Acute

Respiratory
Distress
Syndrome
DR LALIT SINGH
HEAD AND PROFESSOR OF
DEAPARTMENT
DEPT OF PULMONARY MEDICINE
AN CRITICAL CARE
SRMS-IMS, BARIELLY
INTRODUCTION
• ARDS is defined as an acute diffuse, inflammatory lung injury, leading to
increased pulmonary vascular permeability, increased lung weight, and loss
of aerated lung tissue.

• Suspect in patients with progressive symptoms of dyspnoea, an increasing

requirement of oxygen and alveolar infiltrates on chest radiograph within 6-
72 hours of an inciting event.

• Despite >50yrs of research and clinical experience, management of ARDS

still remains a challenging front associated with high mortality as well as
requiring ICU admission and early and prolonged mechanical ventilation.
(MV) 1
DEFINITIONS
• First described in 1967 by Ashbaugh- described 12 patients with acute
respiratory distress, refractory cyanosis, decreased lung compliance,
diffuse infiltrates.

• Modified in 1994 by AECC 1994- as an acute onset condition with PaO2/

FiO2<300 and bilateral infiltrates observed on frontal chest radiograph
and no direct or clinical evidence of LV Failure i.e. PAWP <18 mm Hg

• 2012- The Berlin Diagnostic criterion- modified in 2016– the Kigali

modification.
2023 THE NEW DEFINITION AND WHY
WAS IT NEEDED
• Since 2012, there has been new development of non invasive pulse
oximetric methods for evaluating oxygenation criterion for ARDS and
applied in various studies and clinical trials.
• Use of HFNO to manage severe hypoxaemic respiratory failure
increased after FLORALI trial and its use became widespread during
COVID 19 pandemic . (Patients with acute hypoxaemic injury
managed with HFNO do not meet the criterion of the berlin
definition. )
• Berlin definition is problematic in resource limited setting as requires
use of all chest X-Ray, ABG , and mechanical ventilation
• Use of USG imaging increasingly useful in critically ill patients with
hypoxaemic respiratory failure
Addition and modifications to
berlin criterion
1. acute inflammation leading to lung edema, primarily from an
increase in lung vascular and epithelial permeability, is emphasized

2. predisposing risk factors are specified, although the list is not

comprehensive

3. explicit acknowledgment that ARDS physiology and outcomes are

influenced by gravity-dependent atelectasis, as demonstrated by
the established benefit of prone positioning in moderate-to- severe
ARDS
4. for clarity, the concept of venous admixture is replaced by increased
shunting and increased ratio of physiologic to alveolar dead space

5. “increased lung weight” is no longer included because of limited

feasibility of measurement

6. the potential effects of clinical management on the presentation of

ARDS have been added to improve the bedside relevance of the
conceptual model

7. the language regarding histological findings of diffuse alveolar

damage has been modified because not all patients with clinical
ARDS have histological findings of diffuse alveolar damage and it is
rare to obtain lung biopsies in patients with ARDS
DIAGNOSIS OF
ARDS
APPROACH TO ARDS
• PATIENTS AT RISK: no strong evidence or concensus regarding risk
stratification has been validated.
• ARDS occurs in minority and develops quickly-within 12-24 hrs of
hospitalisation- posing a challenge for risk prediction.
• Clinical scores have been developed to predict ARDS in at-risk
patients, most prominently the Lung Injury Prediction Score (LIPS)
• Higher scores indicate greater risk for developing ARDS.
• Alternative approach – EALI or early acute lung injury score- aims to
identify patient with incipient lung injury before frank ARDS.
LIPS (Lung Injury Prediction
Score)
Predisposing conditions Lung contusion 1.5
Shock 2 Multiple fractures 1.5
Aspiration 2 Risk modifiers
Sepsis 1 Alcohol abuse 1
Pneumonia 1.5 Obesity (BMI > 30) 1
High risk surgery Hypoalbuminemia 1
Orthopedic spine 1 Chemotherapy 1
Acute abdomen 2 FiO2 > 0.35 (> 4 L/min) 2
Cardiac 2.5 Tachypnea (RR > 30) 1.5
Aortic vascular3.5 SpO2 < 95% 1
Acidosis (pH < 7.35) 1.5
High risk trauma
Diabetes mellitusb −1
Traumatic brain injury 2
Smoke inhalation 2
(Add 1.5 for emergency surgery)0
Near drowning 2
What's new?
Biomarkers!
WHATS NEW? SUB
PHENOTYPES!
WHATS NEW? SUB
PHENOTYPES!
Sub phenotypes based on
FACTT trial
CHEST IMAGING
The committee agreed that chest imaging criteria should include
• bilateral radiologic(chest radiography or computedtomography) or
• ultrasound findings suggestive of loss of lung aeration that are not
fully explained by effusions, atelectasis,or nodules/masses.
Although the identification of bilateral opacities by chestradiography has poor interrater
reliability, chest radiography is the most common imaging modality in critically ill patients
USE OF USG THORAX
According to the newer guidelines, criterion should include USG
findings as a diagnostic modality for ARDS-
• for identifying signs of loss of lung aeration consistent
with(noncardiogenic) pulmonary edema or lung consolidation.
• when Chest X—Ray or CT are not available.
• Useful, In resource limited settings.
• Training in the use of lung ultrasound should be emphasized to detect
bilateral consiolidationa nd non cardiogenic pulmonary edema.
 The LUNG
SAFE (Large
Observational
Study to
Understand
the Global
Impact of
Severe Acute
Respiratory
Failure)
 • A major finding was the underrecognition of ARDS by
clinicians,

• The low use of contemporary ventilatory strategies and

adjuncts.
CONCLUSIONS
FROM THE • The limited effect of physician diagnosis of ARDS on
treatment decisions.
LUNG SAFE
STUDY
• Although the reasons for this are unclear, clinicians do
not appear influenced by the presence or absence of
ARDS for setting tidal volume and may be motivated by
other factors (eg, perceived comfort, pH, PaCO2, etc).

• higher driving pressure is associated with increased risk

of death
Updates in treatment-
oxygenation
MANAGEMENT OF ARDS
• Focuses on
• the diagnosis and treatment of infection – appropriate antmicrobrial therapy)
• Respiratory support (o2 supplementation and PPV)
• Fluid management
• Supportive treatments– TPN

• Use of drugs such as Statins have not yet been approved and show no
clear benefits in outcome (except in some sub-phenotypes in a few
recent RCT’s.
Pharmacological management
current status
DRUG RATIONALE FOR USE IN ARDS CURRENT STATUS- use
NMBAs – Paralyse skeletal muscle by blocking Early and severe ARDS
NeuroMuscular neural transmission at N-M Junction With deep sedtaion + mechanical
Blocking agent ventilation + prone positioning
within 48 hr

CORTICOSTEROIDS Reduce inflammation by upregulating Not approved, no clear evidence.

anti inflammatory protein expression Research- may be significant
at receptor complex junction. patient benefit and low
incidence of adverse evnts.

STATINS Acts via inhibition of HMG Co-A Not approved, no clear benefits.
reductase. Also has anti-inflammatory May have different effects
and antiproliferative property according to patient’s
phenotype.
OTHER DRUGS – THAT ARE NOT YET
APPROVED AND HAVE NO CLEAR
BENEFIT IN THE OUTCOME
• ASPIRIN- in ARDS, aspirin reduces • SIVELESTAT - inhibitor of human
pulmonary neutrophil infiltration as well as neutrophil elastase. In ARDS, it
alveolar inflammation and injury. improves oxygenation and reduces
• INTERFERONS- are anti-inflammatory inflammation
cytokines, promote bacterial clearance and
promote lung repair • VASODILATORS- increases perfusiona
and reduces inflammation.
• VITAMINS- immunomodulator effect
• N- ACETYLCYSTEINE- acts as an antioxidant • SURFACTANT- reduces alveolar surface
tension prevent alveolar collapse,
• Beta Agonists- improve symptomsand
thus, limiting pulmonary edema.
stimulate endothelial repair benefitting
pulmonary mechnaics • Others – Dilmapimod, Solnatide,
• NEBULISED HEPARIN- improves Mesenchymal Stomal Cells, Growth
oxygenation and reduceds edema Factors.
MECHANICAL VENTILATION
STRATEGIES
• LOW TIDAL VOLUME- ~6ml/Kg Body Weight. Increase in Vt results in increased
mortality (every 1 ml increase in VT ws associated with 23% increase in morality.(-
LUNG SAFE study. Current guidelines- VT of 4–6 mL/kg and target Pplat of ≤ 30
cmH2O

• PEEP - low levels >5cm H2O. The category of nonintubatedARDS comprises patients
on HFNO or NIV at the time of diagnosis. The committee agreed on a threshold of
oxygen delivery of30L/min with HFNO because 30L/min can provide low levels of
PEEP.

• DRIVING PRESSURE AND PLATEAU PRESSURE- ΔP < 14 cmH2O was associated with
decreased risk of hospital mortality in patients with moderate to severe ARDS
• RESPIRATORY RATE <30
• MECHANICAL POWER <17J/min
• Prone position for 12-18 hrs if PaO2/FiO2 <150-
• NMBA in severe ARDS
• USE OF ECMO and EECO2R- Extra Corporeal CO2 Removal- can be
used in both hypoxaemic and hypercapnic respiratory failure. Used as
a rescue therapy in sever ARDS
• FLUID MANAGEMENT with use of NIVs/ HFNO/ Mechanical
Ventilation
Severe ARDS
treatment
Green section- treatment that
improves outcomes (supported
by RCTs)
Orange section – treatment s
that may improve outcome-
based on retrospective data
Grey section - treatments that
may improve oxygenation but
have not demonstrated
sustained clinical benefit in trials
Purple section - treatments that
likely derive benefit in a subset
of patients