22ND FECAVA. Eurocongress. 31. VÖK Jahrestagung. 31ST VOEK Annual Meeting June 2016 Hofburg, Vienna.

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1 22ND FECAVA Eurocongress 31. VÖK Jahrestagung 31ST VOEK Annual Meeting June 2016 Hofburg, Vienna Proceedings Proceedings

2 22. FECAVA Eurocongress 31 st Annual Congress of the Association of Austrian small animal veterinarians Soft Tissue Surgery - Shunts Soft Tissue Surgery - Wounds Hofburg, Vienna June 22-25,

3 Table of content Speakers... 4 Portosystemic Shunts: Where Are We At?... 5 Imaging of portosystemic shunts...8 Portosystemic Shunts: Prognosis and Outcome Hepatic Vascular Anomalies Basic Tenets of Initial Open Wound Management Favorite wound dressings Advanced Wound Dressing Modalities

4 Speakers Univ. Prof. Dr. Gilles Dupré, Dipl. ECVS Austria Dr. med. vet. Tobias Schwarz MA DipECVDI DACVR DVR MRCVS United Kingdom Ass. Prof. Surgery Bryden Stanley, Surgery Section Chief USA Professor of Surgery Karen Tobias, DVM, MS, DACVS USA Chick (Charles) Weisse, Staff Surgeon, Director of Interventional Radiology Services USA 4

5 Portosystemic Shunts: Where Are We At? Karen Tobias, DVM, MS DACVS University of Tennessee, Knoxville TN Anatomy The portal vein is the major draining to the abdominal digestive tract and is formed from the cranial mesenteric vessels, caudal mesenteric vein, splenic vein, and gastroduodenal vein. It provides 75-80% of the afferent blood and 50% of the oxygen supply to the liver. Before reaching the liver, the portal vein divides into right and left portal branches, about 1 cm beyond the entry of the gastroduodenal tributary. The right portal vein is a short trunk that most commonly supplies the right lateral liver lobe and caudate process of the caudate lobe. The left portal vein gives off a right ventrolateral branch (the central portal vein), which supplies the right medial lobe; a papillary branch to the papillary process of the caudate lobe; and then branches to the quadrate, left medial, and left lateral lobes. Cats usually have 3 portal vein branches: right, central, and left. Within the liver portal vein branches divide into smaller and smaller tributaries. At the edge of hepatic lobules, the portal vein, bile duct, and hepatic artery lie adjacent to one another and are termed a portal triad. Four to 6 portal triads surround a single central vein, which is separated from these structures by sheets of hepatocytes and the capillaries between them, known as sinusoids. Blood from the portal venule enters the sinusoid at its outer end; it is joined downstream by arterial blood. This blood flows toward the central vein passing hepatocytes lining the space of Disse adjacent to the sinuoids. Bile and lymph in the opposite direction, toward the hepatic lobule s periphery. Congenital portosystemic shunts develop from patency of the ductus venosus (left intrahepatic shunt) or abnormalities in development or degeneration of embryologic cardinal and vitelline systems. Portocaval shunts empty directly or indirectly into the caudal vena cava. These shunts can be intrahepatic (right, left, or central IHPSS) or extrahepatic (e.g., portocaval, gastrophrenic, splenocaval, colonocaval EHPSS). Portoazygos veins connect a tributary of the portal vein (e.g., splenic or left gastric vein) to the azygos vein, usually crossing into the thorax between the crus of the diaphragm or at the aortic hiatus. Shunts that are intermittently compressed because of their location (e.g. portoazygos and portophrenic) may be associated with fewer clinical signs, lower fasting ammonia concentrations, and larger portal vein size. This may lead to diagnosis of these animals at a later age. Classification and Epidemiology of Congenital Hepatic Vascular Anomalies Congenital hepatic vasculary anomalies can be divided into several classifications, including congenital portosystemic shunts (usually single vessels); congenital portal vein hypoplasia without hypertension; congenital portal vein hypoplasia with portal hypertension (also called idiopathic noncirrhotic portal hypertension); congenital portal vein hypoplasia without portal hypertension (sometimes called microvascular dysplasia, based on histologic findings); and hepatic arteriovenous malformations, which cause portal hypertension and therefore result in development of multiple acquired shunts. 5

6 Congenital portosystemic shunts are reported in 0.18% of all dogs, with certain breeds at greater risk. Purebred dogs have a greater likelihood of diagnosis with congenital PSS. Congenital extrahepatic shunts are usually found in small breed dogs, although about 5% of large breed dogs with congenital PSS have extrahepatic shunts. In the United States, Yorkshire terriers have a risk at least 30 times greater than all other breeds. In one study of a US veterinary referral hospital, congenital PSS were diagnosed in 11% of Yorkies, 7.4% of Norwich terriers, 5% of pugs and Maltese, 4% of havanese, and 0.04% of mixed breed dogs. Congenital intrahepatic shunts are usually found in large breed dogs. In Europe, Irish wolfhounds were reportedly at greater risk for this condition, with a prevalence rate of %. Hereditary Aspects of Congenital Hepatic Vascular Anomalies In a recent study, the Maltese was found to have a suspected inherited predisposition for both congenital extrahepatic PSS and PVH-MVD, with a suspected partially penetrant, recessive mode of inheritance. Test matings of affected animals resulted in 25% of offspring with PSS, while test matings of affected and unaffected dogs resulted in 9% of offspring with PSS. In that study, 67% of all tested Maltese had bile acids >40 micromoles,l. In a study of Cairn terriers, the prevalence of congenital extrahepatic PSS (0.6%) was significantly higher than in the general population, and test matings of affected and unaffected related animals produced a higher prevalence (20%) of affected offspring. In that study, inheritance was considered autosomal and most likely polygenic or monogenic with variable expression. Shunts produced from those matings were portocaval (67%) or potoazygos, indicating a common genetic basis for abnormalities in cardinal and vitteline system transformation. In Irish wolfhounds, IHPSS has a digenic or polygenic mode of inheritance. Dogs with PSS have alterations in expression of multiple genes. Changes in expression of VCAM1, which is involved in angiogenesis, could result in inappropriate regression or remodeling of the embryonic vitelline system, an important factor in EHPSS development. Increased expression of WEE1 could result in a lack of response of the ductus venosus to changes in altered oxygen tension. Whether these genes are the direct cause of PSS development has yet to be elucidated. In other studies Irish wolfhounds were shown to have decreased expression of AHR, which is thought to play a role in ductus venosus closure. Expression did not differ in Irish wolfhounds with and without IHPSS, so this alteration alone is not the cause of IHPSS development. Hepatic Encephalopathy When 70% of liver function is lost, either through cell destruction or shunting of blood around the liver, neurologic abnormalities will manifest because of loss of brain function, known as hepatic encephalopathy. Although the pathogenesis of hepatic encephalopathy is not fully understood, a myriad of toxins are suspected to be involved, including ammonia, aromatic amino acids, endogenous benzodiazepines, GABA, glutamine, tryptophan, inflammatory cytokines, and others. Central effects if these toxins include cell swelling, inflammation, decreased electrical activity, impaired blood-brain barrier, decreased metabolism, and impaired cerebral function. Ammonia is one of the key measureable toxins; however, its concentrations does not always correlate with severity of clinical signs. In fact, although most dogs with hepatic encephalopathy from congenital PSS have hyperammonemia, some dogs have normal ammonia concentrations. 6

7 Dogs with congenital PSS have dramatic increases in whole blood manganese, a neurotoxin that is likely involved with development of hepatocephalopathy. A systemic inflammatory response can be associated hepatic encephalopathy: dogs with hepatic encephalopathy from congenital PSS are more likely to have increases in monocytes, neutrophils, and C-reactive protein and decreases in lymphocytes than dogs with PSS that have no neurologic signs. Other Clinical Findings Neurologic signs in young dogs can occur secondary to congenital or acquired PSS. Palpable ascites is more common in young dogs with acquired PSS (45%) than young dogs with congenital PSS (2%). Dogs with congenital PSS do not have hypergastrinemia or hyperinsulinemia. In terms of coagulation, some studies show no significant difference in bleeding times, platelet function analysis, and platelet counts of dogs with congenital PSS, while others show alterations in platelet function or agglutination. Overall most dogs with congenital PSS do not have clinically relevant abnormalities in hemostasis before surgery. 7

8 The Royal (Dick) School of Veterinary Studies The University of Edinburgh IMAGING OF PORTOSYSTEMIC SHUNTS: PROS AND CONS FOR EACH MODALITY T. Schwarz 1. INTRODUCTION Portosystemic shunts (PSS) are abnormal communications between the portal circulation and other venous vascular systems causing hepatic encephalopathy, raised bile acids and other abnormalities that relatively frequently occur in dogs and less commonly cats. PSS can occur as a congenital anomaly or as an acquired compensatory mechanism secondary to increased portal vein pressure due to a variety of hepatic conditions. Anatomically PSS can be divided into single and multiple, hepatic and extrahepatic shunt vessels. The three major categories are congenital single intrahepatic PSS, mostly seen in young large breed dogs, congenital single extrahepatic PSS, mostly seen in small breed dogs, and acquired multiple extrahepatic PSS secondary to a primary hepatic condition. However an increasing number of animals are now diagnosed with a shunt pattern that crosses over these boundaries, such as congenital multiple extrahepatic PSS, multiple intrahepatic PSS, shunts with intra- and extrahepatic component, PSS with several entrances but only one exit, PSS with a single entrance and several exits, a combination of intra- and extrahepatic shunts, and a combination of PSS with other vascular anomalies such as arteriovenous malformation and segmental caudal vena cava aplasia. 2. VASCULAR ANATOMY AND NORMAL VARIATIONS Abdominal aorta and branches The abdominal aorta runs in the left dorsal retroperitoneal spaces and gives off in caudal succession the celiac, right and left phrenicoabdominal, cranial mesenteric, right and left renal, right and left testicular/ ovarian, caudal mesenteric, right and left deep circumflex iliac, left and right external iliac arteries before dividing into right and left internal iliac arteries. These branches are all visible on arterial-phased low pitched CT angiography studies. Caudal vena cava and tributaries 8

9 The caudal vena cava (CVC) runs in the right dorsal abdomen from the right dorsal aspect of the liver towards the right ventral margin of the aorta in the caudal abdomen. Further caudally the CVC moves right and then dorsal to the aortic bifurcation. The CVC is formed by the confluence of the common iliac veins. In cranial succession the deep circumflex iliac, right testicular / ovarian, left and right renal, left and right phrenicoabdominal and hepatic veins join the CVC. There are usually two right hepatic veins entering the CVC separately, and the majority of left hepatic veins form a large vessel, the hepatic ampulla than joins the CVC from the left. These tributaries are all visible on low pitched CT angiography studies, best during the arterial phase where they are negatively contrasted against the enhancing hepatic parenchyma. Portal vein, tributaries and branches The jejunal and ileal veins form the cranial mesenteric vein, which makes an S-shaped dorsal and then cranial turn to receive the much smaller caudal mesenteric vein (usually from dorsal) at which point they form the portal vein. The portal vein then receives the large splenic vein from the left and just caudal to the porta hepatis the small gastroduodenal vein from right ventral. With each tributary the portal vein enlarges in diameter. Directly cranial to the gastroduodenal vein entrance the portal vein enters the liver and immediately gives off the short smaller right branch, that supplies the right lateral and caudate lobe, and continues as the larger left branch supplying the remaining lobes of the liver. The hepatic arteries run parallel to the portal veins in the caudal aspect of the liver. The hepatic veins run separately in the cranial aspect of the liver. There is great variation in the feeding pattern of the caudal mesenteric vein. In cats the portal vein can have a bulbous distension prior to the liver entrance. The portal veins can already be seen during the arterial phase, where they run adjacent to the contrast enhancing arteries, as non-enhanced vessels. 3. ABDOMINAL VASCULAR DISEASES Arterioportal hepatic fistula This is a are rare congenital abnormality in dogs in which the hepatic arteries feed into the portal vein with a single vessel or multiple (synonym arteriovenous malformation) tortuous shunt vessels, resulting in portal hypertension, hepatic encephalopathy and ascites. They are often combined with portosystemic shunts, complicating diagnosis. Imaging features Almost always peritoneal effusion 9

10 Test bolus shows portal vein time-attenuation graph similar to aorta with minimal delay. Single or multiple enlarged tortuous hepatic vessels that contrast enhance immediately after abdominal arteries May have abruptly decreasing aortic diameter caudal to celiac artery Distended portal vein branches Microhepatia Portosystemic shunts Portosystemic shunts can be classified according to different criteria: The classification of PSS is an evolving process, as more and more shunt types and combinations according to the different criteria are being identified with advanced imaging modalities. PSS are relatively common in dogs, and the most common shunt types are single extrahepatic in small breed dogs and single intrahepatic in large breeds. The left-divisional intrahepatic shunt is synonymous with a patent ductus venosus Arantii. PSS are rare in cats, the most common type here is an extrahepatic portoazygos shunt. Intrahepatic PSS are usually of assumed congenital origin, whereas extrahepatic shunts can be congenital or secondary to some form of portal hypertension. The assumption that multiple extrahepatic shunts are always acquired is not correct. Microvascular portal vein dysplasia is a condition where shunting only occurs at microscopic level, requiring a liver biopsy for confirmation. CT is used to rule out a macroscopic shunt. Dynamic CT has potential to aid in further diagnostic by calculation of the hepatic perfusion index. Imaging features General features Microhepatia Renomegaly (inconsistent) Urolithiasis Cachexia Enlarged tortuous hepatic arteries Periportal oedema (unknown significance) Gastric foreign bodies (allotriophagia) 10

11 Reduced portal vein diameter cranial to shunting portal tributary vein (extrahepatic shunt) Cessation or reduction of portal enhancement distal to intrahepatic shunt origin. Single right-divisional intrahepatic portosystemic shunt Wide tortuous intrahepatic shunt vessels in right lateral lobe Originates from right portal branch directly at liver entrance Connects to CVC from right with one ore multiple connections Single central-divisional intrahepatic portosystemic shunt Short bulbous intrahepatic shunt vessel in central part of liver Connects left branch with CVC Usually narrowed lumen at either shunt end Single left-divisional intrahepatic portosystemic shunt Wide tortuous intrahepatic shunt vessel in left liver half Originates from left portal branch, curves lateral, then dorsal, to connect to the hepatic ampulla Common single extrahepatic shunt types Originating from the left gastric vein, curving along the minor curvature of the stomach, continuing over the dorsal liver margin to connect to the CVC between liver and diaphragm. Originating from the gastroduodenal and left gastric veins, merging to feed in the CVC from the left, cranial to the kidneys. Originating from the splenic vein and connecting to the azygos vein. Common multiple extrahepatic shunt types Multiple small chaotic vessels between great vessels and left kidney and around left kidney, less commonly right kidney Oesophageal vascular enlargement with varix formation Segmental caudal vena cava aplasia This is an increasingly frequently reported congenital anomaly in dogs in which the pre-renal CVC segment between the kidneys and the liver has not been formed. Post-renal caval blood is shunted to a right or anomalous left azygos vein. The condition can be incidental as the cavo-azygos shunt is a functional conduit, but it is associated with significant morbidity in about 25% of cases, due to either thrombosis in the aneurismal cavo-azygos shunt vessel or associated portosystemic shunts. In some cases the portal vein completely connects to the 11

12 azygos vein making it inoperable. CT-angiography is therefore an excellent modality to assess the need for and possibility of surgical intervention. 4. COMPARISON OF IMAGING MODALITIES Diagnostic Ultrasound Pros: Only sedation is required, no general anaesthesia Very effective in experienced hands Relatively quick procedure Non-invasive US contrast medium can improve sensitivity and specificity Cons: Experienced ultrasonographer required Patient compliance and GI gas may prevent complete diagnosis Difficult to confirm absence of shunt even for experienced sonographer Other body parts such as brain and thorax which may be related to clinical signs are not examined Difficult to confidently diagnose complex and combined vascular anomalies Insufficient for sizing for interventional procedures Potential side effects from US contrast media Mesenteric or splenic portography Pros: Can be done as intraoperative procedure in time efficient manner Very efficient in experienced hand Relatively quick procedure Shows detailed pattern of portal branching Absence of a shunt can be confirmed confidently Sufficient for sizing for interventional procedures Often part of interventional procedure Cons: Requires general anaesthesia Invasive procedure Two views are often required which can be difficult to achieve in an operating theatre Potential side effects from iodinated contrast medium Experienced operator required Other body parts such as brain and thorax which may be related to clinical signs are not examined Other vascular anomalies will only be diagnosed if they are looked for For sizing, magnification needs to be calculated 12

13 Scintigraphy Pros: Only sedation is required, no general anaesthesia Very quick procedure Absence or presence of a shunt can be confirmed confidently Non-invasive Easy to interpret Cons: Requires usually at least 1 day of preparation to order radiopharmaceutical Only gives diagnosis PSS yes / no Animal is radioactive for at least 6h, precluding contact in that time Not sufficient for most planned surgical or interventional procedures Computed Tomography Pros: Relatively quick procedure Absence or presence of a shunt can be confirmed confidently Exact shunt anatomy can be described in detail Other vascular anomalies can be detected and characterised excellently Excellent detail to screen for other abdominal and thoracic procedures Ideal for sizing for interventional procedures Non-invasive Cons: Requires general anaesthesia Potential side effects of iodinated contrast medium Brain can be examined for neurologic conditions, however sensitivity and specificity for brain diseases is only moderate Magnetic Resonance Imaging Pros: Relatively quick procedure Non-invasive Excellent modality for examination of nervous system With 3T magnet MR Spectroscopy can be helpful differentiating hepatic encephalopathy from other neurologic conditions Cons: Requires general anaesthesia Absence of a PSS cannot be determined confidently 13

14 Relatively poor detail of shunt anatomy and limited anatomic reference structures visible Potential side effects of Gadolinium contrast medium Inadequate for sizing of interventional procedures 5. FURTHER READING Frank P, Mahaffey M, Egger C, Cornell KK. Helical computed tomography in 10 normal dogs and 10 dogs with a portosystemic shunt. Vet Radiol Ultrasound 2003;44: Schwarz T, Rossi F, Wray JD, Åblad B, Beal MW, Kinns J, et al. Computed tomographic and magnetic resonance imaging features of canine segmental caudal vena cava aplasia. J Small Anim Pract 2009;50: Zwingenberger AL, McLear RC, Weisse C. Diagnosis of arterioportal fistulae in four dogs using computed tomographic angiography. Vet Radiol Ultrasound 2005;46: Zwingenberger AL, Schwarz T. Dual-phase CT angiography of the normal canine portal and hepatic vasculature. Veterinary Radiol Ultrasound 2004;45: Zwingenberger AL, Schwarz T, Saunders HM. Helical CT angiography of canine portosystemic shunts. Vet Radiol Ultrasound 2005;46: Address of the author: Dr. Tobias Schwarz Diagnostic Imaging Service Royal (Dick) School of Veterinary Studies The University of Edinburgh, Easter Bush Roslin, EH25 9RG, UK Tobias.Schwarz@ed.ac.uk 14

15 Portosystemic Shunts: Prognosis and Outcome A literature review Karen Tobias, DVM, MS, DACVS University of Tennessee, Knoxville TN In their review article Treatment of extrahepatic congenital portosystemic shunts in dogs- what is the evidence base? (JSAP 2012,53:3-11), Dr. Tivers et al provided an excellent review of the literature. Most notable was the variability in evaluating outcome amongst studies and the lack of evidence for treatment and short- and long-term outcomes of dogs with portosystemic shunts. In general, perioperative mortality rates for congenital extrahepatic (EH) PSS range from 2-32% after suture ligation, about 7% after ameroid constrictor placement, and 6-9% after cellophane banding. In dogs with intrahepatic (IH) PSS, mortality rates are 6-23% after suture ligation, 0-9% after ameroid constrictor placement, and 27% after cellophane banding if the shunt is purposefully attenuated during surgery. In general dogs undergoing suture ligation of portosystemic shunts (PSS) have a reported mortality rate of 2-28%. Portal hypertension occurs in 2-14% of dogs undergoing ligation, and is less common in dogs undergoing gradual occlusion of EHPSS. Seizures are reported in 3-18% of dogs and 8-22% of cats undergoing PSS attenuation. Recurrence of clinical signs is more difficult to analyze, since many patients are still on medical management at the time of follow-up, even if none is actually need. Of dogs surviving surgery for attenuation of EHPSS, 78-94% have no clinical signs. Outcome is best for dogs undergoing complete attenuation. For dogs with IHPSS, good to excellent short term outcomes are reported in 70% to 89% of dogs with intrahepatic portosystemic shunts that underwent ameroid constrictor placement, 76% to 100% of dogs that underwent ligation, and 50% of dogs that underwent cellophane banding with intraoperative attenuation. Probability of long-term survival without recurrence was 60% to 61% at 1 year and 55% to 56% at 2 to 4 years. Previously reported preoperative predictors of a positive outcome include absence of neurologic signs, albumin or total protein, and greater liver volume for the body weight. In general, age is not related to outcome. Variable correlations with outcome have been noted with other factors such as white blood cell count, packed cell volume, and shunt location. In the more recent literature, other factors have been evaluated in terms of predicting or effecting outcome: Effects of Shunt Location Intermittent compression of the shunt, based on its location, likely reduces occurrence of clinical signs in dogs with congenital PSS. In dogs with portophrenic shunts, portal vein diameter is larger and ammonia concentrations lower than with other shunts. Preoperative clinical signs are more common in dogs with caval, rather than azygos, insertions and with subdiaphragmatic (e.g. splenocaval), vs portophrenic, insertions. Urinary signs were more common with right gastric shunts, rather than gastrosplenic. Dogs with shunts crossing or travelling within the diaphragm had fewer neurologic signs. MB Kraun et al, J Am Vet Med Assoc. September 1, 2014;245(5): In one study, 64/172 shunts were splenophrenic, and one dogs had 2 shunts. Dogs with splenophrenic shunts have lower fasting ammonia concentrations than those with splenocaval shunts and have larger portal vein/aortic ratios than dogs with splenoazygos, gastrocaval, or splenocaval shunts. K Fukushima et al, Vet J. March 2014;199(3):

16 Predictive Value of Diagnostics: The absence of vessels on preattenuation vascular studies does NOT mean they will not be present after the shunt has been attenuated. Dogs that had no visible vasculature on preoperative CT angiography had visible portal vasculature after ameroid constrictor placement. Allison L Zwingenberger et al, Vet Surg. November 2014;43(8): At this time, liver biopsies cannot be used to predict outcome after congenital PSS attenuation, including whether dogs develop portal hypertension and multiple acquired shunts..hepatic steatosis is associated with age of the dog but is not associated with development of multiple acquired shunts after shunt attenuation. Geraldine B Hunt et al, Vet Surg. November 2014;43(8): Certain factors can be used to predict which dogs can be ligated completely. Vascular endothelial growth factor increases after shunt attenuation; dogs that can be ligated completely have a significantly greater expression of VEGF2 mrna. MS Tivers et al, J Vet Intern Med Sep-Oct;28(5): Dogs that underwent complete ligation had significantly greater MAT2, VEGFR2, and TGFbetaR2 R=mRNA expression. MS Tivers et al, Gut 2012, 61 (Suppl 2):A127. Coagulopathies, while present in some dogs, do not usually cause clinical problems. Dogs with CPSS had significantly prolonged PT, lower platelet counts, lowere AT and protein C activity, indreased d-dimers and factor VIII, more TEG abnormalities. 9/21 dogs were considered hypercoagulable; these dogs were more likely to have hepatic encephalopathy. D Kelley et al, J Vet Intern Med Sep-Oct;27(5): Certain factors can be used to predict outcome, particularly when combined with other variables. Albumin, methionine adenosyltransferase 2 alpha and HGF activator are positively associated with complete recoverey after congenital PSS ligation. The cut-off value for albumin was 19.5 g/; albumin alone was not a good predictor, nor were.other tested genes/gene products. Anne Kummeling; Vet J. March 2012;191(3): Surgery Surgery is still the treatment of choice, and age at surgery does not affect survival. Survival is significantly longer with surgical treatment (median>2156 days) versus medical management (836 days). Survival was not associated with the age at diagnosis or the shunt type. SN Greenhalgh et al, J Am Vet Med Assoc. September 1, 2014;245(5): Dogs improve after surgery because of increased portal flow to hepatic sinusoids and subsequent hepatocellular regeneration. 16

17 Shunt attenuation results in increase hepatic growth factor concentration, likely a reflection of hepatocellular proliferation and regeneration in response to improved blood supply. MS Tivers, Vet J. May 2014;200(2): Intravascular coiling techniques, when performed by an experienced surgeon, can be extremely successful for treatment of intrahepatic PSS, as long as dogs are maintained lifelong on medications that reduce gastric acid production. Use of an intravascular (Amplatz) device was also possible in 5 of 7 dogs with extrahepatic PSS. One hundred dogs with IHPSS (38% right, 33% left, 19% central, and 10% complex) were evaluated for endovascular repair. Of 95 dogs that underwent 11 episodes of endovascular coiling of IHPSS, 14/111 developed major acute complications (most commonly seizures or hepatoencephalopathy) and 3 developed intraoperative complications (temporary portal hypertension or gastrointestinal bleeding). Full occlusion was possible in 3 dogs. Median survival was 2204 days, with 57/86 having an excellent survival. Dogs with IHPSS commonly have gastrointestinal ulceration and must be kept on omeprazole for life. C Weisse et al, J Am Vet Med Assoc. January 1, 2014;244(1): Of 7 dogs weighing kt, one could not tolerate complete temporary occusion. Of 6 remaining dogs, complete occlusion was attained in 5, and 4 of those 5 had resolution of signs and laboratory abnormalities. DF Hogan et al, JVIM 2010;24: Ameroid constrictors are successful in resolving clinical signs in many patients. Closure of congenital portosystemic shunts after ameroid constrictor placement relies on development of inflammation and fibrosis stimulated by the device. Ameroid constrictors themselves do not close completely. Residual flow is detected in 18% of dogs, although it is not significant enough to increase the shunt fraction in most dogs. Geraldine B Hunt et al, Vet Surg. October 2014;43(7): Of 206 dogs that underwent ameroid constrictor placement on single congenital EHPSS, mortality rates (<1 month postop) were 7.3%. Follow-up was available on 112 dogs (median, 54 months); 92% had no clinical signs. Long term, intact dogs and those with higher WBC counts and lower bile acids were more likely to survive. Those in the later study group had a better survival rate. EL Falls et al, Vet Surg. November 2013;42(8): Cellophane banding also relies on fibrous tissue formation to cause shunt attenuation. The difficulty with evaluating outcome of cellophane banding is that there is no medical grade cellophane available commercially for shunt occlusion. Thin films used for cellophane banding are not usually true cellophane but some sort of plastic. RR Smith et al, Vet Surg. May 2013;42(4): Besides classic findings of microvascular dysplasia, cats with congenital PSS may also have fibrosis and hepatocellular swelling. Partial attenuation of shunts will not encourage histologic improvement of the liver in cats. In cats with CPSS, liver biopsies are similar to dogs (portal vein hypoplasia and arteriolar hyperplasia), but other findings included hepatocyte swelling (50%) and fibrosis (42.5%), which 17

18 was usually mild. After partial attenuation, there was no significant change in histologic features of the liver. This is different from in dogs, where 44% had histologic improvement after surgery. However, in the cat study, biopsies were performed on cats that had partial shunt ligation and needed a second surgery or had a post mortem, so that may be the reason histologic abnormalities persisted. F Swinbourne et al, Vet Rec. April 2013;172(14):362. Anticonvulsants and Postoperative Outcome Some clinicians recommend levatiracetam (Keppra) before and after surgery to reduce the risk of seizures. Although one retrospective study supported its use, there have been no randomized, controlled studies. Surgeons anecdotally have reported postoperative seizures in dogs pretreated with Keppra before shunt attenuation. In a retrospective study of 176 dogs, 50 received preattenuation anticonvulsant drugs other than levetiracetam (Keppra) and were excluded from the study; 42 received Keppra, none of which had seizures after surgery; and 84 received no anticonvulsant drugs, 5% of which had postattenuation seizures. Duration of Keppra treatment ranged from 1 to 210 days, and dose ranged from 30 to 83 mg/kg/day (divided in some cases?). Postoperative treatment with levatiracetam ranged from 0-99 days. Dogs that received Keppra preoperatively tended to have neurologic dysfunction and higher ammonia at presentation. Postoperative diarrhea was more common in dogs receiving Keppra. All the dogs that received Keppra were admitted during 2007 or later, and preoperative and intraoperative management of patients was not evaluated to see whether it changed over the time period. KJ Fryer et al J Vet Intern Med Nov- Dec;25(6):

19 22 nd FECAVA Eurocongress June 2016 Hofburg, VIENNA HEPATIC VASCULAR ANOMALIES: RECENT LESSONS LEARNED USING INTERVENTIONAL RADIOLOGY Chick Weisse, VMD, DACVS Animal Medical Center, NY,NY INTRODUCTION Interventional Radiology uses fluoroscopy to guide minimally-invasive therapies. There is currently expanding investigation into the use of these techniques in various areas of veterinary medicine, including but not limited to the arterial and venous systems. The morbidity associated with certain open surgical procedures in these areas, particularly in compromised patients, makes these minimally-invasive approaches increasingly appealing. Moreover, the lack of treatment alternatives available for more complex, terminal, or end-stage diseases when traditional therapies have failed has inspired research into potential uses for these techniques, many of which have become the standard-of-care in human medicine. This lecture will review some of the interventional procedures currently performed in the hepatic arterial and venous systems of veterinary patients and some of the lessons learned or more importantly the new questions raised using these techniques. HEPATIC VASCULAR ANOMALIES The categorization of liver vascular anomalies is often confusing and but the most recent classification suggests three separate categories of liver vascular disease: (1) Congenital portosystemic shunts (IHPSS and EHPSS), (2) Disorders associated with abnormal hepatic bloodflow or portal hypertension, currently termed Primary Hypoplasia of the Portal Vein (PVH), and (3) Disturbances in outflow. The second category (PVH) remains the most confusing, and includes processes that may or may not result in portal hypertension. These are termed PVH with portal hypertension and PVH without portal hypertension. Examples of PVH with portal hypertension include non-cirrhotic portal hypertension (NCPH), and hepato-portal fibrosis/veno-occlusive disease. PVH without portal hypertension was previously termed microvascular dysplasia (MVD). IHPSS (and EHPSS): Single, extrahepatic PSSs are amenable to relatively uncomplicated surgical attenuation, however surgical repair of intrahepatic PSSs are consistently more challenging. Numerous techniques have been described for intrahepatic PSS attenuation, however morbidity and mortality rates can be very high, even for the most experienced surgeons. The goal of IR techniques for IHPSSs is to reduce the unacceptably high, peri-operative mortality rates associated with traditional open surgical techniques and hopefully improve the outcome for these cases. The author has performed over 100 percutaneous transvenous coil embolizations (PTCE) with a vena caval stent and thrombogenic coils placed within the shunt. Peri-operative complications were mostly minor and peri-operative mortalities were comparatively low versus that reported for traditional surgery. PROCEDURE: Percutaneous Transvenous Coil Embolization- All dogs are treated medically initially following diagnosis of the IHPSS for a period of weeks to months. When possible, CT or MR angiography is performed to delineate the shunt anatomy and obtain caval and shunt measurements under a separate anesthetic episode. All PTCE procedures are performed under general anesthesia using standard liver dysfunction protocols and often neuromuscular blockade to minimize respiratory artifact during digital subtraction angiography. Shunts are typically accessed by a percutaneous right jugular approach. Contrast venography is performed to delineate the portal vein, portosystemic shunt, and caudal vena cava anatomy. Intravascular pressure measurements are obtained in the caudal vena cava and portal vein. Shunt attenuation involves placement of a stent within the caudal vena cava, positioned so as to traverse the shunt entrance into the vena cava. Shunt PTCE is subsequently performed by passage of a catheter through the stent interstices and deposition of the coils within the shunt lumen. Coils are subsequently added with intermittent shunt pressure measurements taken to avoid creating portal hypertension. Coils are typically added until the shunt mouth is covered with coils or the shunt pressures have increased between 6 and 10cm H 2O or maximal pressures approached 20cm H 2O. Ultimate shunt and caval pressures are recorded, the jugular sheath is exchanged for a 7Fr multi-lumen catheter, and the animal is recovered from anesthesia. Following the initial procedure, medications are gradually weaned over the following 4-8 weeks. Additional PTCE is recommended if clinical signs returned. LESSONS LEARNED: Lessons learned or questions raised concerning DIAGNOSTIC IMAGING include: -CT and MR angiography are well tolerated and facilitate identifications of uncommon shunt anatomy, however certain abnormalities are underestimated using these techniques. For instance, multiple small intrahepatic shunts are often not identified on standard cross-sectional imaging. These abnormalities are better identified with traditional contrast portography. It is not clear if dual phase CT provides us with additional important information at this time (as compared to single-phase). -MRA(using gadolinium) may permit single procedure IHPSS imaging and treatment in order to avoid excessive iodinated contrast use associated with CT angiography following by angiography. 19

20 22 nd FECAVA Eurocongress June 2016 Hofburg, VIENNA -Even typical IHPSS have variant hepatic vein anatomy. Does location of HV entrance into the PSS affect results of attenuation? It is conceivable that intra-hepatic vein shunting (acquired intrahepatic PSS) may occur ore readily in these patients. Examples will be discussed. Lessons learned or questions raised concerning TREATMENT include: -A certain small population of IHPSS patients have significant portal:systemic venous pressure gradients (or resting portal pressures) before treatment. This is counter-intuitive in animals with PSS in that reduced portal pressure gradients would be anticipated, and this has prevented treatment in some cases. Are there small vascular windows or narrowings present that are not identified on cross sectional imaging with relatively wide slices? This suspicion has been raised as pull-out pressure tracings confirm short, focal areas where pressure gradients exist. The presence of a developed portal system may suggest a narrowing of the shunt in some location making access more difficult. This may be the same for EHPSS suggesting intermittent shunt compression in phrenic shunts for instance!! -Which is more important in preventing the development of complications associated with portal hypertension following IHPSS treatment; Total portal pressure or pressure gradients? During surgery we rarely measured CVP and using IR techniques, we always measure CVP. -During portography, when multiple small intrahepatic shunts are identified, this is almost exclusively associated with and elevated portal pressure and/or pressure gradient. Are these congenital shunts or acquired IHPSS resulting from a congenitally narrowed IHPSS? -Acquired Intrahepatic Portosystemic shunts: Originally believed to only acquire EHPSS, there is more evidence that IHPSS can be acquired as well. Do the same criteria for shunt attenuation (no greater than ~10cmH2O rise in portal pressure and/or no greater than ~20cmH2O total portal pressure) hold for attenuation of IHPSS? Although there is no documented difference between HV attenuation and PV attenuation, the vascular bed receiving the congestion is intrahepatic with the former and extrahepatic with the latter. Does this matter? -DO NOT PERFORM IHPSS SHUNT ATTENUATION IN THE FACE OF GI ULCERATION/HEMORRHAGE. The authors currently perform endoscopy and biopsy of all IHPSS cases before treatment and the overwhelming majority of these dogs have some degree of inflammatory bowel disease, sometimes including GI ulceration. Approximately 17% of patients have evidence of GI bleeding before treatment. Elevation of portal pressures with the presence of GI ulceration can lead to severe GI hemorrhage and death. All animals are maintained on omeprazole therapy for life. Initially a long-term mortality rate of 30% in IHPSS PTCE animals was caused by GI bleeding in ~50% of deaths. Lifelong antacid therapy has reduced the mortality rate to 12.5% with fewer than 4% secondary to GI bleeds. Is lifelong omeprazole therapy safe? Lessons learned or questions raised concerning FOLLOW-UP include: -Is return to normal bile acids concentrations necessary? Should this be the goal of therapy? The majority of patients receiving IHPSS PTCE do not have return to normal liver function and some have even been identified to have no development of portal branching, although pressure gradients continue to exist. Is hepatic vein congestion and reduced portal bloodflow drainage consistent with improved portal bloodflow? Maintenance of a portal gradient appears to coincide with improved clinical signs. Can this be adequate or should additional interventional/surgical treatment be instituted? -Development of longer term (greater than 2-4 weeks) post-procedural ascites is most commonly associated with hypoproteinemia and NOT excessive portal hypertension (although they can occur simultaneously). In our population of cases, this has most commonly been associated with a GI bleed and subsequent hypoalbuminemia and hypoglobulinemia and the resultant reduction in oncotic pressure. This has not always been confirmed but aggressive medical therapy with GI protectants has resulted in resolution of the clinical signs in most of the few patients we have identified with this complication. No therapy for portal hypertension has been necessary. -Approximately 18% (13/73) of cases required additional coiling procedures HEPATIC AVMS: The WSAVA liver study group has recently reclassified circulatory disorders of the liver. One of the less common congenital vascular anomalies present within the liver previously termed, arteriovenous fistula (AVF), is more appropriately termed hepatic arteriovenous malformation (HAVM) due to more recent evidence and a better understanding of the anatomy of such lesions. Little veterinary information exists on the nature of AVMs so most of the information presented here is based upon human experiences. Although both forms of high-flow vascular anomalies, an AVF is a single communication between an artery and vein and can typically be easily identified using cross-sectional imaging or angiography. A more common example of such a lesion could be considered a patent ductus arteriosus. On the other hand, an AVM is composed of multiple small communications involving a nidus, or nest, of vessels and can be more difficult to identify and treat. Treatment is often much more complicated, aimed at embolizing the nidus rather than the feeders, and inappropriate treatment can exacerbate the lesion by stimulating growth and making future treatments more difficult. In addition, treatment of AVMs is often considered more palliation than cure as repeat treatments can 20

21 22 nd FECAVA Eurocongress June 2016 Hofburg, VIENNA be anticipated in the human experience. AVMs are believed to be congenital lesions in veterinary patients even though the diagnosis may not be made until later in life depending upon location. AVFs can be congenital or acquired following trauma (bite wound or biopsy), ligation of an artery to a vein, etc. HAVMs are most often diagnosed in young dogs (or less often cats) and typically involve too numerous to count communications between the hepatic artery and portal vein in the right or central divisions of the liver. Consequently, arterialization of the portal vein (rather than the substantially lower venous pressures of 7-9mmHg) results in development of multiple acquired extrahepatic portosystemic shunts, a similar clinical syndrome to that seen with IHPSS/EHPSS, and often ascites. The author s experience covering only approximately 20 cases has not identified a hepatic artery to hepatic vein communication. Clinical signs are typically associated with ascites (75% of dogs) and/or hepatoencephalopathy (less common than with PSS). As such, these patients are often misidentified as IHPSS dogs as the bloodwork changes and clinical syndrome is similar and a large intrahepatic vessel is identified on ultrasonography. The presence of ascites should raise suspicion (rare in IHPSS cases as these patients have portal hypotension while HAVM dogs have portal hypertension). While 25% of dogs will not have ascites presumptively due to the acquired EHPSS decompressing the portal system, a reliable diagnostic tool seems to be identification of hepatofugal (retrograde) portal bloodflow that is always present in these dogs examined to date by the author. Other clinical signs include GI signs (diarrhea, vomiting), stunted growth, lethargy, and heart murmurs (present in ~20% of dogs). The author has rarely appreciated the reportedly identified audible bruit when the AVM is ausculted. Potential treatment options for HAVM have included nutrient artery ligation, surgical resection (liver lobectomy or lobectomies, and more recently trans-arterial embolization (TAE) with glue (cyanoacrylate). It is the author s opinion that nutrient artery ligation should not be performed for AVMs as there are numerous contributing vessels and this limits access to the AVM in the future if necessary. Ligation is a reasonable option for AVFs although this form of vascular anomaly is exceedingly rare in the animal liver and embolization would likely be much easier. The latter two treatments are both reasonable options for discussion with the owner. As the majority of HAVMS are located in the right and central divisions of the liver (often surrounding or involving the gall bladder or caudal vena cava), and approximately 25% involve more than one lobe, surgery can be challenging. In addition, keep in mind the entire portal circulation is arterialized so there are no minor bleeds from the omentum or mesentery. When surgery is performed, temporary vascular occlusion has been recommended 4 but the author has found that the cranial mesenteric artery needs to be temporarily attenuated along with both the celiac artery and portal vein to limit otherwise substantial intra-operative hemorrhage that has lead to a reported 39% intra-operative hemorrhage occurrence. Other reported surgical complications besides hemorrhage include portal hypertension, systemic hypotension, bradycardia, and portal or mesenteric vein thrombus formation. In dogs undergoing surgical therapy alone, peri-operative survival rates were 77% and long-term outcome was fair or good for 38% to 57%. Overall 75% of dogs continue to require dietary or medical management of clinical signs due to patent acquired EHPSS that will always persist. Transcatheter therapies typically involve cyanoacrylate glue (or more recently Onyx, (ethylene-co-vinyl alcohol [(EVOH] in dimethyl sulfoxide [DMSO]) a slower polymerizing agent. While sclerosants such as alcohol and particles such as PVA or microspheres have been described, these are not less typically used for high-flow lesions such AVMs. The observations below have been made following surgery or glue embolization of approximately 20 HAVMs. Lessons learned or questions raised concerning DIAGNOSTICS include: -These animals often present for clinical signs associated with PSS and are often mistaken for IHPSS due to the ultrasonographic identification of a large intrahepatic vascular structure along with clinical signs consistent with PSS. -While all of these animals have SEVERE PORTAL HYPERTENSION, about 25% of these cases will not present with ascites. This is presumably due to the multiple extrahepatic PSS that are acquired (along with other physiologic changes taking place) and have decompressed the portal system sufficiently to relieve the excessive hydrostatic pressure. -Clinical signs are often less severe with HAVM than standard PSS presumably because the portal system is more developed in the former patients than in the latter ones. -Other diagnostic signs that are less commonly discussed include hepatofugal portal blood flow (ALWAYS PRESENT), a reduction in aortic diameter caudal to the level of the celiac artery, and differing systemic blood pressures obtained from the forelimbs (higher) and the hindlimbs (lower) that is occasionally present. Identifiable abdominal bruit is rarely present in the author s experience. Lessons learned or questions raised concerning TREATMENT include: -It has been suggested in the human literature that while AVFs can be ligated or coil embolized, multiple AVFs or AVMs should receive glue embolization (or alcohol ablation) in order to destroy the nidus that will otherwise recruit additional vessels over time. This has not been confirmed in the veterinary population but angiograms shown may support this notion. -Initial angiography (and cross sectional imaging) often underestimates the extent of the disease. Following initial embolization, additional previously unidentified contributing vessels open up demonstrating the true infiltrative nature of these vascular anomalies. 21