Definitions, etiology, pathophysiology, clinical features, investigations, management, ventilator strategies

1. J.J.M MEDICAL COLLEGE
DEPARTMENT OF
ANESTHESIOLOGY
ACUTE RESPIRATORY DISTRESS
SYNDROME
MODERATOR: DR. SHILPASHRI A.M PRESENTER: DR.
PRIYA R.
PROFESSOR POST
GRADUATE

2. INTRODUCTION
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) - A
major clinical problem worldwide, carrying a high
morbidity and mortality burden.
• Severe arterial hypoxemia being resistant to treatment
with supplemental O2 therapy
• Acute lung injury characterized by diffuse alveolar
damage
• Non-cardiogenic pulmonary oedema.
ARDS is the leading cause for acute hypoxemic failure /
lung failure

3. INCIDENCE AND EPIDEMIOLOGY
• First described by Ashbaugh et al in 1967 at Denver. 12
patients with acute onset of tachypnea, hypoxemia, loss
of compliance
• LUNG SAFE trial 2014 - Higher incidence rates were
reported in North America, and Europe, compared to
South America, Asia And Africa
• clinical recognition, ventilator management, use of
adjunctive interventions
• 30.0% of patients had mild ARDS, 46.6% moderate ARDS
and the remaining 23.4% had severe ARDS

4. DEFINITIONS – A TIMELINE
• 1994 - AMERICAN–EUROPEAN CONSENSUS CONFERENCE (AECC)
DEFINITION.
Inter-clinician variability in interpretation of radiography, onset, and
cardiac status.
• 2011 – BERLIN’S CRITERIA
Identification of a known risk factor and a positive end expiratory
pressure (PEEP) >5 cm H2O. Acute lung injury (ALI) is obsolete. Mild,
moderate, or severe based on paO2 /FIO2 ratio
• 2016 – KIGALI’S MODIFICATION OF BERLIN’S DEFINITION
Resource-constrained settings. PEEP removed, hypoxemia assessed
using pulse oximetry (SpO2)/inspiratory oxygen fraction (FiO2)

6. DEFINITIONS – A TIMELINE
• 1994 - AMERICAN–EUROPEAN CONSENSUS CONFERENCE (AECC)
DEFINITION.
Inter-clinician variability in interpretation of radiography, onset, and
cardiac status.
• 2011 – BERLIN’S CRITERIA
Identification of a known risk factor and a positive end expiratory
pressure (PEEP) >5 cm H2O . Acute lung injury (ALI) is obsolete. Mild,
moderate, or severe based on paO2 /FIO2 ratio
• 2016 – KIGALI’S MODIFICATION OF BERLIN’S DEFINITION
Resource-constrained settings. PEEP removed, hypoxemia assessed
using pulse oximetry (SpO2)/inspiratory oxygen fraction (FiO2)

8. DEFINITIONS – A TIMELINE
• 1994 - AMERICAN–EUROPEAN CONSENSUS CONFERENCE (AECC)
DEFINITION.
Inter-clinician variability in interpretation of radiography, onset, and
cardiac status.
• 2011 – BERLIN’S CRITERIA
Identification of a known risk factor and a positive end expiratory
pressure (PEEP) >5 cm H2O. Acute lung injury (ALI) is obsolete. Mild,
moderate, or severe based on paO2 /FIO2 ratio
• 2016 – KIGALI’S MODIFICATION OF BERLIN’S DEFINITION
Resource-constrained settings. PEEP removed, hypoxemia assessed
using pulse oximetry (SpO2)/inspiratory oxygen fraction (FiO2)

10. THE STATUS QUO
• Overdiagnosed but undertreated
• Not optimally ventilated
• Adjunctive treatments were underutilized
• False positive patients confound results in research trials
“THERE IS A POTENTIAL FOR IMPROVEMENT IN THE MANAGEMENT OF ARDS
PATIENTS”

11. ETIOLOGY
DIRECT LUNG INJURY INDIRECT LUNG INJURY
Pneumonia
Aspiration of gastric
contents
Pulmonary contusion
Fat emboli
Near drowning
Inhalational injury
Reperfusion injury
Sepsis
Trauma associated with
shock
Multiple blood transfusions
Cardiopulmonary bypass
Drug overdose
Acute pancreatitis

12. PATHOGENESIS – 3 PHASES
• ACUTE/EXUDATIVE
• PROLIFERATIVE/SUBACUTE,
• FIBROTIC/ CHRONIC

13. ACUTE/ EXUDATIVE PHASE
• First 7 days
• Activation of neutrophils
• Diapedesis into alveoli
• Release of proteolytic enzymes and
reactive oxygen metabolites
• Cell injury and damage of epithelial
barriers
• Edema fluid – collapse – decreased
compliance
• Release of cytokines and mediators
• Inactivated surfactants
• Hyaline membrane formation
• Activation of coagulation and

14. SUBACUTE / PROLIFERATIVE PHASE
• Day 7 to day 21
• Marked interstitial and alveolar inflammation
• Initiation of lung repair,
• Organization of alveolar exudates,
• A shift from neutrophil → lymphocyte-
predominant infiltrates
• New surfactant synthesis
• Most patients recover
• Progressive lung injury and fibrosis

15. CHRONIC/ FIBROTIC PHASE
• Extensive alveolar-duct and interstitial fibrosis.
• Marked disruption of acinar architecture.
• Intimal fibroproliferation
• Progressive vascular occlusion and pulmonary
hypertension
• Increased risk of pneumothorax.
• Reductions in lung compliance.
• Increased pulmonary dead space.

16. CLINICAL FEATURES
• Dyspnoea and tachypnea
• Tachycardia
• Wheeze and Crackles
• Progressive hypoxemia
• Decreased paO2 /fiO2 ratio

17. DIFFERENTIAL DIAGNOSES

19. DIAGNOSIS
• Predominantly a clinical diagnosis
• Hematological
• Arterial blood gas analysis
• Imaging studies
• Bronchoalveolar lavage

20. HEMATOLOGICAL
• Complete hemogram - Indicators of sepsis – leucopenia or
leukocytosis
- Endothelial injury, dic – thrombocytopenia
• Renal function tests
• Liver function tests
• BNP < 100 rules out pulmonary edema of cardiac origin

21. ABG ANALYSIS
• Helps in finding the extent of derangement and is useful to judge
the effect of alteration in respiratory therapy
• Adjustment of PEEP must be followed by an ABG to assess its
effects, efficiency and complications.

22. IMAGING

23. LUNG ULTRASOUNDS

24. BRONCHOALVEOLAR LAVAGE

25. • Normal - <5% neutrophils
• > 80% of the recovered cells
are neutrophils
• Protein (lavage/serum) <0.5 =
hydrostatic edema
• Protein (lavage/serum) >0.7 =
lung inflammation

26. MANAGEMENT OF ARDS
• Treatment is mainly supportive and includes both
pharmacological and non – pharmacological strategies
• LUNG PROTECTIVE VENTILATION
• Neuromuscular blockade
• Sedation and analgesia
• Fluid and hemodynamic management
• Adjunctive treatment

27. INVASIVE MECHANICAL VENTILATION
• Guarantees sufficient gas exchange
• Increase in paO2
• CO2 removal
• Reduces respiratory muscle activity
• Allows titration of fiO2
• Positive pressure to open up collapsed pulmonary units

28. COMPLICATIONS OF CONVENTIONAL
MECHANICAL VENTILATION - VILI
• Mechanical ventilation itself is a source of lung
injury in patients with ARDS
• Initially, TV of 12 – 15 ml/kg were used to
reduce atelectasis during mechanical
ventilation
• High inflation volumes delivered to small
functional portions of the lungs
• Excessive inflation of distal air spaces 
rupture  volutrauma
• Release of pro inflammatory cytokines 
inflammatory infiltration  biotrauma
• Cyclic opening and closing of small airways 
damage airway epithelium  loss of

29. BABY LUNG CONCEPT AND LUNG
PROTECTIVE VENTILATION
• The lung of a patient with ARDS is modelled as a small aerated
lung
• Respiratory system compliance is linearly related to the “baby
lung” dimensions
• The ARDS lung is not “stiff” but instead small
• The size of the baby lung determines the lung susceptibility to
VILI. Smaller the baby lung, greater the potential for unsafe
mechanical ventilation
• Lung protective ventilator strategy ensures adequate
oxygenation and CO2 clearance and minimizes excessive
mechanical power applied to the lungs

30. VENTILATION STRATEGIES
• PRIMARY TARGET: To ensure adequate gas
exchange while minimizing the risk of VILI.
• Tidal volume setting
• PEEP selection
• Oxygen and carbon dioxide target
• Lung recruitment
• Other modes of ventilation

31. PREFERRED MODE OF VENTILATION
• ASSIST CONTROL MODES OVER PARTIALLY SUPPORTED MODES
• VOLUME LIMITED ASSIST CONTROL MODE – STABLE TIDAL VOLUME
• PRESSURE LIMITED ASSIST CONTROL MODE – STABLE AIRWAY PRESSURE

32. TIDAL VOLUME
• SETTINGS:
A low tidal volume setting – 6ml/kg
predicted body weight
Predicted body weight is based on
height and sex
Men: 50 + [2.3 × (height in inches
- 60)]
Female: 45.5 + [2.3 × (height in
inches - 60)]
• PURPOSE:
Reduces alveolar overdistension
and further injury to lung
• ADVANTAGE:
Reduces VOLUTRAUMA
Lower mortality rates as
compared to conventional
mechanical ventilation [ vt of 12
ml/kg PBW]
• DISADVANTAGE:
Hypercapnia
Increased work of breathing
Dyssynchrony
Increased requirement of

33. PEEP
• SETTINGS:
Ideal level of PEEP is difficult to
set
Needs to be titrated frequently
Start with 5 cm of H2O
and even go up to 15 cm of H2O
• PURPOSE:
To prevent collapse of airways at
the end of expiration and
maximize recruitment
• ADVANTAGES:
Reduces the risk of atelectrauma
Improves lung compliance, gas
exchange and arterial
oxygenation
Limits oxygen toxicity
• DISADVANTAGES:
When there is negligible volume
of recruitable lung, peep may
cause overdistension
Reduce cardiac output 
reduced systemic oxygen
delivery

34. PEEP FIO2 TABLE

35. PLATEAU PRESSURE
• Peak airway pressure and plateau
pressure need to be monitored while
setting the tidal volume
• Persistent breath to breath peak
pressures < 45 cm of H2O
• PLATEAU PRESSURE ≤30 CM OF H2O
• Measuring pplat: inspiratory hold
maneuver
• Excess pressures can cause barotrauma

36. OXYGEN TARGET
• SETTING:
INITIAL FiO2 = 100% and reduced to the lowest level of
FiO2 which achieves a saturation of 88-95%
PaO2 – 60-80 mm hg
• Increase PEEP to maintain SpO2 levels at low FiO2
• PURPOSE:
To correct hypoxemia
DISADVANTAGE:
Oxygen toxicity

37. PERMISSIVE HYPERCAPNIA
• Consequence of low volume
ventilation - reduction in CO2
elimination – respiratory acidosis
• PERMISSIVE HYPERCAPNIA: Arterial
carbon dioxide levels of 60-70 mm
Hg with a pH of 7.20
• SETTINGS:
If pH < 7.15 :
1. Increase RR (upto 35 breaths per
min)
2. Increase TV by 1ml/kg until pH
increases
3. Correct with sodabicarb
• EFFECTS OF HYPERCAPNIA:
Potentiation of hypoxic pulmonary
vasoconstriction,
Increase in cardiac output,
Anti-inflammatory effect
Rightward shift in the oxygen-
hemoglobin dissociation curve.
• DISADVANTAGES:
Increased respiratory drive – needs
more NMBA
• CONTRAINDICATIONS:
Raised ICP, cerebral edema, mass
lesions, Right heart failure

38. COURSE OF THE DISEASE
PATIENT MAY IMPROVE
MEDICAL THERAPY OF UNDERLYING CAUSE OPTIMISED
WEAN FIO2 AND PEEP
WEAN SEDATION AND IONOTROPIC SUPPORT
SWITCH TO PARTIALLY ASSIST MODES/ SPONTANEOUS MODES
PLAN FOR SPONTANEOUS BREATHING
TRIAL AND EXTUBATION
PATIENT MAY NOT IMPROVE
PERSISTENT HYPOXEMIA
HIGH AIRWAY AND PLATEAU PRESSURES
DYSSYNCHRONY
ACUTE CHANGES IN COMPLIANCE
ALTERNATE MODES OF VENTILATION
CONSIDER ALTERNATE DIAGNOSES OF UNDERLYING DISORDER
LOOK FOR COMPLICATIONS OF ARDS
IMPROVE SUPPORTIVE THERAPY

39. RECRUITABILITY - OPEN LUNG
CONCEPT
“OPEN UP THE LUNG, AND KEEP THE LUNG OPEN” - LACHMANN
• ARDS is heterogenous
• Aeration of previously collapsed
or non-aerated lung units
following an increase in alveolar
pressure
• PURPOSE: Improve oxygenation
by opening more functional
lung units
• Sustained recruitment is needed
to prevent atelectotrauma

40. RECRUITMENT MANEUVERS
• Dynamic, transient increase in transpulmonary pressure which in
turn leads to the reopening of lung units.
• Both anatomical (opening of alveolar units) and functional
recruitment (restoration of perfusion) needs to happen to increase
PaO2/FiO2 ratio
• Time doesn’t affect the success of a maneuver but it has an effect
on the hemodynamic alterations
• STEPWISE RM BETTER THAN FAST RM - slowly increasing
transpulmonary pressure instead of the rapid increase used in
sustained inflation – lower mean airway pressure – lesser
hemodynamic compromise and hyperinflation

41. • SIGH: First ever described RM – A high tidal volume or high PEEP is delivered
for a selected number of cycles
3 consecutive sighs/min with pplat of 45 cm of H2O
• SUSTAINED INFLATION : sustained PEEP of 35 to 40 cm of H2O for 40 seconds
– m.c used
• STEPWISE MAXIMUM RECRUITMENT: Sequential increase in Paw in the
increments of 5 cm of H2O till PaO2 +PaCO2 = 400 mm Hg
• STAIRCASE RECRUITMENT MANEUVER: Increasing Paw 15 cm H2O above the
required PEEP in the increments of 10 cm H2O every 2 min
• Voluntarily increasing the transpulmonary pressure transiently (30 sec – 2
min)

42. • ADVANTAGES:
Improved gas exchange
Improved compliance
Cheap, quick and easy
• DISADVANTAGES:
Requires heavy sedation and paralysis
Transient effect
Useful only before the fibro proliferative phase
Patient may desaturate
• CONTRA INDICATIONS:
Hemodynamic instability
Pre existing lung disease susceptible to barotrauma

43. INVERSE RATIO VENTILATION
Inspiratory time exceeds
expiratory time 2:1
Longer the inspiratory phase –
higher the mean airway
pressures - recruitment
Regions of lung which need
more time to open can also
participate in gas exchange
Selective air trapping or intrinsic
peep in underventilated alveoli
[open but no gas exchange]
Oxygenation can be improved

44. PRONE POSITIONING
• RATIONALE:
Redistribution of lung densities
Homogenous distribution of stress and
strain
Recruitment of atelectatic dorsal lung
units
• HOW IT IS DONE:
Reserved for patients with severe ARDS
in the acute phase, refractory to routine
therapies.
Initially a short trial given [6-8hrs]

45. • ADVANTAGES:
Reduction in ventilation perfusion
mismatch
Increase in FRC
Improved CO2 clearance
Improved oxygenation
Prevents VILI
• CONTRAINDICATIONS:
Pregnancy
Hemodynamic instability
Open abdomen treatment
Unstable fractures
• DISADVANTAGES:
Cumbersome,
Patient needs to be completely
paralysed
Accidental endotracheal extubation,
Loss of central venous catheters
Orthopedic
Injury
Facial edema
Pressure
Necrosis

46. EXTRA CORPOREAL MEMBRANE
OXYGENATION
An extracorporeal circuit with a gas
exchange device [oxygenator] removes
CO2 across a semi-peremeable
membrane
• ADVANTAGES
As an artificial lung may provide an
adequate blood CO2 removal and
oxygenation, allowing to reduce
mechanical ventilation and VILI
• DISADVANTAGES:
No difference in quality of life and
spirometric parameters
Superiority over conventional mechanical
ventilation yet to be proven
Hemorrhage, thrombosis, hemolysis,

47. HIGH FREQUENCY OSCILLATION
VENTILATION• HOW ITS DONE
A spl ventilator delivers extremely low VT (1–2
ml/kg) at very high frequencies of pressure
oscillations [4-7 hz]
• RATIONALE:
Low VTs limit VILI and higher mean airway
pressure
improves gas exchange by opening collapsed
alveoli
• ADVANTAGES
Refractory cases where access to extracorporeal
membrane oxygenation (ECMO) is limited.
• DISADVANTAGES:
Barotrauma

48. AIRWAY PRESSURE RELEASE VENTILATION
• Partial support ventilator mode
• A variant of CPAP
• HOW ITS DONE: patient spontaneously breathes
at higher set end expiratory pressures,
interrupted by brief periods of pressure release
to a lower set pressure level.
• Rationale: CPAP improves arterial oxygenation
and the pressure release phase facilitates CO2
removal
• Advantage:
Improved ventilation of dependent areas as
compared to mechanical ventilation
Improved cardiac performance
Less sedation and analgesia requirements
• Disadvantage:

49. PARTIAL LIQUID VENTILATION
Lungs are partially filled with perflurocarbon, a clear inert liquid and
mechanical ventilation is provided with a standard ventilator
PFC improves gas exchange, recruits dependent lung regions, clears
retained secretions
It has low surface tension and anti inflammatory properties – prevents
lung injury
DISAVANTAGES:
Need for heavy sedation and paralysis
Repeated de recruitment of unstable lung units
Repeated evaluation of PFC level in the body
Pneumothorax, hypoxia, hypertension

50. NON INVASIVE VENTILATION
• Not routinely used
• May be of some value in mild ARDS
• Can be used as a bridge to wean
the patient off the ventilator once
oxygenation improves and
spontaneous breathing is allowed
• ADVANTAGES:
Avoid deep sedation,
Lowers the risk of nosocomial
pneumonia
• DISADVANTAGES:
High risk of failure
Risk of delaying intubation and
invasive ventilation

51. FLUID AND HEMODYNAMIC MANAGEMENT
Positive fluid balance is deleterious to gas exchange
“FLUID RESTRICTION” – to reduce pulmonary edema
Use diuretics, albumin
AT THE SAME TIME AVOID DEFICIT TOO – CO decreases in
response to increased intrathoracic pressure settings
Maintain intravascular volume at the lowest level consistent
with adequate organ perfusion
Urine output: 0.5 – 1.0 ml/kg/hr
• Restrict blood transfusions to maintain hemoglobin.
Transfuse blood and products only if it is absolutely
indicated

52. SEDATION AND ANALGESIA
ADVANTAGES:
To initiate mechanical ventilation
To prevent awareness and recall
To tolerate the ET tube, endotracheal suctioning, prolonged
immobility in bed
Deep sedation is required to inhibit the central respiratory drive
especially during prone positioning, ECMO, HFOV etc.
Better adaptation to ventilator during controlled ventilation and
prevents asynchrony
HOW ITS DONE:
Continuous infusions better than repeated intravenous boluses
Always used along with NMBA and ensure sufficient sedation before
paralysis with NMBA
Benzodiazepines and Opioids are the drugs of choice
DISADVANTAGES:
Infections – VAP
Delirium
Post ICU PTSD

53. NEURO MUSCULAR BLOCKADE
• RATIONALE
Spontaneous breathing worsens the extent of lung damage during the initial
phase of ARDS [first 48 hrs]
• ADVANTAGES:
Prevent patient ventilator asynchrony
Reduce oxygen consumption related to respiratory muscle activity
Keep transpulmonary pressure low
Reduces negative increase in pleural pressure – in turn reduces the stress on
the lungs – in turn VILI
To implement prone ventilation, HFOV, ECMO.
• DISADVANTAGES:
Neuromuscular weakness – critical illness myopathy and polyneuropathy

54. NUTRITION
• ARDS is a hyper catabolic state
• Multiple organ dysfunction, hypermetabolism, infectious complications,
malnutrition and impaired immune function
• Nutritional and caloric deficits excarcebate muscle weakness and impede
recovery
• Lack of use of GI tract – translocation of bacteria across gut wall into the
bloodstream
• Enteral preferred over parenteral- less expensive significant reduction in
infectious complication
• Early enteral nutrition [within 48 hrs of ICU admn] even small amounts
[trophic feeds]
• Patients with shock who are being resuscitated can receive nutrition after

55. SUPPORTIVE MEASURES
• REMOVAL OF SECRETIONS: adequate hydration and
humidification of inspired gases, Tracheal suctioning,
chest physiotherapy, postural drainage, bronchoscopy
• CONTROL OF INFECTIONS: A deteriorating pulmonary
functions in an ARDS pt warrants antibiotic therapy
based on sputum culture and sensitivity testing
• Glucose control – insulin
• DVT prophylaxis – heparin, compression stockings
• Gastrointestinal (stress ulcers) prophylaxis - PPI

56. GIVE YOUR PATIENT A “FAST HUG” AT LEAST
ONCE A DAY
• FEEDING
• ANALGESIA
• SEDATION
• THROMBOPROPHYLAXIS
• HEAD UP 30°
• ULCER PROPHYLAXIS
• GLYCEMIC CONTROL

57. OTHER PHARMACOLOGICAL STRATEGIES
• CORTICOSTEROIDS:
Use of systemic glucocorticoids is controversial.
Steroids help in combatting the inflammatory response
Should be initiated before day 14 of ARDS
LOW DOSE METHYL PREDNISOLONE – 1 mg/kg/day and slowly
tapered
Helpful during the fibrotic phase – promotes collagen breakdown

58. • INHALED VASODILATORS
Nitric oxide – local vasodilation effect on pulmonary vasculature –
improved V/Q matching
No strong evidence. No mortality benefit
May even cause renal dysfunction
No role in current treatment
• STATINS:
Have anti – inflammatory and immune modulating effects
RCTS used rosuvastatin and simvastatin
No difference in the incidence/ morbidity/ mortality in ARDS
patients

59. UPCOMING ADJUNCTIVE THERAPIES
• Treatment of clotting system abnormalities with protein C,
antithrombin, tissue plasminogen activator
• Anti oxidants for preventing reactive oxygen species induced
tissue destruction
• Surfactant replacement

60. COMPLICATIONS
Pulmonary Extra pulmonary Iatrogenic
 Pulmonary Fibrosis
 Pulmonary Emboli
 Pulmonary O2 toxicity
CVS
 Myocardial dysfunction
 Low CO
 Hypotension
 Arrhythmias
MODS
 Renal failure
 Hepatic failure
 Neurologic dysfunction
 Endocrine failure
BLOOD
 Anemia
 Tube dislodgement
 Tube kinking
 Nasal necrosis
 Tracheal stenosis
 Hoarseness of voice
 Barotrauma
 Gastric distension

61. WEANING
• When a patient can maintain oxygenation and CO2 elimination without
assistance.
• Spontaneous ventilation without excess tachypnoea, tachycardia or
respiratory distress
• RSBI <100 /min/litre [given by f/VT]
• Trial of withdrawal:
i) SIMV
ii) t-piece trials
iii) decreasing levels of pressure-support ventilation (CPAP)
Can use NIV as a bridge to discontinue mechanical
ventilation

62. EXTUBATION
• Tolerate 2 hours spontaneous breathing during t-piece weaning or when
SIMV rate 1-2bpm tolerated without deterioration of ABG, mental status
and cardiac function.
• Vital capacity >15ml/kg
• PaO2 -pa O2 <350cm H2O while breathing 100% O2
• PaO2 >60mmhg at fi O2 <0.5
• Negative inspiratory pressure >-20cm H2O
• Normal arterial ph (>7.3)
• PACO2<50 mm Hg
• Respiratory rate <20/min
• Dead space ventilation/tidal volume ratio (vd/vt) <0.6
• Active laryngeal reflexes, generate an effective cough and clear secretions
• Oxygen supplementation post extubation

63. PROGNOSIS
• Outcome of the patients is determined by the underlying
causes of ARDS, patient-specific factors such as
comorbidities, clinical management and the severity of
illness.
• Studies on the long-term outcomes of ARDS survivors are
limited, but reductions in functional outcomes are
increasingly recognized
• Significant cognitive and psychiatric sequelae are also
recognized in survivors as is persistent cognitive
impairment in the longer term

64. SEPSIS AND MODS
• The mortality rate is between 40% to 60%
• An ARDS pt rarely dies because of refractory respiratory
failure [only in 20%]
• Sepsis and MODS were the most common cause of death
[40 – 70%]
• Release of inflammatory mediators from the lungs have
systemic effects impairing other organs and leading to
MODS
• Systemic management of the disease focusing on
treating the underlying cause, aggressive and early
treatment of sepsis, remove septic source and start

65. CONCLUSION
• Despite the well-established advances in its supportive treatment,
ARDS remains an oftentimes misdiagnosed syndrome, carrying a
high burden in terms of patient morbidity and mortality, as well as
healthcare costs.
• Even if plentiful literature exists on the pathophysiology and
treatment of this syndrome in human and animal models,
implications in clinical practice are still poor.
• Overall survival rate is improving, thanks to the availability of
diagnostics, and ability to recognize ARDS in the earlier stages
• Future directions of research should focus on identification of the
mechanisms of susceptibility, primary prevention and early
treatment, as well as on targeted pharmacological therapies for this

66. TAKE HOME MESSAGE
• TO VENTILATE WITH LOW TIDAL VOLUME <6ML /KG PREDICTED BODY WEIGHT
• TO KEEP PLATEAU PRESSURE < 30 CM OF H2O
• TO LOOK FOR LUNG RECRUITABILITY
• TO FOLLOW CONSERVATIVE FLUID MANAGEMENT
• GIVE NEUROMUSCULAR BLOCKADE, ADEQUATE SEDATION AND ANALGESICS FOR
INITIAL 48 HOURS
• ANTIBIOTIC COVERAGE BASED ON CULTURE SENSITIVITY TO PREVENT VAP,
CONTROL SEPSIS AND MODS
• SUPPORTIVE MEASURES ARE EQUALLY IMPORTANT IN CARING FOR THE CRITICALLY
ILL
• PRONE, ECMO RECOMMENDED IN SEVERE ARDS WHEN ALL OTHER STRATEGIES HAVE
FAILED
• CONVENTIONAL VENTILATION, HFOV, NIV, INHALED NO ARE NOT ROUTINELY USED

67. REFERENCES
• The Icu Book, 4th Edition - Paul Marino
• Clinical Application Of Mechanical Ventilation, 4th Edition – David W. Chang
• Stoelting’s Anesthesia And Co-existing Disease – 2nd South Asia Edition
• Clinics In Chest Medicine – Acute Respiratory Distress Syndrome – 2006, 2014
• Acute Respiratory Distress Syndrome: BJA Education, 17 (5): 161–165 (2017)
• Current Concepts Of ARDS: A Narrative Review, Int. J. Mol. Sci. 2017, 18, 64
• A Review Of Acute Respiratory Distress Syndrome, Eur Respir Rev 2017; 26:
160116
• Ventilator Management Strategies For Adults With Acute Respiratory Distress
Syndrome –www.uptodate.com
• ARDS Clinical Network Mechanical Ventilation Protocol – www.ardsnet.org