,” JAVM  JAVMA A ,   November 15, 2005, Vol. 227, No. 10). Two years later, Trouble was diagnosed with osteosarcoma, and when his leg was amputated, its metal implant was found to  be corroded. The biopsy report linked the cancer to his 2004 TPLO surgery. As a precaution, Kazsimer had Fly’s implant removed. “But by then ve years had passed and it was too late,” she says. “The damage was already done.” done.” Within



Surgical Options



Debbie Kazsimer, who lives in Pennsylvania, knows a lot about cruciate ligaments. Trouble, her Shepherd/Husky mix, had TPLO surgeries at ages six and seven, and her Shepherd/Malamute mix, Fly, had a TPLO when she was two. In 2005, the  Journal of the American Veterinary Medical Association published the case of a German Shepherd Dog who developed bone cancer after her implant



While it is not possible to repair canine ligaments surgically, lateral suture stabilization or LSS techniques can stabilize knee joints so that they function well. In the extracapsular repair procedure, torn or partially torn ligament tissue and bone spurs are removed along with the damaged portion of the meniscus. Through a hole drilled in the front of the tibia, a large, strong suture is passed around the fabella behind the knee, which tightens the joint and replaces the cruciate ligament. The intracapsular repair method,  which is no longer  popular  popul ar in the Unit United ed Stat States es but stil stilll wide widely ly used in the United Kingdom, replaces the cruciate ligament with a strip of connective tissue after the damaged meniscus and ligament fragments are removed. This “new ligament” is sewn into place



developed in 2002 at the University of Zurich, repositions the top of the tibia by separating and then anchoring it with titanium or steel implants. Like TPLO surgery, TT TTA A requires special equipment and expertise.  None of these procedures work for every patient and all carry risks associated with the use of general anesthetics, postoperative infections, and other complications. The TPLO and TTA TT A are most expensive and most invasive. Which surgical method is best? Every procedure has its advocates and many veterinary surgeons claim high success rates, but the results of research studies can be sobering. In 2005, the  Journal of the American Veterinary Medical As sociation published a study* comparing the results of lateral suture stabilization (LSS), intracapsular stabilization ( ICS),



or attached to an implant. A new ligament repair technique called the Tightrope procedure  utilizes a ber tape suture material developed for human ankle and shoulder reconstruction. This material replaces the damaged cruciate ligament and stabilizes the stie joint. Tibial Plateau Leveling Osteotomy or TPLO surgery involves breaking and resetting the tibia. The meniscus cartilage is removed and, if badly damaged, the remains of the cruciate ligament may be removed as well. The repositioned bone is held in place with a metal plate and screws. This procedure treats an estimated 50 percent of all cruciate ligament injuries inj uries in the U.S. and its popularity helped double the number of American veterinary surgeons in a single decade (1995-2005). TPLO surgery requires a specialist and typically costs twice tw ice as



and TPLO surgery on 131 Labrador Retrievers with ruptured cranial cruciate ligaments and injury to the t he medial meniscus. Limb function was measured before surgery and again two and six months after. Treated dogs were also compared to 17 clinically normal Labrador Retrievers. Compared with the clinically normal dogs, only 14.9 percent of the LSS-treated dogs, 15 percent of ICS-treated dogs, and 10.9 percent of TPLO-treated dogs had normal limb function. Overall im provement was seen in only 15 percent of dogs treated with ICS, 34 percent of those treated with TPLO, and 40 percent of those treated with LSS.



much as extracapsular repair. Tibial Tuberosity Advancement  or TTA,  which was



the American Veterinary Medical Association, January 15, 2005, Vol. Vol. 226, No. 2, p. 232-236.



16|FEBRUARY 2010



* “Effect of surgical technique on limb function after surgery for rupture of the cranial cruciate ligament in dogs,” by Michael G. Conzemius, DVM, PhD, DVACS, et al. Journal of



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TO SUBSCRIBE, CALL (800) 829-9165



 



months, both dogs died of osteosarcoma. Four weeks after Fly’s death, Kazsimer’s Kazsimer ’s six-year-old 100-pound Shiloh Shepherd, Kimber, tore a cruciate ligament. By then, Kazsimer had learned about conservative management and knew she didn’t want to  put another dog through a TPLO surgery. Because of her experiences with Fly and Trouble, she was familiar with range-ofmotion and physical therapy exercises, and she studied massage with her husband, Ken, an Integrated To Touch uch Therapy canine massage therapist. She spent an hour or two daily on Kimber’s rehabilitation. “I thought a leg brace would be a big help to her,” she says, “but my veterinarian refused to t her for one because he was convinced it wouldn’t work. So my husband and son helped me to cast her leg with a casting kit from Orthopets. The  brace supports the knee externally, externally, just as surgery supports it internally.” Kimber went from walking on three legs to walking on four, then swimming, then nally bearing full weight on her leg. Eight months after her injury, Kimber’s regimen of supplements, physical therapy therapy,, massage, swimming, and wearing the brace have enabled her to recover well without surgery. “She runs around like a wild girl!” says Kazsimer, who has posted videos of Kimber online, where you can see her running, swimming, and playing with and without her brace on. “It’s wonderful,” she says. “Kimber is able to do everything she did before she got hurt.”



The most popular “hands-on” treatments for injured dogs include acupuncture, acu pressure, chiropractic, and massage. Dr. Hershman, a certied veterinary



Co-moderator Ansley Newton of Pownal, Maine, became interested in conservative management when her chocolate Lab, Dooley, injured his second knee. “The rst knee had TPLO surgery,” she says, “so I was excited to try conservative management with the second knee. Unfortunately after four months he did not get better and I chose to have a traditional surgery, which was very successful for this 90-pound dog. Then one day my large chocolate Lab,  Nutmeg, came inside with that familiar limp. I again decided to try conservative management along with a knee brace, acupuncture, massage, swimming, and some other supportive techniques. Within six months she was back to normal with very little arthritis. “After three ligament injuries, I thought I was done. But no, two years later Nutmeg came in limping again. I again went the conservative management route and things were going fine until the second month when Nutmeg had an oops  Online support Thanks to the Internet, anyone whose Nutmeg recovered moment. She was limpdog suffers a cruciate ligament injury from two   ACL tears ing again, so I decided can find a wealth of information without surgery. to do surgery but had to about canine anatomy, surgical op postpone it for a couple tions, and alternative therapies online. of months because I tore my own anterior The conservative management forum cruciate ligament and damaged my meniscus at the same time! that Faith Rubenstein founded ve years ago now has more than 2,000 members “So here I was running a farm by myaround the world. Paola Ferraris, who self on crutches and wearing a knee brace lives in Italy, is one of its moderators. with a dog in a knee brace. What a sight “What I would like to stress is that we both were. I wish I had taken a picture. pi cture. conservative management is not an easy We were forced to stay with conservative (and often not cheap) alternative to management because there was no one to surgery,” says Ferraris. “Successful take care of the farm and I couldn’t drive



acupuncturist, treats patients with acupuncture to alleviate pain and enhance healing of the torn ligament. “I do this once or twice per week for the rst two weeks,” she says, “depending on the dog’s level of pain, then once a week for ve to six weeks, then once every two weeks, and nally once a month. When the dog is weight-bearing and in less pain, I stop.” Dr. Hershman is also a certied veterinary homeopath who  prescribes homeopathic remedies according to the patient’s symptoms. In their article “Post-op Acupressure” (August 2006), Nancy Zidonis and Amy Snow describe how stimulating specic



conservative management requires just as much commitment as post-op care. It’s tough love and careful management. Your work is basically the same as rehabbing a dog who has had surgery; in fact, a number of our members have had surgery done on their dogs and use the list for pre-op and  post-op support.” When her own dog suffered a ligament injury,, Ferraris had to make decisions with injury little information. “The best way to discuss treatment with your veterinarian is when you understand the available options and their pros and cons,” she says. “I had to educate myself by spending nights doing



 Nutm eg to get her surgery. We limp ed  Nutmeg through several months together and lo and behold, we both healed. Nutmeg was good to go in six months and it took me closer to 10. Nutmeg recently passed away from lymphoma. She was 14 years old and despite those two ligament injuries, her legs were still ne.”



acupressure withmanagement, a thumb or nger  tip can help points with pain clearthe effects of anesthesia, minimize the



research online, aftermore the fact. I wouldinforhave appreciated having available mation, which is what we now offer.”



and Natural  Natural PetCats. Care For Remedies for Dogs and more information on her books, see page 24.



Holistic therapies



TO SUBSCRIBE: whole-dog-journal.com



 building of scar tissue, and reduce swelling. Acupressure can be learned at home and applied whenever needed. Veterinary chiropractors help speed the healing of injuries and surgeries by making adjustments that improve skeletal alignment and musculoskeletal function. (See “Chiropractors for Canines,” March 2008.) Chiropractic adjustments help restore normal nerve activity by gently moving  bones, ligaments, and tendons back into alignment, and when ligaments are injured, adjustments help realign the body to im prove balance and speed healing. Canine massage therapists used to be unusual, but now they play an important role in maintaining and improving our dogs’ health. Efflurage, passive touch, kneading techniques, and stroking increase circulation, release muscle tension, reduce pain and soreness, relieve stress, and accelerate the repair process. Massage  books and how-to videos make it easy for caregivers to apply these same techniques at home.



Copyright © 2010, Belvoir Media Group, LLC 



 For further information on organizations and products mentioned in this article, see page 23. CJ Puotinen is a long-time contributor to WDJ and author of The Encyclopedia of



THE WHOLE DOG JOURNAL | 17



FACULTEIT DIERGENEESKUNDE



Vakgroep Medische Beeldvorming van de Huisdieren



CRANIAL CRUCIATE LIGAMENT DISEASE IN THE DOG: CONTRIBUTIONS TO ETIOLOGY, DIAGNOSIS AND TREATMENT



Hilde de Rooster



Proefschrift voorgedragen tot het behalen van de graad van Doctor in de Diergeneeskundige Wetenschappen aan de Faculteit Diergeneeskunde Universiteit Gent 2001



Promotor: Prof. Dr. H. van Bree Copromotor: Prof. Dr. E. Cox



“Those who study the cruciate ligaments and the methods of repair when injured, are descendants of the discoverer of the wheel and of those who rediscovered the wheel. All take great pride in their discoveries.”



Charlie Bild



TABLE OF CONTENTS List of abbreviations



GENERAL INTRODUCTION



1



AIMS OF THE STUDY



11



CHAPTER 1.



15



REVIEW OF THE LITERATURE



1.1. Basic science of the cruciate ligaments 1.1.1. 1.1.2. 1.1.3. 1.1.4. 1.1.5. 1.1.6. 1.1.7.



Introduction Insertion points Fibre bundle anatomy Functional anatomy and aspects Microanatomy and ultrastructure Microvascularity Neurology



17 19 20 22 25 30 34 38



1.2. Predisposing and etiological factors in canine cranial cruciate disease. A long list of possible contributors



49



1.3. Cranial cruciate ligament rupture in the dog. A review of diagnostic techniques



57



(Adapted from: Vlaams Diergeneeskundig Tijdschrift 1995;64:42-46)



1.4. Cranial cruciate rupture in the dog. A review of treatments



71



(Adapted from: Vlaams Diergeneeskundig Tijdschrift 1995;64:47-51)



CHAPTER 2.



THE TIBIAL COMPRESSION TECHNIQUE AS A RELIABLE RADIOGRAPHIC TEST FOR CRANIAL CRUCIATE INSTABILITY IN DOGS



89



2.1. Diagnosis of cranial cruciate ligament injury in dogs by tibial compression radiography



91



(Adapted from: Veterinary Record 1998;142:366-368)



2.2. Use of compression stress radiography for the detection of partial tears of the canine cranial cruciate ligament (Adapted from: Journal of Small Animal Practice 1999;40:573-576)



103



TABLE OF CONTENTS



2.3. Radiographic measurement of craniocaudal instability in stifle joints of clinically normal dogs and dogs with injury of a cranial cruciate ligament



115



(Adapted from: American Journal of Veterinary Research 1999;60:1567-1570)



2.4. Popliteal sesamoid displacement associated with cruciate rupture in the dog



127



(Adapted from: Journal of Small Animal Practice 1999;40:316-318)



CHAPTER 3.



BIOMECHANICAL BEHAVIOUR OF THE CANINE CRANIAL CRUCIATE LIGAMENT AND ITS SYNTHETIC SUBSTITUTES



137



3.1. Load-controlled tensile tests



139



3.2. Displacement-controlled tensile tests



151



3.2.1. Biomechanical properties of artificial cranial cruciate ligaments



153



(Adapted from: Textile Research Journal 2001;71:213-219)



3.2.2. Biomechanical properties of braided polyester tapes intended for use as intra-articular cranial cruciate ligament prostheses in dogs



167



(Adapted from: American Journal of Veterinary Research 2001;62:48-53)



CHAPTER 4.



TREATMENT OF CRANIAL CRUCIATE LIGAMENT RUPTURE IN DOGS USING AN INTRA-ARTICULAR POLYESTER PROSTHESIS



185



4.1. Retrospective study evaluating patient data and clinical features in dogs affected by cranial cruciate ligament disease



187



4.2. Intra-articular treatment of cranial cruciate ligament rupture with a polyester prosthesis. Surgical technique



201



4.3. Intra-articular treatment of cranial cruciate ligament rupture with a polyester prosthesis. Longterm follow-up



211



CHAPTER 5.



IMMUNOPATHOLOGICAL MECHANISMS IN CANINE CRANIAL CRUCIATE LIGAMENT DISEASE



235



5.1. Prevalence and relevance of antibodies to type-I and -II collagen in synovial fluid of dogs with cranial cruciate ligament damage



237



(Adapted from: American Journal of Veterinary Research 2000;61:1456-1461)



TABLE OF CONTENTS



GENERAL DISCUSSION



253



SUMMARY



265



SAMENVATTING



271



DANKWOORD



277



CURRICULUM VITAE



283



LIST OF ABBREVIATIONS



ACL



Anterior Cruciate Ligament



CaCL Caudal Cruciate Ligament CCL



Cranial Cruciate Ligament



DJD



Degenerative Joint Disease



ELISA Enzyme-Linked Immunosorbent Assay EO



Ethylene Oxide



H&E



Hematoxylin-Eosin Stain



Ig



Immunoglobulin



OA



Osteoarthrosis



OD



Optical Density



TPLO Tibial Plateau Levelling Osteotomy



GENERAL INTRODUCTION



1



2



GENERAL INTRODUCTION The stifle joint is one of the most complex joints of the skeletal system. The cruciate ligaments are ligamentous structures in the center of the stifle, upon which various species depend for craniocaudal joint stability.1,2 The stifle is relatively susceptible to injury. It must transmit forces of a much larger magnitude than other joints.3 Hind limb lameness in dogs often is associated with the stifle joint.4-12 Cruciate rupture has first been recognised as a serious cause of chronic lameness in 1926.13 All breeds and all sizes of dogs appear to be at risk. The cranial cruciate ligament (CCL) is the most frequently torn ligament of the stifle for it is primarily subjected to excessive forces during extremes of joint motion.14-16 In contrast, rupture of the caudal cruciate ligament (CaCL) is rarely encountered in the dog.6,17-19 Meniscal pathology is often seen concurrently with or as a consequence of rupture of the CCL. It is mainly the medial meniscus which shows disease.20-27



The dog is an important species both clinically and in studies of comparative pathology. In several studies, the dog is choosen as an experimental animal for human stifle arthropathies.28-32 An intriguing similarity in the anatomic features is seen between the canine stifle joint and the human knee, considering - of course - their difference in gait being quadrupedal versus bipedal.18,31,33 The same peri- and intra-articular ligaments are found and their positions in the joint are similar. A different nomenclature is used in dogs and men. The cranial cruciate ligament (CCL) in the canine stifle is the equivalent structure of the anterior cruciate ligament (ACL) in the human knee.33,34



Injury to the CCL causes craniocaudal instability of the affected stifle joint. Because of the difference in gait, the greater joint flexion throughout weight bearing, and the steeper slope of the tibial plateau, the dog’s stifles are more CCL-dependent for their stability and proper function than the human knees.35,36 However, a lot of the clinical signs and pathological changes in and around the affected joint following damage to the cruciate ligament are in common. Transsection of the CCL in the dog serves as a standard experimental model of osteoarthritis for human research.28 As in dogs, insufficiency of the human ACL leads to progressive deterioration of the unstable joint including stretching of secondary restraints, premature degenerative changes, and possible damage to the medial meniscus.37-40 Only the etiology of cranial cruciate rupture seems to differ between dogs and men. Pure traumatic rupture of the canine CCL is only rarely reported.41-45 In the dog, most CCL seem to rupture spontaneously under physiological loading as a result of progressive degeneration of the 3



GENERAL INTRODUCTION ligament itself.9,46-48 Such form of nontraumatic ACL lesions is not well documented in the human literature. Men mostly sustain injury to their cruciates during strenuous sport activities.4952



The first bottleneck comprises the diagnosis of CCL rupture in dogs. Damage to the ligament must often be diagnosed based on signs of degenerative changes in and around the affected stifle joint and not by the instability itself. Two clinical tests are well-known to check for the presence of craniocaudal instability in a cranial cruciate-deficient stifle joint, the classical cranial drawer test13 and the tibial compression test53. In both cases, a positive test result is pathognomonic for a torn CCL. Special attention should also be given to the interpretation of the cranial drawer movement in skeletally immature dogs. A certain degree of cranial drawer of the proximal tibia is normal but it comes to an abrupt stop and is not associated with pain or effusion.54



Unfortunately, false negative results of the manual



instability tests are rather common in dogs. Craniocaudal drawer motion might be masked by increased muscle tone9,54,55 or by tension in the remaining ligament bundle in cases of partial CCL rupture only56,57. In those cases surgical intervention is often unnecessarily delayed. Arthrosis will rapidly progress. An extra diagnostic tool with a higher degree of accuracy and sensitivity, applicable in general practice, is badly needed to aid in early detection and prevention of CCL injury.



The second sore subject we try to deal with in this study is how to manage a rupture of the CCL in the dog. The questions whether and how to optimally reconstruct the CCL have stimulated lively and endless debate among veterinary surgeons. The described surgical interventions can be grossly divided into extra-articular or intra-articular procedures. In excess of 100 methods of surgical repair for cranial cruciate rupture in dogs have been reported.58-60 All reconstruction techniques published so far only provide temporary stability to the operated stifle joint. Furthermore, surgical intervention does not seem to be able to stop any further formation of osteoarthrosis (OA), but slows down the degenerative process at most.25,61,62 On the other hand, there does not seem to be a direct relation between the clinical outcome of a surgical procedure and the degree of postoperative OA. It has been postulated that intra-articular reconstruction using a strong synthetic prosthesis would decrease surgical morbidity and increase stability in the immediate postoperative period.



4



GENERAL INTRODUCTION A third problem concerns the etiopathogenesis of CCL rupture in dogs. Known causes are severe trauma or relatively minor trauma to a previously weakened ligament. In contrast to human beings,63 most of the injuries in dogs are a result of degeneration of the CCL itself.6,9,46-48 Degenerative changes within the microstructure of the ligaments might be due to a loss of elasticity because of increasing age46-48 or due to chronic abnormal loading because of skeletal abnormalities or patellar luxation.9,15,64-70 Immune-mediated inflammation of the canine CCL as a cause of ligament weakening and destruction has been reported by Niebauer and Menzel.71 A better knowledge of the disease mechanisms in canine CCL rupture would enable us to accurately alter the degenerative processes. Maybe, prophylactic measures could be taken in the future.



5



GENERAL INTRODUCTION REFERENCES 1.



Heffron LE, Campbell JR. Morphology, histology and functional anatomy of the canine cranial cruciate ligament. Vet Rec 1978;102:280-283.



2.



Cabaud E, Chatty A, Gildengorin V, et al. Exercise effects on the strength of the rat anterior cruciate ligament. Am J Sports Med 1980;8:79-86.



3.



Haut RC, Little RW. Rheological properties of canine anterior cruciate ligaments. J Biomech 1969;2:289-298.



4.



Vaughan LC, Bowden NLR. The use of skin for the replacement of the anterior cruciate ligament in the dog: A review of thirthy cases. J Small Anim Pract 1964;5:167-171.



5.



Pond MJ, Campbell JR. The canine stifle joint. I. Rupture of the anterior cruciate ligament. An assessment of conservative and surgical treatment. J Small Anim Pract 1972;13:1-10.



6.



Arnoczky SP. Surgery of the stifle - The cruciate ligaments (Part I). Comp Cont Ed 1980;2:106-116.



7.



Hulse DA, Michaelson F, Johnson C, et al. A technique for reconstruction of the anterior cruciate ligament in the dog: Preliminary report. Vet Surg 1980;9:135-140.



8.



Gambardella PC, Wallace LJ, Cassidy F. Lateral suture technique for management of anterior cruciate ligament rupture in dogs: A retrospective study. J Am Anim Hosp Assoc 1981;17:33-38.



9.



Arnoczky SP. The cruciate ligaments: the enigma of the canine stifle. J Small Anim Pract 1988;29:71-90.



10.



Johnson JA, Austin C, Breur GJ. Incidence of canine appendicular musculoskeletal disorders in 16 veterinary teaching hospitals from 1980 through 1989. Vet Comp Orthop Traumatol 1994;7:56-69.



11.



Ness MG, Abercromby RH, May C, et al. A survey of orthopaedic conditions in small animal veterinary practice in Britain. Vet Comp Orthop Traumatol 1996;9:43-52.



12.



Necas A, Zatloukal J, Kecova H, et al. Predisposition of dog breeds to rupture of the cranial cruciate ligament. Acta Vet Brno 2000;69:305-310.



13.



Carlin I. Ruptur des Ligamentum cruciatum anterius im Kniegelenk beim Hund. Arch Wissensch Prakt Tierh 1926;54:420-423.



14.



Singleton WB. The diagnosis and surgical treatment of some abnormal stifle conditions in the dog. Vet Rec 1957;69:1387-1394.



15.



Arnoczky SP, Marshall JL. Pathomechanics of cruciate and meniscal injuries. In: Bojrab MJ, ed. Pathophysiology of Small Animal Surgery. Philadelphia:Lea and Febiger, 1981;590-603.



16.



Thomson LA, Houlton JEF, Allen MJ, et al. Will the cranial cruciate ligament-deficient caprine stifle joint develop degenerative joint disease? Vet Comp Orthop Traumatol 1994;7:14-17.



17.



Reinke JD. Cruciate ligament avulsion injury in the dog. J Am Anim Hosp Assoc 1982;18:257-264.



18.



Pournaras J, Symeonides PP, Karkavelas G. The significance of the posterior cruciate ligament in the stability of the knee. An experimental study in dogs. J Bone Joint Surg (Br) 1983;65-B:204-209.



19.



Johnson AL, Olmstead ML. Caudal cruciate ligament rupture. A retrospective analysis of 14 dogs. Vet Surg 1987;16:202-206.



20.



Flo GL. Modification of the lateral retinacular imbrication technique for stabilising cruciate ligament injuries. J Am Anim Hosp Assoc 1975;11:570-576.



6



GENERAL INTRODUCTION 21.



Flo GL, DeYoung D. Meniscal injuries and medial meniscectomy in the canine stifle. J Am Anim Hosp Assoc 1978;14:683-689.



22.



Shires PK, Hulse DA, Liu W. The under-and-over fascial replacement technique for anterior cruciate ligament rupture in dogs: A retrospective study. J Am Anim Hosp Assoc 1984;20:69-77.



23.



Drapé J, Ghitalla S, Autefage A. Lésions méniscales et rupture du ligament croisé antérieur: étude rétrospective de 400 cas. Point Vét 1990;22:467-474.



24.



Bennett D, May C. Meniscal damage associated with cruciate disease in the dog. J Small Anim Pract 1991;32:111-117.



25.



Elkins AD, Pechman R, Kearny MT, et al. A retrospective study evaluating the degree of degenerative joint disease in the stifle joint of dogs following surgical repair of anterior cruciate ligament rupture. J Am Anim Hosp Assoc 1991;27:533-539.



26.



Bellenger CR. Knee joint function, meniscal disease, and osteoarthritis. Vet Quart 1995;17:S5-S6.



27.



Moore KW, Read RA. Cranial cruciate ligament rupture in the dog - a retrospective study comparing surgical techniques. Austr Vet J 1995;72:281-285.



28.



Pond MJ, Nuki G. Experimentally-induced osteoarthritis in the dog. Ann Rheum Dis 1973;32:387-388.



29.



Bennett D. Immune based erosive inflammatory joint disease of the dog. Rheumatoid arthritis 2. Pathological investigations. J Small Anim Pract 1987;128:799-819.



30.



Carter SD, Makh SR, Ponsford FM, Elson CJ. Rheumatoid factor has increased reactivity with IgG from synovial fluids of patients with rheumatoid arthritis and osteoarthritis. Brit J Rheum 1989;28:233-238.



31.



Arnoczky SP, BrinkerWO. The functional anatomy of the knee: A comparative analysis between the dog and man. Proceedings Comparative aspects on hip and knee joint lesions in dog and man, Uppsala Sweden 1992;16-19sept:25-29.



32.



Arican M, Carter SD, Bennett D, May C. Measurement of glycosaminoglycans and keratan sulphate in canine arthropathies. Res Vet Sc 1994;56:290-297.



33.



Korvick DL, Pijanowski GJ, Schaeffer DJ. Three-dimensional kinematics of the intact and cranial cruciate ligament-deficient stifle of dogs. J Biomech 1994;27:77-87.



34.



Rich FR, Glisson RR. In vitro mechanical properties and failure mode of the equine (pony) cranial cruciate ligament. Vet Surg 1994;23:257-265.



35.



Arcand MA, Rhalmi S, Rivard C-H. Quantification of mechanoreceptors in the canine anterior cruciate ligament. Int Orthop 2000;24:272-275.



36.



Wingfield C, Amis AA, Stead AC et al. Cranial cruciate stability in the rottweiler and racing greyhound: an in vitro study. J Small Anim Pract 2000;41:193-197.



37.



McDaniel WJ, Dameron TB. Untreated ruptures of the anterior cruciate ligament. A follow-up study. J Bone Joint Surg (Am) 1980;62-A:696-705.



38.



Brandt KD, Braunstein EM, Visco DM, et al. Anterior (cranial) cruciate ligament transection in the dog: A bona fide model of osteoarthritis, not merely of cartilage injury and repair. J Rheumatol 1991;18:436446.



39.



Johnson RJ, Beynnon BD, Nichols CE, et al. The treatment of injuries of the anterior cruciate ligament. J Bone Joint Surg (Am) 1992;74-A:140-151.



40.



Clatworthy M, Amendola A. The anterior cruciate ligament and arthritis. Clin Sports Med 1999;18:173199.



7



GENERAL INTRODUCTION



41.



Arnoczky SP, Rubin RM, Marshall JL. Microvasculature of the cruciate ligaments and its response to injury. An experimental study in dogs. J Bone Joint Surg 1979;61-A:1221-1229.



42.



Brünnberg L. Klinische Untersuchungen zu Ätiologie und Pathogenese der Ruptur des Ligamentum cruciatum craniale beim Hund. 2. Mitteilung: Zur Ätiologie und Diagnose der Ruptur des Ligamentum cruciatum craniale beim Hund. Kleintierprax 1989;34:445-449.



43.



Doverspike M, Vasseur PB, Harb MF, et al. Contralateral cranial cruciate ligament rupture: Incidence in 114 dogs. J Am Anim Hosp Assoc 1993;29:167-170.



44.



Whitehair JG, Vasseur PB, Willits NH. Epidemiology of cranial cruciate ligament rupture in dogs. J Am Vet Med Assoc 1993;203:1016-1019.



45.



Bruce WJ. Multiple ligamentous injuries of the canine stifle joint: a study of 12 cases. J Small Anim Pract 1998;38:333-340.



46.



Zahm H. Die Ligamenta decussata in gesunden und arthrotischen Kniegelenk des Hundes. Kleintierprax 1965;10:38-47.



47.



Nieubauer GW, Niedermüller H, Skalicky M. Die Kollagenquervernetzung im Ligamentum cruciatum des Hundes und ihre Beziehung zur pathologischen Kreuzbandruptur. Zbl Vet Med A 1983;30:688-693.



48.



Vasseur PB, Pool RR, Arnoczky SP, et al. Correlative biomechanical and histologic study of the cranial cruciate ligament in dogs. Am J Vet Res 1985;46:1842-1854.



49.



Palmer I. On injuries of the ligaments of the knee joint. A clinical study. Acta Chir Scand 1938 ;suppl 53.



50.



Abbott LC, Saunders JB, De CM, et al. Injuries toe the ligaments of the knee joint. J Bone J Surg 1944;26:503-521.



51.



Kennedy JC, Weinberg HW, Wilson AS. The anatomy and function of the anterior cruciate ligament. As determined by clinical and morphological studies. J Bone Joint Surg (Am) 1974;56-A:223-235.



52.



Ascherl R. Cruciate and meniscal injuries. Proceedings 10th ESVOT Congress, Munich 2000;23-26th March:18.



53.



Henderson RA, Milton JL. The tibial compression mechanism: a diagnostic aid in stifle injuries. J Am Anim Hosp Assoc 1978;14:474-479.



54.



Bennett D, Tennant D, Lewis DG, et al. A reappraisal of anterior cruciate ligament disease in the dog. J Small Anim Pract 1988;29:275-297.



55.



Johnson JM, Johnson AL. Cranial cruciate ligament rupture. Pathogenesis, diagnosis, and postoperative rehabilitation. Vet Clin North Am (SAP) 1993;23:717-733.



56.



Tarvin GB, Arnoczky SP. Incomplete rupture of the cranial cruciate ligament in a dog. Vet Surg 1981;10:94-95.



57.



Scavelli TD, Schrader SC, Matthiesen DT, et al. Partial rupture of the cranial cruciate ligament of the stifle in dogs: 25 cases (1982-1988). J Am Vet Med Assoc 1990;196:1135-1138.



58.



Knecht CD. Evolution of surgical techniques for cruciate ligament rupture in animals. J Am Anim Hosp Assoc 1976;12:717-726.



59.



Jevens DJ, DeCamp CE, Hauptman J, et al. Use of force-plate analysis of gait to compare two surgical techniques for treatment of cranial cruciate ligament rupture in dogs. Am J Vet Res 1996;57:389-393.



8



GENERAL INTRODUCTION 60.



Fox SM, Baine JC. Anterior cruciate ligament repair: New advantages from changing old techniques. Vet Med 1986;31-37.



61.



Heffron LE, Campbell JR. Osteophyte formation in the canine stifle joint following treatment for rupture of the cranial cruciate ligament. J Small Anim Pract 1979;20:603-611.



62.



Vasseur PB, Berry CR. Progression of stifle osteoarthrosis following reconstruction of the cranial cruciate ligament in 21 dogs. J Am Anim Hosp Assoc 1992;28:129-136.



63.



Gillquist J. Repair and reconstruction of the ACL: Is it good enough? Arthroscopy 1993;9:68-71.



64.



Rudy RL. Stifle joint. In: Archibald J, ed. Canine surgery. Santa Barbara:American Veterinary Publications Inc, 1974;1104-1115.



65.



Hohn RB, Newton CD. Surgical repair of ligamentous structures of the stifle joint. In: Bojrab MJ, ed. Current Techniques in Small Animal Surgery. Philadelphia:Lea and Febiger, 1975;470-479.



66.



Read RA, Robins GM. Deformity of the proximal tibia in dogs. Vet Rec 1982;295-298.



67.



Slocum B, Devine T. Cranial tibial thrust: A primary force in the canine stifle. J Am Vet Med Assoc 1983;183:456-459.



68.



Robins GM. The canine stifle. Anatomy, function and kinesiology. In: Whittick WG, ed. Canine Orthopaedics. Philadelpia:Lea and Febiger, 1990;693-702.



69.



Hulse DA. Surgery of the knee (part 1): Basic concepts and treatment of CCL injury. Proceedings SAVAB Flanders WE 1998;9-11 May.



70.



Duval JM, Budsberg SC, Flo GL, et al. Breed, sex, and body weight as risk factors for rupture of the cranial cruciate ligament in young dogs. J Am Vet Med Assoc 1999;6:811-814.



71.



Niebauer GW, Menzel EJ. Immunological changes in canine cruciate ligament rupture. Res Vet Sc 1982;32:235-241.



9



3



SCIENTIFIC AIMS



11



12



SCIENTIFIC AIMS



The frequency and importance of cranial cruciate ligament (CCL) injury in dogs has become widely known. Although reports have been published on virtually every aspect of the cruciate ligaments in both man and dog, knowledge has not advanced greatly, and still no unanimity of opinion exists as to various conditions with regard to the CCL. More objective diagnostic means with a higher degree of accuracy and sensitivity are needed and the ideal method of dealing with cranial cruciate instability is still far from being established. Furthermore, it is still largely unclear why that many canine CCL rupture without a definite traumatic injury.



The aim of this study is to come as close as possible to the ultimate answers on those challenging questions.



Diagnostic aspect:



1. To develop and evaluate a new, clinically useful diagnostic method for early detection of CCL disease.



If there is damage to the CCL, a cranial displacement of the proximal tibia in respect to the distal femur is expected during clinical laxity testing. The classical instability tests may reveal false negative results, and the impression of relative displacement and rotation during clinical examination is often not very accurate. Stress radiographs under tibial compression are routinely taken of all dogs suspected of CCL injury.



Therapeutic aspect:



1. To evaluate the suitability of polyester as CCL substitute by its in vitro characteristics.



The structural and material properties of braided multifilament polyester used for intraarticular stabilisation of CCL deficient stifle joints in dogs are determined. The suitability



13



SCIENTIFIC AIMS of CCL prostheses does not depend solely on tensile behaviour. The recoverable elastic characteristics are equally important. Load-to-failure tests are used to mimic acute overload of the CCL. Additionally, a cyclic loading test method is designed to match the dynamic loading conditions of the CCL of a walking dog.



2. To evaluate an intra-articular stabilisation method using polyester in canine CCL-deficient patients.



For many years, polyester has been implanted in the canine stifle joint to substitute the ruptured CCL. The clinical value of new stabilisation techniques can only be assessed by longterm follow-ups. Detailled questionnaires provide data before surgery, at 6 weeks after the operation, and several months postoperatively. Data are collected by telephone interviews and by clinical and radiographic re-examinations.



Etiopathogenetic aspect:



1. To evaluate immune-mediated phenomena as a possible contribution to CCL rupture in dogs.



Synovial fluid from cruciate-deficient stifles and from joints in which the osteoarthritis was unrelated to cruciate disease is screened for antibodies against collagen. The menisci as well as the intra-articular cruciate ligaments are mainly composed of collagen type I. Collagen type II is the major constituent of articular cartilage. If anti-collagen antibodies can be detected, it has to be examined whether these autoantibodies to collagen play an active role in the initiation of CCL disease in dogs or not.



14



CHAPTER



REVIEW OF THE LITERATURE



1.1. Basic science of the cruciate ligaments 1.1.1. 1.1.2. 1.1.3. 1.1.4. 1.1.5. 1.1.6. 1.1.7.



Introduction Insertion points Fibre bundle anatomy Functional anatomy and aspects Microanatomy and ultrastructure Microvascularity Neurovascularity



1.2. Predisposing and etiological factors in canine cranial cruciate disease A long list of possible contributors



1.3. Cranial cruciate ligament rupture in the dog A review of diagnostic techniques



1.4. Cranial cruciate rupture in the dog A review of treatments



15



1



16



CHAPTER 1



1.1.



Basic science of the cruciate ligaments



17



18



CHAPTER 1.1: Review



1.1.1. INTRODUCTION The cruciate ligaments are both morphologically and functionally complex, dynamical structures, strongly connecting the femur to the tibia.



They run intra-articularly but



extrasynovially in the stifle joint of all terrestrial mammals species.1,2 In the early literature, the cruciate ligaments were referred to as crucial ligaments merely because of their crossed arrangement.3 Only later on, the crucial role of the cruciate ligaments to the well-being of the physiological kinematics of the stifle joint, has been appreciated.4 The cruciate ligaments function as major constrains of stifle joint motion although they are only one facet of the restraining system of the stifle joint. By their anatomy and spatial arrangement, the two crossing cruciate ligaments provide the primary ligamentous support of craniocaudal and axial stability of the stifle through the functional range of motion. The importance of the cruciate ligaments to provide primary ligamentous support of craniocaudal stability of the stifle has been generally recognised for a long while.5 Roughly, the cranial cruciate ligament (CCL) controls the cranial drawer motion, whereas the caudal cruciate ligament (CaCL) acts as major stabiliser against caudal drawer motion. Furthermore, the CCL can be looked at as fine-tuner of proper stifle joint kinematics.6 Data appearing in the literature have been focused merely on the CCL particularly for it is the most vulnerable and most important ligament of the stifle joint.7-9 It has been studied extensively with regard to its morphological appearance and its relationship to other joint structures. Several comparative studies on CCL characteristics in mammals have been published and reinforce the importance of this structure. It may be assumed that only minimal differences between different species do exist anatomically, physiologically and biomechanically.10,13 Over the past decades, the clinical importance of the CCL became more and more obvious, for the different species themselves but even so for further development of animal models to compare with human circumstances.



A correct understanding of normal anatomy of the stifle joint, and in particular normal cruciate anatomy, is essential to both diagnosis and rational treatment for CCL damage.



19



CHAPTER 1.1: Review



1.1.2.



INSERTION POINTS



The intercondylar notch between the femoral condyles is almost completely filled by the two cruciate ligaments and some fat (Fig 1 A). In dogs, the normal anatomy of the cranial outlet of the intercondylar notch is bell-shaped, obliqued a mean of 7 degrees.14 The CCL and the CaCL both attach to the intercondyloid area of the tibia.7,15-17 Although the length of both canine cruciate ligaments is nearly equal, their distal insertion points on the tibia lay almost twice that far apart as their femoral origins.11 At the attachment sites of the cruciate ligaments, extensive interdigitation of collagen fibres of the ligament with those of the adjacent bone ensures strong anchorage.18,19



PL CCL



TT



CCL



CaCL



MCL



MM MCL



LM



MM



LM



LCL



PL CaCL



T



LCL



T



F



B



A Fig 1.



F



Ligaments and structures associated with the stifle joint in the dog A. Cranial view B. View on the tibial plateau after removal of the femur CaCL Caudal cruciate ligament, CCL Cranial cruciate ligament, F Fibula, LCL Lateral collateral ligament, LM Lateral meniscus, MCL Medial collateral ligament, MM Medial meniscus, PL Patellar ligament, T Tibia, TT Tibial tubercle



20



CHAPTER 1.1: Review Within the centre of the stifle joint, the cruciate ligaments form a cross from caudal to cranial, and also from outside to inside, connecting the femur with the tibia.20 The entire CCL and CaCL begin to wrap around each other, checking against each other when the stifle flexes.7 Meanwhile, the fibres of both ligaments begin to twist upon themselves to a varying degree.16



The cranial cruciate ligament



The cranial (or lateral) cruciate ligament originates on the axial aspect of the lateral femoral condyle, very close to the articular margin and extends diagonally across the joint space.16,20 It runs cranially, medially and distally in an outward spiral as it passes from the femur to the tibia.20,21 The amount of twist can vary in different parts of the CCL and the bundles can spiral up to 180 degrees.22 The long axis of the CCL is vertical.16 The tibial attachment is to the cranial intercondyloid area of the tibial plateau.7,15,16,20 This insertion point is cranially bordered by the cranial meniscotibial ligament of the medial meniscus and caudally by the similar-called ligament of the lateral meniscus (Fig 1 B).1,15,23 There are no fibres connecting the ligament to one of the menisci.16



The attachment areas are considered important when considering



landmarks for intra-articular techniques of cranial cruciate substitutions.24



The caudal cruciate ligament



The fibres of the femoral attachements of the caudal (or medial) cruciate ligament originate as a broad fanlike band along the fossa on the ventral aspect of the axial side of the medial femoral condyle.16,20 The ligament transverses caudodistally across the femorotibial joint with only a slight inward helical angle, and attaches to the medial aspect of the popliteal notch of the tibia.16,20,25 This insertion point is cranially bordered by the caudal meniscotibial ligament of the medial meniscus and caudolaterally by the similar-called ligament of the lateral meniscus.23 Both sites of attachment of the CaCL lay behind the axis of flexion of the stifle joint, and the ligament lies medial to and crosses the CCL.16 The band is slightly longer but also broader than the CCL.7,15-17,26,27 In more than half of the dogs, fibres of the femoral ligament to the lateral meniscus are found within the CaCL.16



21



CHAPTER 1.1: Review



1.1.3.



FIBRE BUNDLE ANATOMY



The cruciate ligaments have not just a single strand configuration of longitudinally orientated collagen fibres.16 They contain twisted collagenous fascicles and fiber bundles subdivided into fascicles, subfascicular units, fibres and fibrils.19,28-30 In the dog, the CCL as well as the CaCL can be divided in two functional components because they adhere to individual attachment zones.16



The cranial cruciate ligament The canine CCL is the narrowest in its middle portion and fans out proximally and distally.1,22 The shape of the entire CCL changes through the normal range of motion of the stifle joint.1,16 The decrease of the cross-sectional area is also greatest at the midportion of the CCL when forces are acting.31 The length of the canine CCL is positively correlated with the body weight of the dog. A mean of 13.5 to 18.7mm has been calculated.32-35 In man, the ACL wrinkles into three fibre components as the stifle flexes.36,37 The human ACL was first anatomically subdivided as a two-part ligament in a so-called craniomedial and a caudolateral bundle, based on reference to their relative tibial insertion sites.38,39 Later on a third, smaller bulk was identified, and got the name of intermediate bundle.36 The separate parts are the most demonstrable within the region of the intercondylar notch in a fully flexed stifle.36,40 The appearance of three discrete fibre bundles can not always be confirmed, especially not in specimens derived from younger individuals because of thicker envelopment of the ACL in the synovial covering.40 Some workers even failed to identify a separable interface between portions of the ACL in cadaver knees from some human adults.41,42 There is general agreement regarding functional subdivision of the ACL, although there is not neccesarily macroscopic evidence of separate entities. The spiral in the canine CCL gives the gross appearance of distinct anatomic bands. Apparent are two demonstrably separate bundles in the dog (Fig 2).1,16 The bands are designated as craniomedial and caudolateral, based upon their relative insertional points onto the tibial plateau as their human counterparts. The craniomedial subdivision is the most spiral, the longest but the smallest component of the two.1 It arises more proximally from the femur and also inserts more cranially on the tibial insertion area, as compared to the remainder caudolateral band



22



CHAPTER 1.1: Review of the CCL.1,16 The fibres of the latter component originate from the most lateral and distal part of the insertion area of the lateral femoral condyle, have a more straight path, and insert on the most caudal part of the tibial area.



Fig 2.



Cranial view of the stifle joint. The cranial cruciate ligament (CCL) in the dog is composed of two separate bundles. A forceps has been pushed bluntly between these bundle parts to insert a double suture, demonstrating the separate components EDL Tendon of long digital extensor muscle, MM Medial meniscus, PL Patellar ligament



The geometry of the reciproce attachment sites of the component parts of the cruciate ligament is responsible for their slackening and tensioning due to relative rotations of the attachments through the normal functional range of motion of the stifle joint.16,22,40,42 Different morphological components of the CCL appear to attach to different locations within the insertional area of each bone. Reciprocal tension and thus functional difference does occur because of the arrangement of their individual attachment points.16 In the extended stifle joint, the long axis of the CCL runs along the axis of the femur, and the femoral attachments of both the craniomedial and the caudolateral fibre bundle are almost perpendicular to the joint surface and both bundle parts are taut.1,22 In flexion, the craniomedial part of the CCL curves and twists around the remaining caudolateral part, while meanwhile its femoral attachment area moves distally and caudally.1,16 This reorientation of the femoral attachment sites during flexion of the stifle results in an increased distance between the areas of femoral origin and tibial insertion of



23



CHAPTER 1.1: Review the craniomedial bundle. Therefore, this bulk remains tense in flexion. The inverse shift happens to the femoral insertion of the caudolateral component so as to bring the femoral attachment area of the CCL almost horizontal to the joint.1 Relative relaxation of the fibres of the caudolateral bundle can be explained by the same principles, since the bone attachments move closer together as the stifle is flexed. The caudolateral component is slack in flexion.1,16



The caudal cruciate ligament The canine CaCL is longer and broader than the CCL.7,15-17,26,27 Even its collagen fibrils are thicker in comparison with the CCL.43,44 The total diameter of the ligament in its midsection is the smallest as it fans out from the centre making the femoral and to a lesser extent tibial attachments larger.15 As its cranial counterpart, the CaCL as well is a two-part ligament26 although they are not as distinct as those of the CCL and often inseparable.1 The cranial bulk is heavier than the caudal band.25,45 Also here, the restraining effect of both bundles varies with the position of the stifle, and the component parts perform reciprocal functions at different angles of flexion because of the location of their points of attachment.16,26 In similarity with the CCL, the geometry of the femoral attachment is responsible for tensioning or not.1 The cranial band is taut in flexion and loose in extension whereas the situation is reversed for the caudal part.16,26



24



CHAPTER 1.1: Review



1.1.4.



FUNCTIONAL ANATOMY AND ASPECTS



The cruciate ligaments have specific functions directly related to their anatomic locations and orientations within the stifle joint. Although the main functions of other intra-articular and periarticular structures and ligaments differ from those of the cruciate ligaments, they complement them as constraints of stifle joint motion in various planes.23,46 There is a ranked hierarchy of structures neutralising specific forces acting on the stifle joint and resisting different kinds of joint laxity.



Not only the real ligamentous structures but also muscle forces and joint



compression contribute to joint stability.47,48 Stifle joint function is complemented by a static support from a complex (passive) restraining system consisting of bony and musculotendineous structures, menisci and several ligaments.



Passive control is largely dependent on the



femorotibial ligaments, i.e. the cruciate and collateral ligaments, which interact to prevent excessive motion, in concert with all other anatomical structures.49,50



The conception of



ligaments as passive ropelike structures with purely biomechanical functions is outmoded.51 They also serve as more refined sensors.52 Stifle stability is dynamic as far as muscle control (active forces) is concerned.15,48,49,53,54 Cranially, the quadriceps muscle and the patellar tendon provide support.



The popliteal muscle and probably also the hamstring muscles and the



gastrocnemii provide additional support to the stifle on its caudal aspect.55 In the dog, both cruciate ligaments are composed of two component parts which behave independently and differently from one another at different portions of the loading cycle.16 The loading of the various bundles varies as some fibres are stressed and others are not depending on the angle of the stifle joint. The particular role of the cruciate ligaments and especially the importance of their separate bundle parts as restraints of stifle joint motion have been studied mostly in human and canine cadavers.38,39,40,42,47,56-62 Most assessments of ligamentous function have been based on the changes in laxity observed after sequential cutting selected ligaments. The actual proportion of their combined contributions to sustaining load varies with the angle of stifle flexion. Because of combined interactions, an isolated lesion of any of the component parts of any of the cruciate ligaments does not necessarily provoke clinically detectable instability.39,59 Hyperflexion of the stifle joint will normally not occur because of the contact between the thigh muscles and the gastrocnemius muscle.7 The cruciate ligaments spiral on themselves, and they are naturally twisted upon each other when the stifle is flexed. Since the normal standing angle of the stifle in a dog is about 140 degrees, stifle collapse during the stance phase is also prevented by this twisting.16,63,64 The other extreme of motion of the stifle, overextension, is



25



CHAPTER 1.1: Review completely borne by the tension in the cruciate ligaments.7 Hereby, the cranial cruciate acts as a primary restraint whereas the slightly longer CaCL can be considered to be only a secondary restraint.7,16,25 Because of their anatomic relationship, both cruciate ligaments constitute in the physiological rotatory action of the tibia during craniocaudal motion, although they are anatomically close to the axis of tibial rotation.60



In subtle balance with the capsular structures, the collateral



ligaments, muscles, the condylar geometry and joint surface contact, the cruciate ligaments control and produce rotatory motion of the tibia relative to the femur.8,15,25,26,36,60,65,66 An increased angle of flexion of the stifle joint is also accompanied by increased internal rotation of the tibia if unrestricted.8,23,24,65,67 A portion of valgus load is transformed into an axial rotatory force as the lateral collateral band begins to relax.12,25,68,69 As the stifle flexes, the cruciate ligaments are not only wrapped upon each other but also spiral on themselves.7,16,25 The natural twist of the cruciate ligaments is tightened even more by initiation of increased internal rotation.47 The higher strain in the ligaments limits the amount of normal internal rotation of the tibia on the femur.16,20,25,26 As the stifle extends, the lateral collateral ligament tightens. The lateral femoral condyle moves cranially, causing external rotation of the tibia. This motion has classically been described as the screw-home mechanism.65,68-70 In extension, the medial and lateral collateral ligaments become the primary restraints of rotation, and the cruciate ligaments can only provide a secondary check due to the tension in both ligaments.15,20,65 No singular limiting effect on external rotation is provided by the cruciate ligaments in dogs, even not as secondary restraint structures.16,26,65,71 By external rotation of the tibia, the fibres of the cruciate ligaments start to unwrinkel, and strain decreases.8,20,65 Therefore these ligaments can not provide any restraint against external rotation. Axial tibial rotation of the canine stifle joint is coupled with varus-valgus rotation.12 In a stable stifle joint, the collateral ligaments are considered to be the cardinal primary ligamentous stuctures to provide sideways restraining moments when stifle motion is restricted. In fact, they share their function by the other joint structures and ligaments.12,59,65,66 The degree of stresses on the cruciate ligaments during medial and lateral opening of the joint space generally increases slightly with the degree of flexion of the stifle joint, for the collateral ligaments begin to relax as the stifle is flexed.12,65 Both cruciate ligaments together are important secondary complements against varus and valgus angulation. They become primary restraints if there is a tear of one of the collateral ligaments.59,61,65 In the fully hyperextended stifle joint, the cruciate ligaments, by themselves, can block joint opening.59 In cases of varus force, the CCL will always have to sustain larger strains than the CaCL although these forces are still much lower than these 26



CHAPTER 1.1: Review sustained by the lateral collateral ligament. For medial restraints (valgus force), the proportion of contribution of the CaCL becomes greater with increase of the flexion angle.12,59



The cranial cruciate ligament



The CCL is the fine-tuner of stifle joint motion and guides the stifle through its helicoid of motion.6 The structural characteristics of the CCL clearly play an important part in the rather complex behaviour of the ligament. It has long been realised that maintaining the integrity and stability of the stifle joint could hardly be accomplished by a CCL, constituting only one single band of fibres with constant tension as the stifle moves.1 Tension in the cranial cruciate varies greatly in various positions of stifle flexion. Every change of the joint angle alters the tension on the separate bands and indicates the suitability of the cranial cruciate to withstand the multi-axial stresses of normal function and range of motion. By weigth bearing, active forces are generated that create cranial tibial thrust.49,67 In a sound joint, the intact CCL opposes cranial projecting of the proximal tibia.46,48 During normal daily function, however, the CCL carries only small loads.72 Joint compression and muscle actions greatly contribute to the achieved joint stabilisation.54,73 By CCL-muscle reflexes, direct loading of the ligament causes inhibition of the quadriceps muscles and simultaneously increases the activity of the hamstring muscles in order to reduce CCL loading.74 The CCL has to limit extremes of motion about the stifle.4,6 The CCL is twisted through approximately 90 degrees, as the stifle is flexed from full extension to a right joint angle.42 In concert with the CaCL, hyperflexion is limited.16,63,64 As the joint extends, hyperextension of the stifle is limited by contact of the CCL with the osseous wall of the intercondylar fossa.14 The cranial cruciate serves as the primary check against hyperextension of the stifle joint.7,16,25,75 The entire ligament, both the craniomedial and the caudolateral bundle component, is taut at full extension.1,16 The contribution to restraining hyperextension of the stifle is larger for the caudolateral component which is under the greatest tension in extension.1,39 More important and more specific than its limiting functions, the ligament has to provide a stabilizing effect of the tibia on the femur throughout the whole range of motion, resisting forces that would cause the tibia to translate cranially relative to the femur and, to a lesser degree, resisting forces that would cause tibial rotation during flexion of the stifle.25,61 The chief function of the CCL is to resist cranial drawer movement of the tibia with respect to the 27



CHAPTER 1.1: Review femur.16,57 A primary restraint is provided against straight cranial drawer as well as against cranial drawer combined with internal tibial rotation.60,76 The dog’s stifle is CCL-dependent during the stance phase of gait.54 According to Slocum and Devine48,77, the CCL is only a backup mechanism for control of the cranial projecting of the proximal tibia as a dog walks, and experiences no stresses as long as the cranial tibial thrust is effectively opposed by the caudal pull of the biceps femoris and hamstring muscle group. Only if these active muscle forces are insufficient to counteract cranial translation of the tibia, the cranial cruciate will provide the first passive restraint. Since there will not be a perfect balance at all times and due to the functional cranial to caudal slope of the tibial plateau, the CCL must intermittently resist cranial tibial thrust.67,76,78 With the stifle in extension, the entire CCL is taut. As such, both component parts are limiting cranial translation of the tibia relative to the femur.1,16 Near full extension, the CCL is the sole structure to limit cranial drawer motion, since tension in the hamstring muscles lacks to provide extra restraint.75 The craniomedial part of the CCL is the major contributor to craniocaudal stability in all positions of flexion.8,76 Because of slackening of the caudolateral bulk during flexion, only the craniomedial part which thightness continues, is primary responsible for maintaining craniocaudal stability. Meanwhile, the other joint structures seem to contribute less to craniocaudal stability as the joint flexes.79 The relaxed caudolateral component only acts as a weak secondary restraint to this unidirectional cranial translating force. It only starts to play a role when the craniomedial band is damaged or severely stretched.39,71 The caudolateral component is responsible for restraint of internal rotation.76



A correct understanding of these matters is imperative if reconstructions are to restore normal stifle physiology. The goal of reconstructive methods should not only be to alleviate the existing instability of the symptomatically unstable stifle, but also to mimic normal kinematics as closely as possible.



The caudal cruciate ligament



The significance of the CaCL in the stability of the stifle in dogs is far less important than that of the CCL.80-83 During the extremes of joint motion, the component parts of the CaCL are alternately taut or slackenend. In the extended stifle joint, the cranial bundle will be loose whereas the caudal will be tight. The inverse situation happens in flexion.16,26 In contrast with the individual functions of the CCL, the functional anatomy of the caudal cruciate bundles is not 28



CHAPTER 1.1: Review clinically important. Selective cutting of only one of the component parts does not allow caudal drawer under any joint angle.16,26 Although the caudal component of the caudal cruciate is taut in extension, the bundle functions to limit hyperextension of the stifle only should the somewhat shorter and slightly stouter cranial cruciate be damaged, and thus can be considered to be a secondary restraint against hyperextension.7,16 Prevention of caudal displacement of the tibia on the femur is the cardinal and only primary role of the CaCL.8,16 The clinical importance of this cruciate ligament in the dog is somewhat under discussion because of the angle of the stifle during stance and gaiting.80 In a flexed stifle joint, the cranial component of the CaCL is a primary restraint against caudal instability owing to looseness of the collateral ligament in this joint position.25,26,65 Although being advocated previously15, the canine CaCL alone does not seem to limit external rotation of the tibia when the stifle is not fully extended and the lateral collateral is relaxed.80,82 Experimental isolated damage to this ligament does not lead to rotatory instability at any joint angle.



29



CHAPTER 1.1: Review



1.1.5. MICROANATOMY AND ULTRASTRUCTURE Both cruciate ligaments are covered by a fairly uniform fold of the synovial membrane which incompletely divides the stifle joint in the sagittal plane.17,84 This layer of synovial tissue continues over the horns of the menisci.85 Synovial lining of the cruciate ligaments is only not discernible on the surface in direct contact with the other cruciate ligament.33 The synovial envelope makes the cruciate ligaments extrasynovial structures, protected from the degradative effects of the synovial environment, although they are in fact intra-articular.16,17,86 The envelope originates at the caudal synovial membrane proximally and extends to the cranial joint capsule distally, and is richly endowed with branches of vessels originating from both the cranial and caudal aspect of the stifle joint.84,87 The enveloping paraligamentous membranes mainly consist of dense connective tissue, small fibroblasts, and some adipocytes.1,88 An intima and a thin subintimal layer can be histologically distinguished. The former is presented as a single layer of synoviocytes, and the latter as areolar tissue containing small vascular structures.33 Relative to the enveloping membranes, the cruciate ligaments are rather hypocellular.1 The cruciate ligaments are composite collagenous tissues in which the collagen is arranged in a typical hierarchical structure.



The collagen fibrils, being the smallest visible structure by



electron microscopy, are organised into fibres, then subfascicles, and finally fascicles are formed.19,28-30 Sheaths of loose connective tissue are enclosing the respective collagenous entities.



The cranial cruciate ligament



The synovial fold covering the CCL originates caudally at the intercondylar notch and extends to the cranial aspect of the tibial insertion.87 At that point, the paraligamentous tissue communicates with a fold of the distal joint capsule. On the gross level, the canine cranial cruciate is traditionally described as a twocomponent band.1,16 This uncomplicated and distinct subdivision certainly does not carry through to its intricate microarchitecture.1



Each ligament bundle is a multifascicular



structure, and contains many wavy fascicular subunits. The fascicles located at the periphery of the CCL appear to follow a spiral path of waviness around the fascicle axis.22,30,40,89 The helical angle approximates 25 degrees, being nearly optimal regarding to tensile strength.31



30



CHAPTER 1.1: Review Fascicles are composed of numerous subfascicles.19,28-30 In the canine CCL, there is a great variability in the elliptical shaped fascicle size, since fascicles may be composed of one to ten subfascicles, subdivided by loose endoligamentous tissue.1,30 In humans, the fascicular units are bundles with a diameter ranging from 0.25 to 3 mm.28,89 Small fascicles are found embedded in loose connective tissue with ovoid cells. The thicker ones, in contrast, often are densely arranged and the surrounding cells are fusiform.29,30,88 There is also a considerable range of variation for the subfascicular density and for the amount of loose areolar connective tissue in which the subfascicles are embedded according to distinct fuctional regions within the same ACL.29 Subfascicles contain bundles of collagen fibres, the major constituents of the CCL. Each fibre bundle is not oriented such that it is isometric during stifle joint motion.40 Every subtle threedimensional change in the position of the stifle joint therefore differently recruits fibres of the CCL.90 Individual fibres do change length by straightening of their waveforms as they are recruited into tension. Such is not visible at a gross anatomical level, but is conformed by histological assessment.30,40 Fibrils, composed by organisation of repeated collagen subunits, are joined form the fibres.1,33,87,88 The collagen fibril morphology and architecture is also characterised by uniform waveforms parallel to the long axis of the fascicle (Fig 3 A). The internal collagen fibrils are nearly straight while the fibrils undergo a maximum undulation at the fascicular periphery. At the osseous attachment sites of the CCL, the collagen fibres are not arranged entirely parallel to the longitudinal axis of the ligament and, especially in younger specimens, columns of chondroid cells do penetrate into the CCL (Fig 3 B).20,87 At the contact point of the CCL with the caudal cruciate, the collagen fibres are more dense and oriented tangential to the surface instead of parallel to the long axis.33 Ultrastructurally, the CCL is a heterogenic composite structure formed by an extracellular matrix composed of macromolecules with highly specific arrangements and interactions.88,91 Collagen is the chief macromolecule prevalent in the framework of the CCL. In excess of 90 percent of the collagen content of the CCL is type I collagen, the remaining collagen constituent being of type III.92-94 The molecules are produced by the fibroblasts in the loose supporting connective tissue. The cells are present in long parallel columns between the collagen fibres, their axes parallel to the surrounding collagen fibres. Neurovascular components follow the same longitudinal orientation.1,84,87,89 The complex micro-architecture of the viscoelastic CCL is further composed by about 5 percent of elastin.88 Delicate elastic fibres can be found in the narrow spaces separating the primary collagen bundles.33 Furthermore, the tightly packed longitudinally running collagen fibres are associated with a very small portion of proteoglycan 31



CHAPTER 1.1: Review and glycoprotein macromolecules.88



The functional contribution of these components is



extremely important for maintaining the viscoelastic properties of the CCL.



Continuous



interactions of the cells with the macromolecules of the ligament monitor the normal maintenance of the matrix in spite of load, aging, and injury.88 Collagen fibres submitted to mechanical forces act as electrochemical transducers to the constituent connective tissue cells. The cellular metabolic activity and thus the organisation of the extracellular matrix and the maintenance of its glycosaminoglycan content are modulated indirectly by mechanical factors.95



TibialBone Cartilage B



CCL A



A Fig 3.



B



Normal cranial cruciate ligament (CCL) of a 4-month-old Riezenschnauzer, harvested at its tibial attachment site (H&E stain) A. Along the CCL, dense collagen is aligned parallel to the longitudinal axis of the ligament (bar=100µm) B. At the osseous attachment site of the CCL, the collagen fibres are not arranged entirely parallel to the long axis of the ligament. Columns of chondroid cells (arrow) do penetrate into the CCL (bar=100µm)



32



CHAPTER 1.1: Review The caudal cruciate ligament The CaCL is ensheathed by two folds of the synovial membrane. The cranial envelope originates proximally from the cranial aspect of the joint capsule, while distally the caudal fold originates from the caudal aspect of the joint capsule.87 When compared to the CCL, the CaCL is more heavily structured.43 A dense arrangement of collagen fibres is found in the area in contact with the CCL. Those fibres maintain an orientation tangential to the surface of contact, even when the cruciate ligaments start to twist about one another.33



33



CHAPTER 1.1: Review



1.1.6. MICROVASCULARITY The normal vascular anatomy of the canine stifle is similar to that reported in the human knee.84 The major vascular contribution to the centre of the stifle joint occurs via branches of the middle genicular artery.96-99 This vessel arises from the popliteal artery, penetrates the caudal joint capsule, and passes craniodistally to the fossa intercondylaris, running cranially between the cruciate ligaments (Fig 4).100



Fig 4.



Caudal view of the major blood supply to the stifle joint in the dog 1. Femoral artery 2. Popliteal artery 3. Descending genicular artery 4. Proximal medial genicular artery 5. Middle genicular artery 6. Cranial tibial artery 7. Caudal tibial artery



The blood supply to both cruciate ligaments is predominantly of soft tissue origin. The infrapatellar fat pad and the well-vascularised synovial membranes which form an envelope around the cruciate ligaments are the most important sources of vessels and the major pathway for delivery of nutrients.84,87,101-103



The synovial vessels arborise into a finely



meshed network of paraligamentous vessels which ensheaths the cruciate ligaments throughout their entire lengths (Fig 5, Fig 6).84 The contribution to the blood supply to the cruciate ligaments from the osseous attachments is negligible.19,84,98,99,101



34



CHAPTER 1.1: Review



3 1 2



A



B



4 Fig 5. Superficial vascularisation of normal cruciate ligaments in the dog A. Macroscopic view after injection of latex in a canine cadaver specimen B. Arthroscopic view of a stifle joint in a normal dog 1. Cranial cruciate ligament 2. Caudal cruciate ligament 3. Lateral femoral condyle 4. Tibial plateau Arrow: Artery originating from infrapatellar fat pad



1



4



2



CCL



CCL



SM 1



3



Fig 6.



A



B



Normal cranial cruciate ligament (CCL) of an adult dog (H&E stain) A. The CCL is ensheathed by paraligamentous vessels (bar=100µm) B. The well-vascularised synovial membrane (SM) forms an envelope over the CCL (bar=100µm) 1. Paraligamentous vessels 2. Anastomosis between paraligamentous and endoligamentous vessels 3. Hypovascular zone 4. Synovial vessels



35



CHAPTER 1.1: Review In the inner part of the cruciate ligaments, around and along the bundles of collagen fibres, an endoligamentous vascular network is found along its supporting connective tissue.84,87 The larger vessels, usually one artery accompanied by two veins, mainly course in a longitudinal direction both proximally and distally and lie parallel to the collagen fascicles.87 Some of them have a tortuous path in the interfascicular areolar tissue.89



Only small capillaries



branched off from the longitudinal endoligamentous vessels are seen to run in a transverse direction, encircling the collagen bundles.87 Anastomoses exist between extra- and intraligamentous blood networks. Paraligamentous vessels penetrate transversely into the cruciate ligaments (Fig 6 A). Their branches ramify and anastomose with the endoligamentous vessels. In contrast, the endosteal vessels do not often anastomose with the endoligamentous network, especially not at the tibial insertion site.87,103,104 Most endosteal and endoligamentous vessels terminate in loops without crossing the ligamentous-osseous junction.84,87 The cruciate ligaments are not only nourished by microvessels. Significant nutrient uptake also occurs by passive permeation from the synovial fluid.103,105,106



The cranial cruciate ligament



The vascular roots of the CCL lie in the surrounding soft tissues. The vast majority of vessels originates from the infra-patellar fat pad cranially and from the fold of the synovial membrane caudally.84,101,102,104 The vascular structures at the proximal part of the CCL are more numerous and have a larger diameter compared with those at the tibial side.20,87 Most of them originate from a branch of the middle genicular artery and from some branches of the distal genicular arteries.97-99,102,107 In humans, the largest branch of the middle genicular artery descends along the cranial surface of the ACL.98 There are numerous endosteal vessels at the ligamentous-osseus junctions. However, communications with intrinsic endoligamentous vessels are quite poor. Especially at the tibial insertion area most of the endosteal vessels seem to terminate in subchondral loops instead of crossing the ligamentous-osseous junction.84,87 A number of endosteal vessels communicate with the paraligamentous vascular network overlying the CCL.87 There are also vessels from the menisci anastomosing with the paraligamentous vascular plexus.87 The core of the midportion of the CCL is less well vascularised in comparison with the remainder of the ligament.8,20,33,84,87,101,102,104,108 36



This anatomical feature of a relatively



CHAPTER 1.1: Review hypovascular mid-zone might contribute to the pathogenesis of cranial cruciate disease as discussed later.



The caudal cruciate ligament



The caudal synovial fold also provides the major contributing vessels to the CaCL. Most of them originate from branches of the middle genicular artery and from some branches from the other genicular arteries.97,98 A twig divides halfway the CaCL into an upper and a lower branch, which both continue along the ligament.102,104 In general, the vascular arrangement and the structural characteristics of the vasculature inside the CaCL and the CCL are similar.84,87,104 The web-like network of paraligamentous and synovial vessels surrounding the CaCL appears to be slightly more extensive than the vascular plexus seen around the CCL.84,101,102 However, the CaCL does not have a more abundant intrinsic vascular supply than the CCL.19,98,99,107 Endosteal vascular communications are present proximally and distally, although they are rare.87,104



37



CHAPTER 1.1: Review



1.1.7. NEUROLOGY Three major articular nerves arise from the saphenous nerve, the tibial nerve, and the common peroneal nerve to innervate the periarticular tissues of the canine stifle joint (Fig 1).109



Besides purely anatomic studies on the nerve supply to the stifle joint, a lot of



neurophysiologic experiments have been carried out. Most investigations of the innervation of the cruciate ligaments have been performed on cats or in human corpses. Between various mammals, however, the similarities seem in this respect to be far more prominent than the differences.51,97,110 In the dog, the medial articular nerve is the largest supply to the stifle joint. It branches from the saphenous nerve at about mid-thigh. Some of its branches course through the infrapatellar fat pad to terminate within the proximal or distal attachments of the cruciate ligaments or within the meniscal horns.109 The posterior articular nerve is variably present in dogs. Its branches arise either directly from the tibial nerve or from a muscular branch of the tibial nerve.109 The posterior articular nerve runs to the caudal aspect of the joint capsule, where it may communicate with branches of the medial articular nerve.109 In cats and humans, the posterior articular nerve arises from the tibial nerve usually below the popliteal fossa, and is the most constant and the largest of the stifle joint articular nerves, and the cruciate ligaments are mainly innervated by its branches.111-113 The lateral articular nerve branches from the common peroneal nerve at the level of the fibular head, deep to the biceps femoris muscle.109 It supplies the lateral portion of the stifle joint.109 The main trunk of the nerve bundles is found at the femoral end of the cruciate ligaments, an area that becomes strained only at high loads.19,109,114,115 Other nerves may also contribute afferent fibers to a variable extent to the cruciate ligaments.109,116 Most of the nerve fibres within the cruciate ligaments course along the perilagamentous and endoligamentous blood vessels in their passage through the interfascicular areolar spaces. Therefore, it was previously believed that their function was primarily associated with autonomic nervous regulation of blood flow19,89 what later proved to be a misunderstanding.51 Mechanoreceptors have been described in human as well as animal cruciate ligaments, while their exact role in proprioception is not completely elucidated. Proprioceptive receptors are found within most soft tissues of the stifle and its surrounding.115,117,118 The sensory network within the cruciate ligaments plays an extremely important role in the neurosensory system around the stifle joint. By reflex arches, periarticular muscle groups are triggered to contract in order to avoid ligamentous injury by extremes of motion.51,74,89,113,115,119,120 It is not a



38



CHAPTER 1.1: Review



A



Fig 1.



B



The major nerve supply to the stifle joint in the dog A. Medial view B. Lateral view 1. Saphenous nerve 2. Medial articular nerve 3. Posterior articular nerve 4. Common peroneal nerve 5. Tibial nerve 6. Lateral articular nerve



matter of conscious perception, but rather a reaction to mechanically-evoked electrical signals. The middle third of the cruciate ligaments is less densely equipped with sensory endings and is the primary viscoelastic component of the ACL, providing resistance to deformation at low- and moderate-load levels.51,112,116,119 Sensation of pain might be transmitted by a small population of free nerve endings which ramify in the cruciate ligaments.89,117,121,122 However, the synovia seem to serve as primary pain receptors.119 The cruciate ligaments contain both rapidly- and slowly-adapting receptors with low and high thresholds to mechanical deformation.51,117,123



39



Mechanoreceptors are



CHAPTER 1.1: Review located near the surface of the cruciate ligaments and respond to longitudinal extension and deformation of the ligament, monitoring proprioceptive information.117,123



The cranial cruciate ligament The cranial cruciate muscle reflex plays a physiologic role during stifle function.120 When the CCL is loaded in cranial drawer, hamstring reflex activity is observed.74,120 In dogs, the load threshold to trigger the CCL-muscle reflex is well within the working range of motion of the stifle and appears to be only 1 to 10 per cent of the loading required to rupture the CCL.113 In humans, loss of ACL proprioceptive function is thought to contribute to increased joint laxity over time through loss of dynamic stabilising reflexes.89,121,124 Of course, lesions to other structures in and around the joint contribute to the proprioceptive deficits encountered in an ACL-deficient knee.125 Neural elements associated with the CCL are located primarily in its richly vascularised synovial coverings.114



Mechanoreceptors within the cruciate ligament itself provide



proprioceptive information and indicate local reflex patterns to protect the ligament from tearing and warn against possible joint damage.116,119



In men, there is particularly rich



innervation of the tibial origin of the ACL114, while in dogs a higher number of receptors is encountered in the proximal third of the CCL.122 The CCL is relatively insensitive to pain because it only contains rare free nerve endings.117



The caudal cruciate ligament



In dogs, some branches of the medial articular nerve pass cranially through the joint capsule to supply an extensive innervation of the femoral attachment of the CaCL.109 An independent twig of the posterior articular nerve enters the joint capsule after giving off smaller branches to the fat pad, and finally terminates in the attachment of the CaCL to the tibia.112 As for the CCL, the mechanoreceptor organs in the CaCL were found primarily at either extremity close to the attachments of the ligament.112,115



40



CHAPTER 1.1: Review REFERENCES 1.



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41



CHAPTER 1.1: Review



21. Haut RC, Little RW. Rheological properties of canine anterior cruciate ligaments. J Biomech 1969;2:289298. 22. Stouffer DC, Butler DL, Kim H. Tension-torsion characteristics of the canine anterior cruciate ligament – Part I: Theoretical framework. Trans ASME: J Biomech Engin 1983;105:154-159. 23. Robins GM. The canine stifle. Anatomy, function and kinesiology. In: Whittick WG, ed. Canine Orthopaedics. Philadelpia:Lea and Febiger, 1990;693-702. 24. Arnoczky SP. The cruciate ligaments: the enigma of the canine stifle. J Small Anim Pract 1988;29:71-90. 25. Hulse DA, Shires PK. The stifle joint. In: Slatter DH, ed. Textbook of Small Animal Surgery. Philadelphia:WB Saunders, 1985;2193-2235. 26. Harari J. Caudal cruciate ligament injury. Vet Clin NA:SAP 1993;23:821-829. 27. Payne JT, Constantinescu GM. Stifle joint anatomy and surgical approaches in the dog. Vet Clin NA:SAP 1993;23:691-701. 28. Danylchuk KD, Finlay JB, Krcek JP. Microstructural organisation of human and bovine cruciate ligaments. Clin Orthop Rel Res 1978;131:294-298. 29. Yahia L-H, Drouin G. Collagen structure in human anterior cruciate ligament and patellar tendon. J Mater Sci 1988;23:3750-3755. 30. Yahia L-H, Drouin G. Microscopical investigation of canine anterior cruciate ligament and patellar tendon: Collagen fascicle morphology and architecture. J Orthop Res 1989;7:243-251. 31. Alm A, Ekström H, Strömberg B. Tensile strength of the anterior cruciate ligament in the dog. Acta Chir Scand 1974;suppl 445:15-23. 32. Dorlot J-M, Ait Ba Sidi M, Tremblay GM, et al. Load elongation behavior of the canine anterior cruciate ligament. Trans ASME 1980;120:190-193. 33. Vasseur PB, Pool RR, Arnoczky SP, et al. Correlative biomechanical and histologic study of the cranial cruciate ligament in dogs. Am J Vet Res 1985;46:1842-1854. 34. Coetzee GL. An in vitro comparison of two replacement techniques utilizing fascia lata after cranial cruciate ligament transection in the dog. Vet Comp Orthop Traumatol 1993;6:85-92. 35. Wingfield C, Amis AA, Stead AC et al. Comparison of the biomechanical properties of rottweiler and racing greyhound cranial cruciate ligaments. J Small Anim Pract 2000;41:303-307. 36. Norwood LA, Cross MJ. Anterior cruciate ligament: Functional anatomy of its bundles in rotatory instabilities. Am J Sports Med 1979;7:23-26. 37. Dawkins GPC, Amis AA. A functional study of the structure of the anterior cruciate ligament, related to knee stability, injury mechanisms and prosthetic ligament reconstructions. J Bone Joint Surg (Br) 1985;5:844. 38. Girgis FG, Marshall JL, Monajem ARS. The cruciate ligaments of the knee joint. Anatomical, functional and experimental analysis. Clin Orthop 1975;106:216-231. 39. Furman W, Marshall JL, Girgis FG. The anterior cruciate ligament. A functional analysis based on postmortem studies. J Bone Joint Surg (Am) 1976;58-A:179-185. 40. Amis AA, Dawkins GPC. Functional anatomy of the anterior cruciate ligament. Fibre bundle actions related to ligament replacements and injuries. J Bone Joint Surg (Br) 1991;73-B:260-267.



42



CHAPTER 1.1: Review 41. Welsh RP. Knee joint structure and function. Clin Orthop 1980;147:7-14. 42. Odensten M, Gillquist J. Functional anatomy of the anterior cruciate ligament and a rationale for reconstruction. J Bone Joint Surg (Am) 1985;67-A:257-262. 43. Brünnberg L. Klinische Untersuchungen zu Ätiologie und Pathogenese der Ruptur des Ligamentum cruciatum craniale beim Hund. 2. Mitteilung: Zur Ätiologie und Diagnose der Ruptur des Ligamentum cruciatum craniale beim Hund. Kleintierprax 1989;34:445-449. 44. Neurath MF, Stofft E. Collagen ultrastructure in ruptured cruciate ligaments. An electron microscopic investigation. Acta Orthop Scand 1992;63:507-510. 45. Harari J. Huidige inzichten in de behandeling van voorste kruisbandlaesies. Waltham Focus 1995;5:24-31. 46. Frank CB, Jackson DW. The science of reconstruction of the anterior cruciate ligament. J Bone Joint Surg (Am) 1997;79-A:1556-1576. 47. Shoemaker SC, Markolf KL. Effects of joint load on the stiffness and laxity of ligament-deficient knees. J Bone Joint Surg (Am) 1985;67-A:136-146. 48. Slocum B, Devine T. Tibial plateau leveling osteotomy for repair of cranial cruciate ligament rupture in the canine. Vet Clin NA:SAP 1993;23:777-795. 49. Markolf KL, Bargar WL, Shoemaker SC, et al. The role of joint load in knee stability. J Bone Joint Surg (Am) 1981;63-A:570-585. 50. Ascherl R. Cruciate and meniscal injuries. Proceedings 10th ESVOT Congress, Munich 2000;23-26th March:18. 51. Johansson H, Sjölander P, Sojka P. A sensory role for the cruciate ligaments. Clin Orthop Rel Res 1991;268,161-178. 52. Smith B. Viewpoints in surgery: Cruciate ligament rupture. Extracapsular stabilisation. Austr Vet J 2000;78 :382-383. 53. Shires PK. Intracapsular repairs for cranial cruciate ligament ruptures. Vet Clin NA:SAP 1993;23:761-775. 54. Korvick DL, Pijanowski GJ, Schaeffer DJ. Three-dimensional kinematics of the intact and cranial cruciate ligament-deficient stifle of dogs. J Biomech 1994;27:77-87. 55. Aron DN. Traumatic dislocation of the stifle joint: Treatment of 12 dogs and one cat. J Am Anim Hosp Assoc 1988;24:333-340. 56. Abbott LC, Saunders JB, De CM, et al. Injuries toe the ligaments of the knee joint. J Bone J Surg 1944;26:503-521. 57. Marshall JL, Wang JB, Furman W, et al. The anterior drawer sign: What is it? J Sports Med 1975;3:152158. 58. Butler DL, Noyes FR, Grood ES. Ligamentous restraints to anterior-posterior drawer in the human knee. J Bone Joint Surg (Am) 1980;62-A:259-270. 59. Grood ES, Noyes FR, Butler DL, et al. Ligamentous and capsular restraints preventing straight medial and lateral laxity in intact human cadaver knees. J Bone Joint Surg (Am) 1981;63-A:1257-1269. 60. Fukubayashi T, Torzilli PA, Sherman MF, et al. An in vitro biomechanical evaluation of anterior-posterior motion of the knee. Tibial displacement, rotation, and torque. J Bone Joint Surg (Am) 1982;64-A:258-264.



43



CHAPTER 1.1: Review 61. Markolf KL, Wascher DC, Finerman GAM. Direct in vitro measurements of forces in the cruciate ligaments. Part II: The effect of section of the posterolateral structures. J Bone Joint Surg (Am) 1993;75A:387-394. 62. Sakane M, Fox RJ, Woo SL-Y, et al. In situ forces in the anterior cruciate ligament and its bundles in response to anterior tibial loads. J Orthop Res 1997;15:285-293. 63. Amis AA. Anterior cruciate ligament replacement: knee stability and the effects of implants. J Bone Joint Surg (Br) 1989;71-B:819-824. 64. Moore KW, Read RA. Rupture of the cranial cruciate ligament in dogs - Part I. Comp Cont Educ 1996;18:223-233. 65. Vasseur PB, Arnoczky SP. Collateral ligaments of the canine stifle joint: Anatomic and functional analysis. Am J Vet Res 1981;42:1133-1137. 66. Inoue M, McGurk-Burleson E, Hollis JM, et al. Treatment of the medial collateral ligament injury. I: The importance of anterior cruciate ligament on the varus-valgus knee laxity. Am J Sports Med 1987;15:15-21. 67. Slocum B, Devine T. Cranial tibial thrust: A primary force in the canine stifle. J Am Vet Med Assoc 1983;183:456-459. 68. Arnoczky SP, Torzilli PA, Marshall JL. Biomechanical evaluation of anterior cruciate ligament repair in the dog: An analysis of the instant center of motion. J Am Anim Hosp Assoc 1977;13:553-558. 69. Smith GK, Torg JS. Fibular head transposition for repair of cruciate-deficient stifle in the dog. J Am Vet Med Assoc 1985;187:375-383. 70. Hulse DA, Michaelson F, Johnson C, et al. A technique for reconstruction of the anterior cruciate ligament in the dog: Preliminary report. Vet Surg 1980;9:135-140. 71. Meinen JJ, Verbeek M. Voorste kruisbandlaesies bij de hond: een evaluatie van therapie, klinisch en röntgenologisch verloop bij 215 patiënten. Referaat. Geneeskunde van het Kleine Huisdier, Vakgroep Radiologie, Rijksuniversiteit te Utrecht 1980. 72. Holden JP, Grood ES, Korvick DL, et al. In vivo forces in the anterior cruciate ligament: Direct measurements during walking and trotting in a quadruped. J Biomech 1994; 27:517-526. 73. Kellis E. Quantification of quadriceps and hamstring antagonist activity. Sports Med 1998;25:37-62. 74. Solomonow M, Baratta R, Zhou BH, et al. The synergistic action of the anterior cruciate ligament and thigh muscles in maintaining joint stability. Am J Sports Med 1987;15:207-213. 75. More RC, Markolf KL. Measurement of stability of the knee and ligament force after implantation of a synthetic anterior cruciate ligament. In vitro measurement. J Bone Joint Surg (Am) 1988;70-A:1020-1031. 76. Slocum B, Devine T. Algorithm for diagnosis and treatment of the stifle for cranial cruciate ligament rupture. In: Bojrab MJ, ed. Current techniques in small animal surgery. Baltimore:Williams and Wilkins, 1998;1187-1193. 77. Slocum B, Devine T. Tibial plateau leveling osteotomy for cranial cruciate ligament rupture. In: Bojrab MJ, ed. Current techniques in small animal surgery. Baltimore:Williams and Wilkins, 1998;1209-1215. 78. Hulse DA. Surgery of the knee (part 1): Basic concepts and treatment of CCL injury. Proceedings SAVAB Flanders WE 1998;9-11 May. 79. Wingfield C, Amis AA, Stead AC et al. Cranial cruciate stability in the rottweiler and racing greyhound: an in vitro study. J Small Anim Pract 2000a;41:193-197. 80. Arnoczky SP. Surgery of the stifle - The cruciate ligaments (Part I). Comp Cont Ed 1980;2:106-116.



44



CHAPTER 1.1: Review



81. Reinke JD. Cruciate ligament avulsion injury in the dog. J Am Anim Hosp Assoc 1982;18:257-264. 82. Pournaras J, Symeonides PP, Karkavelas G. The significance of the posterior cruciate ligament in the stability of the knee. An experimental study in dogs. J Bone Joint Surg (Br) 1983;65-B:204-209. 83. Johnson AL, Olmstead ML. Caudal cruciate ligament rupture. A retrospective analysis of 14 dogs. Vet Surg 1987;16:202-206. 84. Arnoczky SP, Rubin RM, Marshall JL. Microvasculature of the cruciate ligaments and its response to injury. An experimental study in dogs. J Bone Joint Surg 1979;61-A:1221-1229. 85. Arnoczky SP, Warren RF. The microvasculature of the meniscus and its response to injury. experimental study in the dog. Am J Sports Med 1983;11:131-141.



An



86. Amiel D, Billings E, Harwood FL. Collagenase activity in anterior cruciate ligament: protective role of the synovial sheath. J Appl Physiol 1990;69:902-906. 87. Alm A, Strömberg B. Vascular anatomy of the patellar and cruciate ligaments. A microangiographic and histologic investigation in the dog. Acta Chir Scand 1974;suppl 445:25-35. 88. Jackson DW, Heinrich JT, Simon TM. Biologic and synthetic implants to replace the anterior cruciate ligament. Arthroscopy 1994;10:442-452. 89. Kennedy JC, Weinberg HW, Wilson AS. The anatomy and function of the anterior cruciate ligament. As determined by clinical and morphological studies. J Bone Joint Surg (Am) 1974;56-A:223-235. 90. Butler DL, Guan Y, Kay MD, et al. Location-dependent variations in the material properties of the anterior cruciate ligament. J Biomech 1992;25:511-518. 91. Figgie HE, Bahniuk EH, Heiple KG, et al. The effects of tibial-femoral angle on the failure mechanics of the canine anterior cruciate ligament. J Biomech 1985;19:89-91. 92. Amiel D, Frank C, Harwood F, et al. Tendons and ligaments: A morphological and biochemical comparison. J Orthop Res 1984;1:257-265. 93. Morgan K, Clague RB, Collins I, et al. Incidence of antibodies to native and denaturated cartilage collagens (types II, IX, and XI) and to type I collagen in rheumatoid arthritis. Ann Rheum Dis 1987;46:902-907. 94. Wildey GM, McDevitt CA. Matrix protein mRNA levels in canine meniscus cells in vitro. Arch Biochem Biophys 1998;353:10-15. 95. Gillard GC, Merrilees MJ, Bell-Booth PG, et al. The proteoglycan content and the axial periodicity of collagen in tendon. Biochem J 1977;163:145-151. 96. Davies DV, Edwards DAW. The blood supply of the synovial membrane and intra-articular structures. Ann R Coll Surg Engl 1948;2:142-156. 97. Müller A. Topographisch-anatomische Grundlagen zu den Kniegelenkoperationen des Hundes. InauguralDissertation. Veterinär-Chirurgischen Klinik, Universität Zürich, Sweiss, 1968. 98. Scapinelli R. Studies on the vasculature of the human knee joint. Acta Anat 1968;70:305-331. 99. Marshall JL, Arnoczky SP, Rubin RM, et al. Microvasculature of the crucite ligaments. Phys Sports Med 1979;7:87-91. 100. de Vos NR, Simoens PJ. Angiologia. In: Schaller O, ed. Illustrated Veterinary Anatomical Nomenclature. Stuttgard:Ferdinand Enke Verslag, 1992;322-325.



45



CHAPTER 1.1: Review 101. Rubin RM, Marshall JL. Vascular anatomy of the cruciate ligaments in the dog - normal and injured states. Trans 22nd Annual Meeting of Orthop Res Soc 1976;1:148. 102. Tirgari M. The surgical significance of the blood supply of the canine stifle joint. J Small Anim Pract 1978;19:451-462. 103. Whiteside LA, Sweeney RE. Nutrient pathways of the cruciate ligaments. An experimental study using the hydrogen wash-out technique. J Bone Joint Surg (Am) 1980;62-A:1176-1180. 104. Clancy WG, Narechania RG, Rosenberg TD, et al. Anterior and posterior cruciate ligament reconstruction in rhesus monkeys. J Bone Joint Surg (Am) 1981;63-A:1270-1284. 105. Skyhar MJ, Danzig LA, Hargens AR, et al. Nutrition of the anterior cruciate ligament. Effects of continuous passive motion. Am J Sports Med 1985;13:415-418. 106. Kanda T, Ochi M, Ikuta Y. Adverse effects on rabbit anterior cruciate ligament after knee immobilization: changes in permeability of horseradish peroxidase. Arch Orthop Trauma Surg 1998;117:307-311. 107. Arnoczky SP. Blood supply to the anterior cruciate ligament and supporting structures. Orthop Clin North Am 1985;16:15-28. 108. Hohn RB, Newton CD. Surgical repair of ligamentous structures of the stifle joint. In: Bojrab MJ, ed. Current Techniques in Small Animal Surgery. Philadelphia:Lea and Febiger, 1975;470-479. 109. O’Connor BL, Woodbury P. The primary articular nerves to the dogs knee. J Anat 1982;134:563-572. 110. Langford LA, Schmidt RF. Afferent and efferent axons in the medial and posterior atricular nerves of the cat. Anat Rec 1983;206:71-78. 111. Gardner E. The distribution and termination of nerves in the knee joint of the cat. J Comp Neurol 1944;80:11-32. 112. Freeman MAR, Wyke B. The innervation of the knee joint. An anatomical and histological study in the cat. J Anat 1967;101:505-532. 113. Miyatsu M, Atsuta Y, Watakabe M. The physiology of mechanoreceptors in the anterior cruciate ligament. An experimental study in decerebrate-spinalised animals. J Bone Joint Surg (Br) 1993;75-B,653-657. 114. Kennedy JC, Alexander IJ, Hayes KC. Nerve supply of the human knee and its functional importance. Am J Sports Med 1982;10:329-335. 115. Schultz RA, Miller DC, Kerr CS, et al. Mechanoreceptors in human cruciate ligaments. A histological study. J Bone Joint Surg (Am) 1984;66-A:1072-1076. 116. Krauspe R, Schmidt M, Schaible H-G. Sensory innervation of the anterior cruciate ligament. J Bone Joint Surg (Am) 1992;74-A:390-397. 117. Schutte MJ, Dabezies EJ, Zimmy ML, et al. Neural anatomy of the human anterior cruciate ligament. J Bone Joint Surg (Am) 1987;69-A:243-247. 118. Schenk I, Spaethe A, Halata Z. The structure of sensory nerve endings in the knee joint capsule of the dog. Ann Anat 1996;178:515-521. 119. Biedert RM, Stauffer E, Friederich NF. Occurrence of free nerve endings in the soft tissue of the knee joint. A histologic investigation. Am J Sports Med 1992;20:430-433. 120. Gómez-Barrena E, Nuñes A, Martinez-Moreno E, et al. Neural and muscular electric activity in the cat’s knee. Acta Orthop Scand 1997;68:149-155.



46



CHAPTER 1.1: Review 121. Barrack RL, Skinner HB, Buckley SL. Proprioception in the anterior cruciate deficient knee. Am J Sports Med 1989;17:1-6. 122. Arcand MA, Rhalmi S, Rivard C-H. Quantification of mechanoreceptors in the canine anterior cruciate ligament. Int Orthop 2000;24:272-275. 123. Boyd IA, Roberts TDM. Proprioceptive discharges from stretch-receptors in the knee-joint of the cat. J Physiol 1953;122:38-58. 124. Corrigan JP, Cashman WF, Brady MP. Proprioception in the cruciate deficient knee. J Bone Joint Surg (Br) 1992 ;74-B :247-250 ; 125. Fridèn T, Roberts D, Zätterström, et al. Proprioceptive defects after an anterior cruciate ligament rupture the relation to associated anatomical lesions and subjective knee function. Knee Surg, Sports Traumatol, Arthrosc 1999;7:226-231.



47



48



CHAPTER 1



1.2.



Predisposing and etiological factors in canine cranial cruciate ligament disease. contributors



49



A long list of possible



50



CHAPTER 1.2: Review Traditionally, injury to the cranial cruciate ligament (CCL) in dogs has been classified in 2 main modes: a degenerative syndrome in middle-aged to older, small to medium-sized dogs and a traumatic condition in young large breed dogs.1,2 Current observations have challenged these traditional views of CCL disease. Both groups are incontestably interrelated and various causes of CCL damage are not mutually exclusive. Pure traumatic CCL rupture in dogs is only an incidental event, occurring in any breed and at any age.3-6



More often, the dog is



performing daily activities within the physiological loading range at the time of rupture.5,7-9 This form of nontraumatic rupture is termed spontaneous CCL rupture. The integrity of the CCL may be lost due to direct trauma of the stifle joint if the breaking strength of the CCL is exceeded.1,10-14 A few mechanics of traumatic CCL damage are recognised in the dog. Sudden hyperextension may occur when a dog steps into a hole while running, or when it is caught in a fence or gate.12 The CCL will rupture as the distance between its attachment sites exceeds the length of this ligament.15 A sharp turn while the foot is weight-bearing produces excessive internal rotation of the tibia. The CCL becomes very tightly twisted, and fibres are torn loose by rotation against the lateral femoral condyle.11,12,16 Extreme cranial tibial thrust is stressing the CCL during landing after a jump from a height.17,18 The purely traumatic form of ACL rupture predominates in men as a clipping injury in football or an hyperextension injury during skiing.19-21,a In dogs, it does not often seem to be the sole causative factor.3,5,6,18 The complete etiopathogenesis of spontaneous CCL rupture in dogs remains largely enigmatic in the majority of cases although much attention has already been focused on trying to identify factors that might predispose to injury. Mechanical strength is gradually decreased by progressive and apparently irreversible degenerative changes within the cruciate ligament itself and the susceptibility to damage due to minimal trauma or even normal loading becomes greater.22-26 Before rupture of the CCL becomes clinically apparent, previous episodes of incremental partial tearing due to imbalance of forces causing tissue fragility to mechanical tension have been considered.15,24,27 Several surveys attempted to gain information of the type of dog affected by cruciate disease.2,6,16,28-31 Age, breed, body weight, and gender all have been considered as risk factors in the development of CCL rupture. Comparison with the normal canine population is mostly lacking in these studies. Therefore, it might be questioned whether most reported data are genuine differences in the prevalence of spontaneous CCL rupture.6,32 Other contributing factors responsible for ligament degeneration and weakening are numerous. The microstructure of the collagen fibrils composing the CCL deteriorates when the 51



CHAPTER 1.2: Review dogs get older.22-24 The central core of the cruciate is the most vulnerable part because of its poorer vascularisation.11,12,22,24,33-38 If normal aging processes were a primary and sole cause of spontaneous CCL rupture, however, the frequency of bilateral cruciate disease would be higher than actually observed.39 A high percentage of patients are overweight and inactive.32 In obese dogs, the ligament is repeatedly submitted to higher stresses what might accelerate degenerative processes.40-42 A sedentary life style weakens the collagen of the CCL itself but also the other secondary soft tissue stabilisers.16,26 Skeletal abnormalities have been associated with increased strain placed on the CCL and predisposition of dog to CCL rupture. Chronic patellar luxation, angular shaft deformities, and conformationally straight in the hind limbs may all contribute to extra stress on the CCL.2,11,12,17,25,43-47 Inappropriate sloping of the tibial plateau is also hypothised as a factor in the pathogenesis of CCL rupture.15,48-50 Because there is a contact between the intercondylar fossa and the CCL, a narrowing of the intercondylar notch might also contribute to ligament fibres impingement and subsequent CCL failure in dogs,51-53 as has been reported in human beings.54-57 Such intercondylar notch stenosis may be a primary congenital or a developmental abnormality, or may be secondary to degenerative changes in the stifle joint. Nontraumatic ACL rupture is not well documented in the human literature.21



The



degenerative processes that occur in spontaneous tendon rupture in men,58 however, appear similar, histologically, to that occurring in the CCL of dogs.24 Many provoking factors remain unidentified to date.



Evidence raised that immune



phenomena play a role in several types of joint pathologies in dogs.59-61 In cases of immunemediated synovitis, a gradual relaxation of the cruciate ligaments can be encountered.36,40,62,63 Elevated auto-antibody titers to collagen were detected in dogs with cruciate disease.59 However, the presence of anti-collagen auto-antibodies does not necessarily imply that the initiation of CCL rupture is immune-mediated. Exposure of ligamentous collagen from a torn cranial cruciate might incite an antigenically stimulated joint inflammation. Further research in this field is highly required to explain all unanswered questions.



a



Ascherl R. Personal communication 2000



52



CHAPTER 1.2: Review REFERENCES 1.



Bennett D, Tennant D, Lewis DG, et al. A reappraisal of anterior cruciate ligament disease in the dog. J Small Anim Pract 1988;29:275-297.



2.



Duval JM, Budsberg SC, Flo GL, et al. Breed, sex, and body weight as risk factors for rupture of the cranial cruciate ligament in young dogs. J Am Vet Med Assoc 1999;6:811-814.



3.



Arnoczky SP, Tarvin GB, Marshall JL, et al. The over-the-top procedure: A technique for anterior cruciate ligament substitution in the dog. J Am Anim Hosp Assoc 1979;15:283-290.



4.



Brünnberg L. Klinische Untersuchungen zu Ätiologie und Pathogenese der Ruptur des Ligamentum cruciatum craniale beim Hund. 2. Mitteilung: Zur Ätiologie und Diagnose der Ruptur des Ligamentum cruciatum craniale beim Hund. Kleintierprax 1989;34:445-449.



5.



Doverspike M, Vasseur PB, Harb MF, et al. Contralateral cranial cruciate ligament rupture: Incidence in 114 dogs. J Am Anim Hosp Assoc 1993;29:167-170.



6.



Whitehair JG, Vasseur PB, Willits NH. Epidemiology of cranial cruciate ligament rupture in dogs. J Am Vet Med Assoc 1993;203:1016-1019.



7.



Niebauer GW, Wolf B, Bashey RI, et al. Antibodies to canine collagen types I and II in dogs with spontaneous cruciate ligament rupture and osteoarthritis. Arthr Rheum 1987;30:319-327.



8.



Scavelli TD, Schrader SC, Matthiesen DT, et al. Partial rupture of the cranial cruciate ligament of the stifle in dogs: 25 cases (1982-1988). J Am Vet Med Assoc 1990;196:1135-1138.



9.



Dupuis J, Harari J. Cruciate ligament and meniscal injuries in dogs. Comp Cont Educ 1993;15:215-232.



10. Loeffler K. Kreuzbandverletzungen im Kniegelenk des Hundes. Anatomy, Klinik und experimentele Untersuchungen. Verslag. Hannover:M and H Schaper, 1964. 11. Hohn RB, Newton CD. Surgical repair of ligamentous structures of the stifle joint. In: Bojrab MJ, ed. Current Techniques in Small Animal Surgery. Philadelphia:Lea and Febiger, 1975;470-479. 12. Arnoczky SP, Marshall JL. Pathomechanics of cruciate and meniscal injuries. In: Bojrab MJ, ed. Pathophysiology of Small Animal Surgery. Philadelphia:Lea and Febiger, 1981;590-603. 13. Hulse DA, Shires PK. The stifle joint. In: Slatter DH, ed. Textbook of Small Animal Surgery. Philadelphia:WB Saunders, 1985;2193-2235. 14. Brinker WO, Piermattei DL, Flo GL. Diagnosis and treatment of orthopedic conditions of the hindlimb. In: Brinker WO, Piermattei DL, Flo GL, eds. Handbook of small animal orthopedics and fracture treatment. Philadelphia:WB Saunders, 1990;341-470. 15. Slocum B, Devine T. Tibial plateau leveling osteotomy for repair of cranial cruciate ligament rupture in the canine. Vet Clin NA:SAP 1993;23:777-795. 16. Johnson JM, Johnson AL. Cranial cruciate ligament rupture. Pathogenesis, diagnosis, and postoperative rehabilitation. Vet Clin North Am (SAP) 1993;23:717-733. 17. Slocum B, Devine T. Cranial tibial thrust: A primary force in the canine stifle. J Am Vet Med Assoc 1983;183:456-459. 18. Drapé J, Ghitalla S, Autefage A. Rupture du ligament croisé antérieur (L.C.A.) chez le chien: pathologie traumatique ou dégénérative? Point Vét 1990;22:573-580. 19. Palmer I. On injuries of the ligaments of the knee joint. A clinical study. Acta Chir Scand 1938;suppl 53.



53



CHAPTER 1.2: Review 20. Kennedy JC, Weinberg HW, Wilson AS. The anatomy and function of the anterior cruciate ligament. As determined by clinical and morphological studies. J Bone Joint Surg (Am) 1974;56-A:223-235. 21. Miyasaka KC, Daniel D, Stone ML, et al. The incidence of knee ligament injuries in the general population. Am J Knee Surg 1991;4:3-7. 22. Zahm H. Die Ligamenta decussata in gesunden und arthrotischen Kniegelenk des Hundes. Kleintierprax 1965;10:38-47. 23. Niebauer GW, Niedermüller H, Skalicky M. Die Kollagenquervernetzung im Ligamentum cruciatum des Hundes und ihre Beziehung zur pathologischen Kreuzbandruptur. Zbl Vet Med A 1983;30:688-693. 24. Vasseur PB, Pool RR, Arnoczky SP, et al. Correlative biomechanical and histologic study of the cranial cruciate ligament in dogs. Am J Vet Res 1985;46:1842-1854. 25. Arnoczky SP. The cruciate ligaments: the enigma of the canine stifle. J Small Anim Pract 1988;29:71-90. 26. Narama I, Masuoka-Nishiyama M, Matsuura T, et al. Morphogenesis of degenerative changes predisposing dogs to rupture of the cranial cruciate ligament. J Vet Med Sci 1996;58:1091-1097. 27. Smith B. Viewpoints in surgery: Cruciate ligament rupture. Extracapsular stabilisation. Austr Vet J 2000;78 :382-383. 28. Barnes AJ. Rupture of the anterior cruciate ligament of the dog: a survey from practices in the Kent region BSAVA. J Small Anim Pract 1977;18:55-59. 29. Elkins AD, Pechman R, Kearny MT, et al. A retrospective study evaluating the degree of degenerative joint disease in the stifle joint of dogs following surgical repair of anterior cruciate ligament rupture. J Am Anim Hosp Assoc 1991;27:533-539. 30. Metelman LA, Schwarz PD, Salman M, et al. An evaluation of three different cranial cruciate ligament surgical stabilization procedures as they relate to postoperative meniscal injuries. A retrospective study of 665 stifles. Vet Comp Orthop Traumatol 1995;8:118-123. 31. Necas A, Zatloukal J, Kecova H, et al. Predisposition of dog breeds to rupture of the cranial cruciate ligament. Acta Vet Brno 2000;69:305-310. 32. Shires PK, Hulse DA, Liu W. The under-and-over fascial replacement technique for anterior cruciate ligament rupture in dogs: A retrospective study. J Am Anim Hosp Assoc1984;20:69-77. 33. Alm A, Ekström H, Strömberg B. Tensile strength of the anterior cruciate ligament in the dog. Acta Chir Scand 1974b;suppl 445:15-23. 34. Alm A, Strömberg B. Vascular anatomy of the patellar and cruciate ligaments. A microangiographic and histologic investigation in the dog. Acta Chir Scand 1974;suppl 445:25-35. 35. Rubin RM, Marshall JL, Wang J. Prevention of knee intability. Experimental model for prosthetic anterior cruciate ligament. Clin Orthop Rel Res 1976;113:212-237. 36. Tirgari M. The surgical significance of the blood supply of the canine stifle joint. J Small Anim Pract 1978;19:451-462. 37. Arnoczky SP, Rubin RM, Marshall JL. Microvasculature of the cruciate ligaments and its response to injury. An experimental study in dogs. J Bone Joint Surg 1979;61-A:1221-1229. 38. Clancy WG, Narechania RG, Rosenberg TD, et al. Anterior and posterior cruciate ligament reconstruction in rhesus monkeys. J Bone Joint Surg (Am) 1981;63-A:1270-1284. 39. Moore KW, Read RA. Rupture of the cranial cruciate ligament in dogs - Part I. Comp Cont Educ 1996a;18:223-233.



54



CHAPTER 1.2: Review



40. Pedersen NC, Pool RR, Morgan JP. Joint diseases in dogs and cats. Meniscal disorders and cruciate ligament rupture. In: Ettinger SJ, ed. Textbook of Veterinary Internal Medicine. Diseases of the Dog and Cat. London:WB Saunders 1983;2197-2198. 41. Edney ATB, Smith PM. Study of obesity in dogs visiting veterinary practices in the United Kingdom. Vet Rec 1986;118:391-396. 42. Vasseur PB. The stifle joint. In: Slatter DH, ed. Textbook of Small Animal Surgery 2nd ed. Philadelphia:WB Saunders, 1993;1817-1866. 43. Rudy RL. Stifle joint. In: Archibald J, ed. Canine surgery. Santa Barbara:American Veterinary Publications Inc, 1974;1104-1115. 44. Read RA, Robins GM. Deformity of the proximal tibia in dogs. Vet Rec 1982;295-298. 45. Robins GM. The canine stifle. The diagnosis and management of acquired abnormalities. In: Whittick WG, ed. Canine Orthopaedics. Philadelpia:Lea and Febiger, 1990;724-752. 46. Hulse DA, Aron DN. Advances in Small Animal Orthopaedics. Comp Cont Ed Pract Vet 1994;16:831-832. 47. Hulse DA. Surgery of the knee (part 1): Basic concepts and treatment of CCL injury. Proceedings SAVAB Flanders WE 1998;9-11 May. 48. Schwarz PD. Tibial plateau leveling osteotomy (TPLO): a prospective clinical comparative study. Proceedings 27nd Ann Meet ACVS Vet Symp 1999;379-380. 49. Morris E, Lipowitz AJ. Comparison of tibial plateau angles in dogs with and without cranial cruciate ligament injuries. Am J Vet Res 2001;218:363-366. 50. Selmi AL, Padilha Filho JG. Rupture of the cranial cruciate ligament associated with deformity of the proximal tibia in five dogs. J Small Anim Pract 2001;42:390-393. 51. Aiken SW, Kass PH, Toombs JP. Intercondylar notch width in dogs with and without cranial cruciate ligament injuries. Vet Comp Orthop Traumatol 1995;8:128-132. 52. Fitch RB, Montgomery RD, Milton JL, et al. The intercondylar fossa of the normal canine stifle: An anatomic and radiographic study. Vet Surg 1995;24:148-155. 53. Wingfield C, Amis AA, Stead AC et al. Comparison of the biomechanical properties of rottweiler and racing greyhound cranial cruciate ligaments. J Small Anim Pract 2000;41:303-307. 54. Anderson AF, Lipsocomb AB, Liudahl KJ, et al. Analysis of the intercondylar notch by computed tomography. Am J Sports Med 1987;15:547-552. 55. Souryal TO, Moore HA, Evans JP. Bilaterality in anterior cruciate ligament injuries: Associated intercondylar notch stenosis. Am J Sports Med 1988;16:449-454. 56. Harner CD, Paulos LE, Greenwald AE, et al. Detailed analysis of patients with bilateral anterior cruciate ligament injuries. Am J Sports Med 1994;22:37-43. 57. Shelbourne KD, Davis TJ, Klootwyk TE. The relationship between intercondylar notch width of the femur and the incidence of anterior cruciate ligament tears. A prospective study. Am J Sports Med 1998;26:402408. 58. Kannus P, Jozsa L. Histopathological changes preceeding spontaneous rupture of a tendon. A controlled study of 891 patients. J Bone Joint Surg (Am) 1991;73-A:1507-1525. 59. Niebauer GW, Menzel EJ. Immunological changes in canine cruciate ligament rupture. Res Vet Sc 1982;32:235-241.



55



CHAPTER 1.2: Review



60. Bari ASM, Carter SD, Bell SC, et al. Anti-type II collagen antibody in naturally occurring canine joint diseases. Brit J Rheum 1989;28:480-486. 61. Arican M, Carter SD, Bennett D, May C. Measurement of glycosaminoglycans and keratan sulphate in canine arthropathies. Res Vet Sc 1994;56:290-297. 62. Hopper PE. Immune-mediated joint diseases. In: Slatter D, ed. Textbook of Small Animal Surgery, 2nd edn. Philadephia:W.B. Saunders, 1993;1928-1937. 63. Galloway RH, Lester SJ. Histopathological evaluation of canine stifle joint synovial membrane collected at the time of repair of cranial cruciate ligament rupture. J Anim Hosp Assoc 1995;31:289-294.



56



CHAPTER 1



1.3. Cranial cruciate ligament rupture in the dog. A review of diagnostic techniques



57



58



CHAPTER 1.3: Review



SUMMARY Different techniques are available for diagnosing cranial cruciate ligament (CCL) rupture in the dog. A review is given on clinical features and laxity tests. Direct and indirect radiographic signs are described. Less available diagnostic modalities that may be useful in the diagnosis and diffential diagnosis of cruciate insufficiency are briefly discussed.



INTRODUCTION Sometimes, the clinician will suspect a cranial cruciate ligament rupture (CCL) based on the history reported by the dog owner. However, individual clinical signs can vary greatly. In the vast majority of cases, the dog becomes acutely lame following rupture of the CCL. It refuses to use the affected limb which is held in a flexed position. Thereafter, the limb will be carried in a walking position, without putting weight on it.1 After a week to 10 days, the dog start using the leg but walks with a distinct limp. At rest, only the toes touch the ground. In more than half of the cases, the owner is not aware of a real cause of the injury. If he is, most of the dogs were jumping or running on uneven territory.2-4 Quite often, the problems are more insidious. In the early disease state, the only clinical signs are a stiffer hindlimb gait, an irregular pace, or excercise intolerance. Sometimes, the affected leg is dragged.5 During the last decade, an increasing number of young, large breed dogs have been presented with intermittent hind limb lameness. Often the problem can be attributed to stifle instability due to partial tearing of the CCL.5-7 Particularly bilateral rupture of the CCL is often erroneously attributed to neurologic disorders.8,9



DIAGNOSIS Clinical examination



Inspection—The dog has to be viewed from behind and from the side at rest in the standing position to assess the position and angle of the stifle joint and to assess the degree of



59



CHAPTER 1.3: Review weight-bearing.10 The patient’s stance should be carefully screened for skeletal abnormalities which may predispose to CCL rupture.11 Some affected dogs are not able to sit in a full squat. They hold the affected limb in a nonphysiological way beside the body because pain or fibrosis impede full flexion of the stifle.12,13 Most of the dogs are presented with a well-defined unilateral lameness.3 In some cases, the dog is bilaterally stiff without an obvious limp.5 A change in limb angulation might be detected.14,15 At touchdown, the stifle joint is often kept in extension to avoid pain due to impingement on the menisci.16



Palpation—The exact clinical diagnosis of stifle lameness is not an easy matter and requires experience and skill. As in humans,17,18 CCL rupture is overlooked initially in a rather high proportion. Palpation of the affected stifle usually elicts a painful response.10,19,20



The joint is



obviously swollen what causes indistinct margins of the patellar tendon. The patellar tendon might be relaxed due to cranial displacement of the tibia.21 A firm medial swelling due to capsular fibrosis or even new bone formation can be felt in longstanding cases.2,9,20,22 Atrophy of the quadriceps muscle group can be appreciated very soon after the start of the problems.1,5,11,23,24



In cases with serious pain and crepitation during passive motion,



osteophytosis is almost always present on the preoperative radiographs.25 It is not imperative for concurrent meniscal damage to produce a clicking noice or a snap as the medial condyle is forced over the caudal edge of the medial meniscus. An audible click can be produced by the femorotibial instability only as well.26-28 Classically, increased endorotation of the tibia in combination with a cranial drawer sign are pathognomonic features for rupture of the CCL.3,29-31 The stifle is tested in an unloaded condition so that only the ligamentous contribution to joint stability is to be detected. The drawer sign has been described on a semi-flexed stifle, by exerting cranial pressure on the fibular head (Fig 1 A).



Correct positioning of the examiner’s hands is important in



performing the test properly.9 Meanwhile, one should avoid inward rotation at the tarsal level and the femur has to be immobilised.10 The goal of the drawer test is to evaluate the integrity of the CCL by determining cranial translation of the tibia (‘drawer sign’). The amount of abnormal displacement depends of course upon the choice of the original neutral position of the tibia.32 Since testing is often painful, the dog’s resistance to manipulation and increased muscle tone might mask the cranial shifting of the proximal tibia. In inconclusive cases, 60



CHAPTER 1.3: Review sedation or even general anaesthesia will be necessary to make a correct diagnosis of subtle instability.5,11,19 Additionally, the same test should be repeated with the stifle joint under a greater angle of flexion. In cases where there is only partial rupture of the CCL, only the craniomedial bundle might be damaged. On a quite straight leg, tension in the intact fibres of the caudolateral band can provide enough craniocaudal stability to give negative test results.20,33 Special attention should also be given to the interpretation of the cranial drawer movement in skeletally immature dogs. A certain degree of cranial drawer of the proximal tibia is normal but it comes to an abrupt stop and is not associated with pain or effusion.5 Therefore, comparison with the clinical findings in the opposite hind leg often is helpful.



A Fig 1.



B



Manual tests to check for cranial cruciate instability in the dog A. Cranial drawer test B. Tibial compression test



61



CHAPTER 1.3: Review In addition to the cranial drawer test, the tibial compression test is a reliable alternate diagnostic tool whenever the craniocaudal instability is difficult to diagnose.3 It is tested on the stifle joint in a weight-bearing position, by placing the index finger on the tibial crest while the palm of the hand contours the femoral condyles. The other hand alternately extends and flexes the tibiotarsal joint (Fig 1 B). This movement mimics the contractions of the gastrocnemius muscles. In cases of rupture of the CCL, the tibia displaces cranially in respect to the femur what can be seen or palpated. Sedation is hardly ever necessary. Less pressure is exerted on the peri-articular tissues, which makes the subluxation of the proximal tibia less painful than when elicted by the cranial drawer test. A slight mechanical advantage is also encountered by counteracting the muscle tone since a conscious patient is less able to resist these forces. Another advantage is the ease of testing in larger dogs as compared to the classical cranial drawer test.3,34 In the early post-traumatic phase, similar results on instability are found by the classical cranial drawer test and the tibial compression test.



In chronic situations of cruciate



deficiency, both tests are less reliable. Thickening of the joint capsule and fibrosis increase the stability of the stifle joint and obscure the diagnosis of cruciate deficiency.3,10 Cranial displacement of the proximal tibia can also be blocked by the presence of a torn meniscus.10,26 During the manual tests, relatively small forces are excerted. Especially in cases of partial rupture and in heavy dogs, a false negative test result can be found, although the patient suffers clinically from joint laxity during normal activities.11 Whenever rupture of the CCL is complicated by tearing of the collateral ligament, a varus or valgus deviation is created by exerting stresses.34,35



In such cases, there is also a



tremendous increase in rotational instability on the extended stifle.30



Radiographic examination



Radiographs are a helpful adjunct to a careful history and a meticulous physical exam to support a tentative diagnosis.21 Pathologies other than cruciate disease can be ruled out by studying soft tissues and bony structures. A standard lateral projection of the affected stifle is indicated in the diagnosis of CCL rupture. mandatory.5,36



62



In very few cases, a craniodorsal view is



CHAPTER 1.3: Review Direct signs—In some cases, a certain degree of displacement of the tibia relative to the femoral condyles can be appreciated on the lateral projection, even when no special appreciation of this area is made.2 Backward sliding of the proximal tibia due to tension in the hamstring muscles might be blocked by a bucket-handle tear of the meniscus.16 In smaller breeds with prominent tibial tuberosities, a false impression can be given that the femur is articulating abnormally far backwards.23



Indirect signs—The first radiographic signs following CCL rupture are mainly situated in the soft tissues: the infrapatellar fat pad is no longer visible and the caudal joint capsule is distended.5,11 Apart from thickening of the capsular shadow, osteoarthrotic changes become visible.37 Larger dogs have consistently more severe radiographic signs of DJD.38,39 Within three to four weeks after experimental sectioning of the CCL, macroscopically visible arthrosis is present.40 The first changes are a sharpening of the distal and proximal rim of the patellar bone, followed by irregular bony proliferation on these spots and osteophyte formation alongside the ridges of the trochlear groove (Fig 2).2,5,39,41



3 2



1



4



Fig 2.



Localisation of the osteoarthrotic changes in cruciate-deficient stifle joints in the dog 1 2 3 4



63



lipping of the distal and proximal patella osteophyte formation on the fabellae sclerosis of the trochlear groove sclerosis of the tibial plateau



CHAPTER 1.3: Review Radiographic signs of DJD are not exclusively specific for CCL pathology, unless avulsion fragments are seen.42,43 When blurring and osteophyte deposits are seen at the tibia site of attachment of the CCL, they can be considered pathognomonic of ligament pathology.44,45 Increased sclerosis along the tibial plateau and on the rims of the femoral condyles can become apparent.46 In longstanding cases, osteophytes form a ‘balcony’ caudal to the tibial plateau. In contrast with humans,47-50 assessing the dimensions of the intercondylar notch is not commonplace in dogs.41,51,52 It is also mandatory to screen radiographically the contralateral stifle joint. Certain early changes encountered on radiographs can contribute to the prediction of bilateral cruciate problems.5,53 Normal cruciate ligaments were screened succesfully in dogs’ stifles by contrast arthrography but the technique did not appear helpful in evaluating cruciate pathology.54,55



Arthroscopy



If the diagnosis on clinical and radiological findings remains tentative, arthroscopy is a useful diagnostic tool. It is relatively atraumatic compared to exploratory arthrotomy.56,57 Dogs, like human patients,58,59 regain a normal gait much faster following an arthroscopic procedure than after an arthrotomy.56,60 Especially in the diagnosis of partial cranial cruciate rupture, arthroscopy can be very useful.56,61,62 During the procedure, specific flexion and extension angles, rotation, and varus and valgus stresses have to be used to augment the efficacy and reliability of this examination method.60



In cases of severe inflammation,



hypertrophic villi might blur the view.62,63 To detect simultaneous meniscal lesions, new portals should still be evaluated as arthroscopy fails to detect damage to the menisci in 50 per cent of the dogs.57,61,64 The increasing popularity of intra-articular reconstructive techniques means that exploratory arthrotomy remains somewhere between diagnosis and treatment.56 In dogs, arthroscopic-assisted CCL reconstructions are still in the experimental phase.65,66



64



CHAPTER 1.3: Review Other techniques Ultrasonography of the stifle can be used as completion of radiographic examination.67-69 Although a diagnosis of CCL rupture in dogs is possible by ultrasound, it can be very difficult to reproduce sonographic findings in the canine stifle.68,69 Scintigraphy provides an indication of disease processes in many joint disorders.



It



appears to be a useful method for staging OA in unstable canine stifle joints, supplying additional information to that seen on radiographs.70 Even in human medicine, however, scintigraphical findings do generally not provide information on the status of the ACL unless there is an avulsion of the attachment.71 Computed tomography is also superior to standard radiography in the detection of very small avulsion fragments.a Magnetic resonance imaging is becoming more and more popular in the diagnosis of cruciate ligament and meniscal injuries in man and has proven to be extremely accurate.72-78 Being totally non-invasive, the technique also does not expose the patient to ionising radiation. Magnetic resonance has an accuracy exceeding that of arthrography and has been demonstrated to be as sensitive and specific as arthroscopy whenever the ACL can be brought clearly into view.11,73 In dogs, normal cruciate ligaments were screened successfully by magnetic resonance.79-81 However, only limited information was given on their clinical relevance as diagnostic tools in pathological joints.81



CONCLUSION In the majority of cases, a thorough clinical examination of the dog leads to a tentative diagnosis of CCL rupture. The injury is often not recognised early in the disease process. Radiography of both stifle joints is a particularly useful supplement to clinical examination. To avoid the risk of morbidity associated with an unnecessary arthrotomy, the diagnosis can be confirmed by viewing the CCL with an arthroscope.



a



van Bree H. Personal communication 2001



65



CHAPTER 1.3: Review REFERENCES 1.



Lieben NH. Intra-articulaire kniestabilisatie met synthetisch stabilisatietechniek. Tijdschr Diergeneesk 1986;23:1160-1166.



materiaal.



Een



praktijkgerichte



2.



Pond MJ, Campbell JR. The canine stifle joint. I. Rupture of the anterior cruciate ligament. An assessment of conservative and surgical treatment. J Small Anim Pract 1972;13:1-10.



3.



Henderson RA, Milton JL. The tibial compression mechanism: a diagnostic aid in stifle injuries. J Am Anim Hosp Assoc 1978;14:474-479.



4.



Drapé J, Ghitalla S, Autefage A. Rupture du ligament croisé antérieur (L.C.A.) chez le chien: pathologie traumatique ou dégénérative? Point Vét 1990b;22:573-580.



5.



Bennett D, Tennant D, Lewis DG, et al. A reappraisal of anterior cruciate ligament disease in the dog. J Small Anim Pract 1988;29:275-297.



6.



Denny HR, Barr ARS. A further evaluation of the ‘over the top’ technique for anterior cruciate ligament replacement in the dog. J Small Anim Pract 1987;28:681-686.



7.



Scavelli TD, Schrader SC, Matthiesen TD. Incomplete rupture of the cranial cruciate ligament of the stifle joint in 25 dogs. Vet Surg 1989;18:80-81.



8.



Wheeler SJ, Sharp NJH. Patient examination. In: Wheeler SJ and Sharp NJH, eds. Small Animal Spinal Disorders. Diagnosis and Surgery. London:Mosby-Wolfe, 1994;21-30.



9.



Muir P. Physical examination of lame dogs. Comp Contin Educ 1997;19:1149-1160.



10. Rudy RL. Stifle joint. In: Archibald J, ed. Canine surgery. Santa Barbara:American Veterinary Publications Inc, 1974;1104-1115. 11. Johnson JM, Johnson AL. Cranial cruciate ligament rupture. Pathogenesis, diagnosis, and postoperative rehabilitation. Vet Clin North Am (SAP) 1993;23:717-733. 12. Schawalder P, Gitterle E. Eigene Methoden zur operativen Rekonstruktion bei Ruptur des vorderen und hinteren Kreuzbandes. Kleintierpraxis 1989;34:323-330. 13. Slocum B, Devine T. Tibial plateau leveling osteotomy for repair of cranial cruciate ligament rupture in the canine. Vet Clin NA:SAP 1993;23:777-795. 14. Korvick DL, Pijanowski GJ, Schaeffer DJ. Three-dimensional kinematics of the intact and cranial cruciate ligament-deficient stifle of dogs. J Biomech 1994;27:77-87. 15. Vilensky JA, O’Connor BL, Brandt KD, et al. Serial kinematic analysis of the unstable knee after transection of the anterior cruciate ligament: temporal and angular changes in a canine model of osteoarthritis. J Orthop Res 1994;12:229-237. 16. Slocum B, Devine T. TPLO: Tibial Plateau Leveling Osteotomy for treatment of cranial cruciate ligament injuries. Proceedings 10th ESVOT Congress, Munich, 23-26th March 2000;37-38. 17. Strand T, Sörensen FK, Solheim E. Undiagnosed anterior cruciate ligament rupture. A common problem with poor prognosis. Ann Chir Gynaec 1997;86:244-247. 18. Bollen S. Ligament injuries of the knee - Limping foward? Br J Sports Med 1998;32:82-84. 19. Arnoczky SP. The cruciate ligaments: the enigma of the canine stifle. J Small Anim Pract 1988;29:71-90. 20. Scavelli TD, Schrader SC, Matthiesen DT, et al. Partial rupture of the cranial cruciate ligament of the stifle in dogs: 25 cases (1982-1988). J Am Vet Med Assoc 1990;196:1135-1138.



66



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21. Keller WF. Diagnosing stifle lameness in dogs. J Am Vet Med Assoc 1965;146:1069-1072. 22. Tomlinson J, Constantinescu GM. Two methods for repairing ruptures of the cranial cruciate ligament in dogs. Vet Med 1994;32-41. 23. Singleton WB. The diagnosis and surgical treatment of some abnormal stifle conditions in the dog. Vet Rec 1957;69:1387-1394. 24. Meutstege FJ, Arnoczky SP, Hazewinkel HAW, et al. Canine cruciate and meniscal problems. Proceedings. Voorjaarsdagen 1980;PAO 12:68-74. 25. Heffron LE, Campbell JR. Osteophyte formation in the canine stifle joint following treatment for rupture of the cranial cruciate ligament. J Small Anim Pract 1979;20:603-611. 26. Flo GL, DeYoung D. Meniscal injuries and medial meniscectomy in the canine stifle. J Am Anim Hosp Assoc 1978;14:683-689. 27. Drapé J, Ghitalla S, Autefage A. Lésions méniscales et rupture du ligament croisé antérieur: étude rétrospective de 400 cas. Point Vét 1990;22:467-474. 28. Bennett D, May C. Meniscal damage associated with cruciate disease in the dog. J Small Anim Pract 1991;32:111-117. 29. Carlin I. Ruptur des Ligamentum cruciatum anterius im Kniegelenk beim Hund. Arch Wissensch Prakt Tierh 1926;54:420-423. 30. Arnoczky SP, Marshall JL. The cruciate ligaments of the canine stifle: an anatomical and functional analysis. Am J Vet Res 1977;38:1807-1814. 31. Heffron LE, Campbell JR. Morphology, histology and functional anatomy of the canine cranial cruciate ligament. Vet Rec 1978;102:280-283. 32. Burstein AH, Wright TM. Joint stability. In: Passano III WM, Mason D, eds. Fundamentals of Orthopaedic Biomechanics. Baltimore:Publication Services Inc, 1994;63-93. 33. Tarvin GB, Arnoczky SP. Incomplete rupture of the cranial cruciate ligament in a dog. Vet Surg 1981;10:9495. 34. Kirby BM. Decision-making in cranial cruciate ligament ruptures. Vet Clin North Am:SAP 1993;23:797819. 35. Egger EL. Collateral ligament injuries. In: Bojrab MJ, ed. Current Techniques in Small Animal Surgery. Philadelphia:Lea and Febiger, 1990;700-701. 36. Meinen JJ, Verbeek M. Voorste kruisbandlaesies bij de hond: een evaluatie van therapie, klinisch en röntgenologisch verloop bij 215 patiënten. Referaat. Geneeskunde van het Kleine Huisdier, Vakgroep Radiologie, Rijksuniversiteit te Utrecht 1980. 37. Brünnberg L. Klinische Untersuchungen zu Ätiologie und Pathogenese der Ruptur des Ligamentum cruciatum craniale beim Hund. 2. Mitteilung: Zur Ätiologie und Diagnose der Ruptur des Ligamentum cruciatum craniale beim Hund. Kleintierprax 1989;34:445-449. 38. Vasseur PB. Clinical results following nonoperative management for rupture of the cranial cruciate ligament in dogs. Vet Surg 1984;13:243-246. 39. Elkins AD, Pechman R, Kearny MT, et al. A retrospective study evaluating the degree of degenerative joint disease in the stifle joint of dogs following surgical repair of anterior cruciate ligament rupture. J Am Anim Hosp Assoc 1991;27:533-539.



67



CHAPTER 1.3: Review



40. Tirgari M. The surgical significance of the blood supply of the canine stifle joint. J Small Anim Pract 1978;19:451-462. 41. Vasseur PB, Berry CR. Progression of stifle osteoarthrosis following reconstruction of the cranial cruciate ligament in 21 dogs. J Am Anim Hosp Assoc 1992;28:129-136. 42. Park RD. Radiographic evaluation of the canine stifle joint. Comp Cont Ed 1979;1:833-841. 43. Reinke JD. Cruciate ligament avulsion injury in the dog. J Am Anim Hosp Assoc 1982;18:257-264. 44. Tirgari M, Vaughan LC. Arthritis of the canine stifle joint. Vet Rec 1975;96:394-399. 45. Tirgari M. Changes in the canine stifle joint following rupture of the anterior cruciate ligament. J Small Anim Pract 1977;19:17-26. 46. Brünnberg L, Rieger I, Hesse EM. Sieben Jahre Erfahrung mit einer modifizierten “Over-the-Top”Kreuzbandplastik beim Hund. Kleintierprax 1992;37:735-746. 47. Anderson AF, Lipsocomb AB, Liudahl KJ, et al. Analysis of the intercondylar notch by computed tomography. Am J Sports Med 1987;15:547-552. 48. Souryal TO, Moore HA, Evans JP. Bilaterality in anterior cruciate ligament injuries: Associated intercondylar notch stenosis. Am J Sports Med 1988;16:449-454. 49. Harner CD, Paulos LE, Greenwald AE, et al. Detailed analysis of patients with bilateral anterior cruciate ligament injuries. Am J Sports Med 1994;22:37-43. 50. Shelbourne KD, Davis TJ, Klootwyk TE. The relationship between intercondylar notch width of the femur and the incidence of anterior cruciate ligament tears. A prospective study. Am J Sports Med 1998;26:402408. 51. Aiken SW, Kass PH, Toombs JP. Intercondylar notch width in dogs with and without cranial cruciate ligament injuries. Vet Comp Orthop Traumatol 1995;8:128-132. 52. Fitch RB, Montgomery RD, Milton JL, et al. The intercondylar fossa of the normal canine stifle: An anatomic and radiographic study. Vet Surg 1995;24:148-155. 53. Doverspike M, Vasseur PB, Harb MF, et al. Contralateral cranial cruciate ligament rupture: Incidence in 114 dogs. J Am Anim Hosp Assoc 1993;29:167-170. 54. Atilola MA, Pennock PW, Sumner-Smith G. Evaluation of analytical grade of metrizamide for canine stifle arthrography. J Am Vet Med Assoc 1984;185:436-439. 55. Hay CW, Aon DN, Roberts R et al. Evaluation of positive contrast arthrography in canine cranial cruciate ligament disaese. Vet Comp Orthop Traumatol 1996;9:10-13. 56. Miller CW, Presnell KR. Examination of the canine stifle: arthroscopy versus arthrotomy. J Am Animl Hosp Assoc 1985;21:623-629. 57. Van Ryssen B, van Bree H, Missine S. Een overzicht van 200 arthroscopieën bij 150 kleine huisdieren. Vlaams Diergeneeskd Tijdschr 1993;62:87-94. 58. Gillquist J, Oretorp N. Arthroscopic partial meniscectomy: technique and long term results. Clin Orthop Rel Res 1982;167:29-33. 59. Patel D, Fahmy N, Sakayan A. Isokinetic and functional evaluation of the knee following arthroscopic surgery. Clin Orthop 1982;167:84-91.



68



CHAPTER 1.3: Review



60. Person MW. A procedure for arthroscopic examination of the canine stifle joint. J Am Anim Hosp Assoc 1985;21:179-186. 61. van Gestel MA. Diagnostic accuracy of stifle arthroscopy in the dog. J Am Anim Hosp Assoc 1987;23:305315. 62. Van Ryssen B. The stifle. In: Arthroscopy in the diagnosis and treatment of osteochondrosis in the dog. Thesis. Department of Diagnostic Imaging of Domestic Animals, Faculty of Veterinary Medicine, Ghent University, Belgium 1996;111-124. 63. Lewis DD, Goring RL, Parker RB, et al. A comparison of diagnostic methods used in the evaluation of early degenerative joint disease in the dog. J Am Anim Hosp Assoc 1987;23:305-315. 64. Fehr M, Behrends I, Meyer-Lindenberg A. Die arthroskopische untersuchung des Kniegelenkes des Hundes. Tierärztl Prax 1996;24:137-143. 65. Person MW. Prosthetic replacement of the cranial cruciate ligament under arthroscopic guidance. A pilot project. Vet Surg 1987;16:37-43. 66. Puymann K, Knechtl G. Behandlung der Ruptur des kranialen Kreuzbandes mittels Arthroskopie und minimal-invasiver Haltebandtechnik beim Hund. Kleintierprax 1997;42:601-612. 67. Reed AL, Payne JT, Constantinescu GM. Ultrasonographic anatomy of the normal canine stifle. Vet Radiol Ultrasound 1995;36:315-321. 68. Engelke A, Meyer-Lindenberg A, Nolte I. Die Ultraschalluntersuchung des inneren Kniegelenkes bei Hunden mit Kreuzbandriss. Dtsch Tierärztl Wschr 1997;104:114-117. 69. Kramer M, Stengel H, Gerwing M, et al. Sonography of the canine stifle. Vet Radiol Ultrasound 1999;40:282-293. 70. Innes JF, Barr ARS, Patteson MW, et al. Scintigraphy in the evaluation of osteoarthritis of the canine stifle joint. Vet Comp Orthop Traumatol 1996;9:53-59. 71. Murray IPC, Dixon J, Kohan L. SPECT for acute knee pain. Clin Nuclear Med 1990;15:828-840. 72. Reicher MA, Hartzman S, Bassett LW, et al. MR Imaging of the knee. Part I. Traumatic disorders. Radiol 1987;162:547-551. 73. Polly DW, Callaghan JJ, Sikes AA, et al. The accuracy of selective magnetic resonance imaging compared with the findings of arthroscopy of the knee. J Bone Joint Surg (Am) 1988;70-A:192-198. 74. Mink JH, Levy T, Crues JV. Tears of the anterior cruciate ligament and menisci of the knee : MR Imaging evaluation. Radiol 1988;167:769-774. 75. Boeree NR, Watkinson AF, Ackroyd CE, et al. Magnetic resonance imaging of meniscal and cruciate injuries of the knee. J Bone Joint Surg (Br) 1991 ;73-B :452-457. 76. Fisher SP, Fox JM, Delpizzo W, et al. Accuracy of diagnosis from magnetic resonance imaging of the knee. J Bone Joint Surg (Am) 1991;73-A:2-10. 77. Boeree NR, Ackroyd CE. Magnetic resonance imaging of anterior cruciate ligament rupture. A new diagnostic sign. J Bone Joint Surg (Br) 1992;74-B:614-616. 78. Lee K, Siegel MJ, Lau DM, et al. Anterior cruciate ligament tears: MR Imaging-based diagnosis in a pediatric population. Rad 1999;213:697-704. 79. Widmer WR, Bucbwalter KA, Braunstein EM, et al. Principles of magnetic resonance imaging and application to the stifle joint in dogs. J Am Vet Med Assoc 1991;198:1914-1922.



69



CHAPTER 1.3: Review



80. Baird DK, Hathcock JT, Rumph PF, et al. Low-field magnetic resonance imaging of the canine stifle joint : Normal anatomy. Vet Radiol Ultras 1998;39:87-97. 81. Konar M, Kneissl S. Magnetic resonance imaging of the cruciate ligaments in the dog. Vet Radiol Ultrasound 1999;40:557-558.



70



CHAPTER 1



1.4. Cranial cruciate ligament rupture in the dog. A review of treatments



71



72



CHAPTER 1.4: Review



SUMMARY A review of treatment of cranial cruciate ligament (CCL) rupture is outlined. Conservative treatment as well as extra- and intra-articular techniques are considered. Many surgical procedures have been listed. Among veterinarians, there is no consensus on the techniques for repairing a torn CCL in the dog.



INTRODUCTION Surgical repair of a ruptured cranial cruciate ligament (CCL) in dogs has been wellassimilated into veterinary publications. Nevertheless, a lot of controversy is still evoked by treating ruptured CCLs in the dog. The fundamental rationale of surgery is to restore stifle stability and to prevent further deterioration of the joint after debridement. The enormous variety of surgical techniques described in the literature indicates that none has proved to be totally satisfactory.1,2



Outcome is variable and seems to be relatively independent of



technique. Until now, more than one hundred techniques have been documented.3 Roughly, the surgical procedures can be divided into three major categories (extracapsular, intracapsular, and tibial plateau leveling techniques). The main principle of the extracapsular techniques is to buttress the tissues lateral to the joint by craniocaudally oriented sutures.1 Another extra-articular way of stabilising the cruciate deficient stifle joint is fibular head transposition.4 Plenty of materials have been studied for intracapsular replacement of the damaged CCL. A strip of the fascia lata was the first prosthesis ever used.5 Other autografts such as skin,6 the tendon of the peroneus longus muscle7 or the long digital extensor muscle,8 and a part of the patellar bone attached to the straight patellar ligament9 are described as natural substitute materials. considered.



On the other hand, synthetic prostheses have also been



In one study, nylon10 was implanted, followed by Teflon11 and Terylene12



implants. Recently, there has been more interest in collagen-inducing materials e.g. carbon fibres13 and polyester14.



The tibial plateau leveling techniques require orthopaedic



reconstructions of the proximal tibia to neutralise cranial tibial thrust during weight bearing.1517



73



CHAPTER 1.4: Review



THERAPY In 1926, Carlin first mentioned CCL rupture in the stifle joint of the dog.18 It was the start of a whole cascade of studies and reports on possible causes and methods of treatment.2 The first really extensive scientific study was published in 1952.5



Conservative treatment According to Paatsama and Arnoczky, conservative treatment in dogs is a waste of time.1,5 They recommended immediate surgical stabilisation. However, other researchers found a 90% success rate after non-surgical treatment in dogs weighing less than 15kg. Heavier dogs did not do so well, with only 1 in 3 having an acceptable clinical outcome.9,19,20



The



surprisingly good results of non-surgical treatment in small dogs might be attributed to the lower demands and the smaller loads on the unstable stifle. Most often, those patients are geriatric and thus less active as well.20 Conservative treatment should be considered a viable alternative to surgical stabilisation for these patients, at least initially.21 In the presence of generalised joint disorders such as rheumatoid arthritis and lupus erythematosus, operative treatment of the ruptured ligament is completely contra-indicated.22 Restricted activity (short walks on the leash) for 3 to 6 weeks, weight control and analgesic medication during periods of discomfort are part of the conservative protocol.20



Anti-



inflammatory drugs might be administered for short periods to treat arthritis pain.19,22,23



Surgical correction



Instability leads to progressive degenerative changes within the affected stifle joint shortly after the injury. For this reason, conservative treatment is often a waste of time.1,5 Whether or not the CCL rupture should be treated surgically, depends on functional as well as on objective criteria.24 In cases of severe instability, especially in large breed dogs or working animals, or when problems are present for more than 6 to 8 weeks, surgery is strongly recommended.19,22



74



CHAPTER 1.4: Review There is no unanimous opinion on possible regeneration and healing of partially ruptured CCLs.25-28 It is not fully clear whether such cruciate ligaments have to be replaced or whether further tearing can be avoided.26 Several investigations show that lameness and pain during manipulation of the affected stifle joint are also present in cases of partial tearing of the CCL, even when there is minimal or no detectable instability.25,27,28 Therefore, surgical intervention is also required in these cases. Meniscal pathology is often seen concurrently with or as a consequence of rupture of the CCL and always requires surgical intervention. It is mainly the medial meniscus which shows disease.29-36 Meniscal surgery is performed following the arthrotomy and before the CCL is repaired.



Most mensical injuries are amendable to partial resection, removing only the



abnormal section (Fig 1 A). Partial meniscectomy is to be preferred where possible over total meniscectomy because it has been shown to produce less degenerative joint changes (DJD).33,35,37,38 Other surgeons prefer total meniscectomy due to the smaller risk of iatrogenic laceration of the joint cartilage or CaCL with the scalpel blade (Fig 1 B).30,39 Quite recently, meniscal release was introduced to prevent meniscal damage in cruciate deficient stifles with intact menisci at the time of arthrotomy.40 The caudal horn of the medial meniscus is freed by a sagittal incision just medial to its lateral attachment on the intercondyloid eminence (Fig 2 A) or by an incision caudal to the medial collateral ligament (Fig 2 B). The purpose of meniscal release is to allow the medial meniscus to move away from the crushing action of the medial femoral condyl during cranial translation of the tibia.40-42



The first surgical method of treating CCL rupture in dogs was introduced in 1952 and was based on the concept of ligament replacement with autologous tissue.5 Many years later, a new surgical concept was developed where the craniocaudal joint instability was corrected without any attempt to replace the ruptured CCL.43 Several comparative studies document the efficacy of different stabilisation techniques.9,44-46



In 1976, Knecht published a



comprehensive review of the surgical methods of treatment.2 Several modifications have been developed since.3 According to Arnoczky, no one technique has been proven to be superior in all categories of patients.22



75



CHAPTER 1.4: Review



A Fig 1.



B



Principle of meniscectomy in the dog in case of a damaged medial meniscus A. Partial meniscectomy. A curved hemostat is attached to the torn strip of the meniscus and the remaining peripheral attachments are dissected free B. Total meniscectomy. Incision of ligament and capsule attachments CaCL Caudal cruciate ligament, CCL Cranial cruciate ligament, LM Lateral meniscus, MM Medial meniscus, TT Tibial tubercle



A Fig 2.



B



Principle of meniscal release in the dog in case of an intact medial meniscus A. Incision just medial to the lateral attachment of the caudal horn of the medial meniscus B. Incision caudal to the medial collateral ligament



76



CHAPTER 1.4: Review Extra-articular techniques—In cats and small dogs, satisfactory postoperative results are achieved following extra-articular stabilisation of cruciate-deficient stifle joints.43,47 Even in heavier dogs, lateral imbrication techniques are used.48,49 While there are many extra-articular techniques, the basic principle is to stabilise the joint by reinforcing and thickening periarticular soft tissue by craniocaudally oriented sutures.1 Generally, these procedures are easy to perform.



Biomechanically, these extra-articular



procedures are far from ideal.50,51 The normal degree of inward tibial rotation in respect to the femur is also prohibited and abnormal loading can occur. Complications, such as tearing of soft tissues or of the suture material, are encountered.52,53 One of the first techniques described uses multiple Lembert sutures in chromic catgut on the lateral aspect of the joint capsule.43 Pearson and others improved this technique by placing three layers of sutures.54 Meanwhile, De Angelis and Lau described a single mattress suture in Polydek, from the lateral fabella sesamoid to the lateral third of the straight patellar ligament or through a bone tunnel in the tibial crest (lateral fabellotibial loop).55



In a



modification of this technique, an extra medial suture was placed.52 The synthetic material can be replaced by an extra-articular fascia lata strip to restore normal stifle biomechanics in dogs under 15 kg of body weight.56 Olmstead published on 5 years experience with stainless steel wire as lateral buttress in dogs of various weights.57 A few years ago, a crimp clamp system has been developed for nylon leader material to avoid large bulky knots when creating the loop.58 Irrespective of the material used, however, all lateral fabellotibial sutures may break or loosen after surgery.



But it is believed that short-time stabilisation allows



periarticular fibrosis to become established, which provides long-term stifle joint stability.57,59 In practice, lateral suture stabilisation is still the preferred method of repair in small dogs.49 Another technique providing lateral and medial support was developed by Hohn and Newton in 1975.60 A medial arthrotomy is performed, the caudal belly of the sartorius muscle is transected and reattached more cranially to the straight patellar ligament. Laterally, 2 mattress sutures are placed on the capsule. Then, the biceps and its fascia lata are plied over the patellar ligament and sutured. More recently, an easy extra-articular procedure has been introduced by Meutstege. He recommends low imbrication of the lateral fascia using a resorbable suture material, after cleaning-up of the affected joint.48 In a last extra-articular technique, the head of the fibula is attached in a more cranial position, by a tension band wire or by the use of a cortical screw.4,61 In this way, the lateral collateral ligament is reorientated and tensioned to stabilise the cruciate-deficient stifle joint. 77



CHAPTER 1.4: Review Intra-articular techniques—The intra-articular techniques are theoretically preferable over the extra-articular as they allow for more accurate substitute of the ruptured CCL.62 Even in cases of fresh tearing and perfect apposition, the CCL will not regain its original strength.63 Only by anatomic restoration of recent CCL avulsion fractures, normal ligament function during all positional changes of the stifle joint can be restored.64 Extensive studies examined the properties of ideal substitue materials and the true anatomical position.65 The prosthesis should mimic the original cruciate in preventing cranial displacement of the tibia and in controlling hyperextension of the stifle.22



Incorrect



orientation of the graft might result in wearing of the material leading to a definite failure.66 In 1952, a modification on the human Hey Groves technique67 was described as a method of treatment in cranial cruciate deficient dogs.5 A fascia lata strip is created to construct a transplant ligament. It is pulled through the joint via a hole drilled in the lateral femoral condyle to the intercondylar groove and a tunnel drilled from the point of attachment of the CCL to a point medial to the tibial crest. The strip is tightened and reattached to the straight patellar ligament.



Small changes in the technique have been described since the first



publication.2 Singleton fixed the graft at the proximal and at the distal end of the bone tunnels by use of orthopaedic screws.68



A major modification was introduced by Rudy.37



Osteophytes are removed, meniscectomy is performed whenever there is damage, and an orthopaedic wire is applied from the lateral fabella to the tibial tuberosity to act as an internal splint. Instead of using the fascial graft, Gibbens lead chemically treated skin through bone tunnels oriented as originally described by Paatsama.6



Meanwhile a patellectomy is



performed if concurrent patellar luxation has to be corrected. Other experiments were carried out: Leighton tested untreated skin,69 Foster and colleagues drilled the bone tunnels more cranially without opening up the joint.70 For the ‘Over-the-Top’ technique, the medial third of the patellar ligament, the craniomedial part of the patella and fascia lata are all included in the flap.66 The freed strip is pulled proximally through the intercondylar groove and it is attached to the soft tissue above the lateral femoral condyle. To better mimic the anatomical insertion place, the graft can be lead under the intermeniscal ligament first.71 Another possibility is to prepare a lateral strip, as Denny and Barr did, which can be lead through an oblique tunnel in the tibia, starting from the original place of insertion of the CCL.72,73 Other tendon transpositions have been used: the tendon of the peroneus longus muscle,7 the long digital flexor tendon74 and the long digital extensor tendon8,75,76. In experimental trials, 78



CHAPTER 1.4: Review reconstruction of the cruciate ligaments was done by fresh and freeze-dried allografts of patellar tendon and fascia lata.77,78 Freeze-dried specimens are well-tolerated, while fresh allografts may induce a foreign body response.



Implantation of frozen bone-CCL-bone



allografs is clinically not yet supported.79 Alternative methods of stabilisation of the CCL deficient stifle such as popliteal tendon transposition are still in the experimental phase.80 Veterinary surgeons as well as human orthopaedists became very interested in the possible use of different synthetic materials to substitute a ruptured CCL.22 Notwithstanding the positive results of preliminary studies, synthetic prostheses are still infrequently used in the veterinary world.81 Reconstructive materials have to be at least as strong as the original ligament, and preferably even stronger.82 Of course, biological inertia of the prostheses is also necessary, and only minimal tissue reaction may be provoked by the implantation.83,84 Removal of a synthetic implant may become obligatory at any time postoperatively.85 Another drawback is the relatively high cost of the implants.86 Support for double-bundle reconstructions for clinical use are so far not found.87,88 Several synthetic substitute materials have been tested. In 1960, Johnson started to use braided nylon.10 In the same year, a publication appeared on the use of Teflon-tubes.11 A lot of materials followed, although a large number of them were used without preliminary studies.2 Besides Teflon meshes,89 supramide,90,91 Terylene12 and Dacron14 were implanted. For use in dogs, a special Polydek prosthesis was developed.83 Fragmentation of carbon fibre substitutes has stimulated two opposing interpretations.92 According to some researchers, a neoligament develops progressively within the gradual weakened meshwork,13 others argue that only a constant inflammatory response is stimulated.93 Polyester also acts as a scaffoldtype device.14,94 It can be used as a fibre bundle or as a tape.94-97 More recently, arthroscopically-assisted intra-articular replacement of a ruptured CCL also gains more popularity in the veterinary world.97,98



Tibial plateau leveling techniques—The common objective of the classical extra- and intra-articular procedures is the elimination of the cranial drawer sign.22 In 1984, a new concept was introduced by the study on cranial tibial wedge osteotomy.15 To gain joint stability, an orthopaedic reconstruction is required which enhances the action of the stifle flexors of the thigh. It has to be followed by another stabilising technique to control internal rotation of the tibia. Tibial plateau leveling osteotomy (TPLO), using a curved osteotomy and a special plate for fixation, has been introduced in 1993.16 In a modification, a wedge osteotomy to the level of the tibial plateau and screws for fixation are used.17 The goal of 79



CHAPTER 1.4: Review TPLO surgery is to neutralise cranial translation of the tibia during weight bearing and ambulation. The cranial drawer sign during passive manipulation is not eliminated. The principle of the surgery is to rotate the sloped tibial plateau until it is level, thus causing the weight bearing forces to be compressive only. It is recently postulated, however, that the procedure generates caudal tibial thrust making stifle stability dependent on CaCL integrity.99 In order to avoid excessive stress on and damage to the caudal horn of the medial meniscus, a medial meniscal release is performed by transection of the lateral attachment of the caudal horn as adjunct procedure.40,42



In humans, the importance of rehabilitation programs is well-understood. Conditioning of the antagonist muscles (hamstrings) seem to play an important role to stabilise a knee lacking the original ACL.100 Little note is taken to the benefits of postoperative rehabilitation on the final outcome of surgery in dogs so far.23,98,101,102



PROGNOSIS AFTER TREATMENT Conservative treatment gives a satisfactory clinical improvement in about 85 per cent of dogs weighing less than 15 kg but only in 19 per cent of heavier patients.9,19,20 All animals develop osteoarthritis (OA).1,103 Furthermore, there is an increased risk of future damage of the medial meniscus.104 The success rate of surgical treatment is multi-factorial and depends on surgeon experience and on the studied population. The subjectivity of the surgeon in assessing clinical and radiographic results influences the outcome as well.73 Most of the authors report a satisfactory functional recovery in 80 to 98 per cent of the dogs operated on. After successful surgery, the limb is fully functional within 8 to 12 weeks postoperatively.71,72,91,94,105 According to others, however, optimal results are only achieved after 12 months.3,106 No correlation can be shown between postoperative stability and the progression of osteophytes.107-110 It is clear that OA increases in the postoperative period. Until now, no technique is able to stop this evolution.109,110 On the other hand, the clinical success seems independent of the degree of radiographic OA.23,28,107,108



80



CHAPTER 1.4: Review The percentage of patients with concomitant meniscal injury seems related to the chronicity of the untreated cruciate injury.104 This phenomenon is not related to the age nor to the sex of the dogs. The firmly attached medial meniscus runs the risk of being compressed between the moving joint surfaces in the unstable stifle joint.111 The final prognosis is negatively influenced by the concurrent damage to the medial meniscus. The progression of OA changes is sped up, before and after surgery, when meniscal damage is present.4,104,112 There is no unanimity on the success in chronic cases with severe OA. Some studies do not show a significant increase in recovery.113



Others suggest that pre-operative DJD



adversely affects the final results.22,69,76 Older dogs also carry a poorer prognosis and might benefit more from conservative treatment with anti-inflammatory drugs and painkillers.22



In some cases, rupture of the contralateral CCL is encountered due to chronic overload.12,106 A bilateral problem is seen in about one third of the cruciate patients, with an interval of a few months.9,12,16,26,114,115 This relatively high incidence of contralateral damage within a year, further supports the hypothesis of degenerative etiology.26,114,115



CONCLUSION The plethora of techniques and prosthetic materials indicates that the ideal therapy for CCL rupture has not yet been invented. All surgical treatments only provide temporary stability. Meanwhile, periarticular fibrosis is responsible for the final stability of the stifle joint, notwithstanding the technique used. Little improvement has been made in preventing the progression of DJD after surgery. However, clinical success seems independent of the degree of joint changes. Cruciate disease remains an enigma on which a lot will be said and published in the future. The choice of treatment will greatly depend on the surgeon’s preference, since the ideal technique has yet to be discovered.



81



CHAPTER 1.4: Review REFERENCES 1.



Arnoczky SP. The cruciate ligaments: the enigma of the canine stifle. J Small Anim Pract 1988;29:71-90.



2.



Knecht CD. Evolution of surgical techniques for cruciate ligament rupture in animals. J Am Anim Hosp Assoc 1976;12:717-726.



3.



Brünnberg L, Rieger I, Hesse EM. Sieben Jahre Erfahrung mit einer modifizierten “Over-the-Top”Kreuzbandplastik beim Hund. Kleintierprax 1992;37:735-746.



4.



Smith GK, Torg JS. Fibular head transposition for repair of cruciate-deficient stifle in the dog. J Am Vet Med Assoc 1985;187:375-383.



5.



Paatsama S. Ligament injuries of the canine stifle joint: A clinical and experimental study. Thesis Helsinki 1952.



6.



Gibbens R. Patellectomy and a variation of Paatsama’s operation on the anterior cruciate ligament of a dog. J Am Vet Med Assoc 1957;131:557-558.



7.



Rathor SS. Experimental studies and tissue transplants for repair of the canine anterior cruciate ligament. MSU Vet 1960;20:128-134.



8.



Hohn RB, Miller JM. Surgical correction of rupture of the anterior cruciate ligament in the dog. J Am Vet Med Assoc 1967;150:1133-1141.



9.



Strande A. Repair of the ruptured cranial cruciate ligament in the dog. MS Thesis, University of Oslo, Baltimore:Williams and Wilkins Co 1967.



10. Johnson FL. Use of braided nylon as a prosthetic anterior ligament of the dog. J Am Vet Med Assoc 1960;137:646-647. 11. Emery MA, Rostrup O. Repair of the anterior cruciate ligament with 8mm tube Teflon in dogs. Canad J Surg 1960;4:11-17. 12. Singleton WB. Observations based upon the surgical repair of 106 cases of anterior cruciate ligament rupture. J Small Anim Pract 1969;10:269-278. 13. Jenkins DHR. Repair of cruciate ligaments with flexible carbon fibre. J Bone Joint Surg (Br) 1978;60B:520-524. 14. Hinko PJ. The use of a prosthetic ligament in repair of a torn anterior cruciate ligament in the dog. J Am Anim Hosp Assoc 1981;17:563-567. 15. Slocum B, Devine T. Cranial tibial wedge osteotomy: A technique for eliminating cranial tibial thrust in cranial cruciate ligament repair. J Am Vet Med Assoc 1984;184:564-569 16. Slocum B, Devine T. Tibial plateau leveling osteotomy for repair of cranial cruciate ligament rupture in the canine. Vet Clin NA:SAP 1993;23:777-795. 17. Koch DA. Anterior cruciate ligament (ACL) injury – Indications and methods of extraarticular reconstruction. Proceedings 1st Surgical Forum ECVS, Velbert 2001;7-8th July:284-290. 18. Carlin I. Ruptur des Ligamentum cruciatum anterius im Kniegelenk beim Hund. Arch Wissensch Prakt Tierh 1926;54:420-423. 19. Pond MJ, Campbell JR. The canine stifle joint. I. Rupture of the anterior cruciate ligament. An assessment of conservative and surgical treatment. J Small Anim Pract 1972;13:1-10.



82



CHAPTER 1.4: Review 20. Vasseur PB. Clinical results following nonoperative management for rupture of the cranial cruciate ligament in dogs. Vet Surg 1984;13:243-246. 21. Scavelli TD, Schrader SC. Nonsurgical management of rupture of the cranial cruciate ligament in 18 cats. J Am Anim Hosp Assoc 1987;23:337-340. 22. Arnoczky SP. Surgery of the stifle - The cruciate ligaments (Part I). Comp Cont Ed 1980;2:106-116. 23. Chauvet AE, Johnson AL, Pijanowski GJ, et al. Evaluation of fibular head transposition, lateral fabellar suture, and conservative treatment of cranial cruciate ligament rupture in large dogs: A retrospective study. J Am Anim Hosp Assoc 1996;32:247-255. 24. Franklin JL, Rosenberg TD, Paulos LE, et al. Radiographic assessment of instability of the knee due to rupture of the anterior cruciate ligament. J Bone Joint Surg (Am) 1991;73-A:365-372. 25. Ström H. Partial rupture of the cranial cruciate ligament in dogs. J Small Anim Pract 1990;31:137-140. 26. Bennett D, Tennant D, Lewis DG, et al. A reappraisal of anterior cruciate ligament disease in the dog. J Small Anim Pract 1988;29:275-297. 27. Scavelli TD, Schrader SC, Matthiesen TD. Incomplete rupture of the cranial cruciate ligament of the stifle joint in 25 dogs. Vet Surg 1989;18:80-81. 28. Kirby BM. Decision-making in cranial cruciate ligament ruptures. Vet Clin North Am:SAP 1993;23:797819. 29. Flo GL. Modification of the lateral retinacular imbrication technique for stabilising cruciate ligament injuries. J Am Anim Hosp Assoc 1975;11:570-576. 30. Flo GL, DeYoung D. Meniscal injuries and medial meniscectomy in the canine stifle. J Am Anim Hosp Assoc 1978;14:683-689. 31. Shires PK, Hulse DA, Liu W. The under-and-over fascial replacement technique for anterior cruciate ligament rupture in dogs: A retrospective study. J Am Anim Hosp Assoc 1984;20:69-77. 32. Drapé J, Ghitalla S, Autefage A. Lésions méniscales et rupture du ligament croisé antérieur: étude rétrospective de 400 cas. Point Vét 1990;22:467-474. 33. Bennett D, May C. Meniscal damage associated with cruciate disease in the dog. J Small Anim Pract 1991;32:111-117. 34. Elkins AD, Pechman R, Kearny MT, et al. A retrospective study evaluating the degree of degenerative joint disease in the stifle joint of dogs following surgical repair of anterior cruciate ligament rupture. J Am Anim Hosp Assoc 1991;27:533-539. 35. Bellenger CR. Knee joint function, meniscal disease, and osteoarthritis. Vet Quart 1995;17:S5-S6. 36. Moore KW, Read RA. Cranial cruciate ligament rupture in the dog - a retrospective study comparing surgical techniques. Austr Vet J 1995;72:281-285. 37. Rudy RL. Stifle joint. In: Archibald J, ed. Canine surgery. Santa Barbara:American Veterinary Publications Inc, 1974;1104-1115. 38. Cox JS, Nye CE, Schaefer WW, et al. The degenerative effects of partial and total resection of the medial meniscus in dog’s knees. Clin Orthop 1975;109:178-183. 39. Schaefer SL, Flo GL. Meniscectomy. In: Bojrab MJ, ed. Current techniques in small animal surgery. Baltimore:Williams and Wilkins, 1998;1193-1197.



83



CHAPTER 1.4: Review 40. Slocum B, Devine T. Meniscal release. In: Bojrab MJ, ed. Current techniques in small animal surgery. Baltimore:Williams and Wilkins, 1998;1197-1199. 41. Slocum B, Devine T. TPLO: Tibial Plateau Leveling Osteotomy for treatment of cranial cruciate ligament injuries. Proceedings 10th ESVOT Congress, Munich, 23-26th March 2000;37-38. 42. Watt P. Smith B. Viewpoints in surgery: Cruciate ligament rupture. Tibial plateau levelling. Austr Vet J 2000;78:385-386. 43. Childers HE. New method for cruciate ligament repair. Modern Vet Pract 1966;47:59-60. 44. Loeffler K, Reuleaux IR. Zur Chirurgie des Ruptur des Ligamentum discussatum laterale. DTW 1962;69:6972. 45. Loeffler K. Kreuzbandverletzungen im Kniegelenk des Hundes. Anatomy, Klinik und experimentele Untersuchungen. Verslag. Hannover:M and H Schaper, 1964. 46. Geyer H. Die Behandlung des Kreuzbandrisses beim Hund. Vergleichende Untersuchungen. Vet Dissertation Zürich 1966. 47. Fox SM, Baine JC. Anterior cruciate ligament repair: New advantages from changing old techniques. Vet Med 1986;31-37. 48. Allgoewer I, Richter A. Zwei intra-extraartikuläre Stabilisationsverfahren zur therapie der Ruptur des Ligamentum Cruciatum Craniale im Vergleich. Proceedings 43st Jahrestagung des Deutschen Veterinärmedizinischen Gesellschaft Fachgruppe Kleintierkrankheiten, Hannover 1997;29-31st August:158. 49. Leighton RL. Preferred method of repair of cranial cruciate ligament rupture in dogs: A survey of ACVS Diplomates specializing in canine orthopedics. Letter to the Editor. Vet Surg 1999;28:194. 50. Arnoczky SP, Torzilli PA, Marshall JL. Biomechanical evaluation of anterior cruciate ligament repair in the dog: An analysis of the instant center of motion. J Am Anim Hosp Assoc 1977;13:553-558. 51. Vasseur PB. The stifle joint. In: Slatter DH, ed. Textbook of Small Animal Surgery 2nd ed. Philadelphia:WB Saunders, 1993;1817-1866. 52. Flo GL. Modification of the lateral retinacular imbrication technique for stabilising cruciate ligament injuries. J Am Anim Hosp Assoc 1975;11:570-576. 53. Hulse DA, Michaelson F, Johnson C, et al. A technique for reconstruction of the anterior cruciate ligament in the dog: Preliminary report. Vet Surg 1980;9:135-140. 54. Pearson PT, McCurnin DM, Carter JD, et al. Lembert suture techniques to surgically correct ruptured cruciate ligaments. J Am Anim Hosp Assoc 1971;7:1-13. 55. DeAngelis M, Lau RE. A lateral retinacular imbrication technique for the surgical correction of anterior cruciate ligament rupture in the dog. J Am Vet Med Assoc 1970;157:79-85. 56. Aiken SW, Bauer MS, Toombs JP. Extra-articular fascial strip repair of the cranial cruciate deficient stifle: technique and results in seven dogs. Vet Comp Orthop Traumatol 1992;5:145-150. 57. Olmstead ML. The use of orthopedic wire as a lateral suture for stifle stabilization. Vet Clin NA 1993;23:735-753. 58. Anderson CC, Tomlinson JL, Daly WR, et al. Biomechanical evaluation of a crimp clamp system for loop fixation of monofilament nylon leader material used for stabilization of the canine stifle joint. Vet Surg 1998;27:533-539.



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CHAPTER 1.4: Review 59. Brinker WO, Piermattei DL, Flo GL. Diagnosis and treatment of orthopedic conditions of the hindlimb. In: Brinker WO, Piermattei DL, Flo GL, eds. Handbook of small animal orthopedics and fracture treatment. Philadelphia:WB Saunders, 1990;341-470. 60. Hohn RB, Newton CD. Surgical repair of ligamentous structures of the stifle joint. In: Bojrab MJ, ed. Current Techniques in Small Animal Surgery. Philadelphia:Lea and Febiger, 1975;470-479. 61. Schäfer H-J, Heider H-J, Köstlin RG, et al. Zwei Methoden für die Kreuzbandoperation im Vergleich: die Over-the-Top- und die Fibulakopfversetzungstechnik. Kleintierpraxis 1991;36:683-686. 62. Kudnig ST. Viewpoints in surgery: Cruciate ligament rupture. Intra-articular replacement. Austr Vet J 2000 ;78 :384-385. 63. O’Donoghue DH, Rockwood CA, Frank GR, et al. Repair of the anterior cruciate ligament in dogs. J Bone Joint Surg (Am) 1966;48-A:503-519. 64. Reinke JD. Cruciate ligament avulsion injury in the dog. J Am Anim Hosp Assoc 1982;18:257-264. 65. Arnoczky SP, Marshall JL. The cruciate ligaments of the canine stifle: an anatomical and functional analysis. Am J Vet Res 1977;38:1807-1814. 66. Arnoczky SP, Tarvin GB, Marshall JL, et al. The over-the-top procedure: A technique for anterior cruciate ligament substitution in the dog. J Am Anim Hosp Assoc 1979;15:283-290. 67. Hey Groves EW. Operation for the repair of the crucial ligaments. Lancet 1917;11:674-675. 68. Singleton WB. The diagnosis and surgical treatment of some abnormal stifle conditions in the dog. Vet Rec 1957;69:1387-1394. 69. Leighton RL. Repair of ruptured anterior cruciate ligaments with whole thickness skin. Small Anim Clin 1961;1:246-259. 70. Foster WJ, Imhoff RK, Cordell JT. Closed joint repair of anterior cruciate ligament rupture in the dog. J Am Vet Med Assoc 1963;143:281-283. 71. Shires PK, Hulse DA, Liu W. The under-and-over fascial replacement technique for anterior cruciate ligament rupture in dogs: A retrospective study. J Am Anim Hosp Assoc1984;20:69-77. 72. Denny HR, Barr ARS. An evaluation of two ‘over the top’ techniques for anterior cruciate ligament replacement in the dog. J Small Anim Pract 1984;25:759-769. 73. Bennett D, May C. An ‘over-the-top with tibial tunnel’ technique for repair of cranial cruciate ligament rupture in the dog. J Small Anim Pract 1991;32:103-110. 74. Strande A. A study of the replacement of the anterior cruciate ligaments in the dog. Nord Vet Med 1964;16:820-827. 75. Frost GE. Surgical correction of rupture of the cranial cruciate ligament in the dog. J S-Afr Vet Med Assoc 1973;44:295-296. 76. Lewis DG. A modified tendon transfer technique for stabilizing the canine stifle joint after rupture of the cruciate ligament(s). Vet Rec 1974;94:3-8. 77. Curtis RJ, Delee JC, Drez DJ. Reconstruction of the anterior cruciate ligament with freeze dried fascia lata allografts in dogs. A preliminary report. Am J Sports Med 1985;13:408-414. 78. Arnoczky SP, Warren RF, Ashlock MA. Replacement of the anterior cruciate ligament using a patellar tendon allograft. J Bone Joint Surg (Am) 1986;68-A:376-385.



85



CHAPTER 1.4: Review 79. Thorson E, Rodrigo JJ, Vasseur P, et al. Replacement of the anterior cruciate ligament. A comparison of autografts and allografts in dogs. Acta Orhtop Scand 1989;60:555-560. 80. Monnet E, Schwarz PD, Powers B. Popliteal tendon transposition for stabilization of the cranial cruciate ligament deficient stifle joint in dogs: An experimental study. Vet Surg 1995;24:465-475. 81. Dupuis J, Harari J. Cruciate ligament and meniscal injuries in dogs. Comp Cont Educ 1993;15:215-232. 82. Butler DL, Grood ES, Noyes FR, et al. On the interpretation of our anterior cruciate ligament data. Clin Orthop Rel Res 1985;196:26-34. 83. Leighton RL, Brightman AH. Experimental and clinical evaluation of a new prosthetic anterior cruciate ligament in the dog. J Am Anim Hosp Assoc 1976;12:735-740. 84. Robello GT, Aron DN, Foutz TL, et al. Replacements of the medial collateral ligament with polypropylene mesh or a polyester suture in dogs. Vet Surg 1992;21:467-474. 85. Beckman SL, Wadsworth PL, Hunt CA, et al. Technique for stabilizing the stifle with nylon bands in cases of ruptured anterior cruciate ligaments in dogs. J Am Anim Hosp Assoc 1992;28:539-544. 86. Person MW. Prosthetic replacement of the cranial cruciate ligament under arthroscopic guidance. A pilot project. Vet Surg 1987;16:37-43. 87. Zaricznyj B. Reconstruction of the anterior cruciate ligament of the knee using a doubled tendon graft. Clin Orthop Rel Res 1987;220:162-175. 88. Radford WJP, Amis AA, Kempson SA et al. A comparative study of single- and double-bundle ACL reconstructions in sheep. Knee Surg, Sports Traumatol, Arthrosc 1994;2:94-99. 89. Butler HC. Teflon as a prosthetic ligament in repair of ruptured anterior cruciate ligaments. Am J Vet Res 1964;25:55-59. 90. Lampadius WE. Vergleichende klinische und histologische Untersuchungen des Heiluorgange nach Transplantion synthetischer und homoioplastischer Bander bei der Ruptur des Liggamenta decussata des Hundes mit der Operationmethode nach Westhues. Vet Dissertation Giessen, 1964. 91. Zahm H. Operative treatment of crucial ligament injuries in dogs with synthetic material. Berl Munch Tierarztl Wochenschr 1966;79:1-4. 92. Stead AC. Recent advances in the repair of cruciate ligaments. In: Grunsell and Hill, eds. Vet Annual 23th issue Bristol:Scientechnica.1983. 93. Amis AA, Campbell JR, Kempson SA, et al. Comparison of the structure of neotendons induced by implantation of carbon or polyester fibres. J Bone Joint Surg (Br) 1984;66-B:131-139. 94. Stead AC, Amis AA, Campbell JR. Use of polyester fibre as a prosthetic cranial cruciate ligament in small animals. J Small Anim Pract 1991;32:448-454. 95. Amis AA, Campbell JR, Miller JH. Strength of carbon and polyester fibre tendon replacements. Variation after operation in rabbits. J Bone Joint Surg (Br) 1985;67-B:829-834. 96. Lieben NH. Intra-articulaire kniestabilisatie met synthetisch stabilisatietechniek. Tijdschr Diergeneesk 1986;23:1160-1166.



materiaal.



Een



praktijkgerichte



97. Puymann K, Knechtl G. Behandlung der Ruptur des kranialen Kreuzbandes mittels Arthroskopie und minimal-invasiver Haltebandtechnik beim Hund. Kleintierprax 1997;42:601-612. 98. Hulse DA. Rehabilitation of the reconstructed cranial cruciate deficient stifle joint in the dog. Proceedings 10th ESVOT Congress, Munich 2000;23-26th March:34-35.



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CHAPTER 1.4: Review 99. Perry R, Warzee C, Dejardin L, et al. Radiographic assessment of tibial plateau leveling osteotomy (TPLO) in canine cranial cruciate deficient stifles: An in vitro analysis. Vet Radiol Ultrasound 2001;42:172. 100. Solomonow M, Baratta R, Zhou BH, et al. The synergistic action of the anterior cruciate ligament and thigh muscles in maintaining joint stability. Am J Sports Med 1987;15:207-213. 101. Johnson JM, Johnson AL, Pijanowski GJ, et al. Rehabilitation of dogs with surgically treated cranial cruciate ligament-deficient stifles by use of electrical stimulation of muscles. Am J Vet Res 1997;58:14731478. 102. Millis DL, Levine D. The role of exercise and physical modalities in the treatment of osteoarthritis. Vet Clin N Am SAP 1997;27:913-930. 103. Pond MJ, Nuki G. Experimentally-induced osteoarthritis in the dog. Ann Rheum Dis 1973;32:387-388. 104. Ehrismann G, Schmokel HG, Vannini R. Meniskusschaden beim Hund bei geleichzeitigem Riss des vorderen Kreuzbandes. Wien Tierärztl Mschr 1994;81:42-45. 105. Denny HR, Barr ARS. A further evaluation of the ‘over the top’ technique for anterior cruciate ligament replacement in the dog. J Small Anim Pract 1987;28:681-686. 106. Schnell EM. Drei Jahre Erfahrung mit einer modifizierten Kreuzbandplastik beim Hund. Dissertation, Munchen 1896. 107. McCurnin DM, Pearson PT, Wass WM. Clinical and pathological evaluation of ruptured cranial cruciate ligament repair in the dog. Am J Vet Res 1971;32:1517-1524. 108. Heffron LE, Campbell JR. Osteophyte formation in the canine stifle joint following treatment for rupture of the cranial cruciate ligament. J Small Anim Pract 1979;20:603-611. 109. Elkins AD, Pechman R, Kearny MT, et al. A retrospective study evaluating the degree of degenerative joint disease in the stifle joint of dogs following surgical repair of anterior cruciate ligament rupture. J Am Anim Hosp Assoc 1991;27:533-539. 110. Vasseur PB, Berry CR. Progression of stifle osteoarthrosis following reconstruction of the cranial cruciate ligament in 21 dogs. J Am Anim Hosp Assoc 1992;28:129-136. 111. Flo GL. Meniscal injuries. Vet Clin NA:SAP 1993;23:831-843. 112. Innes JF, Bacon D, Lynch C, et al. Long-term outcome of surgery for dogs with cranial cruciate ligament deficiency. Vet Rec 2000;147:325-328. 113. Vaughan LC, Bowden NLR. The use of skin for the replacement of the anterior cruciate ligament in the dog: A review of thirthy cases. J Small Anim Pract 1964;5:167-171. 114. Drapé J, Ghitalla S, Autefage A. Rupture du ligament croisé antérieur (L.C.A.) chez le chien: pathologie traumatique ou dégénérative? Point Vét 1990;22:573-580. 115. Doverspike M, Vasseur PB, Harb MF, et al. Contralateral cranial cruciate ligament rupture: Incidence in 114 dogs. J Am Anim Hosp Assoc 1993;29:167-170.



87



88



CHAPTER



2



THE TIBIAL COMPRESSION TECHNIQUE AS A RELIABLE RADIOGRAPHIC TEST FOR CRANIAL CRUCIATE INSTABILITY IN DOGS



2.1. Diagnosis of cranial cruciate ligament injury in dogs by tibial compression radiography



2.2. Use of compression stress radiography for the detection of partial tears of the canine cranial cruciate ligament



2.3. Radiographic measurement of craniocaudal instability in stifle joints of clinically normal dogs and dogs with injury of a cranial cruciate ligament



2.4. Popliteal sesamoid displacement associated with cruciate rupture in the dog



89



90



CHAPTER 2



2.1. Diagnosis of cranial cruciate ligament injury in dogs by tibial compression radiography H. de Rooster, B. Van Ryssen, H. van Bree



Department of Medical Imaging, Faculty of Veterinary Medicine, Ghent University Salisburylaan 133, 9820 Merelbeke, Belgium



Adapted from: Veterinary Record 1998;142:366-368.



91



92



CHAPTER 2.1: Diagnosis



SUMMARY Stress radiographs were taken of 42 sound stifle joints, of 5 stifles with pathologies other than cruciate disease, and of 72 stifles with surgically confirmed cranial cruciate ligament (CCL) damage. The stifles were also examined by the cranial drawer test. No false positive compression radiographs were obtained.



In the 72 stifles with cranial cruciate damage,



instability was diagnosed on the stressed view in all but two cases. The sensitivity of the radiographic tibial compression test was 97 per cent, compared with 86 per cent for the cranial drawer test; the specificities of the tests were 100 per cent and nearly 98 per cent, respectively. The tibial compression radiograph is a simple, objective aid in the diagnosis of cranial cruciate damage in dogs.



INTRODUCTION Cranial cruciate ligament (CCL) injury is a common problem in dogs, and is generally evaluated by physical examination.



The most consistent findings are joint swelling and



instability of the stifle. To assess the instability two tests - the cranial drawer test and the tibial compression test - are often used in veterinary practice. For the cranial drawer test,1 the stifle is slightly flexed and gentle cranial pressure is exerted on the head of the fibula with the thumb. At the same time the femur is supported with the other hand, the thumb behind the lateral fabella, so that counter-pressure can be applied.2 A positive sign is obtained when the tibia can be pushed cranially. The tibial compression test3 mimics the contraction of the gastrocnemius muscle group, whereby the stifle joint is fully extended. The tip of the index finger of the hand that immobilises the femur, rests on the tibial tuberosity, and the hock joint is repeatedly flexed and extended with the other hand. This test is positive when a cranial displacement of the tibial tuberosity can be felt under the index finger of the upper hand. CCL injuries can be difficult to diagnose by these classical clinical tests alone.2,4,5 The cranial drawer test can sometimes not be elicted or fully assessed, and the impression of relative displacement and rotation during clinical examination is often not very accurate.6,7



A



combination of several manual and radiological biomechanical tests has been recommended for the clinical diagnosis of cruciate ligament instability in humans.5 A radiograph shows the spatial



93



CHAPTER 2.1: Diagnosis relationship between the bones at the joint level. The position of the tibia in relation to the femur will be related directly to the status of the supporting ligaments which originate on one bone, and insert on the other.8



On a neutral view of a normal canine stifle in 90° of flexion, the



perpendicular on the femoral axis that runs just cranial to the fabellae, will be almost tangential to the caudal projection of the lateral tibial condyle.9 In a small number of cases, the cranial displacement of the proximal tibia may be visible on a standard lateral radiograph, without any special stresses being applied to the leg during the positioning.10-13 This particular sign is called ‘Cazieux-positive’, and always indicates a ruptured CCL.9



The abnormalities will be



accentuated on stressed views.14 A technique for obtaining a tibial compression radiograph has been designed for dogs suspected of having damage to the CCL. For this technique, the stifle is fixed at an angle of 90° of flexion, while manual stress is exerted on the metatarsals in order to flex the hock joint maximally. A ruptured CCL will then allow the proximal tibia to move cranial in relation to the distal femur. This study was designed to evaluate the accuracy and usefulness of the tibial compression radiographic technique.



MATERIALS AND METHODS Dogs—The stifle joints of two groups of dogs were used to provide control tibial compression radiographs. Ten sound control dogs were radiographed bilaterally, and in addition the normal stifle of 22 unilaterally affected patients was radiographed, to provide a total of 42 compression radiographs of normal stifles. These 32 dogs had a mean age of 5.7 years and a mean bodyweight of 26.0 kg. Five other dogs were screened, three during an arthrotomy procedure to correct medial patellar luxation, one dog with chondromalacia, and one with idiopathic synovitis which was screened during diagnostic arthroscopy of the affected stifle. The five dogs all had intact ligaments. Tibial compression radiographs were taken in all dogs suspected of having damage to the CCL which were submitted to the Department of Medical Imaging from November 1992 until June 1995 (Table 1). The cranial drawer test was assessed by several examiners with different levels of experience. In general, it was first applied while the dog was conscious. Whenever the result was negative or uncertain, it was repeated after the dog had received a sedative (Thalamonal), before the radiological examination.



94



CHAPTER 2.1: Diagnosis Table 1.



Numbers and breeds of dogs suspected of having damage to their cranial cruciate ligament



Breed



Number of cases



Rottweiler Labrador Retriever Poodle Boxer Berner Sennen Crossbred Golden Retriever Husky Maltese Dobermann Pointer Great Dane St Bernard Stafforshire Bull Terrier Yorkshire Terrier Other breeds



17 9 8 7 6 5 5 5 4 4 3 2 2 2 2 12



Total



93



Confirmation of damage to the CCL was obtained during the arthrotomy or arthroscopy of 72 joints, 59 with complete, and 13 partial ruptures of the CCL. The dogs with surgically confirmed cruciate injuries ranged in age from one to 12 years (mean 4.8 years) and in body weight from 5.5 to 70 kg (mean 30.9 kg). The findings during surgery were correlated with the results of the cranial drawer test and the radiographic tibial compression test.



Positioning—A sedative (Thalamonal) was administered intramuscularly before the radiographic examination. The dog was positioned in lateral recumbency, with the affected stifle resting on the x-ray cassette. A standard lateral view was taken of both stifles with the joints in 90° of flexion (‘neutral’). For the stressed position (‘tibial compression’), the stifle was fixed at the same angle of flexion, while manual stress was exerted on the metatarsals by an assistant, in order to flex the hock joint maximally (Fig 1). Care was taken not to twist the leg during this procedure, so that both femoral condyles were maximally superimposed on to each other. The xray beam was collimated as much as possible and lead protection was applied to the hands of the assistants.



95



CHAPTER 2.1: Diagnosis



Fig 1.



Diagram showing the principle of tibial compression radiography by manual positioning



Interpretation of tibial compression views—The radiographs were read separately by two of the authors (HdR and PvB) before the outcome of the arthrotomy or arthroscopic procedure was known. The following criteria were used to assess the instability of the joint on the stressed radiographs. In obviously positive cases, the vertical line tangential to the caudal margin of the femoral condyles ran far behind the caudal projection of the tibial plateau (Fig 2). When less displacement was present, the position of the lateral intercondylar tubercle of the tibia in relation to the contour of the lateral femoral condyle helped to assess the cranial shifting of the proximal tibia. The position of the popliteal sesamoid was also helpful.



96



CHAPTER 2.1: Diagnosis



A



Fig 2.



B



Radiographic images of a cruciate-deficient stifle joint showing A. a neutral view and B. a stressed view



RESULTS Of the 72 joints with known cruciate problems, 13 (18%) had CCLs which were partially torn, and the other 59 were completely ruptured (Table 2). In six dogs, damage to the CCL was diagnosed in both stifle joints. However, only the tibial compression radiographs of the second injured stifle were included in this study. The stress radiographic analysis has a specificity of 100 per cent; no false positive tibial compression radiographs were obtained and no displacement was apparent in the stifle joints of either the control group, or in the group with stifle pathology other than cruciate injury. In contrast, a cranial drawer test was positive in one case of medial patellar luxation, although the CCL was found to be completely intact during arthrotomic inspection of the joint. The manual test has a specificity of nearly 98 per cent. The sensitivity of stress radiography was 97 per cent. In the 72 stifles with cranial cruciate damage, instability was apparent on the stressed radiographic view in all but two cases (one complete and one partial rupture). In the latter case, the popliteal sesamoid appeared far more distal on the stressed radiograph of the affected stifle than on the tibial compression view of the



97



CHAPTER 2.1: Diagnosis unaffected stifle. The probability of making a correct diagnosis of cruciate injury (accuracy) based on tibial compression radiography was 98 per cent. The manual cranial drawer test were applied to 64 of the 72 joints with cranial cruciate disease (Table 2). The test was not always done by one of the authors, but by several clinicians with varying degrees of experience. The test gave false negative results in nine cases (six complete ruptures and three of 11 partial ruptures), giving a sensitivity of 86 per cent for diagnosing cruciate injury in affected joints. Tibial compression radiographs were positive in six of the joints which gave a negative cranial drawer test. Finally, in two CCL-deficient stifle joints, both the cranial drawer test and the radiographic tibial compression test were negative.



Table 2.



Results of the radiographic tibial compression test and the manual cranial drawer test on the 72 stifle joints shown to have either partial or complete rupture of the cranial cruciate ligament by arthrotomy or arthroscopy



Test result Positive Negative Uncertain Not recorded



Partial rupture CCL (13) Intact MM MM tear (10) (3) TC-RX CD-DR TC-RX CD-DR 9 1 0 0



3 3 3 1



3 0 0 0



1 0 1 1



Complete rupture CCL (59) Intact MM MM tear (45) (14) TC-RX CD-DR TC-RX CD-DR 44 1 0 0



29 5 5 6



14 0 0 0



13 1 0 0



CCL Cranial cruciate ligament, TC-RX Tibial compression radiographic test, CR-DR Cranial drawer test, MM Medial meniscus



DISCUSSION In contrast with the physical tibial compression test,3 the stifle is held at an angle of 90° while making the tibial compression radiograph. The canine CCL is formed by a craniomedial and a caudolateral bundle; the former is under tension during the whole range of motion of the stifle, while the latter is loose when the joint is flexed.15 These features can have an effect in cases of partial rupture of the cranial cruciate. At full extension, a false negative result is likely if only the craniomedial bundle of the ligament has ruptured, because the caudolateral bundle can mask the



98



CHAPTER 2.1: Diagnosis instability. In flexion, however, the caudal bundle of the cranial cruciate will always be loose, regardless of the state of the cranial bundle. As a result, fewer cases of incomplete damage will be missed when the tibial compression stress is exerted on a flexed stifle joint. Great care has to be given to certain aspects of radioprotection during the tibial compression technique, because the dog has to be restrained while the radiograph is taken. Sedation is advisible so that minimal restraint is necessary, and the x-ray beam should be carefully collimated and the handlers' hands should be protected by lead. Investigations are underway to modify the technique and eliminate the necessity for manual positioning of the limb. Under general anaesthesia, a figure-of-eight dressing with an elastic gauze bandage has been applied to span the tarsal joint. More clinical cases need to be studied first before the value of the modification can be assessed. Stress radiographs are positive whenever there is an abnormal spatial relationship between the proximal and distal components. In the case of a positive tibial compression radiograph, the proximal tibia will appear too far cranially in relation to the distal femur when stress is applied. The sesamoid bone in the tendon of the popliteus muscle will also often appear to be displaced distally. A distomedial displacement of the popliteal sesamoid has only been reported twice, and both cases suffered avulsion of the popliteus muscle.16,17 To the authors’ knowledge, distal displacement due to rupture of the CCL has not previously been reported. They consider that the sesamoid bone appears more distally on tibial compression radiographs when there is damage to the cruciate ligament. In a small number of dogs the popliteal sesamoid does not ossify, and therefore remains invisible on radiographs.18 In this study, the popliteal sesamoid was not ossified in 6 per cent of the dogs radiographed. They were all small breed dogs, with an average bodyweight of 9.2 kg. The cranial drawer test, rather than the clinical tibial compression test, was used for the clinical assessment of joint laxity. General clinicians are less familiar with the latter test and some of the clinical data were obtained from records which, in most cases, included only the results of the cranial drawer test. No false positive tibial compression radiographs were obtained, because no displacement was apparent in any of the stifles in the control group. Similarly, among the dogs with problems other than cruciate disease, only negative stressed views were encountered. Thus, a positive radiographic test always indicates either a partial or complete tearing of the CCL. False negative results were obtained in only two cases and the test had a sensitivity of 97 per cent. In comparison, the diagnosis would have been missed in about 14 per cent if only the cranial drawer test had been applied. This test had a sensitivity of 86 per cent. Furthermore, this test 99



CHAPTER 2.1: Diagnosis gave a false positive result in one out of the five cases of stifle pathology other than cranial cruciate disease. For this study, no special attention was paid to the existence of degenerative changes in the affected joints and their possible influence on the outcome of the clinical and radiological tests. Several types of arthrometers (‘gonylaxometers’ or ‘goniometers’) have been tested on human knees in order to define the normal and pathological craniocaudal stability of the knee joint during loading of the proximal tibia.7,19-22 Their main disadvantage is the high cost of the specially instrumented devices, and a second drawback is the low accuracy that can be achieved owing to the interposition of soft tissue and relative movement around the stifle other than pure translation.8,22-24



On radiographs these problems are eliminated by working with bony



landmarks. On the basis of these observations, the tibial compression technique is a reliable radiographic test for cranial cruciate instability in dogs. A positive result always indicates either partial or complete rupture of the CCL.



100



CHAPTER 2.1: Diagnosis REFERENCES 1.



Carlin I. Ruptur des Ligamentum cruciatum anterius im Kniegelenk beim Hund. Arch Wissensch Prakt Tierh 1926;54:420-423.



2.



Robins GM. The canine stifle. The diagnosis and management of acquired abnormalities. In: Whittick WG, ed. Canine Orthopaedics. Philadelpia:Lea and Febiger, 1990;724-752.



3.



Henderson RA, Milton JL. The tibial compression mechanism: a diagnostic aid in stifle injuries. J Am Anim Hosp Assoc 1978;14:474-479.



4.



Kennedy JC, Fowler PJ. Medial and anterior instability of the knee. J Bone Joint Surg (Am) 1971;53A:1257-1270.



5.



Torzilli PA., Greenberg RL, Hood RW, et al. Measurement of anterior-posterior motion of the knee in injured patients using a biomechanical stress technique. J Bone Joint Surg (Am) 1984;66-A:1438-1442.



6.



Torg JS, Conrad W, Kalen V. Clinical diagnosis of anterior cruciate ligament instability in the athlete. Am J Sports Med 1976;4:84-93.



7.



Torzilli PA, Greenberg RL, Insall JN. An in vivo biomechanical evaluation of anterior-posterior motion of the knee. Roentgenographic measurement technique, stress machine, and stable population. J Bone Joint Surg (Am) 1981;63-A:960-968.



8.



Jacobsen K. Stress radiographical measurement of the anteroposterior, medial and lateral stability of the knee joint. Acta Orthop Scand 1976;47:335-344.



9.



Meinen JJ, Verbeek M. Voorste kruisbandlaesies bij de hond: een evaluatie van therapie, klinisch en röntgenologisch verloop bij 215 patiënten. Referaat. Geneeskunde van het Kleine Huisdier, Vakgroep Radiologie, Rijksuniversiteit te Utrecht 1980.



10. Singleton WB. The diagnosis and surgical treatment of some abnormal stifle conditions in the dog. Vet Rec 1957;69:1387-1394. 11. Pond MJ, Campbell JR. The canine stifle joint. I. Rupture of the anterior cruciate ligament. An assessment of conservative and surgical treatment. J Small Anim Pract 1972;13:1-10. 12. Park RD. Radiographic evaluation of the canine stifle joint. Comp Cont Ed 1979;1:833-841. 13. Kirby BM. Decision-making in cranial cruciate ligament ruptures. Vet Clin North Am:SAP 1993;23:797-819. 14. Farrow CS. Stress radiography: Applications in small animal practice. J Am Vet Med Assoc 1982;181:777-784. 15. Arnoczky SP, Marshall JL. The cruciate ligaments of the canine stifle: an anatomical and functional analysis. Am J Vet Res 1977;38:1807-1814. 16. Pond MJ, Losonsky JM. Avulsion of the popliteus muscle in the dog: A case report. J Am Anim Hosp Assoc 1976;12:60-63. 17. Eaton-Wells RD, Plummer GV. Avulsion of the popliteal muscle in an Afgan Hound. J Small Anim Pract 1978;19:743-747. 18. McCarthy PH, Wood AKW. Anatomical and radiological observations of the sesamoid bone of the popliteus muscle in the adult dog and cat. Anat Histol Embryol 1989;18:58-65. 19. Daniel DM, Malcom LL, Losse G, et al. Instrumented measurement of anterior laxity of the knee. J Bone Joint Surg (Am) 1985;67-A:720-726. 20. Bach BR, Warren RF, Flynn RF, et al. Arthrometric evaluation of knees that have a torn anterior cruciate ligament. J Bone Joint Surg (Am) 1990;72-A:1299-1307.



101



CHAPTER 2.1: Diagnosis



21. Granberry WM, Noble PC, Woods GW. Evaluation of an electrogoniometric instrument for measurement of laxity of the knee. J Bone Joint Surg (Am) 1990;72-A:1316-1322. 22. Franklin JL, Rosenberg TD, Paulos LE, et al. Radiographic assessment of instability of the knee due to rupture of the anterior cruciate ligament. J Bone Joint Surg (Am) 1991;73-A:365-372. 23. Hooper GJ. Radiological assessment of anterior cruciate ligament deficiency: a new technique. J Bone Joint Surg (Br) 1986;68-B:292-296. 24. Edixhoven P, De Graaf R, Van Rens TJG, et al. Accuracy and reproducibility of instrumented knee-drawer tests. J Orthop Res 1987;5:378-387.



102



CHAPTER 2



2.2. Use of compression stress radiography for the detection of partial tears of the canine cranial cruciate ligament H. de Rooster, H. van Bree



Department of Medical Imaging, Faculty of Veterinary Medicine, Ghent University Salisburylaan 133, 9820 Merelbeke, Belgium



Adapted from: Journal of Small Animal Practice 1999;40:573-576.



103



104



CHAPTER 2.2: Diagnosis



SUMMARY Twenty-three cases of partial rupture of the cranial cruciate ligament (CCL) were reviewed.



All of these patients were evaluated for clinical and radiographic signs of



instability. Nine cases showed a negative drawer sign on manual assessment. A positive radiographic tibial compression test was obtained for all stifle joints with a partially ruptured CCL. In 13 cases, the site of injury and the appearance of the torn ends were evaluated. The final diagnosis of partial CCL rupture was made by direct visualisation and probing of the CCL during arthrotomy (22 cases) or arthroscopy (one case).



INTRODUCTION Damage to the cranial cruciate ligament (CCL) in the dog is the stifle injury most commonly encountered in any small animal practice.1 Originally, partial rupture of the CCL was considered to be rare in the dog.2 The clinical importance of partial tearing of the cranial cruciate has been questioned by Zahm3 and by Heffron and Campbell4 among others, because of the often relatively minor joint instability. More recently, there has been more unanimity of opinion concerning the generation of lameness, pain on manipulation and stifle joint effusion associated with incomplete damage to the CCL, even though no or only slight instability might be demonstrable clinically.5,6 Nevertheless, clinical reports with a special emphasis on partial CCL rupture are rather sparse in veterinary literature.5-8 CCL injuries, and in particular partial tearing of the ligament, are still often overlooked at the time of the initial injury.



In a large number of cases, the veterinarian encounters



difficulties in eliciting instability by a physical examination only, with no detectable cranial drawer sign in response to the small manual forces used on manipulation of the affected stifle joint. Exploratory surgery of the affected stifle joint has been necessary to disclose partial rupture of the CCL in the past.6,7 In obscure cases of knee injury in human orthopaedics, arthroscopic investigation following careful physical examination is a direct standard diagnostic procedure and a valuable tool to determine the rational treatment.9-11 Arthroscopy of the canine stifle joint allows direct visualisation and careful probing to reveal minor surface fraying or subsynovial tears.12-14



Unfortunately, the basic equipment needed to perform arthroscopy, and



105



CHAPTER 2.2: Diagnosis veterinarians with sufficient experience of arthroscopy, are not widely found in veterinary practices.12,15 The purpose of the present study was to investigate the use of compression stress radiography for the clinical diagnosis of partial CCL tearing in dogs.



MATERIALS AND METHODS The surgical reports of all dogs that underwent orthopaedic surgery of the stifle joint at Ghent University Veterinary School from the beginning of February 1996 to the end of January 1998 were reviewed. Partial tearing of the CCL was diagnosed in 23 stifles (23 dogs). For these dogs, the records were reviewed for data such as breed, age at time of presentation, bodyweight and gender. Furthermore, data on history and findings during the physical examination were carefully studied. For each case, neutral and stress radiographs were available for both the injured and contralateral stifle joints. Whether or not cranial drawer was noted during the physical examination, stress views were performed in cases of stifle lameness using a technique previously described by de Rooster and others.16,17 Briefly, the dog is positioned in lateral recumbency. A standard lateral radiograph of the stifle joint is first taken at 90° flexion. While maintaining this angle of flexion of the stifle joint, the hock joint is maximally flexed by manual stress and a second picture is taken.



(The technique of tibial compression



radiographs is not possible in the UK because the Ionising Radiation Regulations forbid manual holding of animals for radiography.



Currently, investigations are under way to



modify the technique [elastic gauze figure-of-eight dressing] and hence eliminate the need for manual positioning of the limb.) For the present study, the radiographs were all re-read in a blinded manner by the principal investigator (HdR) to grade osteoarthrotic (OA) changes and to assess radiographic displacement. The OA scoring system used was based on a global score (grade 0 to 3), according to the criteria of Brünnberg and others18 (Fig 1).



106



CHAPTER 2.2: Diagnosis



Fig 1.



Radiographic grading of osteoarthritic (OA) changes (based on Brünnberg et al. 1992) 0. No signs of OA 1. Mild signs of OA, lipping of the distal patella, sclerosis of the trochlear groove 2. Moderate signs of OA, lipping of the distal and proximal patella, osteophyte formation on the fabellae, sclerosis of the trochlear groove, sclerosis of the tibial plateau 3. Severe signs of OA, all above-mentioned signs, osteophyte proliferation caudal to the tibial plateau, sclerosis in the long digital extensor muscle groove



Surgical findings were compared. Macroscopic inspection of the CCL occurred at the time of arthrotomy in all but one case. If no obvious tearing was seen, careful probing of the individual bundles, comprising the CCL, was carried out with a curved haemostat to detect any incompetent fibres. In the last 13 cases, the main staff surgeon was asked to assess the location of tearing of the CCL. The site of the injury was recorded by the region of the tear (proximal, central, distal or interstitial), and the nature of the remnants (absorbed, unchanged or granulated) was also recorded. Data on which of the two functional components of the CCL was damaged were not available from the surgical reports. Precise determination of the percentage of tearing of the CCL proved not to be possible, since the original thickness of the ligament can only roughly be estimated.



107



CHAPTER 2.2: Diagnosis



RESULTS Thirteen different breeds were presented with partial tearing of the CCL.



Mean



bodyweight of the patients was 33.9 kg (range 8 to 65 kg). The mean age at time of presentation was 3.9 years (range 0.6 to 12 years). Only five of the 23 dogs were male. The mean period from initial lameness to examination was 3.7 months (range 0.2 to 104 months). A negative cranial drawer sign was encountered in nine cases, whereas the radiological tibial compression test was positive for cruciate instability in all the cases. OA changes were present in all but one dog. Only mild degenerative changes were seen radiographically in 14/23 dogs, moderate arthrosis in a quarter of the cases and severe signs of OA in the remaining two patients. The final diagnosis of partial CCL damage and possible meniscal injury was made during surgical examination at arthrotomy performed by the same surgeon in all but one dog. This individual had only a diagnostic arthroscopic examination, which was not followed by any stabilising surgery. Upon entering the joint, the CCL was found partially ruptured in 18 out of the 23 cases. In the remaining five joints, no obvious tears were found instantaneously, but careful probing revealed a fibrillated and torn component (interstitial tearing) and a badly stretched ligament in three cases. One further ligament showed minor surface fraying of its fibres, but no detectable laxity, and the remaining dog showed calcifications within the ligament on its preoperative radiographs, although the bulk of the CCL appeared to be grossly intact by anatomical inspection at the time of arthrotomy. In five cases, simultaneous tearing of the medial meniscus was encountered. The anatomic location of the tearing was recorded in 13 cases. A femoral avulsion fragment was seen in the only case which involved the origin of the CCL, while distal tearing of a ligament bundle occurred in five other cases. In two cases, the rupture was located in the mid-portion of a ligament band and, in the remaining five cases, the tearing was interstitial. The ruptured ends were found to be rounded but almost unchanged in five of the 13 cases, and the torn ends of the partially ruptured CCL were totally atrophied in one further dog. In two other cases the stumps were abundantly granulated. With the limited number of cases available, associations between the presence or absence of a detectable cranial drawer sign and factors such as the degree of radiographic OA, the duration of the clinical signs of lameness, meniscal damage and the region of the ligament



108



CHAPTER 2.2: Diagnosis injury could not be made (data not shown).



The same was true for associations with



background variables, such as patient age and body weight (data not shown).



DISCUSSION The prevalence of partial CCL damage is very difficult to assess accurately. Subclinical tearing may occur more frequently than is realised. It is postulated that quite some cases of partial rupture are only presented to the veterinarian once the damage has become already complete.18 The aetiopathogenesis of partial tearing of the CCL remains obscure. For most of the dogs with partial CCL, a history of trauma is absent.5 The loads that account for partial rupture of ligaments probably do not reach the level of ultimate breaking strength.20,21



Increased



fragility of degenerated ligament tissue under physiological loading conditions is suggested.22 Microfailure is the beginning of a serial process that progresses to involve major fibre bundles. Tearing of the CCL is the result of the initiation of this continuing process of successive overload of the collagen fibres.23 Spontaneous healing of the torn mature ligaments seems an unlikely event.21,24,25 Furthermore, in the human knee it has been stated that weakening of the anterior cruciate ligament will stress the secondary restraints and, in time, stretch them as well.26 There can be difficulty in arriving at a diagnosis of partial CCL tear. Difficulties in establishing the diagnosis of cruciate instability by physical examination alone are especially encountered in long-standing cases of cruciate disease, in cases with only partial tearing of the ligament or if the CCL is incompetent but not truly ruptured.13 Capsular thickening and joint distension may contribute to a false impression of stability.5,27 The cranial drawer test demands a certain portion of the CCL to be torn. The remaining intact portion of a partially ruptured ligament might obscure existing laxity at certain joint angles and resists drawer motion to varying degrees.4,6 Despite testing for a clinical cranial drawer sign at various angles of joint flexion, the test remained negative in nine of the 23 dogs with partial rupture in the present study. In an attempt to improve the diagnostic accuracy of clinical evaluation of cranial cruciate instability, tibial compression radiography has been introduced.16,17 Tibial compression stress radiography is a valuable asset in the diagnosis of canine stifle instability due to cranial



109



CHAPTER 2.2: Diagnosis cruciate tearing. It is a useful technique to prove (or disprove) a tentative diagnosis of CCL damage, especially when there is a lack of cranial drawer sign on clinical examination. All cases of partial rupture in the present study showed a positive tibial compression radiograph, although in nine dogs the cranial drawer test was negative. The accuracy of the radiographic tibial compression test was calculated to be 98 per cent in canine cruciate disease.17 However, diagnostic arthroscopy or exploratory arthrotomy might still be indicated if radiographic examination is not suggestive of CCL damage, but no further abnormalities can be detected. Arthroscopy provides an accurate means of detecting tearing of the CCL whenever a doubtful diagnosis remains after physical and radiological evaluation of the affected stifle joint.13 Gross anatomic inspection of arthritic joints at the time of arthrotomy will not always reveal obvious macroscopic damage to the CCL, although histological examination of such apparently undamaged CCLs does often disclose rupture of individual fibrils.2 The canine CCL is composed of two functional bands.4,28 The craniomedial subdivision is more spiral and longer than the caudolateral division, and remains taut during both flexion and extension of the stifle joint. The caudolateral portion is taut in the extended joint, but becomes relaxed as the stifle joint is flexed. In the case of an isolated partial rupture in the dog, the more common bundle part to be injured seems to be the craniomedial band.5-7,19,29 Because of its smaller size and its permanent tension, the craniomedial bundle is more prone to damage, especially during flexion when accompanied by internal rotation.5,8,30 Unfortunately, there were no data available for the studied cases on which of the two functional bands of the CCL was ruptured. In 13 dogs in the present study, the region of ligament damage was recorded. During tensile tests on canine bone-CCL-bone units, the mid-portion of the ligament is the predominant area of failure.21,31 In the studied cases of partial rupture, only two out of 13 partial ruptures occurred in the central area. A possible explanation is given by the lower force levels acting on the ligament, resulting in incomplete tearing. From clinical observations, it has been established that torn ends often remain normal after partial rupture, whereas they most often disintegrate after complete rupture. In only one case of partial damage of the CCL in the present study did the torn ligament ends seem to be completely absorbed by the time of corrective surgery. Disruption of their major blood supply is the most common reason for prompt disintegration of the stumps.24 In the other cases, CCL tissues have been removed for further histopathological and immunohistopathological investigations. 110



CHAPTER 2.2: Diagnosis Tibial compression stress radiography is able to detect partial tears of the CCL. It is an easy and reliable technique which does not require expensive equipment or a high level of technical proficiency.



111



CHAPTER 2.2: Diagnosis



REFERENCES 1.



Pond MJ, Campbell JR. The canine stifle joint. I. Rupture of the anterior cruciate ligament. An assessment of conservative and surgical treatment. J Small Anim Pract 1972;13:1-10.



2.



Tirgari M, Vaughan LC. Arthritis of the canine stifle joint. Vet Rec 1975;96:394-399.



3.



Zahm H. Die Ligamenta decussata in gesunden und arthrotischen Kniegelenk des Hundes. Kleintierprax 1965;10:38-47.



4.



Heffron LE, Campbell JR. Morphology, histology and functional anatomy of the canine cranial cruciate ligament. Vet Rec 1978;102:280-283.



5.



Scavelli TD, Schrader SC, Matthiesen DT, et al. Partial rupture of the cranial cruciate ligament of the stifle in dogs: 25 cases (1982-1988). J Am Vet Med Assoc 1990;196:1135-1138.



6.



Ström H. Partial rupture of the cranial cruciate ligament in dogs. J Small Anim Pract 1990;31:137-140.



7.



Tarvin GB, Arnoczky SP. Incomplete rupture of the cranial cruciate ligament in a dog. Vet Surg 1981;10:9495.



8.



Williams J, Fitch RB, Lemarié RJ. Partial avulsion of the origin of the cranial cruciate ligament in a 4 yearold dog. Vet Rad Ultrasound 1997;38:380-383.



9.



Noyes FR, Bassett RW, Grood ES, et al. Arthroscopy in acute traumatic hemarthrosis of the knee. J Bone Joint Surg (Am) 1980;62-A:687-695,757.



10. Odensten M, Lysholm J, Gillquist J. The course of partial anterior cruciate ligament ruptures. Am J Sports Med 1985;13:183-186. 11. Noyes, FR, Mooar, LA, Moorman III, CT et al. Partial tears of the anterior cruciate ligament. Progression to complete ligament deficiency. J Bone Joint Surg (Br) 1989;71-B:825-833. 12. Kivumbi CW, Bennett D. (1981) Arthroscopy of the canine stifle joint. Vet Rec 1981;109:241-249. 13. Miller CW, Presnell KR. Examination of the canine stifle: arthroscopy versus arthrotomy. J Am Animl Hosp Assoc 1985;21:623-629. 14. Van Ryssen, B. The stifle. In: Arthroscopy in the diagnosis and treatment of osteochondrosis in the dog. Thesis. Department of Diagnostic Imaging of Domestic Animals, Faculty of Veterinary Medicine, Ghent University, Belgium 1996;111-124. 15. Puymann K, Knechtl G. Behandlung der Ruptur des kranialen Kreuzbandes mittels Arthroskopie und minimal-invasiver Haltebandtechnik beim Hund. Kleintierprax 1997;42:601-612. 16. de Rooster H, Van Ryssen B, van Bree H. Ruptuur van de craniale gekruiste band bij de hond: radiografische diagnose met de tibilae compressietechniek en behandeling met behulp van een polyesterligament. Dissertation. Department of Diagnostic Imaging of Domestic Animals, Faculty of Veterinary Medicine, Ghent University, Belgium, 1993. 17. de Rooster H, Van Ryssen B, van Bree H. Diagnosis of cranial cruciate ligament injuries in dogs by tibial compression radiography. Vet Rec 1998;142:366-368. 18. Brünnberg L, Rieger I, Hesse EM. Sieben Jahre Erfahrung mit einer modifizierten “Over-the-Top”Kreuzbandplastik beim Hund. Kleintierprax 1992;37:735-746. 19. Bennett D, Tennant D, Lewis DG, et al. A reappraisal of anterior cruciate ligament disease in the dog. J Small Anim Pract 1988;29:275-297.



112



CHAPTER 2.2: Diagnosis 20. Riemersma DJ, Schamhardt HC. In vitro mechanical properties of equine tendons in relation to crosssectional area and collagen content. Res Vet Sci 1985;39:263-270. 21. Vasseur PB, Pool RR, Arnoczky SP, et al. Correlative biomechanical and histologic study of the cranial cruciate ligament in dogs. Am J Vet Res 1985;46:1842-1854. 22. Narama I, Masuoka-Nishiyama M, Matsuura T, et al. Morphogenesis of degenerative changes predisposing dogs to rupture of the cranial cruciate ligament. J Vet Med Sci 1996;58:1091-1097. 23. Noyes FR, DeLucas JL, Torvik PJ. Biomechanics of anterior cruciate ligament failure: an analysis of strainrate sensitivity and mechanisms of failure in primates. J Bone Joint Surg (Am) 1974;56-A:236-253. 24. O’Donoghue DH, Rockwood CA, Frank GR, et al. Repair of the anterior cruciate ligament in dogs. J Bone Joint Surg (Am) 1966;48-A:503-519. 25. Arnoczky SP, Rubin RM, Marshall JL. Microvasculature of the cruciate ligaments and its response to injury. An experimental study in dogs. J Bone Joint Surg 1979;61-A:1221-1229. 26. Butler DL, Noyes FR, Grood ES. Ligamentous restraints to anterior-posterior drawer in the human knee. J Bone Joint Surg (Am) 1980;62-A:259-270. 27. Arnoczky SP. The cruciate ligaments: the enigma of the canine stifle. J Small Anim Pract 1988;29:71-90. 28. Arnoczky SP, Marshall JL. The cruciate ligaments of the canine stifle: an anatomical and functional analysis. Am J Vet Res 1977;38:1807-1814. 29. Denny HR. Stifle lameness. Proceedings General Programme Orthopaedics in Small Animal Practice SAVAB Flanders WE, Belgium, 1998. 30. Arnoczky SP, Marshall JL. Pathomechanics of cruciate and meniscal injuries. In: Bojrab MJ, ed. Pathophysiology of Small Animal Surgery. Philadelphia:Lea and Febiger, 1981;590-603. 31. Alm A, Ekström H, Strömberg B. Tensile strength of the anterior cruciate ligament in the dog. Acta Chir Scand 1974;suppl 445:15-23.



113



114



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2.3



Radiographic measurement of craniocaudal instability in stifle joints of clinically normal dogs and dogs with injury of a cranial cruciate ligament H. de Rooster, H. van Bree



Department of Medical Imaging, Faculty of Veterinary Medicine, Ghent University Salisburylaan 133, 9820 Merelbeke, Belgium



Adapted from: American Journal of Veterinary Research 1999;60:1567-1570.



115



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CHAPTER 2.3: Diagnosis



SUMMARY Craniocaudal laxity of the stifle joint of dogs was determined when joints were positioned in tibial compression or neutral position. Relative displacements of bony landmarks were measured on paired lateral radiographs of 10 normal dogs, 29 stifle joints with varying injury to the cranial cruciate ligament (CCL), and 19 unaffected contralateral stifle joints. Two measuring techniques were customized for use in dogs. A wide range in measurements of laxity was found for stifle joints with intact CCLs. Differences in degree of damage to the ligament and medial meniscus cannot be deduced from the amount of relative displacement measured on radiographs. Pathologic changes to the CCL will not necessarily induce detectable changes in laxity of stifle joints in dogs.



INTRODUCTION Lameness of the hind limbs in dogs is often associated with the stifle joints. Instability resulting from damage to a cranial cruciate ligament (CCL) represents the majority of ligamentous injury to the stifle joints.1 Damage to a CCL in dogs is often overlooked at the time of initial injury. Classically, clinical diagnosis of cruciate disease is made on the basis of results of the cranial drawer2 and tibial compression3 tests.



In many dogs, veterinarians encounter difficulties eliciting



instability during physical examination only. Detection of craniocaudal instability may be masked by factors such as muscle tone caused by pain or stress, effusion, torn menisci, or periarticular fibrosis that develops in chronic cases of cruciate disease.4 Indirect signs of cranial cruciate rupture can be assessed on a standard lateral radiographic view of an affected stifle.5 On a radiograph of a joint in a stressed (tibial compression) position, a cranial shift of the proximal portion of the tibia will be visible in most dogs with CCL rupture.6,a In such dogs, exploratory arthrotomy or diagnostic arthroscopy to disclose CCL rupture can be avoided. The objective of the study reported here was to provide data on laxity of the stifle joint in clinically normal dogs, which could be used by clinicians when attempting to diagnose CCL rupture. The accuracy and usefulness of 2 measuring techniques for dogs with suspected



117



CHAPTER 2.3: Diagnosis damage to the CCL, without obvious radiographic displacement on lateral radiographic view with the joint positioned in tibial compression, was assessed.



MATERIAL AND METHODS Animals—Two distinct groups of intact stifle joints (normal joints in clinically normal dogs and unaffected contralateral joints in dogs with cranial cruciate deficiency) were examined. Careful attention was given to clinical details such as joint effusion, range of motion, signs of pain elicited during passive manipulation, and radiographic evidence of signs of early osteoarthritic (OA) changes. Radiographs of normal stifles were obtained from 10 clinically normal dogs; dogs were screened bilaterally, and none had a history of orthopedic problems. Only 19 radiographs were acceptable for use in the study, because excessive rotation of the femur caused 1 radiograph to be discarded from the group. Radiographs of 19 unaffected stifle joints of dogs with unilateral hind limb lameness were available for inclusion in this study. Of all unilaterally lame dogs, 4 were excluded because of bad radiographic positioning, 3 were not radiographed at the time of initial examination, and 3 were excluded because the dogs developed lameness in the second stifle joint before analysis of the study was completed. Four distinct cruciate pathologic categories were identified in affected joints: complete rupture of the CCL alone; complete rupture of the CCL with concomitant medial meniscal damage; partial rupture of the CCL alone; and partial rupture of the CCL with concomitant medial meniscal damage. The only dogs included in the study were those that had appropriate radiographs, had damage confirmed at the time of arthrotomy, and did not have obvious radiographic displacement. Twenty unilaterally lame dogs were evaluated intitially; 10 had complete rupture of the CCL alone, and 10 others had complete rupture of the CCL with concomitant medial meniscal damage. Six dogs that had stifle joints with partial rupture of the CCL and 3 with partial damage of the CCL and simultaneous tearing of the medial meniscus were also used in the study.



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CHAPTER 2.3: Diagnosis Procedure—Positioning of each dog and radiographic technique have been described in detail elsewhere.6 Briefly, each dog was positioned in lateral recumbency. A standard lateral radiographic view of the stifle joint was obtained with the joint at 90° of flexion (neutral position). While maintaining the angle of flexion of the stifle joint, the tarsal joint was maximally flexed by use of manual pressure, and a second radiograph was obtained (tibial compression position). Measurement of tibial displacement was performed by use of two techniques.



The



techniques were customized from those used in human medicine7-9 to account for canine anatomy (Fig 1) and were used to determine whether either of these procedures would be useful in dogs. The practice of using two transparent templates with vertical and horizontal intersecting lines was adapted from the measuring procedure developed by Kennedy and Fowler.7 In the first technique, the vertical line of template 1 was placed on the radiograph tangential to the fossa extensoria on the lateral femoral condyle. Template 2 was then placed on the radiograph, such that its horizontal line was superimposed on the horizontal line of template 1 and its perpendicular line was placed tangential to the most caudal point of the lateral tibial plateau (Fig 2 A). Distance between the two vertical lines was then recorded (mm).



For the second technique, the horizontal line of template 1 was placed on the



radiograph along the subchondral plate of the medial tibial plateau (ie, parallel to the joint line). The vertical line was placed on the radiograph tangential to the most caudal margin of the lateral tibial condyle. Again, horizontal lines of both templates were superimposed; however, with this technique, the perpendicular line on template 2 passed through the caudal margin of the lateral femoral condyle at the level of the physeal line (Fig 2 B). Both techniques were performed on paired lateral radiographs, with the stifle joint without stress (neutral) and with stress (tibial compression). The difference in distance between the two radiographic landmarks of joints in the neutral and tibial compression positions was regarded as the amount of relative craniocaudal laxity. Additional results were obtained by use of an adjustment made on the basis of size of each dog. This was accomplished by measuring the width of the femoral bone immediately proximal to the femoral groove and perpendicular to the long axis of the femur. Initial measurements were then divided by the diameter of the femur of that particular dog, and each resulting value was multiplied by 100 to achieve an adjusted value.



Radiographic



magnification was not considered, because the stifle joint was in direct contact with the radiographic cassette.



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CHAPTER 2.3: Diagnosis



Fig 1.



Bony landmarks used to determine craniocaudal instability in the stifle joints of dogs with and without injury to the cranial cruciate ligament 1. Fossa extensoria 2. Lateral tibial condyle 3. Subchondral plate medial tibial plateau 4. Lateral femoral condyle 5. Tibial tuberosity 6. Lateral intercondylar tubercle



A Fig 2.



B



Measurement of craniocaudal instability of the stifle joint A. By use of the first technique. Notice that the vertical line of template 1 is placed over the fossa extensoria and the vertical line of template 2 is placed over the caudal margin of the lateral tibial condyle B. By use of the second technique. Notice that the horizontal line of template 1 is placed over the subchondral plate of the medial tibial plateau and caudal margin of the lateral tibial condyle, whereas the vertical line of template 2 is placed over the caudal margin of the lateral femoral condyle



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CHAPTER 2.3: Diagnosis All measurements were made by the principle investigator (HdR). Reported values were the mean of two measurements. Investigators were unaware of the identity of the dog from which each radiograph was obtained, and neither clinical nor joint findings were known prior to obtaining the measurements.



Analysis of data—An initial analysis was made separately for each group of joints (normal, unaffected contralateral, partial rupture without medial meniscal damage, partial rupture with meniscal damage, complete rupture without medial meniscal damage, complete rupture with meniscal damage). On the basis of clinical criteria, initial groups of joints were fused 2 X 2, according to status of the CCL alone without regard for damage to the medial meniscus. Even so, stifle joints with intact CCLs were considered as 1 group when significant differences between normal joints in clinically normal dogs and unaffected joints in dogs with unilateral hind limb lameness could be detected and the statistical tests had sufficient power. A Kruskal-Wallis one-way ANOVA with Bonferroni adjustment was used to evaluate results; a value of P < 0.05 was considered significant. Results were evaluated among the various groups (with and without CCL and medial meniscal injury) for each joint and each group of joints determined on the basis of status of the CCL (intact, partial rupture, complete rupture). In addition, outcomes of sets of measurements (with and without adjustment for body size of each dog) were compared.



RESULTS Means of all measured values were summarized (Table 1).



Measurements in the



unaffected contralateral stifle joint of dogs with any degree of rupture of the CCL did not differ significantly from those in the normal stifles of clinically normal dogs between technique 1 and 2. In neutral rotation with the stifle joint flexed 90°, forward displacement of the tibia with respect to the femur (mean ± SD) was 1.2 ± 0.9 and 1.1 ± 1.0 mm in presumably intact joints (ie, normal joints in clinically normal dogs and unaffected contralateral joints in unilaterally lame dogs) for technique 1 and 2, respectively.



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CHAPTER 2.3: Diagnosis Table 1.



Mean (SD) amount of tibial displacement (mm) obtained from radiographs of various stifle joints of dogs



Techniques



N



Mean



SD



Techniques



N



Mean



SD



Technique 1 Normal Contralateral Intact (all) Partial Partial + MM Partial (all) Complete Complete + MM Complete (all)



19 19 38 6 3 9 10 10 20



1.3 1.1 1.2 4.0 2.0 3.3 3.2 5.2‡ 4.2‡



1.0 0.8 0.9 3.3 1.0 2.8 2.6 3.5 3.2



Technique 1 adjusted Normal Contralateral Intact (all) Partial Partial + MM Partial (all) Complete Complete + MM Complete (all)



19 19 38 6 3 9 10 10 20



7.4 8.0 7.7 16.5 10.9 14.6 22.0 32.6‡ 27.3‡



5.6 6.7 6.1 12.5 3.1 10.4 22.8 31.1 27.1



Technique 2 Normal Contralateral Intact (all) Partial Partial + MM Partial (all) Complete Complete + MM Complete (all)



19 19 38 6 3 9 10 10 20



1.0 1.1 1.1 3.7 4.3 3.9† 5.0‡ 5.9‡ 5.4‡



1.1 0.8 1.0 1.6 2.1 1.7 2.5 2.6 2.6



Technique 2 adjusted Normal Contralateral Intact (all) Partial Partial + MM Partial (all) Complete Complete + MM Complete (all)



19 19 38 6 3 9 10 10 20



5.5 6.6 6.0 17.1 14.0 16.1† 30.5‡ 36.0‡ 33.3‡



5.5 4.4 5.0 10.2 12.8 10.4 15.9 22.9 19.4



Significantly (*P