ISSN 2398-2950      

Acute Respiratory Distress Syndrome (ARDS)

ffelis

Synonym(s): shock lung, traumatic wet lung, adult hyaline membrane disease, capillary leak syndrome


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:
  • Indirect or secondary causes of acute lung injury and ARDS include any process that results in systemic inflammation, including:

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:
    • Upper airway obstruction.
    • Strangulation.
    • Head trauma.
  • Secondary lung injury:
  • 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

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Carpenter D H Jr., Macintire D K & Tyler J W (2001) Acute lung injury and acute respiratory distress syndrome. Comp Contin Edu Pract Vet 23 (8), 712-725 VetMedResource.
  • Mueller E R (2001) Suggested strategies for ventilatory management of veterinary patients with acute respiratory distress syndrome. J Vet Emerg Crit Care 11 (3), 191-197 VetMedResource.
  • Parent C, King L G, Walker L M et al (1996) Clinical and clinicopathological findings in dogs with acute respiratory distress syndrome: 19 cases. J Am Vet Med Assoc 208 (9), 1419-1427 PubMed.
  • Parent C, King L G, Van Winkle T J et al (1996) Respiratory function and treatment in dogs with acute respiratory distress syndrome: 19 cases (1985-1993). J Am Vet Med Assoc 208 (9), 1428 -1433 PubMed.
  • López A, Lane I F & Hanna P (1995) Adult respiratory distress syndrome in a dog with necrotizing pancreatitisCan Vet J 36 (4), 240-241 PubMed.
  • Frevert C W & Warner A E (1992) Respiratory distress resulting from acute lung injury in the veterinary patient. J Vet Int Med 6 (3), 154-165 PubMed.
  • Orsher A N & Kolata R J (1992) Acute respiratory distress syndrome case report and literature review. J Am Anim Hosp Assoc 18 (1), 41-46 AGRIS FAO.
  • Turk J, Miller M, Brown T et al (1990) Coliform septicemia and pulmonary disease associated with canine parvoviral enteritis: 88 cases (1987-1988). J Am Vet Med Assoc 196 (5), 771-773 PubMed.

Other sources of information

  • King L G and Waddell L S (2002) Acute Respiratory Distress Syndrome. In: The Veterinary ICU Book. Eds W E Wingfield and M Raffee. Teton New Media, Jackson Hole, WY. pp 582-589.

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