BAGIAN RADIOLOGI REFERAT

FAKULTAS KEDOKTERAN APRIL 2018

UNIVERSITAS MUSLIM INDONESIA

PNEUMOTHORAX

Disusun Oleh:
Nadrah Zuhriah Amri
111 2017 2085

Supervisor Pembimbing:
dr. Evi S Gusnah, Sp. Rad., M. Kes

DIBAWAKAN DALAM RANGKA TUGAS KEPANITERAAN KLINIK

BAGIAN RADIOLOGI
FAKULTAS KEDOKTERAN
UNIVERSITAS MUSLIM INDONESIA
MAKASSAR
2018

i
 HALAMAN PENGESAHAN

Referat yang berjudul “Pneumothorax” yang dipersiapkan dan disusun oleh:

Nama : Nadrah Zuhriah Amri

NIM : 111 2017 2045

Telah diperiksa dan dianggap telah memenuhi syarat Tugas Ilmiah Mahasiswa
Pendidikan Profesi Dokter dalam disiplin ilmu Radiologi pada,

Waktu : April 2018

Tempat : Rumah Sakit Salewangang Maros

Makassar, April 2018

Menyetujui,

Pembimbing Penulis

dr. Evi S Gusnah, Sp. Rad., M. Kes Nadrah Zuhriah Amri

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 DAFTAR ISI

HALAMAN PENGESAHAN ................................................................................ ii

DAFTAR ISI .......................................................................................................... iii

BAB 1 PENDAHULUAN ...................................................................................... 1

BAB 2 TINJAUAN PUSTAKA ............................................................................. 3

2.1 Definisi Pneumothorax ............................................................................. 3

2.2 Patofisiologi ............................................................................................. 3

2.3 Klasifikasi................................................................................................. 5

2.4 Diagnosis .................................................................................................. 9

2.4.1 Anamnesis ......................................................................................... 9

2.4.2 Pemeriksaan Fisis.............................................................................. 9

2.4.3 Pemeriksaan Penunjang .................................................................. 10

2.5 Komplikasi ............................................................................................. 19

2.6 Penatalaksanaa ....................................................................................... 20

2.7 Prognosis ................................................................................................ 24

BAB 3 KESIMPULAN ......................................................................................... 25

DAFTAR PUSTAKA ........................................................................................... 27

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 BAB 1

PENDAHULUAN

Pleura adalah suatu membrane serosa yang melapisi permukaan dalam

dinding thorax di kanan dan kiri, melapisi permukaan superior diagfragma kanan

dan kiri, melapisi mediastinum kanan dan kiri (semuanya disebut pleura

parietalis), kemudian pada pangkal paru, membrane serosa ini berbalik melapisi

(membungkus) paru (disebut pleura viceralis). Pleura viceralis ini berinvaginasi

mengikuti fisura yang membagi setiap lobus paru. 1

Diantara pleura parietalis dan pleura viceralis terdapat ruang yang disebut

“rongga” pleura. Pada “rongga” pleura terdapat cairan pleura seperti lapisan film

karena jumlahnya sangat sedikit yang hanya berfungsi untuk memisahkan pleura

viceralis dan pleura parietalis.1

Gambar 1. Anatomi Rongga Pleura

Pneumothorax adalah keadaan ketika ditemukannya udara di dalam rongga

pleura. Udara di rongga pleura menyebabkan tekanan di dalam rongga pleura

tidak lagi negative (dalam keadaan normal, tekanannya adalah -5cm H2O). Paru

1
akan menjadi kempis, dan disebut sebagai kolaps atau atelectasis. Penderita akan

mengeluh sesak napas karena tidak terjadi ventilasi pada paru yang kolaps.1

Pneumothorax sendiri terjadi baik secara spontan maupun traumatik.

Pneumothorax itu sendiri dapat bersifat primer dan sekunder. Sedangkan

pneumothorax traumatic dapat bersifat iatrogenik dan non-iatrogenik.2

Insidensi pneumothorax spontan lebih sering terjadi pada laki-laki

daripada perempuan. Kejadian tahunan PSP adalah 18-28 per 100.000 pada laki-

laki dan 1,2-6,0 pada wanita. Pneumothorax sekunder kurang umum, dengan 6,3

untuk pria dan 2,0 untuk perempuan. Kejadian pada anak-anak belum diteliti

dengan baik, tetapi mungkin lebih rendah dari orang dewasa dan sering

mencerminkan mendasari penyakit paru-paru.2

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 BAB 2

TINJAUAN PUSTAKA

2.1 Definisi Pneumothorax

Pneumothorax adalah kumpulan udara atau gas dalam rongga

pleura. 2

Pneumotoraks ditandai dengan dyspnea dan nyeri dada yang

berasal dari paru-paru dan dinding dada dan dapat mengganggu respirasi

normal karena adanya gelembung gas di rongga pleura atau retensi gas di

ruang pleura yang terjadi setelah pecahnya bulla. Pneumothoraks

dikategorikan sebagai kolaps spontan-pulmonal atau disebabkan oleh

trauma.3

Pneumotoraks spontan lebih lanjut diklasifikasikan menjadi

pneumotoraks primer dan pneumotoraks sekunder. Pneumotoraks primer

berkembang setelah pecahnya bula pada orang sehat tanpa penyakit paru

yang mendasari. Pneumotoraks sekunder disebabkan oleh ruptur jaringan

pulmonal yang rusak, dan terjadi terutama pada pasien yang didiagnosis

dengan penyakit paru, seperti emfisema pulmonal.3

2.2 Patofisiologi

Rongga toraks berisi paru-paru, jantung, dan banyak pembuluh

darah utama. Pada setiap sisi rongga, membran pleura menutupi

permukaan paru (pleura visceral) dan juga melapisi bagian dalam dinding

dada (pleura parietal). Antara dua lapisan ada sejumlah kecil cairan serosa

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pelumas. Paru-paru sepenuhnya meningkat di dalam rongga karena

tekanan di dalam saluran udara lebih tinggi daripada tekanan di dalam

rongga pleura. Pneumothoraks hanya dapat berkembang jika udara

diperbolehkan masuk, melalui kerusakan pada dinding dada atau

kerusakan pada paru itu sendiri, atau kadang-kadang karena

mikroorganisme di ruang pleura menghasilkan gas.4

Pneumotoraks spontan pada sebagian besar pasien terjadi akibat

pecahnya bleb dan bula. Meskipun PSP didefinisikan terjadi pada pasien

tanpa penyakit paru yang mendasari, pasien ini memiliki bleb

asimptomatik dan bula yang terdeteksi pada CT-Scan atau selama

torakotomi. Selama respirasi normal, rongga pleura memiliki tekanan

negatif. Ketika dinding dada mengembang keluar, tegangan permukaan

antara pleura parietalis dan visceral memperluas paru ke luar. Jaringan

paru-paru elastis,. Jika rongga pleura diisi oleh gas dari pecahnya bleb,

paru-paru akan kolaps sampai kesetimbangan tercapai. Ketika

pneumotoraks membesar, paru menjadi lebih kecil. Konsekuensi fisiologis

utama dari proses ini adalah penurunan kapasitas vital dan tekanan parsial

oksigen.5

Tension pneumothorax terjadi kapan saja jika terdapat gangguan

yang melibatkan pleura visceral, pleura parietal, atau cabang

trakeobronkial. Kondisi ini berkembang ketika jaringan yang terluka

membentuk katup satu arah (one-way valve), yang memungkinkan aliran

udara masuk selama inhalasi dan melarang aliran udara keluar. Volume

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 udara intrapleural yang tidak dapat diserap ini meningkat setiap inspirasi

karena efek katup satu arah. Akibatnya, tekanan meningkat di dalam

hemitoraks yang terkena. Selain mekanisme ini, tekanan positif yang

digunakan dengan terapi ventilasi mekanis dapat menyebabkan udara

terperangkap.5

Saat tekanan meningkat, paru ipsilateral kolaps dan menyebabkan

hipoksia. Peningkatan tekanan lebih lanjut menyebabkan mediastinum

bergeser ke sisi kontralateral dan menekan kedua paru sehingga

mengurangi alirann balik vena kembali ke atrium kanan. Timbulnya

hipoksia akibat dari kolaps paru-paru ipsilateral dan paru-paru yang

terdesak pada sisi kontralateral yang mengganggu pertukaran gas.

Hipoksia dan penurunan aliran balik vena disebabkan oleh kompresi

dinding atrium yang relatif tipis merusak fungsi jantung. 5

2.3 Klasifikasi

Berdasarkan Klinisnya pneumothorax dapat digolongkan sebagai2 :

a. Pneumothorax Spontan Primer (PSP)

Cenderung terjadi pada orang muda tanpa masalah paru-paru yang

mendasari, biasanya menyebabkan gejala terbatas. Nyeri dada dan

kadang-kadang sesak napas ringan adalah gejala dominan. Setengah

dari mereka dengan pneumothorax spontan primer menunggu beberapa

hari untuk mencari bantuan medis. Hal ini sangat jarang untuk PSP

menyebabkan tension pneumothorax. Gejala biasanya mulai saat

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 istirahat. Laki-laki tinggi terutama perokok, adalah khas pada resiko

yang lebih tinggi PSP.2

b. Pneumothorax Spontan Sekunder (SSP)

Terjadi dengan definisi pada mereka dengan penyakit paru-paru

yang mendasari. Gejala cenderung lebih parah, sebagai paru-paru tidak

terpengaruh pada umumnya tidak mampu menggantikan hilangnya

fungsi dari sisi yang terkena. Hipoksia (penurunan kadar oksigen

dalam darah) biasanya hadir dan dapat diamati sebagai sianosis (warna

biru pada bibir dan kulit). Hypercapnia (akumulasi carbon dioksida

dalam darah) kadang-kadang dihadapi, hal ini dapat menyebabkan

kebingungan dan koma.2

Diketahui penyakit paru-paru yang dapat meningkatkan resiko

untuk pneumothorax adalah2:

a. Penyakit Saluran udara: PPOK (terutama ketika terdapat

emfisema dan bula paru-paru), asma parah akut, fibrosis kistik.

b. Infeksi paru : Pneumonia, TB

c. Kanker : Kanker paru-paru, sarcoma melibatkan paru-paru.

d. Catamenial (terjadi dalam kaitannya dengan siklus haid):

endometriosis di dada.

c. Trauma Penumothorax

Baik terjadi karena lubang di dinding dada, misalnya luka tusuk

atau luka tembak, memungkinkan udara masuk ruang pleura, atau

karena cedera pada paru-paru.2

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 Prosedur medis dada (iatrogenik), seperti pengambilan sampel

biopsy dari jaringan paru-paru, memasukkan kateter vena sentral

menjadi salah satu pembuluh darah dada, dapat menyebabkan cidera

pada paru-paru dan pneumothorax resultan. Pemberian ventilasi

tekanan positif, baik ventilasi mekanis atau ventilasi non-invasif dapat

mengakibatkan barotrauma mengarah ke suatu pneumothorax.2

Pneumotoraks traumatik juga dapat diklasifikasikan sebagai

simple, open dan tension Pneumothorax. 6

Pada simple pneumotoraks, udara dari paru-paru yang rusak

memasuki rongga pleura. tidak banyak gejala pada tipe pneumothorax

ini.6

Open pneumotoraks terjadi ketika luka di thorax cukup besar untuk

memungkinkan udara masuk dan keluar secara bebas di rongga pleura.

Dalam hal ini, tekanan atmosfer sama dengan tekanan intrapleura

sehingga menghalangi inflasi paru-paru dan ventilasi alveolar.

Pneumothorax jenis ini membutuhkan intervensi medis segera.6

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 Tension Pneumotoraks terjadi akibat dari cedera thorax atau paru-

paru. Mekanisme “one-way valve” terjadi, di mana udara yang

memasuki ruang pleura selama inspirasi terperangkap dan tidak bisa

dikeluarkan selama ekspirasi. Peningkatan tekanan interthoracic

menyebabkan paru-paru kolaps. Kolaps pada paru-paru menyebabkan

pergeseran mediastinum menjauh dari sisi yang terluka,

mengakibatkan hipoventilasi, penurunan aliran balik vena ke jantung

dan potensi untuk mengakibatkan syok obstruktif.6

Tabel 1. Klasifikasi Pneumothorax

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2.4 Diagnosis

Diagnosis pneumotoraks didirikan dari riwayat pasien dan

pemeriksaan fisik temuan yang menunjukkan penurunan gerakan

hemitoraks, penurunan atau hilangnya fremitus, hipersonor pada perkusi

dan penurunan atau tidak adanya bunyi nafas pada sisi yang terpengaruh.

2.4.1 Anamnesis

Berdasarkan anamnesis, gejala dan keluhan yang sering muncul

adalah6 :

a. Nyeri dada pleuritik mendadak pada sisi yang sama dengan

paru yang terkena.

b. Dyspnea adalah gejala utama, dan nyeri dada pada sisi yang

sama dengan paru-paru yang terkena hadir di sebagian

besar pasien.

c. Beberapa gejala yang paling signifikan secara klinis yang

mungkin berkembang termasuk hipotensi, takikardia,

sianosis, hipoksemia dengan atau tanpa hiperkapnia, dan

gangguan pernapasan akut.

2.4.2 Pemeriksaan Fisis

Pada pemeriksaan fisik thorax didapatkan7:

a. Takipneu

b. Takikardi

c. Hipersonor saat perkusi dinding dada

d. Suara napas tidak terdengar pada saat Auskultasi

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 e. Pendorongan pada mediastinum dan trakea kearah kontra

lateral dari paru-paru yang kolaps.

f. Distensi vena jugular

2.4.3 Pemeriksaan Penunjang

1. Analisa Gas Darah

Arteri gas darah (ABG) tidak menggantikan diagnosis fisik

maupun pengobatan harus ditunda sambil menunggu hasil jika

pneumotoraks simptomatik dicurigai. Namun, ABG analisis

mungkin berguna dalam mengevaluasi hipoksia, hiperkarbia,

dan asidosis respiratorik.8

2. Foto Thorax

A. Posisi Erect

Ini telah menjadi andalan manajemen klinis

pneumotoraks primer dan sekunder selama bertahun-tahun,

meskipun diakui memiliki keterbatasan seperti kesulitan

dalam mengukur ukuran pneumotoraks secara akurat.

Karakteristik diagnostik adalah displacement pleura line.

Dalam 50% kasus, air fluid level terlihat pada sudut

kostofrenik, dan ini kadang-kadang merupakan satu-

satunya kelainan yag terlihat.9

a. Tepi pleura viseral terlihat sebagai garis putih yang

sangat tipis dan tajam

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b. Daerah perifer radiolusen dan avaskuler dibanding

daerah paru yang berdekatan

c. Paru-paru dapat kolaps sepenuhnya

d. Mediastinum seharusnya tidak menjauh dari

pneumotoraks kecuali ada tension pneumothoraks

tension.

e. Emfisema subkutan dan pneumomediastinum mungkin

juga terlihat

Gambar 2.1. Garis Viceral Pleura (panah putih) Normalnya

pleura visceral dan parietal tidak terlihat. Keduanya
normalnya berdekatan dengan dinding thorax. Ketika udara
masuk ke rongga pleura, pleura visceral beretraksi ke hilus
bersamaan dengan paru yang kolaps dan terlihat seperti garis
tipis putih. Tampak daerah perifer yang hiperlusen avaskuler
( panah merah)10

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 Gambar 2.2. Tension Pneumothorax. Tampak radiolusen paru-
paru (L) dan hiperlusen udara bebas (A) di perifer rongga pleura,
tambahan terdapat pergeseran mediastinum ke kiri (panah
hitam)11

B. Lateral X-ray

Dapat memberikan informasi tambahan ketika

pneumotoraks yang dicurigai tidak dikonfirmasi oleh x-rays

PA tetapi, sekali lagi, tidak lagi digunakan secara rutin

dalam praktek klinis sehari-hari.9

C. Supine dan Lateral Decubitus

Teknik-teknik pencitraan ini sebagian besar

digunakan untuk pasien trauma yang tidak dapat

dipindahkan dengan aman. Posisi ini umumnya kurang

sensitif daripada erect x-rays untuk diagnosis pneumotoraks

dan telah digantikan oleh USG atau CT-scan untuk pasien

yang tidak dapat foto erect.9

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 Posisi supine sering tampak normal, bahkan di saat

terdapat udara yang signifikan. Seringkali, satu-satunya

indikasi adalah tanda “deep sulcus sign”, dinamakan

demikian karena penampilan sulkus costovertebral yang

sangat dalam. 8

Gambar 2.3. Deep Sulcus Sign. Pada Posisi Supine, udara yang
cukup banyak pada pneumothorax dapat meduduki anterior dan
inferior dan bermanifestasi menggeser sulcus costophrenicus dan
meningkatkan lusensi dari sulcus (panah hitam). Bandingkan
dengan sulcus yang lain (panah putih)10
3. USG

Probe harus ditempatkan dalam posisi sagital

(indikator menunjuk cephalad) pada dinding dada anterior

sekitar ruang interkostal kedua, di garis mid-klavikula.12

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Gambar 2.4. Posisi probe yang benar untuk evaluasi pneumothorax.
Probe ditelakkan di dinding anterior thorax dengan orientasi sagittal
mengarah ke kepala pasien pada ICS 2 linea mid-clavicula12

Sonografer harus terlebih dahulu mengidentifikasi

dua costa dengan bayangan posterior di belakang dan

memvisualisasikan garis pleura di antara dua costa. Ini

biasanya disebut „Bat Sign' di mana periosteum costa

melambangkan sayap dan garis pleura hyperechoic terang di

antara mereka mewakili tubuh kelelawar.12

Gambar 2.5. a. Bat Sign. dua costa dengan bayangan posterior

melambangkan sayap kelelawar, dan hiperechoic garis pleura sebagai
tubuhnya.12

Kehadiran pleura sliding (bergeser) adalah temuan

paling penting pada paru-paru dengan aerasi normal. Sliding

paling baik dilihat pada apeks paru pada posisi supine.

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Penggunaan M-mode yang mendeteksi gerakan dari waktu ke

waktu, memberikan lebih banyak bukti bahwa garis pleura

bergeser (sliding). Kursor M-mode ditempatkan di atas garis

pleura dan dua pola yang berbeda ditampilkan di layar: Bagian

dada yang tidak bergerak di atas garis pleura menciptakan

'gelombang' horizontal, dan sliding di bawah garis pleura

menciptakan pola granular, 'pasir'. Gambar yang dihasilkan

adalah gambar yang menyerupai gelombang menghantam pasir

dan oleh karena itu disebut „seashore sign‟dan terdapat di paru-

paru normal.12

Gambar 2.6. M-mode yang menggambarkan tanda „seashore.‟ Garis

pleura membagi gambar menjadi dua: Bagian yang tidak bergerak di
atas garis pleura menciptakan „gelombang‟ horizontal, dan garis
geser di bawahnya menciptakan pola granular, „pasir‟12

Garis-B atau „comet-tail artifact‟ muncul sebagai

garis vertikal hyperechoic yang membentang dari pleura ke tepi

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layar tanpa menghilang. Comet-tail artifact bergerak mengikuti

pleura sliding dan gerakan napas.12

Gambar 2.7. 'B-lines' atau 'comet-tail artefact‟ terlihat berasal dari

garis pleura hyperechoic, memanjang secara vertikal ke tepi layar.
Gerakan „B-lines‟ mengikuti pleura sliding di paru-paru normal.12

Gambaran Paneumothorax dalam USG12 :

1. Hilangnya Pleura Sliding

Dalam pneumotoraks, adanya udara yang

memisahkan pleura viseral dan parietal dan mencegah

tervisualisasinya pleura visceral. Dalam situasi ini, pleura

sliding tidak ada. Teknik menggunakan M-mode dapat

digunakan untuk mengkonfirmasi kurangnya sliding.

Pelacakan M-mode yang dihasilkan dalam pneumotoraks

hanya akan menampilkan satu pola garis horizontal paralel

di atas dan di bawah garis pleura, yang menunjukkan

kurangnya gerakan. Pola ini menyerupai 'barcode' dan

sering disebut 'stratosfer sign'.12

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 Gambar 2.8. M-mode dan tidak adanya pleura sliding ditampilkan
sebagai 'stratosfer sign': Garis horizontal paralel di atas dan di bawah
garis pleura, menyerupai 'barcode'. Tanda ini menunjukkan adanya
pneumotoraks pada ruang intercostal12

2. Hilangnya B-Line atau comet-tail artifact

Ultrasound menunjukkan hilangnya „comet-tail

artifact’ pada pasien dengan pneumotoraks. Gambaran ini

hilang karena udara terakumulasi dalam ruang pleura, yang

menghalangi perambatan gelombang suara dan

menghilangkan gradien impedansi akustik. Selain itu,

artefak „comet-tail‟ dihasilkan oleh pleura visceral, yang

tidak divisualisasikan dalam pneumotoraks, oleh karena itu,

gambaranini tidak dihasilkan.12

3. Munculnya A-line Artifact

„A-lines‟ adalah artefak toraks penting lainnya yang

dapat membantu dalam diagnosis pneumotoraks. Ini juga

merupakan artefak gema yang muncul sebagai garis

hyperechoic horizontal berulang yang sama memantul dari

17
 pleura. Ruang di antara setiap A-line sesuai dengan jarak

yang sama antara permukaan kulit dan pleura parietalis.

Pada pasien normal, ketika terdapat „B-lines‟, maka B-line

mereka memanjang dari garis pleura dan menghapus „A-

lines‟, sampai ke tepi layar.12

Gambar 2.9. A-lines, adalah garis horisontal, berjarak sama

terlihat berasal dari garis pleura hyperechoic putih terang.
Jika „B-lines‟ ditemukan, mereka memanjang keluar dari
garis pleura dan menghapus „A-lines‟ di jalur mereka12

4. Digital Imaging

Radiografi digital (Picture-Archiving Communication

Systems, PACS) telah menggantikan radiografi toraks

konvensional di sebagian besar rumah sakit Inggris dalam 5

tahun terakhir, karena memberikan keuntungan yang cukup

besar seperti pembesaran, pengukuran dan manipulasi kontras,

kemudahan transmisi, penyimpanan dan reproduksi

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 Gambar 2.10. Temuan gambaran pneumothorax dalam radiologi8

2.5 Komplikasi

A. Hemopneumothorax Spontan

Sekitar 5% pasien dengan pneumotoraks akan memiliki

haemothorax bersamaan dengan jumlah darah di ruang pleura.

Mekanisme pendarahan dalam Simple hemopneumothorax (SHP)

akibat robeknya adhesi vaskular apikal antara parietal dan visceral

pleura atau pembuluh darah yang robek antara pleura parietal dan

bulla saat paru-paru kolaps atau karena pecahnya vaskularisasi dari

bulla. Manifestasi tergantung pada jumlah darah yang hilang

selama gangguan ini. Perawatan SHP termasuk thoracostomy tube

untuk drainase haemothorax dan re-ekspansi paru-paru. Jika re-

ekspansi paru-paru tidak tidak menghentikan pendarahan,

torakotomi diperlukan untuk menghentikan pendarahan.6

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 B. Bronchopleural fistula

Fistula bronkopleural dapat terjadi pada pasien dengan

pneumotoraks spontan primer (3% hingga 4%),meskipun lebih

sering terjadi pada pasien dengan pneumotoraks spontan sekunder

atau pneumotoraks traumatik. Terjadi kebocoran udara yang

persistent setelah drainase thorakal untuk pneumothorax adalah

tanda awal dari komplikasi ini. Bronkopleural fistula dapat diatasi

dengan torakotomi, penutupan fistula dan pleurodesis.6

C. Chronic pneumothorax (failure of the lung to re-expand)

Chest tube digunakan pada pneumotoraks untuk

meningkatkan ekspansi paru. Namun dalam beberapa kasus,

prosedur ini gagal. Korteks pada pleura visceral menebal sehingga

mencegah ekspansi paru-paru. Prosedur medis untuk kondisi ini

adalah torakotomi dan dekortikasi.6

2.6 Penatalaksanaa

Tujuan dalam mengobati pneumotoraks adalah untuk

menghilangkan udara dari rongga pleura, memungkinkan paru-paru untuk

ekspansi, dan untuk mencegah kekambuhan. Metode terbaik untuk

mencapai hal ini tergantung pada beratnya kolaps paru-paru, jenis

pneumotoraks, kesehatan pasien secara keseluruhan dan risiko komplikasi.

Ada banyak kemungkinan terapeutik dalam praktik klinis.6

1. Observasi

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 Observasi direkomendasikan untuk pasien dengan PSP yang

kurang dari 1 cm. Pada pasien ini, observasi tetap merupakan

pengobatan lini pertama. Tingkat penyerapan udara adalah 25% setiap

24 jam. Oksigen tambahan dapat diberikan untuk meningkatkan

tingkat penyerapan udara pleura.6

2. Aspirasi (Percutaneous Neddle Aspiration)

Aspirasi mungkin merupakan pengobatan awal untuk pasien

dengan pneumotoraks primer. Ini juga dapat dipertimbangkan untuk

pasien dengan usia kurang dari 50 tahun dengan pneumotoraks

sekunder dengan ukuran sedang (lingkar udara 1-2 cm.6

Needle Aspiration sesuai untuk pasien dengan episode pertama

pneumotoraks spontan primer. Pasien harus tidak memiliki bukti

penyakit paru-paru yang mendasari tetapi harus memiliki sesak nafas

atau pneumotoraks dengan rim udara berukuran minimal 2 cm ketika

dinilai pada tingkat hilus.13

Lokasi pemasangan jarum untuk aspirasi pneumotoraks adalah

ruang interkostal kedua pada garis midclavicular, pada sisi paru

dengan pneumotoraks.13

21
 Gambar 2.11. Lokasi Pesangan Neddle13
Lokasi pemasangan jarum untuk aspirasi pneumotoraks adalah ruang interkostal
kedua pada garis midclavicular, pada sisi paru dengan pneumotoraks.

Gambar 2.12. Konfirmasi Penetrasi Ruang Pleural13

Munculnya gelembung udara di syringe, yang sebagian diisi anestesi lokal,
menunjukkan bahwa kateter telah menembus rongga pleura

Gambar 2.13. Aspirasi Udara dari Pneumothorax13

Setelah udara disedot dari pneumotoraks, ia dikembalikan ke udara
ambient

22
3. Tube thoracostomy/ Chest Tube

Tube thoracostomy adalah prosedur bedah yang paling umum

dilakukan. Tindakan torakostomi diindikasikan untuk PSP bergejala,,

serta untuk SSP simptomatik, pneumotoraks iatrogenik dan traumatic.6

Tujuan chest tube secara keseluruhan adalah untuk mendorong re-

ekspansi paru. Chest tube dimasukkan melalui sayatan pada ICS ke-4

atau ke-5 di linea aksilaris anterior atau mid-aksila, dapat pula di ICS 2

mid clavicula.6

Setelah chest tube terpasang, harus terhubung ke suction atau alat

untuk memungkinkan drainase searah (water seal tanpa suction atau

katup Heimlich). Jika re-ekspansi yang adequat tercapai, kateter dapat

dicabut (setelah 5 hingga 7 hari).6

23
 Gambar 2.14. Tatalaksana Pneumothorax9
2.7 Prognosis

Prognosis pneumothorax tergantung pada tingkat dan jenis

pneumothorax. Sebuah pneumothorax spontan kecil umumnya akan hilang

dengan sendirinya tanpa pengobatan..Sebuah pneumothorax sekunder

yang terkait dengan penyakit yang mendasarinya, bahkan ketika kecil, jauh

lebih serius dan membawa kematian 15%. Sebuah pneumothorax sekunder

membutuhkan perawatan mendesak dan segera. Tingkat kekambuhan

untuk kedua pneumothorax primer dan sekunder adalah sekitar 40%,

kambuh paling banyak terjadi dalam waktu 1,5 sampai 2 tahun.2

24
 BAB 3

KESIMPULAN

Pneumothorax adalah kumpulan udara atau gas dalam rongga pleura dan

dada antara paru-paru dan dinding dada yang dapat mengganggu respirasi normal

karena adanya gelembung gas di rongga pleura atau retensi gas di ruang pleura.

Pneumothoraks dikategorikan sebagai kolaps spontan-pulmonal atau disebabkan

oleh trauma. Pneumotoraks spontan lebih lanjut diklasifikasikan menjadi

pneumotoraks primer dan pneumotoraks sekunder. Pneumotoraks primer

berkembang setelah pecahnya bula pada orang sehat tanpa penyakit paru yang

mendasari. Pneumotoraks sekunder disebabkan oleh ruptur jaringan pulmonal

yang rusak, dan terjadi terutama pada pasien yang didiagnosis dengan penyakit

paru.

Pada anamnesis dan pemeriksaan fisis didapatkan nyeri dada pleuritik

mendadak pada sisi yang sama dengan paru yang terkena, dyspnea, beberapa

gejala yang paling signifikan secara klinis yang mungkin berkembang termasuk

hipotensi, takikardia, sianosis, hipoksemia dengan atau tanpa hiperkapnia,

hipersonor saat perkusi dinding dada, suara napas tidak terdengar pada saat

auskultasi, pendorongan pada mediastinum dan trakea kearah kontra lateral dari

paru-paru yang kolaps.

Prognosis pneumothorax tergantung pada tingkat dan jenis pneumothorax.

Sebuah pneumothorax spontan kecil umumnya akan hilang dengan sendirinya

tanpa pengobatan..Sebuah pneumothorax sekunder yang terkait dengan penyakit

25
yang mendasarinya, bahkan ketika kecil, jauh lebih serius dan membawa kematian

15%. Sebuah pneumothorax sekunder membutuhkan perawatan mendesak dan

segera.

26
 DAFTAR PUSTAKA

1. Darmanto D. 2009 Respirologi (respiratory medicine). Jakarta: Penerbit

Buku Kedokteran EGC 172-183 p.

2. Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiati S 2006. Buku

Ajar Ilmu Penyakit Dalam. VI ed. Jakarta: Pusat penerbitan Departemen Ilmu

Penyakit Dalam FKUI. 1642-1651.

3. Choi W-I 2014. Pneumothorax. Tuberculosis and respiratory diseases, 76,

99-104.

4. Zarogoulidis P, Kioumis I, Pitsiou G, Porpodis K, Lampaki S,

Papaiwannou A, et al. 2014. Pneumothorax: from definition to diagnosis and

treatment. Journal of thoracic disease, 6, 372-375.

5. J Daley B. 2017. Pneumothorax [Online]. Available:

https://emedicine.medscape.com/article/424547-overview#a4 [Accessed 4 April

2018].

6. Slobodan M, Marko S, Bojan M 2015. Pneumothorax—Diagnosis And

Treatment. Sanamed, 10, 221-228.

7. Punarbawa IWA, Suarjaya PP Identifikasi Awal Dan Bantuan Hidup

Dasar Pada Pneumotoraks. 8-10.

8. Sharma A, Jindal P 2008. Principles of diagnosis and management of

traumatic pneumothorax. Journal of Emergencies, Trauma and Shock, 1, 37.

9. MacDuff A, Arnold A, Harvey J 2010. Management of spontaneous

pneumothorax: British Thoracic Society pleural disease guideline 2010. Thorax,

65, 18-31.

27
10. Herring W. 2015 Learning Radiology E-Book: Recognizing the Basics. 3

ed: Elsevier Health Sciences. 76-78 p.

11. Torigian DA, Ramchandani P. 2017 Radiology secrets plus. 4 ed.

Philadelphia: Elsevier. 184 p.

12. Husain LF, Hagopian L, Wayman D, Baker WE, Carmody KA 2012.

Sonographic diagnosis of pneumothorax. Journal of emergencies, trauma, and

shock, 5, 76-81.

13. Pasquier M, Hugli O, Carron P-N 2013. Needle aspiration of primary

spontaneous pneumothorax. N Engl J Med, 2013, 1-3.

28
BAGIAN RADIOLOGI REFARAT
FAKULTAS KEDOKTERAN
UNIVERSITAS MUSLIM INDONESIA

Pneumothorax

DISUSUN OLEH :
Nadrah Zuhriah Amri

PEMBIMBING SUPERVISOR :
dr. Evi S Gusnah, Sp. Rad., M. Kes

FAKULTAS KEDOKTERAN
UNIVERSITAS MUSLIM INDONESIA
MAKASSAR
2018
 BAB 1. ‘
PENDAHULUAN
Plaura
Parietal
Plaura
Rongga Pleura

Plaura Viceral

• Pneumothorax adalah keadaan ketika ditemukannya udara di

dalam rongga pleura.

Darmanto D. 2009 Respirologi (respiratory medicine). Jakarta: Penerbit Buku Kedokteran EGC 172-183 p.
 BAB II.
TINJAUAN PUSTAKA
Pneumothorax adalah kumpulan udara atau gas dalam
rongga pleura.

Spontan Traumatik

Primer (PSP) Sekunder (SSP) Iatrogenik Non-iatrogenik

Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiati S 2006. Buku Ajar Ilmu Penyakit Dalam. VI ed. Jakarta: Pusat
penerbitan Departemen Ilmu Penyakit Dalam FKUI. 1642-1551.

Choi W-I 2014. Pneumothorax. Tuberculosis and respiratory diseases, 76, 99-104.
 Patofisiologi

J Daley B. 2017. Pneumothorax [Online]. Available: https://emedicine.medscape.com/article/424547-overview#a4

[Accessed 4 April 2018].
 Klasifikasi

Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiati S 2006. Buku Ajar Ilmu Penyakit Dalam. VI ed. Jakarta: Pusat
penerbitan Departemen Ilmu Penyakit Dalam FKUI. 1642-1651.
 Diagnosis
Gejala Pemeriksaan Fisis

• Nyeri dada pleuritik • Hipersonor saat

• Dyspnea. perkusi dinding
• Hipotensi, dada
• Takikardia, • Suara napas tidak
terdengar pada saat
• Sianosis,
Auskultasi
• Hipoksemia dengan
• Distensi Vena
atau tanpa
Jugular
hiperkapnia
Slobodan M, Marko S, Bojan M 2015. Pneumothorax—Diagnosis And Treatment. Sanamed, 10, 221-228.
Punarbawa IWA, Suarjaya PP Identifikasi Awal Dan Bantuan Hidup Dasar Pada Pneumotoraks. 8-10.
 Radiologi X-Ray
Posisi Erect Posisi Supine
1.Tepi pleura viseral terlihat 1. Deep sulcus sign karena
sebagai garis putih yang penampilan sulkus
sangat tipis dan tajam
costovertebral yang sangat
2.Daerah perifer radiolusen
dan avaskuler dibanding dalam
daerah paru yang
berdekatan
3.Paru-paru dapat kolaps
sepenuhnya
4.Mediastinum seharusnya
tidak menjauh dari
pneumotoraks kecuali ada
tension pneumothoraks
tension
MacDuff A, Arnold A, Harvey J 2010. Management of spontaneous pneumothorax: British Thoracic Society pleural disease
guideline 2010. Thorax, 65, 18-31.
Herring W. 2015 Learning Radiology E-Book: Recognizing the Basics. 3 ed: Elsevier Health Sciences. 76-78 p.
 Gambaran Foto Thorax
Posisi Erect

Gambar 2.1. Garis Viceral Pleura (panah putih)

Normalnya pleura visceral dan parietal tidak terlihat.
Keduanya normalnya berdekatan dengan dinding
thorax. Ketika udara masuk ke rongga pleura, pleura
visceral beretraksi ke hilus bersamaan dengan paru
yang kolaps dan terlihat seperti garis tipis putih.
Tampak daerah perifer yang hiperlusen avaskuler (
panah merah)
Gambar 2.2. Tension Pneumothorax. Tampak
radiolusen paru-paru (L) dan hiperlusen
udara bebas (A) di perifer rongga pleura,
tambahan terdapat pergeseran mediastinum
ke kiri (panah hitam

Herring W. 2015 Learning Radiology E-Book: Recognizing Torigian DA, Ramchandani P. 2017 Radiology secrets plus. 4
the Basics. 3 ed: Elsevier Health Sciences. 76-78 p. ed. Philadelphia: Elsevier. 184 p.
 Posisi Supine

Gambar 2.3. Deep Sulcus Sign. Pada Posisi Supine, udara yang cukup
banyak pada pneumothorax dapat meduduki anterior dan inferior
dan bermanifestasi menggeser sulcus costophrenicus dan
meningkatkan lusensi dari sulcus (panah hitam). Bandingkan
dengan sulcus yang lain (panah putih)
Sharma A, Jindal P 2008. Principles of diagnosis and management of traumatic pneumothorax. Journal of Emergencies,
Trauma and Shock, 1, 37.
 USG
Pleura Sliding Thorax Normal
Gambar 2.6. M-mode yang
menggambarkan tanda ‘seashore.’
Garis pleura membagi gambar
menjadi dua: Bagian yang tidak
bergerak di atas garis pleura
menciptakan ‘gelombang’ horizontal,
dan garis geser di bawahnya
menciptakan pola granular, ‘pasir’
Pleura Sliding Pneumothorax
Gambar 2.8. M-mode dan tidak
adanya pleura sliding ditampilkan
sebagai 'stratosfer sign': Garis
horizontal paralel di atas dan di bawah
garis pleura, menyerupai 'barcode'.
Tanda ini menunjukkan adanya
pneumotoraks pada ruang intercostal
 Gambaran B-Line Thorax Normal Gambaran A-Line Pnemothorax

Gambar 2.7. 'B-lines' atau 'comet-tail Gambar 2.9. A-lines, adalah garis
artefact’ terlihat berasal dari garis horisontal, berjarak sama terlihat
pleura hyperechoic, memanjang berasal dari garis pleura hyperechoic
secara vertikal ke tepi layar. Gerakan putih terang. Jika ‘B-lines’ ditemukan,
‘B-lines’ mengikuti pleura sliding di mereka memanjang keluar dari garis
paru-paru normal pleura dan menghapus ‘A-lines’ di jalur
mereka

Husain LF, Hagopian L, Wayman D, Baker WE, Carmody KA 2012. Sonographic diagnosis of pneumothorax. Journal of
emergencies, trauma, and shock, 5, 76-81.
 Komplikasi

Hemopneumothorax Bronchopleural
Spontan fistula

Chronic
pneumothorax
(failure of the lung to
re-expand)
Slobodan M, Marko S, Bojan M 2015. Pneumothorax—Diagnosis And Treatment. Sanamed, 10, 221-228.
 Tatalaksana

MacDuff A, Arnold A, Harvey J 2010. Management of spontaneous pneumothorax: British Thoracic Society pleural disease
guideline 2010. Thorax, 65, 18-31.
Prognosis
Prognosis tergantung pada tingkat dan jenis pneumothorax
a) Pneumothorax spontan kecil umumnya akan hilang dengan
sendirinya tanpa pengobatan
b) Pneumothorax sekunder bahkan ketika kecil, jauh lebih
serius dan membawa kematian 15%
c) Tingkat kekambuhan untuk kedua pneumothorax primer
dan sekunder adalah sekitar 40%, kambuh paling banyak
terjadi dalam waktu 1,5 sampai 2 tahun

Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiati S 2006. Buku Ajar Ilmu Penyakit Dalam. VI ed. Jakarta:
Pusat penerbitan Departemen Ilmu Penyakit Dalam FKUI. 1642-1651.
TERIMA KASIH
 http://dx.doi.org/10.4046/trd.2014.76.3.99
REVIEW ISSN: 1738-3536(Print)/2005-6184(Online) • Tuberc Respir Dis 2014;76:99-104

Pneumothorax

Won-Il Choi, M.D., Ph.D.

Department of Internal Medicine, Keimyung University School of Medicine, Daegu, Korea

Pneumothorax—either spontaneous or iatrogenic—is commonly encountered in pulmonary medicine. While secondary

pneumothorax is caused by an underlying pulmonary disease, the spontaneous type occurs in healthy individuals
without obvious cause. The British Thoracic Society (BTS, 2010) and the American College of Chest Physicians (ACCP,
2001) published the guidelines for pneumothorax management. This review compares the diagnostic and management
recommendations between the two societies. Patients diagnosed with primary spontaneous pneumothorax (PSP) may
be observed without intervention if the pneumothorax is small and there are no symptoms. Oxygen therapy is only
discussed in the BTS guidelines. If intervention is needed, BTS recommends a simple aspiration in all spontaneous and
some secondary pneumothorax cases, whereas ACCP suggests a chest tube insertion rather than a simple aspiration.
BTS and ACCP both recommend surgery for patients with a recurrent pneumothorax and persistent air leak. For patients
who decline surgery or are poor surgical candidates, pleurodesis is an alternative recommended by both BTS and
ACCP guidelines. Treatment strategies of iatrogenic pneumothorax are very similar to PSP. However, recurrence is not a
consideration in iatrogenic pneumothorax.

Keywords: Pneumothorax; Pneumothorax, Primary Spontaneous; Plmonary Bullae Causing Pneumothorax

Introduction mary pneumothorax and secondary pneumothorax. Primary

A pneumothorax is characterized by dyspnea and chest
pain originating from the lung and chest wall and may in-
terfere with normal respiration owing to the presence of gas
bubbles in the pleural cavity or gas retention in the pleural
space that occur following bullae ruptures. Pneumothorax is
categorized as either spontaneous-pulmonary collapse with-
out any cause-or induced by trauma.
Spontaneous pneumothorax is further classified into pri-
Address for correspondence: Won-Il Choi, M.D., Ph.D.
Department of Internal Medicine, Keimyung University School of
Medicine, 56 Dalseong-ro, Jung-gu, Daegu 700-712, Korea
Phone: 82-53-250-7572, Fax: 82-53-250-7434
E-mail: wichoi@dsmc.or.kr
Received: Jan. 16, 2014
Revised: Jan. 23, 2014
Accepted: Feb. 3, 2014
cc It is identical to the Creative Commons Attribution Non-Commercial
License (http://creativecommons.org/licenses/by-nc/3.0/).
Copyright © 2014
The Korean Academy of Tuberculosis and Respiratory Diseases.
All rights reserved.
pneumothorax develops following bullae ruptures in healthy
people with no underlying pulmonary disease. Secondary
pneumothorax is caused by rupture of damaged pulmonary
tissue, and occurs primarily in patients diagnosed with pul-
monary disease, such as pulmonary emphysema.
Pathophysiology of Pneumothorax
In a healthy person, the pleural pressure remains negative
relative to atmospheric pressure throughout the entire respi-
ratory cycle. This pressure difference between pulmonary
alveoli and the pleural cavity is called the transpulmonary
pressure, and this pressure causes elastic recoil of lung. In
pneumothorax, the pulmonary alveoli or airway becomes
connected to pleural cavity, and air migrates from the alveoli
to the pleural cavity until the pressures of both areas are in
equilibrium. Similarly, when the chest wall and the pleural
cavity are connected, air moves into the pleural cavity from the
environment until the pressure difference is no longer present
or until the connection is closed. When the air present within
the pleural cavity is sufficient to increase the pleural pressure
from −5 cm H2O to −2.5 cm H2O, the transpulmonary pressure
reduces from 5 cm H2O, to 2.5 cm H2O, and the pulmonary

99

vital capacity decreases by 33%. Space for the influx of pleural
cavity air is created by compressing the lung, which decreases
the vital capacity by 25%. In addition, the intra-pleural cavity
pressure change increases the thoracic volume, resulting in an
alteration of the thoracic wall recoil and an approximately 8%
decline in vital capacity. When the pressure of pleural cavity
increases, the mediastinum moves in the opposite direction,
expanding the thorax of the same side, and depressing the
diaphragm. These changes are observed in tension pneumo-
thorax as well as other types of pneumothorax.
The main physiological change in pneumothorax is a re-
duction of arterial oxygen tension in addition to the reduced
vital capacity. Patients experiencing primary pneumothorax
endure the vital capacity reduction relatively well, but in pa-
tients suffering from secondary pneumothorax and underly-
ing pulmonary disease, the vital capacity reduction can led
to alveolar hypoventilation and respiratory failure. In a study
evaluating 12 patients diagnosed with spontaneous pneumo-
thorax, 9 patients (75%) had a PO2≤80 mm Hg, and 2 patients,
who were both diagnosed with secondary pneumothorax,
had a PO2≤55 mm Hg1.
Reduced oxygen tension may be caused by an anatomic
shunt and, in some cases, alveolar hypoventilation in the
pneumothorax area created from the reduced ventilation−
perfusion ratio in the pulmonary alveoli. In the aforemen-
tioned 12 patient study, right-to-left vascular shunting oc-
curred at a ratio higher than the 10% mean found in normal
patients1. When the pneumothorax encompasses <25% of a
lateral thorax, vascular shunts do not increase. However, when
the pneumothorax increased beyond this size, the shunts also
increased in size.
Generally, once the air retained in the pleural cavity is re-
moved, oxygen saturation increases within a few hours. For
example, in a patient suffering from pneumothorax and a
shunt ≥20%, the shunt decreased to ≤10% within 90 minutes of
evacuating the intra-pleural air, though about 5% of the shunt
still remained1. The slow recovery rate of the shunt was likely
associated with the duration of the pneumothorax.
Causes and Risk Factors
Primary spontaneous pneumothorax (PSP) commonly oc-
curs in tall, thin males aged 10−30 years; a substantial propor-
tion of affected patients have a history of smoking. Smoking is
closely related to the PSP. For example, 91% of patients diag-
nosed with PSP are current or past smokers, and as smoking
increases, the risk of pneumothorax also increases2. Smoking-
associated bronchiolitis likely accounts for the occurrence of
pneumothorax in smokers.
Most PSP cases result from spontaneous rupture of a sub-
pleural bleb or bulla, which leaks air into the pleural cavity. A
pulmonary bleb or bulla is a small air sac formed between the
100
WI Choi
lung tissues and pleura, originating from a pulmonary alveoli
enlargement (diameter 1−2 cm) and usually developing at an
apical area3.
There are two purposed mechanisms for bleb or bulla for-
mation. One mechanism is congenital; the upper pulmonary
lobe grows more quickly than the vasculature, causing a lack
of blood supply and development of a bullae. The second
mechanism is related to the pleural cavity pressure, which be-
comes more negative at the apical region of the lungs. In a tall
individual, the negative pleural cavity pressure is increased at
the upper pulmonary lobe, and the alveolar pressure similarly
increases. This increase can cause the formation of numerous
bullae and pneumothoraxes.
Rarely, PSP occurs in persons with specific inherited genes.
Responsible genes have an autosomal dominant inheritance
with a variety of penetrations. Genetic risk factors include
the HLA haplotype A2B40, alpha-1 antitrypsin phenotypes
M1M2, and FBN1 genetic mutation.
Even in patients that have underlying pulmonary diseases
such as asthma or pneumonia, pulmonary abscess, and per-
tussis, PSP may occur; it can even occur in patients diagnosed
with Marfan syndrome or lung cancer.
Secondary spontaneous pneumothorax (SSP), unlike PSP,
develops in patients diagnosed with a pulmonary disorder.
The most common associated etiology is chronic obstructive
pulmonary disease (COPD), also known as chronic bronchitis
or pulmonary emphysema. Multiple bullae can develop in af-
fected patients accompanied by pneumothorax.
1. Clinical manifestations of spontaneous pneumothorax
Ninety-five percent of affected patients complain of acute
and sudden thoracic pain (chest pain) accompanied by short-
ness of breath. This pain may be more severe at inhalation and
localized to the site that the pneumothorax developed. The se-
verity of symptoms such as dyspnea is proportional to the size
of pneumothorax, but 5% of patients may be asymptomatic;
such patients usually have an overall poor systemic condition.
Spontaneous pneumothorax usually occurs at rest, and only
10% of cases occur during exercise4. In patients suffering PSP,
the pain and dyspnea usually resolve within 24 hours, but pa-
tients experiencing SSP usually have more severe symptoms.
When the pleural cavity gas caused by the PSP occupies less
than 25% of the entire pleural cavity, hypoxemia does not de-
velop easily. However, in patients diagnosed with pulmonary
emphysema, even a small amount of intra-pleural cavity gas
can cause serious hypoxemia and hypercapnia.
2. Evaluation of spontaneous pneumothorax
The guidelines published by the American College of Chest
Physicians (ACCP) define a small pneumothorax as a de-
crease in apical length of less than 3 cm5. However, the British
Tuberc Respir Dis 2014;76:99-104 www.e-trd.org
Pneumothorax
Thoracic Society (BTS) designates a marginal depth mea-
sured from the chest wall to the outer pulmonary edge of less
than 2 cm as a small pneumothorax, while a marginal depth
of ≥2 cm is considered a large pneumothorax6,7. The ACCP
guidelines only consider a pneumothorax at the pulmonary
apex for evaluation, and therefore the method can be inad-
equate in assessing the pneumothorax volume. On the con-
trary, the BTS guidelines are a bit more objective in assessing
the pneumothorax volume. Under ACCP guidelines, a patient
is considered clinically stable when able to maintain a respi-
ratory rate of less than 24 breaths/min, a pulse rate between
60−120 beats/min, a normal blood pressure, SPO2 ≥90% on
room air, and is able to speak an entire sentence5. BTS guide-
lines consider a patient clinically stable state when there is no
respiratory disturbance6,7.
Thoracic computed tomography (CT) is effective at identi-
fying the cause of spontaneous pneumothorax, but the ACCP
does not recommend CT as the basic imaging modality,
whereas BTS does emphasize the technique’s importance in
measuring the pneumothorax volume and differentiating di-
agnoses8,9.
3. Treatment of spontaneous pneumothorax
There are three different treatment strategies in addition to
supplying the patient with oxygen, observation, aspiration, or
chest tube placement. Although both ACCP and BTS guide-
lines discuss detailed treatment guidelines for pneumothorax,
they differ in determination of pneumothorax severity and the
importance of aspiration.
1) Oxygen therapy: Gas within the pleural cavity is ab-
sorbed by diffusion and can be facilitated by changing the
composition of the intra-pleural cavity gas. Oxygen is ab-
sorbed 62 times faster than nitrogen, and carbon dioxide (CO2)
is absorbed 23 times faster than oxygen. When the patient
inhales 100% oxygen, nitrogen will disappear from the pleural
cavity, leaving only oxygen, which is absorbed faster from the
pleural cavity into veins.
The absorption rate of intra-pleural cavity gas is approxi-
mately 1.25% per day in ambient air10; a pneumothorax occu-
pying 25% of the cavity will require 20 days to be completely
absorbed. By contrast, when the patient receives oxygen sup-
plementation, the absorption rate accelerates 3−4 times; this
effect is particularly prominent when a large volume of gas oc-
cupies the pleural cavity11,12. BTS guidelines recommend the
use of high-flow oxygen (10 L/min) in symptomatic patients.
However, caution must be exercised to avoid hypercarbia in
patients with COPD7.
2) Observation: Observation can be performed in both
PSP and SSP cases. Because PSP has a low mortality rate,
stable patients can be carefully observed while the gas is ab-
sorbed passively from the pleural cavity. Both the ACCP and
www.e-trd.org http://dx.doi.org/10.4046/trd.2014.76.3.99
BTS recommend observation only of clinically stable patients
diagnosed with a small volume pneumothorax. According
to ACCP guidelines, clinically stable patients should be ob-
served for 3−6 hours and can be discharged home if a repeat
chest radiograph excludes progression of the pneumothorax,
which indicates that the causal lesion has closed. However,
for patients residing far from a hospital or health care center,
admission for observation is best. Even if the patient is not
admitted, the patient should be provided with careful instruc-
tions for follow-up examination within 2 days, depending on
the circumstances. For patients diagnosed with a SSP, both the
ACCP and BTS recommend hospitalizing patients for treat-
ment, even if the pneumothorax is small.
3) Simple aspiration: Aspiration of a pneumothorax is
performed using a small catheter. The catheter is inserted
into the pleural cavity and either removed immediately after
evacuating the air from the pleural cavity or left inserted while
the patient if observed. When left inserted in the thoracic wall,
the catheter is still considered a chest tube despite its small
size. In patients diagnosed with spontaneous pneumothorax,
the mean success rate of aspiration is between 53% and 58%.
Specifically, the mean success rate for PSP is 75%, which is
comparatively higher than the SSP mean success rate of ap-
proximately 37%13.
(1) Primary spontaneous pneumothorax: ACCP recom-
mends the use of simple aspiration in clinically stable patients
diagnosed with PSP whose conditions worsen under observa-
tion. However, BTS recommends the use of simple aspiration
in all patients diagnosed with PSP who need intervention. The
BTS guidelines were established based on a study conducted
by Noppen et al.14. The study compared clinical outcomes in
patients diagnosed with PSP who received aspiration with a
16G IV catheter and chest tube insertion (16F or 20F); there
was no difference in therapeutic effectiveness between the
two techniques, but the hospitalization duration was reduced
in patients receiving simple aspiration. It is worth noting that
the sample size was very small and the treatment protocols of
the two groups were quite different, and therefore, it is difficult
to conclude that there is no difference between two treatment
methods. The BTS guidelines do consider these limitations
and recommends performing simple aspiration only at facili-
ties possessing practical experience in the procedure and rel-
evant equipment6. Further study is required on the therapeu-
tic effectiveness of the simple aspiration and small diameter
chest tube placement.
(2) Secondary spontaneous pneumothorax: While the
ACCP recommends simple aspiration in patients diagnosed
with SSP in a very limited manner, BTS recommends the pro-
cedure for treating small pneumothorax with mild respiratory
symptoms in patients less than 50 years old. The simple aspi-
ration is quite low in the SSP13, in particular, the failure rate is
high in patients ≥50 years old6. After performing simple aspira-
tion, the patient should be hospitalized for observation during
101

recovery.
4) Chest tube placement
(1) Primary spontaneous pneumothorax: ACCP rec-
ommends the placement of a chest tube in a case of large
pneumothorax, regardless of whether the patient is clinically
stable or unstable, and that in most instances, patients with a
large pneumothorax should be hospitalized. In comparison,
BTS recommends placement of a chest tube when the simple
aspiration procedure fails to resolve the pneumothorax.
(2) Secondary spontaneous pneumothorax: ACCP rec-
ommends either observation or chest tube placement in clini-
cally stable patients diagnosed with a small SSP. In a clinically
stable patient diagnosed with a large pneumothorax or a clini-
cally unstable patient, AACP recommends chest tube place-
ment. BTS also recommends chest tube placement, except in
patients diagnosed with a very small pneumothorax (1−2 cm)
and no respiratory symptoms.
5) Chest tube management
(1) Thickness of chest tube: Both ACCP and BTS recom-
mend physicians avoid placing a thick chest tube in both pri-
mary and SSP. The ACCP does recommend inserting a thick
chest tube (24 to 28F) in a patient experiencing a large-scale
air leak, such as a bronchopleural fistula, or receiving me-
chanical ventilation. In the stable patient diagnosed with PSP,
ACCP recommends a chest tube thickness of 14 to 22F or less.
BTS always recommends using a 14F chest tube, as there is
no evidence that a thick chest tube (20−24F) is more clinically
effective than a thin chest tube (10−14F)7.
(2) Suction of the chest tube: The efficacy of suction after
the placement of chest tube is not well verified; one study re-
ported that suction was not an effective treatment in patients
diagnosed with the primary or the SSP15. In another study in-
vestigating pneumothorax treatment in 71 patients, the lungs
re-expanded and the air leaks dissipated without the clinicians
performing any suction through the chest tube in 77% of the
patients treated16. Similarly, in another report, chest tube suc-
tion did not affect the severity of lung collapse17. ACCP recom-
mends suction only when the lung fails to re-expand following
chest tube placement and observation. BTS does not recom-
mend suction because of the risk pulmonary edema induced
by re-expansion. Alternatively, Suction may be applied if the
air leak lasts ≥ 48 hours or there is no pulmonary re-expansion
after chest tube placement. The BTS also recommends per-
forming suction at a higher velocity and lower pressure (−10
to −20 cm H2O)7.
(3) Chest tube removal: Chest tubes should be removed
only when a chest radiograph demonstrates re-expansion of
lung, complete resolution of the pneumothorax, and no clini-
cal evidence of an ongoing air leak18. ACCP and BTS provide
similar guidelines for the timing of chest tube removal. ACCP
recommends that any suction in progress be suspended
prior to chest tube removal. However, the two organizations
have different recommendations on clamping the chest tube
102
WI Choi
closed before its removal. ACCP has a 47% consensus for us-
ing clamping in PSP and a 59% of consensus in SSP. Those
who support clamping express concern for a potential small
air leak and feel that clamping may be useful in locating a leak.
BTS does not recommend clamping when there is no air leak
visible. However, it recommends additional precautions in
observing the patient if clamping is performed6.
6) Definition of persistent air leaks: Intervention to elim-
inate the leak is generally recommended if the air leak persists
for 2 days up to 14 days19-21. ACCP recommends intervention
for air leaks persisting beyond 4 days in PSP cases and over 5
days in SSP cases. BTS recommends thoracic surgery if the air
leaks persist beyond 2 days or if the lung does not re-expand.
If air leaks caused by spontaneous pneumothorax are allowed
to persist, the cost of treatment increases, and the therapeutic
success rate of thoracoscopy decreases22.
7) Interventional procedure for prevention of recur-
rence and air leaks
(1) Surgery: ACCP and BTC recommend surgical inter-
vention to prevent recurrence or to stop persistent air leaks.
Although the advantage of surgical treatment is not clearly
identified yet, ACCP recommends either parietal pleurectomy
and bullectomy, or parietal pleural abrasion of one pleural up-
per half and bullectomy. BTS recommends several possible
interventions including parietal pleurectomy in addition to
parietal pleural abrasion and talc-utilized pleurodesis.
(2) Pleurodesis and Heimlich valve: ACCP recommends
performing pleurodesis, using medications such as talc and
doxycycline administered through the chest tube, in cases of
primary and SSP if the patient declines surgical intervention
or is not a suitable surgical candidate. Similarly, BTS recom-
mends pleurodesis for patients that are not suitable surgical
candidates. Appropriately sized talc may actually reduce the
risk of respiratory failure23. In patients diagnosed with SSP
who cannot undergo surgery, outpatient treatment with a
Heimlich valve may be considered.
(3) Timing of intervention for recurrence prevention of
spontaneous pneumothorax: Excluding persistent air leaks,
85% of ACCP panel members recommend surgical interven-
tion for the second recurrence of PSP, whereas 81% supported
surgical intervention at the first recurrence in cases of SSP. BTS
recommends surgical treatment when the pneumothorax at
the second occurrence on the same side, the first recurrence
on the opposite site, and in cases of bilateral pneumothorax.
Iatrogenic Pneumothorax
Iatrogenic pneumothorax is increasing owing to the in-
crease in invasive diagnostic and treatment methods. The
most common causes of iatrogenic pneumothorax are trans-
thoracic needle aspiration, subclavian vein catheterization,
thoracentesis, transbronchial lung biopsy, pleural biopsy,
Tuberc Respir Dis 2014;76:99-104 www.e-trd.org
Pneumothorax
and mechanical ventilation. Pneumothorax should always be
suspected if the cardiopulmonary function becomes unstable
after these procedures. In some cases, the pneumothorax can
occur immediately after the procedure, but clinicians should
remember that it also could occur several days later. The
clinical profile of iatrogenic pneumothorax is affected by any
underlying diseases and health conditions of patient, as well
as the pneumothorax etiology. A patient in poor general con-
dition may experience severe symptoms even from a small
volume pneumothorax. In addition, when performing positive
pressure ventilation, the pneumothorax volume can increase
more quickly and a tension pneumothorax may result. Trans-
thoracic needle aspiration increases the risk of pneumothorax
when performed on a small lesion located deep in the lung or
when emphysema is present at the biopsy location.
Unlike spontaneous pneumothorax, there is no concern
about recurrence of iatrogenic pneumothorax. Non-invasive
treatment is recommended, depending on the clinical profile
or underlying disease of the patient. Treatment many include
observation, as well as simple aspiration or the chest tube
placement using a small catheter. If the condition occurs in a
patient diagnosed with large volume pneumothorax or COPD,
or during mechanical ventilation, chest tube placement is the
preferred treatment.
Pneumothorax in Specific Form:
Tension Pneumothorax
In tension pneumothorax, air flows into the pleural cavity
during inhalation but is retained in the pleural cavity during
exhalation and thus cannot exit, leading to a gradual increase
in intra-pleural cavity pressure. Tension pneumothorax can
develop from either a spontaneous pneumothorax or trau-
matic pneumothorax. During tension pneumothorax, the
affected lung ipsilateral to the pneumothorax completely col-
lapses, and the contralateral lung and heart are pressurized.
The result is severe dyspnea, cyanosis, and hypotension, lead-
ing to death. Thus, tension pneumothorax should be treated
with immediate needle decompression.
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8. Engdahl O, Toft T, Boe J. Chest radiograph: a poor method for
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its treatment. J Am Med Assoc 1954;155:24-9.
11. Chadha TS, Cohn MA. Noninvasive treatment of pneumotho-
rax with oxygen inhalation. Respiration 1983;44:147-52.
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mothorax: a more aggressive approach? Chest 1997;112:789-
804.
14. Noppen M, Alexander P, Driesen P, Slabbynck H, Verstraeten
A. Manual aspiration versus chest tube drainage in first epi-
sodes of primary spontaneous pneumothorax: a multicenter,
prospective, randomized pilot study. Am J Respir Crit Care
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15. So SY, Yu DY. Catheter drainage of spontaneous pneumo-
thorax: suction or no suction, early or late removal? Thorax
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16. Minami H, Saka H, Senda K, Horio Y, Iwahara T, Nomura F, et
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17. Sharma TN, Agnihotri SP, Jain NK, Madan A, Deopura G.
Intercostal tube thoracostomy in pneumothorax: factors in-
fluencing re-expansion of lung. Indian J Chest Dis Allied Sci
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18. Baumann MH. Pneumothorax. Semin Respir Crit Care Med
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Tuberc Respir Dis 2014;76:99-104 www.e-trd.org
 Review Article

Pneumothorax: from definition to diagnosis and treatment

Paul Zarogoulidis1, Ioannis Kioumis1, Georgia Pitsiou1, Konstantinos Porpodis1, Sofia Lampaki1,
Antonis Papaiwannou1, Nikolaos Katsikogiannis2, Bojan Zaric3, Perin Branislav3, Nevena Secen3,
Georgios Dryllis4, Nikolaos Machairiotis5, Aggeliki Rapti6, Konstantinos Zarogoulidis1
1
Pulmonary Department, “G. Papanikolaou” General Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece; 2Surgery Department,
University General Hospital of Alexandroupolis, Democritus University of Thrace, Alexandroupolis, Greece; 3Institute for Pulmonary Diseases
of Vojvodina, Clinic for Thoracic Oncology, Faculty of Medicine, University of Novi Sad, Novi Sad, Serbia; 4Hematology Department, “Laiko”
University General Hospital, Athens, Greece; 5Obstetric-Gynecology Department, “Thriassio” General Hospital of Athens, Athens, Greece;
6
Pulmonary Department, “Sotiria” Hospital for Chest Diseases, Athens, Greece
Correspondence to: Paul Zarogoulidis, MD, PhD. Pulmonary Department, “G. Papanikolaou” General Hospital, Aristotle University of Thessaloniki,
Thessaloniki, Greece. Email: pzarog@hotmail.com.

Abstract: Pneumothorax is an urgent situation that has to be treated immediately upon diagnosis.
Pneumothorax is divided to primary and secondary. A primary pneumothorax is considered the one that
occurs without an apparent cause and in the absence of significant lung disease. On the other hand secondary
pneumothorax occurs in the presence of existing lung pathology. There is the case where an amount of air
in the chest increases markedly and a one-way valve is formed leading to a tension pneumothorax. Unless
reversed by effective treatment, this situation can progress and cause death. Pneumothorax can be caused
by physical trauma to the chest or as a complication of medical or surgical intervention (biopsy). Symptoms
typically include chest pain and shortness of breath. Diagnosis of a pneumothorax requires a chest X-ray or
computed tomography (CT) scan. Small spontaneous pneumothoraces typically resolve without treatment
and require only monitoring. In our current special issue we will present the definition, diagnosis and
treatment of pneumothorax from different experts in the field, different countries and present different
methods of treatment.

Keywords: Pneumothorax; medical thoracoscopy; spontaneous; secondary

Submitted Sep 09, 2014. Accepted for publication Sep 10, 2014.
doi: 10.3978/j.issn.2072-1439.2014.09.24
View this article at: http://dx.doi.org/10.3978/j.issn.2072-1439.2014.09.24

Primary spontaneous
Spontaneous pneumothoraces are divided into two types:
primary, which occurs in the absence of known lung disease,
and secondary, which occurs in someone with underlying
lung disease. Until now the cause of primary spontaneous
pneumothorax (PSP) has not been identified, however;
several risk factors have been identified such as; smoking,
male sex, and a family history of pneumothorax. Several
underlying mechanisms have been observed and are
discussed below. Moreover; a PSP tends to occur in a young
adult without underlying lung problems. Symptoms such
as, chest pain and sometimes mild breathlessness are usually
observed. There are several cases where a PSP is a threat for
a patient’s life, however; several patients may wait several
days before seeking medical attention. It has been observed
that it is rare for PSPs to cause tension pneumothoraces.
Secondary spontaneous
Secondary spontaneous pneumothorax occurs due to
underlying chest diseases. Most commonly they are
observed in patients with chronic obstructive pulmonary
disease (COPD), which accounts for approximately 70%
of cases. Other known lung diseases that may increase the
incidence for pneumothorax are; tuberculosis, necrotizing

© Pioneer Bioscience Publishing Company. All rights reserved. www.jthoracdis.com J Thorac Dis 2014;6(S4):S372-S376
Journal of Thoracic Disease, Vol 6, Suppl 4 October 2014
pneumonia, pneumonocystis carini, lung cancer, sarcoma
involving the lung, sarcoidosis, endometriosis, cystic
fibrosis, acute severe asthma, idiopathic pulmonary fibrosis,
Rheumatoid arthritis, ankylosing spondylitis, polymyositis
and dermatomyositis, systemic sclerosis, Marfan’s syndrome
and Ehlers-Danlos syndrome, histiocytosis X and
lymphangioleiomyomatosis (LAM). Secondary spontaneous
pneumothoraces (SSPs), by definition, occurs in individuals
with significant underlying lung disease. The following
symptoms are usually observed; hypoxemia and hypercapnia
in more severe cases. The sudden onset of breathlessness
in patients with known underlying lung diseases such as;
COPD, cystic fibrosis, or other serious lung diseases should
therefore prompt investigations to identify the possibility of
a pneumothorax.
Traumatic pneumothorax
Traumatic pneumothorax occurs when the chest wall
is pierced, such as when a stab wound or gunshot
wound allows air to enter the pleural space. Traumatic
pneumothoraces have been found to occur in up to
half of all cases of chest trauma, with only rib fractures
being more common in this group. The pneumothorax
can be occult in half of these cases, but may enlarge—
particularly if mechanical ventilation is required. This type
of pneumothorax has also been observed to patients already
receiving mechanical ventilation for some other reason.
Mechanism
The thoracic cavity contains the lungs, heart, and
numerous major blood vessels. On each side of the cavity,
a pleural membrane covers the surface of lung (visceral
pleura) and also lines the inside of the chest wall (parietal
pleura). Between the two layers there is a small amount of
lubricating serous fluid. The lungs are fully inflated within
the cavity because the pressure inside the airways is higher
than the pressure inside the pleural space. Pneumothorax
can only develop if air is allowed to enter, through damage
to the chest wall or damage to the lung itself, or occasionally
because microorganisms in the pleural space produce gas.
Treatment
The treatment of pneumothorax depends on a number of
factors, and may vary from discharge with early follow-up
to immediate needle decompression or insertion of a chest
© Pioneer Bioscience Publishing Company. All rights reserved.
S373
tube. Treatment also depends on the physician that is going
to handle the patient; pulmonary physicians usually perform
medical thoracoscopy (minimally invasive) one port, while
thoracic surgeons use a surgery suite and two ports. In some
cases patient preference is requested.
In traumatic pneumothorax, chest tubes are usually
inserted and these patients are handled by thoracic surgeons
as other chest organs might be affected. If mechanical
ventilation is required, the risk of tension pneumothorax
is greatly increased and the insertion of a chest tube is
mandatory. Any open chest wound should be covered with
an airtight seal, as it carries a high risk of leading to tension
pneumothorax.
Tension pneumothorax is usually treated with urgent
needle decompression. There are several cases where
“silent lung” is observed and needle decompression may
be required before transport to the hospital upon the site
of the accident, and can be performed by an emergency
medical technician or other trained professional. The
needle or cannula is left in place until a chest tube can be
inserted. If tension pneumothorax leads to cardiac arrest,
needle decompression is performed as part of resuscitation
as it may restore cardiac output.
Conservative
Small spontaneous pneumothoraces do not always require
treatment, as they are unlikely to proceed to respiratory
failure or tension pneumothorax, and generally resolve
spontaneously. A case by case evaluation is needed and
careful follow up of these patients. This approach is most
appropriate if the estimated size of the pneumothorax is
small (defined as <50% of the volume of the hemithorax),
there is no breathlessness, and there is no underlying lung
disease. A 24-hour observation is optional for these patients
or clear instructions are given to return to hospital if there
are worsening symptoms. Follow up as outpatients require
repeated X-rays to confirm improvement. Secondary
pneumothoraces are only treated conservatively if the size
is very small (1 cm or less air rim) and there are limited
symptoms. Oxygen given at a high flow rate may accelerate
resorption as much as fourfold.
Aspiration
In view of a large PSP (>50%), or in a PSP associated
with breathlessness, guidelines recommend that reducing
the size by aspiration is equally effective as the insertion
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S374
of a chest tube. In order to perform this procedure
administration of local anesthetic is necessary and inserting
a needle connected to a three-way tap; up to 2.5 liters of
air (in adults). Upon follow up if there has been significant
reduction in the size of the pneumothorax on subsequent
X-ray, the remainder of the treatment can be conservative.
It has been observed that when compared to tube drainage,
first-line aspiration in PSP reduces the number of people
requiring hospital admission significantly, without
increasing the risk of complications. The same technique
could be also considered in secondary pneumothorax of
moderate size (air rim 1-2 cm) without breathlessness,
however; ongoing observation in hospital is required even
after a successful procedure.
Chest tube
A chest tube (or intercostal drain) is the most definitive
initial treatment of a pneumothorax. Chest tube is typically
inserted in an area under the axilla (armpit) called the
“safe triangle”, where damage to internal organs can be
avoided. Local anesthetic is applied. Usually there are two
types of tubes used. In spontaneous pneumothorax, small-
bore (smaller than 14 F, 4.7 mm diameter) tubes may be
inserted by the Seldinger technique. Larger tubes do not
have an advantage. It has been observed that for traumatic
pneumothorax, larger tubes (28 F, 9.3 mm) are used.
Chest tubes are required in PSPs that have not responded
to needle aspiration, in large SSPs (>50%), and in cases of
tension pneumothorax. The method indicates that they
are connected to a one-way valve system that allows air
to escape, but not to re-enter, the chest. Several times it
includes a bottle with water that functions like a water
seal, or a Heimlich valve. Moreover; they are not usually
connected to a negative pressure circuit, due to the fact that
this would result in rapid re-expansion of the lung and a
risk of pulmonary edema. The tube is left in place until no
air is seen to escape from it for a period of time (no more
than 2 days), and X-rays confirm re-expansion of the lung.
If after 2-4 days there is still evidence of an air leak, various
options are available. If air leak persists then, surgery may
be required, especially in SSP.
Chest tubes are also used as first-line treatment when
pneumothorax occurs in people with AIDS, usually due to
underlying pneumocystis pneumonia (PCP), due to the fact
that this condition is associated with prolonged air leakage.
Furthermore, when bilateral pneumothorax occurs common
in people with PCP, surgery is often required.
© Pioneer Bioscience Publishing Company. All rights reserved.
Zarogoulidis et al. Pneumothorax: an up-to-date presentation
Pleurodesis and surgery
Pleurodesis is considered the final solution it is a procedure
that permanently obliterates the pleural space and attaches
the lung to the chest wall. The surgical thoracotomy with
identification of any source of air leakage and stapling of
blebs—followed by pleurectomy of the outer pleural layer
and pleural abrasion of the inner layer is considered most
effective. During the healing process, the lung adheres to
the chest wall, effectively obliterating the pleural space.
Recurrence rates are approximately 1%. Post-thoracotomy
pain is usually observed.
A less invasive approach is thoracoscopy, usually in the
form of a procedure called video-assisted thoracoscopic
surgery (VATS). The results of VATS are considered less
effective than thoracotomy, however; smaller scars in the
skin. VATS offers a shorter in-hospital stays, less need
for postoperative pain control, and a reduced risk of lung
problems after surgery. VATS may also be used to achieve
chemical pleurodesis; this involves insufflation of talc.
Insufflation of talc induces an inflammation of the pleura
surfaces. If a chest tube is already in place, various agents
may be instilled through the tube to achieve chemical
pleurodesis, such as talc, tetracycline, minocycline or
doxycycline. Results of chemical pleurodesis tend to be
worse than when using surgical approaches, talc pleurodesis
has been found to have the best results.
Aftercare
If pneumothorax occurs in a smoker, it may be advisable
for someone to remain off work for up to a week after a
spontaneous pneumothorax (1-10). For those who have
undergone pleurodesis it may take up to two to three weeks
off work to recover. Air travel is discouraged for up to
seven days after complete resolution of a pneumothorax if
recurrence does not occur. Underwater diving is considered
unsafe after an episode of pneumothorax unless a preventative
procedure has been performed (11-20). Currently
professional guidelines suggest that pleurectomy should be
performed on both lungs and that lung function tests and CT
scan normalize before diving is resumed. Aircraft pilots may
also require assessment for surgery (12,21-28).
Summary
In conclusion, treatment depends on the training of the
pulmonary physician who handles such a patient, if the
www.jthoracdis.com J Thorac Dis 2014;6(S4):S372-S376
Journal of Thoracic Disease, Vol 6, Suppl 4 October 2014
medical thoracoscopy can be applied then it could be
the first option. In the case where medical thoracoscopy
is available or medical thoracoscopy has not provided
previously a solution for a patient then a thoracic surgeon
or an experienced general surgeon should take over to
provide a solution for the patient.
Acknowledgements
Disclosure: The authors declare no conflict of interest.
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14. Papaioannou M, Pitsiou G, Manika K, et al. COPD
Assessment Test: A Simple Tool to Evaluate Disease Severity
and Response to Treatment. COPD 2014;11:489-95.
15. Boskovic T, Stanic J, Pena-Karan S, et al. Pneumothorax
after transthoracic needle biopsy of lung lesions under CT
guidance. J Thorac Dis 2014;6 Suppl 1:S99-107.
16. Papaiwannou A, Zarogoulidis P, Porpodis K, et al. Asthma-
chronic obstructive pulmonary disease overlap syndrome
(ACOS): current literature review. J Thorac Dis 2014;6
Suppl 1:S146-51.
17. Zarogoulidis P, Porpodis K, Kioumis I, et al.
Experimentation with inhaled bronchodilators and
corticosteroids. Int J Pharm 2014;461:411-8.
18. Bai C, Huang H, Yao X, et al. Application of flexible
bronchoscopy in inhalation lung injury. Diagn Pathol
2013;8:174.
19. Zarogoulidis P, Kioumis I, Porpodis K, et al. Clinical
experimentation with aerosol antibiotics: current and
future methods of administration. Drug Des Devel Ther
2013;7:1115-34.
20. Zarogoulidis P, Pataka A, Terzi E, et al. Intensive care unit
and lung cancer: when should we intubate? J Thorac Dis
2013;5 Suppl 4:S407-12.
21. Hohenforst-Schmidt W, Petermann A, Visouli A, et
al. Successful application of extracorporeal membrane
oxygenation due to pulmonary hemorrhage secondary to
granulomatosis with polyangiitis. Drug Des Devel Ther
2013;7:627-33.
22. Zarogoulidis P, Kontakiotis T, Tsakiridis K, et al. Difficult
airway and difficult intubation in postintubation tracheal
stenosis: a case report and literature review. Ther Clin Risk
Manag 2012;8:279-86.
23. Zarogoulidis P, Tsakiridis K, Kioumis I, et al. Cardiothoracic
diseases: basic treatment. J Thorac Dis 2014;6 Suppl 1:S1.
24. Kolettas A, Grosomanidis V, Kolettas V, et al. Influence of
apnoeic oxygenation in respiratory and circulatory system
under general anaesthesia. J Thorac Dis 2014;6 Suppl
1:S116-45.
25. Turner JF, Quan W, Zarogoulidis P, et al. A case of
pulmonary infiltrates in a patient with colon carcinoma.
www.jthoracdis.com J Thorac Dis 2014;6(S4):S372-S376
S376 Zarogoulidis et al. Pneumothorax: an up-to-date presentation

Case Rep Oncol 2014;7:39-42.
26. Machairiotis N, Stylianaki A, Dryllis G, et al. Extrapelvic
endometriosis: a rare entity or an under diagnosed
condition? Diagn Pathol 2013;8:194.
27. Tsakiridis K, Zarogoulidis P. An interview between a
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Cite this article as: Zarogoulidis P, Kioumis I, Pitsiou G,

Porpodis K, Lampaki S, Papaiwannou A, Katsikogiannis N,
Zaric B, Branislav P, Secen N, Dryllis G, Machairiotis N, Rapti
A, Zarogoulidis K. Pneumothorax: from definition to diagnosis
and treatment. J Thorac Dis 2014;6(S4):S372-S376. doi:
10.3978/j.issn.2072-1439.2014.09.24

© Pioneer Bioscience Publishing Company. All rights reserved. www.jthoracdis.com J Thorac Dis 2014;6(S4):S372-S376
4/7/2018 Pneumothorax: Practice Essentials, Background, Anatomy

This site is intended for healthcare professionals

Pneumothorax
Updated: Dec 11, 2017
Author: Brian J Daley, MD, MBA, FACS, FCCP, CNSC; Chief Editor: Mary C Mancini, MD, PhD, MMM
more...

OVERVIEW

Practice Essentials
Pneumothorax is defined as the presence of air or gas in the pleural cavity (ie, the potential space
between the visceral and parietal pleura of the lung), which can impair oxygenation and/or ventilation.
The clinical results are dependent on the degree of collapse of the lung on the affected side. If the
pneumothorax is significant, it can cause a shift of the mediastinum and compromise hemodynamic
stability. Air can enter the intrapleural space through a communication from the chest wall (ie, trauma)
or through the lung parenchyma across the visceral pleura. See the image below.

Radiograph of a patient with a complete right-sided pneumothorax due to a stab wound.

View Media Gallery

Signs and symptoms

The presentation of patients with pneumothorax varies depending on the following types of
pneumothorax and ranges from completely asymptomatic to life-threatening respiratory distress:

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Spontaneous pneumothorax: No clinical signs or symptoms in primary spontaneous

pneumothorax until a bleb ruptures and causes pneumothorax; typically, the result is acute onset
of chest pain and shortness of breath, particularly with secondary spontaneous pneumothoraces
Iatrogenic pneumothorax: Symptoms similar to those of spontaneous pneumothorax, depending
on patient’s age, presence of underlying lung disease, and extent of pneumothorax
Tension pneumothorax: Hypotension, hypoxia, chest pain, dyspnea
Catamenial pneumothorax: Women aged 30-40 years with onset of symptoms within 48 hours of
menstruation, right-sided pneumothorax, and recurrence
Pneumomediastinum: Must be differentiated from spontaneous pneumothorax; patients may or
may not have symptoms of chest pain, persistent cough, sore throat, dysphagia, shortness of
breath, or nausea/vomiting

See Clinical Presentation for more detail.

Diagnosis
History and physical examination remain the keys to making the diagnosis of pneumothorax.
Examination of patients with this condition may reveal diaphoresis and cyanosis (in the case of
tension pneumothorax). Affected patients may also reveal altered mental status changes, including
decreased alertness and/or consciousness (a rare finding).

Findings on lung auscultation vary depending on the extent of the pneumothorax. Respiratory findings
may include the following:

Respiratory distress (considered a universal finding) or respiratory arrest

Tachypnea (or bradypnea as a preterminal event)
Asymmetric lung expansion: Mediastinal and tracheal shift to contralateral side (large tension
pneumothorax)
Distant or absent breath sounds: Unilaterally decreased/absent lung sounds common, but
decreased air entry may be absent even in advanced state of pneumothorax
Minimal lung sounds transmitted from unaffected hemithorax with auscultation at midaxillary line
Hyperresonance on percussion: Rare finding; may be absent even in an advanced state
Decreased tactile fremitus
Adventitious lung sounds: Ipsilateral crackles, wheezes

Cardiovascular findings may include the following:

Tachycardia: Most common finding; if heart rate is faster than 135 beats/min, tension
pneumothorax likely
Pulsus paradoxus
Hypotension: Inconsistently present finding; although typically considered a key sign of tension
pneumothorax, hypotension can be delayed until its appearance immediately precedes
cardiovascular collapse
Jugular venous distention: Generally seen in tension pneumothorax; may be absent if
hypotension is severe
Cardiac apical displacement: Rare finding

Common findings among the types of pneumothoraces include the following:

Spontaneous and iatrogenic pneumothorax: Tachycardia most common finding; tachypnea and
hypoxia may be present
Tension pneumothorax: Variable findings; respiratory distress and chest pain; tachycardia;
ipsilateral air entry on auscultation; breath sounds absent on affected hemithorax; trachea may

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deviate from affected side; thorax may be hyperresonant; jugular venous distention and/or
abdominal distention may be present
Pneumomediastinum: Variable or absent findings; subcutaneous emphysema is the most
consistent sign; Hamman sign—a precordial crunching noise synchronous with the heartbeat
and often accentuated during expiration—has a variable rate of occurrence, with one series
reporting 10%

Lab and imaging studies

Although laboratory and imaging studies help determine a diagnosis, tension pneumothorax primarily
is a clinical diagnosis based on patient presentation. Suspicion of tension pneumothorax, especially in
late stages, mandates immediate treatment and does not require potentially prolonged diagnostic
studies.

Arterial blood gas (ABG) studies measure the degrees of acidemia, hypercarbia, and hypoxemia, the
occurrence of which depends on the extent of cardiopulmonary compromise at the time of collection.
ABG analysis does not replace physical diagnosis, nor should treatment be delayed while awaiting
results if symptomatic pneumothorax is suspected. However, ABG analysis may be useful in
evaluating hypoxia and hypercarbia and respiratory acidosis.

When pneumothorax is suspected, confirmation by chest radiography affords additional information

beyond confirmation, such as the extent of pneumothorax, potential causes, a baseline study from
which to go forward, and assistance with the therapeutic plan.

The following radiologic studies may be used to evaluate suspected pneumothorax:

Chest radiography: Anteroposterior and/or lateral decubitus films

Contrast-enhanced esophagography: If emesis/retching is the precipitating event
Chest computed tomography scanning: Most reliable imaging study for diagnosis of
pneumothorax but not recommended for routine use in pneumothorax
Chest ultrasonography

See Workup for more detail.

Management
Although there is general agreement on the management of pneumothorax, a full consensus about
management of initial or recurrent pneumothorax does not exist. Rather, many clinicians use a risk
stratification framework as well as other approaches for choosing among options to restore lung
volume and an air-free pleural space and to prevent recurrences. [1]

The range of medical therapeutic options for pneumothorax includes the following:

Watchful waiting, with or without supplemental oxygen

Simple aspiration
Tube drainage, with or without medical pleurodesis

Surgery

If the patient has had repeated episodes of pneumothorax or if the lung remains unexpanded after 5
days with a chest tube in place, operative therapy such as the following may be necessary:

Thoracoscopy: Video-assisted thoracoscopic surgery (VATS)

Electrocautery: Pleurodesis or sclerotherapy
Laser treatment
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Resection of blebs or pleura

Open thoracotomy

Pharmacotherapy

The following medications may be used to aid in the management of patients with pneumothorax:

Local anesthetics (eg, lidocaine hydrochloride)

Opioid anesthetics (eg, fentanyl citrate, morphine)
Benzodiazepines (eg, midazolam, lorazepam)
Antibiotics (eg, doxycycline, cefazolin)

See Treatment and Medication for more detail.

Background
Pneumothorax is defined as the presence of air or gas in the pleural cavity (ie, the potential space
between the visceral and parietal pleura of the lung). The clinical results are dependent on the degree
of collapse of the lung on the affected side. Pneumothorax can impair oxygenation and/or ventilation.
If the pneumothorax is significant, it can cause a shift of the mediastinum and compromise
hemodynamic stability. Air can enter the intrapleural space through a communication from the chest
wall (ie, trauma) or through the lung parenchyma across the visceral pleura.

Among the topics this article will discuss are several areas of new information in the medical literature:
(1) studies comparing aspiration and tube drainage for treatment of primary spontaneous
pneumothorax, (2) long-term follow-up of surgical treatment of pneumothorax, (3) assessment of the
impact of pleurodesis on transplantation outcomes in patients with lymphangiomyomatosis, (4)
demonstrated utility of ultrasonography in the bedside diagnosis of iatrogenic pneumothorax, and (5)
inability of ultrasonography to distinguish between intrapulmonary bullae and pneumothorax.

See also Restoring an Air-Free Pleural Space in Pneumothorax.

Primary and secondary spontaneous pneumothorax

Spontaneous pneumothorax is a commonly encountered problem with approaches to treatment that
vary from observation to aggressive intervention. Primary spontaneous pneumothorax (PSP) occurs in
people without underlying lung disease and in the absence of an inciting event (see the images
below). [2] In other words, air enters into the intrapleural space without preceding trauma and without
an underlying history of clinical lung disease. However, many patients whose condition is labeled as
primary spontaneous pneumothorax have subclinical lung disease, such as pleural blebs, that can be
detected by CT scanning. Patients are typically aged 18-40 years, tall, thin, and, often, are smokers.

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Radiograph of a patient with a small spontaneous primary pneumothorax

View Media Gallery

Close radiographic view of patient with a small spontaneous primary pneumothorax (same patient as from the
previous image).
View Media Gallery

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Expiratory radiograph of a patient with a small spontaneous primary pneumothorax (same patient as in the
previous images).
View Media Gallery

Secondary spontaneous pneumothorax (SSP) occurs in people with a wide variety of parenchymal
lung diseases. [2] These individuals have underlying pulmonary pathology that alters normal lung
structure (see the image below). Air enters the pleural space via distended, damaged, or
compromised alveoli. The presentation of these patients may include more serious clinical symptoms
and sequelae due to comorbid conditions.

Computed tomography scan demonstrating secondary spontaneous pneumothorax (SSP) from

radiation/chemotherapy for lymphoma.
View Media Gallery

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Iatrogenic and traumatic pneumothorax

Iatrogenic pneumothorax is a traumatic pneumothorax that results from injury to the pleura, with air
introduced into the pleural space secondary to diagnostic or therapeutic medical intervention (see the
following image). Half a century ago, iatrogenic pneumothorax was predominantly the result of
deliberate injection of air into the pleural space for the treatment of tuberculosis (TB). The terminology
evolved to the preference for "induced" or "artificial" pneumothorax to indicate pulmonary TB
treatment, before arriving at the current classification. Pulmonary TB remains a significant cause of
secondary pneumothorax.

Radiograph of an older man who was admitted to the intensive care unit (ICU) postoperatively. Note the right-
sided pneumothorax induced by the incorrectly positioned small-bowel feeding tube in the right-sided bronchial
tree. Marked depression of the right hemidiaphragm is noted, and mediastinal shift is to the left side, suggestive
of tension pneumothorax. The endotracheal tube is in a good position.
View Media Gallery

Traumatic pneumothorax results from blunt trauma or penetrating trauma that disrupts the parietal or
visceral pleura (see the images below). Management steps for traumatic pneumothoraces are similar
to those for other, nontraumatic causes. If hemodynamic or respiratory status is compromised or an
open (communicating to the atmosphere) and/or hemothorax are also present, tube thoracostomy is
performed to evacuate air and allow re-expansion of the lung. There is a subset of traumatic
pneumothoraces classified as occult; that is, they cannot be seen on chest radiographs but can be
seen on CT scans. In general, these can be observed and treated if they become symptomatic.

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Illustration depicting multiple fractures of the left upper chest wall. The first rib is often fractured posteriorly (black
arrows). If multiple rib fractures occur along the midlateral (red arrows) or anterior chest wall (blue arrows), a flail
chest (dotted black lines) may result, which may result in pneumothorax.
View Media Gallery

Radiograph of a patient with a complete right-sided pneumothorax due to a stab wound.

View Media Gallery

Tension pneumothorax
A tension pneumothorax is a life-threatening condition that develops when air is trapped in the pleural
cavity under positive pressure, displacing mediastinal structures and compromising cardiopulmonary
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function. Prompt recognition of this condition is life saving, both outside the hospital and in a modern
ICU. Because tension pneumothorax occurs infrequently and has a potentially devastating outcome, a
high index of suspicion and knowledge of basic emergency thoracic decompression procedures are
important for all healthcare personnel. Immediate decompression of the thorax is mandatory when
tension pneumothorax is suspected. This should not be delayed for radiographic confirmation. Note
the image below.

This chest radiograph has 2 abnormalities: (1) tension pneumothorax and (2) potentially life-saving intervention
delayed while waiting for x-ray results. Tension pneumothorax is a clinical diagnosis requiring emergent needle
decompression, and therapy should never be delayed for x-ray confirmation.
View Media Gallery

Pneumomediastinum
Pneumomediastinum is the presence of gas in the mediastinal tissues occurring spontaneously or
following procedures or trauma (see the following images). A pneumothorax may occur secondary to
pneumomediastinum.

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Pneumomediastinum from barotrauma may result in tension pneumothorax and obstructive shock.
View Media Gallery

This chest radiograph shows pneumomediastinum (radiolucency noted around the left heart border) in this patient
who had a respiratory and circulatory arrest in the emergency department after experiencing multiple episodes of
vomiting and a rigid abdomen. The patient was taken immediately to the operating room, where a large rupture of
the esophagus was repaired.
View Media Gallery

Anatomy
The inner surface of the thoracic cage (parietal pleura) is contiguous with the outer surface of the lung
(visceral pleura); this space contains a small amount of lubricating fluid and is normally under negative
pressure compared to the alveoli. Determinants of pleural pressure are the opposing recoil forces of
the lung and chest wall.

Pathophysiology
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The underlying pathophysiology of pneumothorax is reviewed in this section.

Spontaneous pneumothorax
Spontaneous pneumothorax in most patients occurs from the rupture of blebs and bullae. Although
PSP is defined as occurring in patients without underlying pulmonary disease, these patients have
asymptomatic blebs and bullae detected on computed tomography scans or during thoracotomy. PSP
is typically observed in tall, young people without parenchymal lung disease and is thought to be
related to increased shear forces in the apex.

Although PSP is associated with the presence of apical pleural blebs, the exact anatomic site of air
leakage is often uncertain. Fluorescein-enhanced autofluorescence thoracoscopy (FEAT) is a novel
method to examine the site of air leak in PSP. FEAT-positive lesions can be detected that appear
normal when viewed under normal white-light thoracoscopy. [3]

In normal respiration, the pleural space has a negative pressure. As the chest wall expands outward,
the surface tension between the parietal and visceral pleura expands the lung outward. The lung
tissue intrinsically has an elastic recoil, tending to collapse inwards. If the pleural space is invaded by
gas from a ruptured bleb, the lung collapses until equilibrium is achieved or the rupture is sealed. As
the pneumothorax enlarges, the lung becomes smaller. The main physiologic consequence of this
process is a decrease in vital capacity and partial pressure of oxygen.

Lung inflammation and oxidative stress are hypothesized to be important to the pathogenesis of PSP.
[4] Current smokers, at increased risk for PSP, have increased numbers of inflammatory cells in the
small airways. Bronchoalveolar lavage (BAL) studies in patients with PSP reveal that the degree of
inflammation correlates with the extent of emphysematouslike changes (ELCs). One hypothesis is that
ELCs result from degradation of lung tissue due to imbalances of enzymes and antioxidants released
by innate immune cells. [5] In one study, erythrocyte superoxide dismutase activity was significantly
lower and plasma malondialdehyde levels higher in patients with PSP than in normal control subjects.
[4]

A growing body of evidence suggests that genetic factors may be important in the pathogenesis of
many cases of PSP. Familial clustering of this condition has been reported. Genetic disorders that
have been linked to PSP include Marfan syndrome, homocystinuria, and Birt-Hogg-Dube (BHD)
syndrome.

Birt-Hogg-Dube syndrome is an autosomal dominant disorder that is characterized by benign skin

tumors (hair follicle hamartomas), renal and colon cancer, and spontaneous pneumothorax.
Spontaneous pneumothorax occurs in about 22% of patients with this syndrome. The gene
responsible for this syndrome is a tumor suppressor gene located on band 17p11.2. The gene
encoding folliculin (FLCN) is thought to be the etiology of Birt-Hogg-Dube syndrome. Multiple
mutations have been found, and phenotypic variation is recognized. In one study, eight patients
without skin or renal involvement had lung cysts and spontaneous pneumothorax. [6] A germ-line
mutation to this gene has been found in five patients, and genetic testing is now available.

Tension pneumothorax

Tension pneumothorax occurs anytime a disruption involves the visceral pleura, parietal pleura, or the
tracheobronchial tree. This condition develops when injured tissue forms a one-way valve, allowing air
inflow with inhalation into the pleural space and prohibiting air outflow. The volume of this
nonabsorbable intrapleural air increases with each inspiration because of the one-way valve effect. As
a result, pressure rises within the affected hemithorax. In addition to this mechanism, the positive
pressure used with mechanical ventilation therapy can cause air trapping.
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As the pressure increases, the ipsilateral lung collapses and causes hypoxia. Further pressure
increases cause the mediastinum to shift toward the contralateral side and impinge on and compress
both the contralateral lung and impair the venous return to the right atrium. Hypoxia results as the
collapsed lung on the affected side and the compressed lung on the contralateral side compromise
effective gas exchange. This hypoxia and decreased venous return caused by compression of the
relatively thin walls of the atria impair cardiac function. Kinking of the inferior vena cava is thought to
be the initial event restricting blood to the heart. It is most evident in trauma patients who are
hypovolemic with reduced venous blood return to the heart.

Arising from numerous causes, this condition rapidly progresses to respiratory insufficiency,
cardiovascular collapse, and, ultimately, death if unrecognized and untreated.

Pneumomediastinum
With pneumomediastinum, excessive intra-alveolar pressures lead to rupture of alveoli bordering the
mediastinum. Air escapes into the surrounding connective tissue and dissects further into the
mediastinum. Esophageal trauma or elevated airway pressures may also allow air to dissect into the
mediastinum. Air may then travel superiorly into the visceral, retropharyngeal, and subcutaneous
spaces of the neck. From the neck, the subcutaneous compartment is continuous throughout the
body; thus, air can diffuse widely.

Mediastinal air can also pass inferiorly into the retroperitoneum and other extraperitoneal
compartments. If the mediastinal pressure rises abruptly or if decompression is not sufficient, the
mediastinal parietal pleura may rupture and cause a pneumothorax (in 10-18% of patients).

A wide variety of disease states and circumstances may result in a pneumothorax.

Primary and secondary spontaneous pneumothorax

Risks factors for primary spontaneous pneumothorax (PSP) include the following:

Smoking
Tall, thin stature in a healthy person
Marfan syndrome
Pregnancy
Familial pneumothorax

Blebs and bullae (sometimes called referred to as ELCs) are related to the occurrence of primary
spontaneous pneumothorax. Thoracic computed tomography (CT) scans of patients with PSP shows
ipsilateral ELC in 89% and contralateral changes in 80% compared with a rate of 20% among control
subjects matched for age and smoking. [2] Nonsmokers with PSP had CT scan ELC abnormalities of
80% compared with a rate of 0% among nonsmoker controls without PSP. [2]

Although patients with PSP do not have overt parenchymal disease, this condition is heavily
associated with smoking—80-90% of PSP cases occur in smokers or former smokers, and the relative
risk of PSP increases as the number of cigarettes smoked per day increases; that is, the risk of PSP is
related to the intensity of smoking, with 102 times higher incidence rates in males who smoke heavily
(ie, >22 cigarettes/day), compared with a sevenfold increase in males who smoke lightly (1-12
cigarettes/day). This incremental risk with increasing number of cigarettes smoked per day is much
more pronounced in female smokers.

Typical PSP patients also tend to have a tall and thin body habitus. Whether height affects
development of subpleural blebs or whether more negative apical pleural pressures cause preexisting
blebs to rupture is unclear.
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Pregnancy is an unrecognized risk factor, as suggested by a 10-year retrospective series in which five
of 250 spontaneous pneumothorax cases were in pregnant women. [7] The cases were all managed
successfully with simple aspiration or video-assisted thoracoscopic surgery (VATS), and no harm
occurred to mother or fetus. [7]

Other associations with pneumothorax include increased intrathoracic pressure with the Valsalva
maneuver, though contrary to popular belief, most spontaneous pneumothoraces occur while the
patient is at rest. Changes in atmospheric pressure, proximity to loud music, and low-frequency noises
are other reported factors.

Familial associations have been noted in more than 10% of patients. Some are due to rare connective
tissue diseases, but mutations in the gene encoding folliculin (FLCN) have been described. These
patients may represent an incomplete penetrance of an autosomal dominant genetic disorder. Birt-
Hogg-Dube syndrome is characterized by benign skin growths, pulmonary cysts, and renal cancers
and is caused by mutations in the FLCN gene.

In one family study, nine ascertained cases of spontaneous pneumothorax were reported among 54
members. A review of the literature summarized 61 reports of familial spontaneous pneumothorax
among 22 families. Up to 10% patients with spontaneous pneumothorax report a positive family
history. [8]

Although rare, spontaneous pneumothorax occurring bilaterally and progressing to tension

pneumothorax has been documented.

Diseases and conditions associated with secondary spontaneous pneumothorax include the following:

Chronic obstructive lung disease (COPD) or emphysema - Increased pulmonary pressure due to
coughing with a bronchial plug of mucus or phlegm bronchial plug may play a role.
Asthma
Human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) with PCP
infection
Necrotizing pneumonia
Tuberculosis
Sarcoidosis
Cystic fibrosis
Bronchogenic carcinoma or metastatic malignancy
Idiopathic pulmonary fibrosis
Inhalational and intravenous drug use (eg, marijuana, cocaine) [9]
Interstitial lung diseases associated with connective tissue diseases
Lymphangioleiomyomatosis
Langerhans cell histiocytosis
Severe acute respiratory syndrome (SARS) - A reported 1.7% of SARS patients developed
spontaneous pneumothorax. [10]
Thoracic endometriosis and catamenial pneumothorax
Collagen vascular disease, including Marfan syndrome

SSPs occur in the presence of lung disease, primarily in the presence of COPD. Other diseases that
may be present when SSPs occur include tuberculosis, sarcoidosis, cystic fibrosis, malignancy, and
idiopathic pulmonary fibrosis.

Pneumocystis jiroveci pneumonia (previously known as Pneumocystis carinii pneumonia [PCP]) was a
common cause of SSP in patients with AIDS during the last decade. In fact, 77% of AIDS patients with
spontaneous pneumothorax had thin-walled cavities, cysts, and pneumothorax from PCP infection. [11]
With the advent of highly active antiretroviral therapy (HAART) and widespread use of trimethoprim-
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sulfamethoxazole (TMP-SMZ) prophylaxis, the incidence of PCP and associated SSP has significantly
declined.

PCP in other immunocompromised patients is seen only when TMP-SMZ prophylaxis is withdrawn
prematurely. For practical purposes, if the immunocompromised patient has been taking TMP-SMZ
prophylaxis reliably, PCP is reasonably excluded from the differential diagnosis and should not be a
causative factor for SSP.

In cystic fibrosis, up to 18.9% of patients have been reported to develop spontaneous

pneumothoraces, and they have a high incidence of recurrence on the same side after conservative
management (50%) or intercostal drainage (55.2%). The risk of SSP in these patients increases with
Burkholderia cepacia or Pseudomonas infections and allergic bronchopulmonary aspergillosis (ABPA).
[12] Pleurodesis increases the risk of bleeding associated with lung transplantation but is not an
absolute contraindication.

Many different types of malignancies are known to present with a pneumothorax, especially sarcomas,
but also genitourinary cancers and primary lung cancer; thus, pneumothorax in a patient with
malignancy should prompt a look for metastatic disease. Chemotherapeutic agents, at times, can also
induce SSP. [13]

Interstitial lung diseases are associated with connective-tissue diseases. Ankylosing spondylitis may
be noted when apical fibrosis is present; in fact, the typically low incidence of spontaneous
pneumothorax in patients with ankylosing spondylitis (0.29%) increases 45-fold (to 13%) when apical
fibrotic disease exists. [14]

Lymphangioleiomyomatosis (LAM) may present with spontaneous pneumothorax. This disease is

characterized by thin-walled cysts in women of childbearing age. Respiratory failure may lead to a
need for lung transplantation, and previous pleurodesis is no longer an absolute contraindication for
lung transplantation.

Thoracic endometriosis is a rare cause of recurrent pneumothorax (catamenial pneumothorax) in

women that is thought to arise from endometriosis reaching the chest wall across the diaphragm (ie,
its etiology may be primarily related to associated diaphragmatic defects). In a case series of 229
patients, catamenial pneumothorax caused by thoracic endometriosis was localized to the visceral
pleura in 52% of patients and to the diaphragm in 39% of patients. [15] Before recurrence, this
condition may be initially diagnosed as primary spontaneous pneumothorax.

Iatrogenic and traumatic pneumothorax

Causes of iatrogenic pneumothorax include the following:

Transthoracic needle aspiration biopsy of pulmonary nodules (most common cause, accounting
for 32-37% of cases)
Transbronchial or pleural biopsy
Thoracentesis
Central venous catheter insertion, usually subclavian or internal jugular [16]
Intercostal nerve block
Tracheostomy
Cardiopulmonary resuscitation (CPR) - Consider the possibility of a pneumothorax if ventilation
becomes progressively more difficult.
Acute respiratory distress syndrome ( ARDS) and positive pressure ventilation in the ICU - High
peak airway pressures can translate into barotrauma in up to 3% of patients on a ventilator and
up to 5% of patients with ARDS. [17]
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Nasogastric feeding tube placement

Iatrogenic pneumothorax is a complication of medical or surgical procedures. It most commonly

results from transthoracic needle aspiration. Other procedures commonly causing iatrogenic
pneumothorax are therapeutic thoracentesis, pleural biopsy, central venous catheter insertion,
transbronchial biopsy, positive pressure mechanical ventilation, and inadvertent intubation of the right
mainstem bronchus. Therapeutic thoracentesis is complicated by pneumothorax 30% of the time
when performed by inexperienced operators in contrast to only 4% of the time when performed by
experienced clinicians.

The routine use of ultrasonography during diagnostic thoracentesis is associated with lower rates of
pneumothorax (4.9% vs 10.3%) and need for tube thoracostomy (0.7% vs 4.1%). Similarly, in patients
who are mechanically ventilated, thoracentesis guided by bedside ultrasonography without radiology
support results in a relatively lower rate of pneumothorax.

Causes of traumatic pneumothorax include the following:

Trauma - Penetrating and nonpenetrating injury

Rib fracture
High-risk occupation (eg, diving, flying)

Traumatic pneumothoraces can result from both penetrating and nonpenetrating lung injuries.
Complications include hemopneumothorax and bronchopleural fistula. Traumatic pneumothoraces
often can create a one-way valve in the pleural space (only letting in air without escape) and can lead
to a tension pneumothorax.

Tension pneumothorax
The most common etiologies of tension pneumothorax are either iatrogenic or related to trauma, such
as the following:

Blunt or penetrating trauma - Disruption of either the visceral or parietal pleura occurs and is
often associated with rib fractures, though rib fractures are not necessary for tension
pneumothorax to occur.
Barotrauma secondary to positive-pressure ventilation (PPV), especially when high amounts of
positive end-expiratory pressure (PEEP) are used
Pneumoperitoneum [18, 19]
Fiberoptic bronchoscopy with closed lung biopsy [20]
Markedly displaced thoracic spine fractures
Acupuncture [21, 22, 23]
Preexisting Bochdalek hernia with trauma [24]
Colonoscopy [25] and gastroscopy have been implicated in case reports.
Percutaneous tracheostomy [26]
Conversion of idiopathic, spontaneous, simple pneumothorax to tension pneumothorax
Unsuccessful attempts to convert an open pneumothorax to a simple pneumothorax in which the
occlusive dressing functions as a one-way valve

Tension pneumothorax occurs commonly in the ICU setting in patients who are ventilated with positive
pressure, and practitioners must always consider this when changes in respiratory or hemodynamic
status occur. Infants requiring ventilatory assistance and those with meconium aspiration have a
particularly high risk for tension pneumothorax. Aspirated meconium may serve as a one-way valve
and produce a tension pneumothorax.

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Any penetrating wound that produces an abnormal passageway for gas exchange into the pleural
spaces and that results in air trapping may produce a tension pneumothorax. Blunt trauma, with or
without associated rib fractures, and incidents such as unrestrained head-on motor vehicle accidents,
falls, and altercations involving laterally directed blows may also cause tension pneumothoraces.

Significant chest injuries carry an estimated 10-50% risk of associated pneumothorax; in about 50% of
these cases, the pneumothorax may not be seen on standard radiographs and are therefore deemed
occult. In one study, 12% of patients with asymptomatic chest stab wounds had a delayed
pneumothorax or hemothorax. McPherson et al analyzed data from the Vietnam Wound Data and
Munitions Effectiveness Team study and determined that tension pneumothorax was the cause of
death in 3-4% of fatally wounded combat casualties. [27]

Acupuncture is a traditional Chinese medicine technique used worldwide by alternative medical

practitioners. Acupuncture's most frequently reported serious complication is pneumothorax; in one
Japanese report of 55,291 acupuncture treatments, an approximate incidence of 1 pneumothorax in
5000 cases was documented. [28]

Pneumomediastinum
The following factors may result in pneumomediastinum:

Acute generation of high intrathoracic pressures (often as a result of inhalational drug use, such
smoking marijuana or inhalation of cocaine)
Asthma
Respiratory tract infection
Parturition
Emesis
Severe cough
Mechanical ventilation
Trauma or surgical disruption of the oropharyngeal, esophageal, or respiratory mucosa
Athletic competition

Epidemiology
The epidemiologic data vary among the pneumothorax classifications.

Primary, secondary, and recurring spontaneous pneumothorax

It is likely that the incidence for spontaneous pneumothorax is underestimated. Up to 10% of patients
may be asymptomatic, and others with mild symptoms may not present to a medical provider.

PSPs occur in people aged 20-30 years, with a peak incidence is in the early 20s. PSP is rarely
observed in people older than 40 years. The age-adjusted incidence of PSP is 7.4-18 cases per
100,000 persons per year for men and 1.2-6 cases per 100,000 persons per year for women. [29] The
male-to-female ratio of age-adjusted rates is 6.2:1.

SSPs occur more frequently in patients aged 60-65 years. The age-adjusted incidence of SSP is 6.3
cases per 100,000 persons per year for men and 2.0 cases per 100,000 persons per year for women.
The male-to-female ratio of age-adjusted rates is 3.2:1. Chronic obstructive pulmonary disease
(COPD) is a common cause of secondary spontaneous pneumothorax that carries an incidence of 26
cases per 100,000 persons. [30]

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Smoking increases the risk of a first spontaneous pneumothorax by more than 20-fold in men and by
nearly 10-fold in women compared with risks in nonsmokers. [31] Increased risk of pneumothorax and
recurrence appears to rise proportionally with number of cigarettes smoked.

In men, the risk of spontaneous pneumothorax is 102 times higher in heavy smokers than in
nonsmokers. Spontaneous pneumothorax most frequently occurs in tall, thin men aged 20-40 years.

Iatrogenic and traumatic pneumothorax

Traumatic and tension pneumothoraces occur more frequently than spontaneous pneumothoraces,
and the rate is undoubtedly increasing in US hospitals as intensive care treatment modalities have
become increasingly dependent on positive-pressure ventilation, central venous catheter placement,
and other causes that potentially induce iatrogenic pneumothorax.

Iatrogenic pneumothorax may cause substantial morbidity and, rarely, death. The incidence of
iatrogenic pneumothorax is 5-7 per 10,000 hospital admissions, with thoracic surgery patients
excluded because pneumothorax may be a typical outcome following these surgeries.

Pneumothorax occurs in 1-2% of all neonates, with a higher incidence in infants with neonatal
respiratory distress syndrome. In one study, 19% of such patients developed a pneumothorax.

Tension pneumothorax

Tension pneumothorax is a complication in approximately 1-2% of the cases of idiopathic spontaneous

pneumothorax. Until the late 1800s, tuberculosis was a primary cause of pneumothorax development.
A 1962 study showed a frequency of pneumothorax of 1.4% in patients with tuberculosis.

The actual incidence of tension pneumothorax outside of a hospital setting is impossible to determine.
Approximately 10-30% of patients transported to level-1 trauma centers in the United States receive
prehospital decompressive needle thoracostomies; however, not all of these patients actually have a
true tension pneumothorax. Although this occurrence rate may seem high, disregarding the diagnosis
would probably result in unnecessary deaths. A review of military deaths from thoracic trauma
suggests that up to 5% of combat casualties with thoracic trauma have tension pneumothorax at the
time of death. [27]

The overall incidence of tension pneumothorax in the intensive care unit (ICU) is unknown. The
medical literature provides only glimpses of the frequency. In one report, of 2000 incidents reported to
the Australian Incident Monitoring Study (AIMS), 17 involved actual or suspected pneumothoraces,
and 4 of those were diagnosed as tension pneumothorax.

Catamenial pneumothorax
Catamenial pneumothorax is a rare phenomenon that generally occurs in women aged 30-50 years. It
frequently begins 1-3 days after menses onset. The risk of thoracic endometriosis cannot be predicted
from the site of peritoneal lesions. [15]

Pneumomediastinum

Spontaneous pneumomediastinum generally occurs in young, healthy patients without serious

underlying pulmonary disease, mostly in the second to fourth decades of life. A slight predominance of
pneumomediastinum exists for males. This condition occurs in approximately 1 case per 10,000
hospital admissions.

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Prognosis
The prognosis varies among the pneumothorax classifications.

Primary, secondary, and recurring spontaneous pneumothorax

Complete resolution of an uncomplicated pneumothorax takes approximately 10 days. PSP is typically
benign and often resolves without medical attention. Many affected individuals do not seek medical
attention for days after symptoms develop. This trend is important, because the incidence of
reexpansion pulmonary edema increases in patients whose chest tubes have been placed 3 or more
days after the pneumothorax occurred.

Recurrences usually strike within the first 6 months to 3 years. The 5-year recurrence rate is 28-32%
for PSP and 43% for SSP.

Recurrences are more common among patients who smoke, patients with COPD and patients with
AIDS. Predictors of recurrence include pulmonary fibrosis, younger age, and increased height-to-
weight ratio. In a retrospective study of 182 consecutive patients with a newly diagnosed first episode
of pneumothorax, a higher rate of recurrence was noted in taller patients, thin patients, and patients
with SSP.

Patients who underwent bedside chest tube pleurodesis had cumulative rates of recurrence of 13% at
6 months, 16% at 1 year, and 27% at 3 years compared with 26%, 33%, and 50%, respectively. The
agent used (tetracycline or gentamicin) did not have any significant impact on the recurrence rate.

Bullous lesions found on CT or at thoracoscopy and the presence of ELCs in PSP are also not
predictive of recurrence. However, contralateral blebs were seen by CT scanning in higher frequency
in the patients with contralateral recurrence (33 patients; 14%) than those without a contralateral
recurrence in a retrospective study of 231 patients with PSP. Primary bilateral spontaneous
pneumothorax (PBSP) was significantly more common in patients with lower body mass index (BMI)
and among smokers. [32] In this series, all patients with contralateral recurrence were treated
surgically.

Although some authors view PSP as more of a nuisance than a major health threat, deaths have been
reported. SSPs are more often life threatening, depending on the severity of the underlying disease
and the size of the pneumothorax (1-17% mortality). In particular, compared with similar patients
without pneumothorax, age-matched patients with COPD have a 3.5-fold increase in relative mortality
when a spontaneous pneumothorax occurs, and their risk of recurrence rises with each occurrence.
One study indicated that 5% of patients with COPD died before a chest tube was placed.

Patients with AIDS also have a high inpatient mortality rate of 25% and a median survival of 3 months
after the pneumothorax. These data were derived from an era before highly active antiretroviral
therapy (HAART) was available.

Tension pneumothorax

Tension pneumothorax arises from numerous causes and rapidly progresses to respiratory
insufficiency, cardiovascular collapse, and, ultimately, death if not recognized and treated. Therefore, if
the clinical picture fits a tension pneumothorax, it must be emergently treated before it results in
hemodynamic instability and death.

Pneumomediastinum

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2015; 10(3): 221–228
ISSN-1452-662X
PNEUMOTHORAX — DIAGNOSIS AND TREATMENT
1, 2
Milisavljevic Slobodan,
1
General and Thoracic Surgery Clinic, Clinical Centre Kragujevac, Serbia
2
Faculty of Medical Sciences University of Kragujevac, Serbia
Primljen/Received 20. 09. 2015. god.
Abstract: Introduction: Pneumothorax is defined
as the presence of air in the pleural cavity, ie, the space
between the chest wall and the lung itself. Pneumotho-
rax is classified ethiologically into spontaneous pneu-
mothorax and traumatic pneumothorax. Spontaneous
pneumothorax is further classified into primary and se-
condary. Traumatic pneumothorax may result from eit-
her blunt trauma or penetrating injury to the chest wall.
It can also be caused by iatrogenic injuries. Spontaneo-
us pneumothorax is a significant health problem beca-
use of the high recurrence rate (this is so called recur-
rent pneumothorax).
The aim of the study: the review of modern diag-
nosis and surgical management of pneumothorax.
Methodology: This is a review article. We used Me-
dline and Pubmed databasis for retrieving the literature.
Conclusion: Pneumothorax, either spontaneous
or traumatic, demands urgent intervention in order to
normalize lung function and save life of the patient.
Keywords: pneumothorax, chest drainage, thora-
cotomy.
INTRODUCTION
Pneumothorax is defined as the presence of air in
the pleural cavity, ie, the space between the chest wall
and the lung itself. Itard first recognized pneumothorax
in 1803, and Laennec himself described the full clini-
cal picture of the condition. In the second part of XIX
century it was believed that tuberculosis was the the
main cause of pneumothorax since it was present
mostly in patients with tuberculosis. On the other hand,
Forlanini (Europe, in 1882) and John B. Murphy (the
USA, in 1898) pointed out the useful results of pneu-
mothorax in tuberculosis treatment (collapse therapy)
(1, 2).
Althoug pathophysiological processes of pneu-
mothorax are not fully known, it is is known that pleu-
ral pressure is negative with values –2 to –40 cm H2O.
DOI: 10.5937/sanamed1503221M
UDK: 616.25-003.219
ID: 219460876
Review article
1 1
Spasic Marko, Milosevic Bojan
Prihva}en/Accepted 10. 11. 2015. god.
If a communication developes between the pleural spa-
ce and an alveolus, air will flow into the pleural space
until a pressure gradient no longer exists or until the
communication is sealed. Without the negative intra-
pleural pressure holding the lungs against the chest
wall, their elastic recoil properties cause them to col-
lapse. The main physiologic consequences od pneu-
mothorax are a decrease in the vital capacity and a dec-
rease in the partial pressure of arterial oxygen (PaO2).
In the otherwise healthy individual, the discease and
the vital capacity is well tolerated. If the patient’s lung
function is compromised before the pneumothorax, ho-
wever, the decrease in the vital capacity may lead to re-
spiratoty insufficiency with alveolar hypoventilation
and respiratory acidosis. In a tension pneumothorax,
the intrapleural air pressure exceeds atmospheric pres-
sure. The mechanism by which a tension pneumotho-
rax develops is probably related to some type of a
one-way valve process in which the valve is open dur-
ing inspiration and closed during expiration. If extra
thoracic air pressure remains relatively higher than the
pressure in the pneumothorax over a period of time,
then the air in pleural space and the ambient atmosphe-
re will begin to approach equilibrium. This can cause
mediastinal shift, compression of the superior vena ca-
va, compression of the contralateral lung. The reduced
preload (volume returning to the heart) causes a redu-
ced stroke volume and therefore reduced cardiac out-
put. This may result in hemodynamic collapse and ob-
structive shock (3).
CLASSIFICATION
OF PNEUMOTHORAX
According to aetiology pneumothorax is classi-
fied into spontaneous and traumatic (Table 1). Sponta-
neous pneumothorax is further classified into primary
and secondary. Traumatic pneumothorax may result
from either blunt trauma or penetrating injury to the
222 Milisavljevic Slobodan, Spasic Marko, Milosevic Bojan

Table 1. Classification of pneumothorax le ratio 6:1). Smoking is associated with a risk of devel-
oping pneumothorax in healthy smoking men (5). Be-
Spontaneous
cause the gradient in pleural pressure is greater from
Primary (a rupture of a subpleural bleb) the lung base to the lung apex in taller individuals, the
Secondary alveoli at the lung apex are subjected to a greater mean
Chronic obstructive pulmonary disease (COPD) distending pressure in taller individuals. Over a long
Cystic fibrosis period, this higher distending pressure could lead to the
formation of subpleural blebs (6). The ocurrence of
Bronchial asthma PSP seems to be related to the level of cigarette smok-
Connective tissue diseases (Marfan Syndrome) ing. The relative risk of a pneumothorax is 100 times
Interstitial lung diseases (Eosinophilic granuloma) higher in heavy smokers (more than 20 cigarettes/day)
Pneumocystis carinii pneumonia (in AIDS patients) than in nonsmokers (7).
Some studies suggest that there is a familial ten-
Pneumonia with lung abscess
dency for the development of primary spontaneous
Pulmonary hydatid disease pneumothorax. In some cases of PSP the mode of inhe-
Lung cancer (metastatic sarcoma) ritance for the tendency for primary spontaneous pneu-
Esophageal perforation mothorax is either autosomal dominant with incomple-
te penetrance or X-linked recessive (8). Primary spon-
Catamenial pneumothorax
taneous pneumothoraces are believed to be the result
Neonatal pneumothorax of rupture of sub-pleural blebs (9). Sub-pleural blebs
Traumatic and bullae are found in up to 90% of cases at thoraco-
Iatrogenic scopy or thoracotomy and in up to 80% on computeri-
Central venous catheter insertion sed tomography (CT) scanning of the thorax (10, 11).
The pathogenesis of the blebs remains unclear. There
Pacemaker implantation
are suggestions that they may be congenital or inflam-
Transthoracic needle biopsy matory in origin or the result of disturbance of collate-
Transbronchial needle aspiration ral ventilation (12). According to some studies, preci-
Thoracocentesis pitating factors may be atmospheric pressure changes,
physical activity, and exposure to loud music (13). Sa-
Laparoscopic surgery
dikot et al, study showed a recurrence rate of 39% dur-
Barotrauma ing the first year (14). It also indicated that there was
Blunt trauma 54% risk of recurrence of pneumothorax in 4 years.
Road traffic accident trauma, falls, sports injuries According to their studies, factors that have been pro-
posed to predispose patients to primary spontaneous
Penetrating trauma
pneumothorax (PSP) include smoking and patient’s
Shot wounds, stab wounds height. The peak age for the occurence of primary
Source: Spasi} M, Milisavljevi} S, Gaji} V. Analiza u~estalosti spontaneous pneumothorax is the aerly 20’ and it ra-
javljanja i na~ina le~enja pneumotoraksa u petogodi{njem peri- rely occurs after age 40. Primary spontaneous pneu-
odu u Kragujevcu. Med Pregl 2012; LXV(Vol 5–6): 238–43. mothorax usually develops while the patient is at rest.
chest wall. It can also be caused by iatrogenic injuries Main symptoms are chest pain and dyspnea. This pain
(3). This condition occurs in 7.4 to 18 per 100 000 men may be mild or severe, sharp and steady ache in charac-
each year and 1.2 to 6 per 100 000 women each year. ter, and usually resolves within 24 h even though pneu-
The incidence of secondary spontaneous pneumotho- mothorax still exists (15). It is interesting that many pa-
rax is 6.3 per 100 000 men each year and 2 per 100 000 tients with a primary pneumothorax do not seek medi-
women each year (4). Some British studies that have
been done recently show the incidence of primary
spontaneous pneumothorax of 24 per 100 000 in men
and 9.8 100 000 in women (5).

PRIMARY SPONTANEOUS
PNEUMOTHORAX
Primary spontaneous pneumothorax (PSP) com- Figure 1. 1a Spontaneous pneumothorax
monly occurs in tall, thin, adolescent men (male-fema- in the left lung; 1b Bilateral pneumothorax
 PNEUMOTHORAX — DIAGNOSIS AND TREATMENT
cal attention for several days- more than 50% of pati-
ents waited more than 24 hours after their symptoms
started to seek help, and 18% waited more than a week
after the symptoms appeared (16) (Figure 1a, 1b).
SECONDARY SPONTANEOUS
PNEUMOTHORAX
Secondary spontaneous pneumothorax (SSP) oc-
curs in patients with underlying lung disease.
The incidence of secondary spontaneous pneu-
mothorax is similar to that of primary spontaneous
pneumothorax. It usually occurs in older people, after
the age of 60 (13). Some research show that the peak
incidence for males occures in the seventh decade of li-
fe, 60/100.000 each yearn (5). Many lung diseases can
cause SSP: chronic airway and alveolar diseases
(COPD, bronchial asthma, cystic fibrosis); infectious
lung diseases (tuberculosis, pneumocystis carinii, lung
abscess leading to pneumothorax with pleural
empyema); interstitial lung diseases (idiopathic fibro-
sing alveolitis, sarcoidosis, histiocytosis X, lymphan-
gio leiomyomatosis); systemic connective tissue disea-
ses (rheumatoid arthritis, ankylosing spondylitis, scle-
roderma, Marfan- and Ehlers Danlos-syndrome); ma-
lignant lung and chest diseases (bronchial cancer, sar-
coma) (13). The most common lung disease that causes
spontaneous pneumothorax is chronic obstructive pul-
monary disease (COPD).
Degradation of elastic fibres of visceral pleura
contributes the occurence of pneumothorax in COPD
(15). SSP occurred in many HIV-infected patients.
Pneumocystis carinii (PCP) infection has been
considered to be the main aetiological factor for this
association, because of a severe form of necrotising al-
veolitis that occurs in which the subpleural pulmonary
parenchyma is replaced by necrotic thin-walled cysts
and pneumatoceles. These patients can develop bilat-
eral pneumothorax (15). The relative risk of recurrence
of secondary spontaneous pneumothorax is 45% hig-
her than the one of PSP (15). Risk factors for reccuren-
ce of SSP include age, pulmonary fibrosis and emphy-
sema (17). Because lung function in these patients is
already compromised, secondary spontaneous pneu-
mothorax (SSP) often presents as a potentially life-thre-
atening disease. The clinical signs and symptoms of
secondary pneumothorax are more intense and severe.
Dyspnea is the main symptom, and chest pain on the
same side as the affected lung is present in most pa-
tients. Some of the most clinically significant sym-
ptoms that may develop include hypotension, tachyca-
rdia, cyanosis, hypoxemia with or without hyperca-
pnia, and acute respiratory distress. The physical fi-
ndings are often subtle and may be masked by the under-
223
Figure 2. 2a Hydropneumothorax in the right lung
Tuberculosis “destroyed lung“; 2b Fibrothorax
in the right lung After the thoracic drainage
lying lung disease, especially in patients with COPD (13)
(Figure 2a, 2b).
CATAMENIAL PNEUMOTHORAX
Catamenial pneumothorax is a spontaneous type
of pneumothorax that starts at the onset of or within 24
to72 hours after onset of menses and is usually recur-
rent. Catamenial pneumothorax was first described by
Maurer in 1958. The initial pneumothorax usually does
not occur until the woman is in her thirties. Lillington
introduced in 1972 the term catamenial pneumothorax
to describe the already reported phenomenon (18).
This pneumothorax was considered to be a rare type
with the incidence 1–5% in women in reproductive age
(18). Recent studies have shown that in 25% of cases
the recurrent catamenial pneumothorax was related to
time of menstruation (19), so the incuidence is not so
low as it was believed. These pneumothoraces are usu-
ally right sided (according to some authors, in 95%)
(20). The pathophysiology of catamenial pneumotho-
rax is uncertain. Three distinct mechanisms have been
proposed based on metastatic, hormonal and anatomic
model (18). The metastatic model hypothesizes migra-
tion of endometrian tissue via the peritoneal cavity th-
rough transdiaphragmatic lymphatic channels, via dia-
phragmatic fenestrations, or hematogenously into the
pleural space. Congenital fenestrations are more com-
mon in right hemidiaphragm making intratho- racic
endometriosis right sided. Endometrial deposits have
been identified in in the pleural space in 13% to 62,5%
of t he cases (19, 20, 21). The hormonal hypothesis was
proposed by Rossi and Goplerud in 1974. It suggests
that high serum levels of prostaglandin F2 at ovulation
leads to vasospasmassociated ischemia with tissue in-
jury and alveolar rupture. However this cannot explain
the preponderance of right sided involvement. Also
there are no non-steroidal anti-inflammatory medica-
tions (NSAIDs) capable of preventing recurrence of
catamenial pneumothorax in respective reported series.
Thus, this hypothesis was rejected (18). The anatomic
model for catamenial pneumothorax is based on the in-
flux of air into the pleural space from the peritonela
224 Milisavljevic Slobodan, Spasic Marko, Milosevic Bojan
cavity via diaphragmatic fenestrations (18). Also con-
comitant pneumoperitoneum is found in some patients
with catamenial pneumothorax (18). Diaphragmatic
defects were found in 50%–62,5% of patients. To pre-
vent recurrence, diaphragmatic defects should cer-
tainly be closed (19, 21). Patients with catamenial
pneumothorax develop chest pain and dyspnea within
24 to 72 hours of the onset of the menstrual flow. It is
usually recurrent and correlated with menses (18).
NEONATAL PNEUMOTHORAX
Spontaneous pneumothorax is present shortly af-
ter birth in 1% to 2% of all infants. It is twice as com-
mon in boys as in girls. The incidence of neonatal pne-
umothorax is higher in cases of preterm birth and low
birth weight. (15%). Also, the cases of infants with fe-
tal distress and respiratiry distress syndrom have high-
er incidence (19%) (15). The pathogenesis of neonatal
pneumothorax is related to the mechanical problems of
first expanding the lung. Transpulmonary pressures
have average values 40cm H2O during the first few
breaths of life, with occasional transpulmonary pres-
sures as high as 100 cm H2O. If bronchial obstruction
occurs, high transpulmonary pressures may lead to ru-
pture of the lung (15). The signs vary from none to se-
vere acute respirator distress. In the infant with a small
pneumothorax, mild apneic spells with some irritab-
ility or restelssness may be present. Large pneumotho-
races incur varying degrees of respiratoty distress, and,
in severe cases, marked tachypnea, grunting, retrac-
tions, and cyanosis are present (15). The most reliable
clinical sign of neonatal pneumothorax is a shift of the
apical heart impulse away from the side of the pneumo-
thorax (15) (Figure 3a, 3b)
Figure 3. 3a Neonatal pneumothorax in the left lung;
3b Bilateral neonatal pneumothorax
IATROGENIC PNEUMOTORAX
The leading cause of iatrogenic pneumothorax is
transthoracic needle aspiration (24%), subclavian nee-
dle (22%), thoracentesis (20%), transbronchial biopsy
(10%), pleural biopsy (8%) and positive-pressure ven-
tilation (7%) (13). Other procedures associated with
Figure 4. Iatrogenic pneumothorax in the
right lung. The rupture of membranous tracheal wall
caused by reinforced tubus
the iatrogenic pneumothorax devlopment include tra-
cheostomy, intercostal nerve block, mediastinoscopy,
liver biopsy, the insertion of nasogastric tubes, car-
diopulmonary resuscitation (15). Iatrogenic pneumo-
thorax should be suspected in any patient with respira-
tory distress symptoms as well as in patients who un-
derwent some procedures (15) (Figure 4).
TRAUMATIC PNEUMOTHORAX
Traumatic pneumothorax may result from either
blunt trauma or penetrating injury to the chest wall.
Pneumothorax can occur at the time of the injury, im-
mediately after the injury, or later.The incidence of se-
vere traumatic pneumothorax is higher than 20% (22),
and the incidence of chest injury is 50% (13). With non
penetrating trauma, a pneumothorax may develop if
the visceral pleura is lacerated secondary to a rib frac-
ture, dislocation. Sudden chest compression abruptly
increases the alveolar pressure, which may cause alve-
olar rupture. Blunt trauma can also cause alveolar rup-
ture (23). With penetrating chest trauma, the wound
allows air to enter the pleural space directly through
the chest wall or through the visceral pleura from the
tracheobronchial tree (23). Traumatic pneumothorax
can also be classified as simple, open (“sucking”) and
tension pneumothorax. In simple pneumothorax, the
air from the injured lung enters the pleural space. There
are not many symptoms of this type of pneumothorax
(1). Open pneumothorax occurs when a wound on the
chest is large enough to allow air to pass freely in and
out of the pleural space. In this case, the atmospheric
pressure is in equilibrium with intrapleural pressure,
blocking the lung inflation and alveolar ventilation.
The rush of air through the wound in the chest wall pro-
duces a sucking sound. In such patients the lung colla-
pses. Traumatic open pneumothorax calls for the emer-
gency intervention- sealing the open wound with Vase-
line gauze and placing the chest tube. The wound treat-
ment involves common surgical procedures (1, 23)
(Figure 5). A tension pneumothorax is the result of the
chest wall or lung injury. A one-way valve mechanism
 PNEUMOTHORAX — DIAGNOSIS AND TREATMENT
Figure 5. Traumatic pneumothorax in the right lung
(traffic accident trauma). Serial rib fractures on the
right side Left pulmonary contusion
Figure 6. 6a. Tension pneumothorax in the left lung
6b. Condition after chest tube drainage in the left
lung. Complete re-expansion of the left lung
occurs, where the air that enters the pleural space with
each inspiration is trapped and cannot be expelled du-
rng expiration. Interthoracic pressure increases cau-
sing the lung to collapse. The collapse in the lung
causes a shift in the mediastinum away from the inju-
red side, resulting in hypoventilation, decreased ve-
nous return to the heart and potentialy in development
of obstructive shock. The signs and symptoms associ-
ated with tension pneumothorax include cyanosis, dys-
pnea, tachypnea, tachycardia, hypotension, distended
neck veins, profuse diaphoresis. A tension pneumot-
horax is a life-threatening injury that should be dia-
gnosed and managed urgently. Management is perfo-
rmed by immediate needle decompression. A large
bore needle is inserted in the II intercostal space, at the
midclavicular line (1, 15) (Figure 6a, 6b).
DIAGNOSIS OF PNEUMOTHORAX
The diagnosis of pneumothorax is established
from the patients’ history and physical examination
findings that reveal decreased movement of the hemit-
horax, decreased or absent fremitus, hyper sonority on
percussion and decreased or absent breath sounds on
the affected side. Radiography of the chest in the up-
right position and PA projection of the chest are the
most common methods of diagnosing pneumothorax.
The main feature of a pneumothorax on a chest radiog-
raph is a white visceral pleural line, which is separated
from the parietal pleura by a collection of gas (15). Ra-
diographs that are obtained in the lateral decubitus po-
225
sition can be useful in cases of clinically suspected
pneumothorax, while PA radiograph is normal. CT scan
of the chest is used to differentiate large bulla from
pneumothorax (24). When PA radiograph reveals ab-
normalities, it is possible to calculate the actual
pneumothorax size by using the Light index: PTX% =
3
100 Š1-diameter lung /diameter hemitorax ¹, and it may
be useful for research purposes (15). To calculate the
size of a pneumothorax: is to measure the distance bet-
ween the pleural surface and the lung edge (at the level
of the hilum). If this is 2 cm or more, it represents a
large pneumothorax and if it is < 2 cm it is considered
to be a small pneumothorax (24).
COMPLICATIONS
OF PNEUMOTHORAX
These complications include tension pneumoth-
orax, hemopneumothorax, bronchopleural fistula, pne-
umomedistanium,chronic pneumothorax (failure of the
lung to re-expand).
Spontaneous hemopneumothorax
The incidence of pleural effusion is 15 to 20% in
patients with hydropneumothorax.
Approximately 5% of patients with pneumotho-
rax will have concomitant haemothorax with an amount
of blood in the pleural space. The mechanisms of ble-
eding described in SHP are bleeding either of a torn
apical vascular adhesion between the parietal and vis-
ceral pleura or of torn congenital aberrant vessels be-
tween the parietal pleura and the bulla as the lung col-
lapses or due to rupture of vascularized bullae. Mani-
festations depend on the amount of blood lost during
this disorder. Treatment of SHP includes tube thora-
costomy for drainage of the haemothorax and re-expa-
nsion of the lung. If the re-expansion of the lung does
not stop the bleeding, thoracotomy is needed to stop
the bleeding (15) (Figure 7).
Bronchopleural fistula
A bronchopleural fistula may occur in patients wi-
th primary spontaneous pneumothorax (3% to 4%),
Figure 7. Spontaneous hemopneumothorax
in the right lung. Upright radiography
226 Milisavljevic Slobodan, Spasic Marko, Milosevic Bojan

though it is more common in patients with secondary
spontaneous pneumothorax or traumatic pneumotho-
rax. Persistent air leakage occurring after thoracic drai-
nage for pneumothorax is the early clinical sign of this
complication. It can be managed by thoracotomy, clo-
sng the fistula and pleurodesis (15).
Pneumomediastinum
Pneumomediastinum is a rare complication of
pneumothorax (< 1%). It is the presence of free air wi-
thin the mediastinum. Subcutaneous emphysema is of-
ten associated with pneumomediastinum.This entity is
without significant clinical importance. Pneumomedi-
astinum has rarely been reported to cause some serious
complications (esophageal injuries and injuries in the
large airways) (1).
Chronic pneumothorax
(failure of the lung to re-expand)
Chest tubes are used for pneumothorax to promote
lung re-expansion. But in some cases, this procedure
fails.The thickened cortex on the visceral pleura pre-
vents the re-expansion of the lung. Medical procedures
for this condition is thoracotomy and decortication (1).
thorax after the exsufflation is almost the same as the
one after the chest tube drainage (24).
Tube thoracostomy
Tube thoracostomy is the most commonly perfo-
rmed surgical procedure in thoracic surgery.
Thoracostomy tube placement is indicated for the
PSP and symptomatic patients, as well as for the sym-
ptomatic SSP, iatrogenic and traumatic pneumothorax
(24).
The overall objestive of chest-tube therapy is to
promote lung reexpansion. The chest tube is inserted
via an incision at the 4th or 5th intercostals space in the
anterior axillary or mid-axillary line. It can also be in-
serted via 2nd midclavicular intercostal space (Figure
8). It is inserted near the upper border of the rib. There
are three techniques most commonly used to place a
chest tube: using the trocar, associated with a higher
rate of intrathoracic organ injury, blunt dissection after
skin incision (less comfortable but with lower risk of
complications) (Figure 9), or Seldinger technique in
which a guide wire is inserted through the introducer
needle and a chest tube is inserted into the pleural
space. Once the chest tube has been inserted, it must be

TREATMENT
The objective in treating a pneumothorax is to
eliminate the air from the pleural space, to allow lung
to re-expand, and to prevent recurrences. The best me-
thod for achieving this depends on the severity of the
lung collapse, the type of pneumothorax, patient’s ove-
rall health and on the risk of complications.There are
many therapeutic possibilities in clinical practice.

Observation
Observation is recommended for patients with
PSP occupying less than 15% of the hemithorax. As
with these patients, observation remains the first-line Figure 8. Thoracic trocar drainage in the right lung
treatment in patients with pneumothoraces of less than
1 cm depth or isolated apical pneumothoraces (24).
The rate of air absorption is 1, 25% every 24 hours.
Supplemental oxygen can be administered to increase
the rate of pleural air absorption. A small number of pa-
tients is treated this way (15).

Aspiration- exsufflation
Aspiration may be the initial treatment for the pa-
tients with primary pneumothorax. It may also be con-
sidered for patients younger than 50 with secondary
pneumothorax of moderate size (air rim 1–2 cm). Per-
cutaneous needle aspiration results in complete lung
re-expansion in 59 to 83% patients with PSP and in 33
to 67% patients with SSP. Recurrence rate of pneumo- Figure 9. Tube thoracostomy drainage
 PNEUMOTHORAX — DIAGNOSIS AND TREATMENT
connected to either suction or an apparatus to allow
unidirectional drainage (water seal without suction or a
Heimlich valve). If the adequate expansion is achie-
ved, the catheter can be removed (after 5 to 7 days). The
instillation of sclerosing agents (talc) through chest
tubes can help prevent recurrences of pneumothorax (1).
SURGICAL MANAGEMENT
AND PREVENTION OF RECURRENT
PNEUMOTHORACES
Chemical pleurodesis
Chemical pleurodesis is a procedure to achieve
symphysis between the two layers of pleura by sclero-
sing agents. These agents can be introduced into the
pleural space. The therapeutic action of the agent (tet-
racycline or talc) instilled into the pleural cavity thro-
ugh a chest drain is thought to result from induction of
an inflammatory reaction (24).
Surgical management
and mechanical pleurodesis
Surgical management is the common method for
pneumothoraces with persistent air leak (5 to 7 days of
thoracic drainage), the failure of the lung to expand, re-
currence of pneumothorax (ipsilateral or contralateral),
bilateral sponatenous pneumothorax, hemothorax, high
risk professions (air craft personnel, scuba divers). The
objective of surgical management of pneumothorax is
to remove air from the pleural cavity (resection of
blebs) and to prevent recurrence (obliteration of pleu-
ral space). Small posterolateral thoracotomy, transaxi-
llary mini thoracotomy, minimally invasive endosco-
pic surgery (VATS- Video-assisted thoracoscopic sur-
gery) are the most common surgical procedures (24)
(Figure 10). Bullae can be treated with different sur-
gerical procedures- lung resection, stapled excision,
electrocoagulation, suture ligature. To prevent the re-
currence of pneumothorax, resection is combined with
some of the procedures for obliteration of pleural spa-
ce. This procedure may be parietal pleurectomy (parti-
al-apical or total), parietal pleural abrasion (mechanic-
al pleurodesis), chemical pleurodesis (application of
sclerosing agents). Parietal pleurectomy produces ad-
hesion between visceral pleura and endothoracic fas-
cia; pleural abrasion produces adhesions between vi-
sceral and parietal pleura while anatomic layers are
preserved, reducing the risk of thoracoscopy (24).
Open thoracotomy with bullectomy plus pleural abra-
sion or pleurectomy is effective in diminishig the rate
of recurrence (1%). The rate of mortality after the
procedure is low (3,7%). Compared to VATS, after this
treatment the lung function is compromised and the
227
Figure 10. VATS resection of right-sided bullae
Figure 11. Primary spontaneous pneumothorax.
Excision of the bulla using stapler
hospitalization period is longer. In minimally invasive su-
rgery not all blebs may be detected, and the recurrence
rate is higher (5-10%), while hospitalization period is
shorter, post-surgical pulmonary gas exchange is better
and post-surgical pain is not so severe (240 (Figure 11).
CONCLUSION
Pneumothorax is defined as the presence of air in
the pleural space. It is caused by a rupture in visceral or
the parietal pleura.Pnemothoraces can be divided into
spontaneous pneumothoraces and traumatic pneumo-
thoraces. Spontaneous pneumothoraces are further di-
vided into primary and secondary spontaneous pneu-
mothoraces. Traumatic pneumothorax may result from
either blunt trauma or penetrating injury to the chest
wall.It may also be caused by iatrogenic injuries resul-
ting from diagnostic or therapeutic procedures.
The diagnosis of pneumothorax can be establis-
hed from the patients’ history, physical examination
findings and the chest X-ray. Pneumothorax can be
managed conservatively (rest and observation), exsu-
fflation, and chest tube thoracotomy. Recurrent pneu-
mothorax and complications are managed through sur-
gical procedures (thoracotomy or VATS).
Abbreviations
PaO2 — partial pressure of arterial oxygen
PSP — Primary spontaneous pneumothorax
SSP — Secondary spontaneous pneumothorax
COPD — Chronic obstructive pulmonary disease
PCP — Pneumocystis carinii
SHP — Spontaneous hemopneumothorax
VATS — Video-assisted thoracoscopic surgery
228 Milisavljevic Slobodan, Spasic Marko, Milosevic Bojan
Sa`etak
PNEUMOTORAKS — DIJAGNOSTIKA I LE^ENJE
1, 2
Milisavljevi} Slobodan,
1
Klinika za op{tu i grudnu hirurgiju, Klini~ki centar Kragujevac
2
Medicinski fakultet Univerziteta u Kragujevcu, Kragujevac, Srbija
Uvod: Pneumotoraks predstavlja prisustvo vazdu-
ha u pleuralnom prostoru, odnosno prisustvo vazduha
izme|u plu}a i zida grudnog ko{a. U zavisnosti od etio-
logije pneumotoraks se klasifikuje na spontani i trauma-
tski. Spontani pneumotoraks se dalje deli na primarni i
sekundarni. Traumatski pneumotoraks nastaje kao po-
sledica tupih ili penetrantnih povreda grudnog ko{a, ili
nakon jatrogenih povreda. Recidivantni pneumotoraks
se javlja kao ponovljeni spontani pneumotoraks.
Cilj rada: Prikaz savremene dijagnostike i na~ina
hirur{kog le~enja kod pacijenata sa pneumotoraksom.
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Ponn RB, Rusch VW, editors. General Thoracic Surgery. 6th ed.
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6. West JB. Distribution of mechanical stress in the lung, a
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inheritance of primary spontaneous pneumothorax. Am J Med
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JM. Computed tomography in the aetiological assessment of idi-
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Correspondence to/Autor za korespondenciju
Prof dr Milisavljevi} Slobodan
General and Thoracic Surgery Clinic, Clinical Centre Kragujevac
Phone: 034/505315
e-mail: s.milisavljevic65ªgmail.com
2 2
Spasi} Marko, Milo{evi} Bojan
Metodologija: Ovo je pregledni ~lanak. Kori{}e-
na je literatura uvidom u bazu medicinskih podataka
Medline i Pubmed.
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traumatski predstavlja hitno stanje u medicini i zahteva
brzu i neodlo`nu intervenciju lekara, kako bi se fun-
kcija plu}a {to pre normalizovala i o~uvao `ivot
vitalno ugro`enom pacijentu.
Klju~ne re~i: pneumotoraks, grudna drena`a, to-
rakotomija.
12. Noppen M: Con: blebs are not the cause of primary
spontaneous pneumothorax. J Bronchol and Interv. Pulmology.
2002; 9(4): 319–25.
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tion. 2008; 76(2): 121–7.
14. Sadikot RT, Greene T, Meadows K, Arnold AG. Recur-
rence of primary pneumothorax. Thorax. 1997; 52(9): 805–9.
15. Mason RJ, Broaddus VC, Murray JF, Nadel JA, edi-
tors. Murray and Nadel’s Textbook of Respiratory medicine. 4th
ed. Philadelphia: Elsevier Saunders; 2005.
16. Seremetis MG: The management of spontaneous pneu-
mothorax. Chest. 1970; 57(1): 65–8.
17. Lippert HL, Lund O, Blegvad S, Larsen HV. Indepen-
dent risk factors for cumulative recurrence rate after first sponta-
neous pneumothorax. Eur Respir J. 1991; 4(3): 324–31.
18. Peikert T, Gillespie DJ, Cassivi SD. Catamenial pneu-
mothorax. Mayo Clin. Proc. 2005; 80(5): 677–80.
19. Alifano M, Roth T, Broet SC, Schussler O, Magdelei-
nat P, Regnard JF.Catamenial pneumothorax: a prospective
study. Chest. 2003; 124(3): 1004–8.
20. Joseph J, Sahn SA. Thoracic endometriosis syndrome:
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1996; 100(2): 164–70.
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R, Riquet M. Catamenial pneumothorax: retrospective study of
surgical treatment. Ann Thorac Surg. 2003; 75(2): 378–81.
22. Di Bartolomeo S, Sanson G, Nardi G, Scian F, Miche-
lutto V, Lattuada L. A population-based study on pneumothorax
in severely traumatized patients. J Trauma. 2001; 51(4): 677–82.
23. Feliciano DV, Mattox KL, Moore EE, editors. Trauma.
6th ed. New York: McGraw-Hill; 2008.
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management of spontaneous pneumothorax Thorax. 2003;
58(suppl 2): 1139–52.
 IDENTIFIKASI AWAL DAN BANTUAN HIDUP DASAR PADA
PNEUMOTORAKS
I Wayan Ade Punarbawa1, Putu Pramana Suarjaya2
1,2
Bagian /SMF Ilmu Anestesiologi dan Terapi Intensif, Fakultas Kedokteran, Universitas
Udayana/Rumah Sakit Umum Pusat Sanglah Denpasar

ABSTRAK

Cedera dada merupakan salah satu trauma yang sering terjadi dan perlu penanganan yang
segera dan tepat sehingga menghindarkan penderita dari kematian. Kejadian trauma dada 1/4
dari kejadian trauma yang menyebabkan kematian dan 1/3 dari kematian yang terjadi di rumah
sakit. Salah satu cedera dada yang sering kita dapatkan pada pusat pelayanan kesehatan adalah
pneumotoraks. WHO menyatakan pada tahun 2020 tingkat morbiditas dan mortalitas dari cedera
dada akan meningkat, hingga menjadi penyebab kedua kematian didunia. Dari data itu perlunya
mengetahui tanda dan gejala dari peneumotoraks, mengidentifikasi tanda dan gejalanya
sehingga kita dapat memberikan bantuan hidup dasar pada penderita, sebelum penderita dirujuk
ke pusat pelayanan medis terdekat sehingga dapat menurunkan tingkat morbiditas dan
mortalitas pada penderita pneumotoraks.

Kata kunci: identifikasi awal, pneumotoraks, bantuan hidup dasar

EARLY IDENTIFICATION AND BASIC LIFE SUPPORT FOR

PNEUMOTHORAX
ABSTRACT

Chest injury is one injury that often occurs and need immediate and precise handling that
prevent people from death. Chest trauma 1/4 of the trauma that caused the death and 1/3 of
those deaths occur in hospitals. One chest injury that often we get to the health center is
pneumothorax. WHO declared in 2020 the level of morbidity and mortality from chest injuries
will increase, to become the second leading cause of death in the world. From this data that need
to know the signs and symptoms of peneumotoraks, identify the signs and symptoms so we can
provide basic life support to the patient before the patient was referred to a medical center
nearby so as to reduce the morbidity and mortality in patients with pneumothorax.

Keyword: early identification, pneumothorax, basic life support

1
PENDAHULUAN

Kejadian cedera dada merupakan salah satu trauma yang sering terjadi, jika tidak

ditangani dengan benar akan menyebabkan kematian1,2, kejadian trauma dada terjadi

sekitar seperempat dari jumlah kematian akibat trauma yang terjadi, serta sekitar

sepertiga dari kematian yang terjadi berbagai rumah sakit3. Beberapa cedera dada yang

dapat terjadi antara lain, tension pneumothoraks, pneumotoraks terbuka, flail chest,

hematotoraks, tamponade jantung3,4,5. Kecelakaan kendaraan bermotor paling sering

menyebabkan terjadinya trauma pada toraks. Tingkat morbiditas mortalitas akan

meningkat dan menjadi penyebab kematian kedua didunia pada tahun 2020 menurut

WHO (Word Health Organitation).3 Pneumotoraks merupakan suatu cedera dada yang

umum di temukan pada kejadian trauma diluar rumah sakit, serta merupakan kegawat

daruratan yang harus di berikan penanganan secepat mungkin untuk menghindari dari

kematian3,4,5,6,7,8. Insiden pneumotoraks tidak diketahui secara pasti dipopulasi,

dikarenakan pada literatur literatur, angka insidennya di masukan pada insiden cedera

dada atau trauma dada. Sebuah penelitian mengatakan 5,4% dari seluruh pasien

menderita trauma, merupakan pasien yang mengalami pneumotoraks. 9 Kurangnya

pengetahuan untuk mengetahui tanda dan gejala dari pneumotoraks terdesak

menyebabkan banyak penderita meninggal setelah atau dalam perjalanan menuju

kerumah sakit.6 Sebenarnya penanganan pneumotoraks terdesak dapat dilakukan

dengan bantuan hidup dasar tanpa memerlukan tindakan pembedahan, sebelum

mengirim pasien ke pusat pelayanan medis terdekat, sehingga disini diperlukan

pengatuhan untuk identifikasi awal dari gejala pneuomotoraks terdesak, memberikan

bantuan hidup dasar, dan mengirimnya ke tempat pelayanan medis terdekat, untuk

mengurangi tingkat mobiditas dan mortalitas.3,4,8

2
DEFINISI

Pneumotoraks adalah suatu keadaan dimana terdapatnya udara pada rongga potensial

diantara pleura visceral dan pleura parietal1,2,3. Pada keadaan normal rongga pleura di

penuhi oleh paru – paru yang mengembang pada saat inspirasi disebabkan karena

adanya tegangan permukaaan ( tekanan negatif ) antara kedua permukaan pleura,

adanya udara pada rongga potensial di antara pleura visceral dan pleura parietal

menyebabkan paru-paru terdesak sesuai dengan jumlah udara yang masuk kedalam

rongga pleura tersebut, semakin banyak udara yang masuk kedalam rongga pleura akan

menyebabkan paru –paru menjadi kolaps karena terdesak akibat udara yang masuk

meningkat tekanan pada intrapleura.4,5

Secara otomatis terjadi juga gangguan pada proses perfusi oksigen kejaringan atau

organ, akibat darah yang menuju kedalam paru yang kolaps tidak mengalami proses

ventilasi, sehingga proses oksigenasi tidak terjadi. 1,2

PATOFISIOLOGI

Rongga dada mempunyai dua struktur yang penting dan digunakan untuk melakukan

proses ventilasi dan oksigenasi, yaitu pertama tulang, tulang – tulang yang menyusun

struktur pernapasan seperti tulang klafikula, sternum, scapula. Kemudian yang kedua

adalah otot-otot pernapasan yang sangat berperan pada proses inspirasi dan ekspirasi 6 .

Jika salah satu dari dua struktur tersebut mengalami kerusakan, akan berpengaruh pada

proses ventilasi dan oksigenasi. contoh kasusnya, adanya fraktur pada tulang iga atau

tulang rangka akibat kecelakaan, sehingga bisa terjadi keadaaan flail chest atau

kerusakan pada otot pernapasan akibat trauma tumpul, serta adanya kerusakan pada

organ viseral pernapasan seperti, paru-paru, jantung, pembuluh darah dan organ lainnya

3
di abdominal bagian atas, baik itu disebabkan oleh trauma tumpul, tajam, akibat

senapan atau gunshot.6,8

Tekanan intrapleura adalah negatif, pada proses respirasi, udara tidak akan dapat masuk

kedalam rongga pleura. Jumlah dari keseluruhan tekanan parsial dari udara pada kapiler

pembuluh darah rata-rata (706 mmHg). Pergerakan udara dari kapiler pembuluh darah

ke rongga pleura, memerlukan tekanan pleura lebih rendah dari -54 mmHg (-36

cmH2O) yang sangat sulit terjadi pada keadaan normal. Jadi yang menyebabkan

masuknya udara pada rongga pleura adalah akibat trauma yang mengenai dinding dada

dan merobek pleura parietal atau visceral, atau disebabkan kelainan konginetal adanya

bula pada subpleura yang akan pecah jika terjadi peningkatan tekanan pleura.7,8

KLASIFIKASI DARI PNEUMOTORAKS

Beberapa literatur menyebutkan klasifikasi pneumothoraks menjadi 2 yaitu,

pneumotoraks spontan dan pneumotoraks traumatik4. Ada juga yang

mengklasifikasikannya berdasarkan etiloginya seperti Spontan pneumotoraks (spontan

pneumotoraks primer dan spontan pneumotoraks sekunder), pneumotoraks traumatik,

iatrogenik pneumotoraks. serta ada juga yang mengklasifikasinya berdasarkan

mekanisme terjadinya yaitu, pneumotoraks terbuka (open pneumotoraks), dan

pneumotoraks terdesak (tension pneumotoraks ). 5

Seperti dikatakan diatas pneumotoraks dapat diklasifikasikan sesuai dengan dasar

etiologinya seperti Spontan pneumotoraks, dibagi menjadi 2 yaitu, Spontan

Pneumotoraks primer (primery spontane pneumothorax) dan Spontan Pneumotoraks

4
Sekunder (secondary spontane pneumothorax), pneumotoraks trauma, iatrogenik

pneumotoraks. 4,5

Pneumotoraks Spontan Primer ( primery spontaneous pneumothorax)

Dari kata “primer” ini dapat diketahui penyebab dari pneumotoraks belum diketahui

secara pasti, banyak penelitian dan terori telah di kemukakan untuk mencoba

menjelaskan tentang apa sebenarnya penyebab dasar dari tipe pneumotoraks ini. Ada

teori yang menyebutkan, disebabkan oleh factor konginetal, yaitu terdapatnya bula pada

subpleura viseral, yang suatu saat akan pecah akibat tingginya tekanan intra pleura,

sehingga menyebabkan terjadinya pneumotoraks.4

Bula subpleura ini dikatakan paling sering terdapat pada bagian apeks paru dan juga

pada percabangan trakeobronkial. Pendapat lain mengatakan bahwa PSP ini bisa

disebabkan oleh kebiasaan merokok. Diduga merokok dapat menyebabkan

ketidakseimbangan dari protease, antioksidan ini menyebabkan degradasi dan lemahnya

serat elastis dari paru-paru, serta banyak penyebab lain yang kiranya dapat

membuktikan penyebab dari pneumotoraks spontan primer.4,7

Pneumotoraks Spontan Sekunder ( Secondary Spontaneus Pneumothorax)

Pneumotoraks spontan sekunder merupakan suatu pneumotoraks yang penyebabnya

sangat berhubungan dengan penyakit paru-paru, banyak penyakit paru-paru yang

dikatakan sebagai penyebab dasar terjadinya pneumotoraks tipe ini. Chronic

Obstructive Pulmonary Disease (COPD), infeksi yang disebabkan oleh bakteri

pneumocity carinii, adanya keadaan immunocompremise yang disebabkan oleh infeksi

5
virus HIV, serta banyak penyebab lainnya, disebutkan penderita pneumotoraks tipe ini

berumur diantara 60-65 tahun .4,7

Pneumotoraks Trauma

Pneumotoraks trauma adalah pneumotoraks yang disebabkan oleh trauma yang secara

langsung mengenai dinding dada, bisa disebabkan oleh benda tajam seperti pisau,atau

pedang, dan juga bisa disebabkan oleh benda tumpul.3

Mekanisme terjadinya pneumotoraks trauma tumpul, akibat terjadinya peningkatan

tekanan pada alveolar secara mendadak, sehingga menyebabkan alveolar menjadi ruptur

akibat kompresi yang ditimbulkan oleh trauma tumpul tersebut, pecahnya alveolar akan

menyebabkan udara menumpuk pada pleura visceral, menumpuknya udara terus

menerus akan menyebabkan pleura visceral rupture atau robek sehingga menimbulkan

pneumotorak.3,4

Jika pada mekanisme terjadinya pneumotoraks pada trauma tajam disebabkan oleh

penetrasi benda tajam tersebut pada dinding dada dan merobek pleura parietal dan udara

masuk melalui luka tersebut ke dalam rongga pleura sehingga terjadi pneumotoraks.4

Iatrogenik Pneumotoraks

Banyak penyebab yang dilaporkan mendasari terjadinya pneumotoraks iatrogenic,

penyebab paling sering dikatakan pemasangan thransthoracic needle biopsy.

Dilaporkan juga kanalisasi sentral dapat menjadi salah satu penyebabnya. 4 Pada

dasarnya dikatakan ada dua hal yang menjadi faktor resiko yang menyebabkan

terjadinya pneumotoraks iatrogenic yaitu pertama adalah dalamnya pemasukan jarum

6
pada saat memasukannya dan kedua, ukuran jarum yang kecil, menurut sebuah

penelitian kedua itu memiliki korelasi yang kuat terjadinya pneumotoraks.3,4.

Berdasarkan mekanisme dari terjadinya pneumotoraks dapat diklasifikasikan menjadi

pneumotoraks terdesak (tension pneumotoraks), dan pneumutoraks terbuka (open

pneumothorax),

Pneumotoraks Terdesak (Tension Pneumothorax)

Suatu pneumotoraks yang merupakan salah satu kegawat daruratan pada cedera dada.

Keadaan ini terjadi akibat kerusakan yang menyebabkan udara masuk kedalam rongga

pleura dan udara tersebut tidak dapat keluar, keadaan ini disebut dengan fenomena

ventil ( one –way-valve).1,3,5,9

Akibat udara yang terjebak didalam rongga pleura ssehingga menyebabkan tekanan

intrapleura meningkat akibatnya terjadi kolaps pada paru-paru, hingga menggeser

mediastinum ke bagian paru-paru kontralateral, penekanan pada aliran vena balik

sehingga terjadi hipoksia.1,3

Banyak literatur masih memperdebatkan efek dari pneumotoraks dapat menyebabkan

terjadinya kolaps pada sistem kardiovaskular. Dikatakan adanya pergeseran pada

mediastinum menyebabkan juga penekanan pada vena kava anterior dan superior,

disebutkan juga hipoksia juga menjadi dasar penyebabnya, hipoksia yang memburuk

menyebabkan terjadinya resitensi terhadap vaskular dari paru-paru yang diakibatkan

oleh vasokonstriksi. Jika gejala hipoksia tidak ditangani secepatnya, hipoksia ini akan

mengarah pada keadaan asidosis, kemudian disusul dengan menurunnya cardiac output

sampai akhirnya terjadi keadaan henti jantung.3,5,9

7
Pneumotoraks Terbuka (Open Pneumothoraks)

Keadaan pneumotoraks terbuka ini tersering disebabkan oleh adanya penetrasi langsung

dari benda tajam pada dinding dada penderita sehingga meninmbulkan luka atau defek

pada dinding dada. Dengan adanya defek tersebut yang merobek pleura parietal,

sehingga udara dapat masuk kedalam rongga pleura. Terjadinya hubungan antara udara

pada rongga pleura dan udara dilingkungan luar, sehingga menyebabkan samanya

tekanan pada rongga pleura dengan udara di diatmosper. Jika ini didiamkan akan sangat

membahayakan pada penderita. Dikatakan pada beberapa literatur jika sebuah defek

atau perlukaan pada dinding dada lebih besar 2/3 dari diameter trakea ini akan

menyebabkan udara akan masuk melalui perlukaan ini, disebabkan tekana yang lebih

kecil dari trakea. Akibat masuknya udara lingkungan luar kedalam rongga pleura ini,

berlangsung lama kolaps paru tak terhindarkan, dan berlanjut gangguan ventilasi dan

perfusi oksigen kejaringan berkurang sehingga menyebabkan sianosis sampai distress

respirasi.1,6

IDENTIFIKASI AWAL

Identifikasi awal tentang gejala pneumotorak sangat diperlukan untuk memberikan

bantuan hidup dasar pada pasien pneumotoraks. Karena penanganan awal yang tepat

pada penderita pneumotoraks sangatlah penting untuk mencegah terjadi kematian.

Dikatakan pada sebuah penelitian penanganan awal pada 85 % penderita pneumotorak

dapat ditangani dengan menggunakan manover bantuan hidup dasar tanpa memerlukan

tindakan pembedahan.6

Untuk mengidentifikasi gejala pnemutoraks, terlebih dahulu kita harus mengetahui

manifestasi klinis dan kriteria diagnosis dari pneumotoraks. Pertama kita melihat

8
penyebab dari terjadinya pneumotoraks untuk mengetahui tipe-tipe pneumotoraks apa

yang kemungkinan terjadi ada penderita. Diluar rumah sakit mungkin kita akan

menemukan lebih banyak kejadian pneumotoraks yang diakibatkan oleh terjadinya

trauma, trauma yang terjadi bisa secara langsung melukai dinding dada atau pun secara

tidak langsung. Penyebab tersering dari pneumotoraks yang bisa didapatkan akibat

kecelakaan lalu lintas, akibat tingginya kecepatan kendaraan bermotor mengakibatkan

resiko terjadinya kecelakaa semakin, sehingga trauma yang terjadi akan semakin parah.

Jika kita menemukan penderita ditempat kejadian, identifikasi terlebih dahulu. Akibat

benturan yang keras terhadap dinding dada penderita akan mengeluhkan nyeri pada

dinding dadanya. Disamping itu dilihat juga apakah ada atau tidak perlukaan yang

terjadi pada dinding dada, untuk mengetahui apakah terdapat luka terbuka pada dinding

dada penderita yang bisa menimbulkan pneumotoraks terbuka. Sesak napas akan terjadi

pada penderita pneumotoraks akibat udara yang mulai masuk mengisi rongga pleura.

Jika terus berlanjut penderita akan terlihat gelisah akibat kesulitan bernapas. Usaha dari

tubuh untuk mengkompensasi akibat sesak napas yang terjadi adalah bernapas yang

cepat (takipneu) dan denyut nadi yang meningkat (takikardia). Udara yang masuk

kedalam rongga pleura ini akan menyebakan terjadi pendesakan pada parenkim paru-

paru hingga menjadi kolaps, jadi yang mengisi rongga dada yang mengalami

pneumotoraks adalah udara, pada saat diperiksa dengan mengetuk dinding dada akan

terdengar suara hipersonor, akibat akumulasi udara pada rongga pleura. Kolapsnya

paru-paru yang terdesak oleh udara yang berada di rongga pleura ini menyebabkan

proses ventilasi dan oksigenasi berkurang atau malah tidak terjadi, sehingga jika

didengarkan dengan stetoskop suara napas tidak terdengar.3,5

9
Keadaan diatas akan bertambah parah jika tidak ditangani secara cepat dan tepat.

Penurunan kesadaran akan terjadi akibat perfusi oksigen ke otak yang menurun

(hipoksia). Penumpukan udara yang semakin banyak disana menyebabkan terjadinya

pendorongan pada mediastinum dan trakea kearah kontra lateral dari paru-paru yang

kolaps. Terjadinya pendesakan pada mediastinum juga menyebabkan hambatan pada

aliran vena balik, sehingga terjadi distensi pada vena dileher, dan hipotensi. Semakin

lama gejala ini berlangsung penderita akan jatuh fase sianosis.2,3,5

BANTUAN HIDUP DASAR (BASIC LIFE SUPPORT)

Bantuan hidup dasar merupakan suatu tindakan atau penatalaksanaan awal yang dapat

dilakukan pada saat kita menemukan korban diluar rumah sakit. Penanganan bantuan

hidup dasar ini bertujuan untuk dapat mengembalikan atau mempertahankan oksigenasi

pada korban. Bantuan hidup dasar ini digunakan untuk mempertahankan aliran napas

(airway), memberikan bantuan pernapasan (breathing), dan evaluasi dari sistem

sirkulasi darah (circulation) apakah sudah cukup untuk memberikan perfusi oksigen

yang adequat keseluruh jaringan.10.11

Tahapan-tahapan dari pemberian bantuan hidup dasar kepada korban, jika kita

menemukan seorang korban dijalan atau dimanapun, pertama jika sendiri mintalah

pertolongan dari orang-orang sekitar, serta menghubungi pelayanan kesehatan terdekat.

Sebelum kita menolong korban pastikan diri kita sendiri aman dari lingkungan sekitar,

agar kita tidak menjadi korban selanjutnya. Kemudian setelah meminta pertolongan

kepada orang disekitar barulah kita mendekati korban. Penilaian awal yang dilakukan,

mengevaluasi kesadaran korban dengan memberikan rangsangan suara, seperti

memanggil sambil menepuk-nepuk bahu korban, jika tidak berespon kita berikan

10
rangsangan nyeri seperti cubitan. Jika berespon segera pindahkan pasien ketempat yang

lebih aman. Setelah memberikan rangsangan suara dan nyeri pasien tidak berespon,

pertama kita lihat aliran napasnya (airway) dengan menggunakan manuver head tilt,

menaruh tangan didahi korban kemudian mendorongnya kebelakang, dan chin lift,

mengangkat dagu korban kedua gerakan ini dilakukan secara simultan dan gentle.

Setelah itu kita evaluasi hembusan napas dan apakah terdengar suara napas tambahan

seperti mengorok. Dilihat apa terdapat benda asing pada jalan napas yang menghambat

jalan napas seperti, sisa makanan, lidah yang terjatuh kebelakang, cairan atau darah, jika

terdapat sumbatan kita bersihkan atau hilang benda asing itu dari jalan napas. Jika

korban dicurigai adanya trauma pada leher (cervical) kita gunakan manuver jaw thrus,

yaitu menempatkan dua atau tiga jari pada sudut kedua mandibular kemudian

mengangkatnya keatas dan kedepan. 10,11

Setelah (airway) jalan napas sudah lapang, kemudian kita menilai pernapasan

(breathing), disini kita mengevaluasi dari pergerakan dada korban yang naik turun,

adakah pergerakan dada yang tertingal (asimetris), pergerakan dada yang cepat dan

terdapat retraksi dari otot-otot pernapasan, atau pergerakan dada yang tidak ada. Jika

tidak ada pergerakan dada, kita lakukan pemberian napas bantuan sebanyak dua kali

kepada korban, secara mulut kemulut, 1 kali napas bantuan dalan satu detik. Pada saat

memberi napas bantuan tutup hidung pasien dengan mempertahankan maneuver head

tilt dan chin lift.11 Tujuan dari pemberian napas bantuan ini untuk memberikan napas

pancingan kepada korban yang henti napas, karena penyebab utama terjadinya kesulitan

bernapas adalah kurang lapangnya jalan napas.10

Pada pemberian dua kali napas bantuan, juga tidak berhasil, kita lanjutkan pada evaluasi

dari sirkulasi korban (circulation). Disini kita evaluasi sirkulasi dengan meraba nadi

11
karotis, brakialis, atau femoralis, dievalusi selama 10 detik.11 jika denyut nadi teraba

spontan kita lanjutkan pemberian napas bantuan, satu napas batuan diberikan setiap 5-6

detik, jadi pada satu menit deberikan 10 sampai 12 kali napas buatan.10 jika pada

perabaan tidak teraba denyut nadi dari korban kita langsung melakukan kompresi

(cardiopulmonary resuscitation). Kompresi dilakukan pada sternum, tepatnya dua atau

tiga jari diatas taju pedang (proccesus cipoideus). Kita taruh telapak tangan kita yang

lebih kuat pada titik kompresi dengan tangan yang lain diletakkan diatas tangan yang

menjadi tumpuan, tujannya agar sebagai pengunci, supaya tidak bergeser pada saat

melakukan kompresi. Kompresi dilakukan sebanyak 30 : 2 yaitu, 30 kali kompresi

diselingi dengan pemberian napas bantuan sebanyak 2 kali. Kompresi ini bertujuan

untuk meningkatkan oksigenasi ke jaringan dan mengeluarkan CO2 .10 Kompresi Ini

dilakukan sampai adanya tanda-tanda kehidupan, dating pengganti untuk melakukan

kompresi, ponolong kelelahan, datang petugas medis yang telah dihubungi. 10,11

Fokus utama untuk menilai bagaimana tanda dan gejala klinis dari pneumotoraks serta

untuk memberikan bantuan hidup dasar pada korban di tempat korban tersebut

ditemukan, sebelum membawa korban ke pusat pelayanan medis terdekat.11,12

Pemberian bantuan hidup dasar pada korban yang menderita pneumotoraks secara garis

besar termasuk dalam pemberian bantuan hidup dasar pada penderita trauma dada. Pada

trauma dada ada 3 faktor penyebab yang menyebabkan nyawa korban terancam yaitu,

perdarahan, penurunan cardiac output, dan distress pernapasan. Pada perdarahan sangat

sulit untuk diidentifikasi, akibat trauma tumpul atau trauma tajam yang mengenai

pembuluh darah pada rongga toraks. Penurunan cardiac output mungkin diakibatkan

penekananan yang disebabkan oleh udara yang menumpuk pada rongga pleura dan

12
mendesak mediastinum sehingga menekan dari cabang vena cava, penurunan dari

aliran darah balik vena sehingga cardiac output menurun.3,5,12

Distress respirasi disebabkan oleh desakan dari penumpukan udara pada rongga pleura

sehingga paru-paru yang terdesak akan menjadi kolaps. Penderita dengan dengan

trauma dada, fokus utama yang kita perhatikan pada breathing, gejala harus dapat

ditangani pada awal penilaian.12

Bantuan hidup dasar yang diberikan, pertama, melihat lapang tidaknya jalan napas

(airway), dengan melakukan manuver head tilt, chin lift, dan jaw thrus jika korban

dicurigai mengalami cedera cervical. Disini dilihat apakah ada sumbatan jalan napas,

yang diakibatkan oleh trauma, dilihat pergerakan napas korban ada atau tidak, terdapat

sumbatan atau tidak dari jalan napas korban seperti benda asing atau cairan, sehingga
3,11
sumbatan jalan napas dari benda asing dapat dihilangkan Setelah itu kita berlanjut

pada breathing, disini kita evaluasi dari pergerakan dada korban apakah simetris atau

tidak, kita lihat juga distensi dari pembuluh darah vena pada leher, luka yang terbuka,

penderita biasanya akan terlihat gelisah akibat kesulitan bernapas. Dari gejala –

gejalanya kemungkinan mengarah ke pneumotoraks terdesak (tension pneumothorax)

yang merupakan suatu kegawat daruratan pada trauma dada. Pemberian oksigen terapi

sangat diperlukan pada keadaan ini, karena pemberian terapi oksigen 100% dapat

meningkatkan absropsi udara pada pleura, oksigen terapi 100% diberikan untuk

menurunkan tekanan alveolar terhadap nitrogen, sehingga nitrogen dapat dikeluarkan

dan oksigen dapat masuk melalui sistem vaskular, terjadi perbedaan tekanan antara

pembuluh kapiler jaringan dengan udara pada rongga pleura, sehingga terjadi

peningkatan absorpsi dari udara pada rongga pleura.3,5,8,9 Kemudian penanganan dengan

jarum dekompresi yang dilakukan pada intercostal 2 pada garis midklavikula, ini

13
merupakan metode konvensional. Pada literatur American College Of Chest Physician

(ACCP) dan British Thoracic Society (BTS) dekompersi dapat dilakukan pada

intercosta 5 pada garis anterior aksila.3,4,8 Pengunaan pipa torakostomi digunakan pada

pneumotoraks dengan gejala klinis sulit bernapsa yang sangat berat, nyeri dada,

hipoksia dan gagalnya pemasangan jarum aspirasi dekompresi. Pada penggunaannya

Pipa torakostomi disambungkan dengan alat yang disebut WSD (water seal drainage).

WSD mempunyai 2 komponen dasar yaitu, ruang water seal yang berfungsi sebagai

katup satu arah berisi pipa yang ditenggelamkan dibawah air, untuk mencegah air

masuk kedalam pipa pada tekanan negatif rongga pleura. dan ruang pengendali suction.

WSD dilepaskan bila paru-paru sudah mengembang maksimal dan kebocoran udara

sudah tidak ada.3,4 Pada sirkulasi (circulation) kita menilainya dengan meraba denyut

nadi, untuk mengevaluasi kemungkinan tanda-tanda syok pada korban (denyut nadi

cepat dan lemah, akral dingin, laju pernafasan dll) jika denyut nadi tidak teraba

langsung berikan kompresi sebanyak 30 kali dengan memberikan 2 kali napas

bantuan.11,12 Pemberian terapi cairan secara intravena dilakukan untuk resusitasi awal

pada penderita pneumotoraks dengan keadaan syok, dengan pemasangan kateter

intravena ukuran besar (minimum 16 gauge) dengan pemberian larutan elektrolit

isotonik, untuk menstabilkan volume vasukuler dengan mengganti cairan pada ruang

interstisial dan intraseluler1.

Pada pneumotorak terbuka, yang terdapat luka yang menganga pada dinding dada dan

udara masuk melalui perlukaan tersebut. Penanganan awal yang dapat kita lakukan

adalah tutup luka tersebut dengan menggunakan gaas steril ataupun kain yang bersih

yang ditutup pada tiga sisinya. Fungsi dari penutup ini sebagai katup, udara dapat keluar

melaluin luka, tetapi tidak dapat masuk melalui luka tersebut. Karena jika kita tutup

14
pada ke empat sisinya, pneumotoraks terbuka ini akan berubah menjadi pneumotoraks

terdesak, akibat udara yang masuk tidak dapat keluar, dan terperangkap di rongga

pleura.3,4,6,7,8

15
RINGKASAN

Trauma dada merupakan salah satu kejadian trauma yang sring terjadi dan bila tidak

mendapat penanganan secara tepat dan cepat akan menyebabkan kematian. Dikatakan

pada tahun 2020 menurut WHO trauma dada akan menjadi penyebab mortalitas dan

morbiditas kedua didunia. Pneumotoraks adalah salah satu dari trauma dada yang akan

sering ditemukan pada pusat pelayanan medis. Pneumotoraks didefinisikan sebgagai

suatu keadaan dimana adanya udara pada rongga potensial antara pleura visceral dan

parietal. Pada jenis – jenis pneumotoraks dapat diklasifikasikan berdasarkan etiologi,

mekanisme terjadinya dan akibat trauma atau non trauma. Penanganan atau identifikasi

awal sangat penting untuk dilakukan mengetahui tanda dan gejala awal dari

pneumototaks. Identifikasi awal dari pneumotoraks yang dapat kita lihat dari tanda dan

gejalanya. Pada awal terjadinya pneumotoraks seperti, nyeri dada, sesak napas, gelisah,

takipneu, takikardia, pergerakan dada yang asimetris, hipersonor pada saat kita

melakukan pemeriksaan dada, dan menghilangnya suara napas pada paru yang

mengalami pneumotoraks. Dan tanda dan gejala lanjut yang terjadi seperti, penurunan

kesadaran, deviasi trakea kearah kontralateral, hipotensi, adanya distensi dari vena

leher, sianosis. Semua gejala diatas sangat tergantung dari seberapa banyak udara yang

terperangkap pada rongga pleura. Pemberian bantuan hidup dasar pada penderita sangat

penting dilakukan untuk mengurangi angka morbiditas dan mortalitas. Bantuan hidup

dasar diberikan seperti penatalaksanaan trauma dada pada umumnya airway, breathing,

dan circulation. Ada tiga fokus utama yang perlu diperhatikan pada pemberian hidup

dasar pada pneumotorak yaitu, distress pernapasan, penurunan cardiac output, dan

perdarahan. Prioritas utama pada penanganan pneumotoraks sebernarnya sangat

diperhatikan pada breathing penderita.

16
DAFTAR PUSTAKA

1. American College Of Surgeons Committee On Trauma, Student Course Manual 7th

Edition : advanced Trauma Life Support for Doctors : Bab 5 Trauma Thoraks: 111-

127.

2. De jong W., Sjamsuhidajat R., Karnadihardja W. Prasetyono T.O, Rudiman R. :

Buku Ajar Ilmu Bedah; Bab 28: 498-513

3. Sharma A, Jindal P : Priciples of diagnosis and management of traumatic

pneumothorax. 2008 ; 34 – 40

4. Idress M.M, Ingleby A.M, Wali S.O : Evalution and Managemet of Pneumothorax.

Saudi Med J 2003; vol.24(5):447 – 452

5. Jain D.G, Gosari S.N, Jain D.D : Understanding and Managing Tension

Pneumothorax. JIACN 2008; 9(1) : 42 – 50

6. Anonim. Europan course trauma care thoracic trauma; cited 24 November 2012

available at www.cdu.dc.med.unipi.it/ectc/ethoma.htm

7. Noppen M, Keukeleire T.D : Pneumothorax. Respiration 2008; 76 :121 – 127

8. Currie G.P, Alluri R, Christie G.L, Legge J.S : Pneumothorax : an update. Post

Med J 2007 ; 83 : 461- 465

9. Leigh-smith S, Harris T : Tension pneumothorax – time for a re-think ?. Emerg

Med J 2005;22:8-16.doi: 10.1136/emj.2003.010421.

10. Berg RA, Hemphill R, Abella BS, Aufderheide TP, Cave DM, Hazinski MF,

Lerner EB, Rea TD, Sayre MR, Swor RA. Adult Basic Life Support: 2010

American Heart Association Guidelines for Cardiopulmonary Resuscitation and

Emergency Cardiovascular Care. 2010;122(suppl 3):S685–S705.

11. Handley A.J : Basic Life Support ; British Journal Of Anesthesia 1997; 79: 151-158

17
12. Section of Injury Prevention and EMS Division of Public Health Department of

Health and Social Services: Prehospital Trauma Guidelines For Micps In Alaska,

January, 2007; 10-11 Juneau, AK 99811-0616

18
 Full text online at www.onlinejets.org

Practitioner Section

Principles of diagnosis and management of

traumatic pneumothorax
Anita Sharma1, Parul Jindal1
1
Departments of Postgraduate Medicine and Anaesthesiology, Himalayan Institute of Medical Sciences, Dehradun, Uttarakhand, India

ABSTRACT
Presence of air and fluid with in the chest might have been documented as early as Fifth Century B.C. by a physician in ancient
Greece, who practiced the so-called Hippocratic succession of the chest. This is due to a development of communication
between intrapulmonary air space and pleural space, or through the chest wall between the atmosphere and pleural space.
Air enters the pleural space until the pressure gradient is eliminated or the communication is closed. Increasing incidence of
road traffic accidents, increasing awareness of healthcare leading to more advanced diagnostic procedures, and increasing
number of admissions in intensive care units are responsible for traumatic (noniatrogenic and iatrogenic) pneumothorax.
Clinical spectrum of pneumothorax varies from asymptomatic patient to life-threatening situations. Diagnosis is usually made
by clinical examination. Simple erect chest radiograph is sufficient though; many investigations are useful in accessing the
future line of action. However, in certain life-threatening conditions obtaining imaging studies can causes an unnecessary
and potential lethal delay in treatment.

Key Words: Diagnosis and management, pneumothorax, trauma

Trauma kills approximately 150,000 people each year and is a
primary public health concern.[1] Motor vehicle accidents are
the most common cause of severe injury and the World Health
Organization estimates that by 2020 vehicular injury will be
the second most common cause of mortality and morbidity
worldwide. According to the most recent data, more than 10%
of traumas and accidents terminate in a lethal outcome or a
heavy degree of physical inability.[2] Thoracic trauma accounts
for one-quarter of trauma deaths, and two-thirds of these deaths
occur after the patient reaches hospital.[3] The main problem
is collection of air in the pleural cavity causing shift of the
mediastinum leading to life-threatening emergency. Promptly
recognizing this condition saves lives, both outside the hospital
and in a modern intensive care unit (ICU). Because this condition
occurs infrequently and has potentially devastating effects, a high
index of suspicion and knowledge of basic emergency thoracic
decompression are important for all healthcare personnel.
DEFINITION
condition develops when injured tissue forms a 1-way valve,
allowing air to enter the pleural space and preventing the air
from escaping naturally. This condition rapidly progresses to
respiratory insufÞciency, cardiovascular collapse, and ultimately
death if, unrecognized and untreated. Favorable patient outcomes
require urgent diagnosis and immediate management.
HISTORY
Physicians deÞned pneumothorax during the reign of Alexander
the Great. Many of the early references to pneumothorax may
have been tension pneumothorax, which can be signiÞcantly more
dramatic in its clinical presentation. The term “pneumothorax”
was Þrst coined by a French physician Itard, a student of Laennec
in 1803.[5] Needle decompression of the chest for presumed
tension pneumothorax has been in practice for many years, but
little data exists in the medical literature showing the efÞcacy of
the procedure or reviewing the Þeld-use and incidence of the
procedure.

A pneumothorax is deÞned as the presence of air between INCIDENCE

parietal and visceral pleural cavity.[4] Tension pneumothorax is
the accumulation of air under pressure in the pleural space. This
Correspondence:
Dr. Anita Sharma, E-mail: drjpshims@hotmail.com
The actual incidence outside of a hospital setting is impossible to
determine. In a large study in Israel, spontaneous pneumothoraces
occurred in 723 (60.3%) of 1199 cases; of these, 218 were
primary and 505 were secondary. Traumatic pneumothorax

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34 CMYK

occurred in 403 (33.6%) patients, 73 (18.1%) of whom had
iatrogenic pneumothorax.[6]
In a recent study, 12% of patients with asymptomatic chest stab
wounds had a delayed pneumothorax or hemothorax.[3]
CLASSIFICATION AND TERMINOLOGY OF THE
PNEUMOTHORAX
It is usually classiÞed on the basis of its causes. Pneumothoraces
are classiÞed as traumatic and nontraumatic (spontaneous).[7]
Nontraumatic pneumothoraces are further subdivided into primary
(occurring in persons with no known history of lung disease) and
secondary (occurring in persons with a known history of lung
disease, such as chronic obstructive pulmonary disease).[8]
Pneumothoraces may also be further described as simple
pneumothorax (no shift of the heart or mediastinal structures)
or tension pneumothorax. It can also be classiÞed as open
(“sucking” chest wound) and closed (intact thoracic cage).[7]
PATHOPHYSIOLOGY OF PNEUMOTHORAX
In normal people, the pressure in pleural space is negative with
respect to the alveolar pressure during the entire respiratory cycle.
The pressure gradient between the alveoli and pleural space, the
transpulmonary pressure is the result of the inherent elastic recoil
of the lung. During spontaneous breathing the pleural pressure
is also negative with respect to atmospheric pressure.
When communication develops between an alveolus or other
intrapulmonary air space and the pleural space, air ßows from the
alveolus into the pleural space until there is no longer a pressure
difference or until the communication is sealed.[9]
Tension pneumothorax
Tension pneumothorax develops when a disruption involves
the visceral pleura, parietal pleura, or the tracheobronchial tree.
The disruption occurs when a one-way valve forms, allowing air
inßow into the pleural space, and prohibiting air outßow. The
volume of this nonabsorbable intrapleural air increases with
each inspiration. As a result, pressure rises within the affected
hemithorax; ipsilateral lung collapses and causes hypoxia. Further
pressure causes the mediastinum shift toward the contralateral
side and compresses both, the contralateral lung and the
vasculature entering the right atrium of the heart. This leads to
worsening hypoxia and compromised venous return. Researchers
still are debating the exact mechanism of cardiovascular collapse
but, generally the condition may develop from a combination
of mechanical and hypoxic effects. The mechanical effects
manifest as compression of the superior and inferior vena cava
because the mediastinum deviates and the intrathoracic pressure
increases. Hypoxia leads to increased pulmonary vascular
resistance via vasoconstriction. If untreated, the hypoxemia,
metabolic acidosis, and decreased cardiac output lead to cardiac
arrest and death.[9,10]
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Sharma and Jindal: Traumatic pneumothorax
Traumatic pneumothorax
A traumatic pneumothorax can result from either penetrating or
nonpenetrating chest trauma. With penetrating chest trauma, the
wound allows air to enter the pleural space directly through the
chest wall or through the visceral pleura from the tracheobronchial
tree. With non penetrating trauma, a pneumothorax may develop
if the visceral pleura is lacerated secondary to a rib fracture,
dislocation. Sudden chest compression abruptly increases the
alveolar pressure, which may cause alveolar rupture. Once
the alveolus is ruptured, air enters the interstitial space and
dissects toward either the visceral pleura or the mediastinum.
A pneumothorax develops when either the visceral or the
mediastinal pleura ruptures, allowing air to enter the pleural
space.[11]
MECHANISM OF INJURY
Traumatic
(a) Penetrating trauma (e.g., stab wounds, gunshot wounds, and
impalement on a foreign body) primarily injure the peripheral
lung, producing both a hemothorax and pneumothorax in more
than 80% of all penetrating chest wounds.
(b) Blunt trauma can lead to rib fracture, causes increased
intrathoracic pressure and bronchial rupture. Manifested either
by “Fallen lung sign” (ptotic lung sign), hilum of lung is below
expected level within chest cavity or persistent pneumothorax
with functioning chest tube.
Pulmonary barotraumas
Since the volume of given mass of gas at a constant temperature
is inversely proportional to its pressure, so a given volume of air
saturated at body temperature expand to 1.5 times the volume at
sea level, if it is placed at an altitude of 3050 m, the trapped air
in the pleural bleb may rupture resulting in a pneumothorax as
seen in air crew members.[12] Similarly in scuba divers, compressed
air is delivered to lung by a demand regulators and during ascent
barotraumas may occur as ambient pressure falls rapidly, gas
contain in the lung expand and cause pneumothorax.[13]
Iatrogenic pneumothorax
It depends on the circumstances in which it develops [Table 1].
The leading cause of iatrogenic pneumothorax is transthoracic
needle aspiration. Two factors may be responsible for it, depth
and size of the lesion. If the lesion is deeper and the size is
smaller chances of traumatic pneumothorax increases.
The second leading cause of iatrogenic pneumothorax is central
cannulation, due to the increasing number of patients requiring
intensive care.
Inadvertent subclavian arterial puncture is a relatively common
complication of subclavian venepuncture.[14] The overall reported
incidence is in the range of 1-13% with 2-5% being typical.
This incidence increases to about 40% if multiple attempts
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Table 1: Causes of iatrogenic pneumothorax Table 2: Classic signs of pneumothorax[17]

according to frequency[11] Trachea
#

Transthoracic needle aspiration or biopsy 24% Expansion !

Subclavian or jugular vein catheterization 22% Percussion note "
Thoracentesis 20% Breath sounds !
Closed pleural biopsy 8% Neck veins "
Mechanical ventilation 7%
Cardiopulmonary resuscitation
Nasogastric tube placement IMAGING STUDIES
Transbronchial biopsy
Tracheostomy Chest radiography
Liver biopsy It is diagnostic in majority of the cases and Þndings are classical
Miscellaneous: [Figures 1-3].
Markedly displaced thoracic spine fracture
Acupuncture has been reported to result in pneumothorax in recent years
Colonoscopy and gastroscopy have been implicated in case reports In some patients, it may be preferable to radiologically conÞrm
Intravenous drug abusers if they choose neck veins
and localize tension pneumothorax before subjecting the patient
to potential morbidities arising from decompression. However,
are made. Thoracentesis is probably the third leading cause
of iatrogenic pneumothorax .This can be reduced if it is done
under ultrasound guidance. In a study analyzing outcomes of 418
invasive procedures, the incidence of iatrogenic pneumothorax
was 13% for computed tomography (CT)-guided transthoracic
Þne needle aspiration (TFNA), 7.1% for pleural biopsy, 16.6%
for transbronchial biopsy, 7.1% for ßuoroscopy guided TFNA,
and 1.5% for thoracentesis.[15] Mechanical ventilation causing
pneumothorax has come down because with newer ventilatory
mode it is possible to ventilate patients with lower peak pressures
and lower mean airway pressure. Other procedures which may
be responsible are, transpleural and transbronchial lung biopsies,
cardiopulmonary resuscitation, thoracic acupuncture,[16] and in
intravenous drug abuser using neck veins.

DIAGNOSIS

Diagnosis of pneumothorax is done by thorough clinical Figure 1: Chest X-Ray showing pneumothorax secondary to
blocked chest tube. A. Pleural white line B. Blocked chest tube
examination and investigations. However, clinical interpretation
of the presenting signs and symptoms is crucial for correctly
diagnosing and treating the condition.

Common early findings include[18-22] [Table 2]

Chest pain
Dyspnea
Anxiety
Tachypnea
Tachycardia
Hyper resonance of the chest wall on the affected side
Diminished breath sounds on the affected side

Whereas late findings includes

Decreased level of consciousness
Tracheal deviation toward the contralateral side
Hypotension
Distension of neck veins (may not be present if hypotension
is severe)
Cyanosis Figure 2: Depressed right hemidiaphragm due to pneumothorax

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36 CMYK

Figure 3: Subcutaneous emphysema
this consideration should be limited to patients who are awake,
stable, not in advanced stages of tension and when an immediate
chest Þlm can be obtained, with facilities to perform urgent
decompression if needed.
Serial chest radiographs every 6hrs on the Þrst day after injury
to rule out pneumothorax is ideal, but two or three chest X-ray
taken every 4-6hrs are sufÞcient.
Air in the pleural cavity, with contralateral deviation of mediastinal
structures, is suggestive of a tension pneumothorax. Chest
radiographic Þndings may include increased thoracic volume,
increased rib separation, ipsilateral ßattening of heart border,
contralateral mediastinal deviation, and the midiaphragmatic
depression.
Rotation can obscure a pneumothorax and mimic a mediastinal
shift.
In evaluating the chest radiograph, first impressions of
Table 3: Radiological findings
Visceral pleural white line
Absence of lung markings
Displacement of mediastinum
Deep sulcus sign[19]
Total / subtotal lung collapse
Radiographic signs in upright position
Radiographic signs in supine position (difficult to see)
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Sharma and Jindal: Traumatic pneumothorax
pneumothorax size can be misleading. To assist in determining
the size of pneumothorax on the radiograph, a 2.5-cm margin
of gas peripheral to the collapsing lung corresponds to a
pneumothorax of about 30%. Complete collapse of the lung is
a 100% pneumothorax.
Supine chest AP films are notoriously inaccurate. Because
they result in air spreading out over the anterior chest, supine
Þlms often appear normal, even in the presence of signiÞcant
air. Frequently, the only indication is the “deep sulcus sign,”[19]
so named because of the appearance of an especially deep
costovertebral sulcus.
In rare circumstances when there is bilateral pneumothorax
patient may appear in severe respiratory distress with engorged
neck vein, one may not Þnd signs of mediastinal shift and Þndings
on both sides of the lung will also be same [Tables 3 and 4].
Chest CT scanning
A CT scan is more sensitive than a chest radiograph in the
evaluation of small pneumothoraces and pneumomediastinum,
although the clinical signiÞcance of these occult pneumothoraces
is unclear, particularly in the stable nonintubated patient.[23]
The occult pneumothorax is being diagnosed more frequently as
methods of evaluating and diagnosing trauma patients become
more sensitive. At present, CT scan is the gold standard for
detecting occult traumatic pneumothorax not apparent on supine
chest X-ray radiograph.[24]
Ultrasonography
Use of bedside ultrasonography in the diagnosis of pneumothorax
is a relatively recent development. In some trauma centers,
pneumothorax detection is included as part of their focused
abdominal sonography for trauma (FAST) examination.[25]
Ultrasonographic features used in the diagnosis of pneumothorax
include absence of lung sliding (high sensitivity and speciÞcity),
absence of comet-tail artifact (high sensitivity, lower speciÞcity),
Convexity towards hilum
Distal or peripheral to the visceral pleural white line
Towards opposite side
On frontal view, larger lateral costodiaphragmatic recess than on opposite side
Diaphragm may be inverted on side with deep sulcus
This is passive or compressive atelectasis
! Sharp delineation of visceral pleural by dense pleural space
! Mediastinal shift to opposite side
! Air-ßuid level in pleural space on erect chest radiograph
! White margin of visceral pleura separated from parietal pleura
! Usually seen in the apex of the lung
! Absence of vascular markings beyond visceral pleural margin
! May be accentuated by an expiratory Þlm in which lung volume is reduced while amount of air in
pneumothorax remains constant so that relative size of pneumothorax appears to increase
! Anteromedial pneumothorax (earliest location)
! Outline of medial diaphragm under cardiac silhouette
! Deep sulcus sign
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Sharma and Jindal: Traumatic pneumothorax

and presence of lung point (high speciÞcity, lower sensitivity).
In a study, ultrasonography performed on patients with blunt
thoracic trauma had 94% sensitivity and 100% speciÞcity for
pneumothorax detection compared with spiral CT scanning[26,27]
[Table 5].
Arterial blood gas analysis
Arterial blood gas (ABG) does not replace physical diagnosis
nor should treatment be delayed while awaiting results if
symptomatic pneumothorax is suspected. However, ABG
analysis may be useful in evaluating hypoxia, hypercarbia, and
respiratory acidosis.
CLINICAL DIAGNOSIS OF AN IATROGENIC
PNEUMOTHORAX
The diagnosis of an iatrogenic pneumothorax should be
suspected in any patient treated by mechanical ventilation whose
clinical condition suddenly deteriorates[4] [Table 6].
The diagnosis should be suspected in any patient who become
more dyspneic after a medical or a surgical procedure that
is known to be associated with the development of the
pneumothorax. However, chest X-ray immediately after central
canulation may not show pneumothorax.

Electrocardiography TREATMENT
In left-sided pneumothorax electrocardiogram (ECG) shows:
rightward shift of the frontal QRS axis, diminution of the Management depends not only on the clinical setting, the site
precordial R voltage, decrease in QRS amplitude, and precordial where we treat the patient (site of trauma or in the hospital), any
T-wave inversion. With right pneumothorax ECG may show procedure which is causing pneumothorax, but also on the size
diminution of the precordial QRS voltage, right axis deviation, of pneumothorax, associated co-morbid condition, whether it
and a prominent R wave in V2 with associated loss of S wave is open/closed and simple/tension pneumothorax.
voltage, mimicking posterior myocardial infarction. All these
changes are thought to be due to mechanical effects and should Method to estimate the correct size of pneumothorax are
not be taken for cardiac ischemia or infarction. controversial. There are currently two methods described in
adults, if the lateral edge of the lung is >2cm from the thoracic
cage. Then, this implies pneumothorax is at least 50% and hence
Table 4: Pitfalls in the diagnosis of pneumothorax large in size. Calculate the ratio of transverse radius of the
with chest X-ray pneumothorax (cubed) to the transverse radius of hemithorax
Skin fold Thicker than the thin visceral pleural white (cubed). To express the size as a percentage, multiply the fraction
line size by 100.[28,29]
Air trapped between chest wall Will be seen as a lucency rather than a
and arm visceral pleural white line
First aid
Edge of scapula Follow contour of scapula to make sure it
does not project over chest Airway, breathing, and circulation should be checked in all the
Overlying sheets Usually will extend beyond the conÞnes of patients of chest trauma. Patency of the airway and the adequacy
the lung of the ventilatory efforts should be evaluated with the assessment
Hair braids -
of the integrity of the chest and the circulatory status as
Emphysematous bullae Convexity laterally
pericardial tamponade can also cause signs and symptoms similar
to tension pneumothorax. Upright positioning may be beneÞcial
if there is no contraindication to it like spinal injury.
Table 5: Conventional ultrasonic signs in the lung
Findings Description
Penetrating wounds (also known as ‘sucking chest wounds’)
Pleural line Horizontal hyper-echoic line between upper and lower ribs,
identiÞed by acoustic shadows require immediate coverage with an occlusive or pressure bandage
Lung-sliding Forward-and-back movement of visceral pleura against made air-tight with clean plastic sheeting. The sterile inside
parietal pleura in real-time motion of a plastic bandage packaging can be used in an emergency
Comet-tail artifacts Are hyper-echoic reverberation artifacts arising from the situation. No patient with penetrating chest wound should be
pleural line, laser-beam-like and spreading up to the edge of
the screen left unattended as tension pneumothorax or other immediately
life-threatening respiratory emergency can arise.

Table 6: Occurrence of pneumothorax in a A thin needle can be used for this purpose, to relieve the
mechanically ventilated patient pressure and allow the lung to reinßate in suspected tension
Finding Cause pneumothorax. An untreated pneumothorax is an absolute
Sudden onset of tachycardia, Tension pneumothorax impending venous contraindication for evacuation or transportation by ßight.
hypotension return
Increase in peak airway pressure External lung compression Hemothorax can be associated with pneumothorax, and the
Sudden decline in oxygen saturation Lung collapse
patient may require immediate intravenous infusion hence large-
Distressed patient To Þght ventilator
bore iv canula should be placed.

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38 CMYK

Oxygen therapy
Immediately administer 100% oxygen. Administration of
supplemental oxygen accelerates the rate of pleural air absorption
in clinical and experimental situations. By breathing 100% oxygen
instead of air, alvelolar pressure of nitrogen falls, and nitrogen
is gradually washed out of tissue and oxygen is taken up by
vascular system. This causes substantial gradient between tissue
capillary and the pneumothorax space, this results in multifold
increase in absorption from pleural space. It is recommended
that hospitalized patient with any type of pneumothorax who
is not subjected to aspiration or tube thoracostomy should
be treated with supplemental oxygen at high concentration.
Normally 1.25% of the volume of is absorbed in 24 h, hence
10% of the volume is absorbed in 8 days and 20% would be in
16 days and so on.[30]
Majority of the patients with small pneumothoraces often are
managed with oxygen administration no treatment other than
repeat observation via chest X-rays may be required.
Several prospective studies in both emergency medicine and
surgery literature dating back to the mid-1980s have supported
the use of needle aspiration and/or small-bore catheter placement
for the treatment of pneumothoraces.[31-34]
Complications of tube thoracostomy include death, injury to
lung or mediastinum, hemorrhage (usually from intercostal artery
injury), neurovascular bundle injury, infection, bronchopleural
Þstula, and subcutaneous or intraperitoneal tube placement.
Simple aspiration
It is done by a plastic iv canula instead of traditionally used needle
which was associated with risk of laceration of lung. The site of
second intercostals space in midclavicular line is conventional. It
can also be performed in Þfth intercostals space in anterior axillary
line to prevent life threatening hemorrhage. Available literature
of American College of Chest Physician (ACCP) and British
Thoracic Society (BTS) says that the needle aspiration and/or small
catheter insertion are effective, comfortable, safe, and economical
alternatives to thorcostmy in selected patients.[35,36]
Tube thoracostomy
This procedure is recommended if simple aspiration proves
ineffective and thoracoscopy is not readily available. The site for
the insertion is same as for simple aspiration. It rapidly results
in the re-expansion of the underlying lung and does not require
prolonged hospitalization. Risk of re-expansion pulmonary
edema is greater when the lung is re-expanded rapidly, it is
probably better to use water seal and to avoid suction for the
Þrst 24 h of tube thoracostomy. Now-a-days Malecot’s catheters
are replaced by pre-packed disposable plastic tube with the long
central metal trocar (18-24 Fr Gauge). Correct placement of the
tube is seen as the stream of the bubbles during expiration and
coughing and the rise on the level of ßuid in the under water
seal during inspiration.
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Sharma and Jindal: Traumatic pneumothorax
If the lung remains unexpanded or if there is a persistent air leak
72 h after tube thoracostomy, consideration should be given to
performing thoracoscopy or thoracotomy.[37-39]
Important points to remember
• As tension pneumothorax is a life-threatening condition,
the diagnosis of a tension pneumothorax should be made
based on the history and physical examination Þndings. A
chest radiograph or CT scan should be used only in those
instances where one is in doubt regarding the diagnosis and
when the patient’s clinical condition is sufÞciently stable.
• Premature diagnosis of tension pneumothorax in a patient
without respiratory distress, hypoxia, hypotension, or
cardiopulmonary compromise should not be made. Immediate
portable chest X-ray must be done to conÞrm the diagnosis.
• Consider the diagnosis of a pneumothorax and/or tension
pneumothorax with blunt and penetrating trauma. In the
patient with blunt trauma; mental status changes, hypoxia
and acidosis may be attributed to a suspected intracerebral
injury rather than a tension pneumothorax. Portable
chest radiography should always be included in the initial
radiographic evaluation of major trauma.
• Myocardial rupture with tamponade may clinically mimic
tension pneumothorax.
• Maintain a high index of suspicion for a tension pneumothorax
in patients using ventilators who have a rapid onset of
hemodynamic instability or cardiac arrest, particularly if they
require increasing peak inspiratory pressures.
• Avoid assuming that a patient with a chest tube does not
have a tension pneumothorax if he or she has respiratory or
hemodynamic instability. Chest tubes can become plugged
or malpositioned and cease to function.
• Avoid the “one size Þts all” approach for tube thoracostomy
placement.
• Tube thoracostomy is an extremely painful procedure.
In stable patients, adequate analgesia/sedation should
be administered, followed by generous amounts of local
anesthetics when chest tubes are placed.
• An initial parenteral dose of a Þrst-generation cephalosporin
should be administered for chest tube insertion in the
emergency department to decrease the risk of empyema and
pneumonia.
• Small pneumothoraces should be treated with thoracostomy
tubes if the patient is undergoing mechanical ventilation
or undergoing air transport prior to transfer to another
facility.
PREVENTION
• Advise persons to wear safety belts and passive restraint
devices while driving.
• When subclavian vein cannulation is required, use the
supraclavicular approach rather than the infraclavicular
approach when possible to help decrease the likelihood of
pneumothorax formation.
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Sharma and Jindal: Traumatic pneumothorax
• Transbronchial, transthoracic, and other procedures
preferably be done under ultrasound guidance.
CONCLUSION
Pneumothorax has been recognized condition since ancient times.
Various methods for the diagnosis and treatment are advised
from time to time. Traditional approaches to the diagnosis
and management of pneumothorax are being challenged, and
physicians should keep an open mind regarding new approaches to
this condition. As CT scans have become cheaper and more widely
utilized their role in diagnosing pneumothorax is also evolving and
being more clearly deÞned. More cases of small pneumothorax
are being diagnosed, but management decisions are not necessarily
being altered. Less costly and less painful alternatives (other
than standard tube thoracostomy and admission) exist for many
etiologies, and more patients are being discharged home than in
the past. Understanding these trends is critical to providing optimal
care for patients with pneumothorax.
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26. Zhang M, Liu ZH, Yang JX, Gan JX, Xu SW, You XD, et al. Rapid detection
of pneumothorax by ultrasonography in patients with multiple trauma.
Crit Care 2006;10:R112.
27. Soldati G, Iacconi P. The validity of the use of ultrasonography in
the diagnosis of spontaneous and traumatic pneumothorax. J Trauma
2001;51:423.
28. Choi BG, Park SH, Yun EH, Chae KO, Shinn KS. Pneumothorax size:
Correlation of supine anteroposterior with erect posteroanterior chest
radiographs. Radiology 1998;209:567-9.
29. Axel L. A simple way to estimate the size of a pneumothorax. Invest Radiol
1981;16:165-6.
30. Chadha TS, Cohn MA. Non invasive treatment of pneumothorax with
oxygen inhalation. Respiraiton 1983;44:147.
31. Delius RE, Obeid FN, Horst HM, Sorensen VJ, Fath JJ, Bivins BA. Catheter
aspiration for simple pneumothorax: Experience with 114 patients. Arch
Surg 1989;124:833-6.
32. Vallee P, Sullivan M, Richardson H, Bivins B, Tomlanovich M. Sequential
treatment of a simple pneumothorax. Ann Emerg Med 1988;17:936-42.
33. Talbot-Stern J, Richardson H, Tomlanovich MC, Obeid F, Nowak RM.
Catheter aspiration for simple pneumothorax. J Emerg Med 1986;
4:437-42.
34. Obeid FN, Shapiro MJ, Richardson HH, Horst HM, Bivins BA. Catheter
aspiration for simple pneumothorax (CASP) in the outpatient management
of simple traumatic pneumothorax. J Trauma 1985;25:882-6.
35. Miller AC, Harvey J. Guidelines for the management of spontaneous
pneumothorax. Br Med J 1993;307:114-6.
36. Miller AC, Harvey J. Pneumothorax: What’s wrong with simple aspiration?
Chest 2001;120:1041-2.
37. Johnson G. Traumatic pneumothorax: Is a chest drain always necessary?
J Accident Emerg Med 1996;13:173-4.
Journal of Emergencies, Trauma and Shock | 1:1 | Jan - Jun 2008
 Sharma and Jindal: Traumatic pneumothorax

38. Devanand A, Koh MS, Ong TH, Low SY, Phua GC, Tan KL, et al.
Simple aspiration versus chest-tube insertion in the management of pri-
mary spontaneous pneumothorax: A systematic review. Respir Med 2004;
98:579-90.
39. Andrivet P, Djedaini K, Teboul JL, Brochard L, Dreyfuss D. Spontaneous
pneumothorax: Comparison of thoracic drainage vs immediate or delayed
needle aspiration. Chest 1995;108:335-9.
How to cite this article: Principles of diagnosis and management of
traumatic pneumothorax. Sharma A, Jindal P; 2008:1:1:34-41.
Received: 31.05.08. Accepted: 02.06.08.
Source of Support: Nil. Conflict of Interest: None declared.

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41 CMYK

BTS guidelines
1
Respiratory Medicine, Royal
Infirmary of Edinburgh, UK
2
Department of Respiratory
Medicine, Castle Hill Hospital,
Cottingham, East Yorkshire, UK
3
North Bristol Lung Centre,
Southmead Hospital, Bristol, UK
Correspondence to
Dr John Harvey, North Bristol
Lung Centre, Southmead
Hospital, Bristol BS10 5NB, UK;
john.harvey@nbt.nhs.uk
Received 12 February 2010
Accepted 4 March 2010
ii18
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Management of spontaneous pneumothorax: British
Thoracic Society pleural disease guideline 2010
Andrew MacDuff,1 Anthony Arnold,2 John Harvey,3 on behalf of the BTS Pleural
Disease Guideline Group
INTRODUCTION
The term ‘pneumothorax’ was first coined by Itard
and then Laennec in 1803 and 1819 respectively,1
and refers to air in the pleural cavity (ie, inter-
spersed between the lung and the chest wall). At
that time, most cases of pneumothorax were
secondary to tuberculosis, although some were
recognised as occurring in otherwise healthy
patients (‘pneumothorax simple’). This classifica-
tion has endured subsequently, with the first
modern description of pneumothorax occurring in
healthy people (primary spontaneous pneumo-
thorax, PSP) being that of Kjærgaard2 in 1932. It is
a significant global health problem, with a reported
incidence of 18e28/100 000 cases per annum for
men and 1.2e6/100 000 for women.3
Secondary pneumothorax (SSP) is associated
with underlying lung disease, in distinction to PSP,
although tuberculosis is no longer the commonest
underlying lung disease in the developed world. The
consequences of a pneumothorax in patients with
pre-existing lung disease are significantly greater,
and the management is potentially more difficult.
Combined hospital admission rates for PSP and SSP
in the UK have been reported as 16.7/100 000 for
men and 5.8/100 000 for women, with corre-
sponding mortality rates of 1.26/million and 0.62/
million per annum between 1991 and 1995.4
With regard to the aetiology of pneumothorax,
anatomical abnormalities have been demonstrated,
even in the absence of overt underlying lung
disease. Subpleural blebs and bullae are found at the
lung apices at thoracoscopy and on CT scanning in
up to 90% of cases of PSP,5 6 and are thought to
play a role. More recent autofluorescence studies7
have revealed pleural porosities in adjacent areas
that were invisible with white light. Small airways
obstruction, mediated by an influx of inflammatory
cells, often characterises pneumothorax and may
become manifest in the smaller airways at an earlier
stage with ‘emphysema-like changes’ (ELCs).8
Smoking has been implicated in this aetiological
pathway, the smoking habit being associated with
a 12% risk of developing pneumothorax in healthy
smoking men compared with 0.1% in non-
smokers.9 Patients with PSP tend to be taller than
control patients.10 11 The gradient of negative
pleural pressure increases from the lung base to the
apex, so that alveoli at the lung apex in tall indi-
viduals are subject to significantly greater
distending pressure than those at the base of the
lung, and the vectors in theory predispose to the
development of apical subpleural blebs.12
Although it is to some extent counterintuitive,
there is no evidence that a relationship exists
between the onset of pneumothorax and physical
activity, the onset being as likely to occur during
sedentary activity.13
Despite the apparent relationship between
smoking and pneumothorax, 80e86% of young
patients continue to smoke after their first episode of
PSP.14 The risk of recurrence of PSP is as high as 54%
within the first 4 years, with isolated risk factors
including smoking, height and age >60 years.12 15
Risk factors for recurrence of SSP include age,
pulmonary fibrosis and emphysema.15 16 Thus,
efforts should be directed at smoking cessation after
the development of a pneumothorax.
The initial British Thoracic Society (BTS)
guidelines for the treatment of pneumothoraces
were published in 1993.17 Later studies suggested
that compliance with these guidelines was
improving but remained suboptimal at only
20e40% among non-respiratory and A&E staff.
Clinical guidelines have been shown to improve
clinical practice,18 19 compliance being related to
the complexity of practical procedures20 and
strengthened by the presence of an evidence
base.21 The second version of the BTS guidelines
was published in 200322 and reinforced the trend
towards safer and less invasive management
strategies, together with detailed advice on a range
of associated issues and conditions. It included
algorithms for the management of PSP and SSP
but excluded the management of trauma. This
guideline seeks to consolidate and update the
pneumothorax guidelines in the light of subse-
quent research and using the SIGN methodology.
Traumatic pneumothorax is not covered by this
guideline.
< SSP is associated with a higher morbidity
and mortality than PSP. (D)
< Strong emphasis should be placed on
smoking cessation to minimise the risk of
recurrence. (D)
< Pneumothorax is not usually associated
with physical exertion. (D)
CLINICAL EVALUATION
< Symptoms in PSP may be minimal or
absent. In contrast, symptoms are greater
in SSP, even if the pneumothorax is rela-
tively small in size. (D)
< The presence of breathlessness influences
the management strategy. (D)
< Severe symptoms and signs of respiratory
distress suggest the presence of tension
pneumothorax. (D)
The typical symptoms of chest pain and dyspnoea
may be relatively minor or even absent,23 so that
Thorax 2010;65(Suppl 2):ii18eii31. doi:10.1136/thx.2010.136986
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a high index of initial diagnostic suspicion is required. Many
patients (especially those with PSP) therefore present several
days after the onset of symptoms.24 The longer this period of
time, the greater is the risk of re-expansion pulmonary oedema
(RPO).25 26 In general, the clinical symptoms associated with
SSP are more severe than those associated with PSP, and most
patients with SSP experience breathlessness that is out of
proportion to the size of the pneumothorax.27 28 These clinical
manifestations are therefore unreliable indicators of the size of
the pneumothorax.29 30 When severe symptoms are accompa-
nied by signs of cardiorespiratory distress, tension pneumo-
thorax must be considered.
The physical signs of a pneumothorax can be subtle but, char-
acteristically, include reduced lung expansion, hyper-resonance
and diminished breath sounds on the side of the pneumothorax.
Added sounds such as ‘clicking’ can occasionally be audible at the
cardiac apex.23 The presence of observable breathlessness has
influenced subsequent management in previous guidelines.17 23
In association with these signs, cyanosis, sweating, severe
tachypnoea, tachycardia and hypotension may indicate the
presence of tension pneumothorax (see later section).
Arterial blood gas measurements are frequently abnormal in
patients with pneumothorax, with the arterial oxygen tension
(PaO2) being <10.9 kPa in 75% of patients,31 but are not required
if the oxygen saturations are adequate (>92%) on breathing
room air. The hypoxaemia is greater in cases of SSP,31 the PaO2
being <7.5 kPa, together with a degree of carbon dioxide reten-
tion in 16% of cases in a large series.32 Pulmonary function tests
are poor predictors of the presence or size of a pneumothorax7
and, in any case, tests of forced expiration are generally best
avoided in this situation.
The diagnosis of pneumothorax is usually confirmed by
imaging techniques (see below) which may also yield informa-
tion about the size of the pneumothorax, but clinical evaluation
should probably be the main determinant of the management
strategy as well as assisting the initial diagnosis.
IMAGING
Initial diagnosis
< Standard erect chest x-rays in inspiration are recom-
mended for the initial diagnosis of pneumothorax,
rather than expiratory films. (A)
< The widespread adoption of digital imaging (PACS)
requires diagnostic caution and further studies since the
presence of a small pneumothorax may not be imme-
diately apparent. (D)
< CT scanning is recommended for uncertain or complex
cases. (D)
The following numerous imaging modalities have been
employed for the diagnosis and management of pneumothorax:
1. Standard erect PA chest x-ray.
2. Lateral x-rays.
3. Expiratory films.
4. Supine and lateral decubitus x-rays.
5. Ultrasound scanning.
6. Digital imaging.
7. CT scanning.
Standard erect PA chest x-ray
This has been the mainstay of clinical management of primary
and secondary pneumothorax for many years, although it is
acknowledged to have limitations such as the difficulty in
accurately quantifying pneumothorax size. Major technological
advances in the last decade have resulted in the advent of digital
Thorax 2010;65(Suppl 2):ii18eii31. doi:10.1136/thx.2010.136986
BTS guidelines
chest imaging, so that conventional chest films are no longer
easily available in clinical practice in the UK or in many other
modern healthcare systems. The diagnostic characteristic is
displacement of the pleural line. In up to 50% of cases an air-
fluid level is visible in the costophrenic angle, and this is occa-
sionally the only apparent abnormality.33 The presence of
bullous lung disease can lead to the erroneous diagnosis of
pneumothorax, with unfortunate consequences for the patient.
If uncertainty exists, then CT scanning is highly desirable (see
below).
Lateral x-rays
These may provide additional information when a suspected
pneumothorax is not confirmed by a PA chest film33 but, again,
are no longer routinely used in everyday clinical practice.
Expiratory films
These are not thought to confer additional benefit in the routine
assessment of pneumothorax.34e36
Supine and lateral decubitus x-rays
These imaging techniques have mostly been employed for
trauma patients who cannot be safely moved. They are generally
less sensitive than erect PA x-rays for the diagnosis of pneu-
mothorax37 38 and have been superseded by ultrasound or CT
imaging for patients who cannot assume the erect posture.
Ultrasound scanning
Specific features on ultrasound scanning are diagnostic of
pneumothorax39 but, to date, the main value of this technique
has been in the management of supine trauma patients.40
Digital imaging
Digital radiography (Picture-Archiving Communication Systems,
PACS) has replaced conventional film-based chest radiography
across most UK hospitals within the last 5 years, conferring
considerable advantages such as magnification, measurement and
contrast manipulation, ease of transmission, storage and repro-
duction. Relatively few studies have addressed the specific issue
of pneumothorax and its diagnosis, and these have tended to
focus on expert diagnosis (by consultant radiologists) and the
more discriminating departmental (rather than ward-based)
workstations. Even so, some difficulties were found in the diag-
nosis of pneumothorax in early studies.41 42 Since then there have
been technological advances, such that digital imaging may now
be as reliable as more conventional chest x-rays in pneumothorax
diagnosis, but there have been no more recent studies to confirm
this. Differences exist between the characteristics (screen size,
pixel count, contrast and luminescence) and therefore the sensi-
tivity of the more expensive departmental devices and the
desktop and mobile consoles available in the ward environment.
It is currently recommended that, where primary diagnostic
decisions are made based on the chest x-ray, a diagnostic PACS
workstation is available for image review.
In addition, digital images do not directly lend themselves to
measurement and size calculations; an auxiliary function and
use of a cursor is required, but this is almost certainly more
accurate than using a ruler and is easy to learn to do. Non-
specialist clinicians and trainees may not always be familiar
with these functions.
CT scanning
This can be regarded as the ‘gold standard’ in the detection of
small pneumothoraces and in size estimation.43 It is also useful
ii19
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BTS guidelines
in the presence of surgical emphysema and bullous lung
disease44 and for identifying aberrant chest drain placement45 or
additional lung pathology. However, practical constraints
preclude its general use as the initial diagnostic modality.
Size of pneumothorax
< In defining a management strategy, the size of a pneu-
mothorax is less important than the degree of clinical
compromise. (D)
< The differentiation of a ‘large’ from a ‘small’ pneumo-
thorax continues to be the presence of a visible rim of
>2 cm between the lung margin and the chest wall (at
the level of the hilum) and is easily measured with the
PACS system. (D)
< Accurate pneumothorax size calculations are best
achieved by CT scanning. (C)
The size of pneumothoraces does not correlate well with the
clinical manifestations.29 30 The clinical symptoms associated
with secondary pneumothoraces are more severe in general than
those associated with primary pneumothoraces, and may seem
out of proportion to the size of the pneumothorax.27 28 The
clinical evaluation is therefore probably more important than
the size of the pneumothorax in determining the management
strategy.
Commonly, the plain PA chest x-ray has been used to
quantify the size of the pneumothorax. However, it tends to
underestimate the size because it is a two-dimensional image
while the pleural cavity is a three-dimensional structure. The
2003 BTS guidelines22 advocated a more accurate means of size
calculation than its predecessor in 1993,15 using the cube
function of two simple measurements, and the fact that a 2 cm
radiographic pneumothorax approximates to a 50% pneumo-
thorax by volume. There are difficulties with this approach,
including the fact that some pneumothoraces are localised
(rather than uniform), so that measurement ratios cannot be
applied. The shape of the lung cannot be assumed to remain
constant during collapse.46 The measurement of the ratio of
the lung to the hemithorax diameter is accurate and relatively
easy with the new PACS systems by means of a cursor, once
familiar with the PACS auxiliary functions.
The choice of a 2 cm depth is a compromise between the
theoretical risk of needle trauma with a more shallow pneu-
mothorax and the significant volume and length of time to
spontaneous resolution of a greater depth of pneumothorax.47 48
Assuming a symmetrical pattern of lung collapse, then this
measure is normally taken from the chest wall to the outer edge
of the lung at the level of the hilum (figure 1). Guidelines from
the USA49 estimated the volume of a pneumothorax by
measuring the distance from the lung apex to the cupola, but
this method would tend to overestimate the volume in a local-
ised apical pneumothorax. Belgian guidelines have used yet
another technique for measuring pneumothorax size, and
comparisons between the different techniques have shown poor
agreement.50
CT scanning is regarded as the best means of establishing the
size of a pneumothorax51 and has been calibrated in a lung
model experiment.52
TREATMENT OPTIONS FOR PNEUMOTHORAX
< Patients with pre-existing lung disease tolerate a pneu-
mothorax less well, and the distinction between PSP
and SSP should be made at the time of diagnosis to
guide appropriate management. (D)
ii20
Figure 1 Depth of pneumothorax.
< Breathlessness indicates the need for active intervention
as well as supportive treatment (including oxygen). (D)
< The size of the pneumothorax determines the rate of
resolution and is a relative indication for active
intervention. (D)
Primary pneumothorax occurs in patients with no evidence of
other underlying lung disease. Although histological abnormali-
ties are usually present, associated in particular with cigarette
smoking, they have not been manifested by symptoms or loss of
function. In contrast, secondary pneumothorax usually occurs in
patients with overt underlying lung disease, most commonly
chronic obstructive pulmonary disease (COPD). It is important
to make this fundamental distinction as pneumothorax in COPD
is much less well tolerated by the patient and tends to respond
less favourably to management interventions and because the
underlying lung disease requires appropriate treatment in addi-
tion. Several series have shown a reduced success rate for aspi-
ration in patients aged >50 years as well as for chronic lung
disease. It seems likely that these older patients had unrecognised
underlying lung disease. This age criterion was included in the
flowchart for SSP in the 2003 guidelines and is incorporated into
the new flowchart (figure 2), serving as a prompt to consider the
likelihood of SSP. Further criteria that are important in the deci-
sion-making process are the presence of significant breathlessness
and the size of the pneumothorax. The rate of resolution/reab-
sorption of spontaneous pneumothoraces has been gauged as
being between 1.25% and 2.2% of the volume of the hemithorax
every 24 h,47 48 52 the higher and more recent estimate52 being
derived from CT volumetry. Thus, a complete pneumothorax
might be expected to take up to 6 weeks to resolve spontaneously
and, conceivably, in the presence of a persistent air leak, even
longer.
Management of PSP
< Patients with PSP or SSP and significant breathlessness
associated with any size of pneumothorax should
undergo active intervention. (A)
< Chest drains are usually required for patients with
tension or bilateral pneumothorax who should be
admitted to hospital. (D)
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BTS guidelines

measure the interpleural

# distance at the level of the hilum

MANAGEMENT OF SPONTANEOUS
PNEUMOTHORAX
Spontaneous Pneumothorax ##

If Bilateral/Haemodynamically unstable
proceed to Chest drain

Age >50 and significant

smoking history
Pri m ar y NO Evidence of underlying
YES Secondary
Pneumothorax lung disease on exam or Pneumothorax
CXR?

YES
>2cm or
S i z e> 2 c m YES* Aspirate Breathless
and/or 16-18G cannula
Breathless Aspirate <2.5l

NO
NO

Aspirate YES Si z e
Su c c e s s 16-18G cannula
1- 2 c m
(<2cm and NO Aspirate <2.5l
breathing
improved)
YES
NO
Consider discharge NO Su c c e s s
review in OPD in 2-4 Siz e
weeks now<1cm

YES
Chest drain
*In some patients with a large S i z e 8- 1 4F r
pneumothorax but minimal Admit Admit
symptoms conservative High flow oxygen (unless suspected
management may be oxygen sensitive)
appropriate Observe for 24 hours

Figure 2 Flowchart of management of spontaneous pneumothorax.

< Observation is the treatment of choice for small PSP
without significant breathlessness. (B)
< Selected asymptomatic patients with a large PSP may be
managed by observation alone. (A)
< Patients with a small PSP without breathlessness should
be considered for discharge with early outpatient review.
These patients should also receive clear written advice to
return in the event of worsening breathlessness. (D)
Both tension pneumothorax and bilateral pneumothorax are
potentially life-threatening events that require chest drain
insertion. Because such patients are generally excluded from
trials of spontaneous pneumothorax, there is no evidence upon
which to base recommendations, advice being based on the
grounds of safe practice. Similarly, patients with associated large
pleural effusions (hydropneumothorax) have also been excluded
from trials, but are likely to require chest drain insertion and
further investigation (see separate guideline). A summary of the
management recommendations is shown in the flowchart
(figure 2) with explanatory detail in the text below.
Minimal symptoms
Conservative management of small pneumothoraces has been
shown to be safe,47 53 54 and patients who are not breathless can
be managed as outpatients providing they can easily seek
medical attention if any deterioration in their symptoms occurs.
Up to 80% of pneumothoraces estimated as smaller than 15%
have no persistent air leak, and recurrence in those managed
with observation alone is less than in those treated by chest
drains.55 Early review is advisable to ensure satisfactory resolu-
tion and to reinforce the advice on lifestyle. There is no evidence
that active intervention improves the associated pain, which
simply warrants appropriate analgesia.
Symptomatic pneumothorax
Observation alone is inappropriate for breathless patients who
require active intervention (needle aspiration or chest drain
insertion). Marked breathlessness in a patient with a small PSP
may herald tension pneumothorax.55 If a patient is hospitalised
for observation, supplemental high flow oxygen should be given
where feasible. As well as correcting any arterial hypoxaemia,56
it has been shown to result in a fourfold increase in the rate of
pneumothorax resolution.57 In the presence of a continued air
leak, the mechanism may be a reduction in the partial pressure
of nitrogen in the pleural space relative to oxygen, which is more
readily absorbed. Also, a similar effect in the pleural capillaries
creates a more favourable resorption gradient.58
Needle aspiration or chest drain?
< Needle (14e16 G) aspiration (NA) is as effective as
large-bore (>20 F) chest drains and may be associated
with reduced hospitalisation and length of stay. (A)

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BTS guidelines
< NA should not be repeated unless there were technical
difficulties. (B)
< Following failed NA, small-bore (<14 F) chest drain
insertion is recommended. (A)
< Large-bore chest drains are not needed for pneumo-
thorax. (D)
Needle aspiration (NA) was recommended in the previous
guidelines17 22 as the initial intervention for PSP on the basis of
studies59 60 showing equivalent success to the insertion of large-
bore chest drains, although this was not shown in another
study.61 Seldinger (catheter over guide wire) chest drains have
entered widespread usage since then and further studies have
been published. A randomised controlled trial in a Kuwaiti
population has confirmed equivalence between NA and chest
drains (16 Fr), plus a reduction in hospital admission and length
of stay for NA.62 A smaller study in India has also confirmed
equivalence.63 Two recent case series have reported NA success
rates of 69%64 and 50.5%.65 Several meta-analyses66e68 were
limited by the small numbers of patients and studies69e77 but
confirm equivalence, with NA success rates ranging from 30% to
80% (see evidence table available on the BTS website www.brit-
thoracic.org.uk). If undertaken, NA should cease after 2.5 l of air
has been aspirated, further re-expansion being unlikely59 because
of the likely presence of a persistent air leak.
Guidelines that encourage NA are not always followed78e82
and the ease of insertion of small-bore (<14 F) Seldinger chest
drains may be regarded as a simpler option to NA. Their success
has been documented in several studies,83e89 the attachment of
Heimlich valves facilitating mobilisation and outpatient care.
Small-bore chest drains have been shown to have a similar
success rate to larger drains90 while being less painful,91 92 but
there have been no randomised controlled trials comparing them
with NA. More detail on chest drain insertion and management
and complications of chest drain insertion are found in the
guideline on pleural procedures. Catheter aspiration was
described in the last guideline,22 with success in up to 59%, and
further improvement with the addition of Heimlich valves and
suction.93e95 Seldinger chest drains have also permitted a ‘step-
wise’ approach to PSP management, following a predefined
pathway that culminates in surgical referral where there is
a persistent air leak.96
The choice of initial intervention for PSP should take into
account operator experience and patient choice; NA is less
painful than chest drain insertion60 but failure in approximately
one-third of patients will require a second procedure. Other
national and consensus guidelines recommend either NA or
small-bore chest drain insertion,97 or chest drain insertion
alone.49 We believe that NA remains the procedure of first choice
in most cases. Repeat NA is unlikely to be successful unless there
were technical difficulties such as a blocked or kinked catheter.
There is some limited evidence that VATS is the preferred
‘salvage’ strategy after failed NA,98 but this is not the usual
practice currently in the UK where small-bore chest drain
insertion is usually employed. Following successful NA, the
patient can be considered for hospital discharge.
Suction
< Suction should not be routinely employed. (B)
< Caution is required because of the risk of RPO. (B)
< High-volume low-pressure suction systems are recom-
mended. (C)
A persistent air leak with or without incomplete re-expansion of
the lung is the usual reason for consideration of the use of
suction, although there is no evidence for its routine use.99e101 It
ii22
is arbitrarily defined as the continued bubbling of air through
a chest drain after 48 h in situ. A retrospective review of 142
cases of pneumothorax102 found a median time to resolution of
8 days which was not related to the initial size of pneumo-
thorax, but longer for SSP. A persistent air leak was observed in
43 cases, 30 of which were treated with suction. The theory that
underpins the role of suction is that air might be removed from
the pleural cavity at a rate that exceeds the egress of air through
the breach in the visceral pleura and to subsequently promote
healing by apposition of the visceral and parietal pleural layers.
It has been suggested that optimal suction should entail pres-
sures of 10 to 20 cm H2O (compared with normal intra-
pleural pressures of between 3.4 and 8 cm H2O, according to
the respiratory cycle), with the capacity to increase the air flow
volume to 15e20 l/min.103 Other forms of suction are not
recommended. High-pressure high-volume suction may lead to
air stealing, hypoxaemia or the perpetuation of air leaks.104
Likewise, high-pressure low-volume systems should be
avoided.105 High-volume low-pressure systems such as Vernon-
Thompson pumps or wall suction with low pressure adaptors
are therefore recommended.
The addition of suction too early after chest drain insertion
may precipitate RPO, especially in the case of a PSP that may
have been present for more than a few days,106 and is thought to
be due to the additional mechanical stress applied to capillaries
that are already ‘leaky’.107 The clinical manifestations are cough,
breathlessness and chest tightness after chest drain insertion.
The incidence may be up to 14% (higher in younger patients
with a large PSP), although no more than a radiological
phenomenon in the majority of cases.106 Sometimes pulmonary
oedema is evident in the contralateral lung.108 Fatalities have
been reported in as many as 20% of 53 cases in one series,108 so
caution should be exercised in this particular group of patients.
Specialist referral
< Referral to a respiratory physician should be made
within 24 h of admission. (C)
< Complex drain management is best effected in areas
where specialist medical and nursing expertise is avail-
able. (D)
Failure of a pneumothorax to re-expand or a persistent air leak
should prompt early referral to a respiratory physician, prefer-
ably within the first 24 h. Such patients may require prolonged
chest drainage with complex drain management (suction, chest
drain repositioning) and liaison with thoracic surgeons. Drain
management is also best delivered by nurses with specialist
expertise. Surgical referral is discussed in a later section.
Surgical emphysema
This is a well-recognised complication of chest drainage.109
Generally it is of cosmetic importance only, although alarming
for patients and their relatives, and subsides spontaneously after
a few days. It is usually seen in the context of a malpositioned,
kinked, blocked or clamped chest drain. It can also occur with an
imbalance between a large air leak and a relatively small-bore
chest drain. Occasionally, acute airway obstruction or thoracic
compression may lead to respiratory compromise109 110 in which
case tracheostomy, skin incision decompression and insertion of
large-bore chest drains have all been used.109 For most, the
treatment is conservative.
Management of SSP
< All patients with SSP should be admitted to hospital for
at least 24 h and receive supplemental oxygen in
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compliance with the BTS guidelines on the use of
oxygen. (D)
< Most patients will require the insertion of a small-bore
chest drain. (B)
< All patients will require early referral to a chest
physician. (D)
< Those with a persistent air leak should be discussed
with a thoracic surgeon at 48 h. (B)
As stated previously, SSP is less likely to be tolerated by
patients than PSP because of co-existing lung disease.
Furthermore, the air leak is less likely to settle spontane-
ously,111 112 so that most patients will require active inter-
vention. Oxygen is indicated,56 57 but caution is required for
patients with carbon dioxide retention.113 Aspiration is less
likely to be successful in SSP (see evidence table available on the
BTS website at www.brit-thoracic.org.uk) but can be consid-
ered in symptomatic patients with small pneumothoraces in an
attempt to avoid chest drain insertion. Otherwise, the inser-
tion of a small-bore chest drain is recommended, a study in
SSP114 having found equivalent success to the use of large
drains. Early referral to a chest physician is encouraged for all
patients with SSP, both for management of the pneumothorax
and also of the underlying lung disease. Similarly, those with
a persistent air leak should be discussed with a thoracic surgeon
after 48 h,112 115 even though many will resolve spontaneously if
managed conservatively for as long as 14 days.111
Patients with SSP but unfit for surgery
< Medical pleurodesis may be appropriate for inoperable
patients. (D)
< Patients with SSP can be considered for ambulatory
management with a Heimlich valve. (D)
These patients are at heightened risk of a persistent air leak but
may not be fit for surgical intervention by virtue of the severity
of their underlying lung disease, or they may be unwilling to
proceed. Their optimal management is challenging and requires
close medical and surgical liaison. Medical pleurodesis is an
option for such patients, as is ambulatory management with the
use of a Heimlich valve.86
DISCHARGE AND FOLLOW-UP
< Patients should be advised to return to hospital if
increasing breathlessness develops. (D)
< All patients should be followed up by respiratory
physicians until full resolution. (D)
< Air travel should be avoided until full resolution. (C)
< Diving should be permanently avoided unless the
patient has undergone bilateral surgical pleurectomy
and has normal lung function and chest CT scan
postoperatively. (C)
All patients discharged after active treatment or otherwise
should be given verbal and written advice to return to the
Accident and Emergency department immediately should they
develop further breathlessness. It is recommended that all
patients should be followed up by a respiratory physician to
ensure resolution of the pneumothorax, to institute optimal care
of any underlying lung disease, to explain the risk of recurrence
and the possible later need for surgical intervention and to
reinforce lifestyle advice on issues such as smoking and air travel.
Those managed by observation alone or by NA should be
advised to return for a follow-up chest x-ray after 2e4 weeks to
monitor resolution. Those with successful lung re-expansion
before hospital discharge will also require early review because
recurrence may occur relatively early.
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BTS guidelines
Since there is no evidence to link recurrence with physical
exertion, the patient can be advised to return to work and to
resume normal physical activities once all symptoms have
resolved, although it is reasonable to advise that sports that
involve extreme exertion and physical contact should be deferred
until full resolution. Patients should be made aware of the
danger of air travel in the presence of a current closed pneu-
mothorax, and should be cautioned against commercial flights at
high altitude until full resolution of the pneumothorax has been
confirmed by a chest x-ray. While there is no evidence that air
travel per se precipitates pneumothorax recurrence, the conse-
quences of a recurrence during air travel may be serious. Many
commercial airlines previously advised arbitrarily a 6-week
interval between the pneumothorax event and air travel, but
this has since been amended to a period of 1 week after full
resolution. The BTS guidelines on air travel116 emphasise that
the recurrence risk only significantly falls after a period of 1 year
from the index pneumothorax so that, in the absence of
a definitive surgical procedure, patients with SSP in particular
may decide to minimise the risk by deferring air travel accord-
ingly. After a pneumothorax, diving should be discouraged
permanently117 unless a very secure definitive prevention
strategy has been performed such as surgical pleurectomy. The
BTS guidelines on respiratory aspects of fitness for diving118 deal
with this in greater detail. Smoking influences the risk of
recurrence,12 15 so cessation should be advised. Pregnancy is an
issue to be discussed with younger female patients.
MEDICAL CHEMICAL PLEURODESIS
< Chemical pleurodesis can control difficult or recurrent
pneumothoraces (A) but, since surgical options are
more effective, it should only be used if a patient is
either unwilling or unable to undergo surgery. (B)
< Chemical pleurodesis for pneumothorax should only be
performed by a respiratory specialist. (C)
Chemical pleurodesis has generally been advocated by respira-
tory physicians experienced in thoracoscopy. The instillation of
substances into the pleural space should lead to an aseptic
inflammation, with dense adhesions leading ultimately to
pleural symphysis. There is a significant rate of recurrence of
both primary and secondary pneumothoraces,12 and efforts to
reduce recurrence by instilling various sclerosantsdeither via
a chest drain, video-assisted thoracoscopic surgery (VATS) or
open surgerydare often undertaken without clear guidelines to
direct physicians in their use. In the vast majority of cases the
prevention of recurrent pneumothoraces should be undertaken
surgically using either an open or VATS approach, as the rate
of recurrence following surgical pleurodesis via thoracotomy
or VATS is far less than following simple medical pleurodesis
with chemical agents,32 119e121 although direct comparative
trials are lacking. A small number of patients are either too
frail or are unwilling to undergo any surgical treatment and,
in these situations, medical chemical pleurodesis may be
appropriate.
Many sclerosing agents suitable for instillation into the
pleural space have been studied.32 119 122e125 Tetracycline used to
be recommended as the first-line sclerosant therapy for both
primary and secondary pneumothoraces as it proved to be the
most effective sclerosant in animal models.123 126 127 Recently,
however, parenteral tetracycline for pleurodesis has become
more difficult to obtain owing to problems with the
manufacturing process. Minocycline and doxycycline have also
been shown to be reasonable alternative sclerosing agents in
animal models.126 127
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BTS guidelines
The rate of recurrence of pneumothorax is the primary indi-
cator for success for any recurrence prevention techniques.
Although tetracycline has been shown to reduce the incidence of
early recurrence, the incidence of late recurrence remains at
10e20% which is unacceptably high when compared with
surgical methods of pleurodesis.119 121 125 128 129 Tetracycline can
be recommended for recurrent primary and secondary pneumo-
thorax when surgery is not an option, and graded talc may also be
used on the grounds that it is the most effective agent in treating
malignant pleural effusion and is also commonly used for surgical
chemical pleurodesis.130e133 There is conflicting evidence as to
whether tetracycline is effective for the treatment of a fully
expanded pneumothorax with a persistent air leak.32 134 135 The
largest of these studies, the Veterans Administration Study, did
not support the use of intrapleural tetracycline to facilitate the
closure of a persistent air leak.31 Macoviak and colleagues135
suggest that intrapleural tetracycline can facilitate the closure of
a persistent air leak provided the lung can be kept expanded so
that symphysis can occur. Likewise, there is conflicting evidence
as to whether intrapleural tetracycline shortens the length of stay
in hospital with pneumothorax.32 119 125
The dosage of intrapleural tetracycline requires clarification.
Almind119 found a reduction in the recurrence rate in a group
receiving 500 mg tetracycline via chest drains compared with
those treated by tube drainage alone. This reduction was not
significant. The Veterans Administration Study,32 which used
1500 mg tetracycline, showed a significant reduction in the
recurrence rate of pneumothorax without significant extra
morbidity. This dose of intrapleural tetracycline is therefore
recommended as the standard dose for medical pleurodesis.
While pain was reported more frequently in the group treated
with tetracycline at a dose of 1500 mg,32 others have reported no
increase in pain with doses of 500 mg provided adequate anal-
gesia is given.119 Adequate analgesia may be achieved with the
administration of intrapleural local anaesthesia. Standard doses
(200 mg (20 ml) of 1% lidocaine) are significantly less effective
than larger doses (250 mg (25 ml) of 1% lidocaine), the higher
doses having been shown to increase the number of pain-free
episodes from 10% to 70% with no appreciable toxicity.136
Chemical pleurodesis using graded talc is an effective alter-
native to tetracycline pleurodesis, but there are no controlled
trials comparing the two in the treatment of pneumothorax.
The issue of talc pleurodesis is discussed in the later section on
surgical chemical pleurodesis as most trials using talc relate to its
use in either thoracoscopic or open surgical techniques. Since we
recognise chemical pleurodesis as an inferior option to surgical
pleurodesis, we recommend that chemical pleurodesis should be
undertaken by respiratory physicians or thoracic surgeons only.
REFERRAL TO THORACIC SURGEONS
< In cases of persistent air leak or failure of the lung to re-
expand, an early (3e5 days) thoracic surgical opinion
should be sought. (C)
There is no evidence on which to base the ideal timing for
thoracic surgical intervention in cases of persistent air leak. A cut-
off point of 5 days has been widely advocated in the past55 but is
arbitrary. Chee et al111 showed that 100% of primary pneumo-
thoraces with a persistent air leak for >7 days and treated by tube
drainage had resolved by 14 days. Also, 79% of those with
secondary pneumothoraces and a persistent air leak had resolved
by 14 days, with no mortality in either group. However, surgical
intervention carries a low morbidity128 129 137e140 and post-
surgical recurrence rates are low.128 129 Surgical intervention as
early as 3 days has advocates,141 142 but there is no evidence that
ii24
intervention before 5 days is necessary for PSP. Each case should
be assessed individually on its own merit. Patients with pneu-
mothoraces should be managed by a respiratory physician, and
a thoracic surgical opinion will often form an early part of the
management plan.
Accepted indications for surgical advice should be as follows:
< Second ipsilateral pneumothorax.
< First contralateral pneumothorax.
< Synchronous bilateral spontaneous pneumothorax.
< Persistent air leak (despite 5e7 days of chest tube drainage) or
failure of lung re-expansion.
< Spontaneous haemothorax.143 144
< Professions at risk (eg, pilots, divers).111 138 145e147
< Pregnancy.
Increasingly, patient choice will play a part in decision-
making, and even those without an increased risk in the event of
a pneumothorax because of their profession may elect to
undergo surgical repair after their first pneumothorax,148 149
weighing the benefits of a reduced recurrence risk against that of
chronic pain,150 paraesthesia151 or the possibility of increased
costs.152
Surgical strategies: open thoracotomy or VATS?
< Open thoracotomy and pleurectomy remain the proce-
dure with the lowest recurrence rate (approximately
1%) for difficult or recurrent pneumothoraces. (A)
< Video-assisted thoracoscopic surgery (VATS) with
pleurectomy and pleural abrasion is better tolerated but
has a higher recurrence rate of approximately 5%. (A)
There are two main objectives in the surgical repair of persistent
air leak from a pneumothorax and in the prevention of recur-
rence. The first objective is to resect any visible bullae or blebs on
the visceral pleura and also to obliterate emphysema-like
changes9 or pleural porosities under the surface of the visceral
pleura.8 The second objective is to create a symphysis between
the two opposing pleural surfaces as an additional means of
preventing recurrence. In the past, surgeons have tended to
favour a surgical pleurodesis with pleural abrasion while others
have stressed the importance of various degrees of pleurectomy
in recurrence prevention.137 153 154 Although there may be slight
advantages of pleurectomy over pleural abrasion,137 a combina-
tion of the two is often used.155e158 Unfortunately there is
a paucity of good comparative case-controlled studies in this
area.128 129 In recent years, less invasive procedures using VATS
have become more popular with lower morbidity although with
slightly higher recurrence rates.
Open thoracotomy with pleural abrasion was the original
surgical treatment for pneumothorax, described by Tyson and
Crandall in 1941.159 In 1956 Gaensler introduced parietal
pleurectomy for recurrent pneumothoraces, encouraging
pleural symphysis through adhesions between the visceral
pleura and the chest wall.153 Closure of the leaking visceral
pleura with direct cautery and ligation or suture of associated
blebs147 is also thought to be important. Although open
thoracotomy has the lowest pneumothorax recurrence rates,
there are also lesser surgical procedures with comparable
recurrence rates but less morbidity.160 These include trans-
axillary minithoracotomy, using a 5e6 cm incision in the
axillary margin with apical pleurectomy and pleural abrasion,
introduced in the 1970s.161 Open thoracotomy is generally
performed with a limited posterolateral approach and single
lung ventilation. This allows for a parietal pleurectomy with
excision, stapling or ligation of visible bullae and pleural abra-
sion.162 Isolated lung ventilation during open thoracotomy
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renders easier visualisation of the visceral pleura than during
a VATS procedure.163e165 Meta-analyses of studies comparing
open with limited or VATS procedures128 129 have shown lower
recurrence rates (approximately 1%) with open procedures but
greater blood loss, more postoperative pain166 and longer
hospital stays.167 Some non-randomised studies have found no
significant differences.168 169 A complicated meta-analysis of
three retrospective studies and one prospective study
comparing the cost of open thoracotomy versus VATS (not
exclusively for pneumothoraces) concluded that the total
economic cost of VATS was lower,170 and it can be undertaken
without general anaesthesia.149 There is a need for better
quality prospective randomised studies in this area. Several
authors suggest that VATS offers a significant advantage over
open thoracotomy, including a shorter postoperative hospital
stay,145 162 167 171e173 less postoperative pain160 162 166 174 175
and improved pulmonary gas exchange postoperatively,176
although not all trials have confirmed shorter hospital stays
with VATS.169 177
Much of the literature contains heterogeneous comparisons
between PSP and SSP, but the most recent ‘clinical bottom
line’129 concludes that VATS pleurectomy is comparable to open
pleurectomy, with several randomised controlled trials showing
reductions in length of hospital stay, analgesic requirement and
postoperative pulmonary dysfunction. Clearly this needs to be
weighed against the slight increase in recurrence rate when using
a less invasive approach.128
Surgical chemical pleurodesis
< Surgical chemical pleurodesis is best achieved by using
5 g sterile graded talc, with which the complications of
adult respiratory distress syndrome and empyema are
rare. (A)
With the advent of VATS for pneumothorax repair and recur-
rence prevention, the use of surgical chemical pleurodesis has
declined significantly. Previous reports have shown that talc can
achieve pleurodesis successfully in 85e90% of cases, similar to
other thoracoscopic techniques for complicated pneumo-
thorax.121 145 171 178 179 A meta-analysis of the success rates of
talc pleurodesis in the treatment of pneumothorax shows an
overall success rate of 91%.178 Graded talc is preferable to tetra-
cycline, which is less available now, and is associated with much
higher recurrence rates.120 Much of the literature concerning the
use of talc in achieving pleurodesis relates to its use in the control
of malignant pleural effusions, although talc poudrage has been
used successfully in secondary pneumothoraces.180 On the basis
of a systematic review of uncontrolled trials, 5 g of intrapleural
talc via VATS achieves a success rate of 87%.178
The adult respiratory distress syndrome has been described
following the use of talc. This probably relates to the size of the
talc particles181 and is unlikely to occur with the use of graded
talc.182 183 If talc is correctly sterilised, the incidence of
empyema is very low.178 184 185 There does not appear to be
a difference between talc poudrage and talc slurry pleurodesis.
The advent of successful and well-tolerated VATS surgery will
lead to less use of surgical chemical pleurodesis with talc. In
those patients who are either unwilling or too unwell to
undergo a VATS procedure, then medical pleurodesis with talc
via a chest drain would be the preferred option.
TENSION PNEUMOTHORAX
< Tension pneumothorax is a medical emergency that
requires heightened awareness in a specific range of
clinical situations. (D)
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BTS guidelines
< Treatment is with oxygen and emergency needle
decompression. (D)
< A standard cannula may be insufficiently long if used in
the second intercostal space. (D)
This is a medical emergency that can arise in a variety of
clinical situations, so a high index of suspicion is required in
order to make the correct diagnosis and to manage it effec-
tively. The most frequent situations are shown in box 1,
although the list does not include all eventualities. It arises as
a result of the development of a one-way valve system at the
site of the breach in the pleural membrane, permitting air to
enter the pleural cavity during inspiration but preventing
egress of air during expiration, with consequent increase in the
intrapleural pressure such that it exceeds atmospheric pressure
for much of the respiratory cycle. As a result, impaired venous
return and reduced cardiac output results in the typical features
of hypoxaemia and haemodynamic compromise.186 187
A recent review188 has emphasised the important differences
between the presentation in ventilated and non-ventilated
patients, where it is typically seen after trauma or resuscitation.
The former group is associated with a uniformly rapid presen-
tation with hypotension, tachycardia, falling oxygen saturation
and cardiac output, increased inflation pressures and cardiac
arrest. This is frequently missed in the ICU setting37 and can
also occur after nasal non-invasive ventilation (NIV). The latter
group of awake patients show a greater variability of presenta-
tions which are generally progressive with slower decompensa-
tion. Tachypnoea, tachycardia and hypoxaemia lead eventually
to respiratory arrest. Apart from these general physical signs, the
most frequent lateralising sign found in a review of 18 case
reports188 was that of decreased air entry (50e75%), with signs
of tracheal deviation, hyperexpansion, hypomobility and
hyperresonance present only in the minority.
In neither group is imaging especially helpful; there is usually
insufficient time to obtain a chest x-ray and, even if available,
the size of the pneumothorax or the presence of mediastinal
displacement correlate poorly with the presence of tension
within a pneumothorax. However, a chest x-ray can, when
time is available, confirm the presence of a pneumothorax (if
uncertain) and the correct side.
Treatment is with high concentration oxygen and emergency
needle decompression, a cannula usually being introduced in the
second anterior intercostal space in the mid-clavicular line. The
instantaneous egress of air through the majority of the respira-
tory cycle is an important confirmation of the diagnosis and the
correct lateralisation. A standard 14 gauge (4.5 cm) cannula may
not be long enough to penetrate the parietal pleura, however,
with up to one-third of patients having a chest wall thickness
Box 1 Typical clinical situations where tension
pneumothorax arises
1. Ventilated patients on ICU.
2. Trauma patients.
3. Resuscitation patients (CPR).
4. Lung disease, especially acute presentations of asthma and
chronic obstructive pulmonary disease.
5. Blocked, clamped or displaced chest drains.
6. Patients receiving non-invasive ventilation (NIV).
7. Miscellaneous group, for example patients undergoing
hyperbaric oxygen treatment.
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BTS guidelines

>5 cm in the second interspace.189 The chest wall may be less
deep in the fourth or fifth interspace, and this could provide an
alternative site for decompression or a chest drain may need to
be inserted if there is an initial treatment failure. In any case,
a chest drain should be inserted immediately after needle
decompression and the cannula left in place until bubbling is
confirmed in the underwater seal system to confirm proper
function of the chest drain.186
PNEUMOTHORAX AND PREGNANCY
< Pneumothorax recurrence is more common in preg-
nancy, poses risks to the mother and fetus, and requires
close cooperation between chest physicians, obstetri-
cians and thoracic surgeons. (C)
< The modern and less invasive strategies of simple
observation and aspiration are usually effective during
pregnancy, with elective assisted delivery and regional
anaesthesia at or near term. (C)
< A corrective surgical procedure (VATS) should be
considered after delivery. (D)
Although less common in women than in men, the occurrence
of PSP in women of childbearing age is not unusual. There
appears to be an increased risk of recurrence during pregnancy
and during parturition,190 with potential risks to the mother and
fetus. The earlier literature consists largely of case reports and
described varied and relatively invasive management strategies
such as prolonged intrapartum chest tube drainage, intrapartum
thoracotomy, premature induction of labour or caesarean
section. A more recent case series and literature review191 has
recommended the use of more modern conservative manage-
ment methods for which favourable outcomes have now been
experienced. Pneumothorax that occurs during pregnancy can be
managed by simple observation if the mother is not dyspnoeic,
there is no fetal distress and the pneumothorax is small (<2 cm).
Otherwise aspiration can be performed, chest drain insertion
being reserved for those with a persistent air leak.
Close cooperation between the respiratory physician, obste-
trician and thoracic surgeon is essential. To avoid spontaneous
delivery or caesarean section, both of which have been associated
with an increased risk of recurrence, the safest approach will
usually be that of elective assisted delivery (forceps or ventouse
extraction) at or near term, with regional (epidural) anaesthesia.
Less maternal effort is required with forceps delivery, which is
therefore preferable. If caesarean section is unavoidable because
of obstetric considerations, then a spinal anaesthetic is preferable
to a general anaesthetic.
Because of the risk of recurrence in subsequent pregnancies,
a minimally invasive VATS surgical procedure should be
considered after convalescence. Successful pregnancies and
spontaneous deliveries without pneumothorax recurrence have
been reported after a VATS procedure.191
CATAMENIAL PNEUMOTHORAX
< Catamenial pneumothorax is underdiagnosed in women
with pneumothorax. (C)
< A combination of surgical intervention and hormonal
manipulation requires cooperation with thoracic
surgeons and gynaecologists. (D)
Catamenial is a term that derives from the Greek meaning
‘monthly’. The typical combination of chest pain, dyspnoea and
haemoptysis occurring within 72 h before or after menstruation
in young women has been thought to be relatively rare. There are
approximately 250 cases described in the medical literature,192
but it is likely that the majority of cases are not reported. Most of
these references are of solitary case reports or small series. The
associated pneumothorax is usually right-sided and there is
a heightened tendency to recurrence coinciding with the
menstrual cycle. Many cases have evidence of pelvic endometri-
osis. Although the aetiology is not fully understood, inspection of
the pleural diaphragmatic surface at thoracoscopy often reveals
defects (termed fenestrations) as well as small endometrial
deposits. These deposits have also been seen on the visceral
pleural surface. Among women undergoing routine surgical
treatment for recurrent pneumothorax, however, catamenial
pneumothorax has been diagnosed in as many as 25%.193 Thus, it
may be relatively underdiagnosed.
Extragenital or ‘ectopic’ endometriosis is an uncommon
condition that can affect almost any organ system and tissue
within the body, the thorax being the most frequent extrapelvic
location. What has been termed the thoracic endometriosis
syndrome (TES) includes catamenial pneumothorax, catamenial
haemothorax, catamenial haemoptysis and lung nodules (purple
or brown coloured). The most accepted theory to explain the
phenomenon of catamenial pneumothorax is that of aspiration
of air from the abdomen and genital tract via the diaphragmatic
fenestrations, but the appearance of endometriosis deposits on
the visceral pleural surface raises the possibility that erosion of
the visceral pleura might be an alternative mechanism.
Haemoptysis is thought to result from intrapulmonary endo-
metriosis deposits, the mechanism by which endometrial tissue
reaches the lung being poorly understood.
The management strategies can be divided into thoracic
surgical techniques and hormonal manipulation although, in the
past, total abdominal hysterectomy and bilateral salpingohys-
terectomy have been employed. Thoracic surgical techniques
have been varied and include diaphragmatic resection or plica-
tion of the fenestrations seen at thoracoscopy, the insertion of
a mesh or patch over these fenestrations, electrocoagulation of
the endometriosis deposits and pleurodesis. This variability
reflects the general lack of success with surgical intervention
alone, recurrence rates of up to 30% being documented.194 When
combined with gonadotrophin-releasing hormone analogues
amenorrhoea results, but recurrence has been avoided with
follow-up approaching periods of 4 years.195 Successful patient
management requires close cooperation between respiratory
physicians, thoracic surgeons and gynaecologists.
PNEUMOTHORAX AND AIDS
< The combination of pneumothorax and HIV infection
requires early intercostal tube drainage and surgical
referral, in addition to appropriate treatment for HIV
and PJP infection. (C)
Over the course of the last 20 years a strong association has
been observed between HIV infection and pneumothorax.
Historically, up to 5% of AIDS patients developed pneumo-
thorax196e198 and up to 25% of spontaneous pneumothoraces
occurred in HIV-infected patients in large urban settings where
a high prevalence occurred.27 28 199 Pneumocystis jiroveci (PJP)d
previously known as Pneumocystis carinii (PCP)dinfection has
been considered to be the main aetiological factor for this
association, because of a severe form of necrotising alveolitis
that occurs in which the subpleural pulmonary parenchyma is
replaced by necrotic thin-walled cysts and pneumatoceles.200 201
The administration of nebulised pentamidine has also been
suggested as a possible independent risk factor.196 The use of
systemic corticosteroids may also contribute to the morbidity in
such patients.202

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Due to the histopathology outlined above, pneumothoraces
caused by PJP have a tendency to more prolonged air leaks,
treatment failure, recurrence and higher hospital mortality.203
Up to 40% of these patients can develop bilateral pneumo-
thorax. Treatment failures have been observed to correlate with
the degree of immunosuppression, as reflected by CD4
counts.203 In view of these features, management strategies have
been evolved that incorporate early and aggressive intervention
including tube drainage, pleurodesis and surgical techniques such
as pleurectomy.197 199 202e205 Observation and simple aspiration
are not likely to suffice, even in the first instance.
Over the last 5 years, and since the last BTS guidelines, the
global spectrum of HIV infection has changed significantly as
a result of the more widespread use of both antiretroviral
therapy and PJP prophylaxis. While the disease burden remains
very high in the underdeveloped world, the prognosis for such
patients in Western societies has greatly improved,206 where this
combination is now much less frequently encountered. As HIV
is now becoming a more chronic disease associated with a high
incidence of smoking and therefore of COPD, pneumothoraces
might become more significant when they occur.
However, the mortality of patients who require intensive care
for PJP in HIV infection remains high, especially when pneu-
mothorax occurs during ventilation. Although antiretroviral
therapy that is commenced before or during hospitalisation can
improve the outcome,207 the potential risk of the ‘immune
reconstitution syndrome’ has to be taken into consideration.
PNEUMOTHORAX AND CYSTIC FIBROSIS
< The development of a pneumothorax in a patient with
cystic fibrosis requires early and aggressive treatment
with early surgical referral. (C)
< Pleural procedures, including pleurodesis, do not have
a significant adverse effect on the outcome of subse-
quent lung transplantation. (D)
Even though long-term survival has improved significantly, spon-
taneous pneumothorax remains a common complication of cystic
fibrosis, occurring in 0.64% of patients per annum and 3.4% of
patients overall.208 It occurs more commonly in older patients and
those with more advanced lung disease, and is associated with a
poor prognosis, the median survival being 30 months.209 Contra-
lateral pneumothoraces occur in up to 40% of patients.209 210 An
increased morbidity also results, with increased hospitalisation
and a measurable decline in lung function.208 While a small
pneumothorax without symptoms can be observed or aspirated,
larger pneumothoraces require a chest drain. The collapsed lung
can be stiff and associated with sputum retention, thus requiring
a longer time to re-expand. During this time other general
measures, such as appropriate antibiotic treatment, are needed.
Chest tube drainage alone has a recurrence rate of 50%, but
interventions such as pleurectomy, pleural abrasion and pleu-
rodesis have lower rates.211e213 With a success rate of 95% and
with little associated reduction in pulmonary function, partial
pleurectomy is generally regarded as the treatment of choice in
patients with cystic fibrosis and recurrent pneumothoraces
who are fit to undergo surgery.209 In those who are not fit for
surgery and in whom re-expansion may take several weeks
with a chest drain and suction, pleurodesis offers an alternative
strategy.209 This had been thought to be a relative contraindi-
cation to later transplantation because of the need for
a lengthier transplant procedure and excessive bleeding.214 A
more recent study215 has concluded that previous pleural
procedures should not be considered as a contraindication for
transplantation, there being no significant effect on surgical
Thorax 2010;65(Suppl 2):ii18eii31. doi:10.1136/thx.2010.136986
BTS guidelines
outcome although more dense pleural adhesions were observed
than in a control population.
IATROGENIC PNEUMOTHORAX
Iatrogenic pneumothorax has been shown to be even more
common than spontaneous pneumothorax in several large
reviews,216 217 the most common causes being transthoracic
needle aspiration (24%), subclavian vessel puncture (22%), thor-
acocentesis (22%), pleural biopsy (8%) and mechanical ventilation
(7%).218 It is also a complication of transbronchial biopsy. During
transthoracic needle aspiration the two primary risk factors are
the depth of the lesion and the presence of COPD.219 A large
retrospective survey in the USA found an incidence of 2.68%
among patients undergoing thoracocentesis.220 No means of
reducing this risk has yet been identified. Positioning of the patient
so that the procedure is performed in a dependent area has had no
beneficial effect.221 Excluding iatrogenic penumothorax that
occurs in intensive care units, the treatment seems to be relatively
simple with less likelihood of recurrence (the underlying risk
factors for SP not usually being present). The majority resolve
spontaneously by observation alone. If intervention is required,
simple aspiration has been shown to be effective in 89% of
patients.94 For the remainder a chest drain is required, this being
more likely in patients with COPD.222
In the intensive care unit iatrogenic pneumothorax is a life-
threatening complication that may be seen in up to 3% of
patients.223 Those on positive pressure ventilation require chest
drain insertion as positive pressure maintains the air leak.224
CONCLUDING REMARKS
These pneumothorax guidelines differ from the last (2003) BTS
guidelines in that they have been produced in accordance with the
SIGN methodology and therefore have necessitated a careful
analysis of the current underlying evidence. Unfortunately there
are relatively few adequate studies that address the main areas of
uncertainty, and few additions to the knowledge base in the last 7
years. Nevertheless, some subtle changes in practice have occurred.
These are incorporated, together with coverage of some additional
topics of relevance such as catamenial pneumothorax and the issue
of pneumothorax in pregnancy. The treatment algorithm is now
illustrated on a single flowchart for both PSP and SSP and places
slightly less emphasis on the size of the pneumothorax and more
on the clinical features. However, the trend towards more
conservative management is maintained, with observation for
many patients with PSP, aspiration for the remainder, and small-
bore chest drains for persistent air leaks. The imaging of pneu-
mothorax has undergone a major change due to the advent of
PACS technology, and the implications of this are now described.
Surgical practice has also developed with the widespread adoption
of less invasive (VATS) procedures rather than open thoracoto-
mies. While the challenge of pneumothorax management in
patients with cystic fibrosis remains, there has been a significant
reduction in pneumothorax in patients with HIV since the
introduction of antiretroviral therapy and PJP prophylactic
therapy, in the countries with advanced healthcare systems at
least. It is hoped that these guidelines build upon their predeces-
sors and lead to improved care for patients with pneumothorax,
and that they inform and support the clinicians who care for them.
Competing interests No member of the Guideline Group is aware of any competing
interests.
Provenance and peer review The draft guideline was available for online public
consultation (July/August 2009) and presented to the BTS Winter Meeting (December
2009). Feedback was invited from a range of stakeholder institutions (see
ii27
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BTS guidelines
Introduction). The draft guideline was reviewed by the BTS Standards of Care
Committee (September 2009).
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Management of spontaneous pneumothorax:

British Thoracic Society pleural disease
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Andrew MacDuff, Anthony Arnold and John Harvey

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Symposium

Sonographic diagnosis of pneumothorax

Lubna F Husain, Laura Hagopian, Derek Wayman, William E Baker,
Kristin A Carmody
Department of Emergency Medicine, Boston Medical Center, Boston, MA, USA

ABSTRACT
Lung sonography has rapidly emerged as a reliable technique in the evaluation of various thoracic diseases. One important,
well-established application is the diagnosis of a pneumothorax. Prompt and accurate diagnosis of a pneumothorax in
the management of a critical patient can prevent the progression into a life-threatening situation. Sonographic signs,
including ‘lung sliding’, ‘B-lines’ or ‘comet tail artifacts’, ‘A-lines’, and ‘the lung point sign’ can help in the diagnosis of a
pneumothorax. Ultrasound has a higher sensitivity than the traditional upright anteroposterior chest radiography (CXR) for
the detection of a pneumothorax. Small occult pneumothoraces may be missed on CXR during a busy trauma scenario,
and CXR may not always be feasible in critically ill patients. Computed tomography, the gold standard for the detection
of pneumothorax, requires patients to be transported out of the clinical area, compromising their hemodynamic stability
and delaying the diagnosis. As ultrasound machines have become more portable and easier to use, lung sonography now
allows a rapid evaluation of an unstable patient, at the bedside. These advantages combined with the low cost and ease of
use, have allowed thoracic sonography to become a useful modality in many clinical settings.

Key Words: Emergency medicine, pneumothorax, diagnosis, thoracic ultrasonography

INTRODUCTION sonographic artifacts created by the interplay of air and fluid

The use of ultrasound (US) in the diagnosis and treatment of
patients is a well-established modality that has existed for many
years. Thoracic sonography is fairly new in comparison to other
accepted ultrasound applications, and is still rapidly evolving. The
use of thoracic ultrasound has gained slow acceptance due to the
traditional teaching that the air-filled lungs are not ultrasound
friendly. Poor imaging is a result of the confinement of air
between the lung and the chest wall, preventing diffusion of the
ultrasound beam into the parietal pleura and deep lung structures,
leading to a production of artifacts. Over the past decade, bedside
lung sonography has developed an established role in literature
for the diagnosis of thoracic diseases. This development is
based on an improved understanding and appreciation of the
Address for correspondence:
Dr. Lubna Farooq Husain, E-mail: lubna.farooq@bmc.org
in the lungs. The first reported use of ultrasound to detect
pneumothorax in humans was by Wernecke et al., in 1987.[1]
The Focused Assessment with Sonography in Trauma (FAST)
examination has now been modified to include lung imaging as
part of the evaluation in a trauma patient. The application has
been renamed as the E-FAST examination, with ‘E’ standing for
extended, including the standard lung views.
A pneumothorax can be divided into two broad categories: traumatic
(including iatrogenic) or atraumatic. Atraumatic pneumothorax
can further be categorized as primary spontaneous or secondary
spontaneous. Pneumothorax is commonly associated with both
blunt and penetrating chest injury and is a leading cause of
preventable morbidity and mortality. Traumatic pneumothorax,
the most common life-threatening outcome in blunt chest trauma,
occurs in over 20% of patients with blunt injuries and about 40%
with penetrating chest injuries.[2]

Access this article online The diagnosis of a pneumothorax is usually made with a
Quick Response Code:
Website:
combination of clinical signs and symptoms, which may be subtle,
www.onlinejets.org and plain chest radiography. Regardless of its presentation, the
early detection and treatment of a pneumothorax is critical. Small-
DOI:
(10% or less) or medium (11 to 40%)-sized pneumothoraces are
10.4103/0974-2700.93116 generally not life-threatening and their management varies.[3-5]
However, a delay in the diagnosis and treatment, especially in those
76 Journal of Emergencies, Trauma, and Shock I 5:1 I Jan - Mar 2012

who are mechanically ventilated, may lead to the progression of a
pneumothorax and resultant hemodynamic instability.[6,7] In these
critical situations where a subtle pneumothorax may be missed,
a quick bedside lung ultrasound may expedite the diagnosis,
treatment, and resuscitation of a patient who may have otherwise
decompensated.
Ultrasound has a well-known established role in the diagnosis
of a traumatic pneumothorax. In one prospective study a
hand-held ultrasound device was used by trauma surgeons
to perform the E-FAST examination in patients with blunt
or penetrating trauma.[8] The utility of thoracic ultrasound
for diagnosing a pneumothorax was compared to chest x-ray
(CXR) alone, a composite standard (CXR, chest, and abdomen
Computed tomography (CT) scans, clinical course, and invasive
interventions), and to the gold standard CT scan (CT only). Their
results showed that the E-FAST examination had a sensitivity of
58.9% with a positive likelihood ratio of 69.7 and a specificity
of 99.1% when compared to the composite standard. The
E-FAST was also compared to CXR, using CT scan as the gold
standard, showing that ultrasound had a higher sensitivity than
CXR, 48.8 and 20.9%, respectively, and a similar specificity of
99.6 and 98.7%, respectively. In addition, they noted that 63%
of all pneumothoraces diagnosed were occult. Traditionally,
these would end up getting diagnosed later on a CT scan.
Although CT scan remains the gold standard, they concluded
that ultrasound was more sensitive in identifying occult traumatic
pneumathoraces compared to CXR.
Similarly, a prospective study by Ball et al., noted that up to 76%
of all traumatic pneumothoraces were missed by the standard
supine AP chest film when interpreted by the trauma team.[9]
This number was much higher than their prior retrospective
study (55%), where image interpretation relied on radiologists.
This stressed the poor sensitivity of CXR in a rushed trauma
scenario and the utility of performing a rapid bedside ultrasound,
to possibly aid in the diagnosis, prior to sending a patient for a
CT scan.[10]
Several other studies highlight the utility of ultrasound compared
to CXR for the diagnosis of pneumothorax in the Emergency
Department.[11-14] The sensitivity of ultrasound in certain studies
has been similar to that found in CT scan, which is still considered
to be the gold standard for the detection of a pneumothorax.[11,15]
Lichtenstein et al., have shown that ultrasound has a sensitivity of
95.3% and a specificity of 91.1% for detecting pneumothorax in
intensive care unit (ICU) patients.[16] However, in this particular
article, the authors cite that the underlying lung process may
have affected the accuracy of ultrasound, resulting in both false-
positive and false-negative cases.
Relevant English language articles and case reports were searched
by using PubMed and Google Scholar (1984–2011). The following
search terms were used: ‘Ultrasonography’, ‘chest sonography,’
‘bedside lung ultrasound,’ ‘pneumothorax,’ and ‘emergency
medicine.’
Journal of Emergencies, Trauma, and Shock I 5:1 I Jan - Mar 2012
Husain, et al.: Sonographic diagnosis of pneumothorax
Probe selection and equipment
The bedside sonographic diagnosis of pneumothorax can be
performed with most ultrasound machines without the need of
any sophisticated functions. Most machines are now portable and
can be brought to the bedside, which is especially helpful in the
critically ill and hemodynamically unstable patient, as it obviates
the need for transport. Also, the physician performing the scan
can interpret the results of the bedside ultrasound immediately.
A straight linear array high frequency probe (5–13 MHz) may
be most helpful in analyzing superficial structures such as the
pleural line and providing better resolution.[17] A microconvex
or curvilinear array probe may be more suitable for deeper lung
imaging as it provides better penetration (1–8 MHz), at the cost of
less resolution. Finally, some advocate the use of the phased array
probe, generally used in cardiac imaging (2–8 MHz), as its flat and
smaller footprint is better suited for imaging in between the ribs.
Technique and normal anatomy
A pneumothorax contains air and no fluid, and therefore, will
rise to the least dependent area of the chest. In a supine patient
this area corresponds to the anterior region of the chest at
approximately the second to fourth intercostal spaces in the
mid-clavicular line. This location will identify the majority of
significant pneumothoraces in the supine patient, which makes
it the recommended initial area for investigation in a trauma.[17,18]
In contrast, air will accumulate in an apicolateral location in an
upright patient.[19]
Based on the above, patients are scanned in a supine or near-to-
supine position. The probe should be placed in a sagittal position
(indicator pointing cephalad) on the anterior chest wall at about
the second intercostal space, in the mid-clavicular line [Figure 1].
The sonographer should first identify the landmarks of two ribs
with posterior shadowing behind them and visualize the pleural
line in between them. This is typically called ‘the bat sign’ where
the periosteum of the ribs represents the wings and the bright
hyperechoic pleural line in between them represents the bats’
Figure 1: Correct probe positioning in the initial evaluation of a
pneumothorax. The probe is placed on the anterior chest wall
in a sagittal orientation, pointing toward the patient’s head at
approximately the second intercostal space in the mid-clavicular line
77
Husain, et al.: Sonographic diagnosis of pneumothorax
body [Figures 2a and 2b].[20] If the ribs are not visualized the
probe should be slowly moved in a caudal direction (inferiorly)
until two ribs appear on the screen. It is in between these two
rib landmarks that the two layers of pleura, parietal and visceral,
are seen sliding across one another. As stated earlier, air will rise
to the anterior chest wall, and therefore a pneumothorax that is
large enough to require a chest tube will appear with this simple
technique.
The presence of pleural sliding is the most important finding
in normal aerated lung. The sonographer should visualize
the hyperechoic pleural line in between two ribs moving or
shimmering back and forth. Lung sliding corresponds to the
to-and-fro movement of the visceral pleura on the parietal
pleura that occurs with respiration. It is a dynamic sign and can
be identified on ultrasound as horizontal movement along the
pleural line.[21] Sliding is best seen at the lung apex in a supine
patient.[21] The use of M-mode, which detects motion over
time, provides more evidence that the pleural line is sliding. It is
beneficial in patients where sliding may be subtle, such as, in the
elderly or in patients with poor pulmonary reserve, who are not
taking large breaths. The M-mode cursor is placed over the pleural
line and two different patterns are displayed on the screen: The
motionless portion of the chest above the pleural line creates
horizontal ‘waves,’ and the sliding below the pleural line creates a
granular pattern, the ‘sand’ [Figure 3]. The resultant picture is one
that resembles waves crashing in onto the sand and is therefore
called the ‘seashore sign’ and is present in normal lung.[13,22,23]
‘B-lines’ or ‘comet-tail artifacts’ are reverberation artifacts that
appear as hyperechoic vertical lines that extend from the pleura
to the edge of the screen without fading [Figure 4]. 'Comet-tail
artifacts' move synchronously with lung sliding and respiratory
movements.[21] A few visualized ‘B-lines’ in dependent regions
are expected in normal aerated lung and are visualized moving
along with the sliding pleura. These artifacts are seen in normal
lung due to the acoustic impedance differences between water
and air.[22] Excessive ‘B-lines’, especially in the anterior lung, are
abnormal and are usually indicative of interstitial edema.
Figure 2: (a) ‘The bat sign.’ Two ribs with posterior shadowing represents the wings of the bat, and the hyperechoic pleural line, its
body (b) A sagittal scan at the upper intercostal spaces depicting normal anatomy
78
The average time to perform this examination varies from two to
three minutes; less than one minute to rule out a pneumothorax
and several minutes to rule it in.[8,12]
Sonographic signs of pneumothorax
Absence of lung sliding
In a pneumothorax, there is air present that separates the visceral
and parietal pleura and prevents visualization of the visceral
pleura. In this situation, lung sliding is absent. This lack of lung
sliding can be visualized by identifying the landmarks discussed
earlier. Two ribs should be identified with the pleural line in
between them. The typical to-and-fro movement or shimmering
of the pleural line will not be present. The same technique using
M-mode can be used to confirm a lack of sliding. The resultant
M-mode tracing in a pneumothorax will only display one pattern
of parallel horizontal lines above and below the pleural line,
exemplifying the lack of movement. This pattern resembles a
‘barcode’ and is often called the ‘stratosphere sign’ [Figure 5].[22,23]
The negative predictive value for lung sliding is reported as
99.2–100%, indicating that the presence of sliding effectively
rules out a pneumothorax.[11,16,24] However, the absence of
lung sliding does not necessarily indicate that a pneumothorax
is present. Lung sliding is abolished in a variety of conditions
other than pneumothorax, including acute respiratory distress
syndrome (ARDS), pulmonary fibrosis, large consolidations,
pleural adhesions, atelectasis, right mainstem intubation, and
phrenic nerve paralysis.[21,25,26] Specificity values range from
60 –99% depending on the patient population, with higher values
in the general population and lower values in the Intensive Care
Unit and in those with ARDS.[11,16,21,24] Although the absence of
lung sliding is not specific for pneumothorax, the combination
of this with other signs improves the accuracy of the diagnosis.
Comet tail artifacts or ‘B-lines’
Ultrasound demonstrates the loss of ‘comet-tail artifacts’ in
patients with a pneumothorax. These reverberation artifacts
are lost due to air accumulating within the pleural space, which
hinders the propagation of sound waves and eliminates the
Journal of Emergencies, Trauma, and Shock I 5:1 I Jan - Mar 2012

Figure 3: M-mode illustrating the ‘seashore sign.’ The pleural
line divides the image in half: The motionless portion above the
pleural line creates horizontal ‘waves,’ and the sliding line below
it creates granular pattern, the ‘sand’
Figure 5: M-mode and the absence of lung sliding are shown
as the ‘stratosphere sign’: Parallel horizontal lines above and
below the pleural line, resemble a ‘barcode.’ This sign indicates
a pneumothorax at this intercoastal space
Figure 7: ‘Lung point sign.’ (Right) B-mode depicting the lung
point: Sliding lung touching the chest wall. (Left) The ‘seashore
sign’ (white arrow) and the ‘stratosphere sign’ (dotted arrow) as
the lung intermittently contacts the chest wall
Journal of Emergencies, Trauma, and Shock I 5:1 I Jan - Mar 2012
Husain, et al.: Sonographic diagnosis of pneumothorax
Figure 4: ‘B-lines’ or ‘comet-tail artifacts’ are seen originating from
the bright white hyperechoic pleural line, extending vertically to
the edge of the screen. ‘B-lines’ move in synchrony with the sliding
pleura in a normal well-aerated lung
Figure 6: ‘A-lines’, a type of reverberation artifact, are horizontal,
equally spaced lines seen originating from the bright white
hyperechoic pleural line. If ‘B-lines’ are present, they extend out
from the pleural line and erase the ‘A-lines’ in their path
acoustic impedance gradient.[20] In addition, ‘comet–tail’ artifacts
are generated by the visceral pleura, which is not visualized in
a pneumothorax, therefore, these artifacts are not generated.[24]
The negative predictive value for this artifact is high, reported
at 98–100%, such that visualization of even one comet-tail
essentially rules out the diagnosis of a pneumothorax.[21,24,27]
‘A-lines’ are other important thoracic artifacts that can help in
the diagnosis of a pneumothorax. These are also reverberation
artifacts appearing as equally spaced repetitive horizontal
hyperechoic lines reflecting off of the pleura [Figure 6].
The space in between each A-line corresponds to the same
distance between the skin surface and the parietal pleura. In the
normal patient, when ‘B-lines’ are present, they extend from
the pleural line and erase ‘A-lines’, as they emanate out to the
edge of the screen. ‘A-lines’ will be present in a patient with a
pneumothorax, but ‘B-lines’ will not. If lung sliding is absent
79
Husain, et al.: Sonographic diagnosis of pneumothorax
with the presence of ‘A-lines’, the sensitivity and specificity for
an occult pneumothorax is as high as 95 and 94%, respectively.[24]
Lung-point sign
The ‘lung-point sign’ occurs at the border of a pneumothorax.
It is due to sliding lung intermittently coming into contact with
the chest wall during inspiration and is helpful in determining
the actual size of the pneumothorax. This sign can further
be delineated using M-mode where alternating ‘seashore’ and
‘stratosphere’ patterns are depicted over time [Figure 7]. The
‘lung-point sign’ is 100% specific for pneumothorax and defines
its border.[21,28] The location of the lung point is beneficial in
determining the size of the pneumothorax. If a lack of lung
sliding is visualized anteriorly, the probe can progressively be
moved to more lateral and posterior positions on the chest wall
searching for the location of the lung-point. The more lateral
or posterior the ‘lung-point sign’ is identified, the larger the
pneumothorax. Therefore, if the ‘lung-point sign’ is seen in
an anterior location on the chest wall, the sonographer can be
assured that the pneumothorax is relatively small.[11,24,29] Although
the specificity is high, the sensitivity of the ‘lung-point sign’
is relatively low (reported at 66%) and is not seen in cases of
total lung collapse.[28] Studies have shown concordance between
pneumothorax size on ultrasound and CT scan, reportedly
within 1.9–2.3 cm.[15,26,29] The determination of the size of a
pneumothorax is important for clinical decision-making, as larger
pneumothoraces are more likely to require thoracostomy.[11,24]
Other signs
The ‘Power Slide’ refers to the use of power (angiography)
Doppler to help identify lung sliding. Power Doppler is very
sensitive and picks up subtle flow and movement. If there is
lung sliding present, power Doppler will light up the sliding
pleural line with color flow [Figure 8]. This technique can be
helpful in cases of subtle sliding when direct visualization may
be difficult. The disadvantage of this type of Doppler is that
due to its increased sensitivity, the probe needs to be held in a
Figure 8: ‘Power slide’ in normal sliding lung. Power (angiography)
Doppler is used at the pleural line, which is visualized lighting up
with color flow as subtle sliding is detected. The probe must be
steady to avoid unwanted color artifacts
80
steady manner and the patient has to be motionless in order to
prevent artifact and erroneous color flow over the pleural line,
when sliding is actually absent.[23,30]
The ‘lung pulse’ refers to the rhythmic movement of the pleura
in synchrony with the cardiac rhythm. It is best viewed in areas
of the lung adjacent to the heart, at the pleural line. The ‘lung
pulse’ is a result of cardiac vibrations being transmitted to the
lung pleura in poorly aerated lung. Cardiac activity is essentially
detected at the pleural line when there is absent lung sliding. In
normal well-aerated lung, the ‘lung pulse’ is not present, as lung
sliding becomes dominant and resistant to cardiac vibrations. [21]
CONCLUSIONS
Thoracic sonography for the detection of pneumothorax has
become a well-established modality in the acute care setting. It
is indispensible in the blunt or penetrating chest trauma patient,
where the identification of a pneumothorax can prevent life-
threatening consequences. The ease of use and portability of
newer machines, combined with the improved training among
physicians has allowed thoracic ultrasound to become a useful
bedside tool in patients with respiratory complaints. The
traditional upright AP radiograph has become less important due
to its poor sensitivity in diagnosing a pneumothorax compared
to ultrasound. Although CT scan remains the gold standard and
may still catch smaller occult pneumothoraces that ultrasound
misses, its disadvantages are becoming more apparent. Bedside
ultrasound obviates the need for patient transport in unstable
situations, it eliminates radiation exposure, it is quicker to perform
and is immediately interpreted at the bedside without unnecessary
delays. In addition, it is more cost-effective and can be repeated
multiple times during a resuscitation.
In addition, ultrasound is the perfect modality in the emergency
and critical care setting after performing certain procedures, such
as a thoracentesis or the placement of a central line, to quickly
confirm the presence of lung-sliding and to rule out an iatrogenic
pneumothorax. It has also been found to be beneficial in the
post-intubation scenario, where a confirmation of bilateral lung
sliding rules out a right mainstem intubation.
The increasing portability of newer ultrasound machines makes
them easier to use in first responder and disaster settings, wilderness
medicine, air medical transport, rural medicine, and even space
explorations. Studies indicate that the recognition of key artifacts
in thoracic ultrasound is readily teachable to both physicians as
well as non-physician health care providers and its uses continue
to expand in the out-of-hospital setting.[31,32]
This article offers a review of the current evidence for the use of
thoracic ultrasound in the diagnosis of a pneumothorax, reviews
the proper techniques used, and highlights its clinical utility.
We conducted a literature search for the latest scientific evidence
on this topic in English language articles and case studies
(1984 - 2011) using PubMed and Google Scholar.
Journal of Emergencies, Trauma, and Shock I 5:1 I Jan - Mar 2012

REFERENCES
1. Wernecke K, Galanski M, Peters PE, Hansen J. Pneumothorax: Evaluation
by ultrasound-preliminary results. J Thorac Imaging 1987;2:76-8.
2. Di Bartolomeo S, Sanson G, Nardi G, Scian F, Michelutto V, Lattuada
L. A population-based study on pneumothorax in severely traumatized
patients. J Trauma 2001;51:677-82.
3. British Thoracic Society Fitness to Dive Group, Subgroup of the British
Thoracic Society Standards of Care Committee. British thoracic society
guidelines on respiratory aspects of fitness for diving. Thorax 2003;58:3-13.
4. Baumann MH, Strange C, Heffner JE, Light R, Kirby TJ, Klein J, et al.
Management of spontaneous pneumothorax: An american college of
chest physicians delphi consensus statement. Chest 2001;119:590-602.
5. de Leyn P, Lismonde M, Ninane V, Noppen M, Slabbynck H,
van Meerhaeghe A, et al. Guidelines belgian society of pneumology.
Guidelines on the management of spontaneous pneumothorax. Acta Chir
Belg 2005;105:265-7.
6. Enderson BL, Abdalla R, Frame SB, Casey MT, Gould H, Maull KI. Tube
thoracostomy for occult pneumothorax: A prospective randomized study
of its use. J Trauma 1993;35:726-30.
7. Bridges KG, Welch G, Silver M, Schinco MA, Esposito B. CT detection
of occult pneumothorax in multiple trauma patients. J Emerg Med
1993;11:179-86.
8. Kirkpatrick AW, Sirois M, Laupland KB, Liu D, Rowan K, Ball CG, et al.
Hand-held thoracic sonography for detecting post-traumatic pneumothoraces:
The extended focused assessment with sonography for trauma (EFAST). J
Trauma 2004;57:288-95.
9. Ball CG, Ranson K, Dente CJ, Feliciano DV, Laupland KB, Dyer D,
et al. Clinical predictors of occult pneumothoraces in severely injured
blunt polytrauma patients: A prospective observational study. Injury
2009;40:44-7.
10. Ball CG, Kirkpatrick AW, Laupland KB, Fox DI, Nicolaou S, Anderson IB,
et al. Incidence, risk factors, and outcomes for occult pneumothoraces in
victims of major trauma. J Trauma 2005;59:917-25.
11. Blaivas M, Lyon M, Duggal S. A prospective comparison of supine
chest radiography and bedside ultrasound for the diagnosis of traumatic
pneumothorax. Acad Emerg Med 2005;12:844-9.
12. Dulchavsky SA, Schwarz KL, Kirkpatrick AW, Billica RD, Williams DR,
Diebel LN, et al. Prospective evaluation of thoracic ultrasound in the
detection of pneumothorax. J Trauma 2001;50:201-5.
13. Zhang M, Liu ZH, Yang JX, Gan JX, Xu SW, You XD, et al. Rapid detection
of pneumothorax by ultrasonography in patients with multiple trauma. Crit
Care 2006;10:R112.
14. Tocino IM, Miller MH, Frederick PR, Bahr AL, Thomas F. CT detection of
occult pneumothorax in head trauma. AJR Am J Roentgenol 1984;143:987-90.
15. Soldati G, Testa A, Sher S, Pignataro G, La Sala M, Silveri NG. Occult traumatic
pneumothorax: Diagnostic accuracy of lung ultrasonography in the emergency
department. Chest 2008;133:204-11.
16. Lichtenstein DA, Menu Y. A bedside ultrasound sign ruling out pneumothorax
in the critically ill. Lung sliding. Chest 1995;108:1345-8.
Journal of Emergencies, Trauma, and Shock I 5:1 I Jan - Mar 2012
Husain, et al.: Sonographic diagnosis of pneumothorax
17. Tocino IM, Miller MH, Fairfax WR. Distribution of pneumothorax in
the supine and semirecumbent critically ill adult. AJR Am J Roentgenol
1985;144:901-5.
18. Ball CG, Kirkpatrick AW, Laupland KB, Fox DL, Litvinchuk S, Dyer DM,
et al. Factors related to the failure of radiographic recognition of occult
posttraumatic pneumothoraces. Am J Surg 2005;189:541-6.
19. Weissberg D, Refaely Y. Pneumothorax: Experience with 1,199 patients.
Chest 2000;117:1279-85.
20. Lichtenstein D, Meziere G, Biderman P, Gepner A. The 'comet-tail
artifact': An ultrasound sign ruling out pneumothorax. Intensive Care Med
1999;25:383-8.
21. De Luca C, Valentino M, Rimondi M, Branchini M, Baleni MC, Barozzi
L. Use of chest sonography in acute-care radiology. J Ultrasound 2008;
11:125-34.
22. Barillari A, Kiuru S. Detection of spontaneous pneumothorax with chest
ultrasound in the emergency department. Intern Emerg Med 2010;5:253-5.
23. Johnson A. Emergency department diagnosis of pneumothorax using
goal-directed ultrasound. Acad Emerg Med 2009;16:1379-80.
24. Lichtenstein DA, Meziere G, Lascols N, Biderman P, Courret JP, Gepner A, et al.
Ultrasound diagnosis of occult pneumothorax. Crit Care Med 2005;33:1231-8.
25. Murphy M, Nagdev A, Sisson C. Lack of lung sliding on ultrasound does
not always indicate a pneumothorax. Resuscitation 2008;77:270.
26. Ball CG, Kirkpatrick AW, Feliciano DV. The occult pneumothorax: What
have we learned? Can J Surg 2009;52:E173-9.
27. Soldati G, Testa A, Pignataro G, Portale G, Biasucci DG, Leone A, et al. The
ultrasonographic deep sulcus sign in traumatic pneumothorax. Ultrasound
Med Biol 2006;32:1157-63.
28. Lichtenstein D, Meziere G, Biderman P, Gepner A. The “lung point”:
An ultrasound sign specific to pneumothorax. Intensive Care Med
2000;26:1434-40.
29. Soldati G, Testa A, Sher S, Pignataro G, La Sala M, Silveri NG. Occult traumatic
pneumothorax: Diagnostic accuracy of lung ultrasonography in the emergency
department. Chest 2008;133:204-11.
30. Cunningham J, Kirkpatrick AW, Nicolaou S, Liu D, Hamilton DR, Lawless
B, et al. Enhanced recognition of “lung sliding” with power color Doppler
imaging in the diagnosis of pneumothorax. J Trauma 2002;52:769-71.
31. Noble VE, Lamhaut L, Capp R, Bosson N, Liteplo A, Marx JS, et al.
Evaluation of a thoracic ultrasound training module for the detection
of pneumothorax and pulmonary edema by prehospital physician care
providers. BMC Med Educ 2009;9:3.
32 Monti JD, Younggren B, Blankenship R. Ultrasound detection of
pneumothorax with minimally trained sonographers: A preliminary study. J
Spec Oper Med 2009;9:43-6.
How to cite this article: Husain LF, Hagopian L, Wayman D,
Baker WE, Carmody KA. Sonographic diagnosis of pneumothorax.
J Emerg Trauma Shock 2012;5:76-81.
Received: 01.06.11. Accepted: 06.06.11.
Source of Support: Nil. Conflict of Interest: None declared.
81
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 The n e w e ng l a n d j o u r na l of m e dic i n e

videos in clinical medicine

summary points

Needle Aspiration of Primary Spontaneous

Pneumothorax
Mathieu Pasquier, M.D., Olivier Hugli, M.D., and Pierre-Nicolas Carron, M.D.

The following text summarizes information provided in the video.

Overview
Primary spontaneous pneumothorax occurs in patients without clinically apparent From the University Hospital of Lausanne,
lung disease or trauma.1-5 Observation may be the only requirement for patients Lausanne, Switzerland. Address reprint
requests to Dr. Carron at Emergency Ser-
with small primary spontaneous pneumothoraxes.5 For a large pneumothorax or vice, University Hospital of Lausanne,
one that causes clinically significant breathlessness, active intervention is required.4 BH06, 1011 Lausanne CHUV, Switzerland,
This intervention may involve simple aspiration, the placement of a chest tube,1,2 or or at Pierre-Nicolas-Carron@chuv.ch.
needle aspiration. Needle aspiration is considered to be as effective and safe as N Engl J Med 2013;368:e24.
chest-tube thoracostomy for the management of primary spontaneous pneumotho- DOI: 10.1056/NEJMvcm1111468
Copyright © 2013 Massachusetts Medical Society.
rax.2-4 Needle aspiration results in less discomfort and pain, a shorter hospital stay,
and fewer hospital admissions than does chest-tube thoracostomy.2-4 Emergency-
department physicians should be familiar with this technique and be able to ex-
plain it to patients as part of the decision-making process involved in determining
the best treatment.3 This supplement reviews the information provided in the video
on the techniques and equipment required to perform needle aspiration of primary
spontaneous pneumothorax in adults. Although needle aspiration may also be in-
dicated for select patients with secondary pneumothorax, its use in patients with
this condition is not addressed here or in the video.

Indications
Needle aspiration is appropriate for patients with a first episode of primary spon-
taneous pneumothorax. Patients should have no evidence of underlying lung dis-
ease but should have either shortness of breath or a pneumothorax with a rim of air
measuring at least 2 cm when assessed at the level of the hilum.4

Contraindications
Needle aspiration is contraindicated when a patient has traumatic pneumothorax,
pneumothorax in each lung, tension pneumothorax, hemodynamic instability, un-
derlying pulmonary disease, a history of recurrent pneumothorax, or a bleeding
disorder. An age older than 50 years is a relative contraindication, because the pro-
cedure is less likely to be successful in patients in this age group.1,4,5

Equipment
Different types of catheters can be used to perform needle aspiration, and you
should be familiar with the specific devices available at your institution. The proce-
dure requires a 16-gauge or 18-gauge over-the-needle catheter, tubing with a three-
way stopcock, and a 50-ml or 60-ml syringe. To administer a local anesthetic agent,
you will need 1% or 2% lidocaine, a 10-ml syringe, and one small-gauge needle (size
25); for anesthetizing deeper layers of tissue, you will also need one larger-gauge
needle (size 22). You will also need sterile gloves, a protective or sterile gown, a face

n engl j med 368;19  nejm.org  may 9, 2013 e24(1)

The New England Journal of Medicine
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Copyright © 2013 Massachusetts Medical Society. All rights reserved.

Figure 1. Site of Needle Insertion.
The preferred location for placement
of a needle for aspiration of pneumo-
thorax is the second intercostal space
at the midclavicular line, on the side
with the pneumothorax.
Figure 2. Confirmation of Penetration
of Pleural Space.
The appearance of air bubbles in the
syringe, which is partially filled with
the local anesthetic, indicates that the
catheter has penetrated the pleural
space.
Figure 3. Aspiration of Air from
a Pneumothorax.
After air is aspirated from a pneumo-
thorax, it is returned to the ambient
air through the side port of a three-way
stopcock.
e24(2)
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Copyright © 2013 Massachusetts Medical Society. All rights reserved.
The new england journal of medicine
mask, chlorhexidine or another antiseptic solution, a sterile preparation kit, and
sterile drapes.
Patient Preparation
To prepare the patient, explain the procedure, confirm the patient’s identity, and
obtain written informed consent. You should also verify the absence of contraindi-
cations, confirm that the patient has no allergy to lidocaine, and verify whether the
pneumothorax is on the right or the left side. Place the patient in a semisupine
position (with the torso at an angle of 30 to 45 degrees) to allow the air to collect
at the apex of the lung. Administer oxygen and monitor the oxygen saturation of
the arterial blood with pulse oximetry. Heart rate and blood pressure should also
be monitored, and an intravenous catheter should be in place. The patient should
be provided with a face mask.
Locating Landmarks
The preferred location for placement of a needle for aspiration of pneumothorax is
the second intercostal space at the midclavicular line, on the side with the pneumo-
thorax. Begin by locating the second and third ribs. The second rib can be felt just
below the collar bone. The second intercostal space is the area between the second
and third ribs. Next, identify the middle of the clavicle and the midclavicular line.
The intersection of the midclavicular line and the second intercostal space is the
correct place to insert the needle for aspiration of pneumothorax (Fig. 1). A skin-
marking pen can be used to mark the insertion site.
Procedure
Put on the face mask, the protective or sterile gown, and the sterile gloves. Use
chlorhexidine or another antiseptic solution to clean the patient’s skin, and then
position the sterile drape. Aspirate lidocaine into the 10-ml syringe. Using the
25-gauge needle, inject a wheal of lidocaine at the superior edge of the third rib, at
the midclavicular line. Switch to a 22-gauge needle and anesthetize the deeper tissue
layers by inserting the needle perpendicular to the skin. Always aspirate the site be-
fore injecting the anesthetic, to make sure the needle has not entered a blood vessel.
With the needle positioned just over the top of the third rib, advance it in the
direction of the pleural space. Placing the needle just above the third rib will pre-
vent injuries to the intercostal vessels and nerves, which lie just below the rib.
Once you have inserted the needle through the intercostal space, continue to aspi-
rate slightly. When you penetrate the pleural space, air bubbles will appear as you
aspirate (Fig. 2). Before you remove the needle, note the depth of the penetration.
You will use the depth as a reference point when you insert the over-the-needle
catheter.
Connect the over-the-needle catheter to the 10-ml lidocaine syringe, which
should be partially filled with the remainder of the local anesthetic. Using the
same landmarks that you used for the local anesthetic, slowly advance the needle
in the direction of the pleural space while continuing to aspirate with the syringe.
Again, when the needle penetrates the pleural space, air bubbles will appear in
the syringe. At this time, advance the needle by a few more millimeters to allow
the catheter tip to fully penetrate the pleural space. Remove both the catheter
needle and the 10-ml syringe as the patient exhales or coughs. Quickly obstruct
the opening of the catheter with your finger to prevent the entry of additional air
into the pleural space.
Attach the tubing with the three-way stopcock to the catheter, and use the 50-ml
or 60-ml syringe to gently aspirate the air from the pleural space (Fig. 3). Manipu-
lation of the three-way stopcock requires close attention, since any opening to the
n engl j med 368;19  nejm.org  may 9, 2013
The New England Journal of Medicine
 needle aspir ation of primary spontaneous pneumothor ax

ambient air can lead to air entrapment in the pleural space and failure of the pro- References
1. Sahn SA, Heffner JE. Spontaneous
cedure. When manipulating the stopcock, be sure that the pleural space is never
pneumothorax. N Engl J Med 2000;342:
open to the environment. Return the air through the side port into the ambient 868-74.
air and measure the volume of the air that is aspirated by counting the number of 2. Wakai A, O’Sullivan RG, McCabe G.
Simple aspiration versus intercostal tube
syringes you evacuate. The evacuation of more than 2.5 liters is an indication that
drainage for primary spontaneous pneu-
there may be an air leak, and the procedure should be stopped.1,4,5 Continue mothorax in adults. Cochrane Database
manual aspiration until you cannot aspirate any more air. Remove the catheter and Syst Rev 2007;1:CD004479.
3. Zehtabchi S, Rios CL. Management of
put a sterile dressing on the site of insertion.
emergency department patients with pri-
A postprocedural chest radiograph should be obtained with the patient in an mary spontaneous pneumothorax: needle
upright position. When needle aspiration is successful, the patient’s symptoms will aspiration or tube thoracostomy? Ann
Emerg Med 2008;51:91-100. [Erratum, Ann
improve, and only minimal residual pneumothorax — or no pneumothorax —
Emerg Med 2008;51:309.]
should be present on the chest film.3,6 Most patients are ready for discharge 6 hours 4. MacDuff A, Arnold A, Harvey J, BTS
after the procedure, provided that a second postprocedural chest radiograph shows Pleural Disease Guideline Group. Manage-
ment of spontaneous pneumothorax: Brit-
no recurrence of the pneumothorax.1,5,6 The time of patient discharge will vary
ish Thoracic Society Pleural Disease Guide-
according to the institution. line 2010. Thorax 2010;65:Suppl 2:ii18-ii31.
5. Kosowsky JM. Pleural disease. In:
Complications Marx JA, ed. Rosen’s emergency medicine:
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Complications from needle aspiration of primary spontaneous pneumothorax may Vol. 1. Philadelphia: Mosby, 2010:939-43.
include localized subcutaneous emphysema, infection, lung laceration, air embo- 6. Ho KK, Ong ME, Koh MS, Wong E,
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lism, or bleeding. You can minimize the risk of bleeding by placing the catheter at
comparing minichest tube and needle as-
the intercostal space just above the third rib, thereby preventing injuries to the in- piration in outpatient management of pri-
tercostal vessels. Technical failure may occur if you cannot reach the pleural space mary spontaneous pneumothorax. Am J
Emerg Med 2011;29:1152-7.
— if the catheter is too short, for instance. This problem most often arises in pa- Copyright © 2013 Massachusetts Medical Society.
tients who are very muscular or obese. Aspiration of more than 2.5 liters of air may
indicate the presence of a persistent air leak, for which the placement of a chest
tube should be considered.1,4,5

Summary
Needle aspiration is an alternative treatment to the placement of a chest tube for
patients with a first episode of primary spontaneous pneumothorax. A careful pre-
procedural evaluation is needed to be certain that there are no contraindications.
All patients should be monitored closely during the procedure. After the anatomical
landmarks have been identified and the local anesthetic agent has been adminis-
tered, the intrapleural air can be evacuated through a large-bore catheter. The success
of the procedure is confirmed by clinical improvement and by a chest film showing
no or minimal residual pneumothorax.
No potential conflict of interest relevant to this article was reported.
Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.

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