ILMU BEDAH KHUSUS VETERINER

“THORACOCENTESIS”

Disusun Oleh :

Kelompok 1

Setio Santoso 1309005128

Baiq Indah Pratiwi 1609511001

Yoga Mahendra Pandia 1609511005

Dimas Norman Medellu 1609511013

Pieter Mbolo Maranata 1609511016

Audrey Febiannya Putri B. 1609511023

Ni Kadek Deasy Pitriyawati 1609511024

Kelas 2016 C

LABORATORIUM BEDAH VETERINER

FAKULTAS KEDOKTERAN HEWAN

UNIVERSITAS UDAYANA

DENPASAR

2019

i
 RINGKASAN

Thoracocentesis merupakan teknik pengeluaran cairan ataupun udara dari

rongga thorax. Indikasi penyakit seperti pyothorax, pneumothorax, chylothora x,
hidrothorax, bilothorax dll. Operasi menggunakan jarum, spuit dan kateter. Anastesi
menggunakan anastesi lokal atau tidak. Operasi dilakukan dengan penetrasi jarum
operasi dan mengeluarkan cairan pada rongga thorax. Komplikasi umumnya rasa nyeri.

Kata kunci: Thoracocentesis, pyothorax, pneumothorax, chylothorax, bilothora x,

hidrothorax

SUMMARY

Thoracocentesis is a technique to remove fluid or air from teh thorac cavity.

Indication disease like pyothorax, chylothorax, hydrothorax, bilothorax, dll. Operation
use surgical needle, spuit, and catheter. Anesthesia with local anesthesia or never.
Operation perform with penetration the needle to remove fluid from thorax cavity.
Generally, complication jut for pain.

Keywords: Thoracocentesis, pyothorax, pneumothorax, chylothorax, bilothora x,

hydrothorax

ii
 KATA PENGANTAR
Om Swastiastu,
Puja dan puji syukur penulis panjatkan kehadirat Ida Sang Hyang Widhi Wasa/
Tuhan Yang Maha Esa karena atas asung kertha wara nugraha dan rahmat-Nya kami
dapat menyelesaikan paper individu dari mata kuliah Bedah Khusus Veteriner yang
berjudul “Thoracocentesis”.
Saya mengucapkan terima kasih kepada semua pihak yang telah membantu
terselesaikanya paper ini dengan baik dan tepat pada waktunya. Penulis menyadari
bahwa paper ini masih jauh dari sempurna dalam penyajian bahasa serta wawasan yang
ada.. Maka dari itu kami mengharapkan saran demi kemajuan dalam penulisan paper
selanjutnya.
Akhir kata penulis berharap agar karya tulis ini dapat bermanfaat dalam
pengembangan ilmu pengetahuan dan bagi pihak-pihak yang memerlukan. Atas
perhatiannya, terima kasih.
Om Santih, Santih, Santih Om

Denpasar, 23 Oktober 2019

Penulis

iii
 DAFTAR ISI

HALAMAN JUDUL ........................................................................................................i

RINGKASAN/SUMARY ............................................................................................... ii
KATA PENGANTAR ..................................................................................................... iii
DAFTAR ISI ................................................................................................................... iv
DAFTAR GAMBAR .......................................................................................................v
BAB I PENDAHULUAN ............................................................................................... 1
1.1 Latar Belakang................................................................................................. 1
1.2 RumusanMasalah ............................................................................................ 2
1.3 Tujuan Penulisan ............................................................................................. 2
1.4 Manfaat Penulisan ........................................................................................... 2
BAB II TINJAUAN PUSTAKA ................................................................................... 3
2.1 Definisi Thoracocentesis ................................................................................. 3
2.2 Indikasi Thoracocentesis................................................................................. 3
2.3 Kontra Indikasi Thoracocentesis..................................................................... 4
BAB III PEMBAHASAN .............................................................................................. 5
3.1 Teknik Preoperasi ............................................................................................ 5
3.2 Teknik dan Prosedur Operasi ............................................................................ 7
3.3 Perawatan Pasca Operasi................................................................................. 15
BAB IV PENUTUP
4.1 Kesimpulan .................................................................................................... 16
4.2 Saran .............................................................................................................. 16
DAFTAR PUSTAKA ................................................................................................... 17

iv
 DAFTAR GAMBAR

Gambar 1.......................................................................................................................... 5

Gambar 2.......................................................................................................................... 6

Gambar 3.......................................................................................................................... 7

Gambar 4.......................................................................................................................... 8

Gambar 5.......................................................................................................................... 8

Gambar 6.......................................................................................................................... 8

Gambar 7.......................................................................................................................... 9

Gambar 8........................................................................................................................ 10

Gambar 9........................................................................................................................ 11

Gambar 10...................................................................................................................... 11

Gambar 11...................................................................................................................... 11

Gambar 12...................................................................................................................... 12

Gambar 13...................................................................................................................... 12

Gambar 15...................................................................................................................... 13

Gambar 16...................................................................................................................... 13

Gambar 17...................................................................................................................... 14

Gambar 18...................................................................................................................... 14

Gambar 19...................................................................................................................... 15

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 BAB I

PENDAHULUAN

1.1 Latar Belakang

Thoraks merupakan rongga tubuh yang didalamnya terdapat beberapa organ vital
bagi makhluk hidup. Beberapa organ diantaranya adalah jantung dan paru-paru, baik
jantung maupun paru-paru dilapisi dengan lapisan yang disebut dengan pleura pada paru-
paru dan pericardium pada organ jantung. Rongga thoraks merupakan cavum dimana pada
keadaan normal tidak terdapat udara maupun cairan pada rongga tersebut. Apabila rongga
ini terdapat udara maupun cairan maka dapat mengganggu fungsi organ pada rongga
tersebut.
Terdapat banyak kelainan atau penyakit yang terkait dengan cavum thoraks
diantaranya adalah adanya athelektasis pada rongga pleura, pneumothorak dan pneumonia.
Beberpa penyakit ini dapat mengganggu aktifitas pada organ thoraks. Athelektasis pada
pleura merupakan kelainan pada pleura dimana pleura melekat pada dinding thorak
sehingga dapat mengganggu proses pernafasan. Penumothiraks meruapakan keadaan
diman rongga thoraks mengalami cedera sehingga terdapat luka yang dapat memungkinka n
terjadinya pemasukan benda asing baik udara maupun benda lain. Sedangkan Pneumonia
adalah kelainan dimana rongga dada terisi cairan yang disebabkan berbagai hal. Untuk
penangananan kelainan ini perlu dilakukan pengeluaran cairan pada rongga dada yang
disebut dengan thoracentesis.
Thoracosentis merupakan tindakan pengeluran cairan dari rongga thoraks, biasanya
dilakuakn pada kasus pneumonia maupun digunakan untuk biopsy jaraingan atau diagnose
dari sutu penyakit. Pada hewan dapat dilukan dengan posisi sternal recumbency dengan
penusukkan jarum pada stringe pada rongga thoraks. Proseduk ini cukup mudah dilukan
namun perlu diperhatikan agar tidak menyebabkan cedera pada pembuluh darah dan
pemasukan udara pada rongga thoraks.

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1.2 Rumusan Masalah
Adapun beberapa rumusan masalah yang dapat kami angkat dalam makalah ini antara lain:
1.2.1 Apa yang dimaksud dengan Thoracocentesis dan apa saja indikasinya?
1.2.2 Bagaimana tahap persiapan operasi dari Thoracocentesis?
1.2.3 Bagaiman Teknik operasi dari thoracocentesis?
1.2.4 Bagaimana penanganan pasca operasi dari thoracocentesis?

1.3 Tujuan
1.3.1 Untuk mengetahui pengertian dari Thoracocentesis.
1.3.2 Untuk mengetahui indikasi dari Thoracocentesis.
1.3.3 Untuk mengetahui tahap persiapan operasi Thoracocentesis.
1.3.4 Untuk mengetahui teknik operasi dari Thoracocentesis.
1.3.5 Untuk mengetahui penanganan pasca operasi dari Thoracocentesis.

1.4 Manfaat
Penulis berharap akalah yang ditulis dapat memberikan pengetahuan dan informas i
kepada pembaca. Sehingga pembaca disini mahasiswa kedokteran hewan dapat
mengetahui bagaimana teknik dan prosedur teknik Thoracocentesis.

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 BAB II

TINJAUAN PUSTAKA

2.1 Pengertian
Thoracocentesis adalah teknik digunakan untuk mengeluarkan cairan atau udara
dari rongga pleura dan biasanya digunakan sebagai diagnosa penyakit. Hal ini digunakan
untuk diagnosa ataupun terapi intervensi (Christ, 2008).
Merupakan prosedur invasif untuk mengeluarkan cairan atau udara dari rongga
pleura untuk tujuan diagnostik atau terapeutik. Menurut Murgia (2015) Thoracocentes is
adalah prosedur sederhana yang memungkinkan menghilangkan cairan atau udara dengan
cepat. Teknik ini dilakukan pada pasien dispnea dengan oksigen.
2.2 Indikasi Operasi Thoracocentesis
Thoracocentesis harus dilakukan pada hewan yang pada pemeriksaan fisik atau
radiogradi toraks menunjukkan efusi pleura (King L. 2008). Biasanya ditemukan cairan
pleura atau udara yang cenderung sangat signifikan. Hal ini dapat merusak respirasi
sehingga penghilangan cairan atau udara tersebut dapat menyelematkan nyawa pasien.
Thoracocentesis diindikasi untuk semua pasein yang memiliki cairan pleura, dan untuk
meredakan gejala pada pasien yang dispnea yang disebabkan oleh efusi pleura yang besar
(Lechtzin. 2016).
Menurut Dennis & Crowe (2002) indikasi dilakukannya thoracentesis dalam
keadaan darurat adalah: 1. Cairan atau udara yang terakumulasi di dalam rongga pleura
menyebabkan peningkatan laju pernapasan. 2. Jika chest tube tidak ditempatkan karena
alasan keuangan dan logistic. Dalam keadaan darurat, pasien yang menunjukkan ganggua n
pernapasan thoracocentesis diagnosis dan terapeutik dalam dilakukan segera tanpa
menunggu dilakukannya radiografi karena dapat menyebabkan pasein stress dan memakan
waktu yang lama. Dalam hal ini tindakan thoracocentesis dilakukan untuk menyikirka n
adanya penumotoraks atau efusi pleura.

3
2.3 Kontra indikasi Operasi Thoracocentesis
Kontra indikasi absolute tidak ada pada thoracocentesis. Namun pada kontra
indikasi relatife meliputi: gangguan pendarahan atau antikoagulasi, lokasi cairan tidak
menentu, volume cairan tidak menentu, volume cairan minimal, anatomi dinding dada
berubah, penyakit paru cukup berat, batuk tidak terkendali

4
 BAB III

PEMBAHASAN

3.1 Teknik Pre-Operasi

Sebelum dilakukanya operasi harus dilakukan evaluasi kelayakan pasien dalam
melakukan thoracocentesis. Anjing atau kucing sebaiknya dirontgen pada bagian thora x
untuk mengetahui posisi cairan atau udaranya. Selain dengan cara rontgen dapat
menggunakan Teknik perkusi untuk mendeteksi akumulasi udara dan cairan pada bagian
thorax.
a. Persiapan Alat
Alat yang digunakan dalam thoracocintesis untuk kepentingan diagnostic adalah
sebagai berikut,
 Kucing ataupun anjing kecil : 19-23 gauge butterfly catheter, spuit, dan 3-way
stopcock
 Anjing dengan ukuran lebih besar : 20-22 gauge, 3-way stopcock, dan spuit

Gambar 1. Butterfly Catheter

Penggunaan jarum tergantung pada bobot ukuran dari pasien, bila pasien lebih
besar maka panjang jarumnya juga berbeda, sehingga jarm dapat menembus musculi
yang tebal. Sedangkan untuk penggunaan terapi alat yang dibutuhkan adalah sebagai
berikut,
 Kucing ataupun anjing kecil : 20-22 gauge over the-needle catheter dengan set
ekstensi, 3way stopcock, dan spuit 20-60 ml
 Anjing dengan ukuran lebih besar : 14-66 gauge over the needle catheter
dengan set ekstensi, 3way stopcock, dan spuit 20-60 ml

5
 Gambar 2. 3way stopcock

b. Persiapan Hewan
Persiapan hewan dapat dilakukan dengan memposisikan pasien dalam posisi sternal
recumbency, hal ini memungkinkan untuk cairan diposisikan diperut dan udara berada
dibagian punggung. Setelah itu perlu dilakukan pembersihan dengan mencukur rambut
disitus yang akan dilakukan penusukan, dengan daerah persegi secukupnya. Setelah
dilakukan pencukuran disterilkan daerah dengan iodine atau chlorhexidine antiseptic.
Pada pneumotoraks dilakukan apsirasi pada ruang 7 dan 9 intercosal, sedangkan bila
adanya cairan diaspirasi pada 7-8 interkostal.
c. Anestesi
Pemberian anestesi dapat digunakan anestesi lokal. Anestesi lokal dapat dilakukan
dengan pemberian lidokain 2-8 mg/kg dosis total infiltrative maksimum, dan pada
kucing tidak boleh lebih dari 2mg/kg. Anestesi lokal dapat dilakukan dimusc ulus
intercostae. Jika hewan galak dapat digunakan anestesi umum, tapi hal ini tidaklah
efisien. Premedikasi dapat menggunakan midazolam (0.2 mg/kg) dan ketamin (
5mg/kg). Untuk maintenance dapat menggunakan isofluorane ataupun halothane
dengan kombinasi oksigen. Tetapi penggunaan sedasi sering tidak dibutuhkan kecuali
pasien dalam kondisi sangat tertekan ataupun gelisah, dalma prosedur hampir semua
hewan dapat dilakukan dengna merestrain pada posisi sternal recumbency ( King et al.
2010).

6
3.2 Teknik Operasi
1. Hewan diposisikan dalam keadaan berdiri atau sternal recumbency. Janga n
memposisikan hewan secara lateral recumbency karena akan menyulitkan hewa n
bernafas.
2. Sebelumnya hewan telah dicukur rambut pada bagian yang akan dioperasi. Kulit
didaerah thorax dibagi menjadi 7-8 bagian kemudian dioleskan dengan cotton ball
yang telah direndam didalam isopropyl alcohol.
3. Jika akan menangani pneumothorax, titik masuknya trocar adalah interspace ke
7-8 pada junction/persimpangan dorsal dan middle ketiga dari lateral dinding
thorax (gambar 3).
4. Jika akan menangani efusi, titik masuk harus tepat diatas costochondral junction

Gambar 3. Daerah/site tempat masuknya jarum pada penanganan pneumothorax

(Sumber : Hansen B, 2016)

5. Setelah menemukan titik masuk yang diinginkan dengan palpasi, kulit dan dinding
tubuh diblok dengan lidokain hingga pleura. Untuk memastikan bahwa jarum
sudah masuk ke pleura, lakukan aspirasi pada plunger untuk menarik/menyedot
udara atau cairan.

7
 Gambar 4. Udara pleural menggelembung masuk kedalam syringe

(Sumber : Hansen B, 2016)

6. Lidokain harus disuntikkan kedalam ruang pleura saat jarum ditarik. Buat goresan
tipis bentuk ‘X’ pada kulit ditempat suntikan, goresan ini akan memb entuk papula
yang akan menandai spot tersebut (Gambar 5)

Gambar 5. Menandai spot dimana lidokain disuntikkan

(Sumber : Hansen B, 2016)

7. Seorang asisten harus mempersiapkan kulit secara aseptic dengan surgical

soap. Povidone-iodine digunakan untuk kucing dan chlorhexidine digunakan pada
anjing, memungkinkan 3 menit untuk kontak basah secara terus menerus dengan
sabun sebelum diolesi/digosok dengan alcohol.
8. Sementara kulit sedang dipersiapkan secara aseptic, operator harus membuat 3 atau
lebih fenestrasi di dinding kateter dengan B.P blade no. 11 atau scalpel, dan
8
 mulai 1 cm proksimal ke ujung kateter. Jika operator terampil dalam teknik ini maka
ini dapat dicapai dengan teknik “no-touch” (Gambar 6). Kalau tidak, operator harus
memakai glove steril untuk memungkinkan operator memegang kateter dekat
dengan tempat fenestrasi dibuat (Gambar 7). Jangan tinggalkan lubang sekitar
1” pada kateter yang dekat dengan hub/pusat, karena ini harus melintasi dinding
tubuh.

Gambar 6. Pembuatan fenestrasi pada dinding kateter dengan teknik no-

touch (Sumber : Hansen B, 2016)

9. Dengan jarum yang dimasukkan kedalam kateter, potongan dibuat pada sudut 45o,
kemudian dilengkapi dengan potongan kedua yang berorientasi 90o ke potong a n
pertama, untuk membuat lekukan berbentuk “V” pada dinding kateter (Ga mba r
8). Lubang harus sekecil mungkin untuk pneumothorax, dan tidak lebih dari
20% lingkar kateter untuk cairan. Hindari kecenderungan alami untuk
“menyendok/scoop” lubang (metode ini akan membuat lubang semakin besar).
Ujung- ujung yang longgar/bergerigi pada potongan harus dikikis dengan
“backsweeping/ menyapu belakang” pisau diatasnya.

9
 Gambar 8. Pembuatan lekukan berbentuk V pada dinding kateter
(Sumber : Hansen B, 2016)

10. Blade no.11 scalpel digunakan untuk menginsisi kulit di lokasi blok lidokain
(tanda X). Kulit tersusun jauh dari dinding tubuh dan insisi dibuat didasar kulit
(Gambar 9). Pastikan insisi tusukan ini sepenuhnya melalui dermis.

Gambar 9. Insisi pada dasar kulit ditempat yang sebelumnya

sudah diberi tanda X (Sumber : Hansen B, 2016)

11. Syringe yang berukuran 3 ml dimasukan dalam jarum/kateter dan kemud ia n

dimasukan ke dalam luka yang dibuat sebelumnya. Jika memakai glove yang
steril (Gambar 10), tangan dominan harus menempel pada dinding tubuh dan
pergelangan tangan serta jari- jari digunakan untuk mendorong kateter menuju
ke ruang pleural. Jika menggunakan clean exam glove (Gambar 11), siku
lengan yang dominan harus menempel pada anjing atau meja, dan kateter maju
dari posisi itu. Pastikan siku dan lengan bawah anda stabil pada anjing atau

10
 meja untuk memungkinkan co ntrol motorik tangan anda untuk bekerja, jangan
memajukan kateter dengan trisep anda. Segera setelah jarum mencapai jaringa n
subkutan, 1-2 ml vakum diaplikasikan pada plunger dan tidak dilepa s ka n
sampai jarum masuk ke rongga pleura. Jangan mengaplikasikan vakum,
release/melepaskan, maju dan uji lagi. Anda ingin vakum terus mene r us
diterapkan. Begitu jarum menembus ruang pleura, vakum akan hilang ketika
udara atau cairan memasuki jarum. Temuan ini menandakan anda harus
menghentikan memajukan jarum lebih jauh ke dalam rongga pleura.

Gambar 10 Gambar 11

12. Setelah jarum menembus ruang pleura, fokuskan semua perhatian anda pada
pusat jarum dan pegang erat stasioner relative pada dinding tubuh sampai
kateter sebagian maju dari posisi itu untuk menutupi ujung jarum. Hal ini
dilakukan dengan menjaga pergelangan tangan atau siku anda stabil pada
dinding thorax atau meja, pegang stasionary jarum pusat d an majukan kateter
I cm ke dada (Gambar 12 dan 13). Focus utama anda selama langkah ini
adalah memegang jarum stasioner. Hindari kesalahan umum saat mena r ik
jarum kembali saat anda memajukan kateter

11
 Gambar 12 Gambar 13

13. Setelah kateter plastik telah menutupi ujung jarum, pusat jarum / kateter
dibawa lebih dekat ke dinding tubuh, untuk membuatnya sejajar dengan dinding
tubuh (Gambar 15). Jika Anda menangani pneumotoraks, kateter harus
berorientasi sejajar dengan tulang belakang. Jika menangani efusi, harus
diarahkan pada thorax cranioventral. Alat ini diletakkan sejajar dengan tulang
rusuk tanpa membengkokkannya secara berlebihan di tulang rusuk di
belakangnya. Selama langkah ini, berhati- hatilah agar tidak secara tidak sengaja
menarik jarum keluar dari ruang pleura. Ujung jarum harus tetap berada di
dalam rongga pleura untuk berfungsi sebagai stylet sampai kateter maju
sepenuhnya ke dada (Gambar 16). Untuk mencapai hal ini, pegang jarum
stasioner dan majukan kateter secara kranial, tinggi untuk udara dan rendah
untuk cairan.

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 Gambar 15. Pusat jarum / kateter dibawa lebih dekat ke dinding tubuh,
untuk membuatnya sejajar dengan dinding tubuh (Sumber : Hansen B,
2016)

Gambar 16. Ujung jarum harus tetap berada di dalam rongga pleura
untuk berfungsi sebagai stylet sampai kateter maju sepenuhnya ke dada
(Sumber : Hansen B, 2016)

14. Setelah pengangkatan jarum, set ekstensi dihubungkan ke kateter dan udara atau
cairan disedot (Gambar 17). Jika kateter akan tetap di tempat, koneksi kateter/
tubing dijembatani dengan ‘butterfly’ dari 1 inch waterproof white tape dan ini
dijahit ke kulit (Gambar 18).

13
 Gambar 17. Setelah pengangkatan jarum, set ekstensi dihubungkan ke
kateter dan udara atau cairan disedot (Sumber : Hansen B, 2016)

Gambar 18. Jika kateter akan tetap di tempat, koneksi kateter / tubing
dijembatani dengan‘butterfly’ dari 1 inch waterproof white tape dan
ini dijahit ke kulit (Sumber : Hansen B,2016)

15. Kateter dapat bekerja dengan baik selama beberapa jam sebelum kusut terlalu
banyak, memberi Anda waktu untuk menstabilkan pasien. Jika Anda berenc a na
untuk radiografi hewan dengan pneumotoraks, pastikan untuk memposisika n n ya
sehingga kateter berada pada aspek tertinggi dari ruang pleura dan benar-
benar kosong sebelum mendapatkan film. Untuk efusi, letakkan kateter sisi
hewan ke bawah dan keringkan semua cairan tepat sebelum melakukan potret.
16. Setelah selesai, jarum trocar dilepas dan lubang kulit segera diolesi atau ditutup
dengan flexible colladion

14
 Gambar 19. Foto menunjukkan penempatan jarum yang tepat dan
teknik untuk thoracentesis. (Maritato et al, 2009)

3.3 Pasca Operasi

Setelah dilakukan tindakan thoracentesis, jarum atau trocar segera dilepas secara
perlahan. Dan lubang kulit segera diolesi atau ditutup dengan flexible colladion.
Karena tidak mengunakan incisi tidak perlu dilakuakn penjahitan namun perlu
diperhatikan adanya abses akibat tertusuknya pembuluh darah pada proseduk ini serta
pemberian antibiotik salep untuk mencegah terjadinya infeksi pada daerah operasi.

BAB IV

15
 PENUTUP

4.1 Kesimpulan
Thoracentesis adalah usaha untuk mengeluarkan cairan dari rongga dada dan
biasanya dilakukan untuk kepentingan diagnosa penyakit. Menurut Murgia (2015)
Thoracocentesis adalah prosedur sederhana yang memungkinkan menghilangkan cairan
atau udara dengan cepat. Teknik ini dilakukan pada pasien dispnea dengan oksigen.
Peralatan yang diperlukan minimal gauge butterfly catheter, 3-way stopcock, dan spuit.
Ukuran disesuaikan dengan tujuan sebagai terapi atau diagnosa. Persiapan anastesi
menggunakan anstesi lokal, untuk terapi usahakan tidak menggunakan anastesi. Persiapan
hewan dengan memposisikan pasien dalam posisi sternal recumbency. Dalam melakukan
operasi kita terlebih dahulu harus menentukan tempat kateterisasi. Setelah itu kateter
dimasukan dan disedot. Pasca operasi tidak diberikan perawatan khusus karena tidak
melakukan incisi. Komplikasi umumnya tidak ada, rasa nyeri dapat terjadi pada daerah
thoracocentesis.

4.2 Saran
Adapun saran yang dapat kami berikan ialah agar penggunaan thoracocentesis ini
dapat ditepakan pada daerah yang tepat. Untuk menghidari terjadinya luka dalam pada
organ, jika terkena organ. Diagnosa radologi ataupu menggunakan USG pada saat operasi
sangat dianjurkan, untuk meminimaliisir resiko.

DAFTAR PUSTAKA

16
Carolina State University – College of Veterinary Medicine. Lechtzin N. 2016. How to do
Thoracentesis. MSD MANUALS
Chris Wong. 2008. Diagnostic of Thoracocentesis. Sacramento Veterinary Referral Center. NAVC
clinician’s brief . june. 2008
Dennis. T & Crowe Jr. 2002. Emergency thoracentesis. DVM360 Magazine.
Hansen B. 2016. Therapeutic Thoracocentesis – Fenestrated Plastic Intravenous Catheter. North
Carolina State University – College of Veterinary Medicine.
King, L. 2008. Basic Respiratory Diagnostic Techniques. School of Veterinary Medicine,
University of Pennsylvania Philadelphia; USA
King, Lesley., Clarke, Dana. 2010. Emergency care of the patient with acute respiratory distress.
Veterinary Focus. Veterinary Focus. Vol 20 No 2.
Lechtzin N. 2016. How to do Thoracentesis. MSD MANUALS
Maritato K.C, Colon J.A, Kergosien D.H. 2009. Pneumothorax. Compendium Vet. Murgia D.
2015. How to drain pleural cavity. Vet Times
Murgia D. 2015. How to drain pleural cavity. Vet Times

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 Trakia Journal of Sciences, Vol. 6, No. 2, pp 61-65, 2008
Copyright © 2007 Trakia University
Available online at:
http://www.uni-sz.bg
ISSN 1312-1723 (print)
ISSN 1313-3551 (online)

Case Report
A CASE OF HYDROTHORAX IN A DOG – CLINICAL, BLOOD
LABORATORY AND ELECTROCARDIOGRAPHIC CHANGES
S. Sabev*, A. Rusenov, N. Rusenova, K. Uzunova

Faculty of Veterinary Medicine, Trakia University, Stara Zagora, Bulgaria

ABSTRACT
The present report describes a clinical case of bilateral hydrothorax in a dog with chronic enteropathy.
Significant deviations in blood biochemical parameters, the radiological and electrocardiographic
findings in the studied punctate are reported. In our view, these alterations were important and could
be successfully used in the diagnosis of this pathological state.

Кey Words: pleural effusion, hydrothorax, dogs, haematology, electrocardiography

INTRODUCTION A breed predisposition has been suspected in

the Afghan hound and Shiba Inu. Among cats,
The visceral pleura is a thin membrane
Oriental breeds such as Siamese and
encompassing the lung parenchyma. It plays a
Himalayan are targets of increased
major role in the absorption of fluids,
prevalence.
produced by the parietal sheet The enhanced
1

release of fluids and/or the reduced absorption

capacity of the visceral pleura result in the
accumulation of excess fluid in the pleural
space (1, 2, 3).
According to the type of accumulated
fluid, pleural effusions could be: accumulation
of serous fluid (hydrothorax), blood
(haemothorax), chyle (chylothorax) and pus
(pyothorax) (4). The mechanisms involved in
these events are capillary pressure,
permeability of pleural capillaries, oncotic
pressure and the lymphatic drainage of the
thorax (1, 5, 6).
Pleural effusion is uncommon in
carnivores (7). Although the cause of the
pleural effusion may be readily apparent, such
as when it is associated with cardiac disease,
oftentimes the underlying disease is obscure
and difficult to ascertain. Despite extensive
diagnostic methods, in the majority of the
pets, the main аetiology is undetermined –
idiopathic effusions (8, 9). Maskell, N. A.
(2003) reports that the aetiology of pleural
effusions remains unknown in up to 15% of
men (10).
Any breed dog or cat may be affected.
* Correspondence to: S. Sabev, Faculty of
Veterinary Medicine, Department of Internal
diseases, Trakia University, Stara Zagora 6000,
Bulgaria; E-mail: s_sab@gbg.bg
Trakia Journal of Sciences, Vol. 6, No. 2, 2008
CASE REPORT
A clinical case of hydrothorax in a dog - 8-
year old female German Shepherd, weighing
30 kg, is described. The dog is owned by a
private owner and was referred to the Small
Animal Clinic of the Faculty of Veterinary
Medicine at the Trakia University at
December 27, 2007. According to the
patient’s history, the dog has been losing
weight for several months, exhibited increased
appetite and thirst, diarrhoeic stools and
general weakness. Subsequently its owner
noticed accelerated and difficult breathing
with rapid emaciation and lack of appetite.
The physical examination of the patient
revealed a marked respiratory distress. The
respiration was labial and difficult in both
phases, mainly of abdominal type. The dog
was reluctant to move and became exhausted
very rapidly. The clinical examination showed
a rectal body temperature of 37.2°С; heart rate
of 150 min-1 weak and hardly perceptible,
respiration rate of 45 min-1; the lymph nodes
appeared healthy. The visible mucous coats
(conjunctival) were markedly cyanotic, and
the capillary refill time was 4-5s. The
elasticity of the skin was reduced, with
marked enophthalm. The auscultation of the
heart revealed dumb and indistinct cardiac
61

tones. The lung auscultation showed lack of
respiratory sounds in the lower half of the
chest with enhanced vesicular breathing in the
dorsal pulmonary areas. The abdomen was
flat, non painful, with firm elastic consistence.
The stools were extremely watery, with a dark
colour, putrefactive odour and mucoid
The electrocardiography (ECG) showed a
sinus tachycardia - HR 167 min-1 with obvious
low-amplitude QRS complex, about 0.3 mV
(Figure 2). The radiographic and ECG
findings guided us to suspect a pleural
effusion. The tentative diagnosis of pleural
62 Trakia Journal of Sciences, Vol. 6, No. 2, 2008
SABEV S., et al.
plaques.
The radiography showed a dense
shadow with horizontal upper margin in the
ventral third of the thorax, an indistinct
cardiac border and enhanced bronchial pattern
(Figure 1)
effusion was confirmed by bilateral
thoracocentesis and the large amount of
aspirated punctate. The latter was determined
as transudate by routine laboratory methods
(Table 1). The bacteriological examination of
punctate was negative.
 SABEV S., et al.

Table 1. Data from the physical, chemical and cytological analyses of punctate.
Amount of Colour Trasparency Specific density Protein Amount of
punctate, ml/kg content, blood cells
body weight g/L
107 straw-yellow transparent 1.013 17 -

The morphological blood analysis established
erythrocytosis with hyperchromaemia and
increased haematocrit values (Table 2).
Leukocyte and thrombocyte counts were
within the reference range. There was
neutrophilia (80%) with a left shift (Table 3).
Blood biochemical analysis showed a
considerable hypoproteinaemia (44 g/l) with
hypoalbuminaemia and increased activities of
liver transaminases (Table 4).

Table 2. Blood morphology

Haemoglobin, Erythrocytes Haematocrit, Leukocytes, Platelets,
g/L T/L % G/L G/L

237 9.39 65.1 13.2 147

Table 3. Differential white blood cell counts

Eo % Ba % Mo % Mm % St % Sg % Ly %

3 1 4 3 5 72 12

Trakia Journal of Sciences, Vol. 6, No. 2, 2008 63

 SABEV S., et al.

Table 4. Blood biochemical parameters

Total Аlbumin, ASAT ALAT Creatinine, Urea, Total Blood
protein, g/L U/L U/L µmol/L mmol/L bilirubin, glucose,
g/L µmol/L mmol/L

44 21 74 115 65.9 4.28 6.54 5.91

DISCUSSION causes exert their effect by a direct influence

on the sinus node (15). The low voltage of the
The commonest cases of hydrothorax are
R peak of 0.3 mV (Figure 2) is a consequence
related to systemic protein deficiency
of the relative higher distance between the
(hypoproteinaemia), following
heart and the electrodes (16). Similar events
glomerulonephropathy, renal amyloidosis,
could be seen in effusions (pericardial, pleural
enteropathy or reduced liver synthesis of
or ascitis), hypothyreosis, hypokalaemia,
albumin (5, 7). Other frequent causes for
pneumothorax and hypovolaemias (17).
transudate effusion in the pleural cavity are
The blood picture revealed a significant
the right-sided heart failure with venous
erythrocytosis, hyperchromaemia and
congestive events and thoracic neoplasm (11).
increased haematocrit. These changes were
The extent of manifested clinical signs
mostly due to the occurring dehydration
in hydrothorax correlates with the amount of
following the accumulation of a large amount
fluid, the systemic compensatory capacity and
of transudate in the thorax. To a certain
the underlying disease that caused the effusion
extent, the changes in these parameters could
(12, 13, 14). The extensive amount of
be attributed to compensatory mechanisms in
transudate in the thorax (Table 1) results in
the attempts of the organism to maintain an
pulmonary compression and collapse and
optimal gas exchange in tissues and cells. The
consequently, to signs of severe respiratory
lack of significant changes in leukocyte
failure. In an insignificant pleural effusion
counts (13 G/l) indicated the lack of
(under 20 ml fluid/kg b.w.) there are no
inflammation. The hypoproteinaemia and
apparent respiratory troubles. The moderate
hypoalbuminaemia are a result of impaired
effusion (20-40 ml/kg b.w.) is accompanied
absorption function of intestinal epithelium
by dyspnoea on physical exertion. The
and the developed chronic enteropathy (18).
massive effusion (over 100 ml/kg b.w.) is
Due to the impaired digestion in the intestinal
accompanied by tachypnoea, shallow
lumen and the formation of a number of toxic
breathing, dyspnoea, barrel-chest and
substances, a damage of liver parenchyma
orthopnoic body position. Also, pale or
occurred that resulted in higher activities of
cyanotic mucous coats, fading or absent heart
transaminases (ASAT and ALAT). The lack
tones and respiratory sounds, dullness with
of changes in blood urea and creatinine
horizontal upper border in percussion could be
concentrations as well as in urinalysis (Table
observed (5).
5), allowed us to reject the hypothesis of
The registered sinus tachycardia is a
nephropathy as a possible cause for
compensatory mechanism of accelerated and
hypoproteinaemia.
difficult breathing, resulting in sympathetic
nervous system excitation. The mentioned

Table 5. Urinanalysis in a dog with hydrothorax

Specific Nitrite pH Protein Glucose Ketones Urobili- Biliru- Leuc Er Hb
density nogen bin
1.030 Neg 6 Neg Normal Neg Normal Neg Neg + Neg

REFERENCES 2. Noone, K. E., Pleural effusion and disease

of the pleura. Vet Clin N Am, 15: 1069-
1. Nakamura, T., Tanaka, Y., Fukabori, T.,
1084,1985.
Iwasaki, Y., Nakagawa, M., Kira, S., The
3. Miserocchi, G., Physiology and
role of lymphatics in removing pleural
pathophysiology of pleural fluid turnover.
liquid in discrete hydrothorax. E R J, 1:
E R J, 10:219-225, 1997.
826-831, 1988.
4. Dinev, D., Simeonova, G., Emergency
Veterinary Medicine. Trakia University –
Stara Zagora, pp147-151, 2007.
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5. Nimand, H., Suter, P., Canine diseases, a
practical guide for veterinarians, pp 406-
407.
6. Turner, W. D., Breznock, E. M.,
Continuous suction drainage for
management of canine pyothorax, A
retrospective study. J A A H A, 24: 485-
494, 1988.
7. Wang N. S., The preformed stomas
connecting the pleural cavity and the
lymphatics in the parietal pleura. Am Rev
Respir Dis, 111: 12-20, 1975.
8. Gould, L., The medical management of
idiopathic chylothorax in a domestic long-
haired cat. Can Vet J, 45: 51-54, 2004.
9. Thompson M. S., Cohn, L. A., Jordan, R.
C., Use of rutin for medical management
of idiopathic chylothorax in four cats. J A
V M A, 215: 345-348, 1999.
10. Maskell, N. A. and Butland, R. J., BTS
guidelines for the investigation of a
unilateral pleural effusion in adults.
Thorax, 58 (Suppl 2): 8-17, 2003.
11. Rahman, N. M., Chapman, S. J., Davies,
R. J. O., Pleural effusion : a structured
approach to care. British Med Bull, 72:
31-47, 2004.
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SABEV S., et al.
12. Hahn, K., Hahn, P. Y., Gadallah, S. F.,
Crockett, J., Hepatic hydrothorax:
Possible etiology of recurring pleural
effusion. Am Fam Physician, 56: 523-527,
1997.
13. Fossum, T. W., Evering, W. N., Miller,
M. W, Severe bilateral fibrosing pleuritis
associated with chronic chylothorax in 5
cats and 2 dogs. J A V M A, 201: 317-324,
1992.
14. Sahn, S. A., Immunologic diseases of the
pleura. Clin Chest Med, 6: 83-102, 1985.
15. Kostov Y., Electrocardiography of
domestic animals – Stara Zagora, pp 67-
69, 1995.
16. Mitov, А., Apostolov, L., Practical
electrocardiography - Plovdiv, pp 216-
217, 1974.
17. Martin, М., Manual of
electrocardiography of small animals.
AQUARIUM Ltd - Moscow, рр 83-85,
2001.
18. Angelov, G., Ibrishimov, N., Milashki, S.,
Clinical laboratory investigations in
veterinary medicine, pp 214-216, 1999.
65
 Emergency care of
the patient with acute
respiratory distress
Lesley King, MVB, Dipl.
ACVECC, Dipl. ACVIM,
Dipl. ECVIM (CA)
Philadelphia School of
Veterinary Medicine, University
of Pennsylvania, Philadelphia,
USA
Dr Lesley King graduated from the Faculty of Veterinary
Medicine, University College Dublin, Ireland, in 1986. After
a year as a House Surgeon in Dublin, she moved to
the School of Veterinary Medicine at the University of
Pennsylvania and completed a residency in small animal
internal medicine in 1989. Following the residency, Dr King
remained on staff in the Intensive Care Unit at the
University of Pennsylvania, and she is currently a Professor
in the Section of Critical Care, and the Director of the
Intensive Care Unit. Her research interests include all
aspects of small animal intensive care medicine, with
special emphasis on pulmonary medicine and outcome
prediction in the critical small animal patient.
KEY POINTS
Respiratory distress is a common presenting sign for
small animals, especially in emergency clinics
Recognizing common respiratory patterns and
routine breed- and age-related problems can help to
narrow the list of differential diagnoses
Emergency management is facilitated by identifying
the anatomic location of the problem
Supplemental oxygen and efforts to minimize
handling and stress are imperative for these patients
Thoracic radiographs, pulse oximetry and blood gas
analysis are the most commonly utilized emergency
diagnostic tests for respiratory disease
Emergency clinicians should be familiar with life-
saving interventions such as endotracheal intubation,
thoracocentesis, and thoracostomy tube placement
36 / / Veterinary Focus / / Vol 20 No 2 / / 2010
Dana Clarke, VMD
Philadelphia School of
Veterinary Medicine, University
of Pennsylvania, Philadelphia,
USA
Dr Dana Clarke attended the School of Veterinary Medicine
at the University of Pennsylvania, graduating in 2006. She
completed a one-year rotating internship at Michigan State
University then returned to the University of Pennsylvania
in 2007 to begin a three-year residency in Emergency &
Critical Care. She is set to complete her residency this
year and would like to continue working in an academic
intensive care unit. Her clinical and research interests
include respiratory disease, mechanical ventilation, care of
critical post-operative patients, and microcirculation.
Introduction, initial assessment
and stabilization
Respiratory distress in small animal patients is a
true emergency which requires rapid stabilization,
prompt recognition and treatment of the under-
lying problem, determination of diagnostic and
therapeutic options, and an assessment of pro-
gnosis. The first steps in the management of the
dyspneic patient include recognizing that the
respiratory system is compromised, performing
a physical examination, providing supplemental
oxygen, and obtaining a brief but focused history
from the owner.
Physical examination
Animals that present in respiratory distress must be
handled carefully to minimize stress and struggling
and the initial physical examination may be limited
to assessment of mucous membranes, capillary refill,
and thoracic auscultation. Commonly the clinician
may note increased respiratory rate and/or effort,
shallow chest excursions, excessive respiratory noise,
extension of the head and neck, nostril flare, mouth
breathing, elbow abduction, and an inability to lie
down or be comfortable. Patients on the verge of
respiratory arrest may have limited movement of
the chest wall and a paradoxical respiratory pattern
due to respiratory muscle fatigue (1-4).
It is imperative to assess airway patency at pre-
sentation by observing that the patient is able to
move air during breathing; the animal should not
be stressed by attempting to open the mouth. If
complete airway obstruction is diagnosed, rapid
sequence sedation, intubation and possibly positive
pressure ventilation are indicated. Cyanosis is
not a reliable indicator of hypoxemia, as it does
not develop until the partial pressure of oxygen in
arterial blood (PaO2) is <50 mmHg, and cannot
be detected in severely anemic or hypoperfused
patients. Therefore the presence of pink mucous
membranes should not be perceived as an indic-
ation of adequate oxygenation (1,4). A brief period
of thoracic auscultation at this time should include
auscultation of the heart to detect arrhythmias or
murmurs, auscultation of the lungs with particular
attention to areas of dullness or abnormal lung
sounds such as crackles or wheezes, and auscult-
ation of the cervical trachea to detect loud sounds
indicating a possible airway obstruction.
Many dyspneic patients, especially cats, are intol-
erant of handling. Therefore supplemental oxygen,
regardless of the cause of respiratory distress,
is imperative for all patients with respiratory
compromise. If possible, a peripheral intravenous
catheter should also be placed at presentation to
provide vascular access.
Methods of oxygen
supplementation
Methods of oxygen support include flow-by, mask,
hood delivery, nasal oxygen catheters, oxygen
cage, and positive pressure ventilation (3-7).
Flow-by oxygen is the provision of oxygen through a
tube held in front of the patient’s face. Inexpensive
and uncomplicated, it does require some patient
restraint and someone to hold the line to the
patient’s mouth and nose. It is most useful for
short-term provision of supplemental oxygen
during the initial assessment of the animal and
during brief procedures such as radiographs and
catheter placement (4-7) but may be insufficient for
patients that are panting or moving. Flow rates
should be between 100-200 mL/kg/min, but
high flow rates may not be well tolerated and are
comparatively wasteful. The effectiveness of flow-
by oxygen can be improved via an oxygen mask: a
plastic cone that attaches to the oxygen line. With
similar flow rates to those given above, this
technique provides higher percentages of inspired
oxygen (especially with a well-fitted mask and a
recumbent patient). Mobile patients will require
restraint to keep the mask in place, and many
distressed animals resist placement of the mask
over their face. An oxygen hood can be fashioned
from an Elizabethan collar partially covered with
plastic wrap. An oxygen line is inserted inside the
collar, with the plastic cover vented to allow expired
heat and gases to escape. Commercially available
hoods, with an adjustable collar and perforated
holes for expired gas release, also exist. Hoods
are generally well tolerated, can achieve high
percentages of inspired oxygen and allow for
patient monitoring and procedures without inter-
rupting oxygen delivery. However, there is no
control over the amount of inspired oxygen and
some patients, especially those that are panting,
may overheat. Humidification should be used
for long term oxygen hood therapy (3-6). Nasal
catheters can provide high percentages of inspired
oxygen via an indwelling catheter (see Table 1)
or human nasal oxygen prongs (which are less
invasive and useful in quiet or recumbent patients -
Figure 1), using flow rates of 0.5-3 L/min. This
technique is useful in patients that are restless or
panting, or too large or intolerant of an oxygen
cage, and is less wasteful than other methods. It
allows patient monitoring and further procedures
without interruption of oxygen therapy, but given
the time needed for catheter placement this
method is usually reserved for more long-term
treatment (rather than initial stabilization) and
humidification should be added in this situation
(3,4,6,7). Oxygen cages are extremely useful
as they provide accurate and (if indicated) high
concentrations of humidified oxygen, allowing
patient observation without restraint. However
cages are expensive and can be wasteful as
Vol 20 No 2 / / 2010 / / Veterinary Focus / / 37
 includes the duration and nature of respiratory
signs, the presence of coughing, gagging, or
exercise intolerance, possibility of toxin or foreign
body ingestion, voice changes, history of heart or
pulmonary disease, use of heartworm prevent-
ative, and the presence of concurrent systemic
illness, such as vomiting, anorexia, and endocrine
diseases. A current medication list should also be
obtained. Once a physical examination has helped
© Dana Clarke

determine the anatomic origin of the respiratory

Figure 1.
The use of human nasal oxygen prongs in a dog with respiratory
disease.
oxygen concentration decreases rapidly when
the door is open. If severe respiratory distress
cannot be relieved using other techniques,
intubation and positive pressure ventilation is
the best way to control the airway, deliver oxygen
or positive end-expiratory pressure, to relieve
the patient’s anxiety and discomfort. Heavy
sedation or light anesthesia, constant intensive
monitoring, specialized equipment and training
are required for this technique (4-7).
Regardless of the method of oxygen supplem-
entation chosen, it is important to remember that
prolonged periods (>24 hours) of high oxygen
concentrations (>60%) should ideally be avoided
to reduce the risk of oxygen toxicity due to free
radical formation (4,6,7).
Obtaining a history
After the patient has been stabilized with supple-
mental oxygen, a preliminary history can be
obtained from the owner. Important information
distress and the animal has been stabilized, a more
complete history can be obtained and a definitive
diagnostic and therapeutic plan reviewed with the
owners.
Localization of respiratory
compromise, diagnostics, and
therapeutics
A more complete physical examination can be
performed to localize the origin of respiratory
distress. Based on this examination, the causes
of respiratory distress can be assigned to one of
five categories: airway obstruction, pulmonary
parenchymal disease, pleural space disease,
thoracic wall abnormalities, and “look-alikes”.
Identification of the probable site of the problem,
combined with the signalment and history, allows
the determination of a list of likely differential
diagnoses, necessary diagnostics and immediate
therapeutic options.
Airway obstruction
These patients may have inspiratory and/or
expiratory stridor or stertor, head and neck
extension, heat and exercise intolerance, pro-
longed inspiration, cyanosis, a honking or dry

Table 1.
Nasal oxygen catheter placement.

To place indwelling nasal oxygen catheters, one or both nostrils should first be infused with lidocaine. A
suitable catheter should be selected, measured to the medial canthus of the eye, and marked at that depth
prior to insertion. With an assistant restraining the dog’s head, the catheter should be advanced into the
nasal passage gently but quickly, as the initial sensation of passing through the rostral part of the ventral
meatus is the most uncomfortable part for the patient. Once inserted to the mark, the catheter should be
secured using tissue glue or sutured with a tape butterfly or a Chinese finger-trap suture pattern. Any
remaining length of catheter should be secured to the top of the patient’s head to avoid irritating the ears or
whiskers. Most patients will also require an Elizabethan collar to prevent them from scratching or dislodging
the catheter.

38 / / Veterinary Focus / / Vol 20 No 2 / / 2010

 EMERGENCY CARE OF THE PATIENT WITH ACUTE RESPIRATORY DISTRESS

a b

© Dana Clarke
c d
Figure 2.
Common sites of pulse oximetry probe placement (a: the tongue, b: lip, c: pinna) and an example of a reliable pulse oximetry wave
(d). A uniform waveform, which matches the patient’s heart rate, must be present in order to accept the pulse oximetry reading
as reliable. Excessive patient movement, poor contact due to fur, and pigmentation can interfere with the generation of a reliable
pulse oximetry value.

cough, respiratory distress, retching, and collapse.
Dogs may be hyperthermic and cats may have
intermittent open mouth breathing. A prolonged
inspiratory phase of respiration (because the
upper airway is sucked closed on inspiration) may
be noted and wheezes may be heard, particularly
on expiration. Coughing is commonly seen in
cats with asthma, and lower airway obstructive
disease is associated with increased expiratory
effort. Referred upper airway noise may be
differentiated from pulmonary parenchymal
sounds as the sound intensity and pitch is
louder on auscultation of the larynx and trachea
(1,2,4,8,9).
Common causes of airway obstruction in dogs
include: brachycephalic airway syndrome, laryngeal
paralysis, inflammation or edema of the pharynx
or larynx, airway infections and/or abscessation,
foreign body, coagulopathy induced hemorrhage,
neoplasia, tracheal and mainstem bronchial
collapse, and bronchitis (1,4,8,9). In cats, the most
common causes of airway obstruction are feline
asthma, nasopharyngeal polyps, pharyngeal and
laryngeal neoplasia, inflammatory and granulo-
matous laryngeal disease, and viral nasal infections
(2,4,8,9).
Since airway obstructions may impede oxygenation,
ventilation, or both, useful diagnostics include pulse
oximetry (Figure 2) and arterial or venous blood
gas analysis. Hypoventilation is defined as arterial
carbon dioxide partial pressure (PaCO2) >43 mmHg
in dogs and >36 mmHg in cats, resulting in primary
respiratory acidosis. PaCO2 >60 mmHg is consistent
with significant hypoventilation and warrants
definitive therapy to relieve the airway obstruction.
When arterial blood gas sampling is not possible,
venous carbon dioxide partial pressure (PvCO2) can
be used. Hypoxemia is defined as arterial partial
pressure of oxygen (PaO2)<80 mmHg and a value
of PaO2 <60 mmHg (which corresponds to <90%
pulse oximetry) is consistent with severe hypo-
xemia and requires therapeutic intervention.

Vol 20 No 2 / / 2010 / / Veterinary Focus / / 39

 In these patients initial stabilization should be aimed
at provision of supplemental oxygen, establishing
vascular access, and applying cooling measures.
Sedative and/or anxiolytic therapies can relieve
respiratory distress and decrease respiratory drive,
thus decreasing the degree of airway collapse.
Intravenous fluid therapy, wetting of the fur and
the use of a fan will aid cooling. Anti-inflammatory
doses of corticosteroid may also be considered; this
can be life-saving in patients with severe airway
edema or inflammation but should be used
selectively as it may impede a definitive diagnosis
of lymphoma (1,8). Cats with feline asthma may
benefit from parenteral bronchodilators such as
terbutaline if they have no evidence of heart
disease. Inhaled drugs (e.g. albuterol, fluticasone)
may be substituted if complicating systemic
disease is present. In the majority of patients,
sedation, cooling and head/neck positioning
to optimize airway patency are sufficient for
stabilization.
For those with complete airway obstruction, or
when cooling and sedative efforts are ineffective,
induction of anesthesia and intubation is required.
If endotracheal intubation cannot be achieved,
an emergency tracheostomy must be performed.
The cause of an upper airway obstruction can
usually be diagnosed by a sedated upper airway/
laryngeal examination, cervical and thoracic radio-
graphs, fluoroscopy, rhinoscopy/laryngoscopy/
tracheoscopy/bronchoscopy, and/or computed
tomography (CT). If a hematoma caused by a
coagulopathy (e.g. secondary to rodenticide) is
suspected, prothrombin time (PT) and partial
thromboplastin time (PTT) should be performed.
Transtracheal lavage, endotracheal lavage,
or bronchoalveolar lavage should be considered
in patients suspected to have lower airway
(bronchial) or concurrent pulmonary parenchymal
disease.
Pulmonary parenchymal disease
Dogs with pulmonary parenchymal disease
are often depressed; signs may include: panting
or breathing open-mouthed, with nostril flare,
coughing, head and neck extension, and anxiety.
Cats only breathe through an open mouth when
they have severe respiratory compromise and (in
40 / / Veterinary Focus / / Vol 20 No 2 / / 2010
contrast to dogs) rarely cough. Physical examin-
ation findings may include weakness, tachypnea,
tachycardia, fever, mucopurulent nasal discharge,
harsh lung sounds, and/or crackles. A heart murmur
and/or arrhythmias are usually heard in dogs
that have respiratory signs due to congestive heart
failure. The same is not always true of cats with
congestive heart failure, when cardiac auscult-
ation may be normal. Pulse quality may be
diminished whilst cyanosis may be seen in severely
hypoxemic patients although hypoperfusion
may produce pallor of the mucous membranes
(1,2,4).
Common causes of pulmonary parenchymal
disease include parasitic or bacterial pneumonia,
pulmonary edema (cardiogenic or non-cardio-
genic), pulmonary contusions, smoke inhalation,
pneumonitis (chemical and uremic), aspiration
pneumonia, fungal or viral infection, pulmonary
thromboembolism, neoplasia, pulmonary fibrosis,
and acute respiratory distress syndrome (ARDS).
Cardiogenic edema occurs frequently in cats,
whereas aspiration pneumonia is uncommon in
this species (1-4,10).
Thoracic radiographs are particularly important
in this situation. For example, classic radiographic
changes associated with pneumonia include a
cranio-ventral alveolar pattern (Figure 3), whereas
cardiogenic pulmonary edema in dogs is generally
associated with a heavy perihilar interstitial to
alveolar pattern (Figure 4). In contrast, non-
cardiogenic pulmonary edema is associated with
a caudo-dorsal interstitial to alveolar pattern
(Figure 5).
Pulmonary parenchymal disease causes hypo-
xemia primarily by mismatch of ventilation and
perfusion, but also due to diffusion impairment and
intrapulmonary shunt. Pulse oximetry and blood
gas analysis are important in determining the
severity of disease, and hematology and bio-
chemistry may assist diagnosis. Lower respiratory
tract sampling via transtracheal, endotracheal, or
bronchoalveolar lavage can be important diagnostics
to determine the origin of pulmonary parenchymal
disease, especially in patients with atypical radio-
graphic changes or when multiple disease processes
are suspected, and cytology, bacterial culture and
 EMERGENCY CARE OF THE PATIENT WITH ACUTE RESPIRATORY DISTRESS

sensitivity, and fungal culture are usually indicated.

Emergency therapy for patients with pulmonary
parenchymal disease depends on the clinician’s
educated guess about the most likely etiology.

Pleural space disease

Clinical signs in these patients may include a
short, shallow restrictive breathing pattern,
increased respiratory rate, nostril flaring, ortho-

© Dana Clarke
pnea, an abdominal component to respiration,
and a reluctance to lie down. Cats may have
open mouth breathing. The degree of respiratory
Figure 3.
distress depends on the rate of development of
Lateral thoracic radiograph from a dog with aspiration pneumonia
the pleural space-occupying lesion, especially showing the cranioventral alveolar pattern commonly seen in
pleural effusion. Paradoxical respiration may be this disease process.
noted in patients with a diaphragmatic hernia.
Thoracic auscultation may reveal decreased or
dull lung sounds ventrally (pleural effusion) or
dorsally (pneumothorax), an auscultable fluid
line, muffled cardiac sounds, or borborygmi
if stomach or intestines are in the chest. Thoracic
auscultation changes may be unilateral or bilateral
and are not always equal. Cats with a mediastinal
mass have decreased chest wall compressibility
(1,2,4,11,12).

© Lesley King, Dana Clarke

Common causes of pleural space disease include
pneumothorax and pleural effusions. Pleural
effusions may be pure or modified transudates due
to congestive heart failure, vasculitis, and lung lobe
torsion; pyothorax, chylothorax, hemothorax, feline Figure 4.
infectious peritonitis, and neoplastic effusions are Lateral thoracic radiograph in a dog with perihilar cardiogenic
also common. Diaphragmatic hernia and pleural pulmonary edema, cardiomegaly, and pulmonary venous
distension.
space masses also occur (1,2,4,11,12).

If pleural disease is suspected, it is imperative to

evacuate the pleural space as quickly as possible
(Table 2). Oxygen supplementation and vascular
access is established if it can be done without
stress. Thoracocentesis is both therapeutic and
© Lesley King, Dana Clarke

diagnostic, and any fluid obtained submitted for

cytology and culture. Thoracocentesis is not indic-
ated for patients with pleural space masses,
diaphragmatic hernias, or hemothorax secondary
to coagulopathy that is not causing significant
respiratory compromise. Other diagnostics (e.g. Figure 5.
radiography or ultrasound) should be delayed until
Lateral thoracic radiograph from a puppy after being strangled by
after the animal has been stabilized by thoraco- his collar, demonstrating the caudo-dorsal, heavy interstitial to
centesis, allowing the pulmonary parenchyma to alveolar pattern commonly seen in patients with non-cardiogenic
be visualized effectively. pulmonary edema.

Vol 20 No 2 / / 2010 / / Veterinary Focus / / 41

 Table 2.
Thoracocentesis.

Sedation is often not necessary unless the patient is very distressed or agitated; most animals can be restrained
in sternal recumbence for the procedure. The patient’s chest wall should be prepared in the region where the
lung sounds are most muffled. This is generally in the upper third of the caudodorsal thorax between the 8th
and 9th ribs for pneumothorax, and in the ventral two thirds of the thorax between the 6th and 8th intercostal
spaces for pleural effusion. Alternatively, an ultrasound probe can be used to find pockets of fluid amenable
to aspiration. When aspirating air, a 22 or 25 gauge straight needle or butterfly needle is preferred; larger gauge
needles (18 or 20 g) are often needed for pleural fluid aspiration in dogs. The needle is attached to tubing, a
three-way stopcock, and syringe. The cranial border of the rib is palpated, and the needle is advanced through
the skin, bevel up, and slowly into the thoracic cavity on the cranial border of the rib. The needle should be
slowly advanced while an assistant aspirates the system; the needle is then held still as soon as air or fluid is
visible in the tubing. Air and fluid should be aspirated until negative pressure is achieved, at which point the
needle may be advanced further into the thorax, redirected, or repositioned if additional air or fluid is
suspected.

Normally blood aspirated during thoracocentesis
should clot quickly, unless a coagulopathy or a
hemorrhagic effusion (e.g. due to neoplasia or
lung lobe torsion) is present; if this occurs further
testing to confirm these suspicions should be
performed. If unexpected air is aspirated, the
collection system should be checked for leaks.
If no leaks are present, thoracoentesis should
be temporarily aborted as long as the animal is
still stable, because an iatragenic pneumothorax
may have been created (3,4,12,13). If negative
pressure is not achieved during thoracocentesis,
if the patient re-accumulates a significant amount
of air within a short period requiring multiple
thoracocentesis events, or for the medical
management of certain pleural effusions such as
pyothorax, thoracostomy tubes (unilateral or
bilateral) may be needed and are best placed
using general anesthesia (1,3,4,14).
Thoracic wall abnormalities
Abnormalities of thoracic wall function may
occur because of dysfunction at several levels. In
some cases, respiratory distress may be second-
ary to thoracic wall injuries or trauma. Those
patients often demonstrate pain on manipulation
or palpation of the thorax, and may have a flail
chest with paradoxical motion of a segment of
chest wall. Lacerations, bruising or concurrent
pulmonary contusions may occur. Alternatively,
abnormal thoracic wall and diaphragmatic funct-
ion may result from defective neuromuscular
control of breathing, which may be caused by
disease in the brain, spinal cord, peripheral nerves
or neuro-muscular junctions. Such patients
typically lack diaphragmatic and abdominal
muscle movement, and have clinical evidence of
hypoventilation with elevated PaCO2 levels on
blood gas analysis (1,3,15).
Common causes of thoracic wall dysfunction
include traumatic injuries, anesthetics and central
respiratory depressants, severe hypokalemia,
myasthenia gravis, botulism, tick paralysis,
polyradiculoneuritis, congenital abnormalities,
some snake envenomation, thoracic wall neo-
plasia, and spinal cord or phrenic nerve disease
(1,3,15).
Diagnostics for these patients include blood
gas analysis, pulse oximetry, capnography, and
thoracic radiographs. Neurologic examination
findings consistent with cervical spinal cord or
brainstem dysfunction may support a neurologic
origin. Measurement of acetylcholine receptor
antibody titers, edrophonium response testing,
and electromyelography (EMG) can aid in the
diagnosis of myasthenia gravis. EMG and the
confirmation of botulism toxin in serum, feces,
or vomited material can support a diagnosis of
botulism. There are no specific diagnostic tests
for tick paralysis, polyradiculoneuritis, and snake
venoms, though geographic location, signalment,
and history may support a diagnosis (15).

42 / / Veterinary Focus / / Vol 20 No 2 / / 2010

 EMERGENCY CARE OF THE PATIENT WITH ACUTE RESPIRATORY DISTRESS
“Look-alikes”
Whilst rare, some non-respiratory conditions
can mimic respiratory disease. Examples include
hyperthermia, compensation for metabolic acid-
osis, anemia, pain, stress, anxiety, hypovolemia,
abdominal distension (cranial organomegaly
and abdominal effusion), hyperadrenocorticism
or corticosteroid therapy, and certain opioid
medications (16). History, physical examination,
thoracic radiographs, blood gas analysis and
serum chemistry can be helpful to distinguish
these conditions from real respiratory disease.
REFERENCES
1. Lee JA, Drobatz KJ. Respiratory distress and cyanosis in dogs. In: King
LG. Textbook of respiratory disease in dogs and cats. Philadelphia: WB
Saunders 2004; 1-12.
2. Mandell DC. Respiratory distress in cats. In: King LG. Textbook of respiratory
disease in dogs and cats. Philadelphia: WB Saunders 2004; 12-17.
3. Tseng LW, Waddell LS. Approach to the patient in respiratory distress. Clin
Tech Small Anim Pract 2000; 15: 53-62.
4. Macintire DK, Drobatz KJ, Haskins SC, et al. Manual of small animal
emergency and critical care medicine. Philadelphia: Lippencott, Williams
and Wilkins, 2005; 115-159.
5. Rozanski E, Chan DL. Approach to the patient with respiratory distress.
Vet Clin Small Anim Pract 2005; 35: 307-317.
6. Tseng LW, Drobatz KJ. Oxygen supplementation and humidification.
In: King LG. Textbook of respiratory disease in dogs and cats.
Philadelphia: WB Saunders 2004; 205-213.
7. Mazzaferro EM. Oxygen therapy. In: Silverstein DC, Hopper K.
Small Animal Critical Care Medicine. Philadelphia: WB Saunders 2009; 78-81.
8. Costello MF. Upper airway disease. In: Silverstein DC, Hopper K.
Small Animal Critical Care Medicine. Philadelphia: WB Saunders 2009;
67-72.
Conclusion
Respiratory distress is a common and serious
emergency encountered by veterinarians. An
understanding of the need for careful patient
handling and the provision of supplemental
oxygen is vital. Veterinarians should recognize the
signalment, history, and physical examination
findings seen with common respiratory diseases.
An understanding of respiratory disease patho-
physiology and localization as well as the
diagnostic and therapeutic techniques essential
for management of each category of dysfunction
is crucial for successful treatment.
9. Holt DE. Upper airway obstruction, stertor, and stridor. In: King LG.
Textbook of respiratory disease in dogs and cats. Philadelphia: WB
Saunders 2004; 35-42.
10. De Clue AE, Cohn LA. Acute respiratory distress syndrome in dogs
and cats: a review of clinical findings and pathophysiology.
J Vet Emerg Crit Care 2007; 17: 340-347.
11. Suave V. Pleural space disease. In: Silverstein DC, Hopper K. Small Animal
Critical Care Medicine. Philadelphia: WB Saunders 2009; 125-130.
12. Silverstein DC. Pleural space disease. In: King LG. Textbook of respiratory
disease in dogs and cats. Philadelphia: WB Saunders 2004; 49-52.
13. Sigrist NE. Thoracocentesis. In: Silverstein DC, Hopper K. Small Animal
Critical Care Medicine. Philadelphia: WB Saunders 2009; 131-133.
14. Sigrist NE. Thoracostomy tube placement and drainage. In: Silverstein
DC, Hopper K. Small Animal Critical Care Medicine. Philadelphia: WB
Saunders 2009; 134-137.
15. Donahue S. Chest wall disease. In: Silverstein DC, Hopper K.
Small Animal Critical Care Medicine. Philadelphia: WB Saunders 2009;
138-140.
16. Hall K, Lee JA. Nonrespiratory look-alikes. In: Silverstein DC, Hopper K.
Small Animal Critical Care Medicine. Philadelphia: WB Saunders 2009;
141-144.
Vol 20 No 2 / / 2010 / / Veterinary Focus / / 43