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.     

Complications and long-term outcomes of the ligation of congenital portosystemic shunts in 49 cats

Only two of 49 cats undergoing surgical ligation of congenital extra- and intrahepatic portosystemic shunts died perioperatively, a mortality rate comparable with the mortality rates of dogs undergoing surgical attenuation of congenital portosystemic shunts and cats in which the shunts are attenuated with an ameroid ring constrictor. Thirty (83 per cent) of the 36 cats for which long-term information was available were still alive at a median follow-up period of 47 months (range six to 105 months); the outcome was excellent (no clinical signs) in 20 of them (median follow-up 37 months, range six to 105 months) and good (minimal clinical signs) in seven (median follow-up 39 months, range 10 to 73 months) and none of these 27 cats was on any long-term medication or special diet. The only major cause of morbidity was the development of neurological signs in 18 (37 per cent) of the cats. These included seizures and a wide variety of other neurological signs, and their development and persistence was not affected by the presence of preoperative seizures, the type of shunt, the degree of shunt attenuation or the age of the cat. The serum concentrations of ammonia and preprandial bile acids were normal or significantly below normal in the cats with neurological signs. Liver histopathology was similar in the cats with and without neurological signs. Ten (56 per cent) of the 18 cats that developed neurological signs recovered normal neurological function long term.     

Surgical and interventional radiographic treatment of dogs with hepatic arteriovenous fistulae

OBJECTIVE: To report outcome after surgical and interventional radiographic treatment of hepatic arteriovenous fistulae (HAVF) in dogs. STUDY DESIGN: Retrospective study. ANIMALS: Dogs (n=20) with HAVF. METHODS: Medical records of dogs with HAVF were reviewed. Referring veterinarians and owners were contacted by telephone. History, clinical signs, biochemical and hematologic variables, ultrasonographic and angiographic findings, surgical findings, techniques used to correct the HAVF, survival time, and clinical follow-up were recorded. RESULTS: Canine HAVF often appeared to be an arteriovenous malformation rather than a single fistula. Multiple extrahepatic portosystemic shunts were identified in 19 dogs. Surgery (lobectomy or ligation of the nutrient artery) and/or interventional radiology (glue embolization of the abnormal arterial vessels) was performed in 17 dogs. Thirteen dogs were treated by surgery alone, 4 dogs by glue embolization alone, and 1 dog by glue embolization and surgery. Three dogs treated by surgery alone died <1 month later, and 3 dogs were subsequently euthanatized or died because of persistent clinical signs. None of the dogs treated by glue embolization died <1month after the procedure and all were alive, without clinical signs, at follow-up (9-17 months). Overall, 9 of 12 (75%) dogs with long-term follow-up required dietary or medical management of clinical signs. CONCLUSION: HAVF-related death occurred less frequently after glue embolization than after surgery. CLINICAL RELEVANCE: Glue embolization may be a good alternative to surgery for treatment of certain canine HAVF.     

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.     

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.     

Retrospective study of 25 young weimaraners with low serum immunoglobulin concentrations and inflammatory disease

Twenty-five weimaraners with recurrent infections or inflammatory disease were investigated; their median age was four months (range two to 36 months), and 11 of them were male and 14 female. Twenty of them showed signs of lethargy, anorexia or pyrexia, 13 had been vomiting or had diarrhoea, 12 had shown signs of pain in the joints or bones and been lame, five had had reactions at the site of an injection, five had generalised lymphadenopathy, three had urinary tract infections and two had recurrent or severe pyoderma. They all had a lower concentration of one or more classes of serum immunoglobulin (IgG, IgM and IgA) than the standard control ranges, and their mean concentration of IgG was significantly lower (P<0.005) than the mean concentration of IgG in 15 clinically normal weimaraners. Of 10 cases for which a complete vaccination history was available, nine had developed clinical signs within five days of being vaccinated. Follow-up data were available from 21 of the 25 dogs for a median period of 24.5 months. One dog died during a symptomatic episode, three were euthanased, six were alive at follow-up but had continued to show clinical signs and 11 had made a full recovery.     

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.     

Primary hypoparathyroidism in dogs: a retrospective study of 17 cases

OBJECTIVE: To evaluate the clinico-pathological findings, response to treatment and prevalence of complications in dogs with primary hypoparathyroidism. DESIGN: Retrospective study of 17 dogs presenting to the University of Melbourne Veterinary Clinical Centre and Murdoch University Veterinary Hospital over a 15 year period (1990 to 2004). Case records were evaluated for signalment, body weight, diet type, historical and clinical findings, serum total calcium, phosphate, albumin and parathyroid hormone concentrations, urinary fractional excretion ratios of calcium and phosphate, electrocardiogram (ECG) results, treatments administered, outcome and period of follow-up. RESULTS: The most common breeds identified were St Bernard (three dogs), Chihuahua (two dogs), German Shepherd (two dogs) and Jack Russell Terrier (two dogs). Three dogs were cross bred. Seizures, muscle tremors and fasciculations, stiff gait, tetany, muscle cramping, behavioural change and hyperventilation were the most common clinical signs. Vomiting, inappetence, diarrhoea, abdominal pain, hyperthermia, facial pruritus, ataxia, weakness, cataracts, and circling also occurred with less frequency. The mean duration of observed clinical signs preceding diagnosis was 33 days (median 13 days, range 1 to 173 days). All dogs had marked hypocalcaemia with normal or mildly increased serum albumin concentrations. Mean phosphate concentrations were significantly higher in inappetent dogs (P = 0.049). Mean serum calcium concentrations were significantly lower in dogs with cataracts compared to those without (P = 0.046). There were no other significant relationships between serum calcium or phosphate concentrations and the clinical presentation or outcome. No significant correlations were identified between the presence of a particular clinical sign and the duration of clinical signs. ECGs were obtained in four dogs and all exhibited QT interval prolongation due to a ST-segment prolongation. Sixteen of 17 dogs were treated successfully for hypocalcaemia and discharged from hospital. Acute management included parenteral calcium gluconate (10 dogs) and intravenous anticonvulsants (five dogs). Chronic therapy included oral vitamin D analogues and calcium supplementation. Treatment complications occurred in two dogs and included acute renal failure (one dog) and iatrogenic tissue necrosis following subcutaneous calcium administration (one dog). The mean follow-up period was 14.5 months (median 13 months, range 0 to 39 months). Twelve dogs were alive at the last follow up and two dogs were euthanased for unrelated reasons. The type of vitamin D analogue used was not associated with outcome. CONCLUSION: Primary hypoparathyroidism was an uncommon diagnosis in dogs. Saint Bernards, cross bred dogs, German Shepherd dogs and Terrier breeds were most commonly affected. Neurological signs were the most common presenting clinical signs, although alimentary signs may have been more common than previously reported. Dogs with primary hypoparathyroidism appeared to have a good prognosis following initiation of calcium supplementation and vitamin D therapy. Complications of treatment were uncommon and could be minimised with regular monitoring.     

Cellophane banding of congenital intrahepatic portosystemic shunts in two Irish wolfhounds

Two three-month-old, male Irish wolfhound siblings were diagnosed with breed-typical left divisional congenital intrahepatic portosystemic shunts consistent with patent ductus venosus. The shunts were amenable to surgical dissection at a posthepatic location. Both dogs had cellophane banding for shunt attenuation. One dog was euthanased after developing post-ligation neurological dysfunction, which was refractory to treatment. The other dog survived and demonstrated shunt attenuation. Successful surgical management using cellophane banding of a patent ductus venosus has not been previously described in a large-breed dog.     

Congenital portosystemic shunts in toy and miniature poodles

Three male Poodles (two Toy, one Miniature) were presented to their veterinarians for evaluation of urolithiasis and varying degrees of hepatic encephalopathy. All three dogs were diagnosed as having intrahepatic shunts and referred for surgical correction. In each case, shunts arose from the right branch of the portal vein and were amenable to perivascular dissection caudal to where the vessel entered the hepatic parenchyma and to placement of perivascular cellophane bands to achieve shunt attenuation. During the same period, a female Miniature Poodle also presented for treatment of a congenital portosystemic shunt discovered during evaluation for generalised motor seizures. This animal had an extrahepatic portoazygous shunt that was completely ligated. Congenital portosystemic shunts have not previously been identified in Toy and Miniature Poodles at the University Veterinary Centre, Sydney and the anatomical types of shunt seen in this breed have not previously been reported in a consecutive series of cases. The three male dogs are noteworthy for a number of reasons: all had intrahepatic shunts, despite being small breed dogs; all three presented in a similar fashion, and all had shunts of an anatomical type amenable to placement of cellophane bands. One male dog died within 12 hours of surgery, the remaining three dogs survived and their liver function was normal at follow-up between 2 and 3 months after surgery. Use of cellophane bands for successful attenuation of intrahepatic shunts has not been previously reported.     

Thoracolumbar disc disease in large dogs: a study of 99 cases

The records of 99 dogs weighing over 20 kg with thoracolumbar disc disease were reviewed. Two types of disc disease were recognised: degenerative nuclear extrusion (n=63) and degenerative annular protrusion (n=36). Sixty-nine per cent of the affected discs were located between T12-T13 and L2-L3. Of the 63 dogs with degenerative nuclear extrusions, 35 were non-ambulatory and seven had no conscious pain perception at the time of presentation. Decompressive surgery was performed in 55 dogs, four dogs were managed non-surgically and three dogs were euthanased. A successful outcome was achieved in 49 (78 per cent) cases as assessed by the authors and in 53 (84 per cent) cases as assessed by the owners. Mean follow-up time was 11.7 months (range 1.5 to 48 months). Five dogs subsequently lost the ability to ambulate on their hindlimbs. Myelographic investigations in three of these dogs revealed a second thoracolumbar degenerative nuclear extrusion. Of the 36 dogs with degenerative annular protrusions, seven were non-ambulatory at the time of presentation. Fifteen cases had multiple protrusions. Twenty dogs were managed non-surgically, 12 surgically and four were euthanased. A successful outcome was achieved in eight (22 per cent) cases as assessed by the authors and in 19 (52 per cent) cases as assessed by the owners. Mean follow-up time was 9.2 months (range 1.5 to 30 months). The outcome of dogs with annular protrusions was significantly worse compared to the outcome of dogs with nuclear extrusions (P<0.001).     

Myokymia and neuromyotonia in 37 Jack Russell terriers

The clinical and clinicopathological characteristics, treatment and outcome of vermicular muscle contractions (myokymia) and generalized muscle stiffness (neuromyotonia) in 37 Jack Russell terriers were evaluated retrospectively. Thirty dogs were affected by both disorders, whereas seven were presented with myokymia and never developed neuromyotonia. Clinical signs started at the mean age of 8 months. Except for signs of myokymia and neuromyotonia, clinical and neurological examination was normal in all dogs. Thirty dogs demonstrated typical signs of hereditary ataxia.Changes in serum chemistry included increased creatine kinase, aspartate aminotransferase and alanine aminotransferase concentrations. Electromyographic abnormalities, especially in muscles showing macroscopically visible myokymia, consisted of semirhythmic bursts of doublet, triplet, or multiplet discharges of a single motor unit. The amplitudes varied between 80 μV and 1 mV and occurred with an interburst frequency between 10 and 40 Hz and an intraburst frequency between 150 and 280 Hz.Most dogs were treated with a sodium channel blocker with variable results. Seven dogs died (most likely because of hyperthermia) or were euthanased during a neuromyotonic attack; 15 dogs were euthanased due to worsening of clinical signs, or lack of or no long-lasting effect of medication, and three were euthanased for unknown or unrelated reasons. Nine dogs were lost to follow-up and three were still alive 5–10.5 years after the start of clinical signs. In conclusion, young Jack Russell terriers with myokymia and neuromyotonia should undergo a complete blood and electrophysiological examination. Long-term prognosis is not favourable.     

Congenital portosystemic shunts in Maltese and Australian Cattle Dogs

SUMMARY Congenital portosystemic shunts were definitively diagnosed in 62 dogs over a period of 15 years. Maltese and Australian Cattle Dogs were significantly over-represented, accounting for 14 and 13 cases, respectively. Maltese invariably had a single extrahepatic shunt derived from the left gastric or gastrosplenic vein, whereas Cattle Dogs usually had large intrahepatic shunts involving the right liver lobes. The clinical syndromes resulting from anomalous portosystemic communications were indistinguishable in the 2 breeds. Fasting blood ammonia concentration was elevated in 20 of 22 dogs tested, providing a minimally invasive and effective means of diagnosis. Complete or partial shunt attenuation was performed successfully in all 9 Maltese and in 2 of 6 Cattle Dogs in which it was attempted.     

Plasma ammonia concentration in dogs using ion-exchange method of analysis

Laboratory methods for measuring plasma ammonia concentration were reviewed. The ion-exchange method of analysis was evaluated using canine plasma from 15 clinically normal dogs and five dogs with portosystemic shunts. Mean and standard deviation was 40.3 +/- 8.1 microgram NH(3)/dl in normal dogs, and values ranged from 125 to 200 microgram NH(3)/dl in dogs with portosystemic shunts. Handling of blood samples properly for accurate results was found to require pre-chilled collection tubes, chilling the samples in an ice bath, immediate separation of plasma from red blood cells and immediate analysis for ammonia concentration. The ion exchange method was determined to be sufficiently accurate for clinical use and is suggested for any veterinary clinical pathology laboratory.     

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.     

Endogenous Benzodiazepine Activity in the Peripheral and Portal Blood of Dogs With Congenital Portosystemic Shunts

Objective- The purpose of this study was to determine whether an endogenous benzodiazepine receptor ligand (EBZ) was present in the arterial and portal blood of dogs with congenital portosystemic shunts (CPSS).
Study Design- The presence or absence of an EBZ was determined by the collection of systemic and portal blood from dogs with CPSS.
Animals- Fifteen client-owned dogs with a confirmed CPSS. All dogs had historical signs compatible with hepatic encephalopathy. Eight healthy dogs were used as controls.
Methods- In all dogs, systemic blood samples were collected after they were anesthetized. Portal blood samples were collected intraoperatively. EBZ was measured by radioreceptor assay.
Results- In 10 of 15 dogs, the portal blood concentration of EBZ was significantly elevated compared with normal dogs (mean, 13.2 ±18.55 ng/mL). Five dogs had elevated systemic blood EBZ levels (mean, 8.2 ±16.08 ng/mL). Eleven of 15 dogs had a higher portal than systemic blood concentration of EBZ. In contrast, control dogs had extremely low EBZ concentrations detected in their portal blood (mean, 0.16 ±0.3 ng/mL) and systemic blood (0 ng/mL). The mean portal and systemic blood concentrations in dogs with CPSS were significantly greater than in control dogs ( P <.05).
Conclusions- Elevated blood levels of EBZ were found in dogs with CPSS. The portosystemic gradient noted in 11 dogs suggests the gastrointestinal tract as a possible source for the endogenous ligand.
Clinical Relevance- Generalized motor seizures have been reported in dogs after surgical correction of CPSS. If the presence of a CPSS results in stimulation of brain receptors for benzodiazepines, post-CPSS ligation seizures may result from a withdrawal of EBZ after ligation of the portosystemic shunt.     

Results of thoracic duct ligation in dogs with chylothorax

Thoracic duct lymphangiography and ligation were done on 15 dogs with idiopathic chylothorax. Lymphangiography revealed thoracic lymphangiectasia in all dogs; none had a thoracic duct rupture. Lymphangiography immediately after ligation demonstrated missed branches of the thoracic duct in 4 of the 15 dogs. Eleven of the 15 dogs are alive and doing well. Eight of the 11 had no radiographic or clinical signs of pleural effusion (mean follow-up, 31.5 months; range, 4 to 75 months). The other 3 living dogs had persistent effusion; 2 were successfully managed with a pleuroperitoneal shunt (follow-up, 15 months) or pleurodesis (follow-up, 5 months), respectively, and 1 was not treated because the effusion was mild and the dog did not have clinical signs of disease (follow-up, 14 months). Four of the 15 dogs died or were euthanatized because of persistent effusion (mean follow-up, 11.5 months; range, 3 to 24 months). Considering the lack of treatment alternatives for dogs with idiopathic chylothorax, these results support thoracic duct ligation as a treatment method for dogs.     

Long-term survival of dogs after cholecystoenterostomy: a retrospective study of 15 cases (1981-2005)

Fifteen dogs with extrahepatic biliary tract disease underwent cholecystoenterostomy. Long-term survivors were significantly older at presentation (mean age 140.5 months) than dogs that survived the first 20 days after surgery but subsequently died from causes related to the surgery or hepatobiliary disease (mean age 72 months). Dogs that died during the first 20 days had significantly more complications in the hospital than dogs that survived this period. The type of underlying hepatobiliary disease (i.e., benign or malignant) was not associated with either short-term outcome or long-term survival. Eight dogs died from causes related to surgery or hepatobiliary disease. Long-term complications included hepatic abscesses, acquired portosystemic shunts, pancreatitis, and vomiting.     

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.     

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.