ARDS

AECC CRITERIA FOR ALI & ARDS

BERLIN DEFINITION
Precipitating Causes
CLINICAL PRESENTATION AND DIAGNOSIS

- The clinical presentation and diagnosis of ARDS are

fundamentally related to the syndrome’s pathophysiologic
changes, regardless of the underlying etiology.
• Patology and pathophysiology
- Pathologically and clinically, ARDS can be divided into:
- early phase (exudative)
- and late phases of lung injury (proliferative)
Clinical course & pathophysiology
Clinical presentation
- usually follows a rapid course, occurring most often within 12 to 72
hours of the predisposing event.
- At its onset, patients with ARDS often become anxious, agitated, and
dyspneic.
- increased work of breathing, small tidal volumes, and tachypnea.
- patients with ARDS typically have initial ABG results showing a PaO2
less than 50 to 55 mm Hg and pulse oximetry recordings of less than
85% arterial O2 saturation.
- The hallmark of ARDS is hypoxemia that is resistant to oxygen therapy
because of the large right-to-left shunt
APPROACH TO CLINICAL DIAGNOSIS
• Chest radiography
- In cases of established ARDS, the chest radiograph typically
demonstrates findings of diffuse, bilateral alveolar infiltrates
consistent with pulmonary edema
• Laboratory studies
- arterial blood gas analysis is essential for confirming the diagnosis 
acute respiratory alkalosis occur in the early stage
- PaO2 is markedly abnormal in patients with ARDS
• cardiac enzymes (creatine phosphokinase and troponins)  useful for
evaluating the presence of myocardial infarction or cardiac ischemia in
patients at risk because of increased age or other factors

• Echocardiography
- Echocardiography is a useful noninvasive method to evaluate potential
cardiac causes of acute hypoxemic respiratory failure
APPROACH TO TREATMENT
- The general approach to treatment of ARDS includes addressing
precipitating causes and other concurrent clinical issues,
- ensuring adequate oxygenation,
- careful implementation of a lung-protective ventilator strategy,
- prudent fluid and hemodynamic management,
- special patient positioning coupled with the so-called “lung recruitment”
maneuvers,
- and a multitude of other measures, including pharmacologic
considerations.
Limmer D, O'Keefe MF. Emergency Care. 11th ed. Chapter 16.
Limmer D, O'Keefe MF. Emergency Care. 11th ed. Chapter 16.
Limmer D, O'Keefe MF. Emergency Care. 11th ed. Chapter 16.
ACUTE RESPIRATORY FAILURE
Gagal Napas
• Klasifikasi gagal napas :
• Gagal napas tipe 1 (hipoksemia)
• Hipoksemia tanpa disertai hiperkapnia dng PaO2 < 60mmHg krn kegagalan pertukaran
O2
• Ditandai dng PaCO2 N/↓, PaO2 ↓, warna kulit pinkpuffer, hiperventilasi, pernapasan
purse lips, umumnya kurus
• Gagal napas tipe 2 (hiperkapnia)
• Hipoksia dng PaCO2 > 50mmHg krn kegagalan pertukaran atau mengeluarkan CO2
• Ditandai dng PaCO2 ↑, PaO2 ↓, sianosis, hipoventilasi, tremor, CO2, edema, pd org
dng BB berlebih/obese
• Gagal napas tipe campuran

Kapita selekta kedokteran. Edisi ke-4

Gunning KEJ. Pathophysiology of respiratory failure and indications for respiratory support. 2003.
Patfis Gagal Napas Tipe 1
• Fraksi O2 inspirasi rendah : dpt disebabkan krn suplai O2 yg tdk baik atau ↑ dead space paru
• Tek barometrik rendah : tek atmosfer rendah ↓ PO2 lingkungan  PaO2 ↓
• Hipoventilasi berat : hipoventilasi awalnya akan ↑ PaCO2 sebelum ↓ PaO2
• Gangguan difusi : terdapat berbagai lapisan antara rongga alveolar hingga mencapai Hb dlm
eritrosit. Kelainan pd lapisan2 tsb dpt menganggu rpses difusi O2 & CO2. CO2 > mudah alami
difusi 20x drpd O2  kelainan pd lapisan spt fibrosis atau edema tdk selalu disertai hiperkapnia
• Ketidakseimbangan ventilasi/perfusi (V/Q) : penyebab tersering hipoksia pd ps dng keadaan
kritis. Perbandingan ideal  1:1. pd hipoksemia tjd ↓ ventilasi. Biasanya disebabkan o/
atelectasis, emboli paru (perfusi ↓), bronkospasme, obstruksi sal napas, pneumonia, ARDS.
• Pirau kanan-kiri : tjd ketika sbgian darah vena pulmonal tdk melewati alveolus yg kaya O2 
saturasi O2 vena pulmonal ↓. Krn tdk melewati alveolus, hipoksemia akibat pirau tdk membaik
pasca pemberian O2

Kapita selekta kedokteran. Edisi ke-4

Patfis Gagal Napas Tipe 2
• Gangguan pusat pernapasan : dpt menyebabkan depresi napas. Biasa diakibatkan o/ penggunaan agen sedative,
cedera kepala, ↑ TIK, atau infeksi SSP
• Gangguan medulla spinalis : dpt menyebabkan gangguan inervasi N.frenikus pd diafragma (setinggi C 3,4,5) &
M.interkostalis  ganggu prosses ventilasi. Cedera medulla spinalis di atas C3  proses ventilasi bergantung pd
otot bantu napas  perlu ventilasi mekanik. Gangguan dpt disebabkan krn trauma, kelainan saraf motorik atau
polimielitis.
• Gangguan saraf motorik : dpt menyebabkan gangguan fungsi otot pernapasan, terutama diafragma  ganggu
proses ventilasi. Biasanya diakibatkan sindrom Gullain-Barre (↓ kapasitas vital) atau disfungsi bulbar
• Gangguan otot pernapasan : dpt diakibatkan o/ kelainan parenkim otot atau NMJ  ganggu proses ventilasi.
Kelainan sel otot dpt berupa miopati kongenital (distrofi muscular), sementara NMJ berupa miastenia gravis dng
krisis miastenik atau kolinergik, racun botulinum, atau paparan organofosfat (kolinesterase inhibitor)
• Kelainan dinding dada : dpt menyebabkan gangguan mekanik ventilasi, ↑ risiko gagal napas. Dpt disebabkan krn
fraktur iga (nyeri fraktur membuat ps menahan batuk & memperlambat laju pernapasan), pneumotoraks,
hematotoraks, atau efusi pleura masif
• Gangguan sal napas & parenkim paru : gangguan tsb awalnya menyebabkan hipoksemia (gagal napas tipe 1). Jika
keadaan tsb dibiarkan maka akan tjd ↓ laju pernapasan & menimbulkan gagal napas tipe campuran
• ↑ produksi CO2

Kapita selekta kedokteran. Edisi ke-4

Respiratory Failure
• Inadequate blood oxygenation or cabon dioxide removal
• Classified as
• Hypercapnic Respiratory Failure
• Hypoxemic Respiratory Failure
Etiology
• Central nervous system • Perpipheral Nervous system or
• Sedative/narcotic overdose Chest Wall
• Meningoencephalitis • GBS
• Tumirs or vascular abnormalities • Mysathenia Gravis
of medulla • Polymiositis
• Strokes • Muscular dystrophies
• Severe myxedema • Acute Poliomyelitis
• Hepatic failure • Traumatic Spinal Cord Injury
• Advanced Uremia • Severe kyphoscoliosis
• Obesity-hypoventilation syndrome • Flail chest, morbid obesity
Etiology
• Airways • Alveoli
• Epiglotitis • Pulmonary edema
• Foreign body aspiration • Diffuse pneumonia
• Tracheal tumor • Pulmonary hemmorhage
• COPD • Aspiration of stomach contents
• Asthma • Near-drowning
• Advanced cystic fibrosis
Classification
Management
• Blood gas analysis for confirmation
• Triage, based on
• Acuity of the respiratory failure
• Degree of hypoxemia, hypercapnia,
acidemia
• Presence of co-morbidities (cardiac/renal
disease)
• Airway Management
• Emergency intubation or ventilator
depends on clinical condition and arterial
blood gas test
• Search for underlying cause
• Correction of Hypoxemia and Hypercapnia
• Hypoxemia  correction to PaO2 60mmHg,
higher in patients with coronary or CVD
• May use face mask or Venturi Mask (high flow
O2)
• May require intubation or ventilator
• Monitoring
• Acute : RR, tidal volume, use of accessory
muscles, paradoxical breathing movement
• Mechanical ventilation  related
complications
• Status asthmaticus  hypotension due to
intrinsic PEEP  alter ventilator, implement
sedation or paralytic agents
Limmer D, O'Keefe MF. Emergency Care. 11th ed.
Limmer D, O'Keefe MF. Emergency Care. 11th ed.
ASTHMA
Clinical Presentation
• Asthma is a chronic inflammatory disorder of the airways
characterized by marked variability in airflow obstruction that is often
reversible, either spontaneously or with treatment.
• This inflammation presents clinically in susceptible patients with
recurrent symptoms of wheezing, chest tightness, cough, and,
occasionally, dyspnea and contributes to the heightened airway
hyperresponsiveness to specific and nonspecific stimuli  a
pathognomonic feature of asthma.
• Increased airway hyperresponsiveness  intolerance to smoke, dust,
air pollution, and strong odors, where exposure to such agents in
healthy individuals does not induce such symptoms.
Sign & Symptoms
Fishman's Pulmonary Diseases and Disorders, 5e
Classification
Medical History
• The typical symptoms of asthma are paroxysmal wheezing, cough, breathlessness, and chest
tightness, which may temporally be related to exposure to triggers or exercise.
• Cough may be productive of clear or yellow/green discolored sputum
• Breathlessness may occur as a result of the dynamic lung hyperinflation that accompanies acute
asthma episodes and patients may report the sensation of difficulty in “getting air in” their lungs
• In patients with poorly controlled asthma, symptoms may temporally evolve slowly over days or
weeks, or present abruptly.
• Distinguishing whether nocturnal symptoms are due to asthma, angina, or gastroesophageal
reflux may be difficult :
• early-morning asthma symptoms are usually relieved with administration of inhaled bronchodilators
• cardiovascular symptoms which occur at any time during the night and,
• gastroesophageal reflux which tends to usually cause symptoms soon after the patient reclines at night.
• Symptoms after heavy exertion, especially in the cold air, are highly suggestive of exercise-
induced asthma and typically, patients experience symptoms at the end of exercise, rather than
during its performance.
Physical Examination
• The most typical physical finding in asthma is wheezing on
auscultation, which is usually caused by turbulent airflow through
narrowed airways.
• During an acute exacerbation of disease, physical signs of increased
ventilation may be observed with the use of accessory muscles of
respiration and chest signs of hyperinflation.
• A sign of severe airway obstruction is pulsus paradoxus, which is the
exaggerated decrease in systolic blood pressure during inspiration by
>10 mm Hg.
Laboratory Investigation : Lung Function Tests
• Peak flow meters  measure the peak expiratory flow (PEF)
• Spirometry measures the expiratory volume and flow of air using
forced maneuvers from full lung inflation
• Patients with asthma typically show :
• A reduced forced expiratory flow in 1 second (FEV1)
• Reduced PEF preserved forced vital capacity (FVC)
• an FEV1/FVC ratio of 0.7 or greater
• With worsening disease :
• FEV1 less than 60% predicted the FEV1/FVC ratio is more usually <0.7
DD

Fishman's Pulmonary Diseases and Disorders, 5e

Treatment

Fishman's Pulmonary Diseases and Disorders, 5e

Treatment

Fishman's Pulmonary Diseases and Disorders, 5e

Tintinalli's Emergency
Medicine - A
Comprehensive Study
Guide 8th 2016.
Tintinalli's Emergency Medicine - A Comprehensive Study Guide 8th 2016.
COPD
Chronic Obstruction Pulmonary Disease
• COPD: caused by an airway
inflammation  destruction of
alveoli, loss of lung elasticity,
closure of small airways  failure
of gas exchange
• Risk factors
• Cigarette smoking
• Air pollution
• Acute exacerbation of COPD
• Change in symptoms beyond
normal day-to-day variations
• May associated with virus,
bacteria or air pollution
Etiology

Rosen’s emergency medicine. 8th ed..

Signs & symptoms
• Chronic obstructive bronchitis
• Air hunger, anxiety, cyanotic appearance, cough, expectoration, scattered rhonchi & rales, chronic CO2
retention
• Chronic respiratory failure & cor pulmonale  peripheral edema, chronic jugular venous distention
• Emphysema
• Thin, anxious, dyspnea, tachypnea, uses accessory muscle of breathing, pursed lip breathing,
chronically hunched forward
• Low diaphragm, ↑ antero-posterior diameter of the thorax, hyper-resonance on percussion, diminished
breath sounds w/ faint end-expiratory rhonchi on auscultation

Rosen’s emergency medicine. 8th ed..

Chronic Obstruction Pulmonary Disease

Diagnosis Management
• Pulse oximetry • Smoking cessation
• Oxygen therapy
• Arterial blood gas analysis
• Beta-agonist: albuterol 2,5-5 mg
• Chest radiography (nebulization), salmeterol
• Anticholinergic: ipratropium bromide 0,5 mg
• Forced expiratory volume (nebulization), tiotropium
• Sputum examination • Steroid: IV methylprednisolone/oral
prednisone 1-2 mg/kg; oral prednisone 1x40
• ECG mg (discharged patients)
• Antibiotic: amoxicillin, tetracycline, TMP-SMX
(for ↑ sputum purulence, vol., dyspnea)

Rosen’s emergency medicine. 8th ed..

Rosen’s emergency medicine. 8th ed..
Clinical Features in Differentiating COPD
from Asthma
Clinical Feature COPD Asthma
Age Older than 35 years Any age

Persistent, Intermittent, usually

Cough
productive nonproductive

Smoking Typical Variable

Progressive,
Dyspnea Variable
persistent
Nocturnal Breathlessness, late Coughing,
symptoms in disease wheezing
Adapted with permission from Stephens, 2008
Clinical Features in Differentiating COPD
from Asthma (continued)
Clinical Feature COPD Asthma
Family history Less common More common
Atopy Less common More common
Diurnal
Less common More common
symptoms
Irreversible airway Reversible airway
Spirometry
limitation limitation

Adapted with permission from Stephens, 2008

AVIAN INFLUENZA
Avian Influenza
• Influenza virus is an orthomyxovirus—an enveloped,
segmented, negative-sense RNA virus.
• Influenza virus has 3 strains—A, B, and C.
• Avian influenza is caused by influenza A virus, which
has 8 RNA segments.
• The serotypes of influenza A virus are identified based
on the hemagglutinin (H) and neuraminidase (N)
proteins; 16 H serotypes and 9 N serotypes have been
identified.

http://emedicine.medscape.com/article/25
Pathophysiology
• Avian influenza is still primarily a respiratory infection but involves
more of the lower airways than human influenza typically does.
• Avian viruses tend to prefer sialic acid alpha(2-3) galactose, which, in
humans, is found in the terminal bronchi and alveoli.

http://emedicine.medscape.com/article/25
Risk Factors
• Travel to (within the last 2 wk) or location in a country with known
avian influenza cases in animals or humans
• Unusual comorbidities such as encephalopathy or diarrhea
• History of exposure to birds, especially living in close proximity to
birds, contact with sick or dying birds, or consumption of
incompletely cooked bird meat
• History of exposure to individuals with known avian influenza,
especially family, or to sick people in a country with known human
cases of avian influenza

http://emedicine.medscape.com/article/
Sign and Symptoms
• Respiratory symptoms are the most common presentation. More
severe respiratory distress occurs around 5 days from the initial
symptoms. The sputum is sometimes bloody.
• Other symptoms include the following:
• Fever (temperature >38°C)
• Diarrhea (watery, nonbloody) (possibly a poor prognostic sign)
• Vomiting
• Chest and/or abdominal pain
• Encephalitis

http://emedicine.medscape.com/article/
Sign and Symptoms
• Low pathogenic avian influenza (LPAI)
• Conjunctivitis
• Influenza-like illness (e.g., fever, cough, sore throat, muscle aches)
• Lower respiratory disease (pneumonia)
• Highly pathogenic avian influenza (HPAI)
• Conjunctivitis
• Influenza-like illness
• 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
Physical Examination
• Tachypnea and crackles are common.
• Wheeze is occasionally apparent.
• Conjunctival suffusion/conjunctivitis is not uncommon.
• Case reports have described other occasional signs (eg, bleeding
gums, always in the presence of viral pneumonia).

http://emedicine.medscape.com/article/
Ancillary Test
• Laboratory tests and findings include the following:
• Nasal wash specimens for detection of virus and viral subtyping.
• Leukopenia.
• Relative lymphopenia.
• Thrombocytopenia.
• Elevated levels of liver enzymes (SGOT/SGPT).
• Disseminated intravascular coagulation (DIC) is rare.
• Other tests blood cultures, lumbar punctures for CSF
analysis (including polymerase chain reaction [PCR]), and
sputum cultures.
• Chest radiography multifocal consolidation

http://emedicine.medscape.com/article/2
Management
• Supportive care oxygen therapy, intravenous fluids and parenteral
nutrition
• Severe cases ventilatory support with intubation and low-volume
(high-frequency) ventilation
• Antivirals
• Amantadine
• Rimantadine 100 mg PO BID
• Oseltamivir 75 mg PO q12hr x5 days
• Zanamivir 10 mg inhaled q12hr for 5 days

http://emedicine.medscape.com/article/250
0029-treatment
Management
• One option for increasing the immunogenicity an adjuvant agent
such as aluminum hydroxide.
• Travelers who plan to travel to areas of the world affected by avian
influenza outbreaks in birds and/or humans  avoid close contact
with poultry, especially diseased or dead birds, and to consume only
adequately cooked meat.
• If contact with birds in enclosed spaces is unavoidable, an N-95
respirator mask (or equivalent), gloves, and goggles should be used to
minimize contact with droplets or particulates.

http://emedicine.medscape.com/article/250
 Prevention:
• Avoid contamination with feces, secretions birds, animals, materials, and tools suspected contaminated by
the virus.
• Use protection (masks, goggles)
• Poultry feces treated by either
• Disinfectants tools used
• Cages and feces should not be excluded from the farms
• The chicken meat was cooked temperature of 800 C for 10 minutes, poultry eggs heated to 640 C for
5 minutes
• Keep the environment and personal hygiene (personal hygiene)
• Implementation of Standard Universal Precautions need to be done by the application of infection control in
the neighborhood
• Personal hygiene in an attempt to minimize the incidence of the pandemic.
• Oseltamivir single dose for 1 week
• Zanamivir should be considered as a prophylactic therapy on health-care workers in contact with
patients infected with Avian Influenza as well as in the treatment using oseltamivir.
• Vaccination has been no effective vaccine is still in the research and development.
Complication:
• Acute respiratory failure
• Organ failure
• Pneumonia
• Sepsis

World Health Organization, Pedoman pelayanan kesehatan anak di rumah sakit rujukan tingkat pertama di kabupaten/ WHO ; alihbahasa, Tim
Adaptasi Indonesia. – Jakarta : WHO Indonesia, 2008
Pleural Effussion
• Pleural effusions result from fluid accumulating in the • Transudative effusions result from an
potential space between the visceral and parietal imbalance between hydrostatic and oncotic
pleurae pressures  results in the production of an
• Pathophysiology : ultrafiltrate with low protein content into the
pleural space
• A continuous amount of fluid is secreted from the
parietal pleura into the pleural space where it is • Clinical features :
absorbed by the visceral pleural microcirculation, • percussion dullness
averaging about 8 L/d in an adult • ↓ breath sounds
• This fluid reduces friction between the pleural
layers & allows for smooth lung expansion &
contraction with respiration
• Any process that ↑ fluid production or interferes
with fluid absorption will result in accumulation in
the pleural space
• Pleural effusions are traditionally divided into
exudates or transudates
• Exudative effusions result from pleural
disease, usually inflammation or neoplasia
that produces active fluid secretion or leakage
with high protein content
Pleural Effussion
• Diagnosis : • Treatment :
• chest radiography : 150 to 200 mL of pleural • Therapeutic thoracentesis with drainage of
fluid in the hemithorax is required to be 1.0 to 1.5 L of fluid is indicated if the patient
detectable (adult) has dyspnea at rest
• Supine chest radiographs  hazy • Diuretic therapy typically resolves >75% of
appearance of pleural fluid in the posterior effusions due to heart failure within 2 to 3
pleural space days
• CT scan : clarify uncertain findings on chest • Patients with pleural empyema (gross pus or
radiograph organisms on Gram stain) require drainage
• A significant pleural effusion is large enough to with large-bore thoracostomy tubes
produce a pleural fluid strip >10 mm wide on
lateral decubitus radiographic views or by
ultrasonography
• Diagnostic thoracentesis : to obtain pleural
fluid for analysis in cases without a clearly
evident cause, to confirm a suspected
diagnosis, or to detect pleural space infection