This document summarizes portosystemic shunts and their management in dogs. Portosystemic shunts are abnormal blood vessel connections that allow blood to bypass the liver. They can be congenital or acquired. Clinical signs include neurological, gastrointestinal and urinary issues. Diagnosis involves imaging like ultrasound, scintigraphy and portography. Treatment options are medical management to improve health for surgery or surgical attenuation of the shunt vessel. The goal of surgery is to redirect blood flow to the liver without causing excessive portal hypertension. Post-operative care focuses on a low-protein diet and medications to prevent hepatic encephalopathy.

1. PORTOSYSTEMIC SHUNTS
AND ITS MANAGEMENT IN
DOGS.
Submitted by :-
Mageshwar singh Slathia (j-15-bv-918)

2. A direct venous communication between the
portal vein and the systemic circulation,
bypassing the hepatic sinusoids and liver
parenchyma

3. Embryology
FETAL LIVER DEVELOPMENTAL
CHANGES
umbilical, vitelline(omphalomesentric) and caudal cardinal
veins

4. Normal circulation of liver
Portal vein formed by confluence of cranial and
caudal mesenteric veins, providing up to 80% of
blood and 50% of oxygen content to the liver,
with remaining being supplied by the hepatic
arterial blood.

5. When the path is interrupted by an anomalous vessel, blood
is diverted away from the liver, traveling the path of least
resistance, reaching the systemic circulation prior to
transversing the hepatic circulation

6. Portosystemic shunts can be either congenital
or acquired
 Congenital portosystemic shunt - If the ductus
venosus remains patent (?), or other congenital
communications exist, portosystemic shunting
occurs.
-Commonly occurs as a single vessel.
 Acquired portosystemic shunts - Liver
hypertension.
-Multiple in numbers

7.  Congenital portosystemic shunt can be
intrahepatic or extrahepatic.
 Approx. 25% to 33% - intrahepatic in both cats and
dogs
 Extrahepatic PSS most common, constitutes 66%
to 75%.

8. Breed predisposition
 Intrahepatic portosystemic shunts occur
predominantly in large breed dogs, particularly in
 Irish wolfhounds ,
 Bernese mountain dogs,
 golden retrievers and
 medium sized Australian cattle dogs and
Australian shepherds breeds.

9. Contd.
 Extrahepatic portosystemic shunts occur mostly in
small breeds, particularly in
 Maltese dogs,
 miniature schnauzers ,
 dachshunds , poodles and
 small terriers (Yorkshire, Jack Russell), but are
occasionally seen in large breeds.
- Yorkshire terrier is the breed most commonly
affected(35 times greater chances than all other
breeds).

10. Severity of clinical signs
 Some EHPSSs, like splenocaval shunts, may be
associated with less severe clinical signs because
splenic blood is not of GI origin and less portal
blood is being shunted away from the liver.
 Dogs with IHPSSs generally have the largest
volume of diverted portal blood, allowing them to
develop more severe clinical signs at an earlier
age than those with EHPSSs.

11. Acquired portosystemic shunt
 most commonly occur secondary to chronic portal
hypertension in which increased portal pressures lead
to the opening of fetal, vestigial blood vessels.
 usually multiple, tortuous, extrahepatic, and located
near the kidneys.
 Common causes – hepatic fibrosis, portal vein
hypoplasia with portal hypertension.
 They are the compensatory mechanism to prevent or
delay liver failure.

12. History of animals with portosystemic
shunts
 Chronic or acute illness before 1 to 2 years of age,
though some have been older than 10 years of age.
 Small stature
 Failure to gain Weight
 Fever
 Anesthesia or tranquilizer intolerance
 Dysuria ?
 Polyuria ?
 Polydipsia ?

13. Clinical signs
 The three most common systems affected are the
central nervous, GI, and urinary systems.
 GI signs – vomiting, diarrhea, anorexia, pica and
or GI bleeding/ melena/ hematemesis.
 Hypersalivation common in cats
 Urinary tract signs – hematuria, stranguria,
urinary obstruction ( ammonium urate calculi)

14. Hepatic encephalopathy
 How ?
 Occurs when 70% of liver function is lost
 20 different compounds (including ammonia,
tryptophan, glutamine, aromatic amino acids,
short-chain fatty acids, gamma-aminobutyric acid
(GABA), endogenous benzodiazepines etc)
 Ammonia - most important ?
 CNS signs- ataxia, circling, seizures, coma etc.

15. DIAGNOSIS
 Signalment (certain breed predisposition)
 History
 Clinical signs
 Laboratory tests (don't provide definitive
diagnosis)
 Imaging techniques (Porto venography ,
ultrasonography, scintigraphy, computed
tomographic angiography)

16. Laboratory tests
 Microcytosis with or without anemia is found in
60% to 70% of dogs with CPSS.
 Leukocytosis – variable
 Decrease in albumin, total proteins and urea
nitrogen concentration.
 Liver enzymes (alanine transaminase and
aspartate transaminase) may be increased. Dogs
with intrahepatic shunts have significantly higher
alkaline phosphatase than dogs with extrahepatic
shunts.
 Ammonium biurate crystalluria and low urine
specific gravity.

17. Specialized biochemical testing of blood
ammonia and bile acid concentration
 Ammonia tolerance test- ammonium chloride(100
mg/kg b wt.; max. of 3g) is adm. By orogastric
tube, oral capsule, or high colonic
infusion(2ml/kg of a 5% solution inserted 20 to 35
cm into the colon).
 Bile acids (radioimmunoassay- measures only non
sulfated conjugated primary bile acid and
enzymatic assays measure all sulfated and non
sulfated hydroxy bile acids.)

18. Imaging techniques
 Ultrasonography
 scintigraphy
 Computed tomographic angiography
 Porto venography

19. ultrasonography
 Small liver size
 Decreased no. of hepatic and portal veins
 Detection of anomalous vessel
Extrahepatic portosystemic shunts are more
difficult to diagnose with ultrasonography (?)

20. Abdominal ultrasound image using color flow
Doppler documenting a portosystemic shunt.
Abnormal communication between the portal vein
(PV), shunting vessel (S), and caudal vena cava
(CVC).

21. Scintigraphy
 Transcolonic scintigraphy utilizing the
radioisotope technetium pertechnetate bolus
infused per rectally and imaged with gamma
camera.
 Scintigraphy does not provide morphologic
information regarding shunt type or location,
Cannot differentiate IHPSS from EHPSS, single
from multiple

22. Transcolonic portal scintigraphy (radio
isotope reaching directly to heart(H) prior to
liver (L) from colon (C) in image B

23. Computed Tomographic Angiography
 It is noninvasive, fast, and images all portal
tributaries and branches from a single peripheral
venous contrast injection.
 most valuable in animals with suspected IHPSS
 or for which US is not diagnostic and more
invasive imaging such as portography is not
desired.

24. Computed tomography (CT) angiogram of a
young dog with intrahepatic portosystemic
shunt
3d reconstruction of shunt(*) Axial

25. PORTO VENOGRAPHY
 Surgical mesenteric Porto venography is the most
commonly performed angiographic test for
documenting PSSs in dogs and cats.
 But it is invasive technique

26. PORTO VENOGRAPHY

27. TREATMENT
 The type of liver shunt that a dog has and their
age and overall condition determines what type
of treatment is best.
 Medical treatment and surgical treatment
 The goal of medical treatment is to improve the
health of the patient to a point where the risk of
anaesthesia and surgery is low.

28. MEDICAL TREATMENT
 Feeding low protein diet :- lower the protein,
lower the byproducts like ammonia. Soya protein
is beneficial over meat protein and several
smaller meals throughout the day is also
beneficial.
 i/v fluids if animal is dehydrated or refuse to
drink water, RL should be avoided due to the need
of conversion of lactate to bicarbonate.
 Antibiotics
 Lactulose orally or enama- colonic acidifier which
works by decreasing the ammonia in the blood.
(counter HE)

29. SURGICAL TREATMENT
 The goal of surgery for PSSs is to attenuate the
abnormal vessel in order to redirect and reestablish
blood flow to the hepatic parenchyma.
 But Approximately 32% to 52% of EHPSS and
approximately 15% of IHPSS dogs have been reported
to be able to tolerate complete shunt attenuation
only.
 Therefore, a delicate balance remains; shunt
attenuation in order to increase portal blood pressure
sufficiently to encourage development of portal
perfusion without causing excessive portal
hypertension.

30. PROCEDURE
 Following identification and careful dissection
 Application of progressive occlusion devices (e.g.,
ameroid constrictors or cellophane bands) or tying
off the vessels with suture material.
 Ameroid constrictors and cellophane bands cause
the vessels to narrow over time.
 shunt is isolated and an encircling suture is placed
as close to the systemic circulation (at shunt
termination not at shunt origin )

31. Laparotomy in a dog with an extrahepatic portosystemic shunt
Splenocaval EHPSS entering the vena cava (VC)
between liver(L) and pancreas(P)

32. The same dog following placement of a ameroid
constrictor(arrow) at the shunt termination onto the
vena cava

33. Laparotomy in a dog with an extrahepatic
portosystemic shunt after placement of a
cellophane band(CB) around the shunt(*) that
has been secured in place with 4 hemoclips
(HC)

34. Posthepatic dissection of the left hepatic vein
(LHV) between the liver (L) and diaphragm for a left
divisional IHPSS before placement of a suture.

35. Prehepatic dissection caudal to the gallbladder
(GB) and liver (L) of a right divisional IHPSS
following placement of a hydraulic occluder (arrow)
secured in place with polypropylene suture.

36. THANKYOU