Page 746 - Clinical Small Animal Internal Medicine

714 Section 7 Diseases of the Liver, Gallbladder, and Bile Ducts

whether they represent preexisting or acquired vascular ins) is responsible for the cardinal clinical signs of por-
VetBooks.ir communications. tosystemic shunting (Table 66.1).
Neurologic perturbations caused by the liver dysfunc-
Traditional acquired shunts may occur between any
branch of the portal and systemic vasculature, but they
neurologic abnormalities are termed hepatic encepha-
are typically small and tortuous and cluster around the tion resulting from portosystemic shunting leading to
cranial and caudal aspects of the kidneys, especially the lopathy (HE) (see description later).
left kidney. Communications with the remnant ovarian It is becoming increasingly recognized that infection
veins may occur in spayed females; these single vessels and inflammation also play a role in development of
may become particularly large and noticeable, especially encephalopathy in laboratory animals and humans.
in cats. Circulating blood levels of C‐reactive protein (a marker
In PVH-MVD , shunts are considered to be micro- of inflammation) have relatively recently been shown to
scopic, occurring between the hepatic portal and hepatic be elevated in dogs with HE, suggesting that this is also
venous systems, thereby bypassing the sinusoids. likely to be an important mechanism in dogs. HE may be
complicated by hypoglycemia in patients that are inap-
petent or being fasted, as a result of low hepatic glycogen
Pathophysiology reserves in the hypoplastic or damaged liver.
Circulating levels of these substances will fluctuate
Dogs and cats with portosystemic shunting usually have according to whether the animal has eaten, the diet, and
low functional hepatic mass. The liver either fails to grow other factors affecting gastrointestinal transit time, bac-
normally as it is deprived of its normal blood supply, terial flora or the production of ammonia within the gut.
trophic factors (such as insulin and hepatic growth fac- Gastrointestinal hemorrhage is a known risk factor for
tor) and nutrients, or liver function is impaired as a result development of HE, and can be a particular problem in
of a primary hepatopathy (in cases with acquired porto- patients with end‐stage liver disease and portal hyper-
systemic shunts). tension, or dogs with CPSS that develop gastrointestinal
The major clinical signs associated with portosys- ulceration (see later).
temic shunting result from failure of the liver to metab- Deranged nitrogen metabolism causes a tendency for
olize substances being absorbed from the urinary ammonium biurate crystalluria and calculus
gastrointestinal tract, receive pancreatic hormones, formation, which may lead to irritation of the renal
and metabolize other circulating hormones. There is pelvis with hematuria, ureteral obstruction or (more
deranged nitrogen metabolism and the capacity of the commonly) urethral obstruction.
liver to produce urea is diminished, leading to elevated Polyuria and polydipsia are common in patients with
levels of circulating ammonia and low blood urea portosystemic shunts. The mechanism is not completely
nitrogen (BUN) levels. Serum bile acids, which nor- understood but is probably multifactorial. Contributing
mally undergo almost complete enterohepatic circula- factors include low plasma BUN and poor renal concen-
tion, are also elevated in systemic samples. Abnormal trating ability, and increased thirst resulting from sys-
filtering or metabolism of a variety of other substances temic inflammation and fever.
absorbed into the portal venous blood (branched chain Abnormal blood flow within the hepatic sinusoids
and aromatic amino acids, bacteria and bacterial tox- results in impairment of delivery of vital substances to

Table 66.1 Clinical and diagnostic features of different conditions causing biochemical evidence of hepatopathy

Age HE Ascites Jaundice Diarrhea Elevated shunt fraction

CPS Younger Yes Rare * No Rare Yes
PVH‐MVD Any age No No No No No
Noncirrhotic PH Young to middle‐aged Yes # Yes No Yes Yes #
Cirrhotic PH Older Yes # Yes Yes Yes Yes #
* Possible in patients with very low serum albumin.
# Once acquired shunts have developed.
CPS, congenital portosystemic shunts; HE, hepatic encephalopathy; MVD, microvascular dysplasia; PH, portal hypertension; PVH, portal venous
hypoplasia.