1. ADULT RESPIRATORY DISTRESS SYNDROME
Dr. M. SOFI MD; FRCP (London); FRCPEdin; FRCSEdin

2. Respiratory Distress Syndrome ARDS
Acute ARDS is defined by timing (within 1 wk of clinical insult or onset of respiratory symptoms); radiographic changes (bilateral opacities not fully explained by effusions, consolidation, or atelectasis); origin of edema (not fully explained by cardiac failure or fluid overload); and severity based on the PaO2/FiO2ratio on 5 cm of continuous positive airway pressure (CPAP).

3. Berlin modification of the American European Consensus Committee (AECC) definitions 
'Berlin Definition' ARDS
Acute onset (within 1 week of known clinical insult)
Bilateral opacities on CXR (not explained by effusions, collapse, or nodules)
Respiratory failure not fully explained by heart failure or fluid overload.
Decreased PaO2/FiO2 ratio indicates reduced arterial oxygenation from the available inhaled gas)
Severity of ARDS
Mild: mmHg (≤ 39.9 kPa)
Moderate: mmHg (≤ 26.6 kPa)
Severe: 100 ≤ 100 mmHg (≤ 13.3 kPa)
Berlin definition requires a minimum PEEP of 5 cm H2O for consideration of the PaO2/FiO2 ratio. This degree of PEEP may be delivered noninvasively with CPAP to diagnose mild ARDS.

4. ARDS: Common risk factors
Smoke inhalation
Burns
Sepsis
Near drowning
Diabetic ketoacidosis
Pregnancy
Eclampsia
Amniotic fluid embolus
Drugs - paraquat, heroin, aspirin
Massive transfusion
Acute pancreatitis
DIC
Head injury/raised intracranial pressure (ICP)
Fat emboli
Transfusions of blood products
Heart/lung bypass
Tumor lysis syndrome
Pulmonary contusion

5. ARDS: Pathophysiology
Three pathologic stages:
The initial exudative stage, of diffuse alveolar damage.
7 – 10 days later proliferative stage develops - resolution of pulmonary edema, type II alveolar cell proliferation, squamous metaplasia, interstitial infiltration and early deposition of collagen.
Some progress to a fibrotic stage - obliteration of normal lung architecture, diffuse fibrosis, and cyst formation.

6. ARDS: Pathophysiology
Increased permeability of
pulmonary microvascular
leakage of proteinaceous
fluid across the alveolar
capillary membrane.
This may be one
manifestation of a more
generalized disruption of
endothelium, resulting in
hypoxia and multiple organ
failure.
There is also evidence of
inflammation in the lung
tissue which can be seen
on metabolic imaging
methods.
Consequences include
impaired gas exchange
decreased compliance
increased pulmonary
arterial pressure

7. ARDS
MILD
MODERATE
SEVERE
Timing
Acute onset within one week of a known clinical insult or new/worsening respiratory symptoms
Hypoxemia
PaO2/FiO2 201 – 300
With PEEP≥ 5
PaO2/FiO2 ≤200
PaO2/FiO2 ≤100
With PEEP≥ 10
Origin of Oedema
Respiratory failure associated to a known risk factors and not fully explained by cardiac failure or fluid overload. Need objective assessment of cardiac failure or fluid overload if no risk factors are present
Radiological Abnormalities
Bilateral opacities*
Opacities involving 3 quadrants*
Additional physiological Abnormalities
N/A
VE corr > 10 L/min or
CRS < 40 ml/cm H2O
* Not fully explained by effusion, nodules, masses, or lobar/lung collapse ; use of training set of CXRs; VE Corr = VE x PaCO2/40 (Corrected for body surface area).

8. ARDS: Clinical presentation
The clinical features of ARDS usually appear within 6 to 72 hours of an inciting event and worsen rapidly.
Patients typically present with dyspnea, cyanosis (i.e., hypoxemia), and diffuse crackles.
Respiratory distress is usually evident, including tachypnea, tachycardia, diaphoresis, and use of accessory muscles of respiration.
A cough and chest pain may also exist.
Arterial blood gases reveal hypoxemia, which is often accompanied by acute respiratory alkalosis and an elevated alveolar-arterial oxygen gradient.
High concentrations of supplemental oxygen are generally required to maintain adequate oxygenation.

9. Clinical presentation
ARDS ARDS :
Clinical presentation
The initial chest radiograph typically has bilateral alveolar infiltrates, while computed tomography (CT) usually reveals widespread patchy or coalescent airspace opacities that are usually more apparent in the dependent lung zones
The infiltrates do not have to be diffuse or severe, as bilateral infiltrates of any severity are sufficient 
Chest radiograph in a patient with ARDS. The condition evolved over approximately 1 week.

10. ARDS A 57 year-old male with non-Hodgkin’s lymphoma
On admission normal lung fields.
The next day some
consolidations
appeared c, d)
(c) Progressing to
diffuse alveolar
involvement, with
“white lung”
appearance
(d)The normal-sized
heart and vascular
structures help in the
differential diagnosis
of pulmonary oedema
due to heart failure
ARDS

11. Clinical presentation
ARDS:
Clinical presentation
Clinical findings related to the precipitant may also exist at presentation.
As an example, in patients with ARDS due to sepsis, there may be fever, hypotension, leukocytosis, lactic acidosis, and disseminated intravascular coagulation (DIC).
HRCT scan in a patient with respiratory distress syndrome showing: non-homogeneous distribution, a ventro-dorsal gradient of density, more dense consolidation in the dependent regions, widespread ground-glass opacities associated with thickening of interlobular septa

12. ARDS: Clinical course
The first several days of ARDS are characterized by hypoxemia requiring a moderate to high concentration of inspired oxygen.
The bilateral alveolar infiltrates and diffuse crackles are persistent during this period and patients may be tenuous due to severe hypoxemia.
Most patients who survive this initial course begin to exhibit better oxygenation and decreasing alveolar infiltrates over the next several days.
This may permit the amount of ventilatory support to be decreased and weaning to begin.
Some will have severe hypoxemia and remain ventilator-dependent.

13. ARDS: Clinical course
Pulmonary proliferative changes and fibrosis may progressively replace the pathological findings of diffuse alveolar damage as early as ten days after the onset of the respiratory failure.
The fibroproliferative phase of ARDS radiographically shows progression from airspace opacification to a more coarsely reticular pattern of lung infiltration.
These changes are accompanied by persistent hypoxemia, low lung compliance, high dead space, and sometimes by progressive pulmonary hypertension.
The course may become dominated by persistent ventilator dependence and various complications.

14. ARDS: Diagnostic evaluation
Excluding cardiogenic pulmonary edema:
 An absence of S3 or S4 gallop, new or changed murmur, elevated jugular venous pressure, and certain radiographic abnormalities (e.g., pulmonary venous congestion, Kerley B lines, cardiomegaly, and pleural effusions), helps distinguish ARDS from cardiogenic pulmonary edema.
Several additional diagnostic tests may also be helpful, including measurement of plasma brain natriuretic peptide levels, echocardiography, and right heart catheterization
Tracheobronchial aspiration :
The lower respiratory tract can be sampled via tracheobronchial aspiration or mini-bronchoalveolar lavage (mini-BAL).

15. ARDS: Diagnostic evaluation
Flexible bronchoscopy:
Flexible bronchoscopy can obtain lower respiratory samples for microscopic analysis and culture if the noninvasive techniques are unsuccessful.
Identify abnormalities that may not be detected with noninvasive
A reasonable next step if noninvasive sampling is non-diagnostic.
Lung biopsy: Surgical lung biopsy may be considered when alternative causes of acute hypoxemic respiratory failure cannot be excluded on the basis of the clinical context, symptoms, signs, and bronchoscopy

16. ARDS: Differential diagnosis
A variety of conditions may present as acute hypoxemic respiratory failure with bilateral alveolar infiltrates and include:
Cardiogenic pulmonary edema
Diffuse alveolar hemorrhage
Idiopathic acute exacerbation of pre-existing interstitial lung disease
Acute eosinophilic pneumonia
Cryptogenic organizing pneumonia
Acute interstitial pneumonia
Rapidly disseminating cancer

17. ARDS: Differential diagnosis
Cardiogenic pulmonary edema:
Distinguishing cardiogenic pulmonary edema from ARDS can be aided by measurement of a brain natriuretic peptide, echocardiography, less often, right heart catheterization.
Acute exacerbation of idiopathic pulmonary fibrosis or other chronic interstitial lung diseases can closely resemble ARDS in both clinical presentation and chest radiographic abnormalities
Diffuse alveolar hemorrhage may be associated with a large, unexplained drop in the hemoglobin concentration and hematocrit.
The hemosiderin-laden macrophages from bronchoalveolar lavage fluid is strongly suggestive of diffuse alveolar hemorrhage.

18. ARDS: Differential diagnosis
Idiopathic acute eosinophilic pneumonia occurs in previously healthy individuals and is characterized by cough, fever, dyspnea, and sometimes chest pain.
Bronchoalveolar lavage specimens always contain a large number of eosinophils, typically 35 to 55 percent of all recovered cells. Peripheral eosinophilia may or may not be present .
Cryptogenic organizing pneumonia (COP) often mimics community-acquired pneumonia with an onset that is heralded by a flu-like illness with fever, malaise, fatigue, and cough.
The diagnosis is made by ruling out infectious causes of pneumonia and documenting typical pathologic changes in tissue obtained by open lung biopsy

19. ARDS: Differential diagnosis
Acute interstitial pneumonia (Hamman-Rich syndrome) is a rare and fulminant form of diffuse lung injury that has a presentation similar to ARDS.
Many consider AIP a subset of idiopathic ARDS since its clinical manifestations are similar and both demonstrate diffuse alveolar damage on histopathology.
The distinguishing characteristic is that ARDS is often associated with a known risk factor, whereas acute interstitial pneumonia is not

20. ARDS: Differential diagnosis
Cancer can disseminate through the lungs so rapidly that the ensuing respiratory failure may be mistaken for ARDS. This is most often due to lymphoma or acute leukemia, but lymphangitic spread of solid tumors occasionally behaves this way. Cytological preparation of bronchoscopic specimens (eg, brushings, lavage) may reveal malignant cells.

21. THANK
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