Introduction

• First described in human literature in 1967.
• Described in veterinary literature in 1978.

Pathogenesis

Etiology

• Multifactorial etiologies in nature, including primary lung injury:
  • Aspiration pneumonitis.
  • Bacterial pneumonia.
  • Pulmonary contusion secondary to:
    • Trauma Thorax: trauma.
    • Smoke Smoke inhalation.
    • Chemical inhalation.
    • Near-drowning.
    • Pulmonary oxygen toxicity.
• Indirect or secondary causes of acute lung injury and ARDS include any process that results in systemic inflammation, including:
  • Sepsis Shock: septic.
  • Pancreatitis.
  • Shock.
  • Trauma.
  • Parvoviral enteritis Canine parvovirus.
  • Organ torsion.
  • Paraquat intoxication Paraquat poisoning.

Predisposing factors

General

• Many patients have more than one predisposing factor when they develop ARDS.
• Primary lung injury:
  • Pulmonary injury secondary to trauma.
  • Bacterial pneumonia.
  • Aspiration pneumonitis.
  • Smoke inhalation.
  • Chemical inhalation.
  • Near-drowning.
  • Oxygen toxicity.
  • Fat embolism.
  • Non cardiogenic pulmonary edema:
    • Seizures Seizures.
    • Asphyxiation.
  • Upper airway obstruction.
  • Strangulation.
  • Head trauma.
• Secondary lung injury:
  • Sepsis Shock: septic.
    • Pyometra Pyometra.
• Pancreatitis.
• Heat-induced illness.
• Shock.
• Trauma.
• Paraquat intoxication Paraquat poisoning.
• Multiple transfusions.
• Cardiopulmonary bypass surgery.

Pathophysiology

• Pathogenesis of ARDS is very complex. Progresses from an early stage (known as acute lung injury) to ARDS. Late in the course of disease, pulmonary fibrosis occurs.
• Direct injury to the pulmonary vascular endothelium or indirect injury associated with an overabundance of inflammatory cytokines, activated neutrophils Hematology: neutrophil, macrophages Hematology: monocyte, platelets Hematology: platelet count and complement.
• Inflammatory mediators including tumor necrosis factor-alpha, interleukin-1, interleukin-6, interleukin-8 are all important in mediating pulmonary inflammation observed in ARDS.
• Influx of neutrophils into the lungs occurs. Once the neutrophils become activated, cellular release of proteases and lipid peroxidation occurs.
• Breakdown of cell membrane arachidonic acid then occurs. Arachidonic acid is metabolized by the cyclooxygenase, lipooxygenase, and cytochrome P450 enzyme pathways to produce prostaglandins, prostacycline, leukotrienes and oxygen-derived free-radical species.
• These mediators perpetuate inflammation.
• Activated macrophages, too, produce inflammatory cytokines that contribute to inflammation.
• Platelets become activated and aggregate, leading to the formation of pulmonary microemboli. This contributes to ventilation-perfusion mismatch Ventilation perfusion mismatching and hypoxia.
• Inflammatory cytokines and oxygen-derived free-radical species damage the vascular endothelium of the lung capillaries, leading to vascular leakage and leakage of proteinaceous fluid into the alveoli.
• Additionally, type II pneumocytes are destroyed and surfactant becomes depleted, leading to atelectasis. Both lead to patchy interstitial to alveolar pulmonary infiltrates and worsens ventilation-perfusion mismatch and hypoxemia.
• Later in the course of disease, pulmonary fibroblast proliferation contributes to pulmonary fibrosis.

Timecourse

• ARDS typically occurs within 24-72 hours of any process that leads to systemic inflammation (SIRS).

Diagnosis

Treatment

Prevention

Outcomes