SEMINAR

1. ACUTE RESPIRATORY DISTRESS
SYNDROME (ARDS)
Presentor: Naveen Kumar
Moderator: Shaila S Kamath

2. OUTLINE
 History
 Definition
 Causes
 Natural history
 Clinical history
 Diagnosis
 Management-Non ventilatory

3.  Ashbaugh & Petty -1967
 Clinical features described by them were:
Severe dyspnea
Cyanosis refractory to O2
Decreased pulmonary compliance
Diffuse alveolar infiltrates on Chest X- ray
Adv : first discription,summarizes clinical features well
Disadv : lack specific criteria

4.  American - European Consensus Conference,1994
 Criteria:
- Acute onset
- Bilateral infiltrates on CXR
- PCWP =< 18 mmHg
- PaO2 / FiO2 ratio =< 200
( ALI =< 300)

5. BERLIN DEFINITION:2012 JAMA.2012;307(23):2526
2533/DOI:10.1001/JAMA.2012.5669

6. BERLINS CRITERIA
 ALI was eliminated as a clinical entity,
 PaO2/FIO2 for ARDS was set at ″300 mm Hg,
 Requirement was added that the PaO2/FIO2
determination should be conducted at a positive
end-expiratory pressure (PEEP) of 5 cm H2O,
 The wedge pressure measurement was eliminated
(because of the diminished use of pulmonary artery
catheters).

8.  Acute respiratory distress syndrome (ARDS) is a
clinical syndrome of severe dyspnea of rapid onset,
hypoxemia, and diffuse pulmonary infiltrates
leading to respiratory failure.
 The annual incidence of ARDS is estimated to be
as high as 60cases/100,000 population.
 Approximately 10% of all intensive care unit(ICU)
admissions involve patients with acute respiratory
failure; ~20% of these patients meet the criteria for
ARDS.

9. ARDS CAUSES
Direct Injury
Common Causes
 Pneumonia 28%
 Gastric aspiration 14%
Less Common Causes
 Pulmonary contusion
 Fat emboli
 Near drowning
 Inhalational injury

10. ARDS CAUSES
Indirect Injury
Common Causes
•Sepsis 32%
•Shock after severe trauma 5%
Less Common Causes
•Cardiopulmonary Bypass
•Drug overdose
•Acute pancreatitis
•Massive blood transfusions

11. NATURAL HISTORY OF ARDS
 3 phases
- Exudative (0-7 d)
- Proliferative ( 7-21 d)
- Fibrotic ( > 21 days)

12. EXUDATIVE PHASE
 Injury to alveolar endothelium and type 1
pneumocytes occur
 Alveolar edema predominantly involves dependent
portions of the lung leading to decrease lung
compliance in the dependent area.
 Consequently, intrapulmonary shunting and
hypoxemia develop and increases work of breathing
and dyspnea.

15. PROLIFERATIVE PHASE
 Organisation of alveolar exudate
 Initiation of repair
 Lymphocyte predominant infiltrate
 New surfactant synthesis from type 2 pneumocytes

16. FIBROTIC PHASE
 Exudate converted to fibrosis
 Disruption of acinar structure
 Microvascular occlusion
 Pulmonary hypertension

18. CLINICAL HISTORY
 Usually follows a rapid onset within 12 to 48 hours
of the predisposing event.
 The earliest signs of ARDS are the sudden
appearance of hypoxemia and signs of respiratory
distress (e.g., dyspnea, tachypnea).
 Increased work of breathing, small tidal volumes.
 Initial ABG shows PaO2 less than 50mm hg and
SPO2 less than 85%

19.  Hallmark – hypoxemia resistant to oxygen therapy
because of the large right to left shunt
 Initial compensation – by hyperventilating
 There by maintaining acceptable PaO2 with an
acute respiratory alkalosis

20.  Patients deteriorate over several hours, requiring
endotracheal intubation and mechanical ventilation.
 Patients with milder lung injury and a normal level
of consciousness – treated with high flow therapy
with or without continuous positive airway pressure
mask or noninvasive assisted ventilation

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

22. BRONCHOALVEOLAR LAVAGE
 Reliable method for distinguishing ARDS from
cardiogenic pulmonary edema .
 Lavage fluid is analyzed for the presence of neutrophils
and protein.
 Normally neutrophils make up less than 5% of the cells
recovered in lung lavage fluid, whereas in patients with
ARDS, as many as 80% of the recovered cells are
neutrophils.
 Inflammatory exudates are rich in proteinaceous
material, lung lavage fluid that is rich in protein is used
as evidence of ARDS.
 Criteria:
 Hydrostatic Edema: Lavage fluid [protein] / plasma
[protein] <0.5
 ARDS: Lavage fluid [protein] / plasma [protein] >0.7

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

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

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

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

27. 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 pulse oximetry,
and regular blood gases are required

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

29. FLUIDS
 Avoiding a positive fluid balance will prevent
unwanted fluid accumulation in the lungs, which
could aggravate the respiratory insufficiency.
 Reduce the time on mechanical ventilation , and
can even reduce mortality.

30. STEROIDS
 Clinical trials show no consistent survival benefit
associated with steroid therapy.
 Reduction in markers of inflammation , improved
gas exchange, shorter duration of mechanical
ventilation, and shorter length of stay in the ICU.
 Steroid therapy is currently recommended only in
cases of early severe and unresolving ARDS

31. EARLY SEVERE ARDS
 Methylprednisolone:
 IV loading dose of 1 mg/kg (ideal body weight) over
30 minutes,
 1 mg/kg/day for 14 days, then gradually taper.
 Five days after the patient is able to ingest oral
medications, the dose can be given orally (as
prednisone or prednisolone) as a single daily dose.

32. UNRESOLVING ARDS
 High-dose steroid therapy started in the developing
phase of fibrinoproliferation can help to halt the
progression to pulmonary fibrosis.
 Methylprednisolone:
 IV loading dose of 2 mg/kg (ideal body weight) over 30
minutes, then infuse at 2 mg/kg/day for 14 days, and 1
mg/kg/day for the next 7 days. After this, gradually taper
the dose and discontinue therapy.
 Risks of high-dose steroid therapy-worsening glycemic
control and prolonged neuromuscular weakness when
combined with neuromuscular blocking agents. There is
no evidence of an increased risk of nosocomial
infections with the steroid regimens

33. THE FAILED THERAPIES IN ARDS
 Surfactant (in adults),
 Inhaled nitric oxide,
 Pentoxyphylline,
 Ibuprofen,
 Prostaglandin E1, and
 Antifungal agents (to inhibit thromboxane).

34. PROGNOSIS
 Mortality ranges-26 %-44%
 Risk factors
- Advanced age >75 years of age
-Preexisting organ dysfunction
- CKD,CLD
- Chronic immunosuppression
- chronic alcohol abuse
 ARDS arising from direct lung injury has double
mortality

35. REFERENCES
 Harrison's Principles of Internal Medicine, 19E
(2015)
 Marino’s -The ICU Book,4E