FOURTH PROBLEM

GROUP 3

Morning Disaster
• Tutor : dr. Susy
• Ketua : Maria Fransisca
• Sekretaris : Selly Herlia Rudianti
• Penulis : Esteven Tanu Gunawan
• Anggota : Prima Putri P
Imelda Jarisa Arisal
Daniel Filemon Poso
Shynta Amelia
Joshua Kurnia Tandi
Natashia Olivia Christian
Adriani Hartanto
Alvin Rinaldo
Ulmy Auly Hidayati
 Fourth Problem
A 40-years old male is brought to the Emergency Departement by his family with keft side
chest pain and shortness of breath at dawn. He also suffers cough with sputum
especially in the morning, sometimes with blood streak and getting worse since 4 weeks
ago. He was diagnosed with pulomonary tuberculosis 10 years ago but he did not geta
proper treatment. He was also a heavy smoker in his young age.
On vital sign examinations : patient looks severely ill, body height: 167 cm, body weight: 55
kg, Blood pressure: 140/90mmHg, heart rates: 100 beats per minute, respiratory rate:
32 beats per minute, body temperatue : 37,3 C, conjungtiva looks pale.
On physical thorax examination: left thorax larger than the contralateral side. Tactile
fremitus was absent on the left lung. On percussion, his thorax sound hypersonor at the
left lung. Regular heart sounds; murmurs and gallops are not found. Abdominal physical
examination is within normal limits.
Laboratory finding: Hb 10,8 g/dL, leucosit count: 11,100/μL, trombosit 421000/mm3. Liver
and renal function test AST 13 U/L, ALT 12 U/L, ureum 19 mg/dL and creatinin 0,6
mg/dL. Blood electrolit : Na+: 141 mEq/L, K+ : 3,4 mEq/L, Cl- : 101 mEq/L, Ca2+ :1,13
mEq/L, Blood sugar: 114mg/dL
Arterial blood gas analysis: pH: 7,51, pCO2 : 34 mmol/L, pO2=75 mmol, HCO3-=23 mmol/L,
Sat O2: 91% BE : -1
Discuss the case, asses the patients condition. Plan proper diagnostic procedures and
treatment while considering all possibilities
Mind Map

Pneumonia: TB, Permeabilitas Efusi pleura, tension

INFEKSI
pneumonia non dinding alveolar pneumotorax 
spesifik terganggu penumpikan cairan +
edema + gas
COPD
Sesak nafas

I : Hipoksemia PO2
Gangguan saturasi O2 Asma
menurun

II : Hipoventilasi PCO2 Gangguan asam-basa

menurun
Asidosis dan alkalosis
respiratorik
 Learning Issues
• Menjelaskan definisi dan etiologi Respiratory failure dan ARDS
(avian influenza, COPD eksaserbasi akut, efusi pleura, tension
pneumothorax, pneumonia aspirasi, SARS, asma akut,
TB+Komplikasi, aspirasi trakea, ARDS)
• Mengetahui tanda dan gejala gagal nafas dan ARDS pada survey
primer
• DD gagal nafas tipe I, II
• Menjelaskan tatalaksana gagal nafas dan ARDS
• Menjelaskan diagnosa gagal nafas dan ARDS (lab, radiologi/ invasif)
• Menjelaskan komplikasi dan prognosis gagal nafas dan ARDS
• Hasil interpretasi pemeriksaan lab pada pasien pemicu dan
patofisiologi
ASMA
 Definisi
• Asma eksaserbasi akut: ditandai dengan
peningkatan gejala yang progresif seperti
wheeze, nafasnya pendek-pendek, sesak
nafas, dan batuk dan progresif dalam
menurunkan fungsi paru. Eksaserbasi dapat
muncul pada pasien yang sebelumnya sudah
didiagnosis asma atau pertama kali muncul
gejala asma. Eksaserbasi biasa muncul akibat
respon pada paparan agen eksternal dan atau
tanpa mengonsumsi obat.

GINA 2018
 Etiologi
• Penyebab dari asma masih belum diketahui dengan jelas.
Faktor resiko yang paling kuat dari asma adalah kombinasi
presdiposisi genetik dengan exposure lingkungan yang
menginhalasi subtansi dan partikel yang menyebabkan
reaksi alergi atau mengiritasi jalan nafas seperti :
• Alergen di dalam rumah ( misalnya tungau debu rumah di
tempat tidur, karpet, dan bulu hewan peliharaan)
• outdoor allergens (serbuk sari dan jamur)
• chemical irritants in the workplace
• air pollution
• Pencetus lain bisa karna udara dingin, emosi ekstrim
seperti marah atau takut, dan olahraga.
• Obat-obatan seperti aspirin, NSAID, dan beta bloker.

GINA 2018
 Identify patients at risk of asthma-
related death
• Patients at increased risk of asthma-related death
should be identified
– Any history of near-fatal asthma requiring intubation and
ventilation
– Hospitalization or emergency care for asthma in last 12
months
– Not currently using ICS, or poor adherence with ICS
– Currently using or recently stopped using OCS
• (indicating the severity of recent events)
– Over-use of SABAs, especially if more than 1 canister/month
– Lack of a written asthma action plan
– History of psychiatric disease or psychosocial problems
– Confirmed food allergy in a patient with asthma
• Flag these patients for more frequent review
GINA 2017, Box 4-1
GINA 2018
 Managing exacerbations in
primary care
PRIMARY CARE Patient presents with acute or sub-acute asthma exacerbation

Is it asthma?
ASSESS the PATIENT Risk factors for asthma-related death?
Severity of exacerbation?

MILD or MODERATE SEVERE

Talks in phrases, prefers
sitting to lying, not agitated
Respiratory rate increased
Accessory muscles not used
Pulse rate 100–120 bpm
O2 saturation (on air) 90–95%
PEF >50% predicted or best
LIFE-THREATENING
Talks in words, sits hunched
forwards, agitated Drowsy, confused
Respiratory rate >30/min or silent chest
Accessory muscles in use
Pulse rate >120 bpm
O2 saturation (on air) <90%
PEF ≤50% predicted or best URGENT

START TREATMENT
SABA 4–10 puffs by pMDI + spacer, TRANSFER TO ACUTE
repeat every 20 minutes for 1 hour CARE FACILITY
WORSENING
Prednisolone: adults 1 mg/kg, max.
50 mg, children 1–2 mg/kg, max. 40 mg While waiting: give inhaled
SABA and ipratropium bromide,
Controlled oxygen (if available): target O2, systemic corticosteroid
saturation 93–95% (children: 94-98%)

CONTINUE TREATMENT with SABA as needed

WORSENING
ASSESS RESPONSE AT 1 HOUR (or earlier)

IMPROVING

ASSESS FOR DISCHARGE ARRANGE at DISCHARGE

Symptoms improved, not needing SABA Reliever: continue as needed
PEF improving, and >60-80% of personal Controller: start, or step up. Check inhaler
best or predicted technique, adherence
Oxygen saturation >94% room air Prednisolone: continue, usually for 5–7 days
(3-5 days for children)
Resources at home adequate
Follow up: within 2–7 days

FOLLOW UP
Reliever: reduce to as-needed
Controller: continue higher dose for short term (1–2 weeks) or long term (3 months), depending
on background to exacerbation
Risk factors: check and correct modifiable risk factors that may have contributed to exacerbation,
including inhaler technique and adherence
Action plan: Is it understood? Was it used appropriately? Does it need modification?

GINA 2017, Box 4-3 (1/7) GINA 2018

 Managing exacerbations in acute care settings

INITIAL ASSESSMENT Are any of the following present?

A: airway B: breathing C: circulation Drowsiness, Confusion, Silent chest

NO
YES

Further TRIAGE BY CLINICAL STATUS Consult ICU, start SABA and O2,
according to worst feature and prepare patient for intubation

MILD or MODERATE SEVERE

Talks in phrases Talks in words

Prefers sitting to lying Sits hunched forwards
Not agitated Agitated
Respiratory rate increased Respiratory rate >30/min
Accessory muscles not used Accessory muscles being used
Pulse rate 100–120 bpm Pulse rate >120 bpm
O2 saturation (on air) 90–95% O2 saturation (on air) < 90%
PEF >50% predicted or best PEF ≤50% predicted or best

Short-acting beta2-agonists Short-acting beta2-agonists

Consider ipratropium bromide Ipratropium bromide
Controlled O2 to maintain Controlled O2 to maintain
saturation 93–95% (children 94-98%) saturation 93–95% (children 94-98%)
Oral corticosteroids Oral or IV corticosteroids
Consider IV magnesium
Consider high dose ICS

If continuing deterioration, treat as

severe and re-aassess for ICU

ASSESS CLINICAL PROGRESS FREQUENTLY

MEASURE LUNG FUNCTION
in all patients one hour after initial treatment

FEV1 or PEF 60-80% of predicted or FEV1 or PEF <60% of predicted or

personal best and symptoms improved personal best,or lack of clinical response
SEVERE
MODERATE
Continue treatment as above
Consider for discharge planning and reassess frequently

GINA 2017, Box 4-4 (1/4)

 Written asthma action plans
Effective asthma self-management education requires:

• Self-monitoring of symptoms and/or lung function If PEF or FEV1

<60% best, or not
• Written asthma action plan improving after
• Regular medical review 48 hours
All patients Continue reliever

Increase reliever Continue controller

Early increase in Add prednisolone

controller as below 40–50 mg/day

Review response Contact doctor

EARLY OR MILD LATE OR SEVERE

GINA 2017, Box 4-2 (1/2)

 Written asthma action plans –
medication options
• Increase inhaled reliever
– Increase frequency as needed
– Adding spacer for pMDI may be helpful
• Early and rapid increase in inhaled controller
– Up to maximum ICS of 2000mcg BDP/day or equivalent
– Options depend on usual controller medication and type of LABA
– See GINA 2017 report Box 4-2 for details
• Add oral corticosteroids if needed
– Adults: prednisolone 1mg/kg/day up to 50mg, usually 5-7 days
– Children: 1-2mg/kg/day up to 40mg, usually 3-5 days
– Morning dosing preferred to reduce side-effects
– Tapering not needed if taken for less than 2 weeks UPDATED
2017
– Remember to advise patients about common side-effects (sleep
disturbance, increased appetite, reflux, mood changes)

GINA 2017, Box 4-2 (2/2)

 Pemeriksaan Penunjang
• Most patients with an asthma exacerbation do not require laboratory studies. If
ordered, laboratory studies must not result in delay of treatment.
• Laboratory studies are used to detect actual or impending respiratory failure,
theophylline toxicity, or conditions that complicate asthma treatment, such as
cardiovascular disease, pneumonia, or diabetes. For example, arterial blood gas
measurements are helpful for evaluating Paco2 in patients with suspected
hypoventilation, those in severe distress, or those with FEV1 or PEF results of 25%
or less of predicted value after initial treatment.
• A complete blood cell count is rarely needed, but might be appropriate in patients
with fever or purulent sputum, but clinicians should bear in mind that modest
leukocytosis is common in patients with asthma.
• A chest radiograph is not recommended for routine assessment but should be
obtained for patients suspected of having congestive heart failure, pneumothorax,
pneumomediastinum, pneumonia, or lobar atelectasis.
• A baseline electrocardiogram and monitoring of cardiac rhythm are appropriate in
patients older than 50 years and in those who have known coexistent heart
disease or chronic obstructive pulmonary disease.

https://www.atsjournals.org/doi/full/10.1513/
pats.P09ST2
 Komplikasi
• Although most patients respond well to therapy, a small percentage will show
signs of worsening ventilation. Because respiratory failure can progress rapidly
and is difficult to reverse, early recognition and treatment are necessary. Signs
of impending respiratory failure include an inability to speak, altered mental
status, intercostal retraction, worsening fatigue, and a PaCO2 of 42 mm Hg or
greater. The Expert Panel recommends that intubation not be delayed once it
is deemed necessary.
• Because intubation of a severely ill asthmatic patient is difficult and can result
in complications, other treatments, such as intravenous magnesium, and
heliox
• Intravenous magnesium sulfate has no apparent value in patients with
exacerbations of lower severity, but it might be considered (conditional
recommendation) in those with life-threatening exacerbations and those
whose exacerbations remain severe after 1 hour of intensive conventional
treatment . The selective use of intravenous magnesium sulfate already has
been adopted by many academic EDs. The dose is 2 g over 20 minutes in adults
and 25 to 75 mg/kg in children (up to a maximum of 2 g).
• Heliox-driven albuterol nebulization can be used to quickly decrease the work
of breathing.
https://www.atsjournals.org/doi/full/10.1513/
pats.P09ST2
 Intubasi
• Patients presenting with apnea or coma should be intubated immediately. Persistent or increasing
hypercapnia, exhaustion, and depressed mental status strongly suggest the need for ventilatory
support.
• Consultation with or comanagement by a physician expert in ventilator management is essential
because ventilation of patients with severe asthma is complicated and risky.
• Because intubation is difficult in asthmatic patients, it should be done semielectively and before
respiratory arrest occurs. Once intubation is deemed necessary, it should not be delayed and
therefore should be performed in the ED, with the patient transferred to an intensive care unit
appropriate to the patient's age.
• Two issues must be considered at the time of intubation. First, intravascular volume should be
maintained or replaced because hypotension commonly accompanies the initiation of positive
pressure ventilation. In addition, high ventilator pressures, with their associated risks of
barotrauma, should be avoided.
• “Permissive hypercapnia” or “controlled hypoventilation” is the recommended ventilator strategy
because it provides adequate oxygenation while minimizing airway pressures and the possibility of
barotrauma. However, this strategy is not uniformly successful in critically ill asthmatic patients,
and additional therapies are under evaluation.

https://www.atsjournals.org/doi/full/10.1513/
pats.P09ST2
COPD
 COPD Definition

► Chronic Obstructive Pulmonary Disease (COPD) is a

common, preventable and treatable disease that is
characterized by persistent respiratory symptoms and
airflow limitation that is due to airway and/or alveolar
abnormalities usually caused by significant exposure to
noxious particles or gases.

© 2017 Global Initiative for Chronic Obstructive Lung Disease

COPD Etiology, Pathobiology &
Pathology

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Management of Exacerbations

OVERALL KEY POINTS (1 of 3):

► An exacerbation of COPD is defined as an acute worsening of respiratory

symptoms that results in additional therapy.

► Exacerbations of COPD can be precipitated by several factors. The most

common causes are respiratory tract infections.

► Short-acting inhaled beta2-agonists, with or without short-acting

anticholinergics, are recommended as the initial bronchodilators to treat an
acute exacerbation.

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Management of Exacerbations

OVERALL KEY POINTS (2 of 3):

► Maintenance therapy with long-acting bronchodilators should be initiated as

soon as possible before hospital discharge.

► Systemic corticosteroids can improve lung function (FEV1), oxygenation and

shorten recovery time and hospitalization duration. Duration of therapy
should not be more than 5-7 days.

► Antibiotics, when indicated, can shorten recovery time, reduce the risk of
early relapse, treatment failure, and hospitalization duration. Duration of
therapy should be 5-7 days.

► Methylxanthines are not recommended due to increased side effect profiles.

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Management of Exacerbations

OVERALL KEY POINTS (3 of 3):

► Non-invasive mechanical ventilation should be the first mode of ventilation

used in COPD patients with acute respiratory failure who have no absolute
contraindication because it improves gas exchange, reduces work of
breathing and the need for intubation, decreases hospitalization duration
and improves survival.

► Following an exacerbation, appropriate measures for exacerbation

prevention should be initiated (see GOLD 2017 Chapter 3 and Chapter 4).

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Management of Exacerbations

COPD exacerbations are defined as an acute worsening of

respiratory symptoms that result in additional therapy.

► They are classified as:

 Mild (treated with short acting bronchodilators only, SABDs)

 Moderate (treated with SABDs plus antibiotics and/or oral
corticosteroids) or
 Severe (patient requires hospitalization or visits the emergency room).
Severe exacerbations may also be associated with acute respiratory
failure.

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Management of Exacerbations

Classification of hospitalized patients

No respiratory failure:
Respiratory rate: 20-30 breaths per minute; no use of accessory
respiratory muscles; no changes in mental status; hypoxemia
improved with supplemental oxygen given via Venturi mask 28-
35% inspired oxygen (FiO2); no increase in PaCO2.
Acute respiratory failure — non-life-threatening: Respiratory
rate: > 30 breaths per minute; using accessory respiratory
muscles; no change in mental status; hypoxemia improved with
supplemental oxygen via Venturi mask 25-30% FiO2; hypercarbia
i.e., PaCO2 increased compared with baseline or elevated 50-60
mmHg.
© 2017 Global Initiative for Chronic Obstructive Lung Disease
 Management of Exacerbations

Classification of hospitalized patients

Acute respiratory failure — life-threatening:

Respiratory rate: > 30 breaths per minute; using accessory
respiratory muscles; acute changes in mental status; hypoxemia
not improved with supplemental oxygen via Venturi mask or
requiring FiO2 > 40%; hypercarbia i.e., PaCO2 increased compared
with baseline or elevated > 60 mmHg or the presence of acidosis
(pH < 7.25).

© 2017 Global Initiative for Chronic Obstructive Lung Disease

Management of Exacerbations

© 2017 Global Initiative for Chronic Obstructive Lung Disease

Management of Exacerbations

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Management of Exacerbations

Pharmacologic treatment

The three classes of medications most commonly used for COPD

exacerbations are:
► Bronchodilators
 Although there is no high-quality evidence from RCTs, it is recommended that
short-acting inhaled beta2-agonists, with or without short-acting
anticholinergics, are the initial bronchodilators for acute treatment of a COPD
exacerbation.
► Corticosteroids
 Data from studies indicate that systemic glucocorticoids in COPD exacerbations
shorten recovery time and improve lung function (FEV1). They also improve
oxygenation, the risk of early relapse, treatment failure, and the length of
hospitalization.
► Antibiotics

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Management of Exacerbations

Respiratory support

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Management of Exacerbations

Respiratory support

© 2017 Global Initiative for Chronic Obstructive Lung Disease

Management of Exacerbations

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Avian Flu
• viruses are divided into 2 groups based on
their ability to cause disease in poultry: high
pathogenicity or low pathogenicity.
• Highly pathogenic viruses (H5N1) result in
high death rates (up to 100% mortality within
48 hours) in some poultry species.
• Low pathogenicity viruses (H7N9) also cause
outbreaks in poultry but are not generally
associated with severe disease.

http://www.who.int/mediacentre/factsheets/avian_influenza/en/
 Signs and symptoms
• Low pathogenic avian influenza virus infections in humans
have ranged from conjunctivitis to influenza-like illness (e.g.,
fever, cough, sore throat, muscle aches) to lower respiratory
disease (pneumonia) requiring hospitalization
• Highly pathogenic avian influenza virus infections in people
have been associated with a wide range of illness from
conjunctivitis only, to influenza-like illness, to severe
respiratory illness (e.g. shortness of breath, difficulty
breathing, pneumonia, acute respiratory distress, viral
pneumonia, respiratory failure) with multi-organ disease,
sometimes accompanied by nausea, abdominal pain,
diarrhea, vomiting and sometimes neurologic changes
(altered mental status, seizures)
http://www.cdc.gov/flu/avianflu/avian-in-humans.htm
 Diagnosis
• first few days of illness : collecting a swab from the nose or
throat  molecular test, grow the virus
• For critically ill patients : collection and testing of lower
respiratory tract specimens may lead to diagnosis of avian
influenza virus infection
• body's immune response to the virus infection by detecting
specific antibodies*
• PCR
• Hematology  leukopenia, lymphocytopenia
/lymphocytosis, thrombocytopenia
• Radiology  lung infiltrate
• Chemical

http://www.cdc.gov/flu/avianflu/avian-in-humans.htm
Buku ajar Ilmu Penyakit Dalam edisi VI jilid I
 Hospitalized criteria
• Suspect avian flu with severe symptoms:
– Shortness of breath/difficulty breathing (RR > 30)
– Pulse > 100
– Altered mental status
– Weak
• Suspect with leukopenia
• Suspect with pneumonia radiology
• Probable or confirm avian flu patient

Buku ajar Ilmu Penyakit Dalam edisi VI jilid I

 Antiviral treatment
• Give antiviral < 48 hours
• Antiviral :
– M2 inhibitor:
• Amantadin (symadine)
• Rimantidin (flu-madine)
• Dose : 100 mg or 5mg/kgBB twice a day for 3-5 days
– Neuramidase inhibitor:
• Zanamivir (Relenza)
• Oseltamivir (tami-flu)
• Dose : 75 mg twice a day for 1 week

Buku ajar Ilmu Penyakit Dalam edisi VI jilid I

 Depkes RI guideline
• Suspect avian flu
– Oseltamivir 2 x 75 mg for 5 days
– give antibiotics in there is indication
• Probable avian flu
– Oseltamivir 2 x 75 mg for 5 days
– give broad spectrum antibiotics
– give steroids if there is pneumonia, ARDS
• Prophylaxis
– Oseltamivir 75 mg once a day for more than 7 days
(until 6 weeks)

Buku ajar Ilmu Penyakit Dalam edisi VI jilid I

 Complication
• Pneumonia
• Respiratory failure
• Shock
• Altered mental state
• Seizures
• Failure of multiple organs (e.g. kidney failure)
• Death

http://www.flu.gov/about_the_flu/h5n1/
 Tension Pneumothorax
Definition & Etiology Signs & Symptoms
• A tension pneumothorax develops • Chest pain
when a “one-way valve” air leak occurs
from the lung / through the chest wall • Air hunger
• Air is forced into the pleural space w/o • Respiratory distress
any means of escape, eventually • Tachycardia
completely collapsing the affected lung
• Shock results from the marked ↓ in • Hypotension
venous return causing a reduction in • Tracheal deviation away from the
cardiac output side of injury
• Etiology : • Unilateral absence of breath
– Mechanical ventilation w/ positive-
pressure ventilation in patients w/ visceral sounds
pleural injury (most common) • Elevated hemithorax w/o
– Traumatic defects in the chest wall if
incorrectly covered w/ occlusive dressings / respiratory movement
if the defect itself constitutes a flap-valve
mechanism.
• Neck vein distention
– Displaced thoracic spine fractures (rare) • Cyanosis (late manifestation)
Management
ARDS
 Faktor Resiko ARDS
Akibat Sistemik Akibat Paru Sendiri
•Luka berat •Aspirasi asam lambung
•Sepsis •Emboli karna pembekuan darah,
•Pankreatitis lemak,udara atau cairan amnion
•Syok •TBC milliar
•Transfusi berulang •Radang paru difus/luas
•DIC •Trauma paru
•Luka bakar •Ekspose radiasi
•Obat-obatan/OD •Terhisap gas beracun
•Opiat •Obsruksi sal nafas atas
•Aspirin •Radang paru eosinofilik akut
•Phenotiazines •High altitude expossure
•Antidepresan trisiklik •Lung reexpansion or reperfusion
•Amidoarone •Near-drowning
•Kemoterapi
•Nitrofurantoin
•Protamine
•Cardiopulmonaru bypass
 Diagnosa Klinis
• Onset akut berlangsung 3-5 hari sejak ada
faktor resiko ARDS
• Tanda pertama : takipnea, retraksi interkostal,
ronkhi basah kasar yg jelas, hipotensi, febris
• Hipoksia/sianosis yg tidak respon dgn
pemberian oksigen
JAMA. 2018;319(7):698-710.
doi:10.1001/jama.2017.21907
 Pemeriksaan Penunjang
• AGD : hipoksemia, hipokapnia (sekunder karna
ventilasi), hiperkapnia(pada emfisema atau keadaan
lanjut), alkalosis respiratorik pada awal proses, akan
berganti menjadi asidosis respiratorik
• Leukositosis (pada sepsis), anemia, trombositopenia
(refleksi inflamasi sistemik dan kerusakan endotel),
peningkatan kadar amilase (pada pankreatitis)
• Gangguan fungsi ginjal dan hati, tanda koagulasi
intravasklura diseminata (sebagai bagian dari MODS)
PULMONARY TUBERCULOSIS
 LO 6: Tuberculosis
• Etiology : M. tuberculosis
• Sign & symptoms:
 Tuberculosis
• Diagnosis : • Treatment:
– Skin test : Mantoux test
– Chest radiograph :
• parenchymal infiltrates
with enlarged hilar or
mediastinal nodes
• unilateral pleural
effusions
• miliary TB
• Ghon focus
• fibrosis and cavitation
– Cultures : “gold
standard” for diagnosis
 Tuberculosis
• Treatment:
 Tuberculosis
• Treatment :
SARS
 Severe acute respiratory
Syndrome
 Severe acute respiratory syndrome (SARS)
is a respiratory disease in humans which is
caused by the SARS coronavirus Between
November 2002 and July 2003 an outbreak of
SARS in Hong Kong nearly became a
pandemic, with 8,422 cases and 916 deaths
worldwide (10.9% fatality) according to the
WHO. Within weeks SARS spread from Hong
Kong to infect individuals in 37 countries in
early 2003.

5 Dr.T.V.RaoMD
5
 SARS belongs to Corona virus
 Coronaviruses are
positive-
strand, enveloped RNA
viruses that are
important pathogens of
mammals and birds.
This group of viruses
cause enteric or
respiratory tract
infections in a variety of
animals including
4 huDrm.T.Va.RnaosM,Dlivestock and
 SARS - Coronavirus
 SARS coronavirus is a
positive and single
stranded RNA virus
belonging to a family of
enveloped coronaviruses.
Its genome is about
29.7kb, which is one of the
largest among RNA
viruses. SARS is similar to
other coronaviruses in that
its genome expression
starts with translation of
two large ORFs 1a and
1b, which are two
polyproteins.
57 Dr.T.V.RaoMD
 SARS belong to Corona Virus
 SARS (Severe Acute Respiratory Syndrome)
is a viral disease caused by a virus of Corona
respiratory viruses affecting mostly respiratory
organs which is characterized by a fever
(more than 38°C), cough, shortage of breath
and underlying atypical pneumonia
(inflammation of the lungs). This is a disease
which spreads very easily and affecting many
people worldwide (over 5,000 people
worldwide).

58 Dr.T.V.RaoMD
59 Dr.T.V.RaoMD
 When to suspect SARS
 SARS may be suspected in a patient who has:
 Any of the symptoms, including a fever of 38
°C (100.4 °F) or higher, and
 Either a history of:
 Contact (sexual or casual) with someone with a
• diagnosis of SARS within the last 10 days OR
 Travel to any of the regions identified by the WHO as
areas with recent local transmission of SARS (affected
regions as of 10 May 2003[13] were parts of China,
Hong Kong, Singapore and the province of Ontario,
Canada).
Dr.T.V.RaoMD
Dr.T.V.RaoMD
 CDC guidelines for
Confirmatory testing
 Positive RT-PCR test results should be
confirmed in a reference laboratory.
Confirmatory testing is particularly
important in areas with a low prevalence of
SARS-CoV disease, where the positive
predictive value of the assay is likely to be
quite low. CDC will conduct confirmatory
testing during the early phases of an
outbreak.
Dr.T.V.RaoMD
 Protect Healthcare Personnel During
Aerosol-Generating Procedures

 Limit personnel to those essential for

performing procedure
 Wear appropriate personal protective
equipment
 Gowns and gloves
 Sealed eye protection (i.e., goggles)
 Respiratory protection device
Dr.T.V.RaoMD
 Management of SARS
 Antibiotics are ineffective as SARS is a viral disease.
Treatment of SARS so far has been largely
supportive with antipyretics, supplemental oxygen
and ventilatory support as needed.
 Suspected cases of SARS must be
isolated, preferably in negative pressure rooms, with
complete barrier nursing precautions taken for any
necessary contact with these patients.
 There was initially anecdotal support for steroids and
the antiviral drug ribavirin, but no published evidence
has supported this therapy
Dr.T.V.RaoMD
 Isolation and Quarantine the
 SARS needs to be
best options
regarded as a
particularly serious
threat for several
reasons. The disease
has no vaccine and no
treatment, forcing health
authorities to resort to
control tools dating back
to the earliest days of
empirical microbiology:
isolation and quarantine

Dr.T.V.RaoMD
ASPIRATION PNEUMONIA
 INTRODUCTI
•
ON
Aspiration is defined as the inhalation of oropharyngeal or gastric contents into the larynx and lower
respiratory tract.
• Aspiration pneumonitis (Mendelson’s syndrome)
a chemical injury caused by the inhalation of sterile gastric contents,
• Aspiration pneumonia is an infectious process caused by the inhalation of oropharyngeal
secretionsthat are colonized by pathogenic bacteria.
• Both conditions can overlap in one patient
• Other aspiration syndromes include airway obstruction, lung abscess, exogenous lipoid
pneumonia, chronic interstitial fibrosis, and Mycobacterium fortuitum pneumonia.
• Four common problems are:
1) Failure to distinguish aspiration pneumonitis from aspiration pneumonia is usually due to:
2) Tendency to consider all pulmonary complications of aspiration to be infectious,
3) Failure to recognize the spectrum of pathogens in patients with infectious complications, and
4) Misconception that aspiration must be witnessed for it to be diagnosed.
 EPIDEMIOLO
•
GY
Aspiration pneumonia is the most common cause of death
in patients with dysphagia due to neurologic disorders
• 5 to 15 percent of cases of community acquired pneumonia
(CAP) are aspiration pneumonia
• Incidence of aspiration pneumonia is 18 percent in nursing
home acquired pneumonia (HCA)
• Aspiration pneumonitis occurs in approximately 10
percent of patients who are hospitalized after a drug
overdose
• Occurs in approximately 1 of 3000 operations in which
general anesthesia is administered and accounting for 10 to
30 percent of all deaths associated with anesthesia
 ASPIRATION PNEUMONITIS
(Mendelson’s syndrome)
• Acute lung injury after the inhalation of regurgitated
gastric contents
• In 1946, Mendelson first showed that acidic gastric
contents introduced into the lungs of rabbits caused severe
pneumonitis and reported in patients who aspirated while
receiving general anesthesia during obstetrical procedures
• Occurs in patients who have a marked disturbance of
consciousness resulting e.g from intoxication or drug
overdose, seizures, massive stroke, or the use of anesthesia
 ASPIRATION PNEUMONITIS
• Severity of lung injury increased significantly as the volume of the
aspirate increased ((20 to 25 ml in adults) and as its pH decreased
(<2.5)
• Aspiration of particulate food matter may cause severe pulmonary
damage, even if the pH of the aspirate is > 2.5
• Aspiration of gastric contents results in a chemical burn of the
tracheobronchial tree and pulmonary parenchyma, causing an intense
parenchymal inflammatory reaction
• Biphasic pattern of lung injury:
• 1)The first phase peaks at one to two hours after aspiration and results
from the direct, caustic effect of the aspirate on the cells lining the
alveolar-capillary interface.
• 2)The second phase, which peaks at four to six hours, is associated
with infiltration of neutrophils into the alveoli and lung interstitium
 ASPIRATION PNEUMONITIS
• Bacterial infection does not have an important role in the
early stages of acute lung injury after the aspiration since
gastric acid prevents the growth of bacteria
• Infection may occur at a later stage
• Colonization of the gastric contents by pathogenic
organisms may occur when the pH in the stomach is
increased by the use of antacids, histamine H2 receptor
antagonists, or proton-pump inhibitors.
• Gastric colonization by gram-negative bacteria in patients
who receive enteral feedings, patients with gastroparesis or
small-bowel obstruction.
 ASPIRATION PNEUMONITIS
SIGNS & SYMPTOMS
• Patients who have aspirated may present with dramatic signs
• symptoms
and
• Wheezing, coughing, shortness of breath, cyanosis,
•
pulmonary edema, hypotension, and hypoxemia, with rapid
progression to severe acute respiratory distress syndrome
and death
• Silent aspiration, manifests only as arterial desaturation with
•
radiologic evidence of aspiration
• Complications include lung abscesses, necrotizing
•
pneumonia, or empyema
 ASPIRATION PNEUMONITIS
• Aspiration pneumonia develops after the inhalation of colonized
oropharyngeal (Haemophilus influenzae and Streptococcus) (or
gastric- GNB) material
• Approximately half of all healthy adults aspirate small amounts of
oropharyngeal secretions during sleep
• Low burden of virulent bacteria in normal pharyngeal secretions,
together with forceful coughing, active ciliary transport, and
normalhumoral and cellular immune mechanisms, results in clearance
of the infectious material
• Any condition that increases the volume or bacterial burden of
oropharyngeal secretions in a person with impaired defense
mechanisms may lead to aspiration pneumonia.
 ASPIRATION PNEUMONITIS
• Risk of aspiration pneumonia is lower in
patients
• without teeth and in elderly patients
in institutional settings who receive aggressive
oral care
• •The diagnosis is made when a patient at
risk for aspiration has radiographic
evidence of an infiltrate in a characteristic
bronchopulmonary
• segment
• In recumbent position, the most common sites
of involvement are the posterior segments of
the
• upper lobes and the apical segments of the
lower lobes
•In
• upright or semirecumbent position, the
basal
•
segments of the lower lobes are usually
affected.
• Usual course is that of an acute pneumonic
 Risk Factors for Oropharyngeal Aspiration
• Elderly, neurologic dysphagia, disruption of the
•
gastroesophageal junction leads to gastroesophageal reflux
(GERD), or anatomical abnormalities of the upper aerodigestive
tract,
• Poor oral- dental hygiene, resulting in oropharyngeal
•
colonization by respiratory tract pathogens, including
Enterobacteriaceae, Pseudomonas aeruginosa, and
Staphylococcus aureus
• Silent aspiration is common in stroke, as the prevalence of
•
swallowing dysfunction ranges from 40 to 70 percent.
Risk Assessment of Oropharyngeal Aspiration

• Assessment of the cough and gag reflexes at bed side is unreliable

• A comprehensive swallowing evaluation,by speech & language
pathologist, supplemented by either a videofluoroscopic swallowing
study or a fiberoptic endoscopic evaluation, is required
• In patients with swallowing dysfunction, a
• soft diet should be introduced, and the patient should be taught
compensatory feeding strategies (e.g., reducing the bite size, keeping
the chin tucked and the head turned while eating, and swallowing
repeatedly)
• Tube feeding is usually recommended in patients who continue to
aspirate pureed food
 Feeding Tubes and Aspiration Pneumonia

• Aspiration pneumonia is the most common cause of death in

•
patients fed by gastrostomy tube
• PEG (percutaneous endoscopic gastrostomy tube) is more
•
effective than nasogastric tube feeding in delivering nutrition
but is not superior to the use of a nasogastric tube for
preventing aspiration
• Incidence of aspiration pneumonia with post-pyloric tubes
•
(those placed in the small bowel-J-Tube) has been shown to be
similar to that with intragastric tubes
• Feeding tubes offer no protection from colonized oral
•
secretions
 Aspiration in Critically Ill Patients
• Factors increase the risk of aspiration in ICU patients,
including a supine position, gastroparesis, and NG tube
• 30 percent of patients who are kept in the supine position
are estimated to have gastroesophageal reflux
• A high gastric residual volume due to gastroparesis,
leading to gastric distention and regurgitation
• Risk is especially high after removal of an endotracheal
tube, because of the residual effects of sedative drugs, the
presence of a NG tube, and swallowing dysfunction, which
usually resolves within 48 hours post extubation
• Authors recommend the discontinuation of oral feeding for
at least 6 hours after extubation (in case re-intubation is
required), followed by institution of a pureed diet and then
soft food for at least 48 hours
 BACTERIOLOGY
• In early 1970s, anaerobic organisms were considered the
predominant pathogens, alone or with aerobes
• Recent studies shown Strep. pneumoniae, Staph. aureus,
H. influenzae, and Enterobacteriaceae predominated in
patients with a community-acquired aspiration syndrome,
• In patients with hospital acquired aspiration syndrome
gram-negative organisms, including P. aeruginosa,
predominated.
• No anaerobic organisms
 MANAGEMENT
Aspiration Pneumonitis
• The upper airway should be immediately suctioned after a witnessed
aspiration
• Endotracheal intubation for airway protection in patients with a
decreased level of consciousness e-g (seizure,stroke,coma,
intoxication/Overdose)
• Prophylactic antibiotics are not recommended
• Antibiotics shortly after aspiration in patients in whom a fever,
leukocytosis, or a pulmonary infiltrate develops is discouraged
• Empirical antibiotic therapy is appropriate in two conditions::
1)Patients who aspirate gastric contents and have small-bowel
obstruction or other conditions associated with colonization of the
gastric contents
2)Aspiration pneumonitis that fails to resolve within 48 hours
 MANAGEMENT
Aspiration Pneumonitis
• Sampling of the lower respiratory tract (by
•
bronchoalveolar lavage or with a protected
brush specimen) and quantitative culture in
intubated
• patients may allow targeted
antibiotic therapy and, in patients with
•
negative cultures, the discontinuation of
antibiotics
• Corticosteroids have been used for decades,
however, there are limited data on their role
and are not routinely recommended
 MANAGEMENT
Aspiration Pneumonia
• Antibiotic therapy is unequivocally indicated
• The choice of antibiotics should depend on the setting in which the
aspiration occurs
• Broad spectrum antibiotics with activity against gram-negative
organisms, such as third-generation cephalosporins (Rocephin),
fluoroquinolones (Levaquin), and piperacillin-tazobactam (zosyn) are
usually required
• Penicillin and clindamycin, often called the standard antibiotic agents
aspiration pneumonia, are inadequate
• Antibiotic with specific anaerobic activity are not routinely warranted
except in patients with severe periodontal disease, putrid sputum, or
evidence of necrotizing pneumonia or lung abscess
MASSIF PLEURAL EFFUSION
 Pleural effusion

• The accumulation of pleural fluid (whether

osmotic or hydrostatic in nature) can usually be
explained by either increased pleural fluid
formation or decreased pleural fluid absorption,
or both.
• Pleural effusions caused by an increase in
pleural fluid formation can be further
subdivided into elevation in hydrostatic
pressure (e.g., congestive heart failure),
decreased colloid osmotic pressure (e.g.,
cirrhosis, nephrotic syndrome), increased
capillary permeability (e.g., infection,
neoplasm), passage of fluid through openings
in the diaphragm (e.g., ascites), or reduction
of pleural space pressure (e.g., atelectasis).
• An effusion caused by decreased pleural fluid
absorption can be qualified further as either
lymphatic obstruction or elevation of systemic
venous pressure resulting in impaired lymphatic
drainage (e.g., superior vena cava syndrome).
• Pleural effusions produce a restrictive ventilatory
defect and also decrease total lung capacity,
functional residual capacity, and forced vital
capac- ity. They may cause ventilation-perfusion
mismatches and, when large enough,
compromise cardiac output.
causes
Sign symptom
 ETIOLOGI GAGAL NAPAS TIPE I
• Asma akut • Edema paru
• Acute Respiratory (kardiogenik,
Distress Syndrome nonkardiogenik)
(ARDS) • Perdarahan paru
• Pneumonia ekstensif
• Emboli paru • Aspirasi
• Fibrosis paru • Near drowning
• PPOK

Gunning KEJ. Pathophysiology of respiratory failure and indications for respiratory support. UK: The Medicine Publishing Company Ltd.;
2003.
Fishman AP, Elias JA, Fishman JA, Grippi MA, Senior RM, Pack AI, editors. Fishman’s pulmonary diseases and disorders. 4th ed vol 2. New
York: The McGraw-Hill Companies, Inc.; 2008.
 Acute Respiratory Failure
• Hypoxemia- inadequate O2 transfer
PaO2 of 60mmHg or less
• Hypercapnia- insufficient CO2 removal
Increases PaCO2
 Hypoxemic Respiratory Failure-
(Affects the pO2)
• V/Q Mismatch
• Shunt
• Diffusion Limitation
• Alveolar Hypoventilation- inc. CO2 and dec.
PO2
Range of V/Q Relationships

Fig. 68-4
 Shunt
• 2 Types
– 1. Anatomic- passes through an anatomic channel of the
heart and does not pass through the lungs ex: ventricular
septal defect
– 2. Intrapulmonary shunt- blood flows through pulmonary
capillaries without participating in gas exchange ex: alveoli
filled with fluid
– * Patients with shunts are more hypoxemic than those
with VQ mismatch and they may require mechanical
ventilators
 Diffusion Limitations
• Gas exchange is compromised by a process
that thickens or destroys the membrane
– 1. Pulmonary fibrosis
– 2. ARDS

* A classic sign of diffusion limitation is hypoxemia

during exercise but not at rest
Diffusion Limitation

Fig. 68-5
 Hypercapnic Respiratory Failure
Ventilatory Failure- affects CO2

1. Abnormalities of the airways and alveoli- air flow

obstruction and air trapping
– Asthma, COPD, and cystic fibrosis

2. Abnormalities of the CNS- suppresses drive to breathe

drug OD, narcotics, head injury, spinal cord injury
Hypercapnic Respiratory Failure
3. Abnormalities of the chest wall
– Flail chest, morbid obesity, kyphoscoliosis

4. Neuromuscular Conditions- respiratory muscles are

weakened:
Guillain-Barre, muscular dystrophy, myasthenia gravis
and multiple sclerosis
105
 Survei Sekunder
Pemeriksaan fisik Pemeriksaan penunjang
• Sianosis sentral
• Merintih / grunting, pernapasan cuping
• Pulse oximetry
hidung, wheezing, stridor • Foto toraks
• Kepala terangguk2
• ↑ tekanan vena jugularis
• Telapak tangan sangat pucat
• Frekuensi pernapasan cepat
• Tarikan dinding dada bagian bawah ke
dalam
• Denyut apeks bergeser / trakea
terdorong dari garis tengah
• Auskultasi – crackles (ronki) atau suara
napas bronkial
• Irama derap pada auskultasi jantung
• Tanda efusi pleura (redup) atau
pneumotoraks (hipersonor) pada
perkusi
106
 DYSPNEA
• Dyspnea is the term applied to the sensation
of breathlessness and the patient’s reaction to
that sensation.
• Dyspnea results from a variety of conditions,
ranging from nonurgent to life-threatening.