Abstract
(1) Background: Systemic inflammatory response syndrome (SIRS) can occur due to a large number of traumatic or non-traumatic diseases. Hyperbaric oxygen therapy (HBOT) may be used as a main or adjuvant treatment for inflammation, leading to the main aim of this study, which was to verify the applicability of HBOT as a safe and tolerable tool in SIRS-positive dogs. (2) Methods: This prospective cohort study included 49 dogs who showed two or more parameters of SIRS, divided into the Traumatic Study Group (n = 32) and the Non-Traumatic Study Group (n = 17). All dogs were submitted to HBOT for 60–90 min sessions, with 2.4–2.8 ATA. (3) Results: This study revealed that 73.5% (36/49) of dogs showed improvement, and the minimum number of HBOT sessions was two, with a mean of 12.73. The number of days between diagnosis and the beginning of HBOT showed statistical significance (p = 0.031) relative to the clinical outcome. No dogs showed any major side effects. (4) Conclusions: We concluded that HBOT may be safe and tolerable for SIRS-positive dogs, and that it should be applied as early as possible.
Highlights
The development of systemic inflammatory response syndrome (SIRS) can be due to a large number of diseases that evoke activation of the inflammatory cascade, such as sepsis, heatstroke, pancreatitis, immunomediated diseases, cancer, severe trauma, or burns [1,2,3].Ischemia is a frequent complication of traumatic events, and, when reperfusion occurs, an ischemia–reperfusion injury might develop
The study sample was divided between the Traumatic Study Group (TSG) and Non-Traumatic Study Group (NTSG) groups and, when the Shapiro–Wilk test was applied, a p value of >0.05 was obtained in both groups and both categories
In the NTSG, there were no signs of possible sepsis, with negative quick Sepsis Related Organ Failure Assessment (qSOFA) and normal lactate levels, systolic arterial pressure, and modified Glasgow scale values
Summary
Ischemia is a frequent complication of traumatic events, and, when reperfusion occurs, an ischemia–reperfusion injury might develop. This complication is caused by the quick release of toxins and free radicals, which were previously restrained by the lack of perfusion in the ischemic area, into the bloodstream. This is an oxidative injury that is further exacerbated by the release of inflammatory mediators, arterial vasoconstriction, thrombosis, and leucocyte adhesion to the endothelium [4,5]. Metabolic acidosis can occur, due to the metabolic residues withheld in the cells
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