Page 616 - Small Animal Internal Medicine, 6th Edition

588 PART IV Hepatobiliary and Exocrine Pancreatic Disorders

of unidentified toxins. In addition, although poorly doc- eventually ascites. The mechanisms of ascites formation in
umented, it is very possible that herbal and nutraceutical dogs with liver disease are complex but involve activation
VetBooks.ir supplements could cause chronic liver disease in some dogs. of the renin-angiotensin-aldosterone system (RAAS), with
sodium retention in the kidneys and increased circulating
Daily ingestion of cheap, poorly quality-controlled joint sup-
plements based on shellfish has been associated with chronic
If the rise in portal pressure is sustained, multiple acquired
liver disease in humans, likely due to a contaminating toxin. fluid volume (see Chapter 33).
Reports of joint supplement hepatotoxicity in dogs have PSSs will develop by the opening up of previously nonfunc-
only been seen with a large overdose, but chronic low-dose tional vessels; this allows for some of the portal blood to
toxicity remains possible. Because a wide variety of drugs bypass the liver and enter the portal vein directly (Fig. 36.2).
and herbals have been reported as causing hepatic adverse These acquired PSSs differ from congenital PSSs in that they
reactions in humans and dogs, a drug reaction should be are multiple and exist in the presence of increased portal
considered in any dog with chronic hepatitis that is also pressure, whereas in patients with congenital PSSs, the portal
on long-term therapy of any type, and a careful history of pressure is low. Acquired PSSs lead to HE by a mechanism
supplement use should be obtained, although care should be similar to that for congenital PSS (see Chapter 33). However,
taken not to overdiagnose drug reactions. Chronic hepatitis the HE must be medically treated because the ligation of
should be considered as possibly being drug-related only acquired PSSs is contraindicated (see section on treatment
when there is a clear temporal relationship with drug intake of PSS later). This is because acquired PSSs are important
and likely alternative causes have been excluded. escape valves to allow dissipation of some of the portal
hypertension; therefore any attempt to ligate them will result
Shared Pathogenesis of All Forms of in fatal splanchnic congestion. Acquired PSSs in humans are
Chronic Hepatitis also recognized to reduce the risk of serious GI ulceration
The pathogenesis of chronic hepatitis relates to the loss of associated with portal hypertension. Because of this, they are
hepatic mass resulting in loss of function and, late in the sometimes created surgically in humans with cirrhosis to
disease process, development of portal hypertension. In reduce the risk of serious bleeds. The same is likely to be true
many cases hepatocyte swelling, fibrosis, and portal hyper- in dogs; GI ulceration is one of the most common causes of
tension also contribute to cholestasis and jaundice. Ongoing death in dogs with chronic hepatitis, and acquired PSSs will
inflammation may also result in bouts of pyrexia and hepatic help reduce this risk.
pain with associated gastrointestinal (GI) and other signs,
and many dogs with chronic hepatitis develop negative Clinical Features of All Forms of
nitrogen balance and protein-calorie malnutrition. Loss of Chronic Hepatitis
hepatic function accounts for coagulopathies and adverse Dogs of any age or breed can be affected with chronic hepa-
drug reactions in affected dogs. titis, but there is an increased suspicion in middle-aged dogs
Portal hypertension is an important consequence of of the breeds listed in Box 36.1. Some of these breeds may
chronic hepatitis and fibrosis, and its effects contribute to the also be affected by copper storage disease, granulomatous
clinical signs and death of many affected animals. It causes hepatitis, or immune-mediated hepatitis (see earlier and
a typical triad of clinical signs of ascites, GI ulceration, and later sections). The functional and structural reserve capacity
hepatic encephalopathy (HE). In a healthy dog the pressure of the liver implies that dogs with chronic hepatitis usually
in the portal vein is lower than the pressure in the caudal have no clinical signs until late in the disease process, when
vena cava. However, in association with obstruction and more than 75% of liver function has been lost. By this stage,
disruption of the sinusoids by fibrosis and hepatocyte swell- there is already extensive destruction of liver mass, and treat-
ing, portal pressure rises until it exceeds that in the caudal ment will be less effective than it would have been earlier
vena cava (portal hypertension). This results in splanchnic in the disease (Fig. 36.3). It is therefore beneficial to diag-
congestion, with splenic congestion, gut wall edema, and nose the disease earlier, and dogs with persistently high liver

Liver
Azygos Vena cava

Shunt
Shunts

Heart Portal vein
A B

FIG 36.2
Diagrammatic representation of congenital and acquired portosystemic shunts. (A)
Congenital portocaval shunt. (B) Multiple acquired shunts. These develop only if the
pressure in the portal vein is higher than the pressure in the vena cava.