ARDS

DR. T. MOHAN KUMAR, MD, AB, DPPR, FCCP

CHIEF & SENIOR CONSULTANT,
DEPARTMENT OF PULMONOLOGY & CRITICAL
CARE,
SRI RAMAKRISHNA HOSPITAL,
COIMBATORE

DIAGNOSTIC CRITERIA
ARDS

ALI

Acute
PaO2/Fio2<200
mmHg
Bilateral interstitial
or alveolar infiltrates
Pcwp <15-18
mmHg
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Acute
<300 mm Hg
Same
same

DR.T.M.K- ARDS

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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Clinical disorders associated with

ARDS
Direct lung injury

Indirect lung injury

Aspiration of
gastric contents
Pulmonary
contusion
Toxic gas
inhalation
Near drowning
Diffuse pulmonary
infection

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Severe sepsis
Major trauma
Hypertransfusion
Acute pancreatitis
Drug overdose
Reperfusion injury
Post cardiac
bypass/lung
transplants

DR.T.M.K- ARDS

Clinical disorders associated with

ARDS
FREQUENT CAUSES
SEPSIS
BACTEREMIA WITHOUT SEPSIS SYNDROME

4%

SEVERE SEPSIS/SEPSIS SYNDROME

35-45%

MAJOR TRAUMA
MULTIPLE BONE FRACTURES
PULMONARY CONTUSION
HYPERTRANSFUSION
ASPIRATION OF GASTRIC CONTENTS

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5-10%
17-22%
5-36%
22-36%

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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DR.T.M.K- ARDS

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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Leukocytosis/Leukopenia/anemia are common

Renal function abnormalities/or liver function
Von willebrands 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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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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DR.T.M.K- ARDS

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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10

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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11

Therapy -goals
Treatment of the underlying
precipitating event
Cardio-respiratory support
Specific therapies targeted at the lung
injury
Supportive therapies
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12

Respiratory Support

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

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Contd..

14

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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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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Contd..16

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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17

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.
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Contd..
18

The ventilatory rate required to clear CO 2

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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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 (CO 2 removal +Oxygenation) and intravascular oxygenation devices (IVOX)
may be of use but are currently not widely available.

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Cardiovascular Support

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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Contd..

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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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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Treatment of Sepsis

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 multiorgan failure, so entral feeding may not be possible.

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Minimizing lung injury and

treating the cause

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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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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Causes of Sudden deterioration in ARDS

Respiratory

Cardiovascular

Pneumothorax

Arrhythmia

Bronchial

plugging

Cardiac

Displaced

ET tube

Myocardial

tamponade

infarction
Pleural

effusion
(Haemothorax)

Aspiration(Eg

NG

GI

bleed(Stress
Ulcer)
Septicaemia

feed)
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Completed trials
Reducing

lung stretching

Lisophyllin
Corticosteroids
ALVEOLI
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in late ARDS

study
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31

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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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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What is new

Use of surfactant therapy

Liquid ventilation in ALI
CPAP trial
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