Acute respiratory distress syndrome in dogs and cats: a review of clinical findings and pathophysiology

Department of Veterinary Medicine and Surgery, College of Veterinary Medicine, University of Missouri, Columbia, MO
Journal of Veterinary Emergency and Critical Care 11/2007; 17(4):340 - 347. DOI:10.1111/j.1476-4431.2007.00247.x

ABSTRACT Objective: To review the clinical and pathophysiologic aspects of acute respiratory distress syndrome (ARDS) in dogs and cats.Data sources: Data from human and veterinary literature were reviewed through Medline and CAB as well as manual search of references listed in articles pertaining to acute lung injury (ALI)/ARDS.Human data synthesis: Since the term ARDS was first coined in 1967, there has been a abundance of literature pertaining to this devastating syndrome in human medicine. More complete understanding of the complex interactions between inflammatory cells, soluble mediators (e.g., tumor necrosis factor, interleukin (IL)-6, IL-8, platelet activating factor) and the clinical patient has provided for timely recognition and mechanistically based protective strategies decreasing morbidity and mortality in human patients with ARDS.Veterinary data synthesis: Although little is known, ARDS is becoming a more commonly recognized sequela in small animals. Initial case reports and retrospective studies have provided basic clinical characterization of ARDS in dogs and cats. Additionally, information from experimental models has expanded our understanding of the inflammatory mechanisms involved. It appears that the inflammatory processes and pathologic changes associated with ARDS are similar in dogs, cats, and humans.Conclusions: Unfortunately, current mortality rates for ARDS in small animals are close to 100%. As our capability to treat patients with advanced life-threatening disease increases, it is vital that we develop a familiarity with the pathogenesis of ARDS. Understanding the complex inflammatory interactions is essential for determining effective preventative and management strategies as well as designing novel therapies for veterinary patients.

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    ABSTRACT: Cytauxzoonosis, caused by Cytauxzoon felis, is a regionally common, often fatal tick-borne disease primarily affecting the domestic cat. Retrospective analysis of case records from January 1995 to June 2005 identified 148 domestic cats diagnosed with cytauxzoonosis, having suitable archived lung sections. Lung sections were examined and graded on relevant parameters, the chief purpose of which was to characterize the pulmonary lesion of fatal feline cytauxzoonosis. Parameters were scored 0 to 3 for no lesion, mild, moderate, and severe, respectively. Evaluated parameters included the presence of interstitial pneumonia, increases in number of alveolar macrophages, degree of intra-alveolar hemorrhage, neutrophils infiltrating peribronchial and septal interstitium, and degree of vascular occlusion. Overall, interstitial pneumonia was moderate (1.72 +/- 0.65); alveolar macrophage numbers were mild (1.20 +/- 0.60); and intra-alveolar hemorrhage was mild (0.78 +/- 0.75). Neutrophil infiltrates were moderate (1.89 +/- 0.76), and vascular occlusion was moderate to severe (2.26 +/- 0.61). Pulmonary edema was common; its scoring was incorporated into the assessment for interstitial pneumonia. Interestingly, a thrombus was detected in the lung of 1 cat. The current understanding of the pathogenesis of cytauxzoonosis focuses on vascular occlusion by macrophages distended by megaschizont parasite stages within liver, spleen, and lung. These findings corroborate the current understanding yet shed light on the possibility that macrophage activation and inflammatory mediators lead to an interstitial pneumonic process characterized by neutrophilic infiltrates and pulmonary edema. These characterized lesions are likely correlative with the respiratory distress seen in affected cats.
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  • Journal of Veterinary Emergency and Critical Care. 11/2007; 17(4):329 - 332.

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