The document provides information about acute respiratory distress syndrome (ARDS). It begins with a brief history of ARDS and provides the clinical definition. It describes the diagnostic criteria and etiology, including that most cases are caused by sepsis, pneumonia, or trauma. It then discusses the normal lung physiology and pathophysiology of ARDS, which involves three phases: exudative, proliferative, and fibrotic. The management section outlines the principles of therapy to provide adequate gas exchange while avoiding secondary injury, including mechanical ventilation protocols, fluid management, and other strategies. It concludes with a discussion of prognosis and recent advances in ARDS management such as protective ventilation strategies.

1. ARDS
Dr. SOUTRIK SETH
RESIDENT , DEPT OF PEDIATRICS
BMCH .

2. HISTORY ( The first description of ARDS ?? ) :
 1821 – Rene Laennec ( inventor
of stethoscope) described
idiopathic lung anasarca which
is pulmonary edema without
heart failure in his text ‘ A
Treatise on Diseases of Chest ’

3. DEFINITION :
 Clinical syndrome of severe dyspnea of rapid onset , hypoxemia
and diffuse pulmonary infiltrates leading to respiratory failure
principally involving dependant portions of lung.
 May be direct or indirect lung injury
 May be due to medical or surgical cause
 Expert consensus divides into 3 categories (mild, moderate,
severe) depending on degree of hypoxemia
 9% of mechanically ventilated children admitted in PICU fulfill
diagnosis of ALI , of which 80% suffer from ARDS .

4. DIAGNOSTIC CRITERIA FOR ARDS (AECC ’94):

5. ARDS( BERLIN definition ):

6. ETIOLOGY :
 Most cases (>80%) caused by severe sepsis syndrome / bacterial pneumonia ,
transfusion induced lung injury ,aspiration , drug overdose .
 Most common surgical causes include pulmonary contusion , multiple bone
fracture , chest wall trauma /flail chest .

7. NORMAL LUNG PHYSIOLOGY :

8. PATHOPHYSIOLOGY :
 Consists of 3 Phases :
 1. EXUDATIVE ( 0 – 7 DAYS )
 Alveolar capillary endothelium and type 1 pneumocytes(alveolar epithelial cells)
damaged
 Loss of tight alveolar barrier
 Edema rich in protein, cytokines and proinflammatory mediators accumulates in
alveolar and interstitial spaces
 Inactivation of surfactant
 Condensed plasma proteins + cellular debris + dysfunctional pulmonary surfactant
aggregate in air spaces forming hyaline membrane whorls .
 Pulmonary vascular injury in form of microthrombi and fibrocellular proliferation

9. Fig : EXUDATIVE PHASE
(ARDS)

10. HISTOLOGY :
Fig. : Diffuse alveolar damage. Some of the alveoli are collapsed; others are
distended, and many are lined by hyaline membranes (arrows).

11. NORMAL VERSUS ARDS CHEST SKIAGRAMS :

12. PROGRESSION FROM ALI TO ARDS :

13.  Anteroposterior chest x-ray in the
exudative phase of ARDS shows
diffuse interstitial and alveolar
infiltrates

14.  2. PROLIFERATIVE PHASE ( 7-21 DAYS )
 Repair is done by type 2 pneumocytes that proliferate to
synthesize surfactant and differentiate to type 1 pneumocytes .
 Organisation of alveolar exudate and shift from neutrophil to
lymphocyte predominance
 First histological sign of resolution evident in proliferative phase .
Most patients recover rapidly in this phase and extubated
 Still may experience dyspnea , tachypnea and hypoxemia
 Some develop progressive lung injury and early pulmonary
fibrosis

15. Fig : PROLIFERATIVE PHASE (ARDS)

16.  3. FIBROTIC PHASE :
 Some patients enter a fibrotic phase after 3-4 weeks of insult
 May require long term support on mechanical ventilation
/supplemental oxygen
 Alveolar edema and exudates convert to extensive alveolar duct
and interstitial fibrosis
 Acinar architecture disrupted leading to emphysematous
changes with large bullae
 Intimal fibroproliferation in microcirculation causes pulmonary
hypertension and vascular occlusion
 Decreased lung compliance and increased dead space occurs
 Increased morbidity

17. LUNG MECHANICS :
 ALI is recognised as a restrictive lung disease
 Lung compliance is reduced due to accumulation of exudates ,
inactivation of surfactant and alveolar collapse
 Children have smaller airways with higher airway resistance , lower FRC
and more rigid chest wall than adults , so higher risk of hypoxic
respiratory failure.

18. PRINCIPLES OF THERAPY :
Provide adequate gas exchange
Avoid secondary injury

19. VENTILATOR SETUP PROTOCOL :
 Select ventilator mode ( Volume/Pressure limited)
 Set ventilator settings to achieve initial VT= 8 ml/kg PBW ( Predicted Body
Weight )
 PBW [ males -> 50 + 2.3 x ( height in inches – 60 ) ; females -> 45.5 + 2.3 x (
height in inches – 60 )
 Reduce VT by 1 ml/kg at intervals ≤ 2 hours until VT = 6ml/kg PBW
 Set initial rate to approximate baseline minute ventilation
 OXYGENATION GOAL: PaO2 55-80 mmHg or SpO2 88-95% . Use a minimum
PEEP of 5 cm H2O

20.  PLATEAU PRESSURE GOAL: ≤ 30 cm H2O
 If Pplat > 30 cm H2O – decrease VT by 1 ml/kg ;
If Pplat < 25 cm H2O or VT < 6 ml/kg – increase VT by 1 ml/kg until Pplat > 25
cm H2O or VT = 6 ml/kg
If Pplat < 30 cm H2O – increase VT by 1 ml/kg
 pH goal : 7.30 – 7.45
 If pH 7.15 – 7.30 increase RR until pH > 7.30
If pH < 7.15 increase RR  increase VT by 1 ml/kg  can give NaHCO3 .
 I : E ratio goal : Duration of inspiration to be < duration of expiration

21. INITIAL MANAGEMENT FLOWCHART :

22. MANAGEMENT:
 1. GENERAL PRINCIPLES :
 Oxygen supplementation immediately via face mask
 Treatment of underlying medical / surgical condition
 Prophylaxis of venous thromboembolism,aspiration,GI bleed
 Control of nosocomial infection
 Adequate nutrition .

23.  2. MECHANICAL VENTILATION :
 Increased work of breathing and frequent hypoxemia requires
mechanical ventilation
 Mechanical ventilation is however only a supportive measure
 ARDS network conducted study shows low VT ventilation (
6ml/kg) to conventional VT (12ml/kg) causes less damage and
hence less mortality
 DISADVANTAGE : Ventilator induced lung injury due to repeated
alveolar overdistension and recurrent alveolar collapse
 Attempts to fully inflate the consolidated lung may lead to
overdistension of and injury to normal areas .

24. PREVENTION OF ALVEOLAR COLLAPSE :
 There is reduction of lung compliance due to loss of surfactant
 Without an elevation in end expiratory pressure , significant
alveolar collapse can occur at end expiration
 PEEP is set to minimize FiO2 and maximize PaO2
 Optimal PEEP for alveolar recruitment is 12-15 cm H2O
 High PEEP doesnot alter mortality rates

25. OTHER STRATEGIES :
 High frequency oscillatory ventilation ( ventilation at high
respiratory rates @ 60-3600 cycles /min with low VT)
 Partial liquid ventilation (PLV) with perfluorocarbon easily
solubilises O2 and CO2
 Extra membrane corporeal oxygenation (EMCO) can be tried
in selected cases

26.  3. FLUID MANAGEMENT :
 Maintaining a low Left Atrial filling pressure minimises pulmonary
edema and improves pulmonic mechanics
 Aggressive attempts to reduce LA filling pressure should be done
with fluid restriction and diuretics (caution: hypotension and vital
organ hypoperfusion )
 4 . NEUROMUSCULAR BLOCKADE :
 In severe ARDS, sedation and neuromuscular blockade facilitates
better patient – ventilator synchrony .
 Now-a-days NAVA ( neurally adjusted ventilatory assist ) help
synchronisation without sedation or muscle blockade

27.  5. OTHERS :
 Current evidence does not support use of high dose steroids for
reducing inflammation in ARDS .
 Clinical trials of surfactant replacement have shown to improve
oxygenation and reduce mortality (PALISI Network study )
 Inhaled nitric oxide and inhaled epoprostenol sodium can
transiently improve oxygenation but do not improve survival

28. WEANING FROM MV :
 PALISI network criteria :
 1. Minimal tidal volume of 5 ml/kg exhaled measured at the
endotracheal tube
 2. SpO2 > 95 % on PEEP < 5 cm H2O and FiO2 < 50 %
 3. Respiratory rate appropriate for age
 A recent evidence based review says no extubation criteria is
more accurate than expert clinical judgement .

29. RECENT ADVANCES IN MANAGEMENT :
 SMALLER TIDAL VOLUMES AND PERMISSIVE HYPERCAPNIA
ARDS is a diffuse process, it is heterogenous . Higher VT will cause
overdistension and damage of unaffected areas of lung .
Conventional teaching would then dictate an increase in the respiratory rate to
maintain a normal CO2 level . This is acceptable upto a certain limit. Increased
rate will leave insufficient time for the previous breath to be fully expired
before the next is delivered. The physiologic effect is the buildup of intrinsic
PEEP / auto-PEEP
A gradual increase of CO2 over a period of 10 to 12 hours has been advocated to
permit intracellular adjustment to alterations in pH.

30.  PRESSURE-LIMITED VENTILATION
Due to the stiffness of the lungs and fluctuations in airway pressure, minute
ventilation is not predictable. Volume-assured pressure-limited ventilation by
limiting tidal volume and adjusting PEEP is desired .
 INVERSE RATIO VENTILATION
 In the spontaneously breathing patient with normal airways, the ratio of
time spent in inspiration to that in expiration (I/E ratio) is 1:2. As inspiratory
time lengthens, the time remaining for expiration shortens.
 There are 2 potentially beneficial effects. First, because the tidal volume is
delivered more slowly, the driving pressure does not need to be so high and
PIP is reduced. Second, the prolonged inspiratory time may improve
oxygenation in some patients.
 Inverse ratio ventilation typically causes an increase in the mean pressure
which causes more barotrauma,so inverse ratio ventilation is becoming less
popular now .

31.  BEST PEEP AND INFLECTION POINTS
 Positive end-expiratory pressure also provides protection against ventilator-
related lung trauma. The selection of a PEEP level for optimal protection is
best understood in the context of static lung compliance, static pressure-
volume curves,and inflection points (Pflex).
 If a series of static compliance values are calculated for progressively
increasing volumes, a static pressure-volume curve is generated. Most of
the curve is linear. Sites of transition to the linear part of the curve are
called the lower and upper inflection points.

32. Figure : Static pressure-volume curve.

33.  PRONE VENTILATION :
 There is a gravity-dependent distribution of volume loss in the
lungs of patients with ARDS. By turning patients to place the
aerated portion of lung dependent, ventilation-perfusion V/Q
matching and oxygenation has been found to improve.
 Prone positioning is probably not advisable in the setting of a
temporary abdominal closure for abdominal compartment
syndrome and spine trauma. Facial edema is an expected side
effect of prone positioning.
 The safe duration of prone positioning is unknown.
 PALISI network showed no significant benefit.

34.  TRIAL OF ACE INHIBITORS :
 Angiotensin converting enzyme activity in Broncho alveolar
lavage fluid triggers inflammation and apoptosis , pretreatment
with ACE inhibitors can reduce pulmonary inflammation and
apoptosis .

35.  PROTECTIVE VENTILATION :

36. EVIDENCE BASED TREATMENT :

37. PROGNOSIS :
 Mortality recent estimate –> 18 % - 27 %
 Largely attributed to non pulmonary cause with sepsis and MODS
accounting for > 80 %
 Outcomes similar for adults and children
 Early elevation of pulmonary dead space (>0.6) and severe arterial
hypoxemia ( PaO2/FiO2<100) are main predictors of increased
mortality
 Patient usually recover maximum lung function by 6 months after
insult .

38. THINK !!!
It would seem ironic that
the very existence of human
is fully dependant on a gas
that, in excess quantities, is
toxic and lethal
- Lynn D. Martin

39. THANK YOU.