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ARDS

Dr Muhammed Aslam

Objectives• Introduction• Definition• Etiology / Risk Factors• Pathology & Pathogenesis• Clinical presentation• Workup• Management of ALI/ARDS• Conclusion

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.

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.)

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 = ALIPaO2/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

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

The Berlin DefinitionJAMA. 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.

The Berlin Definitioncontinue….• 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.

ARDS Severity PaO2/FiO2 *** Mortality• Mild 200 – 300 27%• Moderate 100 – 200 32%• Severe < 100 45%

• *** on ventilator with PEEP ≥5 cm H2O

Aetiology

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

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

• Over 60 possible causes have been identified but the four most frequent causes include:

• Sepsis (Most common cause )• Aspiration• Pneumonia• Severe Trauma

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

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.

• 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.

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

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

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.

• 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.

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

NORMAL ALVEOLUS

Type I cell

EndothelialCell

RBC’s

Capillary

Alveolarmacrophage

Type IIcell

ACUTE PHASE OF ARDS

Type I cell

EndothelialCell

RBC’s

Capillary

Alveolarmacrophage

Type IIcell

Neutrophils

• Three distinct stages (or phases) of the syndrome including:

• Exudative stage

• Proliferative (or fibroproliferative) stage

• Fibrotic stage

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.

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.

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.

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

• 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.

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

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

Arterial blood gas analysis

• PaO2/FiO2 Ratio

ARDS Severity PaO2/FiO2 • Mild 200 – 300 • Moderate 100 – 200 • Severe < 100

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

To exclude cardiogenic pulmonary edema• Echocardiogram -left ventricular ejection

fraction, wall motion, and valvular abnormalities

• plasma B-type natriuretic peptide (BNP) value.

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

• 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,

MANAGEMENT

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

• 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

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

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”)

Tidal Volumes Over The Years…..

1990’s 2010’s

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.

• 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

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.

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


• 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


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.


• Inhaled NitricOxide• Inhaled prostacyclin• Tracheal Gas Insufflation• Extracorporeal Membrane Oxygenation (ECMO) or

ExtracorporealCO2 Removal (ECCO2R)


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.

“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)

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

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