ARDSDR SUBHAJIT BHAKTA

ADULT RESPIRATORY DISTRESS SYNDROME

ACUTE RESPIRATORY DISTRESS SYNDROME

DEFINITION

• 1967 – Ashbaugh and Petty coined the term.

• 1988 – John Murry – LUNG INJURY SCORES.

• 1994 - AECC definition.

• 2012 – New Berlin definition.

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)

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.

BERLIN DEFINITIONwhat 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

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

THE PROBLEM : LUNG INJURY

ETIOLOGY IN CHILDREN

Infectious Pneumonia 28%

Septic Syndrome 32%

Noninfectious Pneumonia 14%

Cardiac Arrest 12%

Trauma 5%

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.

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.

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)

• 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.

• 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

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

ARDS – PRINCIPLES OF THERAPY

• ADEQUATE GAS EXCHANGE

• AVOID SECONDARY INJURY (to already damaged lung)

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

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

DANGERS OF ATELECTASIS

• compliance

• intrapulmonary shunt

• FiO2

• WOB

• inflammatory response

DANGERS OF OVERDISTENTION

• Repetitive shear stress

• Injury to normal alveoli

• Inflammatory response

• Air trapping

• Phasic volume swings: volutrauma

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.

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.

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.

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.

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.

Recommendation for TV

• Keep tidal volume at minimum (≤ 6 cm H2O)

with provision of permissive hypercapnea

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.

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.

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

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.

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.

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)

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.

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.

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

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 )

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.

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

thank you