Page 1618 - Cote clinical veterinary advisor dogs and cats 4th

Portosystemic Shunt 815

Etiology and Pathophysiology • Serum biochemistry profile: liver ○ Ultrasound contrast bubble study uses
• Congenital PSS is caused by developmental enzymes (alanine aminotransferase [ALT], agitated saline or saline diluted autologous
VetBooks.ir of the liver and splanchnic veins. glutamyltransferase [GGT]) normal or produce microbubbles. This is then injected Diseases and Disorders
alkaline phosphatase [ALP], gamma-
anticoagulated blood that is shaken to
failure of the embryonic circulatory system
into the splenic parenchyma. If microbubbles
○ In utero, the oxygen-rich blood from
increased (ALP normally higher in dogs
the placenta should bypass the liver and
flow into circulation through the ductus < 6 months of age); low blood urea nitrogen are detected in right ventricle, a shunt is
present because normal hepatic sinusoidal
(BUN), hypocholesterolemia, and hypoalbu-
venosus. A failure of the ductus venosus minemia common; hypoglycemia sometimes blood flow would trap microbubbles.
to close causes an intrahepatic shunt. recognized ○ ± Uroliths
○ Extrahepatic shunts are usually a devel- • Urinalysis: specific gravity varies but often ○ ± Ascites (APSS)
opmental abnormality of the vitelline < 1.025 ± ammonium urate (biurate) • CT with contrast angiography has become
veins. They should become the portal crystals ± hematuria the imaging study of choice for noninvasive
vein and its branches that deliver blood • Bile acids: increase often in fasting and confirmation of PSS. It provides location
to the sinusoids. Failure of one or more to postprandial samples, but often a marked and number of shunts and can demonstrate
develop results in a persistent connection increase in postprandial sample compared calculi or concurrent abnormalities.
to the caudal vena cava or, less commonly, with fasted sample. Sensitive but not specific • Contrast mesenteric venous portography or
the azygous vein or another systemic vein. for congenital PSS (p. 1312) splenic portography was a standard method
○ Rarely, primary portal vein hypoplasia • Urine bile acid to creatinine (UBA/UCre) of demonstrating presence and location of
or atresia or hepatic arterioportal fistula ratio: less sensitive for detecting PSS than PSS in past decades. Positive iodinated con-
occur. total serum bile acids (p. 1312) trast is injected into a catheterized mesenteric
• APSSs form as a result of portal hypertension • Blood ammonia (fasting or ammonia or splenic vein or splenic pulp by surgery
due to cirrhotic liver disease (most common), tolerance testing): rarely performed due to or as an ultrasound-guided injection. If the
noncirrhotic portal hypertension, congenital difficulties of proper sample handling (p. most caudal point of shunt is cranial to T13,
portal vein atresia, hepatic AV malforma- 1305) but often increased with HE it is likely intrahepatic.
tions, ductal plate malformations, portal • Coagulation profile: usually normal • MRI with contrast angiography creates
vein thrombosis or stricture, or outflow • Fecal exam: all young dogs and cats to rule diagnostic images but requires more time
obstruction through hepatic veins (Budd- out parasites under anesthesia and is more expensive; CT
Chiari syndrome, veno-occlusive syndrome). • Abdominal radiographs: microhepatica and is preferred in most cases.
• With PSS, venous blood from splanchnic plump kidneys common; although urate • Nuclear medicine/portal scintigraphy:
organs bypasses the hepatic sinusoids and calculi are radiolucent, can be radiopaque technetium pertechnetate isotope delivery
mixes with the systemic venous circulation if complexed with magnesium and phosphate to the liver compared with delivery to the
before detoxification (ammonia, others); hepa- APSS: results overlap with PSS except heart imaged after adminstration per rectum
tocytes are also denied necessary substances. • Hyperbilirubinemia suggests APSS. (less detail but even very caudal abdominal
• Coagulation times may be prolonged. shunts are found) or ultrasound-guided
DIAGNOSIS • Radiographs may show peritoneal effusion. splenic injection (better detail). Answers
broad question of whether a shunt is present
Diagnostic Overview Advanced or Confirmatory Testing but does not give anatomic detail.
• In a young animal with findings suggesting Imaging: selection of techniques is often a Laboratory testing:
HE or a mature (non-Dalmation, non- balanced decision involving availability of the • Protein C levels are commonly < 70% of
bulldog) animal with urate cystoliths, the method, skills, and experience of operator, normal for PSS, whereas dogs with HMD
most useful initial test is measurment of total probability of obtaining actionable information, usually have levels > 70%. Protein C does not
serum bile acids (TSBAs). The combination and potential costs. distinguish between PSS and other hepatobili-
of (12-hour) fasted and (2-hour) postprandial • Abdominal ultrasound confirmation of a ary diseases and liver failure. When PSS is
serum samples represents a bile acid panel, PSS relies on excellent equipment, fortuitous corrected, protein C levels return to normal.
which is preferred to a single TSBA mea- patient echogenic features, and advanced Liver biopsy:
surement. Values of bile acids in younger skills/experience of sonographer (estimated • Biopsy is recommended to determine
patients that are > 200 mmol/L commonly accuracy of 85% for congenital PSS). specific hepatic disease in APSS and during
represent congenital PSS (sensitivity ≈99% ○ Subjectively small liver; often nodular with surgical correction of congenital PSS. For
but false-positives occur). APSS (regenerative nodules) congenital PSS, biopsy can assess the degree
• Most animals with APSS are older, and clini- ○ Intrahepatic PSS is generally easier to of hypoperfusion or presence of other
cal signs of hepatic failure (p. 174) occur in identify than extrahepatic PSS. hepatopathies. Findings that reflect portal
addition to signs of HE. ○ Turbulence of flow within the caudal venous hypoperfusion are nonspecific.
• Imaging studies and/or surgical explorations vena cava has good correlation with an
are necessary to confirm the diagnosis of PSS, intrahepatic or extrahepatic PSS. TREATMENT
but such studies are often not important for ○ ± Increased portal blood flow velocity as
APSS. a calculated value (technically difficult) Treatment Overview
○ Measurements of vascular diameters Address HE with medical management. For
Differential Diagnosis are used to obtain ratios of the major congenital PSS, surgical correction of the
• HMD (for congenital PSS) vessels. Portal vein/aorta (PV/Ao) ratio shunt(s) is the treatment of choice. Treatment
• Any hepatopathy resulting in hepatic failure that is < 0.65 is supportive for presence of APSS includes treatment of the underlying
(for APSS) of extrahepatic PSS or noncirrhotic hepatopathy, and continued medical manage-
• HE must be differentiated from other portal hypertension. If the PV/Ao and ment of HE and complications of liver disease
neurologic disorders. portal vein/caudal vena cava (PV/CVC) (e.g., gastric ulcers, vomiting).
are > 0.75 and > 0.80, respectively, an
Initial Database extraphepatic shunt is much less likely. Acute General Treatment
Congenital PSS: ○ Hepatofugal (reverse) portal blood flow • If present, address HE immediately (p. 440):
• CBC: microcytosis, often with absent or has a high correlation with APSS but can lactulose PO or by enema, antibiotics, other
minimal anemia, poikilocytosis in cats be hard to confirm. treatment

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