7. Portosystemic Shunts Flashcards

1
Q

Portosystemic shunts are Abnormal communications of the portal and _____ vasculature that allow products of _____ absorption to bypass the liver and enter directly into the _____ circulation

A
  • systemic
  • intestinal
  • systemic
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2
Q

The portal ssytem drains the small and large intestine, the _____, pancreas, and _____ which means their are alot of _____ that need to be absorbed and _____ that need to be filtered through the liver before entering this main vessel?

A
  • spleen
  • stomach
  • metabolites (abs)
  • toxins
  • caudal vena cava
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3
Q

What are the only 2 organs not drained by the portal vein?

A

Kidney and adrenal (they are in the retroperitoneum)

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4
Q

What are the 2 main classifications of shunts (simple)?

A
  • Congential
  • Acquired
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5
Q

What different shunts are classifed under congenital?

A

Macrovascular (these can be grossly seen)

  • Intrahepatic
  • Extrahepatic

Microvascular (these cannot be grossly seen)

  • Intrahepatic
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6
Q

What different shunts are classifed under acquired?

A

Single Shunt

  • Trauma, iatrogenic

Mutiple Shunt

  • Diseases that cause portal hypertension, cirrhosis and fibrosis causes portal hypertension and the creation of smaller shunts
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7
Q

What is the common signalement assoicated with MACROVASCULAR extrahepatic PSS (congenital)

A

Small dogs and cats; Yorkies are the poster child!!!

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8
Q

With extrahepatic shunts, veins that join the portal vein enter these vessels? Which veins are most commonly involved?

A

enter the caudal vena cava or azygous vein (azygous more toward the diaphragm)

  • MOST COMMONLY the left gastric vein and splenic vein are most commonly involved
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9
Q

at what location will be the landmark looking for shunts

A

Epiploic foramen

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10
Q

The last vessel to enter the caudal vena cava should be a branch off from the adrenal vein, which is what vein?

A

phrenicoabdominal

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11
Q

Describe the pathology of the abnormal blood flow with a PSS?

A

Portal circulation has a higher pressure than systemic circulation. This is why the blood will shunt away from the liver bc of the pressure differential. (bypasses the liver and heads to the heart)

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12
Q

When I state LARGE breeds, labs, goldens, aussies, and old english sheep dogs what is your top differential for PSS?

A

Congenital MACROVASCULAR intrahepatic PSS

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13
Q

Describe the size of the liver with intrahepatic shunts and what vessel is responsible for this?

A

Liver is very small bc its not getting the blood supply it needs, basically the Ductus venosis is patent (a fetal vein normally suppose to be closed off)

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14
Q

Descibe the blood supply with intrahepatic shunts

A

Intrahepatic branches of portal vein enter vena cava or hepatic vein bypassing the hepatic parenchyma

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15
Q

When you have an absence of a portal vein it’s known as _____ ______ ______ and it affects ________ vessels. What is the top CS we see with this and why?

A

When you have an absence of a portal vein it’s known as PORTAL VEIN ATRESIA an it affects PRE-HEPATIC vessels. What is the top CS we see with this and why? ASCITES MORE COMMON THAN WITH OTHER SUNTS BC OF HYPOPROTEINEMIA

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16
Q

HOW CAN YOU TREAT PORTAL VEIN ATRESIA and state the reason why and prognosis?

A

:-( can’t tie off a shunting vessel and still get blood flow through portal vein, medical management is the only way. Don’t live long until they stop responding to MM which they eventually do

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17
Q
  • State the different names of the congenital intrahepatic microvascular shunt?
  • and state what it is and the forms there are?
  • Who do we often think of with these shunts?
A
  • Names
    • Portal vein Hypoplasia
    • Hepatic Microvascular Dysplasia
  • Basically the portal triads are too small. anatomy outside the liver is normal and there is NO BIG SHUNT within the liver resulting in microvscular shunting within the liver
  • FORMS: Stable and progressive forms (can have both micro and macro happening at the same time
    • Think Older animal bc they do have BF to the liver its just that there is shunting and there isnt as much normal BF
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18
Q

What are some clinical signs of portal vein hypoplasia (microvascular dysplasia)

A
  • May be none bc not a large shunting vessel, may show up in middle age
  • Drug “insensitivity
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19
Q

What are some Lab abnormalities of portal vein hypoplasia (microvascular dysplasia), tell me about protein C too?

A
  • Bile acids often mildly elevates
    • post prandial often less than 100
  • Liver function test abnormal even if doesnt show up on lab tests
  • Protein C
    • over 70% (from higher BF)
    • plasma anticoagulant factor syn. in liver
    • Reflects hepatic synthetic activity and portal blood flow (will tell you if blood flow to liver)
    • ddx between macrovascular shunt and microvascular dysplasia
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20
Q

Tell me about nuclear syntigraphy with portal vein hypoplasia

A

Checks for blood flow, shunt fraction with microvascular near 15% which is close to normal, compared to PSS which is over 70%

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21
Q

What is the treatment for the stable form of portalvein hypoplasia

A

Stable form (vast majority)

  • None
  • Medical Management low protein diet is often enough
  • Nothing surgically we can really do for microvascular probs you cant do a a complete transplant
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22
Q

What is the treatment for the progressive form of portal vein hypoplasia, what is it similar to if not corrected?

A
  • Pathophys simialr to uncorrected macrovascular shunts
  • Diet
  • Medical management
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23
Q

This type of shunt is secondary to diseases that cause portal hypertension

A

Multiple Extrahepatic PSS

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24
Q

Multiple extraheptatic PSS likes to live around what anatomical location

A

Kidneys

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25
Q

What 2 conditions of the liver can cause portal hypertension secondarily causing mutiple extrahepatic PSS?

  • ______
  • Secondary to ______ shunt ligation
A
  • Cirrhosis
  • 2* to macrovascular shunt ligation
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26
Q

Describe the basic pathophys for multiple extrahepatic PSS?

A

Blockage of blood that is able to get to the liver and it backs up into portal circulation. Embryonic vessels in abdomen open up to attempt to relieve portal hypertension and this is where multiple extrahepatic PSS come into play

27
Q

Non cirrotic portal hypertension is responsible for these two diseases?

A
  • Indiopathic portal hypertension
  • Hepatic veno occlusive disease
28
Q

Hepatic AC malformation (fistula) can result in what type of shunt?

A

Multiple Extrahepatic PSS

29
Q

Can you correct multiple extrahepatic shunts surgically (why or why not)?

A

Too many vestigial embryonic communications that open up to prevent lethal portal hypertension from developing so NO Sx is not really an option its more of a medical management

30
Q

What types of general signs will we see with macrovascular shunts?

A

poor growth rate (runts) weightloss, poor doers, prolonged anesthetic recovery

31
Q

What types of nervous signs will we see with macrovascular shunts? What causes them and when do you see them during what activity

A

lethargy, depression wekaness mildly, and severe it could result in seizures.

Not processing toxins and an increase in ammonia causing hepatic encephalopathy especially after eating high protein diets

32
Q

What types of urinary signs will we see with macrovascular shunts?

A

Not conjugating ammonia (ammonia biurate stones) decreased USP makes them develop stones, PU PD etc..

33
Q

What’s unique about cats with macrovascular shunts?

A

Cats-copper colored irises

also hypersalivation, aggressive behavior

34
Q

What main CS do you commonly see with macrovascular shunts and what does it cause? It’s uncommon in ____unless….?

A
  • Ascites (liver makes protein)
    • portal hypertension
    • Uncommon with congentical PSS unless severely hypoproteinemic (poor prog)
      • Severe portal vein hypoplasia
      • Portal vein atresia
35
Q

What is often palpable in the abdomen with macrovascular shunts

A

Bruit (HAV malformation) palpable cardiac murmur within abdomen

36
Q

What types of clinical pathology signs will we see with macrovascular shunts?

A

Hematology

  • Anemia, microcytosis (irondef)

Biochem

  • decreased BUN
  • Increased ALT and ALP
  • hypoproteinemia
  • low albumin
  • low cholesterol

Urinalysis

  • low urine sp gravity

Liver function tests

  • elevated serum bile acids pre and post prandial
  • protein c acvitity is less than 70%
37
Q

What crystals will we see with macrovascular shunts that is highly suggestive?

A

ammonium biurate crystals

38
Q

What types of radiographic signs will we see with macrovascular shunts?

A

Wont see much but maybe a small liver and a plum kidney

39
Q

What type of shunts does ultrasound consistently identify, why not the other type?

A

Intrahepatic shunts consistently identified

Extrahepatic shunts depend on lcation and experience of ultrasonographer and gass/food in the stomach obscuring vision and the weight of it compressing the shunt vessel

40
Q

What is nuclear scintigraphy used for? State what is normal and abnormal and which anatomical location lights up first with normal/abnormal

A
  • Noninvasive method of documenting PSS to distinguish from MICROVASCULAR dysplasia
  • Technetium 99
  • Patient may have to be in radiation isolation after

(cannot tell you intra or extra hepatic even if it can tell macrosome too so doesnt work best for that scenario)

41
Q

What is the most diagnostic gold standard to see where abnormal vessels are (intra or extra hepatic and how many shunts)

A

CT angiography

42
Q

What is 5.5 times more likly to correctly determine presence or abcense of PSS compared to abdominal ultrasound. Is it noinvasive or invasive

A

CT angiography; non invasive

MOST DIAGNOSTIC BEST GOLD STANDARD

43
Q

When no shunt can be indentified during abdominal exploratory and you need to confirm the suspected vessel is indeed a shunt what can we do? is in invasive or noninvasive

A

Portography (invasive you are entering the abdomen)

44
Q

With Portography, what vein is most commonly injected. Is it highly diagnostic or not? What can it differentiate from? When is this not necessary?

A

mesenteric vein most commonly; highly diagnostic, cnn differentiate from PVH, not neccessary if pro op CT angiogrpahy performed

45
Q

Describe the basic medical management steps with PSS?

A
  • Diet (restrict protein)
  • Lactulose to trap ammonia within rectum
  • Antimicrobials (lots of bacteria translocate t intestinal wall)
  • Seizure control and prevention
    • Pheno + KBr
46
Q

Pre op albumin less than 1.5 mg/dl indicates what

A

surgery is more riskier more potential for developing ascites

47
Q

What is the best way to manage macrovascular shunts

A

surgery because eventuall most animals will stop responding to medical management

48
Q

What is the goal of PSS surgery

A
  • Improved liver function
  • to divert blood flow back through portal system without creating portal hypertension severe enough to be life-threatening or high enough or long enough to cause acqured shunts to open

want to gradually restore blood flow back to liver bc its not used to getting blood flow and that high of a volume

49
Q

What locations do we need to look for shunts at upon abdominal exploratory

A
  • Epiploic foramen (most common)
  • Omental bursa (splenic vessels)
  • Esophageal hiatus where azygous vein is
  • Any vesself entering caudal venacava cranial to phrenicoabdominal shunting vessel will show turbulent blood flow
50
Q

What is the idea way to surgically manage PSS

A

Complete ligation

51
Q

Explain what partial attenuation with suture for surgical management of PSS is?

A

Eventually do complete ligation, place a red rubber next to vessel, do transfixing through red rubber catheter with silk bc the silk will cause an inflammatory reaction and vessel will be occluded over time

52
Q

What are 2 ways of surgical management for gradual occlusion

A
  • Ameroid constrictor
  • Cellophane band
53
Q

What does the measurement of portal pressures need to be between pre and post ligation to make sure its not too tight

A

9-10 cm H20 (not over 10!!)

54
Q

Ameroid constrictors gradually occlude blood flow because ____ is proinflammatory. What are some complications

A
  • Casin-proinflamm

(Complications)

Acute

  • rapid closure
  • kinking acutely instead of graduallybc heavyness
  • if portal hypertension post sx may have to take it out

Chronic

  • Incomplete occlusion
  • Acquired shunts (20% of cases)
  • Implant migration
55
Q

With cellophane banding occlusion is entirely by ______ reaction. When is it typically occluded?

A
  • inflammatory
  • typically occludes completely within 8-12 days if occluded to < 3mm
  • if larger-takes longer
  • Variable results in cats use ameroid constrictors in cats
56
Q

What are the advantages of hydraulic occluders?

A

Advantages: Single surgery w/o portal pressures, gradual and total vascular occlusion, reversible

57
Q

What are the disadvantages of hydraulic occluders?

A

Disadvantages: implant leakage or diffusion, potential for add’l manipulations, long-term?

58
Q

Surgical Management of Intrahepatic Shunts

A

Extravascular occlusion – procedure similar to extrahepatic techniques but….

  • Pre-hepatic
  • Post-hepatic

Intravascular occlusion

  • Intracaval
  • Transportal
  • Thrombogenic coils
59
Q

What are some acute post complications?

A
  • Portal hypertension
    • ​too much blood in portal system angry pancreas and intestines hyperactive motility with severe D+ abdominal paon. need to remove whatever you put in ASAP
  • Portal vein thrombosis No BF at all to liver=bad
  • Hypoglycemia
  • Seizures
    • 4-6% incidence in patients with no prior history
  • Hemorrhage
  • Electrolyte disturbances
    • Hyponatremia
      • Often iatrogenic
60
Q

What are some immediate post operative management techniques?

A
  • Continue fluid therapy until recovered from anesthesia
  • Encourage early food intake
  • Monitor vital signs and abdomen for signs of portal hypertension
  • Monitor for seizure activity – eyelid twitching frequent prodromal sign up to 3 days
  • Avoid:
    • Hypothermia
61
Q

Postoperative Care?

A
  • Continue pre-op medical management
  • Recheck in 4-8 weeks - minimum
    • Routine bloodwork
    • Liver function tests
      • Protein c activity
  • May take months for labwork to normalize if it ever does
62
Q

Abnormal lab tests post op are from?

A

Significant continued shunting

  • vessel never completely occluded
  • There was more than one
  • You occluded the wrong vessel
  • Multiple acquired shunts formed due to portal hypertension
  • Significant MVD is present
  • Follow-up ultrasonography and/or nuclear scintigraphy
63
Q

Compare and contrast the outcomes for extrahepatic shunts and intrahepatic shunts and cats?

A
  • Extrahepatic shunts
    • Perioperative mortality
      • Suture ligation 2-32%
      • Ameroid constrictor 7%
      • Cellophane banding 6-9%
    • Long term outcome- good to excellent 78-94%

Intrahepatic shunts

  • Mortality rates up to 27%
  • Long term outcome- good to excellent 50-89%

Cats

  • 5% postop complications
  • Long term- good to excellent 30-80%