BILIARY DUCTAL PLATE MALFORMATION WITH SECONDARY PORTAL HYPERTENSION AND MULTIPLE ACQUIRED SHUNTS IN A LITTER OF AMUR TIGERS (PANTHERA TIGRIS ALTAICA).

Congenital abnormalities in tigers (Panthera tigris) are infrequently reported but have included ectrodactyly, cataracts, and vestibular disease. Primary hepatic disease has been documented in multiple nondomestic felid species but is considered uncommon in tigers. To the authors' knowledge, there are no previous reports of congenital abnormalities of the liver in tigers. In May 2022, two male Amur tiger cubs (Panthera tigris altaica) were born at a zoological institution via cesarean section to address dystocia, following the natural birth of a female cub. Between two and six months of age, all three cubs developed progressive lethargy, inappetence, and neurological signs consistent with hepatic encephalopathy, including obtundation and ataxia. In all three cases, serum biochemical values revealed progressive, marked elevations in hepatic enzyme levels with reduction in hepatic synthetic products (albumin, urea, cholesterol). Computed tomographic imaging showed a large cluster of aberrant tortuous vessels craniomedial to the left kidney in all three tigers, consistent with acquired extrahepatic portosystemic shunts. Histologic examination of the livers identified biliary ductal plate malformations. This report details the presentation, clinical findings, diagnoses, and therapeutic interventions attempted in three Amur tiger cubs with biliary ductal plate malformation and subsequent portal hypertension with multiple acquired portosystemic shunts, an unusual abnormality not previously reported in non-domestic felids.

Copper-associated chronic hepatitis in Cavalier King Charles spaniels.

BACKGROUND: Copper-associated chronic hepatitis (CuCH) is poorly characterised in Cavalier King Charles spaniels (CKCS). METHODS: Hepatic copper accumulation was qualitatively and quantitatively assessed, and blood samples were used for genetic testing to screen for known CuCH-associated genetic variants. RESULTS: The study included 13 CKCS with CuCH and eight unaffected controls. Increased transaminase activities, elevated biliary enzyme concentrations and portal hypertension were documented in 100%, 73% and 38% of dogs with CuCH, respectively. Five dogs had three or more abnormalities in measures of liver function. All 11 dogs with CuCh that underwent genetic testing were homozygous negative for the COMMD1 deletion and ATP7A variant but homozygous positive (n = 7) or heterozygous (n = 4) for the ATP7B variant. Liver histology often demonstrated marked architectural distortion by severe, bridging fibrosis and regenerative nodules with lymphoplasmacytic inflammation. Centrilobular copper accumulation characterised early cases with minimal fibrosis. When fibrosis was significant, copper was often differentially concentrated within regenerative nodules. Chelation therapy resolved laboratory derangements and portal hypertension in five of seven dogs. Of the 7 non-surviving dogs with CuCH, 6 had not received chelation therapy. LIMITATIONS: Limitations include a small cohort size and the lack of pedigree analyses to corroborate heritability. CONCLUSIONS: CuCH should be considered in CKCS with suspected liver disease. Long-term prognosis seems favourable in dogs receiving chelation therapy, notwithstanding the presence of previously reported negative prognostic markers.

Repeated specific canine pancreatic lipase measurements do not identify multiple acquired portosystemic shunts in dogs after extrahepatic portosystemic shunt attenuation.

BACKGROUND: In dogs with portal hypertension (PH), spec cPL is suggested to be increased despite normal pancreatic histology. After attenuation of congenital extrahepatic portosystemic shunts (cEHPSS), multiple acquired portosystemic shunt (MAPSS) can develop as consequence of sustained PH. Presence of MAPSS affects future therapeutic options and prognosis. OBJECTIVE: Evaluate if spec cPL concentrations increase postoperatively in dogs that develop MAPSS and can thus serve as an indicator of PH. ANIMALS: Twenty-four dogs with cEHPSS. METHODS: Dogs classified according to surgical outcome after cEHPSS attenuation (8 with MAPSS [group M], 9 with closed cEHPSS [group C] and 7 with patent blood flow through the original cEHPSS, without evidence of MAPSS [group P]). Spec cPL was measured in preoperative samples (T0), 4 days (T1) and 1 (T2) and 3- to 6-months (T3) after surgery. RESULTS: Spec cPL was within reference interval (<200 µg/L) at all timepoints except at T1. At T1, 2 dogs in group M (321 and >2000 µg/L) and also 1 in group C (688 µg/L) and 1 in group P (839 µg/L) had increased spec cPL concentrations. No differences in spec cPL concentrations between groups or changes over time were identified. CONCLUSIONS AND CLINICAL IMPORTANCE: Spec cPL is not consistently increased in dogs that develop MAPSS after cEHPSS attenuation and has no potential as a biomarker for the identification of MAPSS after cEHPSS attenuation.

Perforated duodenal ulcer in a dog with gallbladder agenesis.

Background: Duodenal ulceration (DU) in dogs derives from different causes but has never previously been related to gallbladder agenesis (GA). GA is a rare congenital disorder in dogs and is considered a predisposing factor for DU in humans. Case Description: A 5-month-old intact female Maltese was presented for acute vomiting and diarrhea. Abdominal ultrasound suggested duodenal perforation and absence of the gallbladder. Exploratory laparotomy was performed to treat the perforation and confirmed GA. Hepatic ductal plate malformation (DPM) was histologically diagnosed in liver biopsy, but no signs of liver dysfunction were detected by blood work at first admission. Two months later, the dog developed signs of portal hypertension and medical treatment was started. However, the clinical condition gradually worsened until liver failure and the dog was euthanized 8 months after surgery. Necropsy confirmed hepatic abnormalities. Conclusion: This report describes a case of DU associated with GA and DPM in a dog. As in humans, GA may represent a hepatobiliary disease predisposing to gastroduodenal ulcerations.

Prognostic indicators in dogs with intra-hepatic portal hypertension.

Objectives: The primary goals of this retrospective study were to describe a population of dogs with portal hypertension secondary to liver disease, and to assess whether prognosis could be inferred from historical, clinical, and clinicopathological data. Animals and procedures: Dogs (N = 76) diagnosed with intrahepatic portal hypertension between 2011 and 2020 were included; dogs with known congenital hepatic anomalies were excluded. Effect on survival was assessed using univariable and multivariable Cox proportional hazards models for historical, clinical, and clinicopathological variables. Results: Dogs survived for a median of 14 d (range: 0 to 2028 d), with 31.6% being euthanized within 2 d of diagnosis and 23.7% surviving longer than 2 mo. Presence of jaundice and duration of clinical signs, expressed in days, were significantly associated with outcome in the univariable analysis (HR = 1.846, 95% CI: 1.094 to 3.117, P = 0.02; HR = 0.995, 95% CI: 0.990 to 1.000, P = 0.033, respectively). However, only presence of jaundice was significantly associated with increased hazard of death in the multivariable analysis. Conclusion: Results of this study show that portal hypertension is associated with a poor prognosis; however, some dogs can show prolonged survival. Clinical relevance: Clinical data can guide decision-making for clinicians and owners.

Indicateurs pronostiques chez les chiens atteints d'hypertension portale intra-hépatique. Objectifs: Les principaux objectifs de cette étude rétrospective étaient de décrire une population de chiens souffrant d'hypertension portale secondaire à une maladie hépatique et d'évaluer si le pronostic pouvait être déduit à partir de données historiques, cliniques et clinicopathologiques. Animaux et procédures: Les chiens (N = 76) diagnostiqués avec une hypertension portale intrahépatique entre 2011 et 2020 ont été inclus; les chiens présentant des anomalies hépatiques congénitales connues ont été exclus. L'effet sur la survie a été évalué à l'aide de modèles de risques proportionnels de Cox univariés et multivariés pour les variables historiques, cliniques et clinicopathologiques. Résultats: Les chiens ont survécu pendant une durée médiane de 14 jours (intervalle : 0 à 2028 jours), 31,6 % ayant été euthanasiés dans les 2 jours suivant le diagnostic et 23,7 % ayant survécu plus de 2 mois. La présence d'ictère et la durée des signes cliniques, exprimées en jours, étaient significativement associées au résultat de l'analyse univariée (HR = 1,846, IC à 95 % : 1,094 à 3,117, P = 0,02; HR = 0,995, IC à 95 % : 0,990 à 1,000, P = 0,033, respectivement). Cependant, seule la présence d'ictère était significativement associée à un risque accru de décès dans l'analyse multivariée. Conclusion: Les résultats de cette étude montrent que l'hypertension portale est associée à un mauvais pronostic; cependant, certains chiens peuvent montrer une survie prolongée. Pertinence clinique: Les données cliniques peuvent guider la prise de décision des cliniciens et des propriétaires.(Traduit par Dr Serge Messier).

Congenital porto-pulmonary shunt in a dog.

Background: Congenital extra-hepatic porto-systemic shunts (CEPS) are a non-rare vascular anomaly observed in dogs, most commonly in small and toy pure breeds. Computed tomographic angiography (CTA) examination is considered the gold standard imaging modality for the diagnosis of anomalous vascular connections. Case Description: An anomalous congenital porto-pulmonary shunt was incidentally diagnosed in a 5-year-old French Bulldog. The anomalous vessel originated from the ventral aspect of the portal vein and went cranially towards the esophageal hiatus, entering the lobar vein of the caudal left pulmonary lobe. The dog did not show any significant clinical or computed tomography angiography-perceived hepatic abnormalities and no signs of portal hypertension were evidenced. No case of porto-pulmonary shunt in veterinary medicine have ever been reported, while in humans it was rarely described secondarily to portal hypertension, severe hepatopathies or complex cardiac malformations. Conclusion: CTA must be considered the best imaging modality for the diagnosis also of unusual CEPS and in the author's opinion the congenital porto-pulmonary shunt described in the patient was of little or no clinical relevance.

Treatment of portal vein thrombosis using vascular access port implantation in a Dalmatian dog: A case report.

Background: Portal vein thrombosis is a disease with potentially deleterious outcomes including portal vein hypertension and intestinal infarction. The factors contributing is various; however, dogs with with acute portal vein thrombosis or multiple thromboses are less likely to survive. Therefore, acute development of portal hypertension has a requires an immediate treatment. Case Description: A 10-year-old Dalmatian was referred for syncope and azotemia, hyperammonemia. After each examinations including computed tomography scan, we diagnosed with acute portal vein thrombosis with unknown cause. A portal vein port was inserted to prevent and control the portal vein thrombus. The port was placed in abdomen subcutaneously after the position of the catheter were stabilized. Low-molecular-weight heparin was injected from the port to manage thrombosis after the operation. This case responded well to this treatment. Syncope and azotemia, hyperammonemia resolved and no relapse of thrombosis was found 6 months after the operation. Conclusion: Implantable vascular access port is a drug delivery system with the advantage of dealing with treatment-resistant acute portal vein thrombosis.

Laparoscopic portosystemic shunt attenuation in 20 dogs (2018-2021).

OBJECTIVE: To describe the technique, complications, and outcome of laparoscopic portosystemic shunt attenuation (LPSSA) in dogs. STUDY DESIGN: Retrospective study. ANIMALS: Twenty client-owned dogs. METHODS: Medical records were searched for dogs with a single congenital extrahepatic portosystemic shunt (CEPSS) that was treated with LPSSA. Signalment, clinical signs, CEPSS location, diagnostic imaging, laparoscopic approach, operative technique, complications, and clinical outcome were reviewed. RESULTS: Fourteen dogs with CEPSS located in the epiploic foramen had a right (13/14) or left (1/14) paramedian approach. In 6 dogs a CEPSS was not located in the epiploic foramen, and a left paramedian approach was used. A 3 or 4-port technique was used in 7 and 13 dogs, respectively. A thin film band was used for CEPSS attenuation in all dogs. The median operating time for LPSSA was 62 min (range 27-98 min). Intraoperative complications requiring conversion to an open technique occurred in 5 dogs. Mild perioperative self-limiting portal hypertension occurred in 3 dogs, while severe portal hypertension with surgical revision occurred in 1 case. The complications were resolved, and all dogs had a good outcome. CONCLUSION: Laparoscopic portosystemic shunt attenuation can be performed in dogs, in particular for a CEPSS located in the epiploic foramen using a right paramedian approach. For CEPSS not located in the epiploic foramen, a left paramedian approach is recommended. Conversion to open celiotomy was required in around a third of cases. CLINICAL SIGNIFICANCE: Laparoscopic attenuation of CEPSSs can be performed in dogs and has a good clinical outcome, particularly for CEPSS located in the epiploic foramen.

Esophageal varices in dogs: A retrospective case series.

BACKGROUND: Esophageal varices (EV) are abnormally dilated veins in the esophagus caused by alterations of blood flow or pressure. Esophageal variceal hemorrhage is a major complication of hepatic disease in humans, but a lack of information exists regarding associated adverse events in dogs. OBJECTIVE: To describe the clinical manifestations and associated etiologies and outcomes of dogs with EV. ANIMALS: Twenty-five client-owned dogs with EV diagnosed via computed tomography (CT), endoscopy, or fluoroscopy. METHODS: Retrospective case series. Cases were identified by review of the hospital imaging records database between 2010 and 2020. Signalment, clinical signs, and outcomes were documented. When present, additional collateral vasculature was also recorded. Cases were subcategorized into suspected etiology based upon the anatomic location or absence of an attributable underlying disease process, as well as the direction of blood flow. RESULTS: Twenty-four of 25 cases were identified via CT, with a prevalence of 0.012% (24/1950 total studies). Presenting clinical signs were nonspecific, and more likely because of the underlying cause as opposed to complications secondary to EV themselves. Etiologic anatomic locations were similar in occurrence between the abdomen (N = 14) and thorax (N = 11). All cases with an abdominal etiologic location had presumed or confirmed portal hypertension and 9/11 cases with a thoracic etiologic location had pulmonary, caval, or systemic hypertension. No cases died or were euthanized as a direct result of EV or associated hemorrhage. CONCLUSIONS AND CLINICAL IMPORTANCE: Esophageal varices are rarely reported in dogs and commonly identified concurrently with portal, pulmonary, and caval hypertension. Hemorrhage is not a common clinical manifestation of EV.

Increased canine pancreatic lipase immunoreactivity (cPLI) and 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6'-methylresorufin) ester (DGGR) lipase in dogs with evidence of portal hypertension and normal pancreatic histology: a pilot study.

The clinical presentations of both liver disease and pancreatitis are nonspecific and overlapping, which may cause difficulty in diagnosis. In our retrospective pilot study, we assessed whether dogs with evidence of portal hypertension and absence of pancreatitis on pancreatic histology have increases in canine pancreatic lipase immunoreactivity (cPLI) and 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6'-methylresorufin) ester (DGGR) lipase. We included dogs that had been presented between 2008 and 2019 if they had normal pancreatic histology, histologically confirmed hepatopathy, and if canine pancreas-specific lipase (Spec cPL; Idexx) or DGGR lipase had been measured. Only dogs with portal hypertension were included. Six dogs fulfilled the inclusion criteria. Four of 6 and 2 of 6 dogs had Spec cPL and DGGR lipase exceeding the upper reference limit, respectively. From the 4 dogs with increased Spec cPL, 2 had concentrations of 200-400 µg/L and 2 had concentrations ≥ 400 µg/L. Our results suggest that canine portal hypertension might lead to increased Spec cPL and DGGR lipase values in the absence of pancreatitis on histology. Until more evidence in a larger number of dogs with portal hypertension is available, both tests should be interpreted cautiously in the presence of portal hypertension.

Vasoactive intestinal peptide in canine portosystemic shunt in the absence of portal hypertension.

Background: The congenital portosystemic shunt (PSS) is a common vascular anomaly in dogs. Vasoactive intestinal peptide (VIP) is produced in various organs (including the small intestine, large intestine, and pancreas), leading to abdominal vasodilation, increased blood flow, increased pancreatic blood flow, and promotion of pancreatic endocrine and exocrine secretions. However, there have been no reports on the concentration of VIP in the portal and peripheral veins in canine PSS. Aim: The aim of this pilot study was to evaluate whether dogs with PSS have a different VIP concentration in their portal system in general. Methods: Six dogs with an extrahepatic portosplenic shunt were included in the study. Blood samples were taken from the saphenous and portal veins during PSS ligation surgery with an amerid constrictor, to evaluate and compare the VIP concentration in both samples. VIP was measured using a commercial canine enzyme-linked immunosorbent assay kit. Results: The breeds included Mongrels (n = 2), Norfolk Terriers (n = 1), Miniature Dachshunds (n = 1), and Maltese (n = 2), and their ages were 9.3 ± 6.5 months; the bodyweight was 3.3 ± 0.8 kg. The concentration of VIP in the saphenous vein was 17.75 ± 13.88 pg/ml; on the contrary, the concentration of VIP in the portal vein was 29.7 ± 20.29 pg/ml. There was no significant difference in the VIP concentration between veins. Conclusion: There was no difference in the VIP concentration between the portal and saphenous veins, suggesting a non-association between VIP and the PSS, in the absence of portal hypertension.

CT angiography identifies collaterals in dogs with splenic vein obstruction and presumed regional splenic vein hypertension.

Occlusion of the splenic vein, without occlusion of the portal vein, can lead to a localized, regional splenic hypertension, referred as sinistral or left-sided portal hypertension in the human radiology literature. In people, may cause gastrointestinal hemorrhages from the esophageal and gastric varices and the primary pathology usually includes pancreatitis and pancreatic neoplasms. The final diagnosis of localized splenic hypertension necessitates accompanying normal liver functions and a patent extrahepatic portal vein. Following obstruction, the resultant elevated splenic bed venous pressure causes formation of collateral routes, the extent of which depends upon the level and degree of obstruction. In this retrospective descriptive study, authors assessed the collateral pathways in dogs with isolated splenic vein occlusion and possible regional splenic vein hypertension. Out of the 46 patients initially recruited, 25 were excluded due to the presence of concomitant portal thrombosis and direct/indirect CT signs of portal hypertension. The remaining 21 dogs had clinicopathological tests suggesting normal liver function. The causes of obstruction identified included splenic pedicle torsion, tumoral splenic vein invasion, and splenic vein thrombosis. Four of 21 dogs with isolated splenic vein obstruction showed collateral pathways through the left gastroepiploic vein (4/4), left gastric vein (2/4), and splenogonadal vein (1/4). The diagnosis of isolated, regional splenic hypertension should be based on clinical, biochemical, and radiological evaluation. Computed tomography is an excellent tool to assess the collateral patterns and to determine the underlying cause.

Assessment of a biofluid mechanics-based model for calculating portal pressure in canines.

BACKGROUND: Portal hypertension is a severe complication caused by various chronic liver diseases. The standard methods for detecting portal hypertension (hepatic venous pressure gradient and free portal pressure) are available in only a few hospitals due to their technical difficulty and invasiveness; thus, non-invasive measuring methods are needed. This study aimed to establish and assess a novel model to calculate free portal pressure based on biofluid mechanics. RESULT: Comparison of each dog's virtual and actual free portal pressure showed that a biofluid mechanics-based model could accurately predict free portal pressure (mean difference: -0.220, 95% CI: - 0.738 to 0.298; upper limit of agreement: 2.24, 95% CI: 1.34 to 3.14; lower limit of agreement: -2.68, 95% CI: - 3.58 to - 1.78; intraclass correlation coefficient: 0.98, 95% CI: 0.96 to 0.99; concordance correlation coefficient: 0.97, 95% CI: 0.93 to 0.99) and had a high AUC (0.984, 95% CI: 0.834 to 1.000), sensitivity (92.3, 95% CI: 64.0 to 99.8), specificity (91.7, 95% CI: 61.5 to 99.8), positive likelihood ratio (11.1, 95% CI: 1.7 to 72.8), and low negative likelihood ratio (0.08, 95% CI: 0.01 to 0.6) for detecting portal hypertension. CONCLUSIONS: Our study suggests that the biofluid mechanics-based model was able to accurately predict free portal pressure and detect portal hypertension in canines. With further research and validation, this model might be applicable for calculating human portal pressure, detecting portal hypertensive patients, and evaluating disease progression and treatment efficacy.

Plasma renin activity and aldosterone concentration in dogs with acquired portosystemic collaterals.

BACKGROUND: The renin-angiotensin-aldosterone system (RAAS) is activated in humans with portal hypertension (PH) associated with liver disease. However, involvement of RAAS in dogs with intrahepatic PH is not clear. OBJECTIVE: To measure plasma renin activity (PRA) and plasma aldosterone concentration (PAC) in dogs with PH (chronic hepatitis [CH] and primary hypoplasia of the portal vein [PHPV]), dogs with extrahepatic congenital portosystemic shunt (EH-CPSS), and healthy dogs and to determine whether the RAAS is activated in dogs with PH. ANIMALS: Twenty-seven dogs with acquired portosystemic collaterals (APSCs; 15 dogs with CH, 12 dogs with PHPV), 9 dogs with EH-CPSS, and 10 healthy dogs. METHODS: Retrospective study. Plasma renin activity and PAC were measured by radioimmunoassay. RESULTS: Plasma renin activity was significantly higher in the CH group (median, 4.4 ng/mL/h) than in the EH-CPSS (median, 1.0 ng/mL/h; P < .01) and the healthy (median, 1.1 ng/mL/h; P < .01) groups. No significant differences were found between the PHPV group (median, 2.2 ng/mL/h) and other groups. Plasma aldosterone concentration was significantly higher in the CH (median, 111.0 pg/mL) and PHPV (median, 89.5 pg/mL) groups than in the EH-CPSS (median, 1.0 pg/mL; P < .001, P < .01, respectively) and healthy (median, 14.5 pg/mL; P < .001, P < .05, respectively) groups. CONCLUSIONS AND CLINICAL IMPORTANCE: Activation of the RAAS contributes to the pathophysiology of intrahepatic PH in dogs, suggesting that spironolactone may not only be effective for the treatment of ascites but also for the suppression of intrahepatic PH.

CT features of extrahepatic arterioportal fistula in two cats.

Two cats presented with large volume ascites and the cause was suspected to be portal hypertension. On contrast CT they both showed enhancement of the main portal vein during the arterial phase and an anomalous connection between the celiac artery and extrahepatic portal vasculature, prompting a diagnosis of extrahepatic arterioportal fistula. An extrahepatic arterioportal fistula is a connection between any artery and the portal vein outside the liver and, to our knowledge, this is the first report in cats.

Canine and feline abdominal arterioportal communications can be classified based on branching patterns in computed tomographic angiography.

Arterioportal vascular anomalies are communications between the splanchnic arteries and the portal system that represent a rare cause of presinusoidal portal hypertension in small animals. There is little information concerning the imaging findings of arterioportal communications in small animals and no classification could be found for radiologists and surgeons. The aims of this retrospective descriptive multicentric study were to describe the computed tomographic characteristics of arterioportal communications in a group of cats and dogs, and to propose a classification based on computed tomography (CT) angiographic anatomy. Computed tomography databases from multiple veterinary hospitals were searched for cats and dogs with a diagnosis of arterioportal communication. A total of 36 animals (33 dogs, three cats) met the inclusion criteria. There were 32 intrahepatic arterioportal malformations and four extrahepatic fistulae. The intrahepatic arterioportal malformations were classified as right divisional (11/32) and left divisional (21/32), and the left divisional were subclassified as left medial (16/21) and left lateral (4/21). One patient showed multiple intrahepatic arterioportal communications with concomitant left medial and left lateral conformations. Two patients with intrahepatic arteriovenous malformation showed concomitant congenital intrahepatic shunts. The proposed anatomical classification based on CT angiography could allow veterinary radiologists to have a more systematic approach and help improve the radiologist-surgeon communication.

Haematology and coagulation profiles in cats with congenital portosystemic shunts.

Objectives The objectives of this study were, first, to report the haematological parameters and coagulation times for cats with a congenital portosystemic shunt (CPSS) and the influence of surgical shunt attenuation on these parameters; and, second, to identify any association between prolongation in coagulation profiles and incidence of perioperative haemorrhage. Methods This was a retrospective clinical study using client-owned cats with a CPSS. Signalment, shunt type (extra- or intrahepatic), degree of shunt attenuation (complete or partial), haematological parameters, prothrombin time (PT) and activated partial thromboplastin time (aPTT) test results, and occurrence of any perioperative clinical bleeding complications were recorded for cats undergoing surgical treatment of a CPSS at the Royal Veterinary College, UK, between 1994 and 2011. Results Forty-two cats were included. Thirty-six (85.7%) had an extrahepatic CPSS and six (14.3%) had an intrahepatic CPSS. Preoperatively, mean cell volume (MCV) and mean cell haemoglobin (MCH) were below the reference interval (RI) in 32 (76.2%) and 31 (73.8%) cats, respectively. Red blood cell count and mean cell haemoglobin concentration (MCHC) were above the RI in 10 (23.8%) and eight (19.1%) cats, respectively. Postoperatively, there were significant increases in haematocrit ( P = 0.044), MCV ( P = 0.008) and MCH ( P = 0.002). Despite the significant increase in MCV postoperatively, the median MCV postoperatively was below the RI, indicating persistence of microcytosis. Preoperatively, PT was above the upper RI in 14 cats (87.5%), and aPTT was above the upper RI in 11 cats (68.8%). No cat demonstrated a perioperative clinical bleeding complication. Conclusions and relevance Cats with a CPSS are likely to present with a microcytosis, but rarely present with anaemia, leukocytosis or thrombocytopenia. Surgical attenuation of the CPSS results in a significant increase in the HCT and MCV. Coagulation profiles in cats with a CPSS are likely to be prolonged, irrespective of shunt type, but do not appear to be associated with an increased risk of clinical bleeding.

Endovascular treatment of a high-flow hepatic arteriovenous malformation with secondary portal hypertension in a dog.

CASE DESCRIPTION A 17-month-old neutered female Labrador Retriever with a 3- to 4-month history of abdominal distention was referred for evaluation and treatment. CLINICAL FINDINGS Evaluation of a peritoneal fluid specimen collected by the referring veterinarian indicated a pure transudate. At admission, transabdominal ultrasonography revealed microhepatica, dilation of the intrahepatic and mesenteric vasculature, peritoneal effusion, and multiple aberrant blood vessels. A large, high-flow hepatic arteriovenous malformation (HAVM) with secondary portal hypertension, peritoneal effusion, multiple acquired portosystemic shunts, and microhepatica was evident on CT angiography. TREATMENT AND OUTCOME Transfemoral hepatic arteriography and staged coil and glue (n-butyl cyanoacrylate) embolization of the complex arteriovenous malformation nidus and central main left hepatic artery resulted in ablation of the lesion, restoration of arterial blood flow to the contralateral hepatic lobes, and resolution of the peritoneal effusion. The dog remained without clinical signs of hepatic disease until it was euthanized 5 months after treatment for an unrelated condition. CLINICAL RELEVANCE Successful endovascular management of a HAVM was accomplished by means of coil and glue embolization in the patient of this report. Dogs with comparable HAVMs may benefit from similar minimally invasive treatment.

An Unusual Case of Portal Hypertension Secondary to Primary Hypoplasia of the Portal Vein.

Primary hypoplasia of the portal vein with secondary portal hypertension and acquired portosystemic collateral circulation is infrequently reported in the veterinary literature. Diagnosis of this condition requires documentation of abnormal hepatocellular function, the lack of intrahepatic or extrahepatic macroscopic congenital portosystemic shunts, and liver histopathology demonstrating portal hypoperfusion in the absence of hepatic inflammation or nodular regeneration. Due to a perceived poor prognosis, many patients with this condition are euthanized; however, those that are spared can be medically managed, in some cases for years. This case report describes the diagnosis and management of a patient with primary hypoplasia of the portal vein and secondary portal hypertension that presented with the severe but typical clinical manifestations of ascites and hepatic encephalopathy, normal liver enzyme concentrations, and normal serum bile acid concentrations.

Portal Vein/Aorta Ratio in Dogs with Acquired Portosystemic Collaterals.

BACKGROUND: The portal vein (PV) diameter increases in humans with portal hypertension (PH). However, there is no evidence of PV enlargement in dogs with PH. OBJECTIVES: To measure the PV-to-aorta (PV/Ao) ratio in dogs with PH (chronic hepatitis [CH], primary hypoplasia of the PV [PHPV]), in dogs with extrahepatic congenital portosystemic shunt (EH-CPSS), and in healthy dogs, and to evaluate the relationship between PV/Ao ratio and splenic pulp pressure (SPP). ANIMALS: Twenty-five dogs with acquired portosystemic collaterals (APSCs; 15 with CH, 10 with PHPV), 32 dogs with EH-CPSS, and 20 healthy dogs. METHODS: Retrospective study. The PV/Ao ratio was calculated with images obtained by computed tomography. SPP was measured at the time of liver biopsy in 45 dogs. RESULTS: Median PV/Ao ratio was similar between dogs with CH (1.35, range 1.05-2.01) and healthy dogs (0.95, 0.80-1.15), but differed significantly between the CH group and both the PHPV (0.40, 0.24-0.67) and EH-CPSS groups (0.30, 0.11-0.64) (P < .001). The PV/Ao ratio was significantly lower in the PHPV group than in healthy dogs (P < .05). It also correlated positively with SPP (rs = 0.71; P < .001). However, there was no intragroup correlation between SPP and the PV/Ao ratio in any group. CONCLUSIONS AND CLINICAL IMPORTANCE: The PV/Ao ratio can be evaluated in dogs with APSCs on computed tomography. Further studies are needed to examine the relationship between SPP and the PV/Ao ratio in larger groups of dogs with PH and to determine its clinical relevance.