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

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).

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: 201 - 300 mmHg (≤ 39.9 kPa) Moderate: 101 - 200 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.

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

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.

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

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).

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.

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.

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

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

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.

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.

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).

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

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

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.

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

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

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.

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