Dynamic computed tomographic quantitation of hepatic perfusion in dogs with and without portal vascular anomalies

OBJECTIVE: To compare hepatic, pancreatic, and gastric perfusion on dynamic computed tomography (CT) scans of clinically normal dogs with those of dogs with portal vascular anomalies. SAMPLE POPULATION: Dynamic computed tomography (CT) scans of 10 clinically normal dogs and 21 dogs with portal vascular anomalies. PROCEDURES: Retrospective analysis of dynamic CT scans. Hepatic arterial perfusion, hepatic portal perfusion, total hepatic perfusion, hepatic perfusion index, gastric perfusion, and pancreatic perfusion were calculated from time attenuation curves. RESULTS: Mean +/- hepatic arterial perfusion was significantly higher in affected dogs (0.57 +/- 0.27 mL/min x mL(-1)) than in clinically normal dogs (0.23 +/- 0.11 mL/min x mL(-1)), and hepatic portal perfusion was significantly lower in affected dogs (0.52 +/- 0.47 mL/min x mL(-1)) than in clinically normal dogs (1.08 +/- 0.45 mL/min x mL(-1)). This was reflected in the hepatic perfusion index, which was significantly higher in affected dogs (0.59 +/- 0.34), compared with clinically normal dogs (0.19 +/- 0.07). Gastric perfusion was significantly higher in dogs with portal vascular anomalies (0.72 +/- 0.44 mL/min x mL(-1)) than in clinically normal dogs (0.41 +/- 0.21 mL/min x mL(-1)), but total hepatic perfusion and pancreatic perfusion were not significantly different. Among subgroups, dogs with congenital intrahepatic portosystemic shunts and dogs with arterioportal fistulae had higher hepatic arterial perfusion than did clinically normal dogs. Dogs with congenital intrahepatic portosystemic shunts also had an increase in gastric perfusion and hepatic perfusion index. CONCLUSIONS AND CLINICAL RELEVANCE: Hepatic perfusion variables measured on CT scans revealed differences in hemodynamics between clinically normal dogs and those with portal vascular anomalies.     

Iron Status and Erythrocyte Volume in Dogs With Congenital Portosystemic Vascular Anomalies

Microcytosis, hypochromasia, and low mean corpuscular hemoglobin are frequent hematologic abnormalities in dogs with portosystemic vascular anomalies (PSVA). The relationship of iron status to these abnormalities is unclear. We evaluated iron status and hematologic and biochemical parameters in dogs with congenital PSVA before (25 dogs) and after (11 dogs) partial ligation of the vascular anomaly. Serum iron concentration and total iron binding capacity were subnormal in 56% and 20% of dogs with PSVA, respectively. Transferrin saturation was normal in 68%, decreased in 20%, and increased in 12% of the dogs. Plasma ferritin concentration was either normal (56%) or high (44%), and was not associated with increases in ceruloplasmin concentration. Hepatic stainable iron was increased in 10 of 16 dogs. Mean corpuscular volume (MCV), mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration were decreased in more than 60% of dogs with PSVA. Serum biochemical abnormalities included high bile acid concentration and alanine transaminase (ALT) and alkaline phosphatase (ALP) activities; and low urea, creatinine, cholesterol, and total protein concentrations. Serum iron concentration and clinical status (normal or PSVA) significantly influenced MCV ( P = .003 and P < .001, respectively), whereas age, ceruloplasmin, ferritin, cholesterol, bile acids, and total iron binding capacity did not. Partial ligation of PSVA was associated with resolution of clinical signs and the return to normal of iron status and all clinicopathologic abnormalities, except total fasting bile acid concentrations. These findings indicate that iron status is frequently abnormal in dogs with PSVA and that low serum iron concentration appears to be related to the development of microcytosis. The normalization of iron status and clinicopathologic abnormalities after treatment suggests that they are direct consequences of PSVA.     

IMAGING DIAGNOSIS—PORTAL VEIN APLASIA AND INTERRUPTION OF THE CAUDAL VENA CAVA IN THREE DOGS

Severe portal vascular anomalies have been reported previously accompanying azygos continuation of the caudal vena cava, polysplenia, and situs anomalies in dogs and people. Three dogs with portal vascular anomalies were identified by means of CT angiography as having portal vein aplasia with portal insertion into the caudal vena cava, azygos continuation of the caudal vena cava, and interruption of the pre‐hepatic caudal vena cava. This information confirms that complex embryological defects may occur in patients presenting for congenital portosystemic shunt, and that CT angiography is a non‐invasive method of completely evaluating these potentially non‐surgical portal vascular anomalies.     

Contrast‐enhanced ultrasonography is a feasible technique for quantifying hepatic microvascular perfusion in dogs with extrahepatic congenital portosystemic shunts

Extrahepatic‐congenital portosystemic shunt is a vascular anomaly that connects the portal vein to the systemic circulation and leads to a change in hepatic microvascular perfusion. However, an assessment of hepatic microvascular perfusion is limited by conventional diagnostic modalities. The aim of this prospective, exploratory study was to assess hepatic microvascular perfusion in dogs with extrahepatic‐congenital portosystemic shunt using contrast‐enhanced ultrasonography (CEUS) using perfluorobutane (Sonazoid^®). A total of 17 dogs were included, eight healthy dogs and nine with extrahepatic‐congenital portosystemic shunt. The time‐to‐peak (TTP), rising time (RT), and rising rate (RR) in the hepatic artery, portal vein, and hepatic parenchyma, as well as the portal vein‐to‐hepatic parenchyma transit time (ΔHP‐PV) measured from time‐intensity curve on CEUS were compared between healthy and extrahepatic‐congenital portosystemic shunt dogs. The RT of the hepatic artery in extrahepatic‐congenital portosystemic shunt dogs was significantly earlier than in healthy dogs (P = 0.0153). The TTP and RT of the hepatic parenchyma were significantly earlier in extrahepatic‐congenital portosystemic shunt dogs than in healthy dogs (P = 0.0018 and P = 0.0024, respectively). ΔHP–PV was significantly shorter in extrahepatic‐congenital portosystemic shunt dogs than in healthy dogs (P = 0.0018). CEUS effectively revealed changes in hepatic microvascular perfusion including hepatic artery, portal vein, and hepatic parenchyma simultaneously in extrahepatic‐congenital portosystemic shunt dogs. Rapid hepatic artery and hepatic parenchyma enhancements may reflect a compensatory increase in hepatic artery blood flow (arterialization) caused by a decrease in portal vein blood flow and may be used as an additional diagnostic test to distinguish extrahepatic‐congenital portosystemic shunt dogs from healthy dogs.     

Effect of breed on anatomy of portosystemic shunts resulting from congenital diseases in dogs and cats: a review of 242 cases

OBJECTIVE: To evaluate the effect of species and breed on the anatomy of portosystemic vascular anomalies in dogs and cats. DESIGN: Retrospective study of 233 dogs and nine cats presenting to the University Veterinary Centre, Sydney. METHODS: Case records were evaluated for breed, sex, age, anatomical and histological diagnosis. Cases were included when a portosystemic vascular anomaly resulted from a congenital or developmental abnormality of the liver or portal venous system. RESULTS: Disease conditions included single congenital portosystemic shunt with patent portal vasculature (214 dogs, nine cats), portal vein aplasia (nine dogs), multiple acquired shunts resulting from portal vein hypoplasia (seven dogs), biliary atresia (one dog) and microvascular dysplasia (one dog). One Maltese had a single, congenital shunt and multiple acquired shunts resulting from hepatic cirrhosis. Breeds that were significantly over-represented included the Maltese, Silky Terrier, Australian Cattle Dog, Bichon Frise, Shih Tzu, Miniature Schnauzer, Border Collie, Jack Russell Terrier, Irish Wolfhound and Himalayan cat. Bichon Frise with shunts were significantly more likely to be female than male (12:2, P < 0.001). Two hundred and fourteen dogs (91.4%), and all cats, had shunts that were amenable to attenuation. Inoperable shunts occurred in 19 dogs (8.2%). Fifty six of 61 (92%) operable shunts in large breed dogs were intrahepatic, versus 10/153 (7%) in small breeds (P < 0.0001). Breeds that were not predisposed to portosystemic shunts were significantly more likely to have unusual or inoperable shunts than dogs from predisposed breeds (29% versus 7.6%, P < 0.0001). No significant relationship between breed and shunt type could be determined in cats. CONCLUSION: Breed has a significant influence on shunt anatomy in dogs. Animals presenting with signs of portosystemic shunting may suffer from a wide range of operable or inoperable conditions. Veterinarians should be aware that unusual or inoperable shunts are much more likely to occur in breeds that are not predisposed to congenital portosystemic shunts.     

CONTRAST‐ENHANCED PORTAL MAGNETIC RESONANCE ANGIOGRAPHY IN DOGS WITH SUSPECTED CONGENITAL PORTAL VASCULAR ANOMALIES

Contrast‐enhanced multiphase magnetic resonance angiography (CE‐MRA) was used in 17 dogs with a suspected congenital portal vascular anomaly. Portal vascular anomalies were identified in 16 of the 17 dogs. Eleven had a single intrahepatic portocaval shunt (two central divisional, three right divisional, and six left divisional), one dog had a double intrahepatic portocaval shunt, one dog had a hepatic arteriovenous malformation, one dog had a complex intrahepatic porto‐caval shunt. Two dogs had an extrahepatic portosystemic shunt and no shunt was identified in one dog. Total imaging time was <10 min and image quality was good to excellent in all dogs. Portal CE‐MRA is a feasible, fast and non invasive technique to diagnose portal vascular anomalies in dogs, with a large field‐of‐view and good anatomic depiction of the abnormal vessels. Based on these results, CE‐MRA is an efficient imaging technique for the diagnosis of portal vascular anomalies in dogs.     

ULTRASONOGRAPHIC DIAGNOSIS OF CONGENITAL PORTOSYSTEMIC SHUNTS IN DOGS: RESULTS OF A PROSPECTIVE STUDY

The aims of this study were to determine if accurate diagnosis of congenital portosystemic shunt was possible using two dimensional, grey-scale ultrasonography, duplex-Doppler, and color-flow Doppler ultrasonography in combination, and to determine if dogs with congenital portosystemic shunts have increased or variable mean portal blood flow velocity. Eighty-two dogs with clinical and/or clinicopathologic signs compatible with portosystemic shunting were examined prospectively. Diagnosis of congenital portosystemic shunt was subsequently confirmed in 38 of these dogs using operative mesenteric portography: 14(37%) dogs had an intrahepatic shunt and 24(63%) had an extrahepatic shunt. Ultrasonography had a sensitivity of 95%, specificity of 98%, and accuracy of 94%. Ultrasonographic signs in dogs with congenital portosystemic shunts included small liver, reduced visibility of intrahepatic portal vessels, and anomalous blood vessel draining into the caudal vena cava. Correct determination of intra - versus extrahepatic shunt was made ultrasonographically in 35/38 (92%) dogs. Increased and/or variable portal blood flow velocity was present in 21/30 (70%) dogs with congenital portosystemic shunts. In one dog with an intrahepatic shunt the ultrasonographic diagnosis was based partly on finding increased mean portal blood flow velocity because the shunting vessel was not visible. Detection of the shunting vessel and placement of duplex-Doppler sample volumes were facilitated by use of color-flow Doppler. Two-dimensional, grey-scale ultrasonography alone is sufficient to detect most intrahepatic and extrahepatic shunts; sensitivity is increased by additional use of duplex-Doppler and color-flow Doppler. Increased and/or variable portal blood flow velocity occurs in the majority of dogs with congenital portosystemic shunts.     

Effect of storage on microcytosis observed in dogs with portosystemic vascular anomalies

Microcytosis is a common laboratory finding in dogs with iron deficiency and congenital portosystemic vascular anomalies (PSVA), however artefactual changes due to blood storage may occur which could mask this feature. This study evaluated the effects of storage on microcytosis in dogs with congenital PSVA. Full haematological parameters were measured on the day of sampling and following 24h storage at room temperature, in unaffected dogs (n=13) and in dogs affected with PSVA (n=24). Storage for 24h resulted in significantly higher MCV values in both groups of dogs (P<0.01). The percentage increase in MCV was greater in the control dogs (median 8.07%, range 5.64-9.31%) compared to affected dogs (median 6.05%, range 3.12-15.21%) (P<0.02). Storage of 1ml EDTA blood samples at ambient temperature for 24h prior to analysis, as occurs when samples are posted to external laboratories, will have significant effects on MCV and may mask microcytosis in dogs with PSVA.     

Evaluation of plasma protein C activity for detection of hepatobiliary disease and portosystemic shunting in dogs

OBJECTIVE: To determine the diagnostic value of protein C (PC) for detecting hepatobiliary disease and portosystemic shunting (PSS) in dogs. DESIGN: Prospective study. ANIMALS: 238 clinically ill dogs with (n = 207) and without (31) hepatobiliary disease, including 105 with and 102 without PSS. PROCEDURES: Enrollment required routine hematologic, serum biochemical, and urine tests; measurement of PC activity; and a definitive diagnosis. Total serum bile acids (TSBA) concentration and coagulation status, including antithrombin activity, were determined in most dogs. Dogs were grouped into hepatobiliary and PSS categories. Specificity and sensitivity were calculated by use of a PC cutoff value of 70% activity. RESULTS: Specificity for PC activity and TSBA concentrations was similar (76% and 78%, respectively). Best overall sensitivity was detected with TSBA, but PC activity had high sensitivity for detecting PSS and hepatic failure. Protein C activity in microvascular dysplasia (MVD; PC > or = 70% in 95% of dogs) helped differentiate MVD from portosystemic vascular anomalies (PSVA; PC < 70% in 88% of dogs). A receiver operating characteristic curve (PSVA vs MVD) validated a useful cutoff value of < 70% activity for PC. CONCLUSIONS AND CLINICAL RELEVANCE: Combining PC with routine tests improved recognition of PSS, hepatic failure, and severe hepatobiliary disease and signified a grave prognosis when coupled with hyperbilirubinemia and low antithrombin activity in hepatic failure. Protein C activity can help prioritize tests used to distinguish PSVA from MVD and sensitively reflects improved hepatic-portal perfusion after PSVA ligation.     

Microcytosis and Iron Status in Dogs With Surgically Induced Portosystemic Shunts

Microcytosis is common in dogs with congenital portosystemic shunts (PSS) and acquired liver disease. The objective of this study was to determine if microcytosis could be induced in normal dogs by surgical creation of PSS, and to characterize the changes in hematology and iron status. Hematocrit, mean cell volume, mean cell hemoglobin, and mean cell hemoglobin concentration decreased linearly from 45.5%. 69.1 fL, 22.8 g/dL and 33.1% to 39.5%. 55.9 fL, 17.8 g/dL and 31.9%. respectively, 18 weeks after creation of PSS. The erythrocyte count did not change, but red cell distribution widths indicated a shift to a heterogenous population with decreased volume. Mean cell volume and mean cell hemoglobin decreased rapidly after induction of PSS and were significantly ( P < .05) different from presurgery values within 2 weeks. Serum iron and copper concentrations and total iron binding capacity were decreased in dogs with PSS. Liver iron concentration doubled after creation of PSS, with the majority of stainable iron located in Kupffer cells. The changes in erythrocyte indices and measures of iron status in dogs with surgically induced PSS were similar to those in dogs with congenital PSS. Microcytosis developed rapidly in dogs after induction of PSS. These results indicate that iron deficiency was not the cause of microcytosis in these dogs.     

Transportal Approach for Attenuating Intrahepatic Portosystemic Shunts in Dogs

A novel surgical approach, using portal venotomy during total hepatic vascular occlusion, was used to locate and attenuate congenital intrahepatic portosystemic shunts in nine dogs. Shunt location was consistent with a persistent ductus venosus in only two dogs. In the remaining seven dogs the shunts were window-like orifices arising from either the left (two dogs) or right portal vein branch (five dogs) and communicating with the ipsilateral hepatic vein or caudal vena cava. The transportal approach using total hepatic vascular occlusion consistently provided good access to the portosystemic shunts, including those with window-like communications. A 7 to 16 minute period of total vascular occlusion was well-tolerated hemodynamically, with few intraoperative complications. Intrahepatic shunts were successfully attenuated in eight dogs, while one dog with portal atresia was euthanatized. The postoperative course was complicated by high protein pulmonary edema (one dog), an encapsulated biliary pseudocyst (one dog) and uncontrollable hemorrhage caused by an uncharacterized coagulopathy (one dog). Three dogs required a second operation to further attenuate their shunts. The clinical condition of all seven surviving dogs was improved after surgery.     

Computed tomographic and magnetic resonance imaging features of canine segmental caudal vena cava aplasia

O bjective : To describe the computed tomographic and magnetic resonance imaging features of segmental caudal vena cava aplasia and associated vascular anomalies in dogs.
M ethods : A retrospective study was performed reviewing computed tomographic and magnetic resonance imaging archives of eight institutions for dogs with segmental caudal vena cava aplasia. Inclusion criteria included a computed tomographic or magnetic resonance imaging study and supportive diagnostic and follow-up information. Abdominal vessels were reviewed for size, shape, location and course (including tributaries and branches) and classified as normal, abnormal or shunt vessels.
R esults : Ten dogs with segmental caudal vena cava aplasia were identified. In all dogs, postrenal caval blood was shunted to either a right or a left azygos vein, with seven different angiographic patterns. Affected dogs were predominantly female (70 per cent) and young (mean 2·6 years). Additional portocaval and porto-azygos shunt vessels were identified in two cases each. Computed tomographic angiography and magnetic resonance angiography depicted details of abdominal vessels including thrombus formation in one dog.
C linical S ignificance : Segmental caudal vena cava aplasia is a vascular congenital anomaly in the dog that can be associated with thrombosis and portosystemic shunts. Computed tomographic angiography and magnetic resonance angiography are excellent tools to demonstrate the complex vascular anatomy and to guide treatment planning for portosystemic shunts and thrombolytic therapy.     

A prospective study of basal insulin concentrations in dogs with congenital portosystemic shunts

Objectives : Hypoglycaemia is a common cause of morbidity in dogs with congenital portosystemic shunts but the aetiology is unknown. The hypothesis of this study was that dogs with congenital portosystemic shunts would have significantly higher insulin concentrations than dogs without congenital portosystemic shunts. The main objective of the study was to compare peripheral glucose and insulin concentrations between dogs with congenital portosystemic shunts and dogs without congenital portosystemic shunts. Methods : Peripheral serum insulin and plasma glucose concentrations were measured in dogs with congenital portosystemic shunts and without congenital portosystemic shunts and compared both between groups as well as to reference intervals derived from healthy dogs. Results : Congenital portosystemic shunts were diagnosed in 41 dogs. Forty‐eight dogs hospitalised with other conditions acted as controls. Serum insulin concentrations were mildly elevated (Ä40 μU/mL) in seven dogs and were markedly elevated in two dogs with congenital portosystemic shunts, yet mild hypoglycaemia (3·3 mmol/L) was detected in only one of these dogs. Four dogs with congenital portosystemic shunts showed fasting hypoglycaemia, yet insulin concentrations were within or below the reference interval in three. There was no difference between the median insulin concentration of dogs with congenital portosystemic shunts and without congenital portosystemic shunts. Clinical Significance : Hyperinsulinaemia is infrequently observed in dogs with congenital portosystemic shunts. The aetiology of hypoglycaemia in dogs with congenital portosystemic shunts merits further investigation.     

Post-prandial serum bile acid concentrations and ammonia tolerance in Maltese dogs with and without hepatic vascular anomalies

SUMMARY: Post-prandial serum bile acid concentrations were measured in 200 Maltese dogs in an attempt to identify those with subclinical portosystemic shunts. Five of these were later shown to have hepatic pathology or abnormal liver function. In the other 195 Maltese bile acid concentrations ranged from 1 to 362 μmol.L^-1 (mean ± SD, 70 ±50 μmol.L^-1; median, 65.0 μmol.L^-1). Of these, 79% were above the reference range (0 to 31 μmol.L^-1) established from 23 mixed-breed control dogs. It was therefore not possible to determine the prevalence of subclinical portosystemic shunts on the basis of bile acid determinations.
Further investigation of liver function was performed to investigate why bile acid concentrations were increased in these dogs. Rectal ammonia tolerance tests were normal in 102 of 106 Maltese tested and liver samples (11 dogs) and plasma biochemistry profiles (9 dogs) demonstrated no significant hepatic disease or dysfunction.
Of 2 Maltese with hyperammonaemia after administration of ammonium chloride, one had a large congenital portosystemic shunt that was confirmed at surgery. In the other there were no macroscopic portosystemic communications, but a liver biopsy showed histological changes consistent with microscopic portovascular dysplasia.
Total serum bile acid concentrations were consistently lower when assessed by highperformance liquid chromatography than by an enzymatic spectrophotometric method. This discrepancy was substantially larger in Maltese than in control dogs, suggesting the presence of an additional reacting substance in the serum of Maltese dogs.     

Congenital Interruption of the Portal Vein and Caudal Vena Cava in Dogs: Six Case Reports and a Review of the Literature

Objective —To describe six dogs with congenital abnormalities involving the portal vein, caudal vena cava, or both.
Animals —Six client-owned dogs with congenital interruption of the portal vein or the caudal vena cava, or both.
Methods —Portal vein and caudal vena cava anatomy was evaluated by contrast radiography and visualization at surgery. Vascular casts or plastinated specimens were obtained in three animals.
Results —Portal blood shunted into the caudal vena cava in four dogs and the left hepatic vein in one. Two of these five dogs also had interruption of the caudal vena cava with continuation as azygous vein, as did an additional dog, in which the portal vein was normally formed. Portal vein interruption was present in 5 of 74 (6.8%) dogs with congenital portosystemic shunts evaluated at the Veterinary Teaching Hospital during the study period.
Conclusions —Serious malformations of the abdominal veins were present in more than 1 in 20 dogs with single congenital portosystemic shunts.
Clinical Relevance —Veterinarians involved in diagnosis and surgery for portosystemic shunts should be aware of these potential malformations, and portal vein continuity should be evaluated in all dogs before attempting shunt attenuation.     

Hepatic gene expression and plasma albumin concentration related to outcome after attenuation of a congenital portosystemic shunt in dogs

In dogs with a congenital portosystemic shunt (CPSS), the outcome after CPSS attenuation is difficult to predict but is most likely related to hepatic and vascular proliferation that follows the attenuation. The aim of this study was to evaluate the prognostic value of shunt localization (extrahepatic vs. intrahepatic), plasma albumin concentration and hepatic mRNA expression of 19 genes involved in hepatic and vascular growth. The study population consisted of 48 dogs that were referred for surgical ligation of a single intrahepatic or extrahepatic CPSS. Gene expression was measured in intraoperatively sampled hepatic tissue with quantitative real-time PCR. Albumin, methionine adenosyltransferase 2α (MAT2α) and HGF activator (HGFac) were positively associated with complete recovery after CPSS attenuation using multivariate statistical analyses. Individual outcome could be correctly predicted in 83% of dogs using albumin, MAT2α and HGFac as high or low values compared to cut-off values of 19.5 g/L, 0.457 and 0.974, respectively. These variables predicted outcome after CPSS ligation better than shunt localization or albumin alone. Other evaluated gene products were not correlated with outcome.     

The sonographic search for portosystemic shunts

The diagnostic investigation of portosystemic shunts (PSS) has evolved over the last few decades, helping to understand and identify these vascular anomalies that affect many dogs and cats. Ultrasonography has become an important tool in small animals and high-resolution systems are now widely available. Several sonographic features are observed with the different types of congenital and acquired PSS. A systematic, stepwise approach is described to facilitate ultrasound diagnosis of PSS in small animals.     

Characterization of Hepatoportal Microvascular Dysplasia in a Kindred of Cairn Terriers

Hepatoportal microvascular dysplasia (MVD), a congenital disorder of the hepatic vasculature, is described in a kindred of Cairn Terrier dogs. Cairn Terrier dogs (n = 165) were evaluated using the serum bile acid test. Affected dogs, identified by abnormal fasting or postprandial serum bile acid concentrations, were divided into 2 groups. Group 1 dogs (n = 147) were used for pedigree analysis. Group 2 dogs (n = 18) were characterized on the basis of history, physical examination, clinicopathologic studies, diagnostic imaging of the liver and portal circulation, and hepatic histopathology. Group 2 contained control dogs (n = 2), dogs with hepatoportal MVD (n = 11), and dogs with macroscopic portosystemic vascular anomalies (PVSA) (n = 5). With the exception of high serum bile acid concentrations, dogs with hepatoportal MVD were indistinguishable from control dogs on the basis of history, physical examination, clinicopathologic findings, survey abdominal radiography, abdominal ultrasound, or transcolonic scintigraphy. Contrast portography in dogs with MVD revealed abnormalities of terminal twigs of the portal vasculature with out large intrahepatic or extrahepatic shunting vessels. Histopathologic abnormalities in dogs with hepatoportal MVD were similar to those reported for dogs with PSVA. Pedigree analysis suggested an autosomal inheritance for MVD. Dogs with MVD had high serum bile acid concentrations, abnormal indocyanine green clearance, and hepatic pathology suggestive of PSVA, but they lacked characteristic clinical findings of PSVA. The clinical significance of MVD is unclear. Dogs with MVD were clinically normal when evaluated but long-term follow-up is not yet available. Dogs with hepatoportal MVD should be identified at an early age to avoid confusion in future diagnostic evaluations. J Vet Intern Med 1996:10:219–230. Copyright © 1996 by the American College of Veterinary Internal Medicine .     

Congenital portosystemic shunts in five mature dogs with neurological signs

Congenital portosystemic shunts are a common cause of hepatic encephalopathy and are typically first identified when dogs are <2 years of age. This case series describes five dogs with congenital portosystemic shunts; the dogs were presented for severe encephalopathic signs during middle or old age. Three dogs had portoazygos shunts, and four dogs had multifocal and lateralizing neurological abnormalities, including severe gait abnormalities and vestibular signs. All five dogs responded to medical or surgical treatment, demonstrating that older animals can respond to treatment even after exhibiting severe neurological signs.     

Intrahepatic Portosystemic Venous Anomaly in the Dog Perioperative Management and Complications

Hypotension, hemorrhage, and acute hepatic congestion were common complications during surgical correction of intrahepatic portosystemic venous anomalies in 13 dogs. Acute splanchnic congestion and hyperthermia were the most serious postoperative complications. Three dogs died within 24 hours; 10 dogs are alive and well after 12 to 46 months.