Acute Respiratory Distress Syndrome (Ards)

Key Features

Essentials of Diagnosis

• 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

General Considerations

• 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)

Clinical Findings

Symptoms

• 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

Pathophysiology

• 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

Diagnosis

• 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

Laboratory Findings

• 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

Imaging

• Phase 1

  • Normal radiograph

• Phase 2

  • Patchy alveolar infiltrates

  • Normal heart size

• Phase 3

  • Diffuse alveolar ...