This document discusses acute respiratory distress syndrome (ARDS), including its etiology, clinical features, and management. ARDS can be precipitated by direct lung injury from inhalation of gastric contents or toxins, or indirect injury from non-pulmonary sepsis or trauma. Clinically, ARDS presents with acute onset dyspnea within 1 week and hypoxemia. Chest imaging shows bilateral infiltrates. Treatment involves identifying and treating the underlying cause, maintaining oxygenation with mechanical ventilation, and treating other organ dysfunction. Rescue therapies for severe ARDS include corticosteroids, prone positioning, and extracorporeal membrane oxygenation.

1. ARDS
ETIOLOGY, CLINICAL FEATURES, MANAGEMENT
DR. RAMKUMAR P P
SENIOR ASSISTANT PROFESSOR
DEPT OF RESPIRATORY MEDICINE
GKMCH-KALLAKURICHI

2. PRECIPITATING CAUSES
• Direct causes:
- Aspiration of gastric fluids (MENDELSON SYNDROME)
- Diffuse Bacterial pneumonia e.g., Legionnaires’ disease
- Pneumonia due to Pneumocystis carinii
- Chest trauma with lung contusion , blast injury

3. - Near drowning
- Toxic inhalation eg- smoke, crack cocaine,phosgene
- Viral pneumonia eg- influenza, SARS - COVID
- Paraquat poisoning
- Radiation
- Lung vasculitis

4. •Indirect causes:
- Acute pancreatitis
- TRALI
- Non-pulmonary sepsis
- Multiple trauma
- Severe burns

5. - Toxic ingestion eg- aspirin , tricyclic antidepressants
- Fat- emboli syndrome
- Disseminated intravascular coagulation(DIC)
- Anaphylaxis
- Postcardiopulmonary bypass
- Primary graft failure of lung transplantation

6. Factors influencing risk of ARDS
• Chronic alcohol abuse
• Hypoproteinemia
• Advanced age
• Increased severity and extent of injury or illness
• Hypertransfusion of blood products
• Cigarette smoking
• Antiplatelet therapy is associated with reduced incidence of ALI

7. Factors influencing mortality from ARDS
• Advanced age
• Lower PaO2/FiO2
• High plateau pressure
• Greater extent of pulmonary infiltrates
• Chronic liver disease
• Nonpulmonary organ dysfunction
• Hypoproteinemia
• Greater length of hospitalization prior to onset of ALI/ARDS

8. CLINICAL PRESENTATION
• Rapid course – within 12 - 72 hours of the predisposing factor
• Dyspnea, tachypnea, tachycardia
• Acute confusion
• Cyanosis, and diaphoresis may be evident.

9. • Pulse oximetry – less than 85%
• Diffuse crackles on auscultation
• Cough, chest pain, wheeze, hemoptysis, and fever are inconsistent
and mostly driven by the underlying etiology.

10. DIAGNOSIS
• A thorough history and clinical examination
• Chest radiograph
• Laboratory studies
• Electrocardiography and echocardiography
• Microbiological studies
• Bronchoalveolar lavage
• Lung biopsy

11. Thorough History taking
• H/S/O infectious or aspiration pneumonia
• H/S/O cardiogenic pulmonary edema
• H/S/O cancer, vasculitis, or alveolar hemorrhage
• Abdominal symptoms (pain, vomiting, or diarrhea)

12. • Evidence of recent trauma, surgery, smoke or other toxin
inhalation, environmental or occupational exposures
• Transplant and transfusion history

13. Thorough clinical examination
Should assess for signs of
• Acute cardiogenic pulmonary edema
• Pneumonia
• Abdominal examination
• Skin
• Lymph nodes
• Dentition - for possible source of sepsis
• Volume status

14. Chest radiograph
• Diffuse bilateral alveolar infiltrates ( not fully explained by
effusion/collape/nodules)
• Infiltrates may be variable –
Mild or dense
Interstitial or alveolar
Patchy or confluent

15. RALE SCORE
(Radiological assessment of lung edema)
Thorax . 2018 Sep;73(9):840-846.

16. RALE score
• To determine the RALE score, each radiograph was divided into
quadrants, defined vertically by the vertebral column and horizontally by
the first branch of the left main bronchus
• RALE score ranging from 0 (no infiltrates) to 48 (dense consolidation in
>75% of each quadrant).
• Excellent diagnostic accuracy for ARDS
• Predict severity, outcomes, and response to therapy in ARDS.

17. PULMONARY EDEMA

24. Diagnosis of ARDS-
Sensitivity: 93–98%, specificity:78–100%
Lung Ultrasonography

25. Extra-pulmonary
ARDS
• The dominant pattern is
ground glass opacity.
• In the dependent parts of
the lung there is also some
consolidation.
• An important finding is the
symmetry of the
abnormalities.

26. Pulmonary ARDS
• Patchy distribution of
lung disease and the
almost complete
distorsion more basal.

27. Laboratory studies
• ABG - Pao2 <50 to 55 mm Hg
• Cardiac enzymes
• Brain natriuretic peptide (BNP)
- >500 pg/ml – Congestive heart failure ( PPV – > 90%)
- <100 pg/ml – CHF is unlikely (NPV - > 90%)

28. BIOLOGICAL MARKERS
• Von Willebrand Factor (VWF)
• Plasma angiopoietin-2
• Surfactant protein –D
• Interleukin -6
• Tumour Necrosis factor
• Interferon gamma

29. Echocardiography
Cause for acute hypoxemic respiratory failure
- Mitral valve stenosis/ regurgitation
- LV dilation or dysfunction
- Left ventricle wall motion abnormalities

30. Microbiological studies
• Respiratory tract sampling (eg, sputum or endotracheal aspirates)
• Blood cultures and sensitivity
• Urine Culture and senitivity

31. Bronchoalveolar Lavage (BAL)
• To evaluate patient who have ARDS of unknown origin
• Can be performed safely in patients with ARDS, except those with very low
PaO2 or those requiring high PEEP
• Principal indication is to rule in or rule out acute processes that may require
specific treatment
Eg- Acute Eosinophilic pneumonia and Diffuse Alveolar Hemmorhage

32. Lung Biopsy
• Not recommended in ARDS
• Reserved for Highly selective group of patients in whom alternate
diagnoses are possible and would significantly change the course of
management and prognosis.

33. 4 O – Onset , Opacity, Origin of Edema and Oxygenation
Onset
Within 1 week of a known clinical insult or new or
worsening respiratory symptoms
Chest imaging
Bilateral opacities — not fully explained by effusions,
lobar/lung collapse, or nodules
Origin of edema
Respiratory failure not fully explained by cardiac failure
or fluid overload. (Echocardiogram)
Oxygenation
Mild
200 mmHg < PaO2/FIO2 ≤300 mmHg with PEEP or CPAP
≥5 cmH2Oc
Moderate
100 mmHg < PaO2/FIO2 ≤200 mmHg with PEEP ≥5
cmH2O
Severe PaO2/FIO2 ≤100 mmHg with PEEP ≥5 cmH2O
THE BERLIN DEFENITION

34. Kigali modification of Berlin Definition of ARDS
• ARDS was defined
• Without the need of positive end expiratory pressure ( PEEP)
• Bilateral opacities on Chest radiograph or lung ultrasound
• Hypoxia SpO2/FiO2 ≤ 315
• Resource limited setting ( No PEEP and ABG )

35. Differential Diagnosis
D/D Characteristics
1. Cardiogenic Pulmonary Edema - H/O cardiac dysfunction
- ECG/ Echo showing LVF
- Chest XRAY – cardiomegaly,
vascular distribution towards
upper lobes, presence of septal
lines or kerley lines, perihilar
distribution of edema
- Rapid response to diuresis

36. D/D CHARACTERISTICS
2. Diffuse Alveolar Hemorrhage - Associated with autoimmune diseases like
vasculitis
- BAL fluid – hemosiderin laden
macrophages
- Responds to apheresis, steroids and other
immunosuppressants
3. Acute eosinophilic pneumonia - Present with cough, fever, pleuritic chest
pain, myalgia
- Do not have peripheral eosinophilia, but
BAL > 15 % of eosinophils
- Responds to high dose of corticosteroid

37. D/D Characteristics
4. Pulmonary alveolar proteinosis - Slower onset
- Crazy paving pattern on HRCT
- Treated with whole lung lavage
5. Disseminated malignancy - H/O malignancy
- Cytological preparations from
Bronchoscopy specimens may
reveal malignant cells

38. D/D Characteristics
6. Acute interstitial pneumonitis and
Hypersensitivity pneumonitis
- Slower onset than ARDS
- Treated with high dose of
corticosteroids
7. Acute major pulmonary embolus - Severe hypoxemia and hypotension
requiring vasopressors
- Risk factors for Pulmonary embolism

39. GOALS OF MANAGEMENT
• Treatment of respiratory system abnormalities
• Treatment of non-respiratory system abnormalities

40. Treatment of respiratory system abnormalities
• Diagnose and treat the precipitating cause
- Finding the foci of infection or the precipitating cause
- Aggressive source control – antibiotics, drainage, debridement
• Maintain oxygenation - preferably using nontoxic Fi O2 (0.70) ,PEEP,
mechanical ventilation

41. • Prevent ventilator-induced lung injury (VILI) by using a low tidal volume
ventilatory strategy (≤ 6 ml/kg) with a limit (≤30 cm H2O) on static end-inspiratory
airway pressure (plateau pressure)
• Keep pH in normal range 7.30–7.45
• Enhance patient-ventilator synchrony and patient comfort - by use of sedation,
amnesia, opioid analgesia, and pharmacologic paralysis, if necessary
• Liberate or wean from mechanical ventilation when patient can breathe without
assisted ventilation

42. Treatment of non-respiratory system
abnormalities
• Support or treat other organ system dysfunction or failure
• General critical care (preventive and homeostatic
measures)
• Adequate early nutritional support

43. Fluid Strategy in ARDS
• ARDSNet FACTT (Fluid and Catheter Treatment Trial) supports the use of a
conservative fluid strategy in managing patients with ARDS who are not in
shock
• For acute resuscitation of adults with shock, the following are suggested:
• Measuring dynamic parameters to assess fluid responsiveness
• Using a conservative fluid administration strategy and using crystalloids
over colloids
• Balanced crystalloids are preferred over unbalanced crystalloids

44. Rescue or salvage
Interventions

45. Corticosteroid
• (SSCM/ESICM) issued a conditional recommendation favoring
glucocorticoids in patients with early (within 14 days of onset)
persistent or refractory moderate to severe ARDS
• Glucocorticoids is not recommended in patients with less severe
ARDS and beyond 14 days after ARDS onset (increase mortality).
• Methylprednisolone - 1 mg/kg/day

46. Prone positioning

47. Mechanism
• Increased functional residual capacity
• Change in regional diaphragmatic motion
• Perfusion redistribution
• Improved clearance of secretions

48. PROSEVA Trial
(Prone positioning for Severe ARDS )
• Multicenter, prospective, randomized, controlled trial
• Prone-positioning sessions of at least 16 hours
• The 28-day mortality was 16.0% in the prone group and 32.8% in the
supine group (P<0.001)
• Unadjusted 90-day mortality was 23.6% in the prone group versus
41.0% in the supine group (P<0.001)
N Engl J Med 2013; 368:2159-2168

49. Proning ventilation recomendation
For adults receiving mechanical ventilation who have moderate to
severe ARDS, prone ventilation for 12 to 16 hours is suggested over no
prone ventilation .

50. • Recruitment maneuvers
• Pressure-controlled inverse ratio ventilation (PC-IRV)
• Airway pressure release ventilation

51. Extracorporeal membrane oxygenation (ECMO)
A technique of life support that consists
of diverting a fraction of the patient’s blood
flow (BF) through an artificial lung for gas
exchange (oxygenation and carbon dioxide
[CO2] removal) and then returning it to the
patient.
Among patients with very severe ARDS, 60-day mortality was not significantly lower with ECMO

52. • Venovenous ECMO - Reduced 60-day mortality.
• Associated with a moderate risk of major bleeding

53. High Frequency Oscillatory Ventilation
• HFOV is the use of very small tidal volumes oscillating around a very high
mean airway pressure, thus limiting both volutrauma and atelectrauma.
• Mild ARDS – not utilised

54. • Inhaled Nitric oxide or Prostacyclin
• Tracheal gas insufflation
• Investigational therapies - Inhaled GM-CSF, mesenchymal stem cells
(MSC).
• Other therapies – statins , beta agonist , macrolide antibiotics

55. ARDS PROGNOSIS
• 1/3rd of deaths - < 7 days
• 2/3rd of death - < 14 days
• Mortality beyond > 28 days - 30 %

56. References
• Allan IP, Robert MS. Fishman’s Pulmonary Diseases and Disorders, 6th ed.USA:McGraw Hill
education:2023,Chp-141, Pg-2177
• Vinay k, Abul KA, Jon CA. Robbins & Cotran Pathologic Basis of Disease, SA edn.India: Elsevier:2015,Chp-15,
Pg-672-4
• Dean ES, John FM, Jay AN. Murray & Nadel’s Textbook of respiratory medicine, 5th edn.India: Elsevier:2010,
Chp-90, Pg-2110
• ATS, ESICM, AND SCCM, Clinical Practice Guideline - Acute Respiratory Distress Syndrome MARCH 2017
• Thorac Dis. 2016 Jun; 8(6): E443–E445
• www.uptodate.com

58. Lung Injury Score ( Murray score)
A four-point lung injury scoring system (Murray
Score or LIS)
the most widely used means of
quantifying ARDS severity.
In our patient
Murray score is at least 3

59. Lung injury prediction score (LIPS)
• Six predisposing conditions
shock
aspiration
 sepsis
 pneumonia
 high-risk surgery
 high-risk trauma
• Nine risk modifiers
alcohol abuse
obesity
hypoalbuminemia
chemotherapy
 need for oxygen
tachypnea
hypoxia
acedemia
diabetes mellitus

60. Permissive hypercapnia
• Definition: Clinician allowed hypercapnia during assisted
ventilation, despite ability to achieve a minute ventilation
sufficient to maintain a normal PaCO2 (36-44mmHG)
Michael AG, Jack AE, Jay AF, Robert MK, Allan IP, Robert MS. Fishman’s Pulmonary Diseases
and Disorders, 5th ed.USA:McGraw Hill education:2015,Chp-141, Pg-2178-90

61. Detrimental effects of hypercapnia:
Myocardial depression
Increased pulmonary vascular resistance
Decreased renal blood flow
Increased intracranial pressure
Robert JM, Courtney B, Thomas RM, Talmadge EK, Dean ES, John FM, Jay AN. Murray &
Nadel’s Textbook of respiratory medicine, 5th edn.India: Elsevier:2010, Chp-90, Pg-2110

62. Agreement on the RALE score between two independent researchers was excellent
Calculate the RALE score in this radiograph ?
Consolidation score : 0-4
Density score : 0-3
Total RALE score :
Q1(4*3 ) +
Q2(4*3)+Q3(1*3 )+Q4(2*3)
=33

63. interstitial syndrome (panel A), alveolar-interstitial syndrome (panel B), more severe alveolar interstitial
syndrome with spared area (star) and thickening of pleural line (panel C) and alveolar-interstitial syndrome
with ground-glass attenuation, irregular pleural line and spared area (star) (panel D).
Ultrasonographic signs
of acute respiratory
distress syndrome
Int J Crit Illn Inj Sci. 2019 Jan-Mar; 9(1): 11–15.