Acute Respiratory Distress Syndrome

1. ARDS
DR SUBHAJIT BHAKTA

2. ADULT RESPIRATORY DISTRESS SYNDROME
ACUTE RESPIRATORY DISTRESS SYNDROME

3. DEFINITION
• 1967 – Ashbaugh and Petty coined the term.
• 1988 – John Murry – LUNG INJURY SCORES.
• 1994 - AECC definition.
• 2012 – New Berlin definition.

4. AECC DEFINITION (AMERICAN EUROPEAN CONSENSUS
CONFERENCE)
ARDS
• ACUTE ONSET
• SEVERE HYPOXEMIA (PaO2 /FiO2 < 200)(irrespective of
PEEP)
• B/L OPACITIES on chest X Rays.
• ABSENCE OF LVF ( clinical examination / Rt heart
catheterise PCWP < 18 mm Hg)
New term – ALI (acute lung injury) – PaO2/FiO2 < 300
(same cause and pathophysiology)

5. LIMITATIONS OF AECC DEFINITION
• Acute onset not defined.
• Degree of hypoxemia may vary with PEEP levels.
• The agreements on interpretation of x-rays remains
modest even with experts.
• Threshold value of PCWP<18 is not always discriminative
since many pts of ARDS exhibits >18 due to increased
intrathoracic pressure/fluid overload.

6. BERLIN DEFINITION
what is finally an ARDS?
• TIMING : Within 1 week of a known clinical insult or new or worsening
respiratory symptoms.
• CHEST IMAGING(CXR/CT CHEST): Bilateral opacities – not fully
explained by effusions, lobar/lung collage, or nodules.
• ORIGIN OF EDEMA: Respiratory failure not fully explained by cardiac
failure of fluid overload. Need objective assessment (eg.echocardiography) to
exclude hydrostatic edema if no risk factor present.
• OXYGENATION:
MILD MODERATE SEVERE
200<PaO2/FiO2 ≤ 300 100<PaO2/FiO2 ≤ 200 PaO2/FiO2 <100
with PEEP/ CPAP ≥5 with PEEP /CPAP ≥5 With PEEP/CPAP ≥5

7. CAUSES OF ARDS
DIRECT LUNG INJURY INDIRECT LUNG INJURY
COMMON CAUSES COMMON CAUSES
Pneumonia Sepsis
Aspiration of gastric contents Severe trauma with shock
Multiple transfusion
UNCOMMON CAUSES UNCOMMON CAUSES
Pulmonary contusion Post cardiac surgery
Near drowning Pancreatitis
Inhalational injury Drug overdose
Fat emboli After massive transfusion
Reperfusion injury

8. THE PROBLEM : LUNG INJURY
ETIOLOGY IN CHILDREN
Infectious Pneumonia 28%
Septic Syndrome 32%
Noninfectious Pneumonia
14%
Cardiac Arrest 12%
Trauma 5%

9. PHASES OF ARDS
• EXUDATIVE (1-7 days) - Acute inflammatory
response,alveolar and endothelial damage.
• PROLIFERATIVE PHASE (1 – 3 Weeks) – Proliferation of
Type 2 pneumocytes,fibroblast,myofibroblast leading to
widening of alveolar septae.
• FIBROTIC PHASE (> 3 Weeks) – remodelling and fibrosis.

11. EXUDATIVE PHASE- PATHOPHYSIOLOGY
INJURY TO LUNG AND EPITHELIAL CELLS (TRIGGER EVENT)
PROTEIN RICH FLUID,NEUTROPHIL,MACROPHAGE IN ALVEOLI
RELEASE OF IL/TNF/other inflammatory markers
SURFACTANT DEF.
MASSIVE ALVEOLAR AND ENDOTHELIAL DAMAGE
PROCOAGULANT CASCADE, SMALL VESSEL THROMBOSIS.

12. SURFACTANT DEFICIENCY
ALVEOLAR FILLING,CELLULAR DEBRIES ATELACTASIS
LUNG INTERSTITIAL EDEMA/PULMONARY EDEMA / LESS COMPLIANCE
NORMAL ALVEOLUS WITH NORMAL COMPLIANCE (may be less than 25%
in severe cases)
HETEROGENOUS LUNG PICTURE
(V:Q MISMATCH, DIFFICULT TO VENTILATE)

13. • HABASHI et al – 3 components of ARDS affected lungs
 Aerated normal lung – susceptible to barotrauma induced in
inappropriate ventilation.
 Airspaces filled with exudates – non recruitable.
 Areas collapsed due to interstitial edema – potentially
recruitable.

14. • PULMONARY HYPERTENTION –
 Hypoxia
 Hypercarbia
 Small vessel vasculitis
• Further complicate V:Q mismatch,
• RV dysfunction
• Buldging of IV septum into left ventricle
• Left ventricular dysfunction
• Low cardiac output – multi organ dysfunction

15. ARDS OUTCOMES
• INCIDENCE – 8.5 – 27 / 1000 PICU admission.
• OVERALL MORTALITY – 35 – 50 %
Death is due to MODS rather than pulmonary failure per se.
RISK FACTOR OF MORTALITY (Vasudevan A et al)
• Liver dysfunction,
• Age
• Sepsis,
• HIV infection
• Oxygenation index (MAP× FiO2/ PaO2)
• Length of mechanical ventilation prior to ARDS,
• Mechanism of lung injury
• Right ventricular dysfunction
• PaO2/FiO2 ratio less than 100

16. ARDS – PRINCIPLES OF THERAPY
• ADEQUATE GAS EXCHANGE
• AVOID SECONDARY INJURY (to already
damaged lung)

17. ADEQUATE GAS EXCHANGE
VENTILATOR OPTION.
Invasive Ventilation/ Non invasive ventilation(CPAP, High flow nasal cannula) –
that provide some sort of PEEP.
(Limitation of HFNC- unpredictable levels of PEEP and humidification promoting
infection)
STRATEGIES THAT IMPROVE OXYGENATION WITHOUT
FAVOURABLE LONG TERM OUTCOME (outcome = 1.reduced mortality,
2.number of ventilator free days)
• Prone positioning.
• Inhaled NO
• Aerosolised prostacyclin
• Sildenafil
RESCUE MEASURES
HFOV
ECMO

18. LIMITING SECONDARY LUNG INJURY
GENTLE VENTILATION
• Low Tidal Volume.
• Optimal PEEP
• Lower PIP
• Minimum possible FiO2
• Permissive hypercapnea
GOAL:
• PaO2- 60 – 80 mm Hg
• SpO2 - > 90%
• pH – 7.30 – 7.45
• Open Lung

19. DANGERS OF ATELECTASIS
• compliance
• intrapulmonary shunt
• FiO2
• WOB
• inflammatory response

20. DANGERS OF OVERDISTENTION
• Repetitive shear stress
• Injury to normal alveoli
• Inflammatory response
• Air trapping
• Phasic volume swings: volutrauma

22. VENTILATOR STRATEGIES
• INDICATION OF INTUBATION:
No clear and specific indication
General indications like : 1) loss of consciousness
2) inability to protect the airways
Decision for intubation remains on individual experience and
expertise of intensivist.

23. FiO2
• No clear evidence to support specific FiO2 threshold
• Standard practice to titrate FiO2 (with objective to maintain
FiO2 <0.6)
• Titrate to keep PaO2 of 60 mm Hg, SpO2 >90%
• But it is vital to note that no child should die of
hypoxia and in such cases 100% FiO2 may be needed.

24. PEEP
• Prevents atelectasis, intrapulmonary shunt
• Three RCTs have evaluated modest vs. high levels of PEEP in
patients with ARDS.
• ARDS Network trial comparing low PEEP(8.3 ± 3.2) vs high
PEEP (13.2 ± 3.8) suggested that though oxygenation improved
with high PEEP there is no significant difference in outcome.
• Canadian Critical Care Trials Group study showed that with high
PEEP there is reduced need for supplementary strategies like prone
positioning/iNO but no survival benefit.

25. PEEP
RECOMMENDATION OF OPTIMISATION
OF PEEP:
In ARDS generally higher PEEP is needed to
improve oxygenation and adequate
recruitment.But PEEP should be optimised to
achieve target PaO2 and SpO2 that doesn’t cause
compromise to cardiac output.

26. TIDAL VOLUME AND PERMISSIVE
HYPERCAPNEA
• Low TV decrease volutrauma
• The Pilot ARDS Net trial comparing low TV(6 ml/kg) vs high TV
(12 ml/kg) showed significant reduction of mortality and ventilator
days.
inevitable result of low TV is hypercapnea.
But it is seen that hypercapnic acidosis is well tolerated and it actually
downregulate inflammatory cascade and oxidative stress.
So, permissive hypercapnea with pH >7.20 is a well known lung
protective strategy.

27. Recommendation for TV
• Keep tidal volume at minimum (≤ 6 cm H2O)
with provision of permissive hypercapnea

28. PIP
• Excess PIP causes more alveolar damage to already
damage alveoli (barotrauma).
• Recommendation is to keep PIP at minimum with
caution not to let increase PIP ≥ 30 cm of H2O.

29. Inspiratory time, I:E ratio
• Relatively long Ti is needed to aerate regions of lung
that have high time constant( product of airway resistance
and compliance).
• So Inverse I:E ratio( i.e -1.5:1 / 2:1) may be needed at
times.
• Disadvantage : Auto PEEP.

30. PRONE POSITIONING
• Tried as a recruitment process
How does it help?
1) More recruitment of atelectatic posterobasal lung area.
2) Decreased abdominal compression of thorax, better
excursion of diaphragm.
3) Mobilisation of secretion

31. Reccomendation on prone
positioning
• A study by Fineman et al. demonstrated an improvement in oxygenation
during prone positioning compared to supine positioning in infants and
children.
• A recent systematic review has however demonstrated no difference on
mortality or duration of ventilation with prone positioning.
Reccomendation about prone positioning -
Prone positioning definitely improve oxygenation though its long term
outcome is debatable,
It’s appropriateness should be considered for each patient and
individualised.

33. Inhaled NO
• Attenuate pulmonary cappilary permeability
• Decrease overproduction of cytokines.
• It increases oxygenation dramatically but its long term outcome is
debatable
• In children with severe hypoxic resp. failure iNO reduced need for
ECMO from 54% to 39%
• RECOMMENDATION: iNO, where available is an option for severe
form of ARDS particularly with HFOV as a rescue measure.

35. HFOV
• One crossover trial comparing rescue high-frequency oscillatory ventilation
with conventional mechanical ventilation in paediatric ALI/ARDS showed
that high-frequency oscillatory ventilation was associated with higher
mean airway pressures, improved oxygenation, and a reduced need for
supplemental oxygen at 30 days.
• There was not enough evidence to conclude whether HFV reduced
mortality or long-term morbidity in these patients.
• RECOMMENDATION: HFOV an effective rescue measure when
conventional ventilation fails (i.e FiO2 > 0.6 and PIP >35)

36. ECMO
• ECMO may be beneficial in children with severe ARDS unresponsive to
maximal conventional therapy. However, it is difficult to define maximal
“conventional” therapy.
• Most studies have shown the survival increases with “early” (7 days or
less of mechanical ventilation) institution of ECMO therapy, presumably
when the disease remains reversible and before ventilator induced lung
injury occurs.
• Ventilator duration for more than 10 days prior to commencing ECMO
is a relative contraindication.

37. ROLE OF SURFACTANT
• A PALISI Network randomized trial of Calf surfactant in
children with ALI/ARDS showed improved oxygenation and
decreased mortality but no improvements in the course of
respiratory failure (ventilator days, hospital, or intensive care
unit length of stay).
• There are two ongoing clinical trials across the PALISI
Network evaluating the effect of endotracheal surfactant
(Calfactant and Lucinactant) in children with ALI.
RECOMMENDATION: It is promising but more evidence
needed.

38. OTHER ADJUNCTIVE THERAPY
ROLE OF FLUID RESTRICTION:
A restrictive fluid management protocol has been proven to increase VFDs
and oxygenation in adults with ALI/ARDS when compared with a more
liberal fluid protocol. Evidence in children lacking.
Fluid restriction should only be implemented after children have been
resuscitated adequately from septic shock.
ROLE OF MAINTAINING TARGET HEMOGLOBIN:
Canadian Critical Care Trials Group and the PALISI Network showed that a
Hb transfusion target of 7.0 g/dL is as safe as a target of 9.5 g/dL in stable
critically ill children.
In unstable (profound hypoxia/shock) target is Hb% ≥ 10 g/dl

39. ROLE OF STEROID
Adult studies suggest steroid in patient with ARDS may
decrease mortality and increase ventilator free days without
increasing risk of infection
But no studies on steroid in treatment of childhood ARDS.
RECOMMENDATION: Steroid may be used in unresolving
ARDS.( ie on ventilator more than 7 days without
improvement) (adult data )

41. PARTIAL LIQUID VENTILATION
• Lungs filled to its FRC with perfluorocarbon and gaseous
mechanical ventilation performed simultaneously.
• PFC , dense volatile liquid with low biological reactivity. It evaporates
from lung with minimal systemic absorbtion.
• PFC has very low surface tention and unusually high solubility for
O2 and CO2.
• EFFECTS:
Splint alveoli open and circumvent the unstable air-fluid interface.
Cochrane review – no evidence of RCT to support/refute the use of PLV in
children with ALI.

42. SUMMARY
• ARDS is relatively common cause of admission
in PICU.
• 2 main strategies – adequate gas exchange, and
prevention of VALI and progression to MODS.
• Some sort of PEEP is to be provided.
• As yet, there is no definite end to support for
routine use of pharmacological adjuncts.
• Mortality remains high even with advanced
mode of ventilation

43. thank you