Acute Respiratory Distress

Syndrome

(ARDS)

Belal Alrajoub
 Definition
There is no one or unified definition that is
used universally.

ARDS can be defined as follow:

a clinical syndrome of severe dyspnea of

rapid onset, hypoxemia, and diffuse
pulmonary infiltrates leading to respiratory
failure.*

2
 Diagnostic Considerations
ARDS is the final pathway of a multi-factorial group of
insults.[1]

It is a diffuse lung disease, but it does not affect lung

tissue uniformly. [1]

Therapeutic management may differ according to the

underling etiology. [1]

There are 2 broad etiologies:

Pulmonary ARDS & Extra-pulmonary ARDS. [1]

3
4
Essential Diagnostic Tests and Procedures

History and physical examination.

Chest radiograph.

ABGs measurements.

Other diagnostic tests based on the clinical

circumstances

5
 Berlin Definition of
ARDS

Fanelli, V., Vlachou, A., Ghannadian, S., Simonetti, U., Slutsky, A., Zhang,H. (2013). Acute 6
respiratory distress syndrome: New definition, current and future therapeutic
ARDS defined by the American European
Consensus Conference

Fioretto, J. R., & Carvalho, W. B. (2013). Temporal evolution of acute respiratory

distress syndrome definitions.Jornal De Pediatria,89(6), 523-530. 7
doi:10.1016/j.jped.2013.02.023 [doi]
8
9
Time course for the development and resolution
of ARDS.

10
 Physical examination
Clinically apparent respiratory failure
may ensue after several hours from
the initial insult. [1]
Some authors divided the PE findings
into 4 categories. [1]
1. Acute injury
2. Latent period
3. Acute respiratory failure
4. Severe abnormalities

11
 1. Acute injury

Normal PE & chest X-ray

Tachycardia.
Tachypnea.
Respiratory alkalosis
develops

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 2. Latent period
Lasts approximately 648 h after injury

Patient appears clinically stable

Hyperventilation and hypocapnia persist

Mild increase in work of breathing

Widening of the alveolar-arterial oxygen gradient

A-a gradient = PAO2- PaO2 ..(1).

PAO2= ( FiO2* (760 - 47) - (PaCO2/ 0.8) ..(2).

Minor abnormalities on physical examination and chest

radiograph

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 3. Acute respiratory failure

Marked tachypnea and

dyspnea.

Decreased lung
compliance.

Diffuse infiltrates on chest

radiograph.

High-pitched crackles
heard throughout all the
lung fields.
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 4.Severe abnormalities

Severe hypoxemia
unresponsive to therapy.

Increased intrapulmonary
shunting.

Metabolic and respiratory

acidosis.

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Diagnostic criteria

16
 General Principles of ARDS
Management
Fluid Management High-frequency
Ventilation
Steroids
Extracorporeal Life
Support
Inhaled NO
Liquid Ventilation
Surfactant Replacement
Prone Positioning
Respiratory Support

17
18
 Respiratory Support
Initial
Goals and
managem
limits
ent

Initiate vent.
parameters
Md: A/C pressure
controlled Titrat
e
TV: Set TV to 8 ml/kg of TV by 1ml/kg @ int. of 2hr till
PBW 6ml/kg
RR: baseline min
volume 25 cm H2O < Pplat 30 cm
(not > 35 bpm) H2O
I flow rate: > pt.
Adjus
demand t pH : 7.30-7.45
(usually > 80L/min)

Special http://www.ardsnet.org/
considerations
 Management Strategies
Recruitment Maneuvers and
High PEEP
C*
200
Prevents alveolar collapse [2], [3] 8
Increases V/Q areas [2]
Improves gas exchange [1]
Improve respiratory system compliance in some patients [2]

Risks
! CT
Circulatory depression & barotrauma [2] 2006
Alveolar fluid clearance [3]
There is extreme variability in the
percentage of potentially recruitable
lung areas. [4]

It is strongly associated with the

SS: 68
response to PEEP. [4]
20
http://www.ardsnet.org/

By adjusting PEEP & FiO2 Target

PaO2
By adjusting TV & RR Target
PaCO2/PH
21
 Management Strategies
High-frequency
Ventilation
D*
Avoiding both excessive inspiratory volumes and repetitive airway 2008
collapse. [1]
Minimizes the risk of VALI. [1]

Risks
! RCT
2013
Pressure injury. [1]
Difficulty with humidification of inspired gas.HFOV
[1] had no significant
Hemodynamic deterioration.[3] effect on 30-days
Need for heavy sedation and mortality. [5]
neuromuscular blockade. [3]
SS:795
multicenter,
randomized

22
 Management Strategies
Fluid
Management
D*
200
Conservative management. 8
Extravascular lung water. [1]
duration of mechanical ventilation. [1]
prevents further decrements in arterial oxygenation and lung
compliance. * RCT
improves pulmonary mechanics. * 2006
No difference in 60-day
mortality.
SS:
Special Researchers supported1000
considerations conservative therapy. [6]

Permeability of the alveolarcapillary membrane pulmonary

edema develops at lower pulmonary capillary pressures. [1]
Adequate intravascular volume must be maintained to avoid tissue
hypoperfusion. [1]
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Mortality in ARDS seems to be associated with net fluid gain. [1]
 Management Strategies
Prone Position

lung volume & the amount of atelectasis & shunt fraction. C*

[2] 2008
Heart weight on the left lung. [2]
RCT
Improvement of V / Q. [2] 2001/
! Clearance and drainage of respiratory secretions. [2]
2009/2013
Underlying mechanism is not clear.
Although [2]
it improves oxygenation, it does
not improve survival. [7] (2001)
SS: 304
SS: 342 multicenter,
multicenter, un- prone positioning does not provide significant
randomized
blinded
survival benefit in pt.s with ARDS . [9] (2009)
Special SS: 466
considerations multicenter,
Early application of prolongedsessions
prospective

significantly decreased 28-day and 90-day

mortality. [8] (2013)
Risk of pressure bearing damage on ventral body structures
24
face, eyes, chest [1]
 Management Strategies
RCT
2006
Steroids C*
200
8
Suppression of the cytokine-mediated inflammatory
response could be therapeutic. [1]
may accelerate the resolution of systemic
inflammation associated Itwith
showed
ARDS.a significant
[2] improvement in lu
mechanics, gas exchange, and ventilator &
2 CT and one meta-analysis of selected trials showed
shock-free days. [10]
that steroids are associated with favorable outcomes
and survival benefit when
Thegiven before
routine use ofday 14. [2]
methylprednisolone for
persistent ARDS isSS:180
not recommended. [10]
Special
considerations double-
blinded
Routine use of corticosteroids is not advocated, especially
in the acute phase of ARDS. [1]
It is ineffective in the early exudative stage. [2]

25
 Management Strategies
Surfactant
Replacement
D*
200
Surfactant replacement is associated with survival improvement
8
In neonatal ARDS. [1]
Phase III trial of protein Cbased surfactant showed improvement
in oxygenation without lowering mortality or the number of
ventilator days in adults. [1] RCT Sample size:
2011 1200.
Prospective RCT,
blinded, 161
center, 22
countries [11]
Recombinant protein Cbased surfactant has no
significant benefit in pt.s with direct sever lung
injury.
RCT[2]
2004

No survival benefit in the use of exogenous

Sample size: 448
surfactant in a heterogeneous population of
multicenter,
26
patients. [3] randomized, double-
blind trial. [12]
 Management Strategies
Inhaled NO
D*
200
It reduces the pulmonary vasoconstriction in patients with ARDS. 8
Improves V/Q matching. [2]
Its effect on PO2 is dose dependent, with a maximal effect seen
between 1 and 10 parts per million. [2]
It is not associated with systemic effects . [2]
Studies failed to prove the benefit of NO on survival rate and days
of mechanical ventilation.[2] RCT &
Review
2012/2013
A recent meta- analysis of 14 RCT showed no deference
in mortality, however, the use of NO resulted in more
ventilator free- days and a decrease in length of ICU stay.
[13]

(RCT) Patients who treated with low-dose iNO had SS: 92

significantly better values for selected lung tests after 6Double-
27
blind,
months post-treatment. [14] Randomized
References
[1]. Gabrielli, A., Layon, A. J., & Yu, M., (2009). Civetta, Taylor, &
Kirby's: Critical Care, 4th Edition. Lippincott Williams & Wilkins, a
Wolters Kluwer Business.
[2]. Dernaika, T. A., Keddissi, J. I., & Kinasewitz, G. T. (2009). Update
on ARDS: Beyond the low tidal volume.The American Journal of
the Medical Sciences,337(5), 360-367.
doi:10.1097/MAJ.0b013e318195493e;
10.1097/MAJ.0b013e318195493e.
[3]. Diaz, J. V., Brower, R., Calfee, C. S., & Matthay, M. A. (2010).
Therapeutic strategies for severe acute lung injury.Critical Care
Medicine,38(8), 1644-1650. doi:10.1097/CCM.0b013e3181e795ee;
10.1097/CCM.0b013e3181e795ee
[4]. Gattinoni, L., Caironi, P., Cressoni, M., Chiumello, D., Ranieri, V.
M., Quintel, M., . . . Bugedo, G. (2006). Lung recruitment in patients
with the acute respiratory distress syndrome.N Engl J
Med,354(17), 1775-1786. doi:10.1056/NEJMoa052052
[6]. Comparison of two fluid-management strategies in acute lung
injury. (2006).N Engl J Med,354(24), 2564-2575.
doi:10.1056/NEJMoa062200
28
[7]. Gattinoni, L., Tognoni, G., Pesenti, A., Taccone, P., Mascheroni, D.,
[9]. Taccone P, Pesenti A, Latini R, et al (2009). Prone positioning in patients with moderate
and severe acute respiratory distress syndrome: A randomized controlled trial. JAMA. Vol
302, No. 18 doi:10.1001/jama.2009.1614
[10]. Efficacy and safety of corticosteroids for persistent acute respiratory distress
syndrome. (2006).N Engl J Med,354(16), 1671-1684. doi:10.1056/NEJMoa051693
[11]. Roger G. Spragg,Friedemann J. H. Taut,James F. Lewis,Peter Schenk,Clemens
Ruppert,Nathan Dean,Kenneth Krell,Andreas Karabinis, andAndreas Gnther (2011).
Recombinant surfactant protein C-based surfactant for patients with sever direct lung
injury. American Journal of Respiratory and Critical Care Medicine. Vol.183, No.8(2011),
pp. 1055-1061. Doi :10.1164/rccm.201009-1424OC
[12]. Spragg, R. G., Lewis, J. F., Walmrath, H., Johannigman, J., Bellingan, G., Laterre, P., . . .
Seeger, W. (2004). Effect of recombinant surfactant protein CBased surfactant on the
acute respiratory distress syndrome.N Engl J Med,351(9), 884-892.
doi:10.1056/NEJMoa033181
[13]. Khan, M., & Frankel, H. (2013). Adjuncts to ventilatory support part 1: Nitric oxide,
surfactants, prostacyclin, steroids, sedation, and neuromuscular blockade.Current
Problems in Surgery,50(10), 424-433. doi:10.1067/j.cpsurg.2013.08.005;
10.1067/j.cpsurg.2013.08.005
[14]. Dellinger, R. P., Trzeciak, S. W., Criner, G. J., Zimmerman, J. L., Taylor, R. W., Usansky,
H., . . . Goldstein, B. (2012). Association between inhaled nitric oxide treatment and long-
term pulmonary function in survivors of acute respiratory distress syndrome.Critical Care
(London, England),16(2), R36. doi:10.1186/cc11215; 10.1186/cc11215
* Fauci, A. S., Braunwald, E., Kasper, D. L., Hauser, S. L., Longo, D. L., Jameson, J. L., &
Loscalzo, L. (2008) . Harison's principles of internal medicine (17ed). The McGraw-Hill
Companies.
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