a complete brief of ARDS

1. Acute Respiratory Distress
Syndrome (ARDS)
Dr. Md. Monirul Islam
MS Resident (Phase –B)
Orthopaedic Surgery , BSMMU

2. Outline
• Introduction
• Definition
• Etiology / Risk Factors
• Pathology & Pathogenesis
• Clinical presentation
• Workup
• Management of ALI/ARDS
• Prognosis
• Conclusion

3. Introduction
 ARDS is a clinical devastating syndrome that
affects both medical and surgical patients.
 Despite great advances in understanding the
pathogenesis of disease mortality rate is still
high.
 Even survivors of ARDS usually experience long
ICU stay, hospital stay and several co-
morbidities.
 Moreover survivors require prolonged
rehabilitation time till full recovery.

4. ARDS: What Is It?
Term Acute respiratory distress syndrome was first
described in 1967 by Ashbaugh and colleagues.
Acute respiratory distress syndrome (ARDS) is a
sudden and progressive form of acute respiratory
failure in which the alveolar capillary membrane
becomes damaged and more permeable to
intravascular fluid resulting in severe dyspnea,
hypoxemia and diffuse pulmonary infiltrates
In brief - Acute respiratory failure with non-
cardiogenic pulmonary edema, capillary leak after
diverse insult

5. ARDS is also referred with variety of
terms like
• Stiff Lung
• Shock lung
• Wet lung
• Post traumatic lung
• Adult respiratory distress syndrome
• Adult hyaline membrane disease
• Capillary leak syndrome &
• Congestive atelectasis.

6. Diagnostic Criteria
 Acute onset
 Bilateral CXR infiltrates
 PA pressure < 18 mm Hg
 PaO2 : FiO2 < 200
- 1994 American - European
Consensus Conference

7. Clinical Disorders Associated with ARDS
Direct Lung Injury Indirect Lung Injury
Common causes Common Causes
Pneumonia Sepsis
Aspiration of gastric
contents
Severe trauma with shock ,
multiple transfusions
Less common causes Less common causes
Pulmonary contusion Cardiopulmonary bypass
Fat emboli Drug overdose
Near-Drowning Acute pancreatitis
Inhalational injury Transfusions of blood products
Reperfusion pulmonary
edema

8. Factors Influencing Risk of ARDS
• Chronic alcohol abuse,
• Hypoproteinemia,
• Advanced age,
• Increased severity, and extent of
injury or illness as measured by injury
severity score (ISS) or APACHE
score,
• Hypertransfusion of blood products,
• Cigarette smoking

9. Pathology and Pathophysiology
• In normal, healthy lungs there is a small
amount of fluid that leaks into the
interstitium. The lymphatic system removes
this fluid and returns it into the circulation
keeping the alveoli dry.

10. • ARDS is a consequence of an alveolar injury
which produces diffuse alveolar damage. The
injury causes the release of pro-inflammatory
“cytokines”.
• Cytokines recruit neutrophils to the lungs,
where they become activated and release toxic
mediators (eg, reactive oxygen species and
proteases) that damage the capillary
endothelium and alveolar epithelium.

11. • Damage to the capillary endothelium and
alveolar epithelium allows protein to escape
from the vascular space.

12. The oncotic gradient that favors resorption of
fluid is lost and fluid pours into the
interstitium, overwhelming the lymphatic
system.

13. Breakdown of the alveolar epithelial barrier allows
the air spaces to fill with bloody, proteinaceous
edema fluid and debris from degenerating cells. In
addition, functional surfactant is lost, resulting in
alveolar collapse.

14. • Healthy lungs regulate the movement of fluid to
maintain a small amount of interstitial fluid and
dry alveoli.
• Lung injury interrupts this balance causing
excess fluid in both the interstitium and
alveoli.

15. Results of the excess fluid include impaired gas
exchange, decreased compliance, and increased
pulmonary arterial pressure.

16. NORMAL ALVEOLUS
Type I cell
Endothelial
Cell
RBC’s
Capillary
Alveolar
macrophage
Type II
cell

17. ACUTE PHASE OF ARDS
Type I cell
Endothelial
Cell
RBC’s
Capillary
Alveolar
macrophage
Type II
cell
Neutrophils

18. SCHEMATIC REPRESENTATION OF PATHOPHYSIOLOGY
OF ARDS
Mr sanjay. M. Peerapur, Principal, KLES Institute of Nursing Sciences, Hubli
18
Lung injury
Release of Vasoactive substances
(serotonin, histamine,
bradykinin)
Damaged Type II alveolar cell
Surfactant production
Alveolocapillary
membrane
permeability
Vascular
narrowing &
obstruction
Alveolar
Compliance and recoil
Bronchoconstriction
Outward migration
of blood cells &
fluids from
capillaries
Atelectasis
Pulmonary Edema
Hyaline membrane
formation
Lung
compliance
Impairment in
gas exchange
ARDS
Pulmonary
hypertension

19. Abnormalities in Gas Exchange
Hypoxemia : HALLMARK of ARDS
• Increased capillary permeability
• Interstitial and alveolar exudate
• Surfactant damage
• Decreased FRC
• Diffusion defect and right to left shunt

20. Stages :
• Three distinct stages (or phases) of the
syndrome including:
 Exudative Stage
 Proliferative (or fibroproliferative) stage
 Fibrotic stage

21. Exudative Stage (0-6 Days)
Characterized by:
• Accumulation of excessive fluid in the lungs due
to exudation (leaking of fluids) and acute
injury.
• Hypoxemia is usually most severe during this
phase of acute injury, as is injury to the
endothelium (lining membrane) and epithelium
(surface layer of cells).
• Some individuals quickly recover from this first
stage; many others progress after about a
week into the second stage.

22. Proliferative Stage (7-10 Days)
• Connective tissue and other structural elements
in the lungs proliferate in response to the
initial injury, including development of
fibroblasts
• The terms "stiff lung" and "shock lung"
frequently used to characterize this stage.
• Abnormally enlarged air spaces and fibrotic
tissue (scarring) are increasingly apparent.

23. Fibrotic Stage ( >10-14 Days)
• Inflammation resolves.
• Oxygenation improves and extubation becomes
possible.
• Lung function may continue to improve for as
long as 6 to 12 months after onset of
respiratory failure, depending on the
precipitating condition and severity of the
initial injury.
• Varying levels of pulmonary fibrotic changes are
possible.

24. CLINICAL PRESENTATION
• Development of acute dyspnea and hypoxemia
within hours to days of an inciting event
• Tachypnea, tachycardia, and the need for a
high fraction of inspired oxygen (FiO2) to
maintain oxygen saturation.
• Confusion
• Extreme tiredness

25. CLINICAL PRESENTATION
• Change in patient’s behavior :Mood
swing,Disorientation ..
• Think frothy sputum
• Febrile or hypothermic.
• Sepsis-hypotension and peripheral
vasoconstriction with cold extremities
• Manifestations of the underlying cause

26. • WORK UP

27. Approach to Clinical Diagnosis
• Chest Radiograph -diffuse, bilateral alveolar
infiltrates consistent with pulmonary edema
• cardiogenic edema: increased heart size,
increased width of the vascular pedicle,
vascular redistribution toward upper lobes,
the presence of septal lines, or a perihilar
(“bat’s wing”) distribution of the edema
• Lack of these findings, in conjunction with
patchy peripheral infiltrates that extend to
the lateral lung margins, suggests ARDS

28. 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.

29. 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

30. ARDS
early late

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

35. Arterial blood gas analysis
• PaO2/FiO2 Ratio
ARDS Severity PaO2/FiO2
• Mild 200 – 300
• Moderate 100 – 200
• Severe < 100
• respiratory alkalosis.
• However, in ARDS occurring in the context of
sepsis, a metabolic acidosis with or without
respiratory compensation may be present.
• As the condition progresses and the work of
breathing increases, the partial pressure of carbon
dioxide (PCO2) begins to rise and respiratory
alkalosis gives way to respiratory acidosis

36. To exclude cardiogenic
pulmonary edema
• Echocardiogram -left ventricular
ejection fraction, wall motion, and
valvular abnormalities
• plasma B-type natriuretic peptide
(BNP) value.
• CT scan of the Chest

37. Hematologic
• Septic patients -leukopenia or leukocytosis.
Thrombocytopenia (DIC).
• Renal function Test - Acute tubular necrosis
• Liver function Test - hepatocellular injury or
cholestasis.
• Von Willebrand factor (VWF) may be elevated
in patients at risk for ARDS and may be a
marker of endothelial injury
• Cytokines - (IL)–1, IL-6, and IL-8, are
elevated

38. • Invasive HemodynamicMonitoring- pulmonary
artery wedge pressure (PCWP
• Bronchoalveolar Lavage- to rule in or rule out
acute processes that may have specific
therapies.(eg: acute eosinophilic pneumonia,
diffuse alveolar hemorrhage,

39. Histologic Findings
• Typical histological
findings in ARDS
 alveolar inflammation,
thickened septal from
protein leak (pink),
congestion and decreased
alveolar volume
www.burnsurgery.com/.../pulmonary/part3/sec4.htm
←←Normal LungNormal Lung Histology—largeHistology—large
alveolar volumes, septal spacesalveolar volumes, septal spaces
very thin, no cellular congestion.very thin, no cellular congestion.
Hyaline Protein in
air spaces
Cellular Congestion

40. MANAGEMENT

41. ARDS - Principles of Therapy
• Provide adequate gas
exchange
• Avoid secondary injury

42. Goals of Management of Patients with
ARDS
• Treatment of respiratory system abnormalities
• Diagnose and treat the precipitating cause of
ARDS
• Maintain oxygenation
• Prevent ventilator-induced lung injury (VILI) by
using a low tidal volume ventilatory strategy
• Keep pH in normal range without compromising
goal to prevent VILI

43. • Enhance patient-ventilator synchrony and patient
comfort by use of sedation, amnesia, opioid
analgesia, and pharmacological paralysis, if
necessary
• Liberate or wean from mechanical ventilation when
patient can breathe without assisted ventilation
• Treatment of non-respiratory system abnormalities
• Support or treat other organ system dysfunction or
failure
• General critical care
• Adequate early nutritional support
• Prophylaxis against deep vein thrombosis (DVT) and
gastrointestinal (GI) bleeding

44. MEDICAL MANAGEMENT
• Persons with ARDS are hospitalized and
require treatment in an intensive care unit.
• No specific therapy for ARDS exists.
• Supportive measures :
 Supplemental oxygen
 Mechanical respirator
 Positioning strategies
Turn the patient from supine to prone.
Another position is lateral rotation
therapy
• Fluid therapy
Mr sanjay. M. Peerapur, Principal, KLES Institute of Nursing Sciences, Hubli

45. MEDICAL MANAGEMENT contd…….
• Medications :
 Antibiotics
 Anti-inflammatory drugs; such as
corticosteroids
 Diuretics
 Drugs to raise blood pressure
 Anti-anxiety
 Muscle relaxers
 Inhaled drugs (Bronchodilators)
Mr sanjay. M. Peerapur, Principal, KLES Institute of Nursing Sciences, Hubli

48. Steroid in ARDS
• The patient should have evidence of ARDS and
require an FiO2 >/= 50%
• The steroid regimen:
 Loading dose 2mg/kg
 Then 2mg/kg/day from day 1 to 14
 Then 1mg/kg/day from day 15 to 21
 Then 0.5mg/kg/day from day 22 to 28
 Then 0.25mg/kg/day on days 29 and 30
 Finally 0.125mg/kg on days 31 and 32.

49. APPLICATION OF SURFACTANT
• PREVENT END-EXPIRATORY COLLAPSE OF
ALVEOLI
• RECRUITMENT OF ATELECTATIC LUNG
AREAS
• IMPROVED COMPLIANCE
• IMPROVED OXYGENATION
• IMPROVED VENTILATION /PERFUSION
RATIO

50. What does surfactant do?What does surfactant do?
Alveoli
without
surfactant
Alveoli
with
surfactant

51. ARDS - Outcomes
• Most studies - mortality 40% to 60%; similar for
children/adults
• Death is usually due to sepsis/MODS rather than
primary respiratory
• Risk factors- - advanced age
- CKD,CLD
- Chronic immunosuppression
- chronic alcohol abuse
• ARDS from direct lung injury has double mortality

52. Conclusion
• ARDS is a multisystem syndrome – not a “disease”
• Characterized by accumulation of excessive fluid in
the lungs with resulting hypoxemia and ultimately
some degree of fibrotic changes.
• The most frequent causes of ARDS include sepsis,
aspiration, pneumonia and severe trauma
• Treatment is primarily supportive and can non-
traditional types of ventilation and oxygenation
strategies.
• Many theoretical therapies
• The best proven strategy to improve survival is
low tidal volume ventilation

53. thank u….