ILMU PENYAKIT DALAM VETERINER II

“Kasus Kematian Mendadak Akibat Pecahnya Aorta Pada Kuda”

Disusun oleh:
Kelompok 5 Kelas C

1. Gusti Putu Ayu Indira Pradnyani 1509005009

2. Luh Made Maha Cahyani 1509005010
3. Ni Luh Putu Diah Septianingsih 1509005017
4. I Wayan Dika Wahyu Hendrawan 1509005018

FAKULTAS KEDOKTERAN HEWAN

UNIVERSITAS UDAYANA
DENPASAR
2018
 PENDAHULUAN

Kematian mendadak pada kuda merupakan masalah serius yang dapat mempengaruhi
industri kuda di seluruh dunia. Kematian mendadak kuda di berbagai disiplin ilmu berkuda
telah dikaitkan dengan penyakit pernapasan dan kardiovaskular akut. Penyakit pernapasan
yang menyebabkan kematian mendadak termasuk latihan yang berat danperdarahan paru.
Kardiovaskular penyebab kematian mendadak termasuk miokarditis, pecahnya korda
tendinea, aorta atau arteri besar lainnya, aneurisma, dysrhythmia atrium, lesi katup, dilatasi
dan hipertrofi kardiomiopati, nekrosis miokard, sclerosing arteriopati koroner dan perdarahan
besar (Boden et al, 2005;. Lyle et al., 2010). Aorta adalah arteri utama yang membawa darah
dari ventrikel kiri jantung (ruang pompa utama) untuk semua arteri lainnya kecuali arteri
pulmonalis (KING; BRIGHT, 1999).

Tugas dari aorta adalah untuk membawa darah beroksigen dari paru-paru (yang
masuk jantung melalui atrium kiri, mengalir melalui katup bikuspidalis ke ventrikel kiri,
kemudian dipompa ke aorta) ke arteri tubuh (KING; BRIGHT, 1999). Air mata spontan atau
pecah terjadi di dinding aorta, menyebabkan suatu kondisi yang dikenal sebagai ruptur aorta
atau pecahnya aorta. Pecah aorta biasanya terjadi sangat dekat dengan persimpangan aorta
dengan hati (KING; BRIGHT, 1999). Pangkal aorta pecah pada kuda yang paling sering
menyebabkan kematian mendadak dikaitkan dengan perdarahan masif ke dalam rongga dada
(Orsini; DIVERS, 2008). Tidak ada obat medis atau bedah untuk pecah aorta pada kuda
(KING; BRIGHT, 1999).

Pecahnya aorta merupakan topik penting pada saat di dunia berkuda (DELESALLE,
2013). Ini telah menghasilkan banyak pendapat dan pertanyaan tentang pecahnya aorta pada
kuda kami bermaksud untuk menjelaskan hal tersebut dalam artikel ini. Tujuan dari
penelitian ini adalah untuk menyelidiki pecahnya aorta pada kuda melalui kajian literatur,
studi kasus dan faktor risiko.

ANATOMI

 Sistem Vaskular
Sistem vaskular mungkin secara acak dibagi ke dalam sistem arterial, mikrosirkulasi,
sistem vena, dan sistem limfatik (JUBB et al., 2007). Sistem arteri dibagi menjadi arteri besar
elastis, menengah dan arteri otot kecil, dan arteriol, dengan bertahap transisi antara divisi ini
(DONALD, 1999). Pembuluh arteri ditandai histopatologi oleh dinding terdiri dari tiga
lapisan: internal, menengah, dan tunika eksternal. Tunika intima ditandai dengan endotelium;
jaringan ikat, yang berisi kolagen, elastin, proteoglikan (substansi dasar), fibroblast, dan sel-
sel otot polos dan membran elastis internal. Media tunika terdiri dari lamina elastis dengan
sel-sel otot polos terletak di antara lamina. Substansi dasar intraseluler terutama menonjol di
media tunika arteri elastis di kuda. Jaringan serat kolagen dalam perluasan batas adventitia
arteri elastis (Jubb et al., 2007).
Respon cedera pembuluh darah melibatkan interaksi kompleks antara elemen seluler
dan nonseluler dari dinding pembuluh darah dan elemen seluler dan nonseluler darah. Sel-sel
utama pembuluh darah dalam reaksi ini sel endotel dan sel otot polos. Sel endotel yang aktif
secara metabolik dan memberikan monolayer thromboresistant pada antarmuka darah dan
dinding pembuluh darah. Arteri mungkin memiliki kelainan bawaan, degenerasi, nekrosis,
hipertrofi, mineralisasi, aneurisma dan pecah, trombosis dan emboli, vaskulitis dan
neoplasma. Aorta adalah batang arterial utama. Dasar ventrikel kiri, bagian pertama adalah
dorsal aorta asenden dan paru batang tengkorak (GETTY, 1996). Aorta dapat dibagi menjadi
toraks dan abdomen. Aorta toraks adalah dalam pericardium dan kemudian ditempatkan di
antara dua kantung pleura. Aorta abdominal bagian punggung berhubungan dengan vertebra
lumbalis, ventral ligamen longitudinal dan otot minor psoas kiri (GETTY, 1996).

 Kelainan Pembuluh Darah

Mengenai degenerasi dan nekrosis arteri, penyakit umum degeneratif pembuluh darah
pada hewan diklasifikasikan dalam tiga kelompok utama: 1) arteriosclerosis (perubahan
arteri kronis yang terdiri dari pengerasan, hilangnya elastisitas dan penyempitan lumen yang
dihasilkan biasanya dari proliferasi dan degeneratif, bukan inflamasi, perubahan media dan
intima); 2) aterosklerosis (iliaka dan arteri otot besar dan menengah, lesi penting adalah
ateroma atau fibrofatty plak, yang merupakan fokus, mengangkat, intima plak dengan inti
kolesterol lipid dan esternya sebagian besar ditutupi fibrosa); 3) arteriolosclerosis
(menggambarkan kelompok heterogen lesi arteriol bahwa mungkin didominasi hialin atau
didominasi hiperplastik).
Mineralisasi (kalsifikasi) cukup sering terjadi di arteri hewan baik sebagai distrofik
yang terjadi di daerah peradangan degenerasi dan trombosis, atau metastasis yang terjadi
sebagai hasil dari hiperkalsemia dan atau hiperfosfatemia. Arteri hipertrofi dapat
mempengaruhi satu atau semua komponen dinding arteri. Hipertrofi arteri telah dikaitkan
dengan penyakit pembuluh darah kolateral dalam menanggapi beban tambahan yang mereka
bawa setelah oklusi arteri (Jubb et al., 2007). Pecahnya pembuluh darah sebagai akibat dari
trauma fisik umum pecah spontan. Pecah terjadi selama periode aktivitas, seperti kuda pacu
atau kuda peternakan, dan mungkin terkait dengan peningkatan tekanan intra-aorta. Pecah
spontan dari arteri pulmonalis juga terjadi pada kuda, tapi bahkan jarang daripada pecahnya
aorta (DONALD, 1999).
Aneurysm adalah pelebaran yang abnormal dari setiap pembuluh darah. Aneurisma
yang paling penting ketika mereka mempengaruhi aorta. Tromboemboli terjadi dalam
berbagai kondisi. Dalam arteritis pada kuda, emboli timbul dari trombus di arteri
mesenterika tengkorak dan menyebabkan iskemia usus, dan mungkin infark. Trombosis
aorta-iliaka menyebabkan intoleransi latihan dan kaki kepincangan pada kuda yang terkena
dampak. Kondisi ini terlihat paling sering pada kuda pacu balap Standardbreds (Jubb et al.,
2007).

Gambar 1 (kiri). Rongga dada kuda terdiri dari organ paru-paru kanan, jantung dan aorta
& Gambar 2 (kanan). Thoracic aorta.
( Sumber : Briceno, 2013 )

 Studi Klinis dan Patologis

Literatur telah melaporkan ada 137 kasus kematian secara tiba-tiba akibat pecahnya
aorta pada kuda selama 28 tahun (1986-2014). Sekitar lima kuda meninggal karena pecahnya
aorta per tahun. Riwayat klinis diklasifikasikan sebagai berikut: Kuda dalam kegiatan atletik,
menunjukkan kolaps dan kematian mendadak (137 kuda), kuda dengan kematian mendadak
dalam kotak (4). Semua kuda dalam kegiatan atletik tanpa gejala sebelum jatuh. Pada kuda
dengan kematian mendadak di dalam kotak, dua kasus disajikan dengan obesitas berat.
Literatur melaporkan tanda-tanda menyajikan lesi jantung terdeteksi selama pemeriksaan
rutin dalam satu kuda. Lima kuda memiliki ventricular tachycardia monomorfik. Lima kuda
memiliki paling keras murmur kontinyu karakteristik di ruang intercostal IV kanan (MARR,
1998). Teknik pencitraan hanya dalam empat laporan kasus Echocardiography
mengungkapkan aneurisma dari sinus kanan aorta. Echocardiography (enam kuda) dan/atau
pemeriksaan post-mortem (empat kuda) mengungkapkan kuda memiliki fistula aorto-jantung
yang timbul dari sinus aorta tepat di semua lima kuda di mana situs itu direkam. Dua kuda
telah pecah dilatatisi aneurisma dari dinding aorta di situs ini. Fistula diperpanjang ke
ventrikel kanan di empat kuda; atrium kanan dalam dua kuda, ventrikel kiri dalam satu kuda,
dan lima kuda telah membedah traktat di septum miokardium (MARR, 1998). Nekropsi: kuda
diperiksa dan di nekropsi dan sampel jaringan dikumpulkan (ALUJA; Constantino, 2002;
BANKS, 1996).
Histopatologi : sampel jaringan difiksasi dalam formalin buffer 10% dan diproses
oleh konvensional teknik H&E (BANKS, 1996). Semua kuda dalam penelitian memiliki
kematian mendadak selama latihan atau selama kegiatan reproduksi, kecuali untuk dua kuda.
Evaluasi klinis semua kuda benar-benar tanpa gejala dan tidak menunjukkan tanda-tanda
klinis yang jelas dari gagal jantung, kecuali empat kuda yang memiliki gagal jantung di
klinik. Dinding aneurisma tipis, dan aneurisma menonjol ke dalam atrium kanan dan
ventrikel pada tingkat katup trikuspidalis (SLEEPER et al., 2001). Warna aliran Doppler
echocardiography tidak mengungkapkan aliran darah di seluruh aneurisma.
Diamati pecahnya aorta toraks menunjukkan fibrin dan bahan nekrotik. Dalam kedua
kasus infestasi oleh Strongylus sp, residu diamati memiliki larva parasit. Dalam Kuda Quarter
dengan aterosklerosis, diamati dermatitis alopecia dengan hiperpigmentasi dan xantomathosis
dari jaringan subkutan. Hemoperitoneum diamati dalam rongga perut, disebabkan oleh
pecahnya aliran aorta. Timbunan lemak (MORALES et al., 2012) yang diamati pada dinding
aorta. Aorta dinilai dalam munculnya dari hati, semua bagian-bagian dari lengkung aorta,
aorta toraks, dan aorta abdominal .
Pemeriksaan histologi dari dinding aorta menunjukkan daerah nekrosis yang tersebar
di seluruh dinding di kedua pembuluh darah. Di beberapa daerah ini, serat otot nekrotik
masih ada, sedangkan di lain serat otot menghilang dan serat elastis yang kental. Neutrofil
dan jaringan fibroangioblastic terlihat di sekitar wilayah nekrosis. Area kalsifikasi ditemukan
pada kuda. Semua kuda memiliki banyak vasa vasorum di media dan adventitia aorta dan
batang paru dengan intima penebalan, fibrosis medial, atau keduanya (LINDESIPMAN et al.,
1985).
 Histopatologi mengungkapkan degenerasi lemak dan nekrosis hati. Pada nekropsi di
dua kuda aorta ditemukan, penyemaian semua bagian-bagian yang muncul dari aorta di
jantung, arkus aorta, aorta toraks, dan aorta abdominal. Diamati diskrit perubahan degeneratif
makroskopik di intima. Evaluasi histologis dari bagian yang muncul dari aorta dengan hati
dibuktikan perubahan degeneratif dengan hilangnya kontinuitas dan distribusi serat elastis.
merinci retikulin khusus noda positif perubahan dari serat elastis dalam elektron proses studi
mikroskopis.

Gambar 3. Akar Aorta berasal dari ventrikel kiri jantung (lokasi

pecah biasanya terjadi).

( Sumber : Briceno, 2013 )

 Faktor Risiko
Pecahnya aorta merupakan penyebab kematian mendadak pada kuda atletik, tanpa
predisposisi untuk ras, usia, jenis kelamin, dan bahkan berkuda disiplin demografi.
Patogenesis pecahnya aorta dijelaskan di bawah ini serta faktor terkait:

1. Ruptur Spontan terkait dengan Hipertensi

Pecah aorta spontan dapat terjadi pada kuda. Fenomena yang terkait dengan hipertensi
selama latihan atau latihan posting masih tidak menjelaskan patogenesis. Ternyata, fenomena
mungkin berhubungan dengan hipertensi. Hal ini dapat disampaikan selama tahun ketika
kapasitas elastis hipertensi pembuluh darah melebihi dinding dinamika fisiologis aorta.
Kejadian ini dapat terjadi tanpa adanya tanda-tanda klinis sebelumnya dan makroskopik
revisionary dan histologi perubahan endotel aorta tidak diamati, hanya tiba-tiba pecah aorta.

2. Cedera Vaskular yang sudah ada sebelumnya (Aneurisma)

Lesi-lesi vaskular seperti aneurisma, dilations, hipertrofi vaskuler aorta, dapat
mempengaruhi aorta kuda pecah. Aneurisma yang berhubungan dengan plak ateromatosa,
aterosklerosis, dan aterosklerosis, dengan kemungkinan perforasi, dapat terjadi berhubungan
dengan sindrom metabolik kuda dan obesitas. Migrasi oleh larva Strongyles dan arteritis
penuh kutu yang umum di kuda dengan parasit usus yang parah, sebagian besar terjadi di
aorta. Perubahan dari vasorum vasa dari pembuluh darah besar dapat mempengaruhi mereka
untuk pecah dari efek tekanan pada dinding pembuluh darah. Diamati lesi parah dari
penebalan aorta dan kekakuan katup aorta. Secara histologis, media tunika aorta, arteri
koroner, dan arteri paru diperluas oleh fokus elastin kalsifikasi serat dan matriks ekstraselular
dengan formasi kekosongan. Lesi vaskuler yang komparatif dengan apa yang telah
digambarkan sebagai kalsifikasi arteri medial, terlihat pada manusia yang menderita gagal
ginjal kronis atau diabetes mellitus. Tidak ada paparan vitamin D yang mengandung atau
bahan pakan bisa didokumentasikan pada saat onset atau selama periode tanda-tanda klinis.
Kasus saat menggambarkan lesi dramatis arteri kalsifikasi medial dari aorta, koroner, dan
arteri paru penyebab belum ditentukan (FALES-WILLIAMS, et al., 2008). Infeksi sekunder
telah dilaporkan pada anak kuda dan pengembangan aneurisma aorta distal (Archer et al.,
2012).

3. Dilatasi Kardiomiopati / Hypertrophic

Cedera jantung yang sudah ada sebelumnya juga dapat mempengaruhi hewan untuk
resiko pecahnya aorta, seperti melebar atau hypertrophic cardiomyopathy. Masalah katup
seperti katup endokarditis oleh vegetatif atau mineralisasi dari katup dapat meningkatkan
risiko pecahnya aorta.

4. Tingkat Tembaga di Endothelium

Pecahnya aorta, arteri pulmonalis, atau arteri koroner terjadi secara eksperimental,
meskipun bukan sebagai kejadian alami, dan telah banyak diteliti karena kesamaan dengan
sindrom Marfan. Sindrom Marfan adalah gangguan yang diturunkan dalam metabolisme
fibrillin pada manusia dan ternak, di mana pembedahan aneurisma aorta terjadi (Jubb et al.,
2007). Degenerasi elastis tampaknya menjadi dasar dari lesi vaskular kekurangan tembaga,
dan karena kekurangan enzim yang mengandung tembaga, lysyl oksidase, yang bertanggung
jawab untuk silang kolagen dan elastin (Jubb et al., 2007 ).

5. Genetik : Predisposisi Rasial Perkawinan Sedarah

Perkawinan sedarah di kuda ras dapat berperan dalam pengembangan malformasi
pembuluh darah dan jantung yang sebagian besar tidak dilaporkan jika terjadi pada tahap
awal kehidupan, tetapi kadang-kadang terlihat di nekropsi. Garis genetik yang signifikan
rentan terhadap fenotipe atau genotipe sifat-sifat tertentu mungkin bisa menjadi rentan
hipertensi vaskular. Karena ruptur kantung aorta dan pulmonal terjadi pada tiga kuda Friesian
yang merupakan keturunan dari pejantan yang sama, penyebab genetik tidak dapat
dikecualikan (LINDE-SIPMAN et al., 1985).

6. Toksisitas / zat asing: Anabolik, stimulan dan obat-obatan lainnya

Steroid anabolik juga memiliki efek langsung pada jantung dan pembuluh darah.
Dalam konsentrasi tinggi mereka membunuh sel-sel jantung dan menghasilkan gumpalan
darah. Ini kecil, gumpalan hampir tak terlihat dapat memotong jaringan dari lapisan
pembuluh darah. Efek negatif lain dari androgen adalah bahwa mereka menyebabkan
penyempitan pembuluh darah (stenosis). Ternyata efek kortikosteroid in vitro tidak melukai
endotel dalam dosis tinggi dan stress. Namun, penelitian lain menunjukkan untuk pertama
kalinya bahwa glukokortikoid mengerahkan efek toksik langsung pada sel endotel melalui
mekanisme kematian sel caspase-independen (VALAMANESH et al., 2009).
Seperti kita ketahui, balap dapat menghasilkan vasokonstriksi perifer dan dengan
volume darah tinggi dan fisiologis jantung stres dengan olahraga dapat menyebabkan
kejenuhan dan kosngesti dari akibat pecahnya aorta. Anabolik steroid nandrolone dapat
menyebaban kerusakan endotel langsung melalui produksi gumpalan kecil dari predisposisi
trombosi yang dapat menyebabkan hipertensi pada kerusakan fisik langsung pada ruptur
endothelium (FERENCHICK, 1991). Nandrolone juga dapat menghasilkan stenosis
pembuluh darah dengan terbatas vasokonstriksi arteri aorta dan vasodilatasi dan berbagai
efek samping beracun termasuk perubahan kardiovaskular (FERENCHICK, 1991).
Korelasi nekropsi dan histopatologi hasil dengan laporan toksikologi dan farmakologi
harus dikaji lebih lanjut untuk aorta pada kuda. Stimulan cardio dan zat-zat asing anabolik
seperti clenbuterol dapat menghasilkan gangguan hipertensi berat pada penyakit gagal
jantung dan pembuluh darah yang mengakibatkan cedera aorta (SLEEPER et al., 2002).
Kafein dan zat-zat lain yang cardiostimulatory mungkin bisa menginduksi kejenuhan aorta.
Meskipun tidak dilaporkan dalam literatur tetapi diamati secara klinis, hsl ini biasa terjadi
pada kuda yang diberi obat L-carnitine untuk antioksidan dan pengembangan massa otot
rangka, mungkin juga dapat mengalami hipertrofi otot jantung. Kekerasan air minum (yaitu,
jumlah konsentrasi kalsium dan magnesium) telah berhubungan dengan konsentrasi cadmium
di korteks ginjal dan tanda-tanda mikroskopis arteriosklerosis dan fibrosis miokard fokus di
50 kuda Swedia yang disembelih untuk produksi daging (ELINDER et al., 1980 ).

7. Kesamaan dengan Perdarahan Paru yang disebabkan oleh latihan

Kematian mendadak akibat arteri bronkial segmental yang pecah pada kuda dengan
pendaharan pulmonal akibat latihan sangat homolog pada pecahnya aorta, yang dianggap
sebagai diagnosis diferensial dalam kasus kematian mendadak. Karakteristik yang terkait
dengan pecahnya aorta kuda telah diuraikan oleh Linde-Sipman et al., (1985). Pecah aorta
terlokalisasi tepat di atas katup aorta adalah penyebab kematian akut yang lebih umum pada
kuda, terutama terjadi pada kuda-kuda yang kelebihan berat badan. Pecahnya di lokasi ini di
aorta mungkin karena fakta bahwa dinding aorta lebih tipis di daerah ini daripada di tempat
lain.
Penjelasan lain mungkin faktor hemodinamik dan mekanik, disertai dengan
degeneratif, nekrotik, peradangan atau sclerosing perubahan dari dinding aorta. Pemeriksaan
histologi dinding aorta dan batang paru-paru dari empat kuda menunjukkan kelainan yang
hampir identik. Perubahan dari vasa vasorum dari pembuluh darah besar, seperti yang
ditemukan di kuda-kuda kami, tidak disebutkan dalam literatur sebagai penyebab pecahnya
aorta dan batang paru. Penghilangan sebagian atau seluruh banyak vasa vasorum mungkin
telah menyebabkan hipoksia atau anoksia dari dinding pembuluh yang mengakibatkan
gangguan sirkulasi, nekrosis, dan akhirnya, dalam pecahnya dinding. Aorta dan arteri
ekstrapulmoner diperiksa secara patologis di 33 kuda pacu ras mulai usia satu sampai lima
tahun. Banyak pembuluh darah besar kuda ini menunjukkan perubahan degerneratif atau
sklerotik di media dengan lipidosis atau endapan kolesterol (Imaizumi et al., 1989). Lesi
berat yang sebagian besar diamati pada bifurkasi dari arteri pulmonalis (Imaizumi et al.,
1989).

8. Trauma Alat Gerak Terkait

Penggerak kuda selama latihan (berderap dan melompat) menghasilkan beberapa
pasukan bongkar efek kompresi massa. Teori ini didasarkan pada kenyataan bahwa selama
berderap, tidak adanya keterikatan tulang kaki depan ke tulang di kuda menyebabkan bahu
untuk kompres tulang rusuk kranial (Schröter et al., 1998). Dengan demikian, permukaan
dampak dengan gerakan yang dihasilkan di organ kranial selama arah ventral dan berderap
kuda melompat entah bagaimana dapat memampatkan aorta di dasar atau di beberapa
bagiannya (dada, perut) dan menghasilkan pecah traumatis.

DISKUSI
Kematian mendadak dan tak terduga pada kuda telah dilaporkan dalam literatur sejak
1982. Dalam beberapa tahun terakhir, laporan telah meningkat secara global tanpa geografis
tertentu daerah, Peristiwa berkuda di Internasional (balap, berkuda, rodeo, daya tahan dan
kompetisi lainnya). Pecahnya aorta pada kuda adalah kondisi patologis yang parah yang telah
diberikan kurang penting tapi sangat mempengaruhi industri kuda. Lesi aorta tampak sangat
umum dalam kinerja tinggi kuda atletik di seluruh dunia.
Beberapa faktor predisposisi dan menentukan pecahnya aorta pada waktu tertentu,
paling sering terjadi selama latihan. Hanya beberapa kasus dapat hadir pertama dengan
intoleransi latihan tapi sebagian besar terjadi tiba-tiba. Ada kecenderungan yang berhubungan
dengan usia jelas dalam kuda lebih dari 10 tahun tetapi ada juga peningkatan risiko untuk
kuda yang berusia 2 tahun, serta mempengaruhi kuda dalam proses reproduksi. Sehubungan
dengan seks, ada banyak kasus di kuda jantan. Keturunan dilaporkan merupakan kasus
tertinggi, diikuti oleh kuda dan Quarter Hourse, Friesians. Keturunan lain termasuk Creole
Venezuela, Halfbreeds Belanda, Standardbreds, Warmbloods dan Trakehners telah
dilaporkan pada skala kecil, ada kemungkinan bahwa ini terkait dengan kondisi genetik di
kuda. Fistula Aortocardiac biasanya ditemukan dalam sinus aorta tepat di kuda, membedah
ke atrium kanan atau ventrikel (MARR et al., 1998). Fistula aortocardiac menyebabkan
kelebihan beban volume yang biventrikular di sebagian besar kuda. Kondisi ini harus
dipertimbangkan sebagai diagnosis diferensial untuk kuda-kuda yang mengalami distress
akut, kolik, denyut jantung cepat dengan takikardia ventrikel monomorfik, melompat-lompat
dan murmur rightsided terus menerus, terutama di kuda setengah baya dan lebih tua.
Fistulation aorta paru-paru dalam hubungannya dengan pecahnya aorta lebih sering
terjadi pada Friesians dari perkiraan sebelumnya (PLOET et al., 2013). Dalam beberapa
kasus, temuan menunjukkan patologi progresif daripada gagal jantung akut dan kematian
mendadak (PLOET et al., 2013). Pada manusia, pecahnya aorta toraks (TAR) diakui sebagai
penyebab kematian pada korban trauma tumpul dan kematian langsung adalah 85% (Conor,
2004). Poin penting untuk diperhatikan adalah kondisi asimtomatik dari kuda-kuda ini. Hal
ini sangat penting karena meskipun setiap kuda dalam kompetisi untuk peraturan Nasional
dan Internasional sehingga mendalam diperiksa sebelum kompetisi oleh dokter hewan resmi.
Tidak mungkin untuk mendiagnosa atau memprediksi kondisi patologis ini.
Evaluasi toksikologi kasus ini dibuat sebagian besar tanpa deteksi zat yang dilarang.
Baru-baru ini di California, USA, laporan dari sejumlah besar kasus kematian mendadak
pasca-ras, yang telah digambarkan sebagai sindrom kematian mendadak kuda. Singkatnya,
pecahnya aorta menyebabkan kematian mendadak dan tak terduga bahwa dalam kebanyakan
kasus tidak menunjukkan tanda-tanda klinis yang jelas, hanya runtuhnya akut dan kematian
mendadak. Tanda-tanda klinis yang kesusahan, takikardia, distensi jugularis, membran
mukosa pucat dan berlari pulsa arteri. Tanda-tanda ini mungkin bingung dengan kolik.
Diagnosis diferensial adalah: EIPH (exerciseinduced perdarahan paru), gagal jantung akut,
kegagalan pernafasan dan kuda sindrom kematian mendadak baru-baru ini. Diagnosis dibuat
dengan evaluasi klinis, elektrokardiogram, ekokardiogram dan post mortem dengan cara
nekropsi. Dalam kebanyakan kasus prognosis dicadangkan.

KESIMPULAN
Pecahnya aorta merupakan penyebab penting kematian mendadak pada kuda atletik.
Kesimpulannya, perubahan degeneratif pada serat elastis diskrit dari intima aorta dalam
munculnya jantung tampaknya mempengaruhi pecahnya dinding aorta pada saat tekanan
darah maksimum selama latihan dan runtuhnya akibat syok hipovolemik dan kematian kuda
atletik. Studi lebih dalam diperlukan untuk menjelaskan etiologi dan menetapkan beberapa
mekanisme kontrol yang mengurangi angka kematian kuda. Hal ini sangat mempengaruhi
industri kuda untuk kerugian ekonomi.
298

Sudden death, aortic rupture in horses, literature review,

case studies reported and risk factors
Morte súbita por ruptura da aorta em cavalos, literatura,
estudos de casos relatados e fatores de risco
Abelardo Morales BRICEÑO¹; Aniceto MENDEZ¹; Kimberly BREWER²;
Charlie HUGHES³; Thomas TOBIN³
¹ University of Cordoba, College of Veterinary Medicine,
Department of Anatomy and Comparative Anatomic Pathology – Córdoba, Spain
² Phoenix Rising Veterinary, Wellington – Florida, USA
³ University of Kentucky, The Maxwell H. Gluck Equine Research Center, Lexington – Kentucky, USA

Abstract
Sudden deaths of horses in multiple equestrian disciplines have been attributed to acute and chronic respiratory and
cardiovascular diseases. The aim of this study was to perform a review of aortic rupture in horses analyzing , case studies
and assessing risk factors. The literature has reported a total of 137 cases of aortic rupture in horses for 28 years (1986-
2014), with approximately five horses dying of aortic rupture per year. Histopathologically, there are observed discrete
macroscopic degenerative changes in the intima layer only in the aorta. The histological evaluation in the beginning
portion of the aorta of the heart evidenced degenerative changes with loss of continuity and distribution of elastic fibers.
Risk factors for the rupture of the aorta are: spontaneous rupture associated with hypertension, preexisting vascular
injury (aneurysm), dilated or hypertrophic cardiomyopathy, copper levels in the endothelium, genetic factors such
as inbreeding, toxicology or pharmacological factors. Aortic rupture shows similarity with pulmonary hemorrhage
induced by exercise especially under the locomotors induced trauma theory of exercise that can induce pulmonary
hemorrhage. In conclusion, degenerative changes to discrete elastic fiber of the intima of the aorta in the emergence
of the heart seem to predispose the aorta wall rupture at the time of maximum blood pressure during exercise and the
consequent collapse and athletic horse’s death.
Keywords: Aorta. Equine. Horse. Sudden dead. Thoroughbreds.

Resumo
As mortes súbitas de cavalos em várias provas equestres têm sido atribuídas a doenças respiratórias e cardiovasculares
agudas e crônicas. O objetivo deste estudo foi efetuar uma revisão de literatura da ruptura da aorta em cavalos analisando
estudos de caso e estabelecendo os possíveis fatores de risco. Na revisão da literatura no período de 28 anos (1986-
2014) foram localizados 137 casos de ruptura da aorta em cavalos com aproximadamente cinco cavalos morrendo por
essa causa por ano. Histologicamente, são observadas alterações macroscópicas discretas degenerativas na camada
íntima da aorta. A avaliação histológica na porção inicial da aorta do coração evidencia alterações degenerativas com
perda de continuidade e distribuição das fibras elásticas. Fatores de risco para a ruptura da aorta dos cavalos são:
ruptura espontânea associada com hipertensão, lesão vascular pré-existente (aneurisma), cardiomiopatia dilatada ou
hipertrófica, níveis de cobre no endotélio, fatores genéticos, tais como a consanguinidade na criação, toxicologia e
aspectos farmacológicos. A ruptura aórtica mostra semelhança com hemorragia pulmonar induzida pelo exercício.
Em conclusão, alterações degenerativas discretas das fibras elásticas da íntima da aorta parecem predispor a ruptura da
parede da aorta, no momento da pressão máxima de sangue durante o exercício determinando o consequente colapso
e morte do cavalo atleta.
Palavras-chave: Aorta. Equino. Cavalo. Morte súbita. Thoroughbreds.

Introduction Correspondence to:

Abelardo Morales Briceño
Sudden death in horses is a serious problem affecting University of Cordoba, College of Veterinary Medicine, Department of
the equine industry worldwide. Sudden deaths of horses Anatomy and Comparative Anatomic Pathology, Edificio de Sanidad Animal
Campus de Rabanales Ctra. de Madrid km 396
in multiple equestrian disciplines have been attributed 14071, Córdoba, Spain
E-mail: aamorales13@gmail.com
to acute respiratory and cardiovascular disease.
Respiratory causes of sudden death include exercise- Received: 18/05/2015
Approved: 21/10/2015
induced pulmonary hemorrhage. Cardiovascular

Braz. J. Vet. Res. Anim. Sci., São Paulo, v. 52, n. 4, p. 298-309, 2015
DOI: 10.11606/issn.1678-4456.v52i4p298-309

causes of sudden death include myocarditis, rupture
of chordae tendineae, aorta or other large arteries,
aneurysm, atrial dysrhythmia, valvular lesions,
dilated and hypertrophic cardiomyopathy, myocardial
necrosis, sclerosing coronary arteriopathy and massive
disseminated hemorrhage (BODEN et al., 2005; LYLE
et al., 2010). The aorta is the main artery that carries
blood from the left ventricle of the heart (the major
pumping chamber) to all the other arteries except
the pulmonary artery (KING; BRIGHT, 1999). Its job
is to bring oxygenated blood from the lungs (which
enters the heart through the left atrium, flows through
the bicuspid, or mitral, valve into the left ventricle,
then is pumped into the aorta) to the arteries of the
body (KING; BRIGHT, 1999). However, sometimes
a spontaneous tear or break occurs in the wall of the
aorta, causing a condition known as an aortic rupture.
Aortic ruptures usually occur very close to the junction
of the aorta with the heart (KING; BRIGHT, 1999).
Aortic root rupture in horses most frequently results in
sudden death associated with massive hemorrhage into
the thoracic cavity (ORSINI; DIVERS, 2008). There
are no medical or surgical cures for aortic ruptures
in horses (KING; BRIGHT, 1999). Aortic rupture is
an important topic at the moment in the equestrian
world (DELESALLE, 2013). Equestrian journals often
report that in competing horses and stallions that
died suddenly, the necropsy report showed they were
diagnosed with a ruptured aorta. This has generated
many opinions and questions about aortic rupture in
horses; we intend to elucidate with this article. The aim
of this study was to investigate aortic rupture in horses
through literature review, case studies and risk factors.
Revised Anatomical
The Vascular System
The vascular system may be arbitrarily divided into
the arterial system, microcirculation, venous system,
and lymphatic system (JUBB et al., 2007). The arterial
system is subdivided into large elastic arteries, medium
and small muscular arteries, and arterioles, with gradual
299
transitions between these divisions (DONALD, 1999).
Arterial vessels are characterized histopathologically
by walls composed of three layers: the internal, middle,
and external tunics. The tunica intern (intima) is
characterized with endothelium; subendothelial
connective tissue, which contains collagen, elastin,
proteoglycan (ground substance), fibroblasts, and
smooth muscle cells and the internal elastic membrane.
The tunica media (media) consists of fenestrated elastic
laminae in elastic arteries, with smooth muscle cells
lying between laminae. Intracellular ground substance
is especially prominent in the tunica media of elastic
arteries in the horse. Contraction of muscular arteries
and arterioles upon an animal´s death forces blood
from the lumina, and causes longitudinal folding that
appears as scalloping of the internal elastic membrane
when seen in cross-section. The adventitia consists
of a network of elastic and collagen fibers continuous
with the surrounding connective tissue. The interlacing
network of collagen fibers in the adventitia limits
expansion of the elastic arteries (JUBB et al., 2007).
The response of vessels to injury involves a complex
interaction among the cellular and noncellular elements
of the vessel wall and the cellular and noncellular
elements of the blood. The key cells of vessels in these
reactions are endothelial cells and smooth muscle cells.
Endothelial cells are metabolically active and provide a
thromboresistant monolayer at the interface of blood
and the vessel wall. The arteries may have congenital
abnormalities, degeneration, necrosis, hypertrophy,
mineralization, aneurysms and ruptures, thrombosis
and embolism, vasculitis and neoplasms. The aorta is
the main arterial trunk. The base of the left ventricle,
its first part is dorsal ascending aorta and pulmonary
trunk cranial (GETTY, 1996). The descending aorta
can be divided into thoracic and abdominal. The
thoracic aorta is within the pericardium and then is
placed between the two pleural sacs. The abdominal
aorta is related dorsally with lumbar vertebrae, ventral
longitudinal ligament and the left psoas minor muscle
(GETTY, 1996).
Braz. J. Vet. Res. Anim. Sci., São Paulo, v. 52, n. 4, p. 298-309, 2015
300
Abnormalities of the blood vessels
Congenital anomalies with minor variations
occur among individuals of a species in the course
and distribution of arteries, but these are of little
significance. Regarding degeneration and necrosis
of arteries, generalized vascular degenerative disease
in animals is classified in three principal groups: 1)
arteriosclerosis (chronic arterial change consisting of
hardening, loss of elasticity and luminal narrowing
resulting usually from proliferative and degenerative,
rather than inflammatory, changes of the media and
intima); 2) atherosclerosis (affects the large and elastic
arteries as aorta, iliac and the large and medium
muscular arteries, the essential lesion is the atheroma
or fibrofatty plaque, which is a focal, raised, intimal
plaque with a core of lipid cholesterol and its esters
largely covered fibrous cap); 3) Arteriolosclerosis
(describes a heterogeneous group of arteriolar lesions
that maybe predominantly hyaline or predominantly
hyperplastic). Mineralization (calcification) occurs
quite frequently in the arteries of animals either as
dystrophic which occurs in areas of inflammation
degeneration and thrombosis, or metastatic which
occurs as the results of hypercalcemia and/or
hyperphosphatemia. Arterial hypertrophy may affect
one or all components of the arterial wall. Arterial
hypertrophy has been associated with high altitude
disease with collateral vessels in response to the extra
load they carry after occlusion of the artery (JUBB
et al., 2007). Vasculitis or inflammation of a vessel
is characterized by the presence of inflammatory
cells within and around the blood vessel wall with
concomitant vessel wall damage as indicated by
fibrin deposition, collagen degeneration and necrosis
endothelial and smooth muscle cells (JUBB et al.,
2007). Rupture of arteries as a result of physical
trauma is common; spontaneous ruptures are not.
Rupture of the aorta is well known, but certainly
uncommon, in the horse. The ruptures occur during
periods of excitement and activity, such as racing or
in stallions while breeding, and are probably related to
Braz. J. Vet. Res. Anim. Sci., São Paulo, v. 52, n. 4, p. 298-309, 2015
increased intra-aortic pressure. Spontaneous rupture
of the pulmonary artery also occurs in horses, but is
even less frequent than aortic rupture (DONALD,
1999). An aneurysm is a localized abnormal dilation
of any vessel. Aneurysms are of most importance
when they affect the aorta. Thromboembolism occurs
in a variety of conditions. In verminous arteritis of
horses, emboli arise from thrombi in the cranial
mesenteric artery and cause intestinal ischemia, and
possibly infarction. Aortic-iliac thrombosis causes
exercise intolerance and hind-leg lameness in affected
horses. The condition is seen most frequently in
racing Thoroughbreds and Standardbreds, especially
among young males (JUBB et al., 2007).
Review of cases of sudden death in horses reported
in the literature (period 1986-2014)
Below are the cases of sudden death associated
with rupture of the aorta, aneurysm and pulmonary
hemorrhage in horses reported in the literature between
1986-2014 are described (Table 1).
Clinical and pathological study
The literature has reported a total of 137 cases of
sudden death aortic rupture in horses for 28 years
(1986-2014). Approximately five horses died of aortic
rupture per year. Clinical history was classified as
follows: Horses in athletic activity, showed collapse
and sudden death (137 horses), horses with sudden
death in the box (04). All horses in athletic activity
were asymptomatic before the collapse. In horses with
sudden death in the box, two cases presented with severe
obesity. The literature report the presenting signs were
acute distress and cardiac lesion was detected during
a routine examination in one horse. Five horses had
monomorphic ventricular tachycardia on admission
and another had a history of this arrhythmia. Five
horses had a characteristic continuous murmur
loudest in the right fourth intercostal space (MARR,
1998). Imaging techniques only in four case reports:
Echocardiography revealed an aneurysm of the right
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Table 1 – Retrospective study of mortality aortic rupture in horses by location and year
YEAR DIAGNOSTIC BREED SEX YEAR OLD COUNTRY REFERENCE
1986 Necrosis and rupture of Dutch halfbreed 3 Mare 15,10,13 Netherlands Linde-Sipman, et al.,1985
the aorta 1 Stallion 12

1987 Necrosis and rupture of Standardbreed 1 Mare 15 USA Roby, et al., 1987
the aorta

1990 Rupture of the aorta Thoroughbred 1Stallion 2 USA California Horse Racing Board
4

1991 Rupture of the aorta Thoroughbred 1 Stallion 3 USA California Horse Racing Board

1993 Rupture of the aorta Thoroughbred 1 Stallion 4 USA California Horse Racing Board

1994 Rupture of the aorta Thoroughbred 2 Mare USA Jhonson, et al., 1994; California
3 Stallion Horse Racing Board

1995 Rupture of the aorta Thoroughbred 1 Stallion 3 USA California Horse Racing Board

1998 Aorto cardiac fistules Thoroughbred 3 Mare 15,10,13 UK Marr, et al. 1998
Arabian Standardbreed 4 Stallion 12,15,18,10

1999 Aneurism aortic Thoroughbred 1 Mare 4 JAPAN Shirai, et al., 1999

and rupture

2000 Rupture of the aorta Thoroughbred 1 Stallion 3 USA California Horse Racing Board

2001 Rupture of the aorta Thoroughbred 5 Stallion 2,4,10,12,14 USA Blood-Horse, 2001
Sleeper, et al., 2001

2002 Rupture of the aorta Thoroughbred 1 Mare 4 USA California Horse Racing Board

2003 Rupture of the aorta Thoroughbred 1 Mare 4 USA Blood-Horse, 2003a, Blood-Horse,
5 Stallion 19,13,18,4,5,2 2003b, Blood-Horse, 2003c,
California Horse Racing Board

2005 Rupture of the aorta Thoroughbred 1 Stallion 15 USA Blood-Horse, 2005

2006 Rupture of the aorta Thoroughbred 2 Stallion 12, 13 USA Blood-Horse, 2006a, Blood-Horse,
2006b

2007 Rupture of the aorta Thoroughbred 2 Stallion 1, 2 USA Blood-Horse, February 25, 2007

2008 Rupture of the aorta Thoroughbred 2 Mare 4,5 USA Lieser&Netzler, May 11, 2008;
and EIPH 2 Stallion 17,2 Venezuela Morales, et al., 2013

2009 Rupture of the aorta Thoroughbred 2 Mare 5,8 USA Blood-Horse, 2009; Morales,
and EIPH Quarter Horse 4 Stallion 26,5,4,7 Venezuela et al., 2013

Thoroughbred Blood-Horse, August 15,

2010 Rupture of the aorta Quarter Horse 8 Mare 2,6,2-6 USA 2010; The Jurga Report 2010;
and EIPH Trakehner 8 Stallion 17,5,7,2-4 Venezuela Morales et al., 2012;
Venezuelan Creole horse Morales, et al., 2013.

2011 Rupture of the aorta Thoroughbred 10 Mare 4-10 USA Blood-Horse, January 9, 2011;
and EIPH Quarter Horse 14Stallion 23-2 Venezuela Blood-Horse, October 18, 2011;
Nir, S. M, et al., 2011; Fortnum,
2011; Lyle, et al., 2011; California
Horse Racing Board.

2012 Rupture of the aorta Thoroughbred 4 Mare 2-8 USA Phyllis Carters journal. 2012;
and EIPH Quarter Horse 8 Stallion 21-10 Venezuela Cbsnews, 2013; Morales, et al.,
2013; California Horse Racing
Board. Graef, 2012.

2013 Rupture of the aorta Thoroughbred 2 Mare 8-12 Japan Lesté-Lasserre, January 2013;
and EIPH Belgian Warmblood 6 Stallion 14, 20-5 France Blood-Horse, February 20,
Rodeo Horse USA 2013; Horsetalk.co.nz,
May 20, 2013; Nye, 2013;
California Horse Racing Board.

2014 Rupture of the aorta Friesian 10 Mare 2-15 Netherlands Ploeg, et al., 2014; Blood-Horse,
Thoroughbred 15Stallion 20-10 USA 2014a; Espn, 2014; The horse,
France 2014b.
Canada

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302
aortic sinus. Echocardiography (six horses) and/
or post-mortem examination (four horses) revealed
the horses had aorto-cardiac fistulas arising from the
right aortic sinus in all five horses in which the site
was recorded. Two horses had ruptured aneurysm
dilatations of the aortic wall at this site. Fistulas
extended into the right ventricle in four horses; the
right atrium in two horses, the left ventricle in one
horse, and five horses had dissecting tracts in the
septal myocardium (MARR, 1998). Necropsy: horses
were examined by necropsy and samples of tissue
were collected (ALUJA; CONSTANTINO, 2002;
BANKS, 1996). Histopathology: the tissue samples
were fixed in formalin buffered 10% and processed
by conventional H&E techniques (BANKS, 1996).
The results are presented in table 1 and are described
below. All horses in study had sudden death during
exercise or during the reproductive activity, except
for two horses (2 Creole Venezuelans and 1 Quarter
Horse). Clinical evaluation: all horses were completely
asymptomatic and showed no apparent clinical signs
of cardiovascular failure, except four horses that had a
cardiovascular failure at the clinic. Imaging: only four
cases revealed an aneurysm of the right aortic sinus by
echocardiography. The wall of the aneurysm was thin,
and the aneurysm bulged into the right atrium and
ventricle at the level of the tricuspid valve (SLEEPER
et al., 2001). Color flow Doppler echocardiography
did not reveal any blood flow across the aneurysm;
however, swirling turbulent flow was evident within
the aneurysm (SLEEPER et al., 2001). A small jet
of mitral regurgitation was detected with color flow
Doppler echocardiography and was deemed to be
clinically insignificant at the time of evaluation
(SLEEPER et al., 2001). Necropsy: on necropsy,
massive hemothorax from severe thoracic aortic
aneurysm was observed with ruptured and fibrin
in all cases. Observed rupture of the thoracic aorta
showed fibrin and necrotic material. In both cases of
infestation by Strongylus sp, rupture of the aorta was
lumbar level, residues were observed to have larvae
Braz. J. Vet. Res. Anim. Sci., São Paulo, v. 52, n. 4, p. 298-309, 2015
of parasites, with fibrin (quitine). In the Quarter
Horses with atherosclerosis, dermatitis alopecic
with hyperpigmentation and xantomathosis of
subcutaneous tissue was observed. Hemoperitoneum
was observed in the abdominal cavity, caused by
rupture of the aorta flow. Fat deposits and plates type
atheroma (MORALES et al., 2012) were observed in
the wall of the aorta. The aorta was assessed in the
emergence from the heart, all portions of the aortic
arch, thoracic aorta, and abdominal aorta (Figures 1
and 2). Discrete macroscopic degenerative changes
in the intima only in the initial portion of aorta were
observed (Figures 3, 4 5 and 6). Histopathology:
histological examination of the wall of the aorta
showed necrotic areas that were scattered throughout
the wall in both vessels. In some of these areas, necrotic
muscle fibers were still present, whereas in others the
muscle fibers had disappeared and the elastic fibers
were condensed (Figures 7, 8 and 9). Neutrophils and
fibroangioblastic tissue were seen around the areas of
necrosis. Areas of calcification were found in horses.
All horses had many vasa vasorum in the media and
adventitia of the aorta and the pulmonary trunk with
intimal thickening, medial fibrosis, or both (LINDE-
SIPMAN et al.,1985). The lumen of many vasa
vasorum was completely obliterated. Histopathology
revealed severed fatty degeneration and hepatic
necrosis. The aorta showed lipid-filled foam cell stage
(fatty streak) into an advanced, complicated lesion
that contains abundant extracellular cholesterol
ester in the atheromatous gruel within the arterial
intima. On necropsy in two horses the aorta was
found, seeding all emerging portions of the aorta in
the heart, aortic arch, thoracic aorta, and abdominal
aorta. Discrete macroscopic degenerative changes in
the intima were observed. The histological evaluation
of the emerging portion of the aorta with the heart
evidenced degenerative changes with loss of continuity
and distribution of elastic fibers. The special reticulin
positive stain details the changes of the elastic fiber in
electron microscopic study process.
 303

Figure 1 – Overview chest cavity (right lung, heart and Figure 4 – Aorta root originating from the left ventricle of
thoracic aorta) the heart (where rupture commonly occurs)
Source: (BRICEÑO, 2013) Source: (BRICEÑO, 2013)

Figure 2 – Thoracic aorta Figure 5 – Aorta root originating from the left ventricle of
Source: (BRICEÑO, 2013) the heart (where rupture commonly occurs),
higher resolution
Source: (BRICEÑO, 2013)

Figure 6 – The histological evaluated in the emerging por-

Figure 3 – Abdominal aorta in each horse tion of the aorta (H&E 4X)
Source: (BRICEÑO, 2013) Source: (BRICEÑO, 2013)

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304
Figure 7 – Evaluated in the emerging portion of the aorta
with the heart evidencing degenerative changes
with loss of continuity and distribution of elastic
fibers (H&E 10X)
Source: (BRICEÑO, 2013)
Figure 8 – Evaluated in the emerging portion of the aorta
with the heart evidencing degenerative changes
with loss of continuity and distribution of elastic
fibers (H&E 20X)
Source: (BRICEÑO, 2013)
Figure 9 – Evaluated in the emerging portion of the aorta
with the heart evidencing degenerative changes
with loss of continuity and distribution of elastic
fibers (H&E 40X)
Source: (BRICEÑO, 2013)
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Risk factors
The rupture of the aorta is a cause of sudden death
in athletic horses, with no predisposition for race, age,
sex, and even equestrian discipline demography. The
pathogenesis of the rupture of the aorta is described
below as well as its associated factors:
Spontaneous rupture associated with hypertension
Spontaneous rupture of the aorta may occur in
horses. Phenomena associated with hypertension
during exercise or post exercise still does not explain
the pathogenesis. Apparently, phenomena may be
associated with hypertension. This can be submitted
during the year when vascular hypertension elastic
capacity exceeds wall physiological dynamics of the
aorta. This event can occur without presentation of
prior clinical signs and revisionary macroscopic and
histology aortic endothelial changes are not observed,
only the abrupt rupture of the aorta.
Preexisting vascular injury (aneurysm)
Preexisting vascular lesions such as aneurysms,
dilations, vascular hypertrophy of the aorta, may
predispose equine aortas to rupture. Aneurysms
associated with atheromatous plaques, atherosclerosis,
and atherosclerosis, with possible perforation, can
occur associated with equine metabolic syndrome
and obesity. Migration by larvae of Strongyles and
verminous arteritis are common in horses with severe
intestinal parasites, mostly occurring in the caudal aorta.
Alterations of the vasa vasorum of the great vessels may
predispose them to rupture from the effect of pressure
on the blood vessel wall. Severe lesions of aortic
thickening and aortic valve rigidity were observed.
Histologically, the tunica media of the aorta, coronary
arteries, and pulmonary arteries were expanded by
foci of elastin fiber calcification and extracellular
matrix with lacunae formation. The vascular lesions
are comparative to what has been described as medial
arterial calcification, seen in humans suffering from
chronic renal failure or diabetes mellitus. No exposure
to vitamin D-containing plants or feedstuff could be

documented at the time of onset or during the period
of clinical signs. The current case describes dramatic
lesions of arterial medial calcification of the aorta,
coronary, and pulmonary arteries of undetermined
cause (FALES-WILLIAMS, et al., 2008). Secondary
infections had been reported in foal and development
of distal aortic aneurysm (ARCHER et al., 2012).
Dilated / hypertrophic cardiomyopathy
Preexisting heart injury can also predispose animals
to risk of rupture of the aorta, such as dilated or
hypertrophic cardiomyopathy. Valvular problems such
as valvular endocarditis by vegetative or mineralization
of the valve can increase the risk of aortic rupture.
Dilated hypertrophic concentric and eccentric mural
endocarditis is also common in horse necropsies.
Thoroughbred athletes tend to show concentric left
ventricular hypertrophy.
Copper levels in the endothelium
Rupture of the aorta, pulmonary artery, or coronary
artery occurs experimentally, though not as a natural
event, in cooper-deficient swine, and has been
extensively investigated because of similarities with
Marfan syndrome. Marfan syndrome is an inherited
disorder in fibrillin metabolism in man and cattle, in
which dissecting aortic aneurysm occur (JUBB et al.,
2007). Degeneration of elastic appears to be the basis of
the vascular lesion of copper deficiency, and is due to a
deficiency of a copper-containing enzyme, lysyl oxidase,
which is responsible for cross-linking of collagen and
elastin (JUBB et al., 2007). Whether hypervitaminosis
D plays a role in the condition in racehorses needs to be
determined by further study (IMAIZUMI et al., 1989).
Genetic: inbreeding racial predisposition
Inbreeding in thoroughbred race horses can somehow
play a role in the development of vascular and cardiac
malformations that mostly go unreported if they occur
in the early stages of life, but are occasionally seen in
necropsies. Significant genetic lines prone to certain
phenotypic or genotypic traits could possibly be prone
305
to vascular hypertension. Since aortic and pulmonary
trunk ruptures occurred in three Friesian horses which
were descendants from the same sire, a genetic cause
cannot be excluded (LINDE-SIPMAN et al.,1985).
Toxicity /Foreign substances: Anabolic, stimulants
and other drugs
Anabolic steroids also have an immediate effect on
heart and blood vessels. In high concentrations they
kill heart cells and produce blood clots. These tiny,
almost invisible clots can cut tissue from the blood
vessel lining. Another negative effect of androgens
is that they cause blood vessels to narrow (stenosis).
Apparently the effect of corticosteroids in vitro does
not injure the endothelium in high doses and stress;
however, other studies demonstrate for the first
time that glucocorticoids exert direct toxic effect
on endothelial cells through caspase-independent
cell death mechanisms (VALAMANESH et al.,
2009). As we know, racing can somehow generate
peripheral vasoconstriction and with a high blood
volume and heart physiologically stressed by exercise
can lead to saturation and congestion of the aorta
with consequent rupture. The anabolic steroid
nandrolone can produce direct endothelial damage
through the production of small clots predispose to
thrombotic MI that can cause hypertension under
direct physical damage on the endothelium with
rupture (FERENCHICK, 1991). Nandrolone can also
produce vascular stenosis with limited aortic arterial
vasoconstriction and vasodilatation and numerous
toxic side-effects including deleterious cardiovascular
changes (FERENCHICK, 1991). Correlation of
necropsy and histopathology results with toxicology
and pharmacology reports should be further studied
for the aorta in horses. Cardio stimulants and anabolic
foreign substances like clenbuterol can produce severe
hypertensive disorders in cardiac and vascular collapse
resulting in injury of the aorta. (SLEEPER et al.,
2002). Caffeine and other substances that are cardio-
stimulatory could possibly induce super-saturation of
the aorta and its subsequent breakup. Although not
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306
reported in the literature but observed clinically, it is
common in horses medicated with L-carnitine for an
antioxidant and development of skeletal muscle mass,
one may also observe cardiac muscle hypertrophy.
The hardness of drinking water (i.e., the sum of
calcium and magnesium concentrations) has been
related to cadmium concentration in kidney cortex
and to microscopic signs of arteriosclerosis and focal
myocardial fibrosis in 50 Swedish horses slaughtered
for meat production (ELINDER et al., 1980).
Similarity with pulmonary hemorrhage induced by
exercise
Sudden death from ruptured segmental bronchial
arteries in horses with exercise induced pulmonary
hemorrhage is highly homologous to the rupture of the
aorta, which is considered as a differential diagnosis in
cases of sudden death. Characteristics associated with
equine aortic rupture have been outlined by Linde-
Sipman et al. (1985). Aortic ruptures localized just above
the aortic valve are a more common cause of acute death
in horses; they occur especially in overweight stallions
after excitement. Rupture in this location in the aorta
may be due to the fact that the aortic wall is thinner in
this area than elsewhere. Another explanation may be
hemodynamic and mechanical factors, accompanied
by degenerative, necrotic, inflammatory or sclerosing
alterations of the aortic wall. Histological examination
of the wall of the aorta and the pulmonary trunk of
the four horses showed almost identical abnormalities.
Alterations of the vasa vasorum of great vessels, as found
in our horses, is not mentioned in the literature as the
cause of ruptures of the aorta and pulmonary trunk.
Partial or total obliteration of many vasa vasorum may
have caused hypoxia or anoxia of the vessel walls which
resulted in local compromised circulation, necrosis,
and finally, in a rupture of the wall. The aorta and
extrapulmonary artery were examined pathologically
in 33 thoroughbred racehorses ranging in age from one
to five years. Many of the great vessels of these horses
exhibited degenerative or sclerotic changes in the
Braz. J. Vet. Res. Anim. Sci., São Paulo, v. 52, n. 4, p. 298-309, 2015
media with neither lipidosis nor deposits of cholesterol
(IMAIZUMI et al., 1989). The severe lesions were
predominantly observed at the bifurcation of the
pulmonary artery (IMAIZUMI et al., 1989).
Locomotor-associated trauma
Locomotion of the horse during exercise (galloping
and jumping) generates multiple loading forces and
mass compression effect. The theory is based on the
fact that during galloping, the absence of any bone
attachment of the forelegs to the spine in the horse
causes the shoulder to compress the cranial rib cage
(SCHROTER et al., 1998). Thus, the impact surface
with the movement generated in cranial viscera during
the ventral direction and galloping horses jumping can
somehow compress the aorta in its base or in some
portion thereof (thoracic, abdominal) and generate a
traumatic rupture.
Discussion
Sudden and unexpected death in horses has been
reported in the literature since 1982. In recent years,
reports have increased globally without a specific
geographical area, in prestigious international
equestrian events (racing, riding, rodeo, endurance
and other competition), major deaths have occurred
in horses recognized for their career and industry
awards. The rupture of the aorta in horses is a severe
pathological condition that has been given less
importance but severely affects the equine industry.
Aortic lesions appear to be very common in high
performance athletic horses worldwide. Multiple
factors predispose and determine the rupture of the
aorta at a given time, most often occurring during
exercise. Only some cases may present first with
exercise intolerance but mostly occur suddenly. There
is an apparent age-related predisposition in horses over
10 years of age but there is also an increased risk for two-
year-old colts, as well as affecting important stallions in
reproduction work. In relation to sex, there are as many
cases in stallions as in mares. Thoroughbreds reported

the highest number of cases, followed by horses and
Quarter Horses, Friesians. Other breeds include the
Creole Venezuelans, Dutch halfbreeds, Standardbreds,
Warmbloods and Trakehners have been reported on
a minor scale, it is possible that this is associated with
a genetic condition in the horse. Aortocardiac fistulas
are usually found in the right aortic sinus in horses,
dissecting into the right atrium or ventricle (MARR et
al., 1998). The aortocardiac fistula causes biventricular
volume overload in the majority of horses. The
condition should be considered as a differential
diagnosis for horses presenting with acute distress,
colic, rapid heart rate with monomorphic ventricular
tachycardia, bounding pulses and a continuous right-
sided murmur, particularly in middle-aged and older
stallions. Echocardiography is the technique of choice
for diagnosis of the aortocardiac fistula (MARR et al.,
1998). Aorto-pulmonary fistulation in conjunction
with aortic rupture is more common in Friesians than
previously estimated (PLOET et al., 2013). In some
cases, findings demonstrate a progressive pathology
rather than acute cardiac failure and sudden death
(PLOET et al., 2013). In humans, thoracic aortic
rupture (TAR) is recognized as a cause of death in
victims of blunt trauma and immediate mortality is
85% (CONOR, 2004). An important point to note is
asymptomatic condition of these horses. This point is
very important because even though every horse in
competition for national and international regulations
is so exhaustively examined before the competition by
an official veterinarian, it is not possible to diagnose or
predict this pathological condition. The toxicological
evaluation of these cases was made mostly without
detection of banned substances. Recently in California,
307
USA, have been reports of a significant number of cases
of sudden death post-race, which have been described
as sudden death syndrome equine. In summary, the
rupture of the aorta causes sudden and unexpected
death that in most cases does not show obvious
clinical signs, only acute collapse and sudden death.
The clinical signs are distress, tachycardia, jugular
distension, pale mucous membranes and bounding
arterial pulse. These signs may be confused with
colic. The differential diagnoses are: EIPH (exercise-
induced pulmonary hemorrhage), acute heart failure,
respiratory failure and the recent equine sudden death
syndrome. The diagnosis is made by clinical evaluation,
electrocardiogram, echocardiogram and post mortem
by necropsy. In most cases the prognosis is reserved.
Conclusion
The rupture of the aorta is an important cause
of sudden death in athletic horses. In conclusion,
degenerative changes to the discrete elastic fiber of the
intima of the aorta in the emergence of the heart seem
to predispose the rupture of the wall of the aorta at
the time of maximum blood pressure during exercise
and the consequent collapse of hypovolemic shock
and athletic horse death. Deeper studies are needed
to elucidate its etiology and establish some control
mechanisms that reduce horse mortality. This severely
affects the equine industry for economic losses and the
direct impact on the spectators.
Acknowledgments
The authors acknowledge the technical assistance of
Mrs. Gema Muñoz and Mr. Antonio Ramirez Career at
necropsy and histological processing.
Braz. J. Vet. Res. Anim. Sci., São Paulo, v. 52, n. 4, p. 298-309, 2015
308
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