BACKGROUND:Congenital portosystemic shunt (cPSS) is one of the most common congenital disorders diagnosed in dogs. Hepatic encephalopathy (HE) is a frequent complication in dogs with a cPSS and is a major cause of morbidity and mortality. Despite HE been a major cause of morbidity in dogs with a cPSS, little is known about the cellular changes that occur in the central nervous system of dogs with a cPSS.OBJECTIVES:The objective of this study was to characterise the histological changes in the cerebral cortex and cerebellum of dogs with cPSS with particular emphasis on astrocyte morphology.METHODS:Eight dogs with a confirmed cPSS were included in the study.RESULTS:Six dogs had substantial numbers of Alzheimer type II astrocytes and all cases had increased immunoreactivity for glial fibrillary acidic protein in the cerebral cortex, even if there were minimal other morphological changes.CONCLUSIONS:This study demonstrates that dogs with a cPSS have marked cellular changes in the cerebral cortex and cerebellum. The cellular changes that occur in the cerebral cortex and cerebellum of dogs with spontaneously arising HE are similar to changes which occur in humans with HE, further validating dogs with a cPSS as a good model for human HE.

Equine pregnancy failure can occur throughout gestation, with causes varying by region. In the UK, umbilical cord torsion (UCT) accounted for 44.0% of pregnancy loss (PL) cases occurring after day 70 of gestation and submitted to a diagnostic laboratory. Limited reports on the features of UCT are available. This study aimed to compare the gross and histological features in PLs resulting from UCT to those with no UC pathology. Cases submitted to a UK diagnostic laboratory diagnosed with definitive or suspected UCT (n=81) were compared to PLs diagnosed as not associated with umbilical cord (UC) pathology (nUCT) (n=33). Logistic regression analysis was used for categorical data and Mann-Whitney U tests for non-parametric continuous data. Median gestation age at loss was significantly lower in the UCT (215 days, inter-quartile range (IQR) 32) group compared to nUCT (325 days, IQR 56), p<0.005, with 83.5% of the UCT abortions occurring prior to day 240 of gestation compared to 10.3% of the nUCT cases. The median fetal weight in the UCT group was significantly lighter than the nUCT group, 11.0kg (IQR 6.4) and 45.4kg (IQR 22.5) respectively, remaining after adjustment for gestational age (p<0.005). The UCT group had a significantly longer median total UC length (UCL) (79cm, IQR 19, p<0.001) and amniotic UCL (45cm, IQR 14, p<0.001) but not allantoic UCL (p=0.32) compared tothe nUCT group (total UCL 61cm, IQR 22 and amniotic UCL 27.5cm, IQR 13). A 7.3-fold (95% confidence interval (CI) 2.9-18.2) increase in the risk of UCT diagnosis was identified when the amniotic:allantoic UCL ratio was >1. There was no significant difference in the fetal sex ratio between the two groups (p=0.79). Seven gross features were associated with UCT diagnosis (p<0.05), with reddening of the chorioallantois leading to the greatest increase in the odds of UCT diagnosis (OR 17.4, 95% CI 5.7, 53.4). Histological assessment of the chorioallantois in a subset of cases (46 UCT and 31 nUCT) identified three features associated with UCT diagnosis: autolysis, villous mineralisation and villous karyorrhexis (p<0.001). No UCT cases (0/46) exhibited a significant inflammatory infiltrate in the chorioallantois, compared to 9/31 cases of nUCT. The presence of karyorrhexis and mineralisation likely reflects ischaemic injury resulting from malperfusion of the chorion, in the case of UCT, as a response to episodes of venous stasis following increased vascular resistance associated with the significant increase in UCL and/or vascular obstruction. Collectively, this suggests a more chronic pathophysiology involving lengthening of the amniotic, not allantoic, UC. Identification of these features enables evidence-based refinement of diagnostic criteria for UCT, which can now undergo consultation to reach a universally accepted consensus.