Clinical outcome of congenital extrahepatic portosystemic shunt attenuation in dogs aged five years and older: 17 cases (1992–2005)

Deanna R. Worley Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104-6010.

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David E. Holt Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104-6010.

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Abstract

Objective—To assess the outcome of extrahepatic portosystemic shunt (EHPSS) treatment in dogs aged 5 years and older.

Design—Retrospective case series.

Animals—17 client-owned dogs.

Procedures—Medical records for dogs (≥ 5 years old) that underwent surgical attenuation of an EHPSS (1992 through 2005) were evaluated; data, including clinical signs, clinicopathologic findings, surgical procedure, and outcome, were recorded. Follow-up information was obtained via patient examination or telephone interview with veterinarians and owners.

Results—Dogs (5 to 9 years old [median age, 6.6 years]) had neurologic (n = 12), urinary tract (8), and gastrointestinal tract (6) EHPSS-associated clinical signs. Serum bile acids and ammonia concentrations were abnormal in all evaluated dogs. Treatment of EHPSSs included complete (n = 6 dogs) or partial (2) suture attenuation or ameroid constrictor placement (9). Two dogs died following surgery. Follow-up information (6 to 120 months) was available for 13 dogs. Deaths were attributable to heart failure (n = 1), bacterial hepatitis (2; with pyelonephritis in 1 dog), and unknown causes (3). At a median of 23 and 25 months, serum bile acids concentrations had almost normalized in 5 of 8 dogs and ammonia concentrations were within reference limits in 3 of 5 dogs, respectively; dogs with abnormal liver function test results had no associated clinical signs. Median long-term survival time was 72 months.

Conclusions and Clinical Relevance—Attenuation of EHPSS in ≥ 5-year-old dogs ameliorated signs of liver dysfunction in surviving dogs, although return of normal liver function occurred less frequently than expected.

Abstract

Objective—To assess the outcome of extrahepatic portosystemic shunt (EHPSS) treatment in dogs aged 5 years and older.

Design—Retrospective case series.

Animals—17 client-owned dogs.

Procedures—Medical records for dogs (≥ 5 years old) that underwent surgical attenuation of an EHPSS (1992 through 2005) were evaluated; data, including clinical signs, clinicopathologic findings, surgical procedure, and outcome, were recorded. Follow-up information was obtained via patient examination or telephone interview with veterinarians and owners.

Results—Dogs (5 to 9 years old [median age, 6.6 years]) had neurologic (n = 12), urinary tract (8), and gastrointestinal tract (6) EHPSS-associated clinical signs. Serum bile acids and ammonia concentrations were abnormal in all evaluated dogs. Treatment of EHPSSs included complete (n = 6 dogs) or partial (2) suture attenuation or ameroid constrictor placement (9). Two dogs died following surgery. Follow-up information (6 to 120 months) was available for 13 dogs. Deaths were attributable to heart failure (n = 1), bacterial hepatitis (2; with pyelonephritis in 1 dog), and unknown causes (3). At a median of 23 and 25 months, serum bile acids concentrations had almost normalized in 5 of 8 dogs and ammonia concentrations were within reference limits in 3 of 5 dogs, respectively; dogs with abnormal liver function test results had no associated clinical signs. Median long-term survival time was 72 months.

Conclusions and Clinical Relevance—Attenuation of EHPSS in ≥ 5-year-old dogs ameliorated signs of liver dysfunction in surviving dogs, although return of normal liver function occurred less frequently than expected.

Extrahepatic portosystemic shunts are a frequently described congenital anomaly in dogs that result from persistence of an abnormal communication between the portal and systemic venous circulations. Affected dogs develop clinical signs of neurologic, gastrointestinal tract, and urinary tract diseases.1-11 Dogs with an EHPSS generally develop clinical signs before they are 2 years old.1-4,6-10,12-25 The preferred treatment for this condition is shunt attenuation. This can be achieved via suture ligation, cellophane banding, or placement of an ameroid ring constrictor, thrombogenic intravascular coil, or hydraulic occluder.26

Several retrospective studies4,8,10 have been undertaken to evaluate the results of surgical attenuation of EHPSSs in dogs. Many of these studies used a cut-off age of 2 years to distinguish between younger and older dogs. Conflicting and limited information exists regarding outcome of EHPSS attenuation in dogs that are > 2 years old. Of 24 previously published retrospective studies,1-4,7-11,13,14,17-19,21-25,27-31 15 included dogs that were > 4 years old,2,3,7-10,18,19,22,24,25,28-31 but it is difficult to discern how many of these older dogs were in each study. The median or mean ages of dogs included in the latter 15 studies were < 2 years. In 3 studies,9,10,22 18% to 27% of the study population dogs were > 2 years old, and in another study,8 18% of the dogs were > 3 years old.

In reports of 3 retrospective studies4,9,30 of dogs with EHPSS that undergo shunt attenuation, it was stated that older dogs have a poorer outcome (including persistence of clinical signs, increased morbidity, or death), compared with younger dogs. Other retrospective studies8,10,17,21-22 revealed that there is no difference in outcome between younger and older dogs with EHPSS that undergo shunt attenuation. To the authors’ knowledge, the results of surgical EHPSS treatment in a cohort of adult dogs have not been previously described.

The purpose of the study of this report was to assess the outcome of EHPSS treatment in dogs aged 5 years and older. The clinical signs, clinicopathologic abnormalities, and treatment methods were also examined. Our hypothesis was that the amelioration of EHPSS-associated clinical signs and long-term outcome in an adult cohort of dogs that underwent surgical shunt attenuation would be similar to findings of previous EHPSS studies.

Materials and Methods

Case selection—Dogs for which a diagnosis of EHPSS had been made in the period of 1992 through 2005 at the University of Pennsylvania were considered for inclusion in the study. Dogs were included if they were ≥ 5 years old at the time of initial evaluation, had a single congenital extrahepatic shunt, and underwent surgical attenuation. Dogs were excluded from the study if they had multiple extrahepatic shunts.

Medical records review—Medical records of dogs that were eligible for inclusion in the study were reviewed. Preoperative data collected included age, sexneuter status, breed, clinical signs, hematologic and serum biochemical findings, and liver function test results (either serum ammonia concentration assessed after withholding of food or pre- and postprandial serum bile acids concentrations). Information from abdominal ultrasonographic and nuclear scintigraphic evaluations was recorded. Details of the surgical treatment and postoperative complications were collected; fol-low-up information was obtained via patient reevaluation or telephone contact with owners and referring veterinarians.

Surgical procedures—A ventral midline laparotomy was performed in all dogs. The shunt was identified by the surgeon. Gross characteristics of portal hypertension, including intestinal hypermotility and pancreatic cyanosis, were monitored in all dogs during shunt dissection and occlusion. At the surgeon’s discretion, a catheter was placed in a mesenteric vein and connected to a water manometer to allow quantifiable measurement of resting portal pressures (assessed before manipulation of the shunt) and attenuated portal pressures. Any additional surgical procedures performed were also recorded.

Postoperative evaluation—Immediate postoperative complications were defined as those that developed in the interval from discontinuation of anesthesia for surgery to suture removal. On the basis of long-term fol-low-up information, median long-term survival time was determined by use of a Kaplan-Meier survival curve.

Results

Study population—From the medical records, 77 dogs that were 5 or more years old were initially eligible for inclusion in the study having a sole diagnosis of EHPSS; however, 38 of these dogs had multiple acquired EHPSSs and were excluded. Thus, medical records of 17 dogs met the criteria for inclusion in the study. Of the 17 dogs, 8 were spayed females, 1 was a sexually intact female, 7 were castrated males, and 1 was a sexually intact male. Median ± SD age of the dogs was 6.6 ± 1.4 years (range, 5.0 to 9.2 years). Breeds included Yorkshire Terrier (n = 5); Miniature Schnauzer (3); and 1 each of Border Terrier, Maltese, Miniature Poodle, Dachshund, Shih Tzu, Standard Schnauzer, Pug, Lhasa Apso, and mixed.

Preoperative findings—In the study population, clinical signs at the initial evaluation were classified as neurologic (n = 12 dogs), urinary (8), and gastrointestinal (6). Median ± SD age of onset of clinical signs was 5.7 ± 2.0 years (range, 4.6 to 9.1 years). Median number of days since the dog was last considered normal was 62 ± 176 days (range, 1 to 731 days). Twelve dogs had ≥ 1 concurrent clinical sign. Of the 12 dogs with neurologic signs, all had abnormal mentation, 8 had ataxia, and 3 had seizures. One dog was treated for seizure activity, and 2 dogs were administered prophylactic medication for seizures. Of the 8 dogs with urinary tract signs, 6 underwent cystotomy because of urate cystic calculi, 1 underwent urethrotomy for an undetermined calculus, and 1 had dysuria. In 6 dogs, gastrointestinal tract signs included hypersalivation, anorexia, vomiting, pica, coprophagy, and weight loss. Seven of 17 dogs had polyuria and polydipsia.

In the 17 dogs, other problems that developed prior to EHPSS diagnosis included otitis externa and otitis media (n = 3), reactions to anesthetic agents (3; prolonged recovery from anesthesia in 2 dogs and an uncharacterized problem in another dog), pyometra (1), medial luxation of the patella (1), femur fracture (1), and masticatory myositis (1). Nine dogs had undergone anesthesia for surgeries other than neutering. Body condition scores were considered normal in 11 dogs, overconditioned in 3 dogs, and underconditioned in 3 dogs.

Selected hematologic and biochemical tests were performed in all 17 dogs. Median ± SD PCV was 44.2% ± 5.3% (range, 37.1% to 55%; reference range, 40.3% to 60.3%); anemia was detected in 3 dogs. Median ± SD corpuscular volume was 65 ± 4.4 fL (range, 56.9 to 70 fL; reference range, 62.7 to 75.5 fL); microcytosis was detected in 6 dogs. Median total WBC count was 15.2 ± 5.8 X 103 cells/μL (range, 7.6 to 28.7 X 103 cells/μL; reference range, 5.3 to 19.8 X 103 cells/μL); leukocytosis was detected in 5 dogs. Median serum albumin concentration was 2.5 ± 0.5 g/dL (range, 1.6 to 3.7 g/ dL; reference range, 2.5 to 3.7 g/dL); hypoalbuminemia was detected in 8 dogs. Median blood glucose concentration was 83 ± 16.6 mg/dL (range, 43 to 105 mg/dL; reference range, 65 to 112 mg/dL); hypoglycemia was detected in 3 dogs. Median BUN concentration was 5 ± 2.5 mg/dL (range, 2 to 12 mg/dL; reference range, 5 to 30 mg/dL); low concentrations were detected in 6 dogs. Median serum alkaline phosphatase activity was 120 ± 216.1 U/L (range, 27 to 734 U/L; reference range, 20 to 155 U/L); high activities were detected in 5 dogs. Median serum alanine aminotransferase activity was 122 ± 171.8 U/L (range, 40 to 559 U/L; reference range, 16 to 91 U/L); high activities were detected in 11 dogs. Median serum aspartate aminotransferase activity was 108 ± 118.4 U/L (range, 35 to 397 U/L; reference range, 23 to 65 U/L); high activities were detected in 10 of 14 dogs for which data were available.

Pre- and postprandial serum bile acids concentrations were abnormal in all 14 dogs that were evaluated; median ± SD preprandial bile acids concentration was 155 ± 68.7 μmol/L (range, 30 to > 200 μmol/L; reference range, 0.0 to 5.0 μmol/L), and postprandial bile acids concentration was 148 ± 38.8 μmol/L (range, 97.7 to > 200 μmol/L; reference range, 0.0 to 15.5 μmol/L). Serum ammonia concentrations assessed after food was withheld were abnormal in all 12 dogs that were evaluated; median serum ammonia concentration was 108 ± 102.7 μmol/L (range, 36 to 298 μmol/L; reference range, 11 to 35 μmol/L).

Prothrombin and activated partial thromboplastin times were within reference limits in all 15 dogs that were evaluated. Four of 17 dogs had urinary tract infections at the initial evaluation.

Shunt characteristics and surgical procedures— Abdominal ultrasonography was performed in all 17 dogs. An EHPSS was detected in 12 dogs. Although a shunt was not definitively identified in 2 dogs, features consistent with an EHPSS, including a small hyperechoic liver, small portal vein, and poor portal vascularization, were detected ultrasonographically. An EHPSS could not be identified in the remaining 3 dogs. In 1 of 3 dogs without an ultrasonographically identified EHPSS, nuclear scintigraphy per rectum was performed with a shunt fraction supportive of an EHPSS.

During surgery, a portocaval shunt was identified in 8 dogs and a portoazygous shunt was identified in 7 dogs. Shunts in the 2 remaining dogs were extrahepatic but were not classified further. Six dogs underwent complete EHPSS ligation with silk suture. Eleven dogs underwent partial shunt attenuation; this was achieved by use of a 5-mm ameroid ring constrictor in 8 dogs, a 7-mm ameroid ring constrictor in 1 dog, and partial silk suture ligation in 2 dogs. Mesenteric portal pressures were quantified in 7 dogs and were qualitatively assessed in 7 other dogs via temporary complete occlusion of the shunt; median ± SD baseline portal pressure was 9.5 ± 3.2 cm H2O (range, 5.5 to 13.5 cm H2O; reference range, 8 to 13 cm H2O). After attenuation, portal pressure was quantitatively assessed in 6 dogs, 4 that underwent complete ligation, 1 that underwent partial ligation, and 1 that underwent ameroid ring placement. Median postattenuation portal pressure was 13.8 ± 4.2 cm H2O (range, 7.5 to 17.0 cm H2O). None of the cohort dogs had portal hypertension prior to manipulation of the shunting vessel. Seven of 14 dogs (all 6 dogs that underwent complete ligation and 1 that underwent ameroid ring placement) had portal vasculature that could tolerate complete occlusion of the shunt. Additional surgical procedures performed at the time of attenuation included cystotomy (n = 7), nephrotomy (1), gastrotomy (1), and tube gastropexy (1).

Liver biopsy specimens were obtained from 7 dogs. Results of histologic examination of those samples were consistent with established liver changes in dogs with portosystemic shunts.32

Postoperative illness and death—The postoperative mortality rate was 12% (2/17 dogs died in the immediate postoperative period). One dog that underwent partial shunt attenuation had persistently low blood pressure values following surgery; cardiac arrest occurred 9 hours after surgery following aggressive treatment including use of multiple vasopressors. Another dog that was treated before surgery for neurologic signs and that underwent ameroid ring constrictor placement developed intractable seizures; the seizures were unresponsive to multimodal anticonvulsant treatment, and the dog was euthanized 7 days after surgery. Three dogs had mild transient neurologic signs following surgery; 2 of those dogs required short-term treatment with antiseizure medication. All 3 dogs had neurologic clinical signs before surgery. Other complications included hematochezia (n = 1), melena (1), vomiting (1), regurgitation (1), and abdominal distention (1). All gastrointestinal tract complications were transient. Duration of postoperative hospitalization ranged from 1 to 5 days (median ± SD duration, 3 ± 1.0 days).

Long-term follow-up data and outcome—Two of the 15 dogs that were discharged from the hospital were lost to long-term follow-up. Data were available for the remaining 13 dogs for a period of 6 to 120 months (median ± SD duration, 42 ± 32 months). All available referring veterinarians and all 13 owners were contacted via telephone. Eight of the 13 dogs were reexamined at the University of Pennsylvania.

Seven of 13 dogs were alive at the conclusion of the study. All 7 dogs were considered to be free of clinical signs by their owners. One dog was receiving prophylactic treatment with s-adenosyl-methionine. Six of 15 dogs that were dead at the end of the study period had survived 22 to 120 months after surgery (median ± SD survival time, 42 ± 36.7 months). Death was attributed to bacterial hepatitis (n = 2) and heart failure (1); causes were unknown for 3 dogs. One of the dogs that died as a result of bacterial hepatitis also had pyelonephritis. For both dogs with bacterial hepatitis, the diagnosis was based on findings of bacterial cultures of liver tissues obtained during surgeries subsequent to EHPSS attenuation. One dog for which the cause of death was unknown was 17 years old at the time of death; it had survived for 10 years following EHPSS attenuation. Of the 13 dogs that were available for follow-up, only 1 had been treated orally with lactulose and fed a restricted protein diet long-term. Median long-term survival timea among the 13 dogs discharged from the hospital was 72 months (Figure 1).

Figure 1—
Figure 1—

Kaplan-Meier survival curve of overall survival in 17 dogs that were each ≥ 5 years old and underwent surgical treat-ment of an EHPSS. Squares indicate patient death.

Citation: Journal of the American Veterinary Medical Association 232, 5; 10.2460/javma.232.5.722

Evaluation of liver function—Assessment of pre- and postprandial serum bile acids concentrations was performed in 8 dogs at 1.3 to 48 months (median ± SD, 23 ± 18.9 months) after surgery. Results were within or near reference limits (postprandial serum bile acids concentration, < 40 μmol/L) in 5 dogs and abnormal in 3 dogs (Table 1). Surgical attenuation in dogs with abnormal bile acids test results included complete ligation (n = 2) and partial ligation (1). Serum ammonia concentration after food was withheld was measured in 5 dogs at 1.3 to 45 months (median ± SD, 25 ± 18.3 months) after surgery, and results were abnormal in 2 dogs (1 each having undergone partial or complete shunt ligation). According to their owners, dogs with evidence of abnormal liver function did not have clinical signs of liver dysfunction.

Table 1—

Results of liver function tests performed before and after surgical shunt attenuation in 17 dogs with EHPSSs and that were aged 5 years or older.

DogBefore surgeryAfter surgery
Preprandial SBAs concentration (μmol/L)Postprandial SBAs concentration (μmol/L)serum ammonia concentration* (μmol/L)Preprandial SBAs concentration (μmol/L)Postprandial SBAs concentration (μmol/L)Time of postsurgical assessment of SBAs concentration (mo)serum ammonia concentration* (μmol/L)Time of postsurgical assessment of serum ammonia concentration (mo)
156160ND10391.3NDND
2> 200> 200NDNDNDNDNDND
3127129159ND213NDND
4> 200> 200NDNDNDNDNDND
5NDND108NDNDNDNDND
6NDND59NDNDNDNDND
7220141298NDNDNDNDND
8489842202430NDND
9183665NDNDNDNDNDND
106521,4585741448NDND
1150128ND5106305525
12NDND92> 200> 2003133
1398ND245NDNDNDNDND
14189227365816301.3
1529469145NDNDND3228
1630148110NDNDNDNDND
1795143128106167456645

Value assessed after food had been withheld.

SBAs = Serum bile acids. ND = Not done.

Liver biopsy specimens were obtained from 3 dogs 23 to 37 months after shunt attenuation. Only 1 of these dogs had a corresponding biopsy performed at the time of shunt attenuation surgery. Histologic examination of that dog’s latter liver biopsy specimen (obtained during abdominal exploratory surgery for septic peritonitis) revealed lipogranuloma necrosis, extensive lipogranulomas, chronic fibrosis, multifocal hepatocellular necrosis, and congestion. Histologic examination of the liver biopsy specimen from 1 of the other 2 dogs (obtained during management of transient thrombocytopenia) revealed steroid hepatopathy. Histologic examination of the liver biopsy specimen from the remaining dog (obtained during abdominal exploratory surgery for acute onset of jaundice) revealed hepatocellular swelling, portal fibroplasia, diffuse hemosiderosis, and severe portal lymphangiectasia with concurrent bacterial hepatitis.

Discussion

The clinical signs and preoperative clinicopathologic abnormalities in this cohort of older dogs with EHPSSs were similar to those reported for younger dogs in previous populations.1-4,7-11,13,14,17-19,21-25,27-31 study Conversely, most of the dogs in the present study did not have clinical signs for a prolonged period and generally the diagnosis had only recently been made prior to evaluation at the hospital for surgery. It is not clear why these dogs did not develop clinical signs at a younger age, as more commonly expected.1-4,6-10,12-25 Although comparison across patient populations in different reports is difficult, the results of liver function tests in the cohort of older dogs in our study were comparable to those reported for younger dogs with EHPSS.4,7-8,21,27,31 Thus, it seems unlikely that the late onset of clinical signs among the older dogs was attributable to less severe liver dysfunction.

In the present study, the immediate postoperative mortality rate in the cohort of older dogs was 12%. This value is similar to mortality rates determined in other studies,3,7-11,17,19,21-25,27,29-31 which have ranged from 0% to 35% (median mortality rate, 13%). Seizures are an uncommon but often fatal postoperative complication of EHPSS surgery, and results of 2 studies10,33 suggest that the risk of postoperative seizures is greater in older dogs with EHPSSs. Only 1 dog in the present study developed seizures that were refractory to aggressive medical treatment. Three other dogs developed abnormal neurologic signs in the postoperative period; however, these signs were only transient and resolved completely. The incidence of seizures and the immediate postoperative mortality rate in the cohort of older dogs in the present study are therefore comparable to findings of previous studies in which most dogs were < 2 years old.

Median long-term survival of dogs with EHPSSs is difficult to gauge from many previous studies. In the present study, dogs with EHPSSs that were 5 to 9 years old at the time of shunt attenuation had a median postoperative survival time of 6 years. Clinical signs of liver dysfunction were not apparent in any surviving dog, although results of postoperative liver function tests were not within reference ranges in some of those dogs. In 5 previous studies4,7,8,11,31 of dogs and cats, serum bile acids concentration did not necessarily correlate with clinical outcome following shunt attenuation. Persistently abnormal liver function tests may be a result of incomplete shunt attenuation, shunt recannulation, an overlooked and untreated second shunt, development of multiple acquired shunts, or concurrent hepatic microvascular dysplasia. Follow-up imaging procedures to evaluate for these abnormalities were not permitted in surviving dogs of the present study.

The return of liver mass and function to apparently normal condition is at the heart of the decision to recommend surgery for treatment of EHPSSs in dogs. Attenuation of the shunt and redirection of portal blood flow to the liver is intended to allow the liver vasculature and parenchyma to develop and overall liver function to improve. In humans and dogs, the incredible regenerative capacity of the clinically normal adult liver34 and the importance of portal blood flow to the liver35,36 have been recognized for many years. Despite extensive research, the mechanisms underlying liver regeneration are still incompletely understood.37 Cytokines, growth factors (especially hepatocyte growth factor), and socalled mitogens, including insulin and glucagon, are vital for liver regeneration.37 It is also known that cells for both the parenchymal38,39 and vascular40 elements of liver regeneration are derived from the bone marrow. Although congenital portosystemic shunts have been identified and treated in dogs for more than 30 years, little is known about the mechanisms of liver regeneration following shunt attenuation. Research into liver regeneration has largely been conducted in adult humans and other animals; it is not known whether the process of regeneration is similar in young animals, especially those in which the liver has not completely developed because of a lack of normal portal blood flow. Although the liver in adult animals retains remarkable regenerative capacity, the regenerative capacity of the liver in older dogs with congenital portosystemic shunts has not been established to our knowledge. In the present study, follow-up liver function tests (pre- and postprandial assessments of serum bile acids concentrations) were not substantially improved, compared with preoperative values, in 3 of 8 dogs. In the remaining 5 dogs (which were 5 to 9 years old), liver function test results were substantially improved, thereby indicating that liver regenerative capacity is retained even in older dogs with congenital EHPSS.

Two dogs in the study of this report developed bacterial hepatitis 22.3 and 27.6 months after surgery. To our knowledge, this has not been reported previously for dogs that underwent attenuation of an EHPSS. It is not clear whether bacterial hepatitis is a potential complication of surgery in older dogs with EHPSSs or was a coincidental development in these 2 study dogs. Portal bacteremia, leukocytosis, and portal hypoxemia were not detected in dogs with EHPSSs and were not correlated with illness and death of those animals in another study.41 The ages of the dogs in that study were not reported, and it is not clear whether findings in older dogs might differ from those in the dogs of that study. It is also possible that reticuloendothelial function may be altered in older dogs with EHPSSs, but information regarding reticuloendothelial function in dogs with EHPSSs is limited. In 2 studies,42,43 there was no reduction in hepatic reticuloendothelial function in dogs with experimentally created portocaval shunts; however, studies of reticuloendothelial function in dogs with congenital EHPSSs are lacking. Other possible etiologies of bacterial hepatitis in dogs without congenital portosystemic shunts include trauma, toxins, other infectious agents (eg, Leptospirosis interrogans, Bartonella spp, and canine adenovirus), bacterial sepsis, heat, or inflammation.

In the present study, activated partial thromboplastin times were within reference limits in all 15 dogs that were evaluated. Before attenuation in another study,44 activated partial thromboplastin times were prolonged by > 25% in 20 of 39 (51.3%) dogs with congenital portosystemic shunts. In another investigation,45 mean activated partial thromboplastin time in dogs with congenital portosystemic shunts before attenuation was greater than the reference range used. Combined ages of dogs from those 2 studies44,45 ranged from 3 months to 3.5 years.For the 15 older dogs in the present study, the activated partial thromboplastin times may not be representative of a larger population of similar dogs; alternatively, the apparently normal activated partial thromboplastin times may be an age-related difference. Further investigation of coagulation profiles in dogs with EHPSSs is warranted.

There are several limitations to the present study, including the retrospective rather than prospective design, variety of surgeons and forms of shunt attenuation, long study period, lack of follow-up image procedures, and small sample size. Nevertheless, results of our study indicated that the immediate postoperative mortality rate in the cohort of older dogs was similar to that previously reported4,8,10 for younger dogs. In addition, median survival time after surgery for the dogs of this report was 6 years; in surviving dogs, clinical signs of liver disease were ameliorated and biochemical indicators of liver function were improved, compared with findings before shunt attenuation. Given the perioperative complication rate and acceptable long-term survival, the authors believe that it is reasonable to recommend surgical attenuation of EHPSSs in dogs ≥ 5 years old.

ABBREVIATION

EHPSS

Extrahepatic portosystemic shunt

a.

The LIFETEST procedure, The SAS System, version 9.1, SAS Institute Inc, Cary, NC.

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    Swalec KM, Smeak DD. Partial versus complete attenuation of single portosystemic shunts. Vet Surg 1990;19:406411.

  • 25

    Bostwick DR, Twedt DC. Intrahepatic and extrahepatic portal venous anomalies in dogs: 52 cases (1982–1992). J Am Vet Med Assoc 1995;206:11811185.

    • Search Google Scholar
    • Export Citation
  • 26

    Sereda CW, Adin CA. Methods of gradual vascular occlusion and their applications in treatment of congenital portosystemic shunts in dogs: a review. Vet Surg 2005;34:8391.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 27

    Vogt JC, Krahwinkel DJ, Bright RM, et al. Gradual occlusion of extrahepatic portosystemic shunts in dogs and cats using the ameroid constrictor. Vet Surg 1996;25:495502.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28

    Youmans KR, Hunt GB. Cellophane banding for the gradual attenuation of single extrahepatic portosystemic shunts in eleven dogs. Aust Vet J 1998;76:531537.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 29

    Harvey J, Erb HN. Complete ligation of extrahepatic congenital portosystemic shunts in nonencephalopathic dogs. Vet Surg 1998;27:413416.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 30

    Wolschrijn CF, Mahapokai W, Rothuizen J, et al. Gauged attenuation of congenital portosystemic shunts: results in 160 dogs and 15 cats. Vet Q 2000;22:9498.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 31

    Hunt GB. Effect of breed on anatomy of portosystemic shunts resulting from congenital diseases in dogs and cats: a review of 242 cases. Aust Vet J 2004;82:746749.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 32

    Tobias KM. Portosystemic shunts and other vascular anomalies. In:Slatter D, ed.Textbook of small animal surgery. 3rd ed. Philadelphia: Saunders Co, 2003;727752.

    • Search Google Scholar
    • Export Citation
  • 33

    Matushek KJ, Bjorling D, Mathews K. Generalized motor seizures after portosystemic shunt ligation in dogs: five cases (1981–1988). J Am Vet Med Assoc 1990;196:20142017.

    • Search Google Scholar
    • Export Citation
  • 34

    Francavilla JA, Porter KA, Benichou J, et al. Liver regeneration in dogs: morphologic and chemical changes. J Surg Res 1978;25:409419.

  • 35

    Mathie RT, Lieberman DP, Harper AM, et al. The role of liver blood flow in the control of liver size. J Surg Res 1979;27:139144.

  • 36

    Starzl TE, Porter KA, Francavilla JA, et al. A hundred years of hepatotrophic controversy. In: Hepatotrophic factors. Wiley, Amsterdam: CIBA Symposium Amsterdam, Elsevier, 1978;111138.

    • Search Google Scholar
    • Export Citation
  • 37

    Court FG, Wemyss-Holden SA, Dennison AR, et al. The mystery of liver regeneration. Br J Surg 2002;89:10891095.

  • 38

    Theise ND, Nimmakayalu M, Gardner R, et al. Liver from bone marrow in humans. Hepatology 2000;32:1116.

  • 39

    Alison MR, Poulsom R, Jeffery R, et al. Hepatocytes from nonhepatic adult stem cells. Nature 2000;406: 257.

  • 40

    Gao Z, McAlister VC, Williams GM. Repopulation of liver endothelium by bone-marrow-derived cells. Lancet 2001;357:932933.

  • 41

    Tobias KM, Besser TE. Evaluation of leukocytosis, bacteremia, and portal vein partial oxygen tension in clinically normal dogs and dogs with portosystemic shunts. J Am Vet Med Assoc 1997;211:715718.

    • Search Google Scholar
    • Export Citation
  • 42

    Edgcomb LP, Knol JA, Strodel WE, et al. Differential effects of portal diversion on hepatocyte function (HF) and hepatic reticuloendothelial cell (HRES) activity in the dog. J Surg Res 1982;33:233244.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 43

    Edgcomb LP, Eckhauser FE, Porter-Fink VL, et al. Effects of portacaval shunt and portacaval transposition on hepatocellular reticuloendothelial cell activity in the dog. J Surg Res 1984;36:446452.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 44

    Niles JD, Williams JM, Cripps PJ. Hemostatic profiles in 39 dogs with congenital portosystemic shunts. Vet Surg 2001;30:97104.

  • 45

    Kummeling A, Teske E, Rothuizen J, et al. Coagulation profiles in dogs with congenital portosystemic shunts before and after surgical attenuation. J Vet Intern Med 2006;20:13191326.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • Figure 1—

    Kaplan-Meier survival curve of overall survival in 17 dogs that were each ≥ 5 years old and underwent surgical treat-ment of an EHPSS. Squares indicate patient death.

  • 1

    Breznock EM. Surgical manipulation of portosystemic shunts in dogs. J Am Vet Med Assoc 1979;174:819826.

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    Rothuizen J, Van DenIngh S, Voorhout G, et al. Congenital portosystemic shunts in sixteen dogs and three cats. J Small Anim Pract 1982;23:6781.

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  • 3

    Johnson CA, Armstrong PJ, Hauptman JG. Congenital portosystemic shunts in dogs: 46 cases (1979–1986). J Am Vet Med Assoc 1987;191:14781483.

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  • 4

    Lawrence D, Bellah JR, Diaz R. Results of surgical management of portosystemic shunts in dogs: 20 cases (1985–1990). J Am Vet Med Assoc 1992;201:17501753.

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  • 5

    Tisdall PL, Hunt GB, Bellenger CR, et al. Congenital portosystemic shunts in Maltese and Australian cattle dogs. Aust Vet J 1994;71:174178.

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  • 6

    Holt DE, Schelling CG, Saunders HM, et al. Correlation of ultrasonographic findings with surgical, portographic, and necropsy findings in dogs and cats with portosystemic shunts: 63 cases (1987–1993). J Am Vet Med Assoc 1995;207:11901193.

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  • 7

    Murphy ST, Ellison GW, Long M, et al. A comparison of the ameroid constrictor versus ligation in the surgical management of single extrahepatic portosystemic shunts. J Am Anim Hosp Assoc 2001;37:390396.

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  • 8

    Winkler JT, Bohling MW, Tillson DM, et al. Portosystemic shunts: diagnosis, prognosis, and treatment of 64 cases (1993–2001). J Am Anim Hosp Assoc 2003;39:169185.

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  • 9

    Hurn SD, Edwards GA. Perioperative outcomes after three different single extrahepatic portosystemic shunt attenuation techniques in dogs: partial ligation, complete ligation and ameroid constrictor placement. Aust Vet J 2003;81:666670.

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  • 10

    Mehl ML, Kyles AE, Hardie EM, et al. Evaluation of ameroid ring constrictors for treatment for single extrahepatic portosystemic shunts in dogs: 168 cases (1995–2001). J Am Vet Med Assoc 2005;226:20202030.

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  • 11

    Frankel D, Seim H, MacPhail C, et al. Evaluation of cellophane banding with and without intraoperative attenuation for treatment of congenital extrahepatic portosystemic shunts in dogs. J Am Vet Med Assoc 2006;228:13551360.

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  • 12

    Ewing GO, Suter PF, Bailey CS. Hepatic insufficiency associated with congenital anomalies of the portal vein in dogs. J Am Anim Hosp Assoc 1974;10:463476.

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  • 13

    Strombeck DR, Breznock EM, McNeel S. Surgical treatment for portosystemic shunts in two dogs. J Am Vet Med Assoc 1977;170:13171319.

  • 14

    Gofton N. Surgical ligation of congenital portosystemic venous shunts in the dog: a report of three cases. J Am Anim Hosp Assoc 1978;14:728733.

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  • 15

    Center SA, Magne ML. Historical, physical examination, and clinicopathologic features of portosystemic vascular anomalies in the dog and cat. Semin Vet Med Surg 1990;5:8393.

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  • 16

    Brockman DJ, Brown DC, Holt DE. Unusual congenital portosystemic communication resulting from persistence of the extrahepatic umbilical vein. J Soc Adm Pharm 1998;39:244248.

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  • 17

    Smith KR, Bauer M, Monnet E. Portosystemic communications: follow-up of 32 cases. J Soc Adm Pharm 1995;36:435440.

  • 18

    Meyer HP, Rothuizen J, VanSluus FJ, et al. Progressive remission of portosystemic shunting in 23 dogs after partial closure of congenital portosystemic shunts. Vet Rec 1999;144:333337.

    • Crossref
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  • 19

    Kummeling A, VanSluijs FJ, Rothuizen J. Prognostic implications of the degree of shunt narrowing and of the portal vein diameter in dogs with congenital portosystemic shunts. Vet Surg 2004;33:1724.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20

    Niles JD, Williams JM, Cripps PJ. Hemostatic profiles in 39 dogs with congenital portosystemic shunts. Vet Surg 2001;30:97104.

  • 21

    Hottinger HA, Walshaw R, Hauptman JG. Long-term results of complete and partial ligation of congenital portosystemic shunts in dogs. Vet Surg 1995;24:331336.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 22

    Hunt GB, Hughes J. Outcome after extrahepatic portosystemic shunt ligation in 49 dogs. Aust Vet J 1999;77:303307.

  • 23

    Komtebedde J, Koblik PD, Breznock EM, et al. Long-term clinical outcome after partial ligation of single extrahepatic vascular anomalies in 20 dogs. Vet Surg 1995;24:379383.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 24

    Swalec KM, Smeak DD. Partial versus complete attenuation of single portosystemic shunts. Vet Surg 1990;19:406411.

  • 25

    Bostwick DR, Twedt DC. Intrahepatic and extrahepatic portal venous anomalies in dogs: 52 cases (1982–1992). J Am Vet Med Assoc 1995;206:11811185.

    • Search Google Scholar
    • Export Citation
  • 26

    Sereda CW, Adin CA. Methods of gradual vascular occlusion and their applications in treatment of congenital portosystemic shunts in dogs: a review. Vet Surg 2005;34:8391.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 27

    Vogt JC, Krahwinkel DJ, Bright RM, et al. Gradual occlusion of extrahepatic portosystemic shunts in dogs and cats using the ameroid constrictor. Vet Surg 1996;25:495502.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28

    Youmans KR, Hunt GB. Cellophane banding for the gradual attenuation of single extrahepatic portosystemic shunts in eleven dogs. Aust Vet J 1998;76:531537.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 29

    Harvey J, Erb HN. Complete ligation of extrahepatic congenital portosystemic shunts in nonencephalopathic dogs. Vet Surg 1998;27:413416.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 30

    Wolschrijn CF, Mahapokai W, Rothuizen J, et al. Gauged attenuation of congenital portosystemic shunts: results in 160 dogs and 15 cats. Vet Q 2000;22:9498.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 31

    Hunt GB. Effect of breed on anatomy of portosystemic shunts resulting from congenital diseases in dogs and cats: a review of 242 cases. Aust Vet J 2004;82:746749.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 32

    Tobias KM. Portosystemic shunts and other vascular anomalies. In:Slatter D, ed.Textbook of small animal surgery. 3rd ed. Philadelphia: Saunders Co, 2003;727752.

    • Search Google Scholar
    • Export Citation
  • 33

    Matushek KJ, Bjorling D, Mathews K. Generalized motor seizures after portosystemic shunt ligation in dogs: five cases (1981–1988). J Am Vet Med Assoc 1990;196:20142017.

    • Search Google Scholar
    • Export Citation
  • 34

    Francavilla JA, Porter KA, Benichou J, et al. Liver regeneration in dogs: morphologic and chemical changes. J Surg Res 1978;25:409419.

  • 35

    Mathie RT, Lieberman DP, Harper AM, et al. The role of liver blood flow in the control of liver size. J Surg Res 1979;27:139144.

  • 36

    Starzl TE, Porter KA, Francavilla JA, et al. A hundred years of hepatotrophic controversy. In: Hepatotrophic factors. Wiley, Amsterdam: CIBA Symposium Amsterdam, Elsevier, 1978;111138.

    • Search Google Scholar
    • Export Citation
  • 37

    Court FG, Wemyss-Holden SA, Dennison AR, et al. The mystery of liver regeneration. Br J Surg 2002;89:10891095.

  • 38

    Theise ND, Nimmakayalu M, Gardner R, et al. Liver from bone marrow in humans. Hepatology 2000;32:1116.

  • 39

    Alison MR, Poulsom R, Jeffery R, et al. Hepatocytes from nonhepatic adult stem cells. Nature 2000;406: 257.

  • 40

    Gao Z, McAlister VC, Williams GM. Repopulation of liver endothelium by bone-marrow-derived cells. Lancet 2001;357:932933.

  • 41

    Tobias KM, Besser TE. Evaluation of leukocytosis, bacteremia, and portal vein partial oxygen tension in clinically normal dogs and dogs with portosystemic shunts. J Am Vet Med Assoc 1997;211:715718.

    • Search Google Scholar
    • Export Citation
  • 42

    Edgcomb LP, Knol JA, Strodel WE, et al. Differential effects of portal diversion on hepatocyte function (HF) and hepatic reticuloendothelial cell (HRES) activity in the dog. J Surg Res 1982;33:233244.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 43

    Edgcomb LP, Eckhauser FE, Porter-Fink VL, et al. Effects of portacaval shunt and portacaval transposition on hepatocellular reticuloendothelial cell activity in the dog. J Surg Res 1984;36:446452.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 44

    Niles JD, Williams JM, Cripps PJ. Hemostatic profiles in 39 dogs with congenital portosystemic shunts. Vet Surg 2001;30:97104.

  • 45

    Kummeling A, Teske E, Rothuizen J, et al. Coagulation profiles in dogs with congenital portosystemic shunts before and after surgical attenuation. J Vet Intern Med 2006;20:13191326.

    • Crossref
    • Search Google Scholar
    • Export Citation

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