Ulmi auly hidayati

405150169
ARF
 Gagal Napas Akut
• Ketidamampuan sistem pernapasan untuk
mempertahankan suatu keadaan pertukaran
udara antara atmosfer dengan sel-sel tubuh yang
sesuai dengan kebutuhan normal
• Peranan sistem pernapasan→mempertahankan
PO2, PcO2, dan pH darah tetap normal
• Dapat diakibatkan→kelainan dari paru, jantung,
dinding dada, otot pernapasan, mekanisme
pengendalian sentral ventilasi di medula
oblongata.
 Klasifikasi

• Gagal napas dibagi menjadi :

– Hipoksemi (tipe I) : PaO2<60mmHg, kegagalan
transfer oksigen dalam paru

– Hiperkapnia ( tipe II) : PaCO2 >45mmHg,

kegagalan ventilasi untuk mengeluarkan CO2
 Efektifitas dan Efisiensi Sistem
Pernapasan
• PaO2 100mmHg→oksigenasi darah arteri yang
efisien →mengukur efektifitias oksigenasi
• PaCO2 <40mmHg →fungsi eliminasi CO2 yang
efektif→mengukur fungsi efektivitas ventilasi.
• Ukuran efektivitias ventilasi : Hubungan antara
PaCO2 dan ventilasi semenit (V e)
ARDS
 ARDS
Acute respiratory distress syndrome (ARDS) occurs
when fluid builds up in the tiny, elastic air sacs (alveoli) in your
lungs. More fluid in your lungs means less oxygen can reach
your bloodstream. This deprives your organs of the oxygen
they need to function.
The signs and symptoms of ARDS can vary in intensity,
depending on its cause and severity, as well as the presence of
underlying heart or lung disease. They include:
• Severe shortness of breath
• Labored and unusually rapid breathing
• Low blood pressure
• Confusion and extreme tiredness
 Diagnosa
There's no specific test to identify ARDS. The diagnosis is based on the
physical exam, chest X-ray and oxygen levels and by ruling out other diseases
and conditions — for example, certain heart problems — that can produce
similar symptoms.
Imaging
• Chest X-ray. A chest X-ray can reveal which parts of your lungs and how
much of the lungs have fluid in them and whether your heart is enlarged.
• Computerized tomography (CT). A CT scan combines X-ray images taken
from many different directions into cross-sectional views of internal
organs. CT scans can provide detailed information about the structures
within the heart and lungs.
Lab tests
• A test using blood from an artery in your wrist can measure your
oxygen level. Other types of blood tests can check for signs of
infection or anemia. If your doctor suspects that you have a lung
infection, secretions from your airway may be tested to determine
the cause of the infection.
Heart tests
• Because the signs and symptoms of ARDS are similar to those of
certain heart problems, your doctor may recommend heart tests
such as:
• Electrocardiogram. This painless test tracks the electrical activity in
your heart. It involves attaching several wired sensors to your body.
• Echocardiogram. A sonogram of the heart, this test can reveal
problems with the structures and the function of your heart.
 Management
The first goal in treating ARDS is to improve the levels of oxygen in your
blood. Without oxygen, your organs can't function properly.
Oxygen
To get more oxygen into your bloodstream, your doctor will likely use:
• Supplemental oxygen.For milder symptoms or as a temporary measure,
oxygen may be delivered through a mask that fits tightly over your nose
and mouth.
• Mechanical ventilation. Most people with ARDS will need the help of a
machine to breathe. A mechanical ventilator pushes air into your lungs
and forces some of the fluid out of the air sacs.
Fluids
• Carefully managing the amount of intravenous fluids is crucial. Too much
fluid can increase fluid buildup in the lungs. Too little fluid can put a strain
on your heart and other organs and lead to shock.
Medication
• People with ARDS usually are given medication to:
• Prevent and treat infections
• Relieve pain and discomfort
• Prevent clots in the legs and lungs
• Minimize gastric reflux
• Sedate
Fishman's Pulmonary Diseases and Disorders, 5e
 Definisi dan etiologi

• Flu burung adalah penyakit yang disebabkan

oleh virus influenza jenis H5N1.

• Virus ini disebarkan oleh unggas. Virus tersebut

menyebar pada unggas hampir di seluruh dunia,
sangat menular terhadap sesama unggas dan
mematikan.
ETIOLOGI FLU BURUNG

Influenza viruses
are highly unstable,
genetically labile, and
well adapted to elude
host defences.
 TANDA & GEJALA
Gejala klinis yang ditemui seperti gejala flu pada umumnya,
yaitu:
• Demam (>380C)
• Kesulitan bernafas
• Batuk
• Sakit tenggorokan
• Hidung berair
• Nyeri otot
• Sakit kepala
• Lemas
Dalam waktu singkat penyakit ini dapat menjadi lebih berat
berupa peradangan di paru-paru (pneumonia), dan apabila
tidak dilakukan penanganan dengan baik dapat menyebabkan
KEMATIAN.
 SIFAT VIRUS INFUENZA
• Virus tersebut dapat bertahan hidup di air sampai
4 hari pada suhu 220C dan lebih dari 30 hari pada
00C.
• Virus mati pada pemanasan 600C selama 30
menit atau 560C selama 3 jam
• Atau dengan detergent, desinfektan misalnya
formalin, serta cairan yang mengandung iodin.
 Faktor Risiko
Seseorang yang selama 7 hari sebelum terkena, telah mengalami salah satu
atau lebih dari keadaan berikut ini:
• Kontak (dalam jarak 1 meter atau kurang) dengan dengan ternak unggas atau
burung liar baik hidup atau mati
• Berada pada tempat dimana ternak unggas pernah atau sedang dikandangkan
selama 6 minggu sebelumnya
• Berhubungan (dalam jarak jangkauan sentuhan atau percakapan) dengan orang
yang didiagnosa menderita influenza A (H5N1)
• Berhubungan (dalam jarak jangkauan sentuhan atau percakapan) dengan orang
yang menderita penyakit pernafasan akut yang tidak dapat dijelaskan yang
kemudian berakhir pada kematian
• Pernah bekerja dalam laboratorium dimana ada pengolahan contoh dari orang
/ binatang yang dicurigai menderita penyakit flu burung.
 Penularan pada manusia
• Virus H5N1 mudah ditularkan lewat kotoran dan cairan tubuh
hewan.
• Virus ini dapat menular melalui udara ataupun kontak melalui
makanan, minuman, dan sentuhan.

• Daging, dan telur hewan yang tidak dimasak dengan

matang.

• Virus dapat bertahan hidup pada suhu dingin. Bahan

makanan yang didinginkan atau dibekukan dapat
menyimpan virus. Tangan harus dicuci sebelum dan setelah
memasak atau menyentuh bahan makanan mentah.
Penularan pada manusia
 Patofisiologi
• Virus respiratory track melekat di bronkus terminal dan
alveoli  mengikat (binding) antara protein virus dengan
jaringan sel-sel tubuh  Injeksi replikasi transkrip 
perakitan  lisis sel
• Virus ini cenderung melekat pada jaringan saluran respirasi
bagian bawah, karena sesuai dengan tempat perlekatan
proteinnya, yaitu sialic acid alpha (2-3) galactose .
• Berbeda dengan jaringan epitel sal. pernapasan atas, yang
merupakan residu sialic acid alpha (2-6) galactose
Demam Biasa vs Flu Burung
 Pemeriksaan Penunjang

• Pemeriksaan serologi
– Hemagglutination Inhibition (HI)
– Uji Fikasasi Komplemen
– ELISA
• Isolasi dan identifikasi virus (swab tenggorok,
sputum)
• RT-PCR
• Rontgen dada
 Gambaran Radiologis Flu Burung
• Kelainan radiologis terjadi pada hari ke 7 setelah
timbul demam (rentang : 3 – 17 hari)
• Infiltrat bilateral yang luas dengan progress yang
cepat
• Kolaps lobar
• Konsolidasi fokal
• Air bronchogram (+)
• Infiltrat intertitial
• Bercak inhomogen ( patchy infiltrate)
• Efusi pleura
 TERAPI
Farmakologis Non-farmakologis
• Amantadine (Symmetrel) – Rawat dalam
– <65 years: 200 mg/hari setelah makan
>65 years: 100 mg/hari setelah makan ruangan isolasi
Hemodialysis: 200 mg setelah makan – Jika parah,
• Rimantadine (Flumadine) gunakan
– 100 mg/hari setelah makan
ventilator
• Oseltamivir (Tamiflu)
– 75 mg setelah makan – Jika pasien
• Zanamivir (Relenza) mengalami
– 10 mg (2 inhalations, 5 mg/inhalation) gangguan ginjal,
setelah makan gunakan dialisis
 Pencegahan
• Menggunakan pelindung (masker , sarung tangan)
• Bahan yang berasal dari saluran cerna unggas seperti tinja harus
dikelola dengan baik (dikubur / dibakar) agar tidak menjadi sumber
penularan bagi orang di sekitarnya
• Mencuci alat-alat dengan desinfektan
• Kandang dan tinja tidak boleh dikeluarkan dari lokasi peternakan
• Mengkonsumsi daging ayam yang telah dimasak pada suhu 800 c
selama 1 menit, sedangkan telur unggas perlu dipanaskan pada suhu
640 c selama 5 menit
• Selalu cuci tangan setelah kontak dengan unggas atau kotorannya
• Setelah kontak dengan unggas yang mati / sakit segera mandi dan
cuci pakaian dan sepatu dengan sabun
• Vaksinasi
 Komplikasi
• Acute Respiratory Distress, Pneumonia, Sepsis
TRACHEAL ASPIRATION
Pneumonitis aspirasi : dri isi lambung msuk ke paru
Aspirasi pneumonia : mukus dll msuk ke paru

ASPIRATION PNEUMONIA
 Aspiration pneumonia
• results from inhalation of stomach contents or
secretions of the oropharynx, leading to lower
respiratory tract infection
• aspiration may cause:
– Chemical pneumonitis
– Obstruction
– Bacterial infection
• The usual site for an aspiration pneumonia is the apical
and posterior segments of the lower lobe of the right
lung
• If the patient is supine then the aspirated material may
also enter the posterior segment of the upper lobe

http://pedsccm.org/FILE-CABINET/Practical/Akron_pdfs/7ASTHMAP.PDF
 Epid
• It is common. One study of elderly patients
implicated aspiration pneumonia in 10% or
cases of community-acquired pneumonia
• Aspiration pneumonia is relatively common in
hospital and usually involves infection with
multiple bacteria, including anaerobes.
• It is more common in men, young children and
the elderly

http://pedsccm.org/FILE-CABINET/Practical/Akron_pdfs/7ASTHMAP.PDF
 Pathogens
• Pathogens of community-acquired aspiration pneumonia are often the
normal flora of the oropharynx, including:
– Streptococcus pneumoniae
– Staphylococcus aureus
– Haemophilus influenzae
– Anaerobes - eg, Peptostreptococcus, Fusobacterium and Prevotella spp.
'Streptococcus milleri' group
– Klebsiella pneumoniae - increasingly seen in those with a history of alcohol
misuse.
• Pathogens of nosocomial aspiration pneumonia include[2]:
– Oral anaerobes - as above
– Gram-positive cocci - eg, Peptostreptococcus spp., Peptococcus spp
– Gram-negative bacilli - eg, enterobacteria (Klebsiella pneumoniae, Escherichia
coli, Enterobacter spp.), Pseudomonas aeruginosa
– Meticillin-resistant S. aureus (MRSA).

http://pedsccm.org/FILE-CABINET/Practical/Akron_pdfs/7ASTHMAP.PDF
 RF
• Impaired consciousness: drug or alcohol misuse, general
anaesthesia, seizures, sedation, acute stroke, central
nervous system lesions, head injury
• Poor mobility, nil by mouth status, increasing age, chronic
obstructive pulmonary disease (COPD), male gender and
increasing number of medications
• Swallowing disorders: oesophageal stricture, dysphagia,
stroke, bulbar palsy, pharyngeal disease (eg, malignancy),
neuromuscular disorders (eg, multiple sclerosis).
• Other: tracheo-oesophageal fistula, ventilator-associated
pneumonia, periodontal disease, gastro- oesophageal
reflux, post-gastrectomy, tracheostomy.

http://pedsccm.org/FILE-CABINET/Practical/Akron_pdfs/7ASTHMAP.PDF
 S/S
• Nonspecific symptoms - eg, fever, headache, nausea,
vomiting, anorexia, myalgia, weight loss.
• Cough.
• Dyspnoea.
• Pleuritic chest pain.
• Purulent sputum.
• Signs may include tachycardia, tachypnoea, decreased
breath sounds and dullness to percussion over areas of
consolidation, pleural friction rub.
• Severe infection may lead to hypoxia and septic shock

http://pedsccm.org/FILE-CABINET/Practical/Akron_pdfs/7ASTHMAP.PDF
 DD
• Other causes of respiratory distress, including:
– Other causes of pneumonia
– Bronchiolitis.
– Croup.
– Epiglottitis.
– Foreign body in respiratory tract
– Asthma.
– Cardiovascular disease.

http://pedsccm.org/FILE-CABINET/Practical/Akron_pdfs/7ASTHMAP.PDF
 Investigations
• Blood count: neutrophil leukocytosis.
• Electrolytes and renal function: dehydration, electrolyte
• imbalance.
• Blood culture.
• Blood gases.
• Culture of sputum: n patients with bacterial aspiration pneumonia, this may show
organisms normally resident in the pharynx.
• CXR:
– Right, middle and lower lung lobes are the most common sites.
– Aspiration when upright may cause bilateral lower lung infiltrates.
– Right upper lobe often shows consolidation in those with a history of alcohol misuse who
aspirate in the prone position.
• Lung CT is only very occasionally required.
• Specimens obtained from bronchoscopy may help to guide choice of antibiotic
treatment

http://pedsccm.org/FILE-CABINET/Practical/Akron_pdfs/7ASTHMAP.PDF
 Management
• Mechanical obstruction: removal of the object, normally by bronchoscopy.
• Tracheal suction if seen early.
• Intubation with positive pressure ventilation may be required.
• Bacterial infection of lower airways (the choice of antibiotics will be
influenced by any recent previous antibiotic treatment, microbiology
culture results and the patient's condition):
– Initial empirical antibiotic therapy while awaiting culture results.
– Antimicrobial therapy should be based on the patient's characteristics, the
setting in which aspiration occurred, the severity of pneumonia, and available
information regarding local pathogens and resistance patterns
– Community-acquired aspiration pneumonia is often initially treated with co-
amoxiclav. Metronidazole may need to be added if there is evidence of
complications - eg, lung abscess
– Hospital-acquired aspiration pneumonia: a suitable combination in patients
who have already recently been treated with antibiotics is piperacillin with
tazobactam.

http://pedsccm.org/FILE-CABINET/Practical/Akron_pdfs/7ASTHMAP.PDF
 • The role of steroids is uncertain and not of
proven benefit.
• Supportive therapy with fluid management,
bronchodilators and physiotherapy may help.
• Referral to speech and language therapists.

http://pedsccm.org/FILE-CABINET/Practical/Akron_pdfs/7ASTHMAP.PDF
 Complication
• Lung abscess / bronchiectasis
• ARD

Prognosis
• This depends on the underlying cause, general well-being of the
patient, presence of complications, speed of diagnosis and effective
treatment.

Prevention
• Keep the head of the bed at a 30° angle: this reduces the risk or
aspiration pneumonia in those at risk
• Nasogastric feeding for at-risk patients - eg, poor gag reflex,
dysphagia.

http://pedsccm.org/FILE-CABINET/Practical/Akron_pdfs/7ASTHMAP.PDF
ACUTE COPD EXACERBATION
 Chronic Obstructive Pulmonary
Disease
• Characterized by persistent airflow limitation that is generally
progressive & associated w/ an abnormal inflammatory
response to noxious particles/ gases
• GOLD: COPD encompasses chronic bronchitis, emphysema,
bronchiectasis, asthma, & knowledges that most patients have a
combination of the different diseases
• 2 main forms:
– Chronic bronchitis:
• defined in clinical terms
• Chronic productive cough for 3 months in each of 2 successive years,
where other causes of chronic cough have been excluded
– Emphysema:
• defined in term of anatomic pathology
• Destruction of bronchioles & alveoli

Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e

 Pathophysiology
• Irritants (tobacco smoke, air
pollutants) increase in
inflammatory cells in the
airways, lung interstitium,
alveoli
• Proteases break down lung
parenchyma  stimulate mucus
secretion mucus-secreting
cells replace cells that normally
secrete surfactant & protease
inhibitor loss of elastic recoil,
narrowing, collapse of the
smaller airways mucus stasis
& bacterial colonization develop
in the bronchi

Tintinalli’s Emergency Medicine: A Comprehensive

• airways secretions, mucosal edema, bronchospasm,
bronchoconstriction airways obstruction
• Emphysema alveolar & capillary surface are distorted/
destroyed alveolar hyperventilation & ventilation-
perfusion mismatch hypoxemia & hypercarbia
• Sleep may blunt the ventilator response to hypercarbia
• RV hypertrophies & dilates pulmonary hypertension &
RV failure
• RV pressure overload atrial & ventricular arrhythmias

Tintinalli’s Emergency Medicine: A Comprehensive

 Clinical features
• Hallmark symptoms chronic & progressive dyspnea, cough, sputum production
• Minor hemoptysis
• Tachypnea
• Accesory respiratory use/ pursed-lip exhalation
• Lower airway obstruction expiratory wheezing, especially during maximum forced
inhalation, prolongation of the expiratory time
• Chronic bronchitis crackles
• Emphysematous disease
– expansion of the thorax
– impeded diaphragmatic motion
– global diminution of breath sounds
– Poor dietary intake & excessive caloric expenditure for the work of breathing weight loos
– Early stages ABG mild to moderate hypoxemia w/o hypercapnia
• Arterial oxygenation worsens during acute exacerbations, exercise, sleep
• Facial vascular engorgement from secondary polycythemia, tremor, somnolence,
confusion from hypercarbia
• RV failure (edema/ ascites)
• Left heart failure cardiac ausculatory may be overshadowed by the pulmonary inflation
abN of COPD

Tintinalli’s Emergency Medicine: A Comprehensive

 Diagnosis

Global Initiative for Chronic Obstructive Lung Disease

• Spirometry:
postbronchodilator FEV1
of <80% predicted, and a
ratio of FEV1 to forced vital
capacity of <0.7
• Chronic bronchitis is not
radiographycally apparent
unless bronchiectasis is
present
• Emphysema
– radiographs show
hyperaeration, seen as
increased anteroposterior
chest diameter
– flattened diaphragms
– increased parenchymal
lucency
– attenuation of pulmonary
arterial vascular shadows

Tintinalli’s Emergency Medicine: A Comprehensive

Differential Diagnosis
Alpha-1 antitrypsin
deficiency (AATD)
screening.
• WHO all patients
w/ dx COPD screened
once especially in
ares w/ high AATD
• A low concentration
(< 20% normal)
highly suggestive of
homozygous
deficiency.
• Family members
should also be
screened.

Global Initiative for Chronic Obstructive Lung Disease

(GOLD)
 Assesment

• Presence & severity of the spirometric abN

• Current nature & magnitude of the patients
symptoms
• Exacerbation history & future risk
• Presence of comorbidities

Global Initiative for Chronic Obstructive Lung Disease

Classification of severity of airflow
obstruction

Global Initiative for Chronic Obstructive Lung Disease

 Assessment of symptoms
Modified British Medical Research Council
(mMRC) Questionnaire

Global Initiative for Chronic Obstructive Lung Disease

Global Initiative for Chronic Obstructive Lung Disease
Global Initiative for Chronic Obstructive Lung Disease
Clinical Emergency
Medicine (LANGE)
ACUTE EXACERBATIONS OF CHRONIC
OBSTRUCTIVE PULMONARY DISEASE
• Worsening of respiratory symptoms beyond normal day-to-day
variations & are usually triggered by an infx/ respiratory irritant
• 75% patients viral/ bacterial infx, half specifically due to
bacteria
• Other triggers hypoxia, cold weather, b-blocker, narcotics,
sedative-hypnotic agents
• Final common pathway for an exacerbation release of
inflammatory mediators that result in bronchoconstriction,
pulmonary vasoconstriction, mucus hypersecretion
• The work of breathing increase due to higher airway resistance
& lung hyperinflation
• The o2 demand of respiratory muscles increase, generating
additional CO & causing hypercapnia physiologic stress
• Primarily due to ventilation-perfusion mismatch rather than the
expiratory aiflow limitation seen w/ asthma exacerbations
Tintinalli’s Emergency Medicine: A Comprehensive
 Clinical features
• Most life-threatening feature of an acute exacerbation hypoxemia
(arterial saturation <90%)
• Sign of hypoxemia tachypnea, tachycardia, systemic HTN, cyanosis,
change in mental status
• Increased work of breathing:
– CO prod increase
– alveolar hypoventilation arterial carbon dioxide retention & respiratory
acidosis
• Severe dyspnea & orthopnea by sitting in an up-and-forward position,
using pursed-lip exhalation, engaging accessory muscle to breathe
• Pulsus paradoxus (a drop of>10 mmHg in SBP during respiratory cycles)
• Complications, such as pneumonia, pneumothorax, pulmonary
embolism, or an acute abdomen may exacerbate COPD
• Other acute triggers include asthma, CHF, pneumonia, pulmonary
embolism, tuberculosis, metabolic disturbance

Tintinalli’s Emergency Medicine: A Comprehensive

 Diagnosis
• Pulse oximetry hypoxemia
• Capnography hypercarbia
• ABG clarify the severity of exacerbation & the probable clinical course
• Respiratory failure is characterized by an arterial Pao2 of <60mmHg or an
arterial Sao2 <90% in room air
• Respiratory acidosis: partial Pco2 >44mmHg
• If the pH <7.35 acute & uncompensated component of respiratory/
metabolic acidosis present
• Acute respiratory acidosis serum bicarbonate rises by 1mEq/L for each
10mmHg increase in Pco2, pH will change by 0.0008x(40-Pco2)
• Chronic respiratory acidosis bicarbonate rises by 3.5 mEq/L for each 10-
mmHg increase in Pco2, pH will change by 0.03x(40-Pco2) (formula 1&2)
• Patients w/ acute COPD exacerbation are too dyspneic to perform bedside
pulmonary fx test inaccurate (also PE)
• Assement of sputum
• Ancillary studies radiographic abN, ECG, CBC, electrolytes, B-type natriuretic
peptide, d-dimers, and CT angiography of the chest

Tintinalli’s Emergency Medicine: A Comprehensive

 • Oxygen
– Raise the Pao2 >60mmHG/
Sao2 >90%

Management – Standart duallong nasal canula,

simple facemask, venturi mask,
nonrebreathing mask w/
reservoir & one-way valve
• B2-adrenergic agonist
– Short-acting b2-agonist &
anticholinergic agents first
line
– Aerosolized forms, using
nebulizer/ metered-dose
inhalers
– Given every 30-60 mnt
– Nebulized aerosols every 20
mnt improve FEV1, but more
side effects: tremor, anxiety,
palpitations
– Continous cardiac monitoring
• Anticholinergics
– Ipratropium bromide single
dose by metered-dpse inhaler
w/ spacer/ as an inhalant
solution by nebulization (0.5
mg or 2.5mL of the 0.02%
inhalant solution)
– Aerosolized glycopyrrolate (2
mg in 10 mL of saline)
– Long-acting inhaled
anticholinergics(tiotropium,
aclidinium, glycopyrronium)
Tintinalli’s Emergency Medicine: A Comprehensivenot used for acute COPD
• Corticosteroid
– Use of a short course (5-7 days) of systemic steroids improve lung fx &
hypoxemia & shorten recovery time in acute COPD
– No clear benefit from a dose >40-60mg PO prednisone daily
– Adverse affect hyperglycemia
• AB
– Choose agents directed at the most common pathogens associated with
COPD exacerbation: Streptococcus pneumoniae, Haemophilus influenzae,
and Moraxella catarrhalis
– Macrolides (azithromycin), tetracyclines (doxycycline), amoxicillin w/ or
w/o clavulanic acid  3 – 14 hari
• Methylxanthines
– Such as theophylline (PO) & aminophylline (parenteral) inhibit
phospodiesterases, enhance respiration in 2 ways: improving the
mechanics of breathing & through an anti-inflammatory effect
– Aminophylline 3-5 mg/kg IV over 20 mnts) third-line

Tintinalli’s Emergency Medicine: A Comprehensive

• Noninvasive ventilation
• Contraindications
– uncooperative or
obtunded patient
– inability of the patient to
clear airway secretions
– hemodynamic
instability
– respiratory arrest
– recent facial or
gastroesophageal
surgery
– Burns
– poor mask fit, or
extreme obesity

Tintinalli’s Emergency Medicine: A Comprehensive

• Assisted Ventilation
– Mechanical ventilation
is indicated if there is
evidence of respiratory
muscle fatigue,
worsening respiratory
acidosis, deteriorating
mental status, or
refractory hypoxemia

Tintinalli’s Emergency Medicine: A Comprehensive

Tintinalli’s Emergency Medicine: A Comprehensive
Tintinalli’s Emergency Medicine: A Comprehensive
PNEUMOTHORAX
 the presence of gas in the
Pneumothorax pleural space

Primary Spontaneous Secondary Traumatic Tension

Pneumothorax Pneumothorax Pneumothorax Pneumothorax

Secondary pneumothorax
• Occurs in patients with underlying lung
disease  chronic obstructive pulmonary
disease (COPD)

Marx JA, Hockberger RS, Walls RM. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 8th Ed. 2014.
Harrison’s Principles of Internal Medicine. 18th Ed. Volume II. Chapter 263.
 Pathophysiology
• Primary spontaneous pneumothorax: rupture of subpleural bullae/bleb
(typically at the lung apex)  disruption of alveolar-pleural barrier
• Subpleural bullae are found in patients who undergo surgical treatment for
PSP, related to the degradation of elastic fibers in the lung
• Secondary spontaneous pneumothorax: underlying disease weaken the
alveolar-pleural barrier
– P. jiroveci pneumonia: the cytotoxic effects of repeated episodes of inflammation
 bullous and cystic changes.
– COPD: chronic exposure to cigarette smoke  development of large, thin-walled
bullae that are at an increased risk for rupture
– Other factors: increased intrabronchial and intra-alveolar pressures generated by
bronchospasm and coughing
• A break in the pleura  air travels down a pressure gradient into the
intrapleural space  until pressure equilibrium occurs with partial or total
lung collapse
• Altered ventilation– perfusion relationships and decreased vital capacity then
contribute to dyspnea & hypoxemia

Marx JA, Hockberger RS, Walls RM. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 8th Ed. 2014.
 Clinical Features
• Symptoms are related:
– Size of the pneumothorax
– Rate of development
– Underlying clinical status of the patient
• Acute pleuritic chest pain that localizes to the side of
the pneumothora
• Large-volume pneumothorax (especially in patients
with COPD)  dyspnea, tachycardia, hypotension,
and hypoxia

Marx JA, Hockberger RS, Walls RM. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 8th Ed. 2014.
 Diagnosis
• Chest radiography
• Chest CT
• Ultrasonography
 Treatment
• The major ED treatment goal: elimination of intrapleural air
• Administration of oxygen  3 L/min nasal cannula - 10 L/min
by mask and should be guided by the patient’s status, with
monitoring for hypercapnia in COPD patients
• Needle or catheter aspiration: small primary, secondary
spontaneous pneumothorax
• Chest tube thoracostomy: large pneumothorax, recurrent or
bilateral pneumothorax, coexistent hemothorax, or if there
are abnormal vital signs or dyspnea, and is an option for small
SSP where large air leak is anticipated

Harrison’s Principles of Internal Medicine. 18th Ed. Volume II. Chapter 263.
SARS
 SARS
• febrile severe lower respiratory illness that is
caused by infection with a novel coronavirus,
SARS-associated coronavirus (SARS-CoV)
• The vast majority of patients with SARS-CoV
disease
1) have a clear history of exposure either to a SARS
patient(s) or to a setting in which SARS-CoV
transmission is occurring, and
2) develop pneumonia
• Laboratory tests are can be helpful but do not
reliably detect infection early in the illness

https://www.cdc.gov/sars/clinical/guidance.html
 • absence of person-to-person transmission of SARS-CoV anywhere
in the world, the diagnosis of SARS-CoV disease should be
considered only in patients who require hospitalization for
radiographically confirmed pneumonia and who have an
epidemiologic history that raises the suspicion of SARS-CoV
disease.
• The suspicion for SARS-CoV disease is raised if, within 10 days of
symptom onset, the patient:
– Has a history of recent travel to mainland China, Hong Kong, or Taiwan
(see Figure 1, footnote 3) or close contact1 with ill persons with a
history of recent travel to such areas, or
– Is employed in an occupation at particular risk for SARS-CoV exposure,
including a healthcare worker with direct patient contact or a worker
in a laboratory that contains live SARS-CoV, or
– Is part of a cluster of cases of atypical pneumonia without an
alternative diagnosis

https://www.cdc.gov/sars/clinical/guidance.html
https://www.cdc.gov/sars/clinical/fig1.html
 • Once person-to-person transmission of SARS-CoV has been
documented in the world, the diagnosis should still be considered
in patients who require hospitalization for pneumonia and who
have the epidemiologic history described above.
• In addition, all patients with fever or lower respiratory symptoms
(e.g., cough, shortness of breath, difficulty breathing) should be
questioned about whether within 10 days of symptom onset they
have had
– Close contact with someone suspected of having SARS-CoV disease,
OR
– A history of foreign travel (or close contact with an ill person with a
history of travel) to a location with documented or suspected SARS-
CoV, OR
– Exposure to a domestic location with documented or suspected SARS-
CoV (including a laboratory that contains live SARS-CoV), or close
contact with an ill person with such an exposure history.

https://www.cdc.gov/sars/clinical/guidance.html
https://www.cdc.gov/sars/clinical/fig2.html
ACUTE SEVERE ASTHMA / STATUS
ASTHMATICUS
 Status asthmaticus
• extreme form of an asthma exacerbation that can
result in hypoxemia, hypercarbia, and secondary
respiratory failure
• acute exacerbation of asthma that remains
unresponsive to initial treatment with
bronchodilators
• vary from a mild form to a severe form with
bronchospasm, airway inflammation, and mucus
plugging that can cause difficulty breathing,
carbon dioxide retention, hypoxemia, and
respiratory failure
RF
• Viral infections
• Air pollutants - Such as dust, cigarette smoke, and
industrial pollutants
• Medications - Including beta-blockers, aspirin,
and nonsteroidal anti-inflammatory drugs
(NSAIDs)
• Cold temperature
• Exercise
Primary survey
• As for all patients, the initial evaluation should center around the “ABCs.”
History taking and a more detailed examination can occur after you assure
adequate airway, breathing, and circulation. This need only takes a few
seconds to minutes, but is essential.
– Airway: Can the patient maintain his/her airway? Is the mental status
adequate to protect the airway?
– Breathing: What is the degree of air exchange? Is the patient cyanotic?
– Circulation: How is the perfusion? The pulses?
History
• Previous history of wheezing?
• If known asthmatic, what are maintenance meds?
Compliance? Time of last
• aerosol?
• Previous office/clinic/ED visits?
• Previous hospitalizations, intubations, last steroid
course?
• When did this exacerbation begin?
• Precipitating factors?
• General medical history, including any medications.
Vital signs
• Temperature: fever may indicate URI, pneumonia, other
source of infection
• Pulse: Usually tachycardic, even before treatment
• Respiratory rate: Usually tachypneic.
• Blood pressure: Pulsus paradoxus over 10-15 correlates
well with moderate to severe disease, as it indicates the
effect that air trapping is having on the cardiac output. It is
best measured with a sphygmomanometer and a
stethoscope, and is the difference in systolic BP between
the pressure at which an observer first hears faint pulse
sounds and the pressure at which all sounds are heard.
Breath sounds / chest exam
• There must be air movement in order to appreciate wheezing, lack or wheezing
does NOT necessarily mean everything is fine!
• I:E ratio is usually 5:2, may be up to 1:4 with a severe attack
• Symmetry of breath sounds
– Some asymmetry may be heard with asthma alone due to mucous plugging and
atelectasis.
– Increased wheezing unilaterally may indicate presence of a foreign body
– Significantly decreased breath sounds unilaterally may indicate pneumonia
– or pneumothorax.
• The use of accessory respiratory muscles(abdominal paradoxic breathing,
• sternocleidomastoid use, nasal flaring, intercostal retractions) correlates with the
severity of airway obstruction. Wheezing is a less sensitive indicator of the degree
of obstruction present.
• Feel for the presence of crepitus in the neck or chest wall, signifying air leak and
significant obstruction
Cardiac exam
• Attention should be paid to rate and blood
pressure, including the presence of pulsus
paradoxus. In addition, are the heart tones
normal, is there a murmur (any evidence of pre-
existing heart disease)
Mental status
• Confusion or obtundation suggest significant
hypercapnia or hypoxemia, and necessitate
immediate action!!!
• Clinical asthma score
Prognosis
• In general, unless a complicating illness such as
congestive heart failure or chronic obstructive
pulmonary disease is present, status asthmaticus
has a good prognosis if appropriate therapy is
administered
• Delays can result from poor access to health care
on the part of the patient or even delays in using
corticosteroids
• with acute asthma should use corticosteroids
early and aggressively
Complications
• Cardiac arrest
• Respiratory failure or arrest
• Hypoxemia with hypoxic ischemic central
nervous system (CNS) injury
• Pneumothorax or pneumomediastinum
• Toxicity from medications
LIGHT criteria

MASSIVE PLEURAL EFFUSION

• Efusi pleura : terdapat
cairan berlebih di dalam
rongga pleura disebabkan
ketidakseimbangan antara
produksi & absorbsi cairan
pleura.
 Diagnosis
• Anamnesis
• Pemeriksaan fisik:
– pergerakan dada tdk simetris
– cairan > 300cc:
• perkusi redup
• fremitus menghilang
• suara nafas melemah-hilang
• trakea terdorong ke kontralateral
• Torakosentesis aspirasi cairan pleura dan analisis cairan:
– Warna cairan:
• Biasa berwarna kekuning-kuningan (serous-santokrom)
• Kemerah-merahan: trauma,infark paru,keganasan, aneurisma aorta
• Kuning kehijauan & purulen: empiema
• Merah coklat: abses krn amuba
• Bakteriologi
• Biopsi Pleura
 Transudat Eksudat
Kadar protein dlm efusi(g/dl) <3 >3
Kadar protein dlm efusi / < 0,5 >0,5
Kadar protein dalam serum
Kadar LDH dalam efusi (I.U) <200 >200
Kadar LDH dalam efusi/ <0,6 >0,6
kadar LDH dalam serum
Berat jenis cairan efusi <1,016 >1,016
Rivalta - +

- Sitologi
 Sel neutrofil: infeksi akut
 Sel limfosit: infeksi kronik (pleuritis tuberkulosa/limfoma maligna
 Sel mesotel: meningkat infark paru
 Sel mesotel maligna: mesetolioma
 Sel-sel besar banyak inti: arthritis reumatoid
 Sel LE: lupus erimatosus sistemik
 Sel maligna: pada paru/metastase
 Diagnosis
• Periksa glukosa& ph
• Kadar amilase
• Foto Toraks dada
– posisi PA tegak (cairan 250-300ml)
– Lateral tegak cairan <250 ml(100-200)ml: ditemukan pengisian
cairan di sudut kostofrenikus posterior.
– posisi dekubitus cairan<100ml (50-100 ml)cairan akan
berkumpul di sisi saping bawah.
 PA/lateral: perselubungan homogen menutupi struktur
paru,radiopak(putih), permukaan atas cekung,terdorongnya
mediastinum kontralteral.
• USG bantu sebagai penuntun waktu aspirasi cairan.
• Ct-scan
 Tatalaksana Efusi Pleura
• Tatalaksana
– Keluarkan segera efusi dgn pipa intubasi.
– Pleuritis tuberkulosa terapi sesuai pengobatan
TB paru
PULMONARY EDEMA
http://www.sgph.ch/tl_files/daten/Medical/High%20Altitude%20PH/53.jpg
http://www.hkma.org/english/cme/onlinecme/201211-fig2.gif
http://www.hkma.org/english/cme/onlinecme/201211-fig2.gif
PULMONARY TB
 Tuberculosis
• TB is a disease caused by a bacterium called
Mycobacterium tuberculosis.
• Infection with M tuberculosis  exposure of
the lungs or mucous membranes to infected
aerosols.
• Person with active pulmonary TB, a single
cough can generate 3000 infective droplets,
with as few as 10 bacilli needed to initiate
infection.
 Patophysiology
• Droplet inhaled  nuclei deposited within the
terminal airspaces of the lung  organisms
grow for 2-12 weeks, until they reach 1000-
10,000 in number  sufficient to elicit a
cellular immune response  can be detected
by a reaction to the tuberculin skin test.
• The infection may be cleared by the host
immune system or suppressed into an inactive
form called latent tuberculosis infection (LTBI)
TB lesions
• Epithelioid granuloma with central caseation
necrosis.
• The most common site  within alveolar
macrophages in subpleural regions of the
lung.
• Bacilli proliferate locally and spread through
the lymphatics to a hilar node, forming the
Ghon complex.
Early tubercles  spherical, 0.5- to 3-mm nodules
with 3 or 4 cellular zones demonstrating the
following features:
• A central caseation necrosis
• An inner cellular zone of epithelioid macrophages
and Langhans giant cells admixed with
lymphocytes
• An outer cellular zone of lymphocytes, plasma
cells, and immature macrophages
• A rim of fibrosis (in healing lesions)
• Initial lesions may heal and the infection become
latent before symptomatic disease occurs.
Smaller tubercles may resolve completely.
• Fibrosis occurs when hydrolytic enzymes dissolve
tubercles and larger lesions are surrounded by a
fibrous capsule.
• Such fibrocaseous nodules usually contain viable
mycobacteria and are potential lifelong foci for
reactivation or cavitation.
• Some nodules calcify or ossify and are seen easily
on chest radiographs.
• Tissues within areas of caseation necrosis have high
levels of fatty acids, low pH, and low oxygen tension, all
of which inhibit growth of the tubercle bacillus.
• If the host is unable to arrest the initial infection, the
patient develops progressive, primary TB with
tuberculous pneumonia in the lower and middle lobes
of the lung.
• Purulent exudates with large numbers of acid-fast
bacilli can be found in sputum and tissue.
• Subserosal granulomas may rupture into the pleural or
pericardial spaces and create serous inflammation and
effusions.
Lesions that develop around mycobacterial foci can be
either proliferative or exudative.
• Proliferative lesions  the bacillary load is small and
host cellular immune responses dominate. These
tubercles are:
- Compact
- With activated macrophages admixed,
- Surrounded by proliferating lymphocytes, plasma cells,
and an outer rim of fibrosis.
• Exudative lesions  large numbers of bacilli and host
defenses are weak. Without treatment, these lesions
progress and infection spreads.
 Risk factors
The following factors help to determine whether
a TB infection is likely to be transmitted:
• Number of organisms expelled
• Concentration of organisms
• Length of exposure time to contaminated air
• Immune status of the exposed individual
 Clinical features
• Cough
• Weight loss/anorexia
• Fever
• Night sweats
• Hemoptysis
• Chest pain
• Fatigue
• Abnormal breath sounds, especially over the
upper lobes or involved areas.
 Diagnosis: Screening method
• Mantoux tuberculin skin test with purified
protein derivative (PPD)  active and latent
TB
• An in vitro blood test based on interferon-
gamma release assay (IGRA) with antigens
specific for Mycobacterium tuberculosis 
latent TB
 Laboratory test
• Acid-fast bacilli (AFB) smear and culture -
Using sputum obtained from the patient
• HIV serology in all patients with TB and
unknown HIV status
 Work up
• Chest radiograph to evaluate for possible
associated pulmonary findings. If chest
radiography findings suggest TB and a sputum
smear is positive for AFB, initiate treatment
for TB.
• A computed tomography (CT) scan of the
chest may help to better define abnormalities
in patients with vague findings on chest
radiography.
 Treatment

Latent TB
• Recommended regimens  isoniazid and rifampin
• An alternative regimen  isoniazid plus rifapentine as directly observed
therapy (DOT) once-weekly for 12 weeks
AVIAN INFLUENZA
 Avian influenza
• infection with avian (bird) influenza (flu) Type
A viruses
• occur naturally among wild aquatic birds
worldwide and can infect domestic poultry
and other bird and animal species
• do not normally infect humans. However,
sporadic human infections with avian flu
viruses have occurred

https://www.cdc.gov/flu/avianflu/avian-in-humans.htm
 Influenza A virus :
• divided into subtypes on the basis of two proteins on the surface of the virus: hemagglutinin
(HA) and neuraminidase (NA)
• All known subtypes of influenza A viruses can infect birds, except subtypes H17N10 and
H18N11, which have only been found in bats.
• Only two influenza A virus subtypes (i.e., H1N1, and H3N2) are currently in general
circulation among people.
• H7N7 and H3N8 virus infections can cause illness in horses, and H3N8 virus infection cause
illness in horses and dogs
• Sporadic H5 virus infection of humans has occurred, such as with Asian lineage HPAI H5N1
viruses currently circulating among poultry in Asia and the Middle East
• The most frequently identified H7 viruses associated with human infection are Asian lineage
avian influenza A(H7N9) viruses, which were first detected in China in 2013
• H7N2, H7N3, H7N7 virus infections have been reported. These viruses have primarily caused
mild to moderate illness in people, with symptoms that include conjunctivitis and/or upper
respiratory tract symptoms.
• Rare, sporadic H9N2 virus infections in people have been reported to generally cause mild
upper respiratory tract illness; one infection has results in death.

https://www.cdc.gov/flu/avianflu/influenza-a-virus-subtypes.htm
 Avian Influenza A Virus Infections in Humans
• Infected birds shed avian influenza virus in their saliva,
mucous and feces
• Human infections with bird flu viruses can happen when
enough virus gets into a person’s eyes, nose or mouth, or is
inhaled
• happen when virus is in the air (in droplets or possibly dust)
and a person breathes it in, or when a person touches
something that has virus on it then touches their mouth,
eyes or nose
• occurred most often after unprotected contact with
infected birds or surfaces contaminated with avian
influenza viruses

https://www.cdc.gov/flu/avianflu/avian-in-humans.htm
https://www.cdc.gov/flu/avianflu/avian-in-humans.htm
 S/S
• Mild – severe
• Conjunctivitis
• Influenza like illness (fever, cough, sore throat, muscle aches)
• Accompanied by nausea, abdominal pain, diarrhea, vomiting
• Severe respi illness (shortness of breath, difficulty breathing,
pneumonia, ARD, viral pneumonia, respi failure)
• Neurologic changes (altered mental status, seizures)
• Involve other organ systems
• Asian lineage H7N9 & HPAI asian lineage H5N1  most serious
illness & highest mortality in humans

https://www.cdc.gov/flu/avianflu/avian-in-humans.htm
 Diagnosis
• collecting a swab from the upper respiratory tract (nose or
throat) of the sick person (more accurate when the swab is
collected during the first few days of illness)  lab :
molecular test, by trying to grow the virus, or both
• possible to diagnose avian influenza A virus infection by
looking for evidence of antibodies the body has produced
in response to the virus (requires two blood specimens
(one taken during the first week of illness and another
taken 3-4 weeks later)  take several weeks to verify the
results, and testing must be performed in a special
laboratory, such as at CDC

https://www.cdc.gov/flu/avianflu/avian-in-humans.htm
 Treatment
• neuraminidase inhibitor
• most viruses are susceptible to oseltamivir,
peramivir, and zanamivir, some evidence of
antiviral resistance has been reported in Asian
H5N1 and Asian H7N9 viruses isolated from
some human cases

https://www.cdc.gov/flu/avianflu/avian-in-humans.htm
 Prevention
• avoid sources of exposure
• had contact with infected birds may be given
influenza antiviral drugs preventatively
• Seasonal influenza vaccination will not
prevent infection with avian influenza A
viruses, but can reduce the risk of co-infection
with human and avian influenza A viruses

https://www.cdc.gov/flu/avianflu/avian-in-humans.htm
https://www.gov.uk/government/u
ploads/system/uploads/attachment
_data/file/358673/Investigation_an
d_management_of_possible_human
_cases_of_avian_influenza_A_H7N9
__flow_diagram_July_new.pdf
https://www.gov.uk/government/uploads/system
/uploads/attachment_data/file/358675/Case_ma
nagement_of_suspected_human_case.pdf
 2 Phase 3 Management of asymptomatic contacts of
confirmed human case(s) of avian influenza A/H5N1
1 January 2009. Please check for updates at:
http://www.hpa.org.uk/webw/HPAweb&HPAwebStandard/HPAweb_C/1195733851442?p=1160495617107

The clinician attending a confirmed human case of avian influenza should notify the local Health Protecti on Unit (HPU) as soon
as possible. The local HPU will advise, in liasion with HPA Centre for Infections (CfI), on the assessment of contacts, clinical
management and use of oseltamivir prophylaxis.

- Start oseltamivir prophylaxis4 as soon as possible

unless more than 7 days have elapsed since last
exposure. Current licensed indication for post-
exposure prophylaxis is a 10-day course of therapy.

- If exposure is ongoing (e.g. caring for the patient)

then prophylaxis to be continued for 10 days after last
Close contacts1 of a symptomatic case or
1 healthcare workers2 caring for a symptomatic case
Yes exposure.

- HPU to provide information leaflets5 and coordinate

active follow up: daily assessments for up to 7 days
after last exposure to the symptomatic case and
passive follow up until the course of oseltamivir is
completed.

- The extent of serological investigation will be agreed

No
by the Incident Management team in discussion with
CfI. However as a minimum, a 10ml clotted blood
specimen should be taken 28 days after last exposure
to the case and sent to CfI for serology.

Casual contact of a symptomatic case - Prophylaxis not indicated.

2 in transit (air/train/ferry/coach/car) Yes

- Provide information and advise on passive follow up
Refer to Port Health algorithm for advice3 for 7 days after last contact with case. HPU to
coordinate.6

No

3 Casual contact of an asymptomatic case Yes No action required however information leaflets may
be helpful.

If a contact becomes unwell, the local HPU should liaise with the Pandemic Influenza Office in the first instance. If
unavailable, contact appr opriate consultant in the Respiratory & Systemic Infections Department or the Virus
Reference Laboratory at CfI to discuss next steps.

Footnotes:

1 A close contact is defined as an individual sharing a household or remaining unprotected whilst within speaking distance (<1 metre) while caring for a patient
with confirmed or strongly suspected H5N1 infection. (adapted from WHO Rapid Advice Guidelines on pharmacological management of humans infected with
avian influenza A(H5N1) virus, May 2006 www.who.int/csr/d isease/avian_influenza/guidelines/pha rmamanagement/en/index.html )

2 Health care worker or anyone else engaged in direct clinical care or examination of symptomatic patient. Ideally, the number of people involved should be
kept to a minimum.
3 Port Health algorithm for information on travel exposures. (to follow)

4 Refer to dosing schedule for oseltamivir prophalyxis. (http://www.bnf.org/bnf/bnf/current/119743.htm)

5 Refer to information leaflets on active follow up. (link to information leaflets to follow)
6 Passive follow up: provision of information to individual (or responsible carer) and request that any febrile respiratory or other unexplained illness within 7
days of last contact be reported (24 hour reporting).
https://www.gov.uk/government/uploads/syst
In case of uncertainty, discuss with local Health Protection Unit.
em/uploads/attachment_data/file/358676/2p
Health Protection Agency www.hpa.org,uk
hase3contactsofconfirmedcasealgorithm20090
101b.pdf