Page 631 - Small Animal Internal Medicine, 6th Edition

CHAPTER 36 Hepatobiliary Diseases in the Dog 603

surgical) should receive antioxidant therapy, preferably with pressure and those with high portal pressure. However, it is
vitamin E (400 IU PO for a 30-kg dog, scaled appropriately important to remember than when two or more congenital
VetBooks.ir to the size of the dog; tablets usually come as 100, 200, or hepatic defects occur concurrently, the differentiation will be
less obvious.
400 IU) and SAM-e (20 mg/kg PO q24h) because it has been
demonstrated that bile reflux in the liver is a potent oxidant
toxin. Dogs should be fed a high-quality diet that is not
protein-restricted: usually, a diet designed for critical care DISORDERS ASSOCIATED WITH LOW
feeding is more appropriate than a manufactured liver PORTAL PRESSURE: CONGENITAL
support diet because the dog is suffering an inflammatory PORTOSYSTEMIC SHUNT
and/or septic process, but hepatocyte function is usually Etiology and Pathogenesis
good.
The prognosis for dogs with EBDO depends on the under- Congenital PSSs are the most common congenital portovas-
lying cause. If the cause can be addressed without surgical cular disorder in dogs. The etiology and pathogenesis are
reconstruction, the prognosis is fair to good. If extensive similar to those in cats; see Chapter 35 for more details.
biliary reconstruction is needed, the prognosis is guarded. Many different types of congenital portovascular anomalies
have been reported in dogs; sometimes they coexist with
Bile Peritonitis intrahepatic or extrahepatic portal vein hypoplasia or intra-
Bile peritonitis usually results from abdominal trauma dam- hepatic MVD (see later). However, a distinguishing feature
aging the CBD (e.g., penetrating injury, horse kick, automo- of isolated congenital PSS is that it results in a low portal
bile accident) or pathologic rupture of a severely diseased pressure because some blood is shunted away from the sinu-
gallbladder, particularly with gall bladder mucocele but also soidal circulation by the shunting vessel(s). Dogs with iso-
which sometimes occurs after diagnostic ultrasonography- lated congenital PSS therefore do not present with ascites
guided aspiration. Early signs of bile peritonitis are nonspe- unless they are severely hypoalbuminemic. This allows dif-
cific, but with progression, jaundice, fever, and abdominal ferentiation from the congenital vascular disorders associ-
effusion are seen. When bile, which is normally sterile, comes ated with increased portal pressure and therefore acquired
into contact with the peritoneal surface, there are resultant PSS (see later) in which portal hypertension and associated
cell necrosis and changes in permeability, which predispose ascites are common at presentation.
to infection with bacteria that move across the intestinal Canine congenital PSSs can be extrahepatic or intra-
wall. Hypovolemia and sepsis may occur in animals with hepatic. Extrahepatic PSSs are anomalous vessels connecting
undetected bile peritonitis. Surgery is essential in bile peri- the portal vein or one of its contributors (left gastric, splenic,
tonitis, both to identify and treat the cause and to lavage cranial or caudal mesenteric, or gastroduodenal vein) to the
the abdomen. Presurgical considerations are the same as for caudal vena cava or azygos vein. They are most commonly
EBDO. If surgery for bile peritonitis is to be delayed, peri- recognized in small-breed dogs and have a high prevalence
toneal drainage should be established to remove noxious, in Cairn Terriers, Yorkshire Terriers, West Highland White
bile-containing abdominal fluid and for lavage. Terriers, Maltese, Havanese, other terriers, and Miniature
Schnauzers (Fig. 36.10). Intrahepatic PSSs may be left-sided,
CONGENITAL VASCULAR DISORDERS in which case they are thought to represent persistence of the
fetal ductus venosus, or they can be right-sided or central, in
Congenital disorders of hepatic vasculature, intrahepatic and which case they likely have a different embryologic origin.
extrahepatic, are more common in dogs than in cats. There An intrahepatic PSS is usually seen in large-breed dogs, but
are some breed-related tendencies, suggesting a genetic basis Collies tend to have extrahepatic PSSs, despite being large
to some disorders, but it is also assumed that most of them dogs. Increased breed prevalence suggests a genetic basis to
result from some type of (as yet undefined) insult in utero. the disease, but this has only been investigated in Irish Wolf-
Experimental reduction in flow in the umbilical vein in hounds, in which an inherited basis of patent ductus venosus
sheep and other species can result in the development of has been demonstrated, in Cairn Terriers with extrahepatic
PSSs and asymmetry of hepatic lobular and vascular sup- PSSs, in which an autosomal polygenic inheritance or mono-
plies; this is likely also true in dogs. This would explain why genic inheritance with variable expression is suspected (van
it is relatively common to see dogs with more than one Straten et al., 2005), and in Maltese dogs, in which a partially
coexistent congenital vascular disorder in the liver (e.g., a penetrant recessive mode of inheritance has been proposed
congenital PSS combined with intrahepatic portal vein (O’Leary et al., 2014). Affected Irish Wolfhounds tend to
hypoplasia or microvascular dysplasia [MVD]) and would have smaller litters and can also produce more than one
also explain why dogs with congenital PSSs have a higher puppy with a PSS in a litter.
prevalence of other congenital defects, such as cryptorchi- One study reported that dogs from breeds that were not
dism and cardiac disorders. usually recognized as having a high risk of PSS were more
For ease of categorization, and because they have different likely to present with unusual anatomic forms of PSS that
clinical presentations, congenital vascular disorders have were less often amenable to surgical management (Hunt,
been divided into disorders associated with low portal 2004).