The document provides information about Acute Respiratory Distress Syndrome (ARDS) including its definition, pathophysiology, diagnosis, management, and prognosis. ARDS is defined as rapid onset hypoxemia and diffuse pulmonary infiltrates leading to respiratory failure. It is caused by direct lung injury from conditions like pneumonia or indirect injury from sepsis or trauma. Diagnosis involves criteria of acute onset, hypoxemia with PaO2/FiO2 ≤200, and no heart failure. Management focuses on treating the underlying cause and providing ventilator support using low tidal volumes per the ARDSNet protocol to reduce ventilator-induced lung injury. Prognosis depends on risk factors and mortality ranges from 26-44%.

1. ACUTE RESPIRATORY DISTRESS
SYNDROME (ARDS)
GUIDE - DR.SHIV.S.SHARMA
- DR.Y. JAMRA
CANDIDATE-DR.SARATH MENON.R
Intensive care unit,Dept.Internal Medicine
MGM MEDICAL COLLEGE & M Y HOSPITAL,INDORE

2. OUTLINE
 Definition
 Clinical history
 Pathophysiology
 Diagnosis
 Management

3. CASE
 35 yr old male met with an RTA was admitted in
surgery icu developed severe tachpnoea,dyspnoea
within 24hrs admission
o/e-
pulse- 110/mt,bp- 80/50mmHg
pallor+ cyanosis + no jvp
S1/S2- NL
Chest b/l rales present in mid/lower area
p/a- soft ,no HSM
Abg analysis- O2 sat 50%,pao2-40%,pco2-45%
ph – 7.3

4. CXR – WHAT’S DIAGNOSIS ?

5. ARDS -DEFINITION
 ARDS is a clinical syndrome of dyspnea of rapid
onset,hypoxemia and diffuse pulmonary infiltrates
leading to respiratory failure.
 Inflammatory cells and proteinaceous fluid
accumulate in the alveolar spaces leading to a
decrease in diffusing capacity and hypoxemia.

6. ALI V/S ARDS
 ALI is the term used for patients with significant
hypoxemia (PaO2/FiO2 ratio of ≤ 300)
 ARDS is the term used for a subset of ALI patients
with severe hypoxemia (PaO2/FiO2 ratio of ≤ 200)

7. ARDS ALI
 Acute  Acute
 PaO2/FiO2 < 200  < 300mmHg
 B/l interstitial /alveolar  Same
infiltrates
 PCWP <18mmHg  Same

8. ARDS DIAGNOSTIC CRITERIA
Acute Onset
Predisposing Condition
Bilateral Infiltrates
PaO2/FiO2 ≤ 200 mm Hg
Pulmonary capillary Wedge Pressure ≤ 18 mm Hg or
no clinical evidence increase in LA pressure.

9. ARDS CAUSES
 Direct Lung Injury:
a) Pneumonia
b) pulmonary contusion
c) near drowning
d) inhalation injury
f) aspiration of gastric contents

10. ARDS CAUSES
 Indirect lung injury
a) sepsis
b) severe trauma w/ shock,
hypoperfusion
c) acute pancreatitis
d) transfusion of multp blood products

11. PATHOPHYSIOLOGY
 Diffuse alveolar damage
 Lung capillaries damage
 Inflammatory cells
 Alveolar edema
 Severe hypoxemia
 Decreased lung compliance & atelectasis
 Pulmonary hypertension

12. NATURAL HISTORY OF ARDS
 3 phases
- exudative (0-7 d)
- proliferative ( 7-21 d)
- fibrotic ( > 21 days)

15. HISTOLOGIC FINDINGS
Hyaline Protein in air
spaces
Cellular Congestion
 Typical histological
findings in ARDS
www.burnsurgery.com/.../pulmonary/part3/sec4.htm
 alveolar inflammation,
thickened septal from protein
leak (pink), congestion and
decreased alveolar volume
←Normal Lung Histology—large alveolar
volumes, septal spaces very thin, no
cellular congestion.

16. CLINICAL HISTORY
 Acute
 Critically ill
 Rapid –tachypnoea,dyspnoea,hypoxia
 Within in 12-48 hr of precipitating event
 Initial respiratory alkalosis
 Respiratory failure

17. LAB INVESTIGATIONS
 Routine blood counts
 RFT
 CXR
 ABG
 CT chest
 BNP
 2D Echo
 BAL
 PCWP

18. HOW TO DETERMINE ARDS BY CXR
 Can be difficult to do. Should always try to make
the diagnosis in light of the clinical picture.
 Need to determine Cardiogenic vs. Non-cardiogenic
edema.

19. Cardiogenic Non-Cardiogenic
Diffuse Bilateral patchy infiltrates
Bilateral infiltrates predominately in
homogenously distributed
lung bases. Kerley B’s.
throughout the lungs. No Kerley
Cardiomegaly.
B’s.

20. CARDIOGENIC V/S NON CARDIOGENIC EDEMA
cardiogenic Non-cardiogenic
 Patchy infiltrates in bases  Homogenous pluffy
 Effusions + shadows
 Kerley B lines +  Effusions –
 Cardiomegaly +  Kerley B lines –
 Pulmonary vascular  Cardiomegaly –
redistribuition  No pulm.vascular
 Excess fluid in alveoli redistribuition
 Protein,inflammatory
cells,fluid

21. ARDS
early late

22. Cardiogenic Non-Cardiogenic
No septal thickening. Diffuse
Septal thickening. More severe in alveolar infiltrates. Atelectasis
lung bases. of dependent lobes usually
seen .

23. THERAPY- GOALS
 Treatment of underlying cause
 Cardio-pulmonary support
 Specific therapy targeted at lung injury
 Supportive therapy.

24. SPONTANEOUSLY BREATHING PATIENT
 In the early stages of ARDS the hypoxia may be
corrected by 40 to 60% inspired oxygen .
 If the patient is well oxygenated on <= 60 % inspired
oxygen and apparently stable without CO2 retention
then ward monitoring may be feasible but close
observation( 15 to 30 Min), continuous oximetry, and
regular blood gases are required

25. INDICATION FOR MECHANICAL VENTILATION
 Inadequate oxygenation ( PaO2- < 60 with FiO2
>=0.6)
 Rising or elevated PaCO2 ( > 50mmHg)
 Clinical signs of incipient respiratory failure

26. MECHANICAL VENTILATION
The Aims are to increase PaO2 while
minimizing the risk of further lung injury
(ventilator induced lung injury)

27. ARDSNET
VENTILATOR PROTOCOL

28. ARDS NET PROTOCOL -WEANING
 Spontaneous breathing trial daily
 PaO2/FiO2-<8/<.4 or <5/ <.5
 PaO2/FiO2 less than previous day
 Systolic BP > 90 without vasopressors
 No neuromuscular blockade
 2 hr trial- with T piece with 1-5cm water CPAP.
 ABG,RR,SPO2 monitoring
 If tolerated for 30 mt,consider extubation

29. EVIDENCE BASED RECOMMENDATIONS FOR
ARDS THERAPY
TREATMENT RECOMMENDATIONS
 MECHANICAL VENTILATION
Low tidal volume
A
Minimize LAFP
B
High PEEP
C
Prone position
Recruitment maneuvers C
High frequency ventilation C
 Glucocorticoids D
 Sufactant D
replacement,inhaled D
NO,others

30. MANAGEMENT: REDUCING VENTILATOR-
INDUCED LUNG INJURY
 Low tidal volume mechanical ventilation
 In ARDS there is a large amount of poorly compliant
(i.e. non-ventilating) lung and a small amount of
healthy, compliant lung tissue. Large tidal volume
ventilation can lead to over-inflation of the healthy
lung tissue resulting in ventilator-induced lung injury
of that healthy tissue.
 PEEP
 Setting a PEEP prevents further lung injury due to
shear forces by keeping airways patent during
expiration

31. ARDS NETWORK CLINICAL TRIALS
 High TV vs low TV (12ml/kg vs 6ml/kg)
- 861 pts
- mortality rate 39.2 % vs 31%
 High PEEP vs low PEEP
13cm H20 vs 8 cm H20 –NO difference
 Amato etal- optimal PEEP- 15cm H20

32.  Inverse ratio ventilation
- reduce peak airway pressure
- I: E – 1:1 & 4:1
- severe hypoxemic resp.failure
 Permissive hypercapnea
- controlled hypoventilation
- PaCO2 upto 55mmhg
- pH upto 7.25
 Proning

33. OTHER METHODS
 High flow ventilation
 ECMO
 Partial fluid ventilation (PLV)

34. EXTRA CORPOREAL MEMBRANE OXYGENATION
(ECMO)

35. MANAGEMENT
 Fluids –
- conservative management
- normal or low LAFP
- reduce icu stay,duration of ventilation
 Steroids
- Meduri et al study
- methyprednisolone-2mg/kg
& taper to .5-1mg/kg in 1-2wk

36. TREATMENT OF SEPSIS
 Empirical antibiotics
 Culture sensitivity & change antibiotics
 Avoid nephrotoxic drug
 Enteral feeding

37. OTHER TREATMENT MODALITIES
 NO
 Ketoconazole
 Albuterol
 Pentoxyphylline
 NSAIDS
 N-acetyl cysteine

38. PROGNOSIS
 Mortality ranges-26 %-44%
 Risk factors-
- advanced age
- CKD,CLD
- Chronic immunosuppression
- chronic alcohol abuse
 ARDS from direct lung injury has double mortality

39. REFERENCES
 Harrison’s text book of medicine-18th edition
 ARDS Network clinical trials
- www.ardsnet.org
 ARDS Foundation
- www.ardsusa.org

40. THANK U….