Page 71 - ONLINE PROCEEDING BOOK WSAVA 2017
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out. In addition, any dilation or abnormally soft,  uid- lled consistency of a liver lobe should raise the suspicion of the presence of an IHPSS passing through it.
Shunt occlusion
Two types of occlusions are used for PSS attenuation: acute and gradual.
Acute surgical attenuation consists of completely or partially ligating the abnormal vessel. In many cases, complete ligation is not possible without life-threatening portal hypertension. Partial occlusion may result in persistent shunting and necessity for a second surgery to ligate the shunt further. Acute attenuation always carries a risk of postoperative portal hypertension, which may cause death or necessitate reintervention to remove the ligature.
Gradual attenuation of a PSS aims at giving time for the intrahepatic portal vasculature to develop as the PSS is progressively attenuated, thereby decreasing the risk of portal hypertension, and can be achieved with ameroid constrictors, cellophane bands or hydraulic occluders.
The author currently prefers cellophane banding over other techniques. Cellophane bands placed around shunt vessel induce in ammation around the vessel, leading to its occlusion. The rate of occlusion is therefore dependant on the amount of in ammation induced. They are reported to induce complete occlusion of
the PSS within 6 months. Cellophane can be used for shunt vessels of any size, as well as for EHPSS and IHPSS. In early reports, it was advocated to attenuate shunts intraoperatively to less than 3mm of diameter for complete occlusion to occur, but more recent evidence suggest that no attenuation is necessary to achieve long- term complete occlusion, regardless of the shunt size7, which avoids the risk of inducing portal hypertension. The cellophane band is therefore just applied around the shunt vessel and secured with 3 or 4 vascular clips.
Postoperative care
If any attenuation has been induced surgically, the patient is monitored for signs of portal hypertension, which may warrant reintervention to relieve the shunt occlusion.
Postoperative hypothermia and hypoglycaemia are frequent, and must be actively monitored and promptly addressed. Postoperative seizures occur in 3% to 7% of dogs and 8% to 22% of cats after PSS attenuation, typically up to 4 days after surgery. Treatments include midazolam, propofol, barbiturate or levetiracetam administration.
Once discharged from the hospital, animals are maintained on a low-protein diet, antibiotics, lactulose and gastrointestinal protectants. Bile acids levels are monitored 1, 3 and 6 months after surgery. In the absence of clinical signs of HE, antibiotics are stopped
An Urban Experience
1 month after surgery and lactulose administration is discontinued a few weeks later. Approximately 3 months after surgery, if tolerated, the diet is progressively returned to normal.
Prognosis
Both short- and long-term, dogs with CPSS treated surgically have better survival rates and less persistent clinical signs than those treated medically8, 9. In dogs, reported mortality rates range from 2% to 32% after EHPSS surgical attenuation and from 0% to 27% after IHPSS surgical attenuation. Good to excellent outcomes in surviving dogs are reported in 84% to 94% for EHPSS and 50% to 100% for IHPSS.
In cats, perioperative mortality ranges from 0% to 23%. Good to excellent long-term outcome is reported in 33% to 80% of surviving cats.
References
1. Gerritzen-Bruning MJ, Ingh TSGAMvd, Rothuizen J. Diagnostic value of fasting plasma ammonia and bile acid concentrations in the identi cation of portosystemic shunting in dogs. Journal of Veterinary Internal Medicine. 2006;20: 13-19.
2. Zwingenberger AL, Schwarz T, Saunders HM. Helical computed tomographic angiography of canine portosystemic shunts. Vet Radiol Ultrasound. 2005;46: 27-32.
3. Parry AT, White RN. Comparison of computed tomographic angiography and intraoperative mesenteric portovenography for extrahepatic portosystemic shunts. J Small Anim Pract. 2017;58: 49-55.
4. Kim SE, Giglio RF, Reese DJ, Reese SL, Bacon NJ, Ellison GW. Comparison of computed tomographic angiography and ultrasonography for the detection and characterization of portosystemic shunts in dogs. Veterinary Radiology & Ultrasound. 2013;54: 569-574.
5. Nelson NC, Nelson LL. Anatomy of extrahepatic portosystemic shunts in dogs as determined by computed tomography angiography. Veterinary Radiology & Ultrasound. 2011;52: 498-506.
6. Fryer KJ, Levine JM, Peycke LE, Thompson JA, Cohen ND. Incidence of postoperative seizures with and without levetiracetam pretreatment in dogs undergoing portosystemic shunt attenuation. Journal of Veterinary Internal Medicine. 2011;25: 1379-1384.
7. Frankel D, Seim H, MacPhail C, Monnet E. Evaluation of cellophane banding with and without intraoperative attenuation for treatment of congenital extrahepatic portosystemic shunts in dogs. Journal of the American Veterinary Medical Association. 2006;228: 1355-1360.
8. Greenhalgh SN, Reeve JA, Johnstone T, Goodfellow MR, Dunning MD, O’Neill EJ, et al. Long-term survival and quality of life in dogs with clinical signs associated with a congenital portosystemic shunt after surgical or medical treatment. Journal of the American Veterinary Medical Association. 2014;245: 527-533.
9. Greenhalgh SN, Dunning MD, McKinley TJ, Goodfellow MR, Kelman KR, Freitag T, et al. Comparison of survival after surgical or medical treatment in dogs with a congenital portosystemic shunt. Journal of the American Veterinary Medical Association. 2010;236: 1215-1220.
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