ARDS

1. ARDS
Dr Muhammed Aslam

2. Objectives
• Introduction
• Definition
• Etiology / Risk Factors
• Pathology & Pathogenesis
• Clinical presentation
• Workup
• Management of ALI/ARDS
• 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. What is ARDS?
• Asbaugh, Bigelow & Petty described ARDS as:
―A syndrome of acute respiratory failure in adults
characterized by non-cardiogenic pulmonary
edema manifested by severe hypoxemia caused by right
to left shunting through collapsed or fluid-filled alveoli.”
• The Berlin Definition: ―An acute, diffuse,
inflammatory lung injury that leads to increased
pulmonary vascular permeability, increased lung weight,
and a loss of aerated tissue.‖
(The ARDS Definition Task Force. Acute Respiratory Distress Syndrome: The Berlin Definition.JAMA 2012; May 21,
2012:Epub ahead of print.)

5. Definition (older)
• American-European Consensus Conference
• An acute condition characterized by bilateral
pulmonary infiltrates and severe hypoxemia in
the absence of evidence for cardiogenic
pulmonary edema.
• PaO2/FiO2* <300 = ALI
PaO2/FiO2 <200 = ARDS
• Cardiogenic pulmonary edema must be
excluded either by clinical criteria or by a
pulmonary capillary wedge pressure (PCWP)
lower than 18 mm Hg

6. Limitations of Consensus Definitions
• The chest radiograph is subject to
variability in interpretation
• PaO2/FiO2 may vary according to
ventilator parameters, e.g., PEEP, and at
extremes of FiO2
• Accuracy in excluding the presence of
heart failure may be influenced by
measurement methodology and timing

7. The Berlin Definition
JAMA. 2012;307:2526-2533
• “Acute lung injury” no longer exists.
• Under the Berlin definition, patients with PaO2/FiO2 200-
300 would now have ―mild ARDS.‖
• Onset of ARDS (diagnosis) must be acute, as defined
as within 7 days of some defined event, which may be
sepsis, pneumonia, or simply a patient’s recognition of
worsening respiratory symptoms.

8. The Berlin Definition
continue….
• Bilateral opacities consistent with pulmonary edema must be
present but may be detected on CT or chest X-ray. These
opacities must not be fully explained by pleural effusions,
lobar collapse, lung collapse, or pulmonary nodules.
• There is no need to exclude heart failure in the new ARDS
definition
• The new criterion is that respiratory failure simply be ―not fully
explained by cardiac failure or fluid overload,‖ in the
physician’s best estimation using available information.
• An ―objective assessment―– meaning an
echocardiogram in most cases — should be performed if
there is no clear risk factor present like trauma or sepsis.

9. ARDS Severity PaO2/FiO2 *** Mortality
• Mild 200 – 300 27%
• Moderate 100 – 200 32%
• Severe < 100 45%
• *** on ventilator with PEEP ≥5 cm H2O

10. Aetiology
Direct Precipitating Cause
• Pneumonia
• Aspiration
• Pulmonary embolism
• Pulmonary contusion
• Inhalation injury
• Reperfusion injury
• Chest trauma with lung contusion
• Near-drowning

11. Indirect (Systemic) Precipitating Cause
• Sepsis
• Blood transfusions with transfusion-related acute lung
injury (TRALI)
• Trauma with multiple fractures and the fat-emboli
syndrome
• Burns
• Acute pancreatitis
• Post-cardiopulmonary bypass
• Toxic ingestions, e.g., aspirin, tricyclic antidepressants

12. • Over 60 possible causes have been identified but the
four most frequent causes include:
• Sepsis (Most common cause )
• Aspiration
• Pneumonia
• Severe Trauma

13. 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

14. 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.

15. • 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.

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

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

18. 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.

19. • 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.

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

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

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

23. • Three distinct stages (or phases) of the syndrome
including:
• Exudative stage
• Proliferative (or fibroproliferative) stage
• Fibrotic stage

24. 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.

25. 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.

26. 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.

27. 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.
• Febrile or hypothermic.
• Sepsis-hypotension and peripheral vasoconstriction with
cold extremities
• Bilateral rales
• Manifestations of the underlying cause

28. • Because cardiogenic pulmonary
edema must be distinguished from
ARDS, carefully look for signs of
congestive heart failure or
intravascular volume overload,
including jugular venous distention,
cardiac murmurs and gallops,
hepatomegaly, and edema.

29. Approach to Clinical Diagnosis
• Chest Radiograph -diffuse, bilateral alveolar infiltrates
consistent with pulmonary edema
• Early in the course of the disorder, the infiltrates
associated with ARDS may be variable: mild or
dense, interstitial or alveolar, patchy or confluent
• Initially, the infiltrates may have a patchy peripheral
distribution, but soon they progress to diffuse bilateral
involvement with ground glass changes or frank alveolar
infiltrates

33. Chest Radiograph
• 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

34. Arterial blood gas analysis
• PaO2/FiO2 Ratio
ARDS Severity PaO2/FiO2
• Mild 200 – 300
• Moderate 100 – 200
• Severe < 100

35. ABG
• In addition to hypoxemia, arterial blood gases often
initially show a 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.

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. MANAGEMENT

40. 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

41. • 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

42. Maintaining Adequate Oxygenation
• Positive end-expiratory pressure
(PEEP) is employed.
• When utilized in sufficient
amounts PEEP allows FiO2 to be
lowered from high potentially toxic
concentrations
• Whether maintenance of PEEP above a certain point improves
clinical outcome is unknown

43. Lung-Protective Mechanical Ventilation
• Mechanical ventilation using limited tidal volumes
• The goals of lung-protective ventilation are to avoid
injury due to overexpansion of alveoli during inspiration
(―volu-trauma‖) and injury due to repetitive opening and
closing of alveoli during inspiration and expiration
(―atelecta-trauma‖)

44. Tidal Volumes Over The Years…..
1990’s 2010’s

45. Low Tidal Volume Ventilation (LTVV)
Initial Settings
• Calculate Ideal Body Weight (IBW) in pounds
• Males = 106 + [6 x (height in inches – 60 in)]
Females = 105 + [5 x (height in inches – 60 in)]
1 lb is equal to 0.45359237 kilogram.

46. • Set initial tidal volume to 8 ml/kg IBW
• Reduce tidal volume to 7 ml/kg IBW
then 6 ml/kg IBW over the next 1-3
hours.
• Set respiratory rate to < 35 bpm to
match baseline minute ventilation

47. Adjusting Settings
• Adjustments to tidal volume are based on the Plateau
pressure reading.
• Goal is to maintain Plateau pressure < 30cmH2O.
• If Plateau pressure rises above 30 cmH2O, the tidal
volume setting is decreased by 1 ml/kg IBW increments
to a minimum of 4 ml/kg IBW.
• Using LTVV when Plateau pressures are not high has
also shown benefit.

48. Adjuncts to Lung Protective Mechanical
Ventilation
Permissive Hypercapnia
• Permissive hypercapnia is defined as clinician-allowed
hypercapnia during assisted ventilation, despite an
ability to achieve a level of minute ventilation sufficient to
maintain a normal

49. Adjuncts to Lung Protective Mechanical
Ventilation
• Fluid Management
Distinction between primary ARDS due to
aspiration, pneumonia, or inhalational injury, which
usually can be treated with fluid restriction, from
secondary ARDS due to remote infection or inflammation
that requires initial fluid and potential vasoactive drug
therapy is central in directing initial treatments to
stabilize the patient.
• Hemodynamic Management

50. Adjuncts to Lung Protective Mechanical
Ventilation
Prone Positioning
• About two-thirds of patients with ARDS improve
their oxygenation after being placed in a prone position.
• Mechanisms that may explain the improvement include:
(1) increased functional residual capacity;
(2) change in regional diaphragmatic motion;
(3) perfusion redistribution;
(4) improved clearance of secretions.

52. Adjuncts to Lung Protective Mechanical
Ventilation
• Inhaled NitricOxide
• Inhaled prostacyclin
• Tracheal Gas Insufflation
• Extracorporeal Membrane Oxygenation (ECMO) or
ExtracorporealCO2 Removal (ECCO2R)

53. Adjuncts to Lung Protective Mechanical
Ventilation
Corticosteroids
• The general consensus among intensivists is that
corticosteroids have little or no role to play in treating the
acute phase of ALI or ARDS.
• However, the role of corticosteroids in later
phases of ALI or ARDS has been controversial.

54. “Rescue” or “Salvage” Interventions Used in ARDS and Resistant
to Conventional Mechanical Ventialation and PEEP
• Corticosteroids
• Extracorporeal CO2 removal (ECCO2R)
• Extracorporeal membrane oxygenation (ECMO)
• High frequency oscillatory ventilation (HFOV)
• Inhaled nitric oxide (NO) or inhaled prostacyclin
(epoprostenol/iloprost)
• Pressure controlled inverse ratio ventilation (PC-IRV)
• Prone positioning
• Recruitment maneuvers
• Tracheal gas insufflation (TGI)

55. 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

56. THANK YOU