1. ARDS
DR. T. MOHAN KUMAR, MD, AB, DPPR, FCCP
CHIEF & SENIOR CONSULTANT,
DEPARTMENT OF PULMONOLOGY & CRITICAL CARE,
SRI RAMAKRISHNA HOSPITAL,
COIMBATORE

2. DIAGNOSTIC CRITERIA
ARDS ALI
Acute Acute
PaO2/Fio2<200 <300 mm Hg
mmHg
Bilateral interstitial Same
or alveolar infiltrates
Pcwp <15-18 same
mmHg
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3. Clinical diagnosis
Rapid
Within 12 to 48 hr of the predisposing event
Awake patients become anxious,agitated &
dyspnoeic
Dyspnoea on exertion proceeding to severe
when hypoxemia intervenes
Stiffening of lung leads to increase work of
breathing,small tidal volumes,rapid respiratory
rate
Initially respiratory alkalosis
Respiratory failure
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4. Clinical disorders associated with ARDS
Direct lung injury Indirect lung injury
 Aspiration of gastric  Severe sepsis
contents  Major trauma
 Pulmonary contusion  Hypertransfusion
 Toxic gas inhalation  Acute pancreatitis
 Drug overdose
 Near drowning
 Reperfusion injury
 Diffuse pulmonary
 Post cardiac
infection
bypass/lung
transplants
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5. Clinical disorders associated with ARDS
FREQUENT CAUSES
SEPSIS
BACTEREMIA WITHOUT SEPSIS SYNDROME 4%
SEVERE SEPSIS/SEPSIS SYNDROME 35-45%
MAJOR TRAUMA
MULTIPLE BONE FRACTURES 5-10%
PULMONARY CONTUSION 17-22%
HYPERTRANSFUSION 5-36%
ASPIRATION OF GASTRIC CONTENTS 22-36%
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6. CLINICAL MANIFESTATIONS
ARDS occurs in the setting of acute severe
illness
Clinical manifestations may vary
Sepsis and trauma most important
Multiple organ failure
Atelectasis and fluid filled lungs
Hypoxemia/dyspnoea
Fever /leukocytosis
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7. Laboratory studies
To date no lab findings pathognomonic of ARDS
X-ray chest shows bilateral infiltrates consistent with
pulmonary edema, may be mild or dense, interstitial
or alveolar, patchy or confluent
ABG shows hypoxemia with respiratory alkalosis.
In late stages hypoxemia, acidosis, hypercarbia may
be seen.
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8. Leukocytosis/Leukopenia/anemia are common
Renal function abnormalities/or liver function
Von willebrand’s factor or complement in
serum may be high
Acute phase reactants like ceruloplasmin or
cytokine (TNF,IL-1,IL-6,IL-8) may be high.
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9. BRONCHOALVEOLAR LAVAGE
Inflammatory mediators like cytokines, reactive oxygen
species, leukotrienes & activated complement fragments
are found in the fluid
Cellular analysis shows more than 60% of neutrophils.
As ARDS resolves neutrophils are replaced with alveolar
macrophages.
Another interesting finding is the presence of a marker
of pulmonary fibrosis called procollagen peptide III
(PCPIII) and this correlates with mortality.
Presence of more eosinophils suggest eosinophilic
pneumonia, high lymphocyte counts may be seen in
hypersensitivity pneumonitis, sarcoidosis, BOOP, or
other acute forms of interstitial lung disease.
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10. Differential diagnosis
Infectious causes
 Bacteria - Gm neg & pos , mycobacteriae, mycoplasma,
rickettsia, chlamydia
 Viruses- CMV, RSV, hanta virus, adeno virus, influenza virus
 Fungi- H.capsulatum, C.immitis
 parasites- pneumocytis carinii, toxoplasma gondii
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11. Differential Diagnosis
Non infectious causes
 CCF
 Drugs & toxins (paraquat, aspirin, heroin, narcotics,
toxic gas, tricyclic anti depressants, acute radiation
pneumonitis)
 Idiopathic (esinophilic pneumonia, Acute interstitial
pneumonitis, BOOP, sarcoidosis, rapidly involving
idiopathic pulmonary fibrosis)
 Immunologic (acute lupus pneumonitis, Good Pastures
syndrome, hypersensitivity pneumonitis)
 Metabolic (alveolar proteinosis)
 Miscellaneous (fat embolism, neuro/high altitude
pulmonary oedema)
 Neoplastic (leukemic infiltration, lymphoma)
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12. Therapy -goals
Treatment of the underlying precipitating
event
Cardio-respiratory support
Specific therapies targeted at the lung injury
Supportive therapies
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13. Respiratory Support

14. Spontaneously Breathing Patient
 In the early stages of ARDS the hypoxia may be
corrected by 40 to 60% inspired oxygen with CPAP
 Peak inspiratory flow rates of >= 70ltrs / min require
a tight-fitting face mask with a large reservoir bag or
a high flow generator
 If the patient is well oxygenated on <= 60 % inspired
oxygen and apparently stable without CO2 retention
and apparently stable, then ward monitoring may be
feasible but close observation( 15 to 30 Min),
continuous oximetry, and regular blood gases are
required
Contd..
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15. Indications for mechanical ventilation
 Inadequate Oxygenation(PaO2 < 8k Pa
on FiO2 >= 0.6)
 Rising or elevated PaCO2(>= 6k Pa)
 Clinical signs of incipient respiratory
failure
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16. Mechanical Ventilation
The Aims are to increase PaO2 while
minimizing the risk of further lung injury
(Oxygen toxicity, Barotrauma). This is the
realm of the IRCU Physician: seek specialist
advice early to prevent complications. The
general principles are the following:
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17.  Start with FiO2 = 1.0, tidal volume 6 to 10 ml
per Kg, PEEP <= 5 cm H2O and inspiratory
flow rates ~ 60 L / min. Subsequent
adjustments are done to try to achieve
arterial oxygen sats. of > 90% with FiO2 <
0.6 and peak airway pressures < 40 to 45 cm
H20
 Controlled Mandatory Ventilation (CMV) with
sedation and neuromuscular blockade (to try
to suppress the respiratory drive and reduce
respiratory muscle oxygen requirement.)
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18. PEEP improves PaO2 in most patients and
allows reduction of FiO2. Increase by 2 to 5 cm
H2O increments every 20 min watching for
hemodynamic deterioration (due to impaired
venous return and decreased cardiac out put).
Optimal PEEP is usually 10 to 15 cm H2O
Inverse Ratio Ventilation may decrease peek
inflation pressures and thus Barotrauma.
Inspiratory time : Expiratory time ratio (I:E
ratio) of between 1:1 and 4:1 may be tried.
Contd..
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19. The ventilatory rate required to clear CO2 and
normalize pH is commonly high (20 to 25
breaths / min). However this may result in
unacceptable airway pressures.
Another strategy is’ permissive hypercapnoea’
which as the name suggests is controlled
hypoventilation. PaCO2 up to 13 kPa is
generally well tolerated; acidosis (pH < 7.25)
may be treated with intravenous bicarbonate
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20.  Changing the patients position (lateral decubitus or
prone instead of supine) can improve oxygenation by
improving perfusion of aerated portion of lung. Consider
this in patients with non uniform or predominantly
posterior and lower lobe infiltrates
 Inhaled nitric oxide (18 ppm) reduces pulmonary artery
pressures, intra pulmonary shunting and improves
oxygenation while not affecting mean arterial pressure
or cardiac output. However studies showing an effect on
mortality are awaited.
 Newer methods such as high frequency jet ventilation,
extra corporeal gas exchange (CO2 removal +-
Oxygenation) and intravascular oxygenation devices
(IVOX) may be of use but are currently not widely
available.
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21. Cardiovascular Support

22.  Invasive monitoring is mandatory(Arterial line, PA
catheter (Swan-Ganz) to measure cardiac outputs and if
available, continuous mixed venous oxygen saturation)
 In order to minimize pulmonary oedema, aim to keep
PCWP low (8 to 10 mm Hg) and support the circulation
with inotropes if necessary
 The role of colloids and albumin is relatively minor: the
increased capillary permeability allows these molecules
to equilibrate with the alveolar fluid with little increase
in net plasma oncotic pressure
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22

23.  Renal failure is common and may require
haemofiltration to achieve a negative fluid
balance and normalize blood chemistry.
 Oxygen consumption (VO2) in patients with
ARDS appears to be delivery dependent. The
current trend is to aim for target levels of
oxygen delivery (DO2 = Cardiac Index(HbXSao2X1.34)X10)
as guided by tissue perfusion (clinically and
serum lactate, pHi from a gastric tonometer).
DO2 may be increased by blood transfusion,
inotropes and vasodilators including
prostacyclin).
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24.  Selection of appropriate inotropes and
vasodilators can only be made by repeated
measurements of haemodynamic parameters
and calculating DO2 and VO2 while evaluating
the effects of the various agents
 Nutritional support must be chosen to try to
avoid fluid overload. Lipid metabolism
produces marginally less CO2 than dextrose
metabolism and thus favourably affects the
respiratory quotient but there is controversy
as to whether lipid can exacerbate lung injury
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25. Treatment of Sepsis

26. Fever, Neutrophil leukocytosis and raised inflammatory
markers (CRP) are common in patients with ARDS and
do not always imply sepsis. However sepsis is common
precipitant of ARDS
A trial of empirical antibiotics guided by possible
pathogens should be given early. Eg Cefotaxime. This
may be modified in light of the results of appropriate
cultures. Avoid nephrotoxic antibiotics.
Enteral feeding seems to carry a lower risk of sepsis
than parenteral feeding and helps maintain the integrity
of the gut mucosa. Ileus is common in multi-organ
failure, so entral feeding may not be possible.
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27. Minimizing lung injury and
treating the cause

28. Look for a precipitant
In general prevention (example of aspiration of gastric
acid) is more effective than trying to treat ARDS.
However there are no effective measures for
prophylaxis in patients at risk ( Eg from Trauma)
Steroids : there is no benefit from treatment early in the
disease. Treatment later (> 7 to 14 days from onset)
especially in patients with peripheral blood eosinophilia
or eosinophils in bronchoalveolar lavage, improves
prognosis
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29. Give 2 to 4 mg / Kg prednisolone or
equivalent: the duration depends on the
clinical response( 1 to 3 weeks)
Other therapies such as inhaled nitric oxide ,
exogenous surfactant, antioxidants
(acetylcysteine), ketoconazole, NSAIDs,
Pentoxifylline and anticytokine antibodies are
still under investigation
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30. Causes of Sudden deterioration in ARDS
Respiratory Cardiovascular
Pneumothorax Arrhythmia
Bronchial plugging Cardiac tamponade
Displaced ET tube Myocardial infarction
Pleural effusion GI bleed(Stress Ulcer)
(Haemothorax)
Aspiration(Eg NG Septicaemia
feed)
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31. Completed trials
 Reducing lung stretching
 Lisophyllin
 Corticosteroids in late ARDS
 ALVEOLI study
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32. Completed trials -II
 Fluids and catheters treatment trial (FACTT)
 Low tidal volume versus high tidal volume
ventilation
 Ketoconazole
 Role of MODS
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33. WHAT IS NEW?
ALI & Gene transfer
New approaches to enhancing lung edema
clearance
Nitric oxide donors
New treatment for altered pulmonary
vascular permeability
Inflammatory & cytokine networks in ARDS
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34. What is new
Use of surfactant therapy
Liquid ventilation in ALI
CPAP trial
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