Mass screening of Irish wolfhound puppies for portosystemic shunts by the dynamic bile acid test.

Five hundred and sixty-six Irish wolfhound puppies aged six to 15 weeks were tested for congenital portosystemic shunts by the dynamic bile acid method. Plasma ammonia concentration was also measured in 165 of the puppies both fasting and postprandially. Nineteen puppies (3.4 per cent), nine males and 10 females, had portosystemic shunts. Smaller litters appeared to be more likely to contain affected puppies. The postprandial bile acid concentration was a reliable predictor of the presence of a shunt, with the highest concentration in a normal puppy being 38 mumol/litre and the lowest in an affected puppy being 43 mumol/litre. In contrast, fasting bile acid concentrations were normal in the majority of the affected puppies. There was considerable overlap in fasting plasma ammonia concentrations between normal and affected puppies (26 puppies, 15.8 per cent of those tested). Postprandial ammonia concentration appeared to give better separation between the two groups, apart from two individuals which produced bizarre results. It was concluded that the postprandial or dynamic bile acid test is an appropriate test for the mass screening of Irish wolfhound puppies for portosystemic shunts, and guidelines are proposed for the interpretation and follow-up of the test.     

Liver function tests in dogs with portosystemic shunts: measurement of serum bile acid concentration

Sulfobromophthalein excretion and plasma ammonia and serum bile acid concentrations were measured in 11 dogs with portal vascular anomalies. The fasting serum bile acid concentration was increased in all 11 dogs (78.9 +/- 16.1 mumol/L; normal, 2.6 +/- 0.4 mumol/L). For values measured in 8 dogs, the 2-hour postprandial serum bile acid concentration was increased further (177.0 +/- 26.4 mumol/L; normal, 7.6 +/- 2.3 mumol/L). The fasting plasma ammonia concentration was markedly increased in all 11 dogs (246.9 +/- 40.3 micrograms/dl; normal, 27 to 15 micrograms/dl). Thirty minutes after the oral administration of ammonium chloride, the plasma ammonia concentration was increased further in the 7 dogs (510.7 +/- 45.5 micrograms/dl; normal, 57.5 to 20.5 micrograms/dl). Results of the sulfobromophthalein excretion test were abnormal in 10 of 11 dogs (12.3 +/- 1.4%; normal, less than 5% retention after 30 minutes).     

Serum hyaluronic acid in dogs with congenital portosystemic shunts

Objectives : To compare the serum level of hyaluronic acid in dogs with congenital portosystemic shunt with that in healthy dogs and to investigate the perioperative change in serum hyaluronic acid following shunt attenuation. Methods : Blood samples were obtained from 29 congenital portosystemic shunt dogs before the operation, and 2 and 4 weeks after the operation from 17 and 7 dogs, respectively. The serum hyaluronic acid level of these dogs was measured and compared with that of 10 healthy beagles. Results : The median preoperative hyaluronic acid level in dogs with congenital portosystemic shunt was significantly elevated compared with that in healthy dogs. Furthermore, the median postoperative hyaluronic acid level significantly decreased compared with the median preoperative levels in congenital portosystemic shunt dogs. Clinical Significance : In the case of dogs with congenital portosystemic shunt, the reduction of intrahepatic portal blood flow might lower the clearance rate of hyaluronic acid in hepatic sinusoidal endothelial cells, so hyaluronic acid clearance could be improved by attenuation of a shunt vessel. Hence, serum hyaluronic acid levels might be useful to evaluate liver function and also have the potential to evaluate successful attenuation of a shunt vessel in dogs with congenital portosystemic shunt. Further investigations are required to clarify whether serum hyaluronic acid offers significant benefits over existing markers such as serum bile acid or ammonia concentrations.     

Surgical manipulation of portosystemic shunts in dogs.

Surgical manipulation to achieve stenosis or occlusion of portocaval shunts in 7 dogs resulted in disappearance of signs of central nervous, gastrointestinal, or urinary dysfunction. Results of blood chemical analyses and hepatic function studies as well as hepatic cellular architecture returned to normal or near normal within several months. Cranial mesenteric angiography was done on 4 dogs following corrective surgery; there was evidence of improved hepatic-portal circulation in 3 of the dogs and complete shunt obstruction in 1 dog.     

Neurological dysfunction in dogs following attenuation of congenital extrahepatic portosystemic shunts

Eleven of 89 dogs (12 per cent) developed neurological signs within six days of surgical attenuation of a congenital extrahepatic portosystemic shunt. Neurological signs were not associated with hepatic encephalopathy or hypoglycaemia. Signs varied in severity from non-progressive ataxia (three dogs) to generalised motor seizures (four dogs), progressing to status epilepticus (three dogs). In a further four cases, ataxia and disorientation were treated vigorously with anticonvulsant medication, presumably preventing the development of seizures. Two dogs that developed status epilepticus died or were eventually euthanased. All other animals survived, although some had persistent neurological deficits. Postligation neurological complications were not prevented by gradual shunt attenuation. Prophylactic treatment with phenobarbitone (5 to 10 mg/kg preoperatively, followed by 3 to 5 mg/kg every 12 hours for three weeks) did not significantly reduce the incidence of neurological sequelae (2/31 [6 per cent] dogs with phenobarbitone vs 9/58 [16 per cent] without phenobarbitone; P = 0.2). However, no animal receiving phenobarbitone experienced generalised motor seizures or status epilepticus. In conclusion, these observations suggest that postligation neurological syndrome comprises a spectrum of neurological signs of variable severity. Perioperative treatment with phenobarbitone may not reduce the risk of neurological sequelae, but may reduce their severity.     

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.     

Congenital portosystemic shunts in the cat: A report of nine cases

The clinical features, diagnosis, management and outcome of nine cases of congenital portosystemic shunt in the cat are reported. Neurological signs associated with hepatic encephalopathy and ptyalism were the main clinical signs. Six cases were presented as kittens less than six months of age and the remaining three cases were presented as adults, although in one of these signs were first noted at eight to 12 weeks of age. Fasting hyperammo-naemia was the only consistent abnormal biochemical finding. Medical management was instituted in all cases and surgical partial ligation was later performed in four with recanalisation of the ligated vessel occurring in three cases. The condition in the cat is compared and contrasted with that in the dog.     

Diagnostic value of fasting plasma ammonia and bile acid concentrations in the identification of portosystemic shunting in dogs

Portosystemic shunting occurs frequently either as congenital anomalies of the portal vein (PVA) or as acquired shunting (AS) due to portal hypertension secondary to parenchymal liver disease or portal vein thrombosis. The 2 most commonly used screening tests for portosystemic shunting are bile acid and plasma ammonia concentrations. The purpose of this study was to compare the 12-hour fasting plasma ammonia (AMM) and bile acid concentration (BA) as tests for diagnosing portosystemic shunting. Medical records of 337 dogs were used in which AMM and BA were measured simultaneously and in which portosystemic shunting was confirmed or excluded. These dogs were divided into 2 groups (group 1: portosystemic shunting present, n = 153, and group 2: portosystemic shunting absent, n = 184). Group 1 was subdivided into 2 subgroups (group 1a: PVA, n = 132 and group 1b: AS, n = 21). The sensitivity of AMM in detecting PVA was 100% and of BA was 92.2%. For portosystemic shunting in general (PVA or AS), the sensitivity of AMM was 98% and that of BA was 88.9%. The specificity in the total population of AMM was 89.1% and that of BA was 67.9%. If only dogs with liver diseases were included with (n = 153) or without (n = 28) shunting, the specificity of AMM to detect shunting was 89.3% and that of BA was 17.9%. In conclusion, AMM is a highly sensitive and specific parameter to detect PVA and portosystemic shunting in a general population and in dogs with liver disease, whereas BA is somewhat less sensitive and considerably less specific.     

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.     

Neurological dysfunction in three dogs and one cat following attenuation of intrahepatic portosystemic shunts

Neurological dysfunction is an uncommon complication following extrahepatic portosystemic shunt ligation. Three dogs and one cat are described that developed neurological signs within 21 to 42 hours of attenuation of intrahepatic portosystemic shunts. None of these cases had biochemical evidence of hepatic encephalopathy postoperatively. Two dogs died during management of status epilepticus following aspiration of food. One dog died six months postoperatively. The cat had persistent neurological dysfunction at discharge, but was alive and had recovered most of its neurological function at the time of writing, 37 months after surgery. This report demonstrates the potential for animals with intrahepatic portosystemic shunts to develop postoperative neurological signs and highlights the difficulty of managing such cases. Two dogs had both intrahepatic and extrahepatic portosystemic shunts. Large intestinal malrotation (partial situs inversus) may have been linked to the development of a portosystemic shunt in the remaining dog.     

Congenital portosystemic shunts in dogs: 46 cases (1979-1986)

Congenital portosystemic shunts (CPSS) were diagnosed in 46 dogs. The historic, physical, and laboratory findings were tabulated. Half of the affected males were cryptorchid. Urolithiasis was detected in 20% of the dogs. The biochemical tests with the best sensitivity for the diagnosis of CPSS were sulfobromophthalein retention, fasting serum ammonia concentration, and serum alkaline phosphatase activity. The survival time and quality of life were assessed by physical and biochemical reevaluation of the dogs and by means of a questionnaire that was completed by the owners. Five dogs were treated medically. Thirty-three dogs were treated surgically. Dogs that had complete surgical occlusion of the CPSS became normal, and quality of life was excellent. Dogs that had partial occlusion of the CPSS improved, and some became clinically normal. Dogs that did not have surgical correction of the CPSS had continuation of signs, but several survived for years.     

Cerebrospinal fluid glutamine,tryptophan, and tryptophan metabolite concentrations in dogs with portosystemic shunts

OBJECTIVE: To determine whether glutamine (GLN), tryptophan (TRP), and tryptophan metabolite concentrations are higher in cerebralspinal fluid (CSF) dogs with naturally occurring portosystemic shunts (PSS), compared with control dogs. ANIMALS: 11 dogs with confirmed PSS and 12 control dogs fed low- and high-protein diets. PROCEDURE: Cerebrospinal fluid and blood samples were collected from all dogs. Serum and CSF concentrations of GLN, alanine, serine, TRP, 5-hydroxyindoleacetic acid (5-HIAA), and quinolinic acid (QUIN) were measured. RESULTS: Cerebrospinal fluid concentrations of GLN, TRP, and 5-HIAA were significantly higher in PSS dogs, compared with control dogs fed high- or low-protein diets. Cerebrospinal fluid QUIN concentration was significantly higher in PSS dogs, compared with control dogs fed the low-protein diet. Serum QUIN concentration was significantly lower in PSS dogs, compared with control dogs fed either high- or low-protein diets. CONCLUSIONS AND CLINICAL RELEVANCE: An increase in CNS GLN concentration is associated with high CSF concentrations of TRP and TRP metabolites in dogs with PSS. High CSF 5-HIAA concentrations indicate an increased flux of TRP through the CNS serotonin metabolic pathway, whereas high CSF QUIN concentrations indicate an increased metabolism of TRP through the indolamine-2,3-dioxygenase pathway. The high CSF QUIN concentrations in the face of low serum QUIN concentrations in dogs with PSS indicates that QUIN production from TRP is occurring in the CNS. High concentrations of QUIN and other TRP metabolites in the CNS may contribute to neurologic abnormalities found in dogs with PSS and hepatic encephalopathy.     

Congenital portosystemic shunts in dogs and cats

Congenital portosystemic shunts (PPS) are abnormal vascular communications that allow blood from the intestine to bypass the liver, and are classified as intrahepatic or extrahepatic. Clinical signs are generally related to the nervous, gastrointestinal or urinary systems, and are often vague. In addition, changes present on routine blood analysis are often mild and non-specific. For this reason, alternative tests are required for a diagnosis. Diagnostic tests include serum bile-acid concentrations, ammonia tolerance test, portography, ultrasonography and/or scintigraphy. Medical therapy involves reducing absorption of encephalopathic toxins from the gastrointestinal tract and may prolong survival. Surgical therapy is aimed at attenuation of the shunting vessel and provides improved survival rates. The traditional approach has been complete or partial ligation of the shunt. More recent approaches have involved slow, progressive attenuation with ameroid constrictors or cellophane banding. Overall, prognosis following surgical therapy is good in dogs and fair in cats.