Acute Respiratory Distress Syndrome

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Acute Respiratory Distress Syndrome:

Ahad Aftab Khan Lodhi , MD Acute Respiratory Distress Syndrome




A.K.A. Adult Respiratory Distress Syndrome Da Nang Lung Transfusion Lung Post Perfusion Lung Shock Lung Traumatic Wet Lung


Acute respiratory distress Cyanosis refractory to oxygen therapy Decreased lung compliance Diffuse infiltrates on chest radiograph Difficulties: lacks specific criteria controversy over incidence and mortality ORIGINAL DEFINITION


1988: four-point lung injury score Level of PEEP PaO 2 / FiO 2 ratio Static lung compliance Degree of chest infiltrates 1994: consensus conference simplified the definition REVISION OF DEFINITIONS

The 1994 NAECCDefinition:

Acute onset may follow catastrophic event Bilateral infiltrates on chest radiograph PAWP < 18 mm Hg Two categories: Acute Lung Injury - PaO 2 /FiO 2 ratio < 300 ARDS - PaO 2 /FiO 2 ratio < 200 The 1994 NAECCDefinition

PowerPoint Presentation:

ARDS Acute PaO2/FiO2 < 200 B/l interstitial /alveolar infiltrates PCWP <18mmHg Acute < 300mmHg Same Same ALI

PowerPoint Presentation:

The 1994 NAECC Definition Limitations Descriptive definition - Permits inclusion of a multiplicity of clinical entities ranging from autoimmune disorders to direct and indirect Pulmonary injury Does not address the cause of lung injury Does not provide guidelines on how to define acute The radiological criteria are not sufficiently specific Does not account for the level of PEEP used, which affects the Pao 2 /Fio 2 ratio Does not specify the presence of nonpulmonary organ system dysfunction at the time of diagnosis Does not include the different specific mechanistic pathways involved in producing lung injury

PowerPoint Presentation:

The 1998 NAECC Updated Recommendations The collection of epidemiologic data should be based on the 1994 NAECC definitions. The severity of ALI/ARDS should be assessed by the Lung Injury Score (LIS) or by the APACHE III or SAPS II scoring systems. The factors that affect prognosis should be taken into account. The most important of these are incorporated into the GOCA stratification system. It will be also useful to record: Information relating to etiology (at a minimum, direct or indirect cause) Mortality,including cause of death,and whether death was associated with withdrawal of care Presence of failure of other organs and other time-dependent covariates Follow-up information, including recovery of lung function and quality of life



Natural history of ards:

Natural history of ards 3 phases - exudative (0-7 d) - proliferative ( 7-21 d) - fibrotic ( > 21 days)


Acute, exudative phase rapid onset of respiratory failure after trigger diffuse alveolar damage with inflammatory cell infiltration hyaline membrane formation capillary injury protein-rich edema fluid in alveoli disruption of alveolar epithelium STAGES


Subacute, Proliferative phase: persistent hypoxemia development of hypercarbia fibrosing alveolitis further decrease in pulmonary compliance pulmonary hypertension STAGES


Chronic phase obliteration of alveolar and bronchiolar spaces and pulmonary capillaries Recovery phase gradual resolution of hypoxemia improved lung compliance resolution of radiographic abnormalities STAGES




Inciting event Inflammatory mediators Damage to microvascular endothelium Damage to alveolar epithelium Increased alveolar permeability results in alveolar edema fluid accumulation PATHOGENESIS

Clinical Disorders Associated with the Development of ALI/ARDS :

Clinical Disorders Associated with the Development of ALI/ARDS


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


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


Target organ injury from host’s inflammatory response and uncontrolled liberation of inflammatory mediators Localized manifestation of SIRS Neutrophils and macrophages play major roles Complement activation Cytokines: TNF- a , IL-1 b , IL-6 Platelet activation factor Eicosanoids: prostacyclin, leukotrienes, thromboxane Free radicals Nitric oxide PATHOGENESIS


Abnormalities of gas exchange Oxygen delivery and consumption Cardiopulmonary interactions Multiple organ involvement PATHOPHYSIOLOGY


Hypoxemia: HALLMARK of ARDS Increased capillary permeability Interstitial and alveolar exudate Surfactant damage Decreased FRC Diffusion defect and right to left shunt ABNORMALITIES OF GAS EXCHANGE


Pathologic flow dependency Uncoupling of oxidative dependency Oxygen utilization by non-ATP producing oxidase systems Increased diffusion distance for O 2 between capillary and alveolus OXYGEN DELIVERY & CONSUMPTION


A = Pulmonary hypertension resulting in increased RV afterload B = Application of high PEEP resulting in decreased preload A+B = Decreased cardiac output CARDIOPULMONARY INTERACTIONS

Clinical Risk Factors Predictive of a Poor Outcome :

Clinical Risk Factors Predictive of a Poor Outcome

Lab investigations:

Lab investigations Routine blood counts RFT CXR ABG CT chest BNP 2D Echo BAL PCWP

How to determine ARDS by CXR:

How to determine ARDS by CXR Can be difficult to do. Should always try to make the diagnosis in light of the clinical picture . Need to determine Cardiogenic vs. Non-cardiogenic edema.

PowerPoint Presentation:

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.

Cardiogenic v/s non cardiogenic edema:

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


ARDS early late

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

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RESPIRATORY SUPPORT Conventional mechanical ventilation Newer modalities: High frequency ventilation ECMO Innovative strategies Nitric oxide Liquid ventilation Exogenous surfactant


Monitoring: Respiratory Hemodynamic Metabolic Infections Fluids/electrolytes MANAGEMENT

Therapy- goals:

Therapy- goals Treatment of underlying cause Cardio-pulmonary support Specific therapy targeted at lung injury Supportive therapy.

Spontaneously Breathing Patient:

Spontaneously Breathing Patient In the early stages of ARDS the hypoxia may be corrected by 40 to 60% inspired oxygen . If the patient is well oxygenated on <= 60 % inspired oxygen and apparently stable without CO 2 retention then ward monitoring may be feasible but close observation( 15 to 30 Min), continuous oximetry, and regular blood gases are required

Indication for mechanical ventilation:

Indication for mechanical ventilation Inadequate oxygenation ( PaO2- < 60 with FiO2 >=0.6) Rising or elevated PaCO2 ( > 50mmHg) Clinical signs of incipient respiratory failure

Mechanical Ventilation:

Mechanical Ventilation The Aims are to increase PaO2 while minimizing the risk of further lung injury (ventilator induced lung injury)

ARDSNet Ventilator protocol:

ARDSNet Ventilator protocol

Ards net protocol -weaning:

Ards net protocol -weaning Spontaneous breathing trial daily PaO2/FiO2 less than previous day Systolic BP > 90 without vasopressors No neuromuscular blockade 2 hr trial- with T piece with 1-5cm water CPAP. ABG,RR,SPO2 monitoring If tolerated for 30 mt,consider extubation


EVIDENCE BASED RECOMMENDATIONS FOR ARDS THERAPY TREATMENT MECHANICAL VENTILATION Low tidal volume Minimize LAFP High PEEP Prone position Recruitment maneuvers High frequency ventilation Glucocorticoids Sufactant replacement,inhaled NO,others RECOMMENDATIONS A B C C C D D D

Management: Reducing Ventilator-Induced Lung Injury:

Management: Reducing Ventilator-Induced Lung Injury Low tidal volume mechanical ventilation In ARDS there is a large amount of poorly compliant (i.e. non-ventilating) lung and a small amount of healthy, compliant lung tissue. Large tidal volume ventilation can lead to over-inflation of the healthy lung tissue resulting in ventilator-induced lung injury of that healthy tissue. PEEP Setting a PEEP prevents further lung injury due to shear forces by keeping airways patent during expiration

ARDS network clinical trials:

ARDS network clinical trials High TV vs low TV (12ml/kg vs 6ml/kg) - 861 pts - mortality rate 39.2 % vs 31% High PEEP vs low PEEP 13cm H20 vs 8 cm H20 –NO difference Amato etal- optimal PEEP- 15cm H20

PowerPoint Presentation:

Inverse ratio ventilation - reduce peak airway pressure - I: E – 1:1 & 4:1 - severe hypoxemic resp.failure Permissive hypercapnea - controlled hypoventilation - PaCO2 upto 55mmhg - pH upto 7.25 Proning

Other methods:

Other methods High flow ventilation ECMO Partial fluid ventilation (PLV)

Extra corporeal membrane oxygenation (ECMO):

Extra corporeal membrane oxygenation (ECMO)


Management Fluids – - conservative management - normal or low LAFP - reduce icu stay,duration of ventilation Steroids - Meduri et al study - methyprednisolone-2mg/kg & taper to .5-1mg/kg in 1-2wk

Treatment of sepsis:

Treatment of sepsis Empirical antibiotics Culture sensitivity & change antibiotics Avoid nephrotoxic drug Enteral feeding

Other treatment modalities:

Other treatment modalities NO Ketoconazole Albuterol Pentoxyphylline NSAIDS N-acetyl cysteine


Prognosis Mortality ranges-26 %-44% Risk factors- - advanced age - CKD,CLD - Chronic immunosuppression - chronic alcohol abuse ARDS from direct lung injury has double mortality

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