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BAB I

PENDAHULUAN

1.1. Latar Belakang


American Lung Association, melaporkan bahwa hingga tahun 1936 pneumonia
menjadi penyebab kematian nomor satu di Amerika. Di Indonesia, pneumonia penyebab
kematian ketiga setelah kardiovaskuler dan tuberculosis (Misnadiarly,2008). Berdasarkan
laporan kabupaten/kota tahun 2011 di Jawa Timur terdapat 75.699 kasus pneumonia dan
dengan jumlah kematian 6 orang (Dinkes Jatim, 2012).
Pneumonia adalah peradangan yang mengenai parenkim paru, distal dari bronkiolus
terminalis yang mencakup bronkiolus respiratorius, dan alveoli, serta menimbulkan
konsolidasi jaringan paru dan gangguan pertukaran gas setempat. Di Negara berkembang
termasuk Indonesia penyebab pneumonia yang paling sering ditemukan adalah disebabkan
oleh bakteri, sedangkan di negara maju disebabkan oleh Mycoplasma Pneumon.
Batuk darah merupakan salah satu gejala pada Pneumonia, namun menjadi penyulit
apabila batuk darah menjadi profuse (Eddy JB,2005). Penanganan batuk darah profuse di
tempat pelayanan kesehatan dalam hal ini Rumah Sakit merupakan jenis pertolongan kegawat
daruratan klinik yang cukup sering dijumpai, sehingga sebagai ujung tombak dokter umum
hendaknya memahami dan mengerti hal hal yang perlu di lakukan pada pertolongan batuk
darah pada umumnya dan batuk darah profuse pada khususnya.

1.2.Rumusan Masalah
Bagaimana penatalaksanaan Pneumonia dengan penyulit batuk darah profuse ?

1.3. Tujuan Penelitian


1.3.1. Tujuan Umum
Mengetahui penatalaksanaan Pneumonia dengan penyulit batuk darah profuse ?
1.3.2. Tujuan Khusus
1. Mempelajari gejala klinis Pneumonia dengan penyulit batuk darah profuse
2. Mempelajari pemeriksaan fisik Pneumonia dengan penyulit batuk darah profuse
3.Mempelajari pemeriksaan penunjang Pneumonia dengan penyulit batuk darah profuse
4. Mempelajari penatalaksanaan Pneumonia dengan penyulit batuk darah profuse

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1.4. Manfaat Penelitian
1.4.1. Manfaat Bidang Akademis
1. Memberi pengalaman pada mahasiswa dalam membuat karya tulis berupa Laporan
Kasus.
2.Meningkatkan pengetahuan mahasiswa tentang penatalaksanaan Pneumonia dengan
penyulit batuk darah profuse

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BAB II
TINJAUAN PUSTAKA

2.1. PNEUMONIA
2.1.1. Definisi Pneumonia
Pneumonia adalah peradangan yang mengenai parenkim paru, distal dari bronkiolus
terminalis yang mencakup bronkiolus respiratorius, dan alveoli, serta menimbulkan
konsolidasi jaringan paru dan gangguan gas setempat (Dahlan,2006 ). Pada Pneumonia
dijumpai sel sel inflamasi dalam alveoli samapai parenkhim paru, berakibat alveoli
mengalami penurunan kemampuan menyerap oksigen yang berefek penurunan kemampuan
imunitas tubuh yang berefek terjadinya penyebaran infeksi ke seluruh tubuh yang dikenal
dengan sepsis yang menjadi penyebab kematian pada pneumonia (Misnadiarly,2008).
2.1.2. Klasifikasi Pneumonia
Pneumonia, maka pneumonia diklasifikasikan berdasarkan kuman penyebab dan ciri radiologis yaitu
Tipical Pneumonia dan Atipikal Pneumoniai (Spicer,WJ,2003). Klasifikasi berdasarkan faktor
lingkungan yaitu Community Acquired Pneumonia, Nosocomial Pneumonia/ Hospital
Aquired Pneumonia (HAP), Aspiration Pneumonia dan Ventilator Associated Pneumonia
(VAP)( Hazinski, Thomas A. 2003)
2.1.2.1. Klasifikasi Pneumonia berdasarkan kuman penyebab dan ciri radiologis
Tipical Pneumonia, dengan gambaran radiologi berupa opasitas pada lobus atau lobularis (
sering disebut sebagai Pneumonia Lobar (Spicer,WJ,2003). Tipical Pneumonia ini disebabkan oleh Str.
Pneumonia , pneumonia jenis ini kadang disebut sebagai Bacterial Pneumonia (Dahlan 2006).
Atipikal Pneumonia, dengan gambaran radiologi berupa infiltrat paru yang bersifat bilateral dan
difus. Secara terperinci di bagi atas (Spicer,WJ,2003):
1. Broncho-pneumonia: diffuse patchy, menyebar sepanjang paru-paru.
2. Interstisial: menyerang interstisium
3. Necrotising: cavitation dan penghancuran dari parenkim, membentuk abses-abses (Spicer,
2008).
Atipikal Pneumonia ini disebabkan oleh H. influenza, S. aureus dan bakteri gram negatif
memberikan sindromklinik yang identik dengan pneumonia oleh Str. Pneumoniae, dan bakteri lain
danvirus dapat menimbulkan gambaran yang sama dengan pneumonia oleh M.pneumoniae. Sebaliknya
Chlamydia pneumoniae atau Legionella spp. dan virus dapat memberikan gambaran pneumonia yang
bervariasi luas karena itu istilah tersebut tidak lagi dipergunakan , pneumonia jenis ini kadang disebut sebagai
Non bacterial Pneumonia (Dahlan 2006).

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2.1.2.2. Klasifikasi Pneumonia berdasarkan faktor lingkungan
Community Acquired Pneumonia (CAP), adalah pneumonia yang terjadi infeksi
diluar rumah sakit, seperti rumah jompo atau Home care. Jenis Pneumonia ini bisa bersifat
bakterial atau viral. Infeksi bakterial terjadi dalam dua pola morfologik yang sering tumpang
tindih (Bronkopneumonia serta Pneumonia Lobaris) dan disebabkan oleh berbagai
mikroorganisme gram positif atau gram negative. Bergantung pada virulensi bakteri dan
resistensi hospes, mikroorganisme yang sama dapat menyebabkan bronkopneumonia,
pneumonia lobaris atau suatu keadaan yang berada diantara kedua pneumonia ini.
Mikroorganisme yang sering dijumpai pada Community Acquired Pneumonia antara lain:
Streptococcus pneumonia atau pneumococcus merupakan mikroorganisme yang paling
sering ditemukan; diplokokus gram positif berbentuk lanset di dalam neutrophil.
Haemophilus influenza merupakan bakteri pleomorfik, gram negative, berkapsul (enam
serotip) atau tidak berkapsul (tidak bisa ditentukan tipenya); mikroorganisme ini
menyebabkan infeksi saluran nafas bawah dan meningitis yang bisa membawa kematian
pada anak-anak dan merupakan penyebab umum pneumonia pada orang dewasa.
Moraxella catarrhalis menyebabkan pneumonia bacterial, khususnya pada manula; infeksi
ini memperberat COPD dan merupakan penyebab umum otitis media pada anak-anak.
Staphylococcus aureus pneumonie sering menjadi komplikasi penyakit virus dan
merupakan infeksi pada para pemakai obat intravena; infeksi oleh mikroorganisme ini
mengakibatkan abses dan empiema.
Klebsiella pneumonie merupakan penyebab paling umum pneumonia gram negatif; infeksi
ini mengenai orang-orang yang keadaan umumnya buruk, khususnya pecandu alcohol
kronik.
Pseudomonas aeruginosa sering ditemukan pada pasien kistik fibrosis dan neutropenia.
Legionella pneumophilia menyebar lewat aerosol; infeksi oleh mikroorganisme ini
menyebabkan pneumonia yang berat pada pasien dengan gangguan imunitas.
Nosocomial Pneumonia/ Hospital Aquired Pneumonia (HAP), adalah Pneumonia
yang didapat selama (batasan yang sering dipakai perawatan > 3 hari) di rumah sakit.
Mikroorganisme yang sering dijumpai pada pasien dengan penyakit dasar yang berat atau
dengan pemakaian alat yang invasive, dan merupakan komplikasi serius yang bisa membawa
kematian. Mikroorganisme yang sering dijumpai pada Nosocomial Pneumonia adalah:
kuman bukan multi drug resistance (MDR) misalnya S.pneumoniae, H. Influenzae,
Methicillin Sensitive Staphylococcus aureus (MSSA) dan kuman MDR misalnya
Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae, Acinetobacter spp dan

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Gram positif seperti Methicillin Resistance Staphylococcus aureus (MRSA). Pneumonia
nosokomial yang disebabkan jamur, kuman anaerob dan virus jarang terjadi
(Hendrickson,2005).
Ventilator Associated Pneumonia (VAP), adalah Pneumonia yang terjadi setelah 48-
72 jam intubasi tracheal atau menggunakan ventilasi mekanik di ICU ( Hazinski, Thomas A.
2003)
Aspiration PneumoniaPneumonia Aspirasi terjadi pada pasien-pasien yang keadaan
umumnya sangat buruk atau yang tidak sadarkan diri; keadaan ini sebagian mengakibat
kan pneumonia kimia (asam lambung) dan sebagian lagi pneumonia bacterial (campuran
dengan flora oral).
2.1.3. Patofisiologi dan Patogenesis Pneumonia
Mekanisme terjadinya Pneumonia secara Patofisiologi dan pathogenesis adalah:
Aspirasi mikroorganisme yang mengkolonisasi sekresi orofarinks merupakan rute infeksi
yang paling sering. Rute inokulasi lain meliputi inhalasi, penyebaran infeksi melalui darah
(hematogen) dari area infeksi yang jauh, dan penyebaran langsung dari tempat penularan
infeksi.
Jalan napas atas merupakan garis pertahanan pertama terhadap infeksi, tetapi, pembersihan
mikroorganisme oleh air liur, ekspulsi mukosiliar, dan sekresi IgA dapat terhambat oleh
berbagai penyakit, penurunan imun, merokok, dan intubasi endotrakeal.
Pertahanan jalan napas bawah meliputi batuk, reflex muntah, ekspulsi mukosiliar,
surfaktan, fagositosis makrofag dan polimorfonukleosit (PMN), dan imunitas selular dan
humoral. Pertahanan ini dapat dihambat oleh penurunan kesadaran, merokok, produksi mucus
yang abnormal (mis., kistik fibrosis atau bronchitis kronis), penurunan imun, intubasi dan
tirah baring berkepanjangan.
Makrofag alveolar merupakan pertahanan primer terhadap invasi saluran pernapaan bawah
dan setiap hari membersihkan jalan napas dari mikroorganisme yang teraspirasi tanpa
menyebabkan inflamasi yang bermakna.
Virulensi mikroorganisme terlalu besar, maka makrofag akan merekrut PMN dan memulai
rangkaian inflamasi dengan pelepasan berbagai sitokin termasuk leukotriene, factor nekrosis
tumor (TNF), interleukin, radikal oksigen , dan protease. Inflamasi tersebut menyebabkan
pengisian alveolus mengalami ketidakcocokan ventilasi/perfusi dan hipoksemia. Terjadi
apoptosis sel-sel paru yang meluas, ini membantu membasmi mikroorganisme intrasel seperti
tuberkolosis atau klamidia, tetapi juga turut andil dalam proses patologis kerusakan paru.

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Infeksi dan inflamasi dapat tetap terlokalisirdi paru atau dapat menyebabkan bacteremia
yang mengakibatkan meningitis atau endocarditis sindrom respons inflamasi sistemik dan/
atau sepsis. Faktor virulensi dan berbagai mikroorganisme dapat mempengaruhi
patofisiologi dan perjalan klinis penyakit. Streptococcus pneumonia (pneumococcus)
merupakan contoh yang sangat tepat (Steinert Don MA,2009)
2.1.4. Faktor Resiko Pneumonia
Individu yang memiliki kecenderungan terjadi Pneumonia antara lain:
Individu yang memiliki daya tahan tubuh lemah, hal ini dijumpai pada: Penderita
HIV/AIDS, Penderita penyakit kronis, seperti sakit jantung, diabetes mellitus, Orang yang
pernah atau rutin menjalani kemoterapi, Perokok dan peminum alcohol. Perokok berat dapat
mengalami iritasi pada saluran pernapasan (bronchial) yang akhirnya menimbulkan sekresi
mucus (riak/dahak). Apabila riak/dahak mengandung bakteri, maka dapat menyebabkan
pneumonia. Alcohol berdampak buruk terhadap sel darah putih sehingga daya tahan tubuh
dalam melawan suatu infeksi menjadi lemah.
Pasien yang berada di ruang perawatan intensif (ICU/ICCU). Pasien yang dilakukan
tindakan ventilator (alat bantu napas) endotracheal tube sanagta berisiko terkena pneumonia.
Di saat mereka batuk akan mengeluarkan tekanan balik isi lambung (perut) kea rah
kerongkongan. Bila hal itu mengandung bakteri dan berpindah ke rongga napas (ventilator).
Ia sangat berpotensi terkena pneumonia.
Menghirup udara yang tercemar polusi zat kimia. Risiko tinggi yang dihadapi para petani
apabila menyemprotkan tanaman dengan zat kimia tanpa memakai masker adalah terjadinya
iritasi dan menimbulkan peradangan paru-paru, dan selanjutnya rentan menderita penyakit
pneumonia.
Pasien yang lama berbaring. Pasien yang mengalami operasi besar biasanya bermasalah
dengan hal mobilisasi. Orang dengan kondisi semacam ini memiliki resiko tinggi terkena
penyakit pneumonia. Pasalnya, saat tidur berbaring statis sangat mungkin riak berkumpul di
rongga paru-paru dan menjadi media berkembangnya bakteri (Torres A,et all,2013)
2.1.5. Diagnosis Pneumonia
2.1.5.1. Tanda dan Gejala Klinis
Tanda-tanda Pneumonia sangat bervariasi, tergantung golongan umur,
mikroorganisme penyebab, kekebalan tubuh (imunologis) dan berat ringannya penyakit.Pada
umumnya, diawali dengan panas, batuk, pilek, suara serak, nyeri tenggorokan. Selanjutnya
panas makin tinggi, batuk makin hebat, pernapasan cepat (takipnea), tarikan otot rusuk
(retraksi), sesak napas dan penderita menjadi kebiruan (sianosis).

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2.1.5.2. Pemeriksaan Fisik
Pada penderita pneumonia hasil pemeriksaan fisik dijumpai antara lain: Keadaan
Umum: umumnya keadaan umumnya nampak kelelahan atau sesak
Kesadaran: compos mentis sampai somnosent
Tanda-Tanda vital :
- Tekanan darah normal atau menurun, Nadi meningkat, Suhu meningkat, Respirasi
meningkat ringan sampai berat
Kepala/Leher:
Mata : Konjungtiva bisa anemis
Hidung: Jika sesak akan terlihat napas cuping hidung
Paru :
Inspeksi: Pengembangan paru berat, tidak simetris jika hanya satu sisi paru, ada pengunaan
otot bantu nafas dan retraksi.
Palpasi: Pengembangan paru tidak sama pada area Konsolidasi, Fremitus Raba pada daerah
Konsolidasi Meningkat
Perkusi: Bunyi redup pada area konsolidasi
Auskultasi: Bunyi nafas berkurang, bisa terdengar wheezing
Jantung: Jika tidak ada kelainan pada jantung, pemeriksaan normal
Ekstermitas: Pada ekstremitas bisa telihat sianosis, turgor kurang jika dehidrasi (Jan
Thompson, 2008)
2.1.6. Pemeriksaan Penunjang
Pemeriksaan penunjang yang dilakukan dalam menegakkan diagnosis Pneumonia al:
Pemeriksaan darah lengkap (Complete Blood Count):
Leukositosis biasanya timbul, meskipun nilai pemeriksaan darah putih (white blood count –
WBC) rendah pada infeksi virus. Pada penderita pneumonia umumnya, jumlah leukosit (sel
darah putih ) dapat melebihi batas normal yaitu 10.000/mikroliter (Christie, 2004)
Pemeriksaan Radiologis :
Pada pemeriksaan radiologis ini memberi gambaran bervariasi yaitu: bercak konsolidasi
merata pada bronkopneumonia, bercak konsolidasi satu lobus pada pneumonia lobaris,
gambaran bronkopneumonia difus atau infiltrat insertitialis pada pneumonia stafilokok.
Pemeriksaan sputum:
Pemeriksaan mikrobiologis pada pneumonia rutin dilakukan untuk memastikan bakteri
penyebab Pneumonia, sehingga antibiotika broadspectrum yang diberikan pada saat penderita
masuk Rumah Sakit (MRS) selanjutnya di ganti sesuai hasil kultur dahak.

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Spesimen pemeriksaan ini berasal dari usap tenggorok, sekret nasofaring, bilasan bronkus,
darah, pungsi pleura, atau aspirasi paru (Said, 2008). Spesimen dari saluran napas atas kurang
bermanfaat untuk kultur dan uji serologis karena tingginya prevalens kolonisasi bakteri
(McIntosh, 2002).
2.1.7. Penanganan Pneumonia
Pengobatan diberikan berdasarkan etiologi dan uji resistensi, akan tetapi, karena hal
itu perlu waktu dan pasien perlu terapi secepatnya maka biasanya diberikan (Navdeep K.
Brar,2011).
Pemberian oksigen tergantung kebutuhan penderita yang disesuaikan dengan kadar oksigen
dalam darah ( saturasi O2 dalam darah)
Cairan intravena untuk Pneumonia dewasa dapat diberikan D5:RL: 2:1. Jumlah dan jenis
cairan yang dibutuhkan penderita tergantung keadaan penderita pada saat sakit dan adanya
penyakit penyerta (Diabetes Melitus, Decomp Cordis, Gagal ginjal, atau keadaan lain yang
memerlukan jenis dan jumlah cairan yang dibatasi atau tertentu)
Antibiotika broad spectrum yang diberikan data dipilih sesuai dibawah ini :
Chefrtiaxon 2 x 1 gram IV atau Chefotaxim 3x1 gram IV atau Levofloxacin 1x 500 mg IV
atau Cyprofloxacin 2 x 1 gram IV. Pemberian antibiotika pada umumnya adalah 5-7 hari
Blood Gas Analisa (BGA), dapat diperiksa karena pasien pneumonia sering jatuh dalam
keadaan asidosis metabolic akibat intake kurang dan hipoksia, maka koreksi sesuai dengan
hasil analisis gas darah arteri.

2.2. BATUK DARAH / HEMOPTISIS


Batuk darah merupakan bagian dari tanda dan gejala pneumonia, namun batuk darah
akan menjadi penyulit apabila terjadi dalam jumlah ( lebih dari 200cc/ hari atau profuse).
Batuk darah pada pneumonia terjadi akibat ulserasi mukosa bronkhus, gangguan pembekuan
darah, peningkatan permeabilitas dinding pembuluh darah dan akibat hipervaskularisasi pada
parenkhim paru (Lordan JL,2003).
2.2.1. Definisi Batuk Darah / Hemoptisis
Hemoptisis adalah dahak yang bercampur darah yang dikeluarkan saat batuk yang
berasal dari saluran pernafasan bagian bawah (glotis ke arah distal). Definisi lain Hemoptisis
adalah setiap proses yang mengakibatkan terganggunya kontinuitas aliran pembuluh darah
paru-paru dapat mengakibatkan perdarahan.

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2.2.2. Klasifikasi Batuk darah
Klasifikasi batuk darah dapat dipandang dari dua sudut yaitu: berdasarkan volume
darah dan berdasarkan frekwensi terjadinya batuk darah (Lordan,JL, 2003)
Berdasarkan volume darah yang dikeluarkan (Lordan,JL, 2003):
Blood Streak Haemoptisis ( darah keluar berupa bercak bercak yang nampak bersama dahak)
Profuse Haemoptisis ( darah yang dibatukkan > 200CC/ 24 jam)
Berdasarkan volume darah yang dikeluarkan (Bidwell Jacob L,2005):
Derajat 1 ( blood streak)
Derajat 2 (1-30 cc/24 jam)
Derajat 3 ( > 30-150 cc /24 jam)
Derajat 4 (> 150-500 cc /24 jam)
Derajat 5 /Massive (> 500 cc/24 jam)
Berdasarkan frekwensi terjadinya Batuk darah
Single haemoptisis (interval kejadian haemopts < 7 hari )
Repetaed haemoptisis (interval kejadian haemopts > 7 hari )
2.2.3. Perbedaan Haemoptisis dan Hematemesis
Dalam penanganan batuk darah (haemoptisis) diperlukan ketepatan dasn kecepatan ,
khususnya pada batuk darah yang massive /profuse, maka hendaknya dapat membedakan
antara batuk darah dan muntah darah, agar tidak melakukan kesalahan dalam penanganan.
Dibawah ini terdapat perbedaan antara batuk darah dan muntah darah (lihat Tab 2.2.3).

Hemoptysis Hematemesis
History History
Absence of nausea and vomiting Preserence of nausea and vomiting
Lung disease Gastric or hepatic of disease
Asphyxia possible Asphyxia unusual
Sputum examination Sputum examination
Frothy Rarely frothy
Liquid or clotted appearance Coffe ground appearance
Bright red or pink Brown to black
Laboratory Laboratory
Alkaline pH Acidic pH
Mixed with macrophages and neutrophils Mixed with food particles
Tab.2.2.3. Dikutip dari: Bidwell Jacob L,2005.Haemoptysis:Diagnosis and management, American Family
Phisician.vol.72,no.7

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2.2.4. Penyebab Batuk Darah
Berdasarkan asal darah yang dibatukkan atau atau berdasarkna sumber
perdarahannya, maka perlu diketahui tentang differential diagnosis pada batuk darah ( lihat
tab.2.2.4)
Differential Diagnosis of Hemoptysis
Source other than the lower Pulmonary parenchymal Primary vascular source
Respiratory tract source Arteriovenous malformation
Upperairway (nasopharyngeal) Lung abscess Pulmonary embolism
Gastrointestinal bleeding Pneumonia Elevated pulmonary venous
Tracheobronchial source Tuberculosis pressure (mitral stenosis)
Neoplasm(bronchogenic Mycetoma Pulmonary artery rupture
carcinoma, endobronchial Goodpasture’s syndrome secondary to balloon-tip
metastatic tumor, Kaposi’s Idiopathicpulmonary pulmonary artery catheter
sarcoma, bronchial carcinoid) hemosiderosis manipulation
Bronchitis (acute or chronic) Wegener’s granulomatosis Misscellaneous and rare causes
Bronchiectasis Lupus pneumonitis Pumonary endometriosis
Broncholithiasis Long contusion Systemic coagulopathy or use
Airway trauma of anticoagulants or
Foreign body thrombolytic agents

Tab.2.2.4.Dikutip dari: Bidwell Jacob L,2005.Haemoptysis:Diagnosis and management, American Family


Phisician.vol.72,no.7

2.2.5. Penanganan Batuk Darah


Tujuan penanganan pasien dengan hemoptisis adalah menghentikan perdarahan,
mencegah aspirasi dan mengobati penyebab yang mendasari. Penanganan pada haemoptisis
profuse lebih diutamakan pada penanganan kegawat daruratannya. Haemoptisis profuse,
merupakan kondisi yang berpotensi serius, maka lakukan evaluasi Airway-Breath-
Circulation (ABC) yaitu: bebaskan saluran napas, periksa fungsi pernapasan dan periksa
fungsi sirkulasi (Bidwell Jacob.L.dkk,2005)
Mencegah aspirasi dengan cara: Posisi tredelendurg, bebaskan jalan napas dan miring
ke posisi paru yang sakit, bertujuan agar tidak terjadi aspirasi ke paru yang sehat dan
membuat pembuluh darah paru sehat terjepit, shg perdarahan cepat teratasi / berhenti, pasang
infuse, penghisapan darah dan pengambilan bekuan yang dijumpai. Cegah kehilangan banyak
darah (Eksanguination) dengan cara: menghentikan sumber perdarahan, memberi obat
koagulansia, fresh-frozen plasma dan tranfusi faktor pembekuan /platelet transfusions, FOB
(suction darah dan cari lokasi perdarahan), Rigid bronchoscopy (penghisapan darah yang
menggumpal an mudah), Endobrachial tamponade (balon kateter tamponade) dan
Embolization (pada a. Bronkialis), Cauterization,Laser photocoagulation dan Reseksi paru
(Lordan,JL, 2003)

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Bahaya utama batuk darah adalah terjadi penyumbatan trakea dan saluran nafas,
sehingga timbul sufokasi yang sering fatal. Penderita tidak nampak anemis tetapi sianosis, hal
ini sering terjadi pada batuk darah masif (600-1000 cc/24 jam). Karena saluran nafas
tersumbat, maka paru bagian distal akan kolaps dan terjadi atelektasis. Pneumonia aspirasi
merupakan salah satu penyulit yang terjadi karena darah terhisap kebagian paru yang sehat
Akibat kehilangan banyak darah sampai syok hipovolemi dan Anemia (Lordan,JL, 2003)

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BAB III
KERANGKA KONSEPTUAL

Demam
Gejala
Batuk
Sesak klinis
Nyeri dada
Batuk Darah

Gerakan paru sakit Inspeksi


tertinggal

Fremitus raba asimetri Pemeriksaan


Palpasi
Fremitus suara meningkat
Fisik
Redup Perkusi

Bronchovesikuler Auskultasi

Konsolidasi infiltrat Foto dada

Darah lengkap
Pemeriksaan
SGOT SGPT Darah
penunjang
Bun Screat
Faal Haemostasis

Sputum smear gram Sputum


Sputum Kultur gram

Posisi trendelenburg
Bebaskan jalan
Kegawatan
napas
Haemoptisis Profuse
Pemberian Cairan Penanganan
Oksigenasi
Koagulansia Konservative
Pneumonia
Antibiotika
Antitusif

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Penjelasan Kerangka Konseptual:
Gejala klinis pada pneumonia antara lain: Demam, malaise, batuk berdahak, sesak
napas dan nyeri dada) merupakan gejala umum. Batuk darah dan wajah pucat merupakan
bagian dari gejala khusus / tambahan.
Pada pemeriksaan fisik pneumonia dijumpai : Inspeksi: pengembangan paru berat,
tidak simetris jika hanya satu sisi paru, ada pengunaan otot bantu nafas dan retraksi;Palpasi:
pengembangan paru tidak sama pada area konsolidasi, fremitus raba pada daerah konsolidasi
meningkat;Perkusi: bunyi redup pada area konsolidasi; Auskultasi: bunyi nafas berkurang,
bisa terdengar wheezing dan ronchi pada daerah konsolidasi.
Pada pemeriksaan penunjang antara lain: Foto thoraks/ chest x ray, sputum smear dan
kultur, darah lengkap. Pada penatalaksanaan dibagi atas penangan kegawat daruratan pada
haemoptisis profuse dan penanganan konservative pada pneumonia pada umumnya. Untuk
penangan kegawat daruratan pada haemoptisis profuse dilakukan pemberian cairan,
membebaskan jalan napas serta mengurangi perdarahan dengan pemberian koagulansia
(transamin). Sedangkan untuk penanganan konservative dengan antibiotika broad spectrum,
terapi simptomatik dengan pemberian Oksigenasi, anti tusive (codein), Antipiretik
(parasetamol).

13
BAB IV
METODE PENELITIAN

4.1. Rancangan Penelitian


Jenis rancangan penelitian ini adalah penelitian observasional yaitu melakukan
pengamatan terhadap subjek dari suatu waktu ke waktu dengan pendekatan cross sectional.
4.2. Sampel Penelitian
Penderita dewasa yang menjalani rawat inap di ruang rawat inap Penyakit Dalam RS X
4.2.1. Kriteria Inklusi :
Penderita dewasa yang didiagnosa oleh dokter spesialis paru sebagai pneumonia dengan
penyulit batuk darah yang menjalani rawat inap di ruang rawat inap Penyakit Dalam RS X
4.2.1. Kriteria Ekklusi :
Penderita menolak menanda tangani Inform concern
4.3. Prosedur dan Tekhnik Pengambilan Sampel
Pasien yang dipilih dalam penelitian ini diambil secara nonprobability sampling dengan
teknik purposive sampling, yaitu teknik penentuan sampel dengan pertimbangan tertentu
(sugiyono, 1999). Adapun pertimbangan tertentu yang dihadapi adalah masalah perijinan
pengambilan data ke rumah sakit yaitu di ruang rawat inap Penyakit Dalam RS X.
4.4. Variabel Penelitian
Variabel dalam penelitian ini meliputi:
Gejala klinis
Pemeriksaan Fisik
Pemeriksaan Penunjang
Pengobatan Konservative dan Kegawat daruratan
4.5. Lokasi dan Waktu Penelitian
Penelitian ini dilakukan di sebuah rumah sakit di kota Surabaya. Waktu penelitiannya yaitu:
Pembuatan Proposal : September 2014
Pengumpulan Data : Oktober 2014
Analis Data : Oktober 2014
4.6. Instrumen Penelitian:
4.6.1. Alat Penelitian
Alat yang digunakan untuk penelitian retrospektif ini adalah table isian untuk
mengolah data, yaitu berisikan anamnesa, pemeriksaan fisik, dan pemeriksaan penunjang.
4.6.2. Bahan Penilitian
14
Bahan yang digunakan adalah rekam medis yang merupakan sumber sekunder.
Rekam medis pasien didapat di rumah sakit maupun informasi dari dokter spesialis sehingga
didapat suatu gambaran dan penatalaksanaan penyakit dari pasien yang diteliti.
4.7. Definisi operasional:
Pneumonia : peradangan yang mengenai parenkim paru, distal dari bronkiolus
terminalis yang mencakup bronkiolus respiratorius, dan alveoli, serta menimbulkan
konsolidasi jaringan paru dan gangguan pertukaran gas setempat
Batuk darah atau hemoptisis: ekspektorasi darah akibat perdarahan pada saluran
napas di bawah laring, atau perdarahan yang keluar melalui saluran napas bawah laring.
Penyulit batuk darah pada Pneumonia: adalah batuk darah menjadi hal yang
menyulitkan dan memberikan perhatian lebih pada penatalaksanaan pneumonia, hal ini
terjadi apabila batuk darah menjadi profuse

15
4.8.Prosedur Penelitian

Pengurusan surat perijinan penelitian laporan kasus


ke ruang rawat inap RS yang bersangkutan

Mendapat ijin melakukan penelitian


laporan kasus

Pengumpulan data

Data dari Data dari Data dari


pasien pemeriksaan Pemeriksaan
(anamnesis) fisik penunjang

Data diolah menggunakan tabel isian

Analisis data

Gejala Pemeriksaan Pemeriksaan


klinis fisik penunjang

Penanganan Pneumonia dengan


penyulit batuk darah

16
DAFTAR PUSTAKA

Bidwell Jacob L,2005.Haemoptysis:Diagnosis and management, American Family


Phisician.vol.72,no.7

Christie, Asih dan Niluh Gede Y, 2004. Keperawatan Medikal Bedah : Klien dengan
Gangguan Sistem Pernapasan. Jakarta : EGC

Dahlan, Zul. 2006. Buku Ajar Ilmu Penyakit Dalam, jilid 2. Pusat Penerbitan Departemen
Ilmu Penyakit Dalam FKUI. Jakarta.

Dinkes Jatim. 2012. Profil Kesehatan Provinsi Jawa Timur Tahun 2010, Pemerintah Provinsi
Jawa Timur Dinas Kesehatan, Surabaya.

Eddy JB,2005. Management Haemoptisis in The Emergency Department. Clinical Review


article. Page 53-59

Hazinski, Thomas A. 2003. Typical and Atypical Pneumonias. In: Rudolph et al (editor).
Rudolph’s Pediatrics, 21st edition. McGraw-Hill. New York. chapter 23.11

Jan Thompson, 2008. A Practical Guide to Clinical Medicine, A comprehensive physical


examination and clinical education site for medical students and other health care
professionals Program Representative, UCSD School of Medicine Center, San Diego,
California 92093-0611.

Lordan JL,2003. The Pulmonary Phisician In Pulmonary Care, Clinical Review. Illustrative
Case 7: Assesment and Management Massive Haemoptysis. Thorax;58: 814-819

McIntosh, Kenneth. 2002. Current Concepts: Community-Acquired Pneumonia .Available


from http://www.nejm.org (Accessed 11th September 2012).

Misnadiarly. 2008. Pneumonia, Penyakit Infeksi Saluran Napas,Edisi 1. Pustaka Obor


Populer. Jakarta.

Navdeep K. Brar,2011. Management of community-acquired Pneumonia.A Review and


Update. Ther Adv Resp Dis. 2011;5(1):61-78.

Spicer,WJ,2003. Clinical Microbiology and Infectious Diseases: An Illustrated Colour Text.


McGraw-Hill. New York. Chapter 125-127

Steinert Don MA, RRT,MT,CRS, 2009. Pathophisiology and Laboratory Identification of


Pneumonia.Clinical Laboratory of Medicine. Focus Journal jan/Feb,p:20-46

Torres A,et all, 2013. Risk factors for community-acquired pneumonia in adults in Europe: a
literature review. Thorax;68:1057-1065.

17
PROPOSAL STUDI KASUS

PENATALAKSANAAN PNEUMONIA
DENGAN PENYULIT BATUK DARAH PROFUSE
DI RUMAH SAKIT MUHAMMADIYAH GRESIK

Untuk Memenuhi Persyaratan


Memperoleh Gelar Sarjana Kedokteran

Oleh :
NASRULLAH NOOR INDRAJANU
NPM : 10700319

PROGRAM STUDI PENDIDIKAN DOKTER


FAKULTAS KEDOKTERAN
UNIVERSITAS WIJAYA KUSUMA SURABAYA
SURABAYA
2014

18
DAFTAR ISI

JUDUL................................................................................................. i
DAFTAR ISI....................................................................................... ii
BAB I PENDAHULUAN ................................................................... 1
A. Latar Belakang.................................................................................. 1
B. Rumusan Masalah .......................................................................... 2
C. Tujuan Penelitian.........................................................................……….. 2
1. Tujuan Umum...........................................................................……… 2
2. Tujuan Khusus...................................................................…….......... 2
D. Manfaat Penelitian........................................................................……… 2
BAB II. TINJAUAN PUSTAKA.......................................................... 3
A. Pneumonia ………………………………………………………….. 3
1. Definisi Pneumonia ............................................... …………… 3
2. Klasifikasi Pneumonia ............................................................... 3
a). Klasifikasi Pnemonia Berdasarkan Kuman Penyebab
dan Ciri Radiologis………….…….…………………………… 3
b). Klasifikasi Pnemonia Berdasarkan Faktor Lingkungan……… 3
3. Patofisiologi dan Patogenesis Pneumonia................................... 6
4. Faktor Resiko Pneumonia.......................................................... 8
5. Diagnosis Pneumonia............................................................... 9
a). Tanda dan gejala klinis ....................................................... 9
b). Pemeriksaan fisik ............................................................... 9
c). Pemeriksaan penunjang ........................................................... 10
6. Penatalaksanaan Pneumonia …………………………………….. 11
7. Komplikasi Pneumonia…………………………………………… 12
8. Penyulit Pneumonia ……………………………………………… 13
B. Batuk darah / Haemoptisis............................................................... 14
1. Definisi Batuk darah / Haemoptisis........................................ ……… 14
2.Perbedaan Haemoptisis dan Hematemesis.................................... 14
3. Klasifikasi Batuk darah / Haemoptisis........................................ 15
4. Diferential Diagnose Haemoptisis........................................... ……… 16
5. Penanganan batuk darah………………………………........... ……… 16

19
BAB III.KERANGKA KONSEP.......................................................... 18
BAB IV.METODE PENELITIAN……………………………………….. 20
A. Rancangan Penelitian ……………............................................ 20
B. Lokasi dan Waktu Penelitian ……………………………………. 20
C. Sampel Penelitian……………………….................................... 20
1. Besar Sampel Penelitian………………………………….. 20
2. Kriteria Inklusi……………………………………………. 20
3. Kriteria Eksklusi …………………………………………. 21
D. Prosedur dan Tehnik Pengambilan Sampel ……………………... 21
E. Variabel Penelitian……………................................................. 21
F. Definisi Operasional …………….............................................. 21
G. Prosedur Penelitian ……………………………………………… 22
H. Instrumen Penelitian……………...........................................……… 23
1. Alat Penelitian……………………………………………. …… 23
2. Bahan Penelitian ...........................................................…………. 23
BAB V. HASIL…………………………………………………………… 25
BAB VI. ANALI SA DAN PEMBAHASAN …………………………… 46
BAB VII.KESIMPULAN………………………………………………… 55
DAFTAR PUSTAKA ........................................................................………
LAMPIRAN

20
DAFTAR PUSTAKA

Bidwell Jacob L,2005.Haemoptysis:Diagnosis and management, American Family


Phisician.vol.72,no.7

Christie, Asih dan Niluh Gede Y, 2004. Keperawatan Medikal Bedah : Klien dengan
Gangguan Sistem Pernapasan. Jakarta : EGC

Dahlan, Zul. 2006. Buku Ajar Ilmu Penyakit Dalam, jilid 2. Pusat Penerbitan Departemen
Ilmu Penyakit Dalam FKUI. Jakarta.

Dinkes Jatim. 2012. Profil Kesehatan Provinsi Jawa Timur Tahun 2010, Pemerintah Provinsi
Jawa Timur Dinas Kesehatan, Surabaya.

Eddy JB,2005. Management Haemoptisis in The Emergency Department. Clinical Review


article. Page 53-59

Hazinski, Thomas A. 2003. Typical and Atypical Pneumonias. In: Rudolph et al (editor).
Rudolph’s Pediatrics, 21st edition. McGraw-Hill. New York. chapter 23.11

Jan Thompson, 2008. A Practical Guide to Clinical Medicine, A comprehensive physical


examination and clinical education site for medical students and other health care
professionals Program Representative, UCSD School of Medicine Center, San Diego,
California 92093-0611.

Lordan JL,2003. The Pulmonary Phisician In Pulmonary Care, Clinical Review. Illustrative
Case 7: Assesment and Management Massive Haemoptysis. Thorax;58: 814-819

McIntosh, Kenneth. 2002. Current Concepts: Community-Acquired Pneumonia .Available


from http://www.nejm.org (Accessed 11th September 2012).

Misnadiarly. 2008. Pneumonia, Penyakit Infeksi Saluran Napas,Edisi 1. Pustaka Obor


Populer. Jakarta.

Navdeep K. Brar,2011. Management of community-acquired Pneumonia.A Review and


Update. Ther Adv Resp Dis. 2011;5(1):61-78.

Spicer,WJ,2003. Clinical Microbiology and Infectious Diseases: An Illustrated Colour Text.


McGraw-Hill. New York. Chapter 125-127

21
Steinert Don MA, RRT,MT,CRS, 2009. Pathophisiology and Laboratory Identification of
Pneumonia.Clinical Laboratory of Medicine. Focus Journal jan/Feb,p:20-46

Torres A,et all, 2013. Risk factors for community-acquired pneumonia in adults in Europe: a
literature review. Thorax;68:1057-1065.

23

Pneumonia: Pathogenesis and


Pathophysiology
Pathogenesis

The lungs are constantly exposed to pathogens through aspiration; however, the lower
airways usually remain sterile related to innate and acquired immunity of the pulmonary
system (Marrie, 2013). Pneumonia can develop after aspiration of oropharyngeal secretions,
inhalation of causative microorganisms, or when bacteria from an infection elsewhere in the
body spreads to the lungs (ex. Bacteremia caused by IV drug use). If pathogens are able to
move past the first line of defense in the upper airway (i.e. cough reflex, mucociliary

22
clearance) to the lower respiratory tract, development of pneumonia depends of virulence of
the microorganism and the host’s defenses (McCance & Heuther, 2010).

Factors that can increase the host’s risk for infection include:

 Advanced age
 Immunocompromise (ex: HIV/AIDS, chemo)
 Underlying lung disease (ex: COPD, cystic fibrosis, bronchiectasis)
 Smoking history
 Alcohol consumption
 Altered LOC
 Impaired swallowing and entotracheal intubation
 Immobilization
 Cardiac and/or liver disease
 Malnutrition
 Medications that decrease gastric pH (ex: H2 receptor blockers)

(Marrie, 2013; McCance & Heuther, 2010)

Pathophysiology

CAP is most commonly caused by aspiration or inhalation of microorganisms through the


nasopharynx or oropharynx. Microorganisms are usually trapped in the mucous-producing
cells and cilia that line the upper airway. Factors that can impair the lungs’ first line of
defense include suppressed cough reflex, decreased ciliary action, decreased activity of
phagocytic cells, and the accumulation of secretions. If the microorganism gets past the upper
airways line of defense, the next line of defense is the airway epithelial cells which contain
alveolar macrophages. Alveolar macrophages release cytokines and cause widespread
inflammation in the lungs in an attempt to activate the immune response. The products of
inflammation (inflammatory mediators, immune complexes) can damage the lung tissue and
cause the terminal bronchioles to fill with infectious debris and exudates. Some
microorganisms also release toxins which can cause further damage to the alveolar walls.
Accumulation of exudates can leads to alveolar edema resulting in dyspnea and hypoxemia
(McCance & Heuther, 2013, Miskovich-Riddle & Keresztes, 2006).

23
Typical bacteria will usually cause lobar pneumonia which is characterized by consolidation
in a portion of the entirety of one lung (Miskovich-Riddle & Keresztes, 2006 ). In lobar
pneumonia, biproducts of inflammation such as cytokines damage the fragile alveoli and
cause edema. This edema becomes are good medium for further bacterial proliferation and
colonization. The inflammatory response results in solidification of the lung tissue as it fills
with exudate of blood, fibrin, bacteria, etc. causing a reddened appearance of the lungs. This
is called red hepatization. Red hepatization eventually progresses to gray hepatization; the
lung tissue turns gray from fibrin deposition and phagocytosis by neutrophils of the
inflammatory biproducts and microorganisms. Resolution follows when neutrophils are
replaced by macrophages, eventually eliminating the infection (McCance & Heuther, 2010).

Atypical pathogens generally cause bronchopneumonia or interstitial infiltrate characterized


by patchy inflammation and edema of both lungs (Miskovich-Riddle & Keresztes, 2006).

24
DAFTAR ISI

JUDUL................................................................................................. i
DAFTAR ISI....................................................................................... ii
BAB I PENDAHULUAN ................................................................... 1
1.1. Latar Belakang.............................................................................. 1
1.2. Rumusan Masalah .......................................................................... 1
1.3. Tujuan Penelitian.........................................................................……… 1
1.3.1. Tujuan Umum......................................................................... 1
1.3.2. Tujuan Khusus...................................................................……... 1
1.4.Manfaat Penelitian........................................................................……… 2
BAB II. TINJAUAN PUSTAKA.......................................................... 3
2.1. Pneumonia ………………………………………………………….. 3
2.1.1.Definisi Pneumonia ............................................... …………… 3
2.1.2.Klasifikasi Pneumonia ............................................................... 3
2.1.2.1. Klasifikasi Pnemonia Berdasarkan Kuman Penyebab
Dan Ciri Radiologis………….…….………………… 3
2.1.2.2.Klasifikasi Pnemonia Berdasarkan Faktor Lingkungan 4
2.1.3. Patofisiologi dan Patogenesis Pneumonia............................ 5
2.1.4. Faktor Resiko Pneumonia.......................................................... 6
2.1.5. Diagnosis Pneumonia ………………………………………… 6
2.1.5.1. Tanda dan Gejala Klinis …… ………………………. 6
2.1.5.2. Pemeriksaan Fisik …………………………………… 7
2.1.6. Pemeriksaan penunjang ........................................................... . 8
2.1.7.Penanganan Pneumonia................................................................ .. 8
2.2.Batuk darah / Haemoptisis............................................................... .. 8
25
2.2.1. Definisi Batuk darah / Haemoptisis........................................ .. 8
2.2.2. Kalsfikasi Batuk darah / Haemoptisis........................................... .. 9
2.2.3. Perbedaan Haemoptisis dan Hematemesis.............................. .. 9
2.2.4. Diferential Diagnose Haemoptisis........................................... . 10
2.2.5. Penanganan batuk darah………………………………........... 10
BAB III.KERANGKA KONSEP.......................................................... 12
BAB IV.METODE PENELITIAN……………………………………….. 14
4.1.Rancangan Penelitian ……………............................................. 14
4.2.Sampel Penelitian……………………….................................... 14
4.2.1. Kriteria Sampel Inklusi…………………………………… 14
4.2.2. Kriteria Sampel Eksklusi ………………………………… 14
4.3.Prosedur dan Tehnik Pengambilan Sampel …………………….. 14
4.4.Variabel Penelitian……………................................................ 14
4.5.Lokasi dan Waktu Penelitian……………................................. 14
4.6. Instrumen Penelitian……………............................................ 14
4.6.1.Alat Penelitian……………………………………………… 14
4.6.2.Bahan Penelitian ...........................................................……… 15
4.7. Definisi Operasional .............................................................……… 15
4.8. Prosedur Penelitian……………................................................ 16
DAFTAR PUSTAKA ........................................................................…….. 17
LAMPIRAN

26
Coughing Up Blood (Hemoptysis)

Share this:

Coughing up blood (hemoptysis) can be a sign of a serious medical condition. Infections,


cancer, and problems in blood vessels or in the lungs themselves can be responsible.
Coughing up blood generally requires medical evaluation unless the hemoptysis is due to
bronchitis.

Causes of Hemoptysis

There are many potential reasons for coughing up blood. Causes for coughing blood include:

 Bronchitis (acute or chronic), the most common cause of coughing up blood. Hemoptysis
due to bronchitis is rarely life-threatening.
 Bronchiectasis
 Lung cancer or non-malignant lung tumors
 Use of blood thinners (anticoagulation)
 Pneumonia
 Pulmonary embolism
 Congestive heart failure, especially due to mitral stenosis
 Tuberculosis

27
 Inflammatory or autoimmune conditions (lupus, Wegener’s granulomatosis, microscopic
polyangiitis, Churg-Strauss syndrome, and many others)
 Pulmonary arteriovenous malformations (AVMs)
 Crack cocaine
 Trauma, such as a gunshot wound or motor vehicle accident
 Dieulafoy’s disease

Hemoptysis can also come from bleeding outside the lungs and airways. Severe nosebleeds or
vomiting of blood from the stomach can result in blood draining into the windpipe (trachea).
The blood is then coughed up, appearing as hemoptysis.

In many people with hemoptysis, no cause is ever identified. Most people with unexplained
hemoptysis are no longer coughing up blood six months later.

Hemoptysis Tests

In people who are coughing up blood, testing focuses on determining the rate of bleeding and
any risk to breathing. The cause for hemoptysis must then be identified. Tests for coughing
up blood include:

History and physical examination. By talking to and examining someone who is coughing
up blood, a doctor gathers clues that help identify the cause.

Chest X-ray. This test may show a mass in the chest, areas of fluid or congestion in the
lungs, or be completely normal.

Computed tomography (CT scan). By producing detailed images of structures in the chest,
a CT scan can reveal some causes for coughing up blood.

Bronchoscopy. A doctor advances an endoscope (flexible tube with a camera on its end)
through the nose or mouth into the windpipe and airways. Using bronchoscopy, a doctor may
be able to identify the cause of hemoptysis.

Complete blood count (CBC). A test of the number of white and red blood cells in the
blood, along with platelets (cells that help blood clot).

Urinalysis. Certain causes of hemoptysis also result in abnormalities on this simple urine
test.

Blood chemistry profile. This test measures electrolytes and kidney function, which may be
abnormal in some causes of hemoptysis.

Coagulation tests. Alterations in blood’s ability to clot can contribute to bleeding and
coughing up blood.

Arterial blood gas. A test of the levels of oxygen and carbon dioxide in the blood. Oxygen
levels can be low in people coughing up blood.

Pulse oximetry. A probe (usually on a finger) tests the level of oxygen in the blood.

28
Pathophysiology Behind Classical
Symptoms of Pulmonary
Tuberculosis |Pathology|
Posted by Prince of Caliph on July 17, 2011

5 Votes

Pulmonary TB has classic symptoms of night sweat, fever, dypsnea and hemoptysis. In order
to correlate the pathogenesis of the disease with the presenting classical symptoms of
pulmonary TB, let me overview the whole picture of the disease.

1. Upon settlement in the alveolar space, after passes through the cough reflex and
mucociliary clearence, mycobacterium tuberculosis (MTB) will initiate an immidiate acute
inflammatory response. Detected foreign particle by macrophage through its distinctive
mannose capped glycolipid, macrophage will start to engulf the MTB. Consequent to that, IL-
1 will be released as soon as possible to stimulate the thermostat of the brain at the
Organum Vasculasum of Lamina Terminalis (OVLT) to increase the level of body temperature
with a hope to fight against the foreign particles. Through increasing the body temperature,
iron serum level will drop significantly this will immobilize bacterial growth as most bacteria
need iron for replication. Therefore, at the early stage of pulmonary TB, patient is presented
with intermittent on and off low grade fever.
2. Upon engulfment of the MTB, macrophage is now susceptible to endosomal manipulation in
which will lead to ineffective digestion of MTB and finally lead to MTB multiplication inside
the alveolar macrophage. Nevertheless, some alveolar macrophages resist the endosomal
manipulation through a protein called Natural Resistance-Associated Macrophage Protein
1 (NRAMP1) which is highly genetic polymorphism. This kind of mcrophage is capable of
digesting the MTB and finally present the antigen in the Major Histocompatibility Complex
(MHC). The MHC will then recognize by the T-cell and APC will in turn release IL-12 to

29
initiate the production of T-cell subtype which is Helper T-cell type 1 (TH1). . In order to elicit
the formation of granuloma in order to settle down and confine the infection, Helper T-cell 1
will produce Tumour Necrosis Factor (TNF). Interestingly, this TNF is produced massively at
night and some extensive experiments have been done and it is believed that the sharp
increase in the serum TNF level causes the classic night sweat in pulmonary TB patient.
Despite of that, the hypothesis is still remained inconclusive and some scienctists are still
debating the basis of TNF pathology towards night sweat.
3. After the confinement of MTB inside granuloma, inflammatory response couldn’t stop to
initiate further destruction over the surrounding tissues as massive inflammatory cells
infiltration has lead to release of tremendous amount of free radicals to fight against the
destructive MTB. Massive tissue damage has lead to destuction of pulmonary capillary
endothelium which causes hemorrhage. In fact, during chronic inflammation, blood vessels
surrounding the infected sites are engorged and highly susceptible to destroy. The leakage
of blood vessel leads the patient to cough out not only pus containing sputum but also
blood.
4. On further destruction, lung function is now at the brink of compromisation as patient is
now can hardly breath air as too many lung parenchyma has been obliterated.
Consequently, more tissue fibrosis takes part and more lung remodelling occurs as a part of
healing process. This further compromises lung function. As at the farther prognosis of the
disease, patient is now starting to present with shortness of breath (dyspnea) as a part of
compensatory mechanism to eleavate the oxygen partial pressure inside the systemic
circulation. Since the patient is at at the state of hypoxia for quite something, total body
metabolism depletes insidiously making the patient to only capable to gasp air instead of
having a long and complete force ventilation (with respect to its reduced energy)

Massive Hemoptysis: Pathogenesis and


Management
1. Stephen M. Winter, MD
1. Pulmonary Section, Yale-New Haven Hospital, New Haven, CT

1. David H. Ingbar, MD
1. Pulmonary Section, Yale-New Haven Hospital, New Haven, CT

Abstract

Massive hemoptysis is a life-threatening complication of many pulmonary disorders, and it


occurs most com monly in association with longstanding inactive tuber culosis,
bronchiectasis, lung abscess, bronchogenic car cinoma, and fungal disease. It is generally a
neovascular change or local erosive effect of chronic pulmonary dis ease and may originate
from either bronchial or pulmo nary circulation. Recurrent bleeding is unpredictable;
therefore, diagnostic and therapeutic intervention must be undertaken with urgency. The
immediate priorities must be protection of the airway to the nonbleeding lung and
localization of the site of hemorrhage prefera bly by bronchoscopy, which has a high yield
when per formed during active hemorrhage. Immediate control of bleeding may be obtained
by local tamponade with a balloon-tipped Fogarty catheter, use of a double-lumen

30
endotracheal tube, or angiographically guided emboliza tion. Surgical resection is the
preferred definitive treat ment for those who meet operative criteria; those who lack adequate
pulmonary reserve are candidates for em bolization of sites with persistent bleeding. The high
mortality of conservatively treated massive hemoptysis and the current inability to predict
which patients will have fatal hemorrhage mandate rapid assessment and intervention.

INTRODUCTION

Hemoptysis, or the expectoration of blood, can range from blood-streaking of sputum to the
presence of gross blood in the absence of any accompanying sputum. Hemoptysis has a broad
differential, but the cause can be determined in the majority of patients (table 1). It is
important to identify the cause and location of bleeding in order to guide treatment.

The evaluation of nonmassive hemoptysis that is not immediately life-threatening will be


reviewed here. The acute evaluation and management of massive (life-threatening)
hemoptysis are discussed separately. (See "Overview of massive hemoptysis" and "Massive
hemoptysis: Causes" and "Massive hemoptysis: Initial management".)

DEFINITION OF MASSIVE HEMOPTYSIS

The term massive hemoptysis is reserved for bleeding that is potentially acutely life-
threatening; it has been defined by a number of different criteria, ranging from 100 mL to
more than 600 mL of blood over a 24 hour period [1,2]. In our clinical practice, we define
massive hemoptysis as either ≥500 mL of expectorated blood over a 24 hour period or
bleeding at a rate ≥100 mL/hour.

Patients with mild-to-moderate hemoptysis and adequate gas exchange generally do not
require hospitalization and the evaluation can proceed in a stepwise fashion as described
below. Massive hemoptysis requires a prompt response to ensure adequate ventilation,
protect the airway, and control the hemoptysis. (See "Overview of massive hemoptysis" and
"Massive hemoptysis: Initial management".)

BRONCHIAL VERSUS PULMONARY VASCULAR ORIGINS OF HEMOPTYSIS

Blood traversing the lungs can arrive from one of two sources: pulmonary arteries or
bronchial arteries. Virtually the entire cardiac output courses through the low-pressure
pulmonary arteries and arterioles en route to being oxygenated in the pulmonary capillary
bed. In contrast, the bronchial arteries are under much higher systemic pressure, but carry
only a small portion of the cardiac output. Bleeding from a bronchial artery is the cause of
massive hemoptysis in 90 percent of cases

31
What is Brain Death?

In the past, it was easy to say when a person was dead. When their heart stopped beating,
they were dead. However, with the development over the last half-century of medical devices
that can artificially maintain blood flow and breathing, the term brain death has come into
use.

By definition, “brain death” is “when the entire brain, including the brain stem, has
irreversibly lost all function.” Removal of assistive devices will result in immediate cardiac
arrest and cessation of breathing.

You already know that the brain is responsible


for all our movement, sensations, senses and speech. But what does the brainstem do?

The brain stem is responsible for regulating most of the automatic functions of the body that
are essential for life, including breathing, maintaining the heartbeat and blood pressure and
swallowing.

The brain stem also relays all information to and from the brain to the rest of the body, so it
plays a fundamental role in the brain’s core functions, such as consciousness, awareness and
movement.

The causes of brain death include:

32
 Trauma to the brain (severe head injury caused by a motor vehicle crash, gunshot wound,
fall or blow to the head)
 Cerebrovascular injury (i.e. stroke or aneurysm)
 Anoxia (a lack or blood flow/oxygen to the brain resulting from a heart attack, drowning,
etc.)
 Brain tumor

How is this different from a coma or vegetative state?

A coma is a deep state of unconsciousness. A patient in a coma is totally unconscious,


unresponsive, unaware, and unarousable. Patients in a coma do not respond to external
stimuli, such as pain or light, and do not have sleep-wake cycles. Although a patient in a
coma does not have a normal EEG, it is not completely flat (see below).

Coma results from widespread trauma to the brain. Coma generally is of short duration,
lasting a few days to a few weeks. After this time, some patients gradually come out of the
coma, some progress to a vegetative state, and others die.

Patients in a vegetative state are unconscious and unaware of their surroundings, but they
continue to have a sleep-wake cycle and can have periods of alertness. Unlike coma, where
the patients eyes are closed, patients in a vegetative state often open their eyes and may
move, groan, or show reflex responses.

A vegetative state can result from diffuse injury to the cerebral hemispheres of the brain
without damage to the lower brain and brainstem. Anoxia, or lack of oxygen to the brain,
which is a common complication of cardiac arrest, can also bring about a vegetative state.

Many patients emerge from a vegetative state within a few weeks, but those who do not
recover within 30 days are said to be in a persistent vegetative state (PVS) . The chances of
recovery depend on the extent of injury to the brain and the patient’s age, with younger
patients having a better chance of recovery than older patients.

After a year, the chances that a PVS patient will regain consciousness are very low and most
patients who do recover consciousness experience significant disability. In general, the longer
a patient is in a PVS, the more severe the resulting disabilities will be.

How is brain death determined?

There are three criteria (and one prerequisite) to determine brain death.

First, you need to know what caused the brain injury and be sure that there are no
circumstances that can complicate or mask the diagnosis. This would include:

 problems with severe electrolyte, acid-base or endocrine disturbances (such as a diabetic


coma)
 no drug intoxication or poisoning
 the patient’s core body temperature must be above 90° F (32° C). Normal body temperature
is 98.6° F (37° C).

The three main criteria in brain death are

33
1. Coma or unresponsiveness:
2. Absence of brainstem reflexes
3. Apnea (inability to breath)

How are these tested?

Coma is tested by looking for a reaction to painful stimuli, such as pressing hard on the
nailbeds or above the eyes.

Lack of brainstem
reflexes are evaluated by:

 No response of the pupils when a bright light is shone into them


 No deviation of the eyes when cold water is put into the ear canal (see right)
 No oculocephalic reflex (dolls eyes manuever- see right)
 No gag reflex
 No cough reflex if the intubated patient has the trachea suctioned
 No corneal reflex- patient blinks when the cornea is touched with a cotton swab
 No facial grimace when the nailbeds are squeezed

A n apnea test is done to determine whether a


patient can breathe on his own.

34
The patient is hooked up to a pulse oximeter ( a machine that determines the amount of
oxygen in the blood). Then the patient is disconnected from the ventilator for a set period of
time.

The amount of oxygen and carbon dioxide in the blood in monitored as well as watching the
patient for any signs that they have started breathing on their own. A drop in oxygen levels
and rise in carbon dioxide without any respiratory effort by the patient confirms that apnea is
present.

Although it may not be legally required, an EEG


(electroencephalogram) which measures the electrical output of the brain may be done to
support the diagnosis.

In brain death, the normal electrical activity of the brain (left side of diagram) becomes flat
(right side). Some localities require two EEG’s 24 hours apart.

Why is it important to determine brain death?


For the patient and family:

For the family, determining brain death confirms that their loved one has, in fact, died. The
heart and lungs are maintained only through medical means and that there is no chance of
recovery. It allows the family to move on to the next stage of their grieving.

For the patient, further unnecessary, invasive and expensive treatment is avoided.

35
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htm

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The Lung Exam

Inspection and Sample Lung


Anatomy Palpation Percussion Auscultation
Observation Sounds

The 4 major components of the lung exam (inspection, palpation, percussion and auscultation) are
also used to examine the heart and abdomen. Learning the appropriate techniques at this juncture
will therefore enhance your ability to perform these other examinations as well. Vital signs, an
important source of information, are discussed elsewhere.

Inspection/Observation: A great deal of information can be gathered from simply watching


a patient breathe. Pay particular attention to:

1. General comfort and breathing pattern of the patient. Do they appear distressed,
diaphoretic, labored? Are the breaths regular and deep?

38
2. Use of accessory muscles of breathing (e.g. scalenes, sternocleidomastoids). Their use
signifies some element of respiratory difficulty.
3. Color of the patient, in particular around the lips and nail beds. Obviously, blue is bad!

Cyanosis of nail beds

4. The position of the patient. Those with extreme pulmonary dysfunction will often sit up-
right. In cases of real distress, they will lean forward, resting their hands on their knees in
what is known as the tri-pod position.

Patient with emphysema bending over in Tri-Pod Position

39
5. Breathing through pursed lips, often seen in cases of emphysema.
6. Ability to speak. At times, respiratory rates can be so high and/or work of breathing so great
that patients are unable to speak in complete sentences. If this occurs, note how many
words they can speak (i.e. the fewer words per breath, the worse the problem!).
7. Any audible noises associated with breathing as occasionally, wheezing or the gurgling
caused by secretions in large airways are audible to the "naked" ear.
8. The direction of abdominal wall movement during inspiration. Normally, the descent of the
diaphragm pushes intra-abdominal contents down and the wall outward. In cases of severe
diaphragmatic flattening (e.g. emphysema) or paralysis, the abdominal wall may move
inward during inspiration, referred to as paradoxical breathing. If you suspect this to be the
case, place your hand on the patient's abdomen as they breathe, which should accentuate
its movement.
9. Any obvious chest or spine deformities. These may arise as a result of chronic lung disease
(e.g. emphysema), occur congenitally, or be otherwise acquired. In any case, they can impair
a patient's ability to breathe normally. A few common variants include:
o Pectus excavatum: Congenital posterior displacement of lower aspect of sternum.
This gives the chest a somewhat "hollowed-out" appearance. The x-ray shows a
subtle concave appearance of the lower sternum.

40
o Barrel chest: Associated with emphysema and lung hyperinflation. Accompanying
xray also demonstrates
increased anterior-posterior diameter as well as diaphragmatic flattening.

41
o Spine abnormalities:
 Kyphosis: Causes the patient to be bent forward. Accompanying X-Ray of
same patient clearly demonstrates extreme curvature of the spine.

42
 Scoliosis: Condition where the spine is curved to either the left or right. In
the pictures below, scoliosis of the spine causes right shoulder area to
appear somewhat higher than the left. Curvature is more pronounced on x-
ray.

43
10. Review of Lung Anatomy: Understanding the pulmonary exam is greatly enhanced
by recognizing the relationships between surface structures, the skeleton, and the
main lobes of the lung. Realize that this can be difficult as some surface landmarks
(eg nipples of the breast) do not always maintain their precise relationship to
underlying structures. Nevertheless, surface markers will give you a rough guide to

44
what lies beneath the skin. The pictures below demonstrate these relationships. The
multi-colored areas of the lung model identify precise anatomic segments of the
various lobes, which cannot be appreciated on examination. Main lobes are outlined
in black. The following abbreviations are used: RUL = Right Upper Lobe; LUL =
Left Upper Lobe; RML = Right Middle Lobe; RLL = Right Lower Lobe; LLL = Left
Lower Lobe.

Anterior View

45
Posterior View

46
Right Lateral
View

47
Left Lateral View

18.

48
19.
20. Palpation: Palpation plays a relatively minor role in the examination of the normal
chest as the structure of interest (the lung) is covered by the ribs and therefore not
palpable. Specific situations where it may be helpful include:
1. Accentuating normal chest excursion: Place your hands on the patient's back
with thumbs pointed towards the spine. Remember to first rub your hands together
so that they are not too cold prior to touching the patient. Your hands should lift
symmetrically outward when the patient takes a deep breath. Processes that lead to
asymmetric lung expansion, as might occur when anything fills the pleural space
(e.g. air or fluid), may then be detected as the hand on the affected side will move
outward to a lesser degree. There has to be a lot of plerual disease before this
asymmetry can be identified on exam.

Detecting Chest Excursion

49
2. Tactile Fremitus: Normal lung transmits a palpable vibratory sensation to the
chest wall. This is referred to as fremitus and can be detected by placing the ulnar
aspects of both hands firmly against either side of the chest while the patient says
the words "Ninety-Nine." This maneuver is repeated until the entire posterior thorax
is covered. The bony aspects of the hands are used as they are particularly sensitive
for detecting these vibrations.

Assessing Fremitus

Pathologic conditions will alter fremitus. In particular:

50
A. Lung consolidation: Consolidation occurs when the normally air filled lung parenchyma becomes
engorged with fluid or tissue, most commonly in the setting of pneumonia. If a large enough
segment of parenchyma is involved, it can alter the transmission of air and sound. In the presence of
consolidation, fremitus becomes more pronounced.
B. Pleural fluid: Fluid, known as a pleural effusion, can collect in the potential
space that exists between the lung and the chest wall, displacing the lung
upwards. Fremitus over an effusion will be decreased.

In general, fremitus is a pretty subtle finding and should not be thought of as


the primary means of identifying either consolidation or pleural fluid. It can,
however, lend supporting evidence if other findings (see below) suggest the
presence of either of these processes.

51
Effusions
and
infiltrates
can perhaps
be more
easily
understood
using a
sponge to
represent the
lung. In this
model, an
infiltrate is
depicted by
the blue
coloration
that has
invaded the
sponge itself
(sponge on
left). An
effusion is
depicted by
the blue
fluid upon
which the
lung is
floating
(sponge on
right).

52
3. Investigating painful areas: If the patient complains of pain at a particular
site it is obviously important to carefully palpate around that area. In addition,
special situations (e.g. trauma) mandate careful palpation to look for evidence of rib
fracture, subcutaneous air (feels like your pushing on Rice Krispies or bubble paper),
etc.

Percussion: This technique makes use of the fact that striking a surface which covers
an air-filled structure (e.g. normal lung) will produce a resonant note while repeating
the same maneuver over a fluid or tissue filled cavity generates a relatively dull
sound. If the normal, air-filled tissue has been displaced by fluid (e.g. pleural
effusion) or infiltrated with white cells and bacteria (e.g. pneumonia), percussion will
generate a deadened tone. Alternatively, processes that lead to chronic (e.g.
emphysema) or acute (e.g. pneumothorax) air trapping in the lung or pleural space,
respectively, will produce hyper-resonant (i.e. more drum-like) notes on percussion.
Initially, you will find that this skill is a bit awkward to perform. Allow your hand to
swing freely at the wrist, hammering your finger onto the target at the bottom of the
down stroke. A stiff wrist forces you to push your finger into the target which will not
elicit the correct sound. In addition, it takes a while to develop an ear for what is
resonant and what is not. A few things to remember:

53
4. If you're percussing with your right hand, stand a bit to the left side of the
patient's back.
5. Ask the patient to cross their hands in front of their chest, grasping the opposite
shoulder with each hand. This will help to pull the scapulae laterally, away from the
percussion field.
6. Work down the "alley" that exists between the scapula and vertebral column, which
should help you avoid percussing over bone.
7. Try to focus on striking the distal inter-phalangeal joint (i.e. the last joint) of your left
middle finger with the tip of the right middle finger. The impact should be crisp so
you may want to cut your nails to keep blood-letting to a minimum!
8. The last 2 phalanges of your left middle finger should rest firmly on the patient's
back. Try to keep the remainder of your fingers from touching the patient, or rest
only the tips on them if this is otherwise too awkward, in order to minimize any
dampening of the perucssion notes.
9. When percussing any one spot, 2 or 3 sharp taps should suffice, though feel free to
do more if you'd like. Then move your hand down several inter-spaces and repeat
the maneuver. In general, percussion in 5 or so different locations should cover one
hemi-thorax. After you have percussed the left chest, move yours hands across and

54
repeat the same procedure on the right side. If you detect any abnormality on one
side, it's a good idea to slide your hands across to the other for comparison. In this
way, one thorax serves as a control for the other. In general, percussion is limited to
the posterior lung fields. However, if auscultation (see below) reveals an
abnormality in the anterior or lateral fields, percussion over these areas can help
identify its cause.

Percussion Technique

10. The goal is to recognize that at some point as you move down towards the
base of the lungs, the quality of the sound changes. This normally occurs when you
leave the thorax. It is not particularly important to identify the exact location of the
diaphragm, though if you are able to note a difference in level between maximum
inspiration and expiration, all the better. Ultimately, you will develop a sense of
where the normal lung should end by simply looking at the chest. The exact
vertebral level at which this occurs is not really relevant.
11. "Speed percussion" may help to accentuate the difference between dull and
resonant areas. During this technique, the examiner moves their left (i.e. the non-
percussing) hand at a constant rate down the patient's back, tapping on it
continuously as it progresses towards the bottom of the thorax. This tends to make
the point of inflection (i.e. change from resonant to dull) more pronounced.

55
Practice percussion! Try finding your own stomach bubble, which should be around the left
costal margin. Note that due to the location of the heart, tapping over your left chest will
produce a different sound then when performed over your right. Percuss your walls (if
they're sheet rock) and try to locate the studs. Tap on tupperware filled with various
amounts of water. This not only helps you develop a sense of the different tones that may
be produced but also allows you to practice the technique.

Auscultation: Prior to listening over any one area of the chest, remind yourself which
lobe of the lung is heard best in that region: lower lobes occupy the bottom 3/4 of the
posterior fields; right middle lobe heard in right axilla; lingula in left axilla; upper
lobes in the anterior chest and at the top 1/4 of the posterior fields. This can be quite
helpful in trying to pin down the location of pathologic processes that may be
restricted by anatomic boundaries (e.g. pneumonia). Many disease processes (e.g.
pulmonary edema, bronchoconstriction) are diffuse, producing abnormal findings in
multiple fields.

12. Put on your stethoscope so that the ear pieces are directed away from you.
Adjust the head of the scope so that the diaphragm is engaged. If you're not sure,
scratch lightly on the diaphragm, which should produce a noise. If not, twist the
head and try again. Gently rub the head of the stethoscope on your shirt so that it is
not too cold prior to placing it on the patient's skin.
13. The upper aspect of the posterior fields (i.e. towards the top of the patient's back)
are examined first. Listen over one spot and then move the stethoscope to the same
position on the opposite side and repeat. This again makes use of one lung as a
source of comparison for the other. The entire posterior chest can be covered by
listening in roughly 4 places on each side. Of course, if you hear something
abnormal, you'll need to listen in more places.

Lung Auscultation

56
14. The lingula and right middle lobes can be examined while you are still
standing behind the patient.
15. Then, move around to the front and listen to the anterior fields in the same fashion.
This is generally done while the patient is still sitting upright. Asking female patients
to lie down will allow their breasts to fall away laterally, which may make this part of
the examination easier.

Thoughts On "Gown Management" & Appropriately/Respectfully Touching


Your Patients:

There are several sources of tension relating to the physical exam in general, which
are really brought to the fore during the chest examine. These include:

o Area to be examined must be reasonably exposed - yet patient kept as covered as


possible
o The need to Palpate sensitive areas in order to perform accurate exam - requires
touching people w/whom you've little acquaintance - awkward, particularly if
opposite gender
o As newcomers to medicine, you're particularly aware that this aspect of the exam is
"unnatural" & hence very sensitive.. which is a good thing!

Keys to performing a sensitive yet thorough exam:

57
o Explain what you're doing (" why) before doing it → acknowledge "elephant in the
room"!
o Expose the minimum amount of skin necessary - this requires "artful" use of gown &
drapes (males & females)
o Examining heart & lungs of female patients:
 Ask pt to remove bra prior (you can't hear the heart well thru fabric)
 Expose the chest only to the extent needed. For lung exam, you can listen to
the anterior fields by exposing only the top part of the breasts (see picture
below).
 Enlist patient's assistance, asking them to raise their breast to a position that
enhances your ability to listen to the heart
o Don't rush, act in a callous fashion, or cause pain
o PLEASE... don't examine body parts thru gown as:
 It reflects Poor technique
 You'll miss things
 You'll lose points on scored exams (OSCE, CPX, USMLE)!

58
Remember - Don't examine thru clothing or "snake" stethoscope down shirts/gowns

Good exam options

A few additional things worth noting.

24. Ask the patient to take slow, deep breaths through their mouths while you are
performing your exam. This forces the patient to move greater volumes of air with
each breath, increasing the duration, intensity, and thus detectability of any
abnormal breath sounds that might be present.
25. Sometimes it's helpful to have the patient cough a few times prior to beginning
auscultation. This clears airway secretions and opens small atelectatic (i.e. collapsed)
areas at the lung bases.
26. If the patient cannot sit up (e.g. in cases of neurologic disease, post-operative states,
etc.), auscultation can be performed while the patient is lying on their side. Get help
if the patient is unable to move on their own. In cases where even this cannot be
accomplished, a minimal examination can be performed by listening
laterally/posteriorly as the patient remains supine.
27. Requesting that the patient exhale forcibly will occasionally help to accentuate
abnormal breath sounds (in particular, wheezing) that might not be heard when
they are breathing at normal flow rates.

What can you expect to hear? A few basic sounds to listen for:

59
28. A healthy individual breathing through their mouth at normal tidal volumes
produces a soft inspiratory sound as air rushes into the lungs, with little noise
produced on expiration. These are referred to as vessicular breath sounds.
29. Wheezes are whistling-type noises produced during expiration (and sometimes
inspiration) when air is forced through airways narrowed by bronchoconstriction,
secretions, and/or associated mucosal edema. As this most commonly occurs in
association with diffuse processes that affect all lobes of the lung (e.g. asthma and
emphysema) it is frequently audible in all fields. In cases of significant
bronchoconstriction, the expiratory phase of respiration (relative to inspiration)
becomes noticeably prolonged. Clinicians refer to this as an increased I to E ratio.
Normal is approximatley 1:2 (i.e. expiration twice as long as inspiration) though
actual timed measurements are neither practical nor reliable. Focus instead on
simple observation, noting whether E seems >> I. The greater the difference, the
worse the obstruction. Occasionally, focal wheezing can occur when airway
narrowing if restricted to a single anatomic area, as might occur with an obstructing
tumor or bronchoconstriction induced by pneumonia. Wheezing heard only on
inspiration is referred to as stridor and is associated with mechanical obstruction at
the level of the trachea/upper airway. This may be best appreciated by placing your
stethescope directly on top of the trachea.
30. Rales (a.k.a. crackles) are scratchy sounds that occur in association with processes
that cause fluid to accumulate within the alveolar and interstitial spaces. The sound
is similar to that produced by rubbing strands of hair together close to your ear.
Pulmonary edema is probably the most common cause, at least in the older adult
population, and results in symmetric findings. This tends to occur first in the most
dependent portions of the lower lobes and extend from the bases towards the
apices as disease progresses. Pneumonia, on the other hand, can result in discrete
areas of alveolar filling, and therefore produce crackles restricted to a specific region
of the lung. Very distinct, diffuse, dry-sounding crackles, similar to the noise
produced when separating pieces of velcro, are caused by pulmonary fibrosis, a
relatively uncommon condition.
31. Dense consolidation of the lung parenchyma, as can occur with pneumonia, results
in the transmission of large airway noises (i.e. those normally heard on auscultation
over the trachea... known as tubular or bronchial breath sounds) to the periphery. In
this setting, the consolidated lung acts as a terrific conducting medium, transferring

60
central sounds directly to the edges. It's very similar to the noise produced when
breathing through a snorkel. Furthermore, if you direct the patient to say the letter
'eee' it is detected during auscultation over the involved lobe as a nasal-sounding
'aaa'. These 'eee' to 'aaa' changes are referred to as egophony. The first time you
detect it, you'll think that the patient is actually saying 'aaa'... have them repeat it
several times to assure yourself that they are really following your directions!
32. Secretions that form/collect in larger airways, as might occur with bronchitis or
other mucous creating process, can produce a gurgling-type noise, similar to the
sound produced when you suck the last bits of a milk shake through a straw. These
noises are referred to as ronchi.
33. Auscultation over a pleural effusion will produce a very muffled sound. If, however,
you listen carefully to the region on top of the effusion, you may hear sounds
suggestive of consolidation, originating from lung which is compressed by the fluid
pushing up from below. Asymmetric effusions are probably easier to detect as they
will produce different findings on examination of either side of the chest.
34. Auscultation of patients with severe, stable emphysema will produce very little
sound. These patients suffer from significant lung destruction and air trapping,
resulting in their breathing at small tidal volumes that generate almost no noise.
Wheezing occurs when there is a superimposed acute inflammatory process (see
above).

Most of the above techniques are complimentary. Dullness detected on percussion, for
example, may represent either lung consolidation or a pleural effusion. Auscultation over
the same region should help to distinguish between these possibilities, as consolidation
generates bronchial breath sounds while an effusion is associated with a relative absence of
sound. Similarly, fremitus will be increased over consolidation and decreased over an
effusion. As such, it may be necessary to repeat certain aspects of the exam, using one
finding to confirm the significance of another. Few findings are pathognomonic. They have
their greatest meaning when used together to paint the most informative picture.

Sample Lung Sounds (courtesy of Dr. Michael Wilkes, MD-- UC Davis and UCLA
Schools of Medicine)

 Bronchial Breath Sounds

61
 Vesicular Breath Sounds

 Crackles

 Wheeze

 Stridor

 Normal Voice E

 Egophony

The Auscultation Assistant -- A limited sampling of lung sounds can be found at this site.

Listen to more lungs sounds from Rales Repository of Lung Sounds.

The Dynamic Lung Exam:

Pulse Oxymeter

62
Oftentimes, a patient will complain of a symptom that is induced by activity or
movement. Shortness of breath on exertion, one such example, can be a marker of
significant cardiac or pulmonary dysfunction. The initial examination may be
relatively unrevealing. In such cases, consider observed ambulation (with the use of a
pulse oxymeter, a device that continuously measures heart rate and oxygen saturation,
if available) as a dynamic extension of the cardiac and pulmonary examinations.
Quantifying a patient's exercise tolerance in terms of distance and/or time walked can
provide information critical to the assessment of activity induced symptoms. It may
also help unmask illness that would be inapparent unless the patient was asked to
perform a task that challenged their impaired reserves. Pay particular attention to the
rate at which the patient walks, duration of activity, distance covered, development of
dyspnea, changes in heart rate and oxygen saturation, ability to talk during exercise
and anything else that the patient identifies as limiting their activity. The objective
data derived from this low tech test can aid you in determining disease and symptom
severity, helping to create a list of possible diagnoses and assisting you in the rational
use of additional tests to further delineate the nature of the problem. This can be
particularly helpful in providing objective information when symptoms seem out of
proportion to findings. Or when patients report few complaints yet seem to have a
cosiderable amount of disease. It will also generate a measurement that you can refer
back to during subsequent evaluations in order to determine if there has been any real
change in functional status.

63