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Key Features

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Essentials of Diagnosis
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  • Severe form of lung injury characterized by hypoxemia, bilateral pulmonary infiltrates, and no clinical evidence of left atrial hypertension

  • Can arise as a consequence of either direct pulmonary injury or systemic conditions that are nonpulmonary in origin

  • Lung protective mechanical ventilation and careful fluid management are crucial to good outcomes in ARDS patients

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General Considerations
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  • Direct lung injury risk factors include

    • Pneumonia

    • Aspiration of gastric contents

    • Inhalation injury

    • Pulmonary contusion

    • Hydrocarbon ingestion or aspiration

    • Near-drowning

  • Systemic conditions that are nonpulmonary in origin

    • Sepsis

    • Shock

    • Burns

    • Trauma

    • Fat embolism

    • Drug overdoses (eg, aspirin, opioids, barbiturates, tricyclic antidepressants)

    • Transfusion of blood products

    • Pancreatitis

  • Can be divided roughly into four clinical phases

    • Phase 1 (early changes)

    • Phase 2 (onset of parenchymal changes)

    • Phase 3 (acute respiratory failure with progression; 2–10 days after lung injury)

    • Phase 4 (pulmonary fibrosis, pneumonia with progression; > 10 days after lung injury)

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Clinical Findings

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Symptoms
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  • Phase 1

    • Dyspnea

    • Tachypnea

    • Normal chest examination

  • Phase 2

    • Dyspnea

    • Tachypnea

    • Cyanosis

    • Tachycardia

    • Coarse rales

  • Phase 3

    • Tachypnea

    • Tachycardia

    • Sepsis syndrome

    • Signs of consolidation

    • Diffuse rhonchi

  • Phase 4

    • Symptoms of phases 1–3

    • Recurrent sepsis

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Pathophysiology
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  • Phase 1

    • Neutrophil sequestration

    • No clear tissue damage

  • Phase 2

    • Neutrophil infiltration

    • Vascular congestion

    • Increased lung permeability

    • Pulmonary edema

    • Fibrin strands

    • Platelet clumps

    • Type 1 epithelial cell damage

  • Phase 3

    • Increased interstitial and alveolar inflammatory exudate with neutrophils and mononuclear cells

    • Type II cell proliferation

    • Beginning fibroblast proliferation

    • Thromboembolic occlusion

  • Phase 4

    • Type II cell hyperplasia

    • Interstitial thickening

    • Infiltration of lymphocytes, macrophages, fibroblasts

    • Loculated pneumonia or interstitial fibrosis

    • Medial thickening and remodeling of arterioles

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Diagnosis

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  • Consensus diagnostic criteria include

    • Acute onset

    • Bilateral pulmonary infiltrates on chest radiograph

    • No clinical evidence of left atrial hypertension

    • Severe hypoxemia in which the ratio of the arterial oxygen level (PaO2) to inspired oxygen concentration (FIO2) is ≤ 300 while receiving a PEEP of at least 5 cm H2O via mechanical ventilation

      • Mild ARDS: PaO2:FIO2 ratio is between 200 and 300

      • Moderate ARDS: PaO2:FIO2 ratio is between 100 and 200

      • Severe ARDS: PaO2:FIO2 ratio is under 100

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Laboratory Findings
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  • Phase 1

    • Mild pulmonary hypertension

    • Normoxemic or mild hypoxemia

    • Hypercapnia

  • Phase 2

    • Moderate to severe hypoxemia

    • Increasing shunt

    • Decreased lung compliance

    • Pulmonary hypertension

    • Normal wedge pressure

  • Phase 3

    • Worsening of shunt fraction

    • Further decrease in compliance

    • Increase minute ventilation

    • Impaired oxygen extraction

  • Phase 4

    • Phase 3 changes persist

    • Recurrent pneumonia

    • Progressive lung restriction

    • Impaired tissue oxygenation

    • Impaired oxygen extraction

    • Multiorgan system failure

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Imaging
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  • Phase 1

    • Normal radiograph

  • Phase 2

    • Patchy alveolar infiltrates

    • Normal heart size

  • Phase 3

    • Diffuse alveolar infiltrates

    • Air bronchograms

    • Decreased lung volume

    • Normal heart size

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