Evaluation of serum bile acid concentrations for the diagnosis of portosystemic venous anomalies in the dog and cat

The serum concentration of bile acids was measured in dogs and cats with portosystemic venous anomalies (PSVA). In 14 dogs, the mean serum bile acid concentration after 12 hours of fasting was 61.7 +/- 68.7 mumol/L (normal, 2.3 +/- 0.4 mumol/L (SEM) and when measured 2 hours after a meal in 15 dogs was 229.9 +/- 87.7 mumol/L (normal, 8.3 +/- 2.2 mumol/L). The fasting serum bile acid concentration was within the normal range in 5 of 14 dogs. The postprandial concentration was determined in 3 of the 5 and in each case increased more than tenfold above the fasting value. The mean fasting serum bile acid concentration in 4 cats was 24.4 +/- 10.1 mumol/L (normal, 1.7 +/- 0.3 mumol/L) and in 2 of the cats increased to a mean of 120.6 mumol/L (normal, 8.3 +/- 0.8 mumol/L) 2 hours after feeding. The bile acid values in patients with PSVA were correlated with values for blood ammonia content, sulfobromophthalein (BSP) retention, and results of conventional tests of hepatic function. Bile acid concentrations were more sensitive than abnormalities in serum enzyme activities or BSP retention and equal in sensitivity to the ammonia tolerance test in detecting hepatobiliary insufficiency. Bile acid measurements were accomplished with less inconvenience to the patient and clinician, than tests of BSP excretion or ammonia tolerance. Used in combination with conventional laboratory tests for hepatic disease, pre- and postprandial serum bile acid concentrations appear to be a sensitive and specific indicator of hepatobiliary dysfunction of value in the diagnosis of PSVA in the dog and cat.     

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.     

Bile acid concentrations in the diagnosis of hepatobiliary disease in the dog

The clinical usefulness of measuring serum bile acid concentrations as a diagnostic test for hepatobiliary disease, was examined in 150 dogs that were suspected of having hepatic disease. Serum values of total bilirubin (TB), alkaline phosphatase (ALP), alanine transaminase (ALT), and albumin were also measured. Fasting serum bile acid (FSBA) values were determined, using a solid-phase radioimmunoassay for total conjugated bile acids or a direct enzymatic spectrophotometric method. A definitive diagnosis was established by histologic examination of the liver. On the basis of histologic findings, dogs were assigned to groups (1 to 8, respectively) including: extrahepatic bile duct obstruction, cirrhosis, portal systemic vascular anastomosis (PSVA), hepatic necrosis, intrahepatic cholestasis, steroid hepatopathy, neoplasia, and secondary disease. Dogs in group 8 had no morphologic evidence of hepatobiliary disease or had mild hepatic lesions. Test efficacies of FSBA, TB, ALP, ALT, and albumin were expressed using 4 indices: sensitivity, specificity, and positive-predictive and negative-predictive values. The diagnostic efficacy of FSBA was examined alone and in combinations with the other tests. There was wide overlapping of FSBA values among dogs in groups 1 to 7, and there was wide overlapping of ALT and ALP values among dogs in all groups. The specificity of FSBA for the diagnosis of liver disease exceeded 90% at values greater than or equal to 30 mumol/L and reached 100% at greater than or equal to 50 mumol/L. Individual liver tests with the best sensitivity for each group were:FSBA and ALP for extrahepatic bile duct obstruction; FSBA for cirrhosis and PSVA; ALT for hepatic necrosis; and ALP for intrahepatic cholestasis, steroid hepatopathy, and neoplasia. Combinations of tests with the best sensitivity for each group were: FSBA + ALP for extrahepatic bile duct obstruction; FSBA + ALT for cirrhosis and PSVA; FSBA + ALT and TB + ALT for hepatic necrosis; and FSBA + ALP for intrahepatic cholestasis, steroid hepatopathy, and neoplasia. Individual tests had the best sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Use of pulmonary hydrogen gas excretion to detect carbohydrate malabsorption in dogs

Pulmonary H2 excretion was measured in 10 healthy dogs, in 6 dogs with pancreatic exocrine insufficiency, and in 6 dogs with chronic small intestinal disease. Concentration of expired H2 in fasted healthy dogs was 0.9 +/- 0.1 ppm (mean +/- SEM) and peak H2 concentration of 1.4 +/- 0.2 ppm was detected up to 8 hours after feeding. Dogs with pancreatic exocrine insufficiency had fasting expired H2 concentrations of 3.3 +/- 0.9 ppm, which increased to a mean peak H2 concentration of 28.8 +/- 2.0 ppm 6.5 hours after feeding. Following xylose administration, expired H2 concentrations increased from fasting concentrations of 3.6 +/- 0.9 ppm to peak at 19.0 +/- 2.0 ppm in 1.5 hours. Blood xylose concentrations were diagnostic for carbohydrate malabsorption in 4 of 6 dogs with pancreatic exocrine insufficiency. Plasma p-aminobenzoic acid concentration identified bentiromide maldigestion in all dogs with pancreatic exocrine insufficiency. In 3 pancreatic exocrine insufficient dogs tested, pancreatic enzyme replacement therapy partially corrected carbohydrate malabsorption. Fasting expired H2 concentration was 5.3 +/- 1.3 ppm in dogs with chronic small intestinal disease and increased to a peak H2 of 72.2 +/- 18.0 ppm 7 hours after feeding. Following administration of xylose to dogs with chronic small intestinal disease, fasting expired H2 concentration increased from 3.0 +/- 1.0 ppm to a peak of 35.5 +/- 7.2 ppm at 2 hours. Blood xylose concentration was abnormal in only 2 of 6 dogs with chronic small intestinal disease. Results of these studies indicate that expired H2 analysis can identify carbohydrate malabsorption in dogs with pancreatic exocrine insufficiency or chronic small intestinal disease, and that pulmonary H2 testing is more sensitive than xylose absorption testing for the identification of carbohydrate malabsorption.     

The utility of uric acid assay in dogs as an indicator of functional hepatic mass

Uric acid was used as a test for liver disease before the advent of enzymology. Three old studies criticised uric acid as a test of liver function. Uric acid, as an end-product of purine metabolism in the liver, deserved re-evaluation as a liver function test. Serum totalbile acids are widely accepted as the most reliable liver function test. This study compared the ability of serum uric acid concentration to assess liver function with that of serum pre-prandial bile acids in dogs. In addition, due to the renal excretion of uric acid the 2 assays were also compared in a renal disease group. Using a control group of healthy dogs, a group of dogs with congenital vascular liver disease, a group of dogs with non-vascular parenchymal liver diseases and a renal disease group, the ability of uric acid and pre-prandial bile acids was compared to detect reduced functional hepatic mass overall and in the vascular or parenchymal liver disease groups separately. Sensitivities, specificities and predictive value parameters were calculated for each test. The medians of uric acid concentration did not differ significantly between any of the groups, whereas pre-prandial bile acids medians were significantly higher in the liver disease groups compared with the normal and renal disease group of dogs. The sensitivity of uric acid in detecting liver disease overall was 65% while the specificity of uric acid in detecting liver disease overall was 59%. The sensitivity and specificity of uric acid in detecting congenital vascular liver disease was 68% and 59%, respectively. The sensitivity and specificity of uric acid in detecting parenchymal liver disease was 63% and 60%, respectively. The overall positive and negative predictive values for uric acid in detecting liver disease were poor and the data in this study indicated uric acid to be an unreliable test of liver function. In dogs suffering from renal compromise serum uric acid concentrations may increase into the abnormal range due to its renal route of excretion.     

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 .     

Endotoxin Concentrations Measured by a Chromogenic Assay in Portal and Peripheral Venous Blood in Ten Dogs With Portosystemic Shunts

A chromogenic Limulus amebocyte lysate assay was used to measure portal and peripheral venous endotoxin concentrations in ten medically managed dogs undergoing surgery for correction of a single extrahepatic portosystemic shunt. In all dogs, both peripheral and portal venous blood samples were obtained at the time of surgical manipulation of the anomalous vessel. In six dogs, peripheral venous samples were obtained an average of 8.0 months after surgery. Five physically normal dogs without biochemical or histologic evidence of liver disease served as controls. Data analysis failed to demonstrate significant differences in peripheral and portal venous endotoxin concentrations between the control and study groups. Postoperatively five of six dogs showed a measurable reduction in peripheral venous endotoxin concentration over intraoperatively obtained values, but the differences were not statistically significant (P = 0.06). Based on results of this study it was concluded that systemic endotoxemia was not present in dogs with a single extrahepatic portosystemic shunt that were medically stable prior to surgery.     

Serum gastrin concentrations in dogs with liver disorders

Dogs with liver disorders often display gastrointestinal signs that may be triggered by ulceration. The liver is important for inactivation of some forms of gastrin. Therefore, hypergastrinaemia has been implicated in the pathogenesis of gastrointestinal ulcerations related to liver dysfunction. The aim of this study was to determine serum gastrin concentrations in dogs with liver disease. Fasted blood samples were collected from 15 dogs with newly diagnosed liver disease and 18 healthy dogs. Gastrin concentrations were significantly lower in dogs with congenital portosystemic shunt compared with healthy dogs (P=0.003). No significant difference (P=0.6) in gastrin concentration was revealed between dogs with hepatocellular disease and healthy dogs. Serum gastrin concentrations were not significantly associated with the occurrence of vomiting, anorexia, diarrhoea, or melaena in dogs with liver disorders. These findings did not provide support for the role of hypergastrinaemia in the development of gastrointestinal signs associated with liver disease in dogs. Decreased serum concentrations of gastrin in a dog with liver disease may suggest the presence of portosystemic shunt. Further investigation is warranted to determine the importance of hyopogastrinaemia in congenital postosystemic shunts in dogs and to evaluate potential alterations in serum gastrin concentrations in specific hepatocellular diseases.     

Congenital dilatation of the bile ducts (Caroli's disease) in young dogs

We describe 8 young dogs with congenital dilatation of the intra- and extrahepatic bile ducts and diffuse cystic kidney disease, compatible with Caroli's disease in humans. The dogs were referred between 1980 and 2000 because of chronic disease at an age of 6 months to 3 years. These dogs included 3 Collies, 2 Frisian Stabyhouns, 2 Jack Russell Terriers, and 1 mixed-breed dog. The most common signs were vomiting (6/6), polyuria and polydipsia (4/6), and anorexia (4/6). Ascites was a common finding (4/6). Clinicopathologic abnormalities were available for 6 dogs. All had increased plasma alkaline phosphatase activity and fasting bile acids: increased alanine aminotransferase activity and urea and creatinine concentrations were present in 50% of dogs. Ultrasound examination of the liver showed severely dilated bile ducts without evidence of obstruction, and calcification in all cases but 1. Postmortem examination revealed severe dilatation of the larger intra- and extrahepatic bile ducts. The common bile duct and gall bladder were normal, and the bile system was patent. The ducts contained a clear viscid fluid often with calcified material. Microscopically, marked portal fibrosis was present, often with abnormally structured dilated bile ducts lined with columnar or cuboid epithelium and regularly small calcifications. The lesion was complicated by ascending cholangitis in 1 dog. The kidneys showed marked cortical and medullary fibrosis with a diffuse radial cystic pattern; only slight renal fibrosis was found in the oldest dog. Seven dogs were euthanized without treatment; the oldest dog was alive and well 5 months after diagnosis and was maintained on a protein-restricted diet.     

Glomerular Filtration Rate and Renal Volume in Dogs with Congenital Portosystemic Vascular Anomalies before and after Surgical Ligation

Glomerular filtration rate (GFR) and renal volume were evaluated in dogs with confirmed portosystemic vascular anomalies (PSVA) before and after surgical ligation of their PSVA. Pre- and postligation CBC, serum biochemistry, urinalysis, abdominal ultrasonography with measurement of renal volume, and per rectal scintigraphy were performed to document resolution of abnormalities consistent with portosystemic shunting. GFR was estimated by plasma 99mTc-diethylenetriaminepentaacetic acid (99mTc-DTPA) clearance before (n = 21) and after (n = 12) surgical correction of PSVA. Preligation 99mTc-DTPA GFR was increased (median, 5.64 mL/minute/kg; range, 3.53-8.49 mL/minute/kg; reference range, 2.83-4.47 mL/minute/kg) in 81% (17/21) of dogs. Postligation 99mTc-DTPA GFR decreased in all 12 evaluated dogs (median change = -42%; P < .001). Preligation renal volume was above the reference range for the left and right kidneys in 71% (10/14) and 69% (11/16) of dogs evaluated, respectively. Right renal volume decreased significantly (n = 5; median change, -45%; P = .03) after surgical ligation of PSVA. These findings document increased GFR and renal volume in dogs with PSVA, which may explain in part the low blood urea nitrogen and serum creatinine concentrations encountered in these dogs. Knowledge of changes in GFR associated with PSVA ligation may prove helpful in the anesthetic, drug, and dietary management of affected dogs.     

Hepatic Volume Measurements in Dogs with Extrahepatic Congenital Portosystemic Shunts before and after Surgical Attenuation

Background: In dogs with congenital portosystemic shunts (CPSS), the ability of the hypoplastic liver to grow is considered important for recovery after surgical shunt attenuation.
Objectives: This study investigated hepatic growth after extrahepatic shunt attenuation in dogs using magnetic resonance imaging (MRI) and computed tomography (CT).
Animals: Ten client-owned dogs with single extrahepatic CPSS.
Methods: Abdominal MRI, CT, or both were performed before and 8 days, 1, and 2 months after shunt attenuation. Liver volumes were calculated from the areas of the MRI or CT images.
Results: Before surgery, median liver volume was 18.2 cm³/kg body weight. Liver volume increased significantly after surgery. Growth was highest between days 0 and 8 and decreased afterward. Median liver volume was 28.8 cm³/kg at 2 months after attenuation. No significant differences in growth were found between dogs with complete or partial shunt closure or between dogs with complete or incomplete metabolic recovery. Volumes measured from consecutively performed MRI and CT images correlated well ( r = 0.980), but volumes from MRI images were significantly larger than volumes from CT images (6.8%; P = .008).
Conclusion and Clinical Importance: After shunt attenuation, rapid normalization of liver size was observed. Hepatic growth was not decreased in dogs after partial closure of CPSS or in dogs with subclinical, persistent shunting 2 months after surgery. CT is the preferred imaging method for volumetric estimation because of speed.     

Use of hepatobiliary scintigraphy in the diagnosis of extrahepatic biliary obstruction in dogs and cats: 25 cases (1982-1989).

Twenty-five animals (21 dogs and 4 cats) in which hepatobiliary scintigraphy (HBS) was performed between 1982 and 1989 were included in a retrospective study to determine the utility of HBS for diagnosis of extrahepatic biliary obstruction. Final diagnoses, which were based on liver biopsy results and surgical findings in all animals, were hepatocellular disease alone (n = 17), hepatocellular disease and extrahepatic biliary obstruction (n = 7), and normal liver (n = 1). Hepatobiliary scintigraphy was performed by use of 99mTc-diisopropyl iminodiacetic acid in all cases. All 7 cases of extrahepatic biliary obstruction were confirmed at surgery. In animals with biliary obstruction, HBS failed to demonstrate radiolabel within either the gallbladder or intestine at any time. Using nonvisualization of the intestine by 180 minutes as the scintigraphic criterion for diagnosis of biliary obstruction, sensitivity was 83% and specificity was 94% in this series. Hepatobiliary scintigraphy was concluded to be an accurate indicator of extrahepatic biliary obstruction in this group of animals. High serum bilirubin concentration at the time HBS was performed did not appear to reduce the diagnostic usefulness of the scintigraphic findings.     

Liver glutathione concentrations in dogs and cats with naturally occurring liver disease

OBJECTIVE: To determine total glutathione (GSH) and glutathione disulfide (GSSG) concentrations in liver tissues from dogs and cats with spontaneous liver disease. SAMPLE POPULATION: Liver biopsy specimens from 63 dogs and 20 cats with liver disease and 12 healthy dogs and 15 healthy cats. PROCEDURE: GSH was measured by use of an enzymatic method; GSSG was measured after 2-vinylpyridine extraction of reduced GSH. Concentrations were expressed by use of wet liver weight and concentration of tissue protein and DNA. RESULTS: Disorders included necroinflammatory liver diseases (24 dogs, 10 cats), extrahepatic bile duct obstruction (8 dogs, 3 cats), vacuolar hepatopathy (16 dogs), hepatic lipidosis (4 cats), portosystemic vascular anomalies (15 dogs), and hepatic lymphosarcoma (3 cats). Significantly higher liver GSH and protein concentrations and a lower tissue DNA concentration and ratio of reduced GSH-to-GSSG were found in healthy cats, compared with healthy dogs. Of 63 dogs and 20 cats with liver disease, 22 and 14 had low liver concentrations of GSH (micromol) per gram of tissue; 10 and 10 had low liver concentrations of GSH (nmol) per milligram of tissue protein; and 26 and 18 had low liver concentrations of GSH (nmol) per microgram of tissue DNA, respectively. Low liver tissue concentrations of GSH were found in cats with necroinflammatory liver disease and hepatic lipidosis. Low liver concentrations of GSH per microgram of tissue DNA were found in dogs with necroinflammatory liver disease and cats with necroinflammatory liver disease, extrahepatic bile duct occlusion, and hepatic lipidosis. CONCLUSIONS AND CLINICAL RELEVANCE: Low GSH values are common in necroinflammatory liver disorders, extrahepatic bile duct occlusion, and feline hepatic lipidosis. Cats may have higher risk than dogs for low liver GSH concentrations.     

Plasma amino acid analysis in dogs with experimentally induced hepatocellular and obstructive jaundice

Plasma amino acid concentrations were determined weekly for 4 weeks in 6 sham-operated control dogs, in 6 sham-operated dogs after induction of liver disease with dimethylnitrosamine (DMNA), and in 6 dogs after surgical ligation of the common bile duct. Results were compared with standard biochemical indices of liver function and with histologic changes in serial liver biopsy specimens. Concentrations of most amino acids increased after 2 weeks in DMNA-treated dogs, whereas they were normal or decreased in bile duct-ligated dogs. With increasing severity of the liver disease, the molar ratio (normal mean +/- SEM = 3.48 +/- 0.14) in DMNA-treated dogs decreased to 2.42 +/- 0.19 by 2 weeks and to 1.17 +/- 0.09 by 4 weeks. The ratio remained normal in bile duct-ligated dogs. Molar ratio and aromatic amino acid concentrations correlated better with hepatic necrosis and inflammation than did standard biochemical indices (eg, bilirubin, liver enzymes). Therefore, plasma amino acid analysis and determination of the molar ratio may be useful in the differential diagnosis of hepatocellular and obstructive jaundice in dogs. A decrease in the molar ratio may reflect portal hypertension and hepatocellular disease.     

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.     

Sensitivity and specificity of fasting ammonia and serum bile acids in the diagnosis of portosystemic shunts in dogs and cats

Background: Portosystemic shunt (PSS) is the most common cause of hepatic encephalopathy in dogs and cats. Fasting ammonia and serum bile acids (SBA) are used to diagnose PSS, but their true sensitivity and specificity have not been fully evaluated, especially in cats. Objectives: The purpose of this study was to determine the diagnostic accuracy of fasting ammonia and SBA concentrations in the diagnosis of PSS in dogs and cats and to compare diagnostic accuracy between species. Methods: A retrospective analysis of data from 373 dogs and 85 cats presented to the clinic from 1996 to 2006 was carried out. Based on clinical, laboratory, and imaging findings, animals were grouped as having PSS, parenchymal hepatic disease, or extrahepatic disease. The sensitivity and specificity of ammonia and SBA concentrations for the diagnosis of PSS were calculated and receiver‐operating characteristic analysis was used to optimize cut‐offs. Results: Using the upper limit of laboratory reference intervals (ammonia, 59 μmol/L; SBA, 20 μmol/L), the sensitivity and specificity of ammonia was 85% and 86% in dogs, and 83% and 76% in cats, respectively. The sensitivity and specificity of SBA was 93% and 67% in dogs, and 100% and 71% in cats, respectively. Using optimal cut‐off points for ammonia (dogs, 57 μmol/L; cats, 94 μmol/L) the sensitivity and specificity was 91% and 84% in dogs and 83% and 86% in cats, respectively. Using optimal cut‐off points for SBA (dogs, 58 μmol/L; cats, 34 μmol/L) the sensitivity and specificity was 78% and 87% in dogs and 100% and 84% in cats. Conclusion: Increased fasting ammonia and SBA concentrations are accurate indicators of PSS. An improvement in diagnostic accuracy can be achieved by using defined optimal cut‐off points for the selective diagnosis of PSS.     

Serum bile acid analysis in dogs with experimentally induced cholestatic jaundice

Serum bile acid (SBA) concentration was determined weekly for 4 weeks in dogs with experimentally induced hyperbilirubinemic liver disease. Obstructive jaundice was created in 6 dogs by surgical ligation of the common bile duct, and hepatocellular jaundice was created in 6 sham-operated dogs by administration of dimethylnitrosamine; 6 other sham-operated dogs served as controls. Serum bile acid concentration increased rapidly after bile duct ligation (from 0.6 +/- 0.1 to 69.2 +/- 15.3 mumol/L at 3 days), peaked at 14 days (247.8 +/- 54.1 mumol/L), and then gradually decreased (179.9 +/- 27.1 mumol/L at 28 days). Serum bile acid concentration in dimethylnitrosamine-treated dogs increased more gradually to 38.9 +/- 10.7 mumol/L at 28 days, at which time the serum bilirubin concentration was comparable with that of bile duct-ligated dogs. Mean total SBA values in bile duct-ligated dogs were significantly (P less than 0.01) higher than those in control and dimethylnitrosamine-treated dogs at days 3 through 28, with no overlap of individual values. Serum bile acid concentration at day 28 correlated positively (P less than 0.01) with cholestasis and bile duct proliferation observed in liver biopsy specimens, but did not correlate with necrosis or inflammation. Serum bile acid concentration also correlated positively (P less than 0.01) with serum bilirubin and cholesterol concentrations and with serum alkaline phosphatase and alanine transaminase activities. Results of the study reported here indicated a relationship between SBA concentration and cholestasis in dogs; extrahepatic bile duct obstruction resulted in the highest SBA values.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hepatic lesions associated with intrahepatic arterioportal fistulae in dogs

Seven cases of hepatic arterioportal fistulae in young dogs (mean age 6 months) are described. All cases were presumed to be congenital in origin. The onset of clinical signs, which frequently included gastrointestinal and neurological disturbances, was usually sudden. All dogs had clinical evidence of portal hypertension in the form of ascites, and all developed multiple extrahepatic portacaval venous shunts consequential to portal hypertension. The neurological disturbances were likely the result of portacaval shunting. The arterial and venous vessels involved in the fistulae had markedly altered wall structure. Hepatic regions adjacent to the fistulae frequently evidenced marked bile duct proliferation. Hepatic parenchymal atrophy, relative collapse of distributing portal veins, dilatation of hepatic arterial branches and proliferation of hepatic arterioles were seen throughout the liver; these changes closely resembled those present with portacaval shunting in the absence of hepatic arterioportal fistulae. The importance of recognizing that hepatic arterioportal fistulae and multiple extrahepatic portacaval shunts usually coexist and separately influence the morphological appearance of the liver is stressed.