Partial portal vein ligation is the experimental model most frequently used to study prehepatic portal hypertension. Different systemic and splanchnic biochemical and histological alterations in short-term (28-45 days) and long-term (12-14 months) evolutive phases which has been described in this experimental model suggest the existence of different pathophysiological mechanisms involved in their production. The enteropathy produced could develop in three phases: an early or acute phase with vasomotor hemodynamic alterations (ischemia-reperfusion associated with intestinal hyperemia, edema and oxidative stress); an intermediate phase with immunological alterations (mesenteric lymphadenopathy, increased mucosal infiltration by mast cells and the hepato-intestinal release of pro-and anti-inflammatory mediators); and a late or chronic phase with intestinal remodeling (vascular and epithelial). The alterations which are produced in these three evolutive phases make it possible to propose an inflammatory etiopathogeny for hypertensive portal enteropathy.

Objective The main aim of this study was to describe complications in dogs weighing < 20 kg treated for medial patellar luxation and to determine risk factors associated with these complications. Materials and Methods Medical records were reviewed and cases were grouped based on four techniques of stabilization for the tibial tuberosity transposition (TTT). Variables including animal signalment, clinical presentation, TTT technique, other concurrent surgical techniques and associated complications were investigated. Multiple logistic regression was used to determine the association of the same variables with specific complications such as tibial tuberosity fractures or avulsions, patellar reluxation and implant-related complications. Results Of the 100 procedures performed, 37 suffered a complication. There were no significant differences in the overall complication rate between TTT stabilization techniques. Preservation of the tibial tuberosity distal cortical attachment was associated with a reduced risk of implant-related complications, whereas adding a medial release to the surgical techniques was associated with an increased risk of medial patellar reluxation. The type of trochleoplasty performed did not affect the complication rate. Conclusions In the current study, a high rate of complications was found in dogs < 20 kg undergoing medial patellar luxation surgery. Performing a medial release and preserving the distal cortical attachment of the tibial tuberosity were the only variables associated respectively with an increase and a reduction in the risk of postsurgical complications.

A LC induces significantly increased ROM in lateral bending to the side of the surgery and in total lateral ROM. Extending the LC to a LC-MH does not change the spinal column stability compared to LC alone, while it provides better access to the spinal canal. The LC-H further destabilizes the VMU. The finding of intervertebral collapse following these surgical procedures confirms the importance of the intervertebral disc and articular facet in the maintenance of spatial integrity.

Portal hypertension induces a splanchnic and systemic low-grade inflammatory response that could induce the expression of three phenotypes, named ischemia-reperfusion, leukocytic, and angiogenic phenotypes.During the splanchnic expression of these phenotypes, interstitial edema, increased lymph flow, and lymphangiogenesis are produced in the gastrointestinal tract. Associated liver disease increases intestinal bacterial translocation, splanchnic lymph flow, and induces ascites and hepatorenal syndrome. Extrahepatic cholestasis in the rat allows to study the worsening of the portal hypertensive syndrome when associated with chronic liver disease. The splanchnic interstitium, the mesenteric lymphatics, and the peritoneal mesothelium seem to create an inflammatory pathway that could have a key pathophysiological relevance in the production of the portal hypertension syndrome complications. The hypothetical comparison between the ascitic and the amniotic fluids allows for translational investigation. From a phylogenetic point of view, the ancestral mechanisms for amniotic fluid production were essential for animal survival out of the aquatic environment. However, their hypothetical appearance in the cirrhotic patient is considered pathological since ultimately they lead to ascites development. But, the adult human being would take advantage of the potential beneficial effects of this “amniotic-like fluid” to manage the interstitial fluids without adverse effects when chronic liver disease aggravates.