Portosystemic Shunt Flashcards
What are portosystemic vascular anomalies?
abnormal communications of the portal and systemic vasculature that allow normal blood draining from the stomach, intestines, spleen, and pancreas to bypass the liver and enter directly into systemic circulation
What are the 2 classifications of congenital portosystemic shunts?
- MACROVASCULAR - intra/extrahepatic
- MICROVASCULAR - intrahepatic
What are the 2 classifications of acquired portosystemic shunts?
- SINGLE - trauma, iatrogenic
- MULTIPLE - diseases that cause portal hypertension, like viral hepatitis or fibrosis of the liver
In what animals are extrahepatic PSS most common?
- DOGS: small breeds; Yorkies, Shih Tzu, Maltese, Poodle, Schnauzer, Dachsund, Lhasa Apso, Bichon Frise, Jack Russel Terrier, Pekingese
- CATS: DSH
What are extrahepatic shunts? What vessel is most commonly involved?
veins that should join the portal vein enter the caudal vena cava or azygous vein instead
left gastric vein
- (gastro)splenic vein
- direct portocaval
- gastroduodenal
- mesenteric (jejunal and colic)
What are the most common causes of extrahepatic and intrahepatic PSS?
EXTRAHEPATIC = portocaval shunt involving the left gastric vein
INTRAHEPATIC = persistent ductus venosus, congenital portal vein hypoplasia (microvascular dysplasia)
At what level in the abdomen is the presence of veins suspicious of PSS?
anything above the kidney entering the caudal vena cava
Extrahepatic PSS:
In what breeds are intrahepatic PSS most common?
large breeds
- Labrador Retrievers
- Golden Retrievers
- Australian Sheperds
- Old English Sheepdofs
What vessel is most commonly responsible for intrahepatic PSS?
patent ductus venosus - intrahepatic branches of the portal vein enter the vena cava or hepatic vein, bypassing hepatic parenchyma
(within the lobes, hard to find and treat)
What is portal vein hypoplasia? What is the most common clinical sign?
hepatic microvascular dysplasia where hepatocytes are bypassed
drug sensitivity - prolonged response to anesthetic agents or tranquilizers
What are the 2 major laboratory tests used to diagnose portal vein hypoplasia (HMD)?
- bile acids often mildly elevated
- protein C activity decreased to > 70% of normal, reflecting a decrease in hepatic synthetic activity and portal bloodflow
How is nuclear scintigraphy used to diagnose portal vein hypoplasia (HMD)? What are the 2 techniques?
technetium 99 is injected into the GIT and followed to see if the liver is skipped
- transcolonic - higher dose needed, confirms shunt, but not type
- transsplenic - smaller dose, can identify type of shunt
How does treatment differ in the stable and progressive forms of portal vein hypoplasia (HMD)?
STABLE = no treatment usually necessary, diet management is usually enough
PROGRESSIVE = extensive liver involvement requiring diet changes and medical management
What are the 5 most common causes of multiple extrahepatic PSS?
- disease causing portal hypertension (virus, toxins)
- macrovascular shunt ligation
- cirrhosis
- non-cirrhotic portal hypertension due to hepatic veno-occlusive disease
- hepatic A-V malformation (fistula)
What are the best diagnostics for diagnosing macrovascular shunts?
- hematology
- biochemistries: increased ammonia
- urinalysis: ammonia stones
- liver function tests
- ultrasonography
What are the most common general signs associated with macrovascular shunts?
- poor growth
- weight loss
- tranquilizer intolerance
What 3 systems are commonly affected by macrovascular shunts?
- NERVOUS - lethargy, depression, weakness, behavior changes, pacing, aggression, ataxia, stupor, head pressing, coma, seizures, blindness
- GI - anorexia, vomiting, diarrhea, ptyalism (cats), pica, ascites
- URINARY - PU/PD, cystitis, hematuria, dysuria, pollakiuria, stranguria, urolithiasis, urethral obstruction
What 3 clinical signs are especially associated with cats in macrovascular shunts?
- copper colored irises
- hypersalivation (ptyalism)
- aggressive behavior (hepatoencephalitis)
Why do patients with macrovascular shunts develop acites? In what patients is this uncommon?
portal hypertension
those with congenital PSS, unless severely hypoproteinemic (poor prognostic sign)
What is commonly seen on hematology in patients with macrovascular shunts?
- anemia
- microcytosis
- hypochromasia
- poikilocytosis
- target cells (codocytes)
- neutrophilia
What is commonly seen on biochemistry in patients with macrovascular shunts?
- decreased BUN
- increased ALT and ALP
- hypoproteinemia
- decreased albumin
- decreased cholesterol
What is commonly seen on urinalysis in patients with macrovascular shunts?
- low USG
- ammonium biurate crystals**
- sediment suggestive or cystitis: hematuria, pyuria, proteinuria
What 3 things are commonly seen on liver function tests in patients with macrovascular shunts?
- elevated serum bile acids (pre- and post-prandial)
- hyperammonemia
- protein C activity < 70% of normal
How can radiography be used to diagnose PSS?
- small liver
- urinary stones
not as helpful —> ultrasound more valuble
What shunts are most commonly and accurately identified via ultrasonography? Which are more difficult?
intrahepatic - stand out amongst hepatocytes (+ turbulent flow)
extrahepatic - depends on experience of the ultrasonographer, location of shunt, and presence of gas or food in the stomach
What is the most common vein used for portography of extrahepatic PSS? What can cause false negatives?
mesenteric vein —> not as commonly done now
positioning
What are 4 options for medical management of PSS?
- diet
- lactulose - decreases ammonia
- antimicrobials - decreases bacterial load, along with their production of ammonia
- seizure control or prevention - Kepra
In what 2 situations is medical management of congenital PSS indicated?
- stabilize patient before surgical correction
- manage cases where surgery is not an option
What is the goal of surgery for PSS?
- divert blood flow back through the portal system without creating portal hypertension
- improved liver function
What are the general steps to surgical management to PSS?
- ventral midline approach
- intra-operative localization of shunt (after it has been located by mesenteric/transplenic portography or Doppler US)
- livery biopsy
(monitor portal pressure during the procedure with manometry via jejunal or splenic vein catheters)
What are the 3 general areas to check of PSS in the abdomen? What will the shunts look like?
- caudal vena cava - only the phrenicoabdominal veins should enter between the renal veins and the hepatic veins
- portal vein - caudal to the liver in the epiploic foramen
- left gastric and splenic veins - greater and lesser curvatures of the stomach
thin-walled vessels with turbulent blood flow
What happens if a shunt cannot be identified visually?
- intra-op portography
- close up and go to radiology for intra-op ultrasound
What are the 3 options for surgical management of PSS?
- complete ligation (not recommended)
- partial attenuation with suture and reoperation to completely close
- gradual occlusion by ameroid constrictor, cellophane bands, thrombogenic coils, hydraulic occluders
What benefits do gradual occlusion and surgical attenuation have over complete ligation?
- reduces risk of life-threatening portal hypertension
- decreases risk of post-ligsation neurologic syndrome
- reduced operative time and monitoring
- improved prognosis
What is an ameroid constrictor? For what shunts do they work best?
hydroscopic compressed casein in stainless steel that SLOWLY compresses in 4-5 weeks due to local tissue reaction and casing swelling to avoid hypertension
What acute and chronic complications are associated with the use of ameroid constrictors?
ACUTE - accidental rapid closure due to kinking
CHRONIC - incomplete occlusion, acquired shunts, implant migration (ring only is not usually a problem)
How is cellophane banding used to treat PSS?
cellophane is placed and closed around the shunt, resulting in occlusion entirely by inflammatory reaction within 8-12 days
- variable results in cats
On what shunts does percutaneous transjugular coil embolization (PTCE) work best? In what 3 ways are they different compared to other gradual occlusion devices?
intrahepatic
- may not incite complete shunt attenuation
- rapid occlusion within 5-7 days
- higher cost
How is percutaneous transjugular coil embolization placed?
nitinol stent is placed into the caudal vena cava to cover the opening of the shunting vessel while the thrombogenic coils are placed through the stent into the shunt using a catheter
On what type of PSS do hydraulic occluders work? How do they work?
intrahepatic
cuff is secured SQ and is gradually inflated every 2 weeks over 8 weeks
What are 3 advantages to using hydraulic occluders? 2 disadvantages?
- single surgery without portal pressures
- gradual and total vascular occlusion
- reversible
- implant leakage or diffusion
- potential for additional manipulations
What are the 6 most common acute postoperative complications associated with surgical treatment of PSS? How are they avoided?
- portal hypertension
- portal vein thrombosis
- hypoglycemia
- neurological signs (seizures)
- hemorrhage
- electrolyte disturbances - hyponatremia
slow/gradual attenuation
What 4 immediate postoperative monitoring are recommended following PSS surgical treatment?
- continue fluid therapy until recovered from anesthesia
- encourage early food intake to monitor glucose
- monitor vital signs and abdomen for signs of portal hypertension
- monitor for seizure activity (eyelid twitching)
What are 5 possible causes of significant continued shunting following surgery for PSS?
- vessel never completely occluded
- there were more shunts than treated
- occluded wrong vessel
- multiple acquired shunts due to portal hypertension
- significant hepatic microvascular dysplasia
What are 4 signs of portal hypertension following surgery?
- abdominal pain and ileus
- hemorrhagic diarrhea
- metabolic acidosis
- endotoxemia and cardiovascular collapse
When can ameroid constrictors cause portal hypertension? What can reduce this risk?
RARE —> weight of the constrictor can twist the shunt
minimal dissection of the shunt
How can seizure activity be controlled following PSS treatment?
- phenobarbital (cats)
- potassium bromide
- levetiracetam (Keppra)
What is a norma common postoperative complication associated with PSS treatment?
ascites —> does not require removal of occluding device!
When is post-operative medical management able to be weaned? What do most animals need to be on chronically?
when ammonia levels and liver function tests are normalized or stable —> wean off of anti-seizures, antibiotics, lactulose, and restricted protein diet one by one
restricted, high quality protein diet in multiple small meals
When is it advised to perform PSS correction?
before 2 years of age
What additional signs are associated with PSS in cats? What additional signs are seen?
GI —> sialorrhea, ptyalism, anorexia, vomiting, diarrhea, sica, polyphagia
- NEURO: grand mal seizures, aggression, behavior changes, cardiac murmur
- copper colored irises
How do laboratory signs in cats with PSS compare to dogs?
- ALB, ALT, ALP often normal
- typically not anemic
- decreased BUN rare
- ammoniun biurate uroliths rare
many have persistent neurological signs post-op even though biochem and bile acids are normal (seizures more likely than dogs)
