Page 622 - Small Animal Internal Medicine, 6th Edition

594 PART IV Hepatobiliary and Exocrine Pancreatic Disorders

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A B

C

FIG 36.5
(A) Nine-year-old neutered female German Shepherd dog with previously stable
noncirrhotic portal hypertension treated medically for 8 years presented very depressed,
with a week-long history of anorexia (same dog as Fig. 36.13). (B) and (C) In spite of
immediate institution of tube feeding on admission, the dog rapidly developed fatal septic
peritonitis as a result of rupture of an ulcer at the gastroduodenal junction. It was found
that the dog had developed asymptomatic pyelonephritis. The referring veterinarian had
recognized the hepatic encephalopathy but tried to manage it by starvation for a week,
which likely increased rather than decreased ammonia production through breakdown of
muscle and also increased the risk of GI ulceration because of a lack of intraluminal gut
nutrition.

Treatment of GI ulceration largely revolves around its of active ulceration and melena, gastric acid secretory inhibi-
prevention (i.e., avoiding triggers as much as possible, such tors are often used in the hope that they will help. In these
as prolonged fasting and the use of steroids or NSAIDs, and circumstances, cimetidine is contraindicated because of its
avoiding hypotension during any surgery). It is particularly effect on hepatic P450 enzymes; therefore ranitidine (2 mg/
important that any dog with portal hypertension that under- kg administered orally or via slow IV administration q12h)
goes a prolonged period of anorexia is fed because they will or famotidine (0.5-1 mg/kg administered PO q12-24h) are
be at high risk of GI ulceration if they do not receive nourish- recommended. The proton pump inhibitor omeprazole is
ment (see Fig. 36.5). Parenteral nutrition is not an effective likely to be more effective in the face of overt bleeding and
alternative in these dogs because it does not supply luminal should be dosed at 1 mg/kg q12h. Likewise, sucralfate (Cara-
nutrients for enterocyte healing—upper GI ulceration is a fate ) is of questionable efficacy; it is most effective against
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common adverse effect of total parenteral nutrition in gastric ulceration (i.e., in association with a low pH), but it
humans, even in those without portal hypertension, and is often used (at a dosage of 500 mg-1 g per dog PO q8h).
some form of enteral support should be instituted as soon as Hemostasis profiles should also be evaluated, and any coagu-
possible. The use of gastric acid secretory inhibitors (H 2 lopathy treated with vitamin K (see the later section on
blockers or proton pump inhibitors) is of questionable coagulopathy) or plasma transfusions.
benefit in patients with portal hypertension because it is Treatment of coagulopathies
usually the duodenum that is ulcerated (rather than the Despite the presence of hemostatic abnormalities, spon-
stomach); also, there have been reports that the gastric pH taneous bleeding is uncommon in patients with chronic liver
in dogs with liver disease may already be higher than normal disease but relatively common in those with acute disease
as a result of changes in gastrin metabolism, although a (see later). Because dogs with portal hypertension and GI
recent study of dogs with newly diagnosed liver disease hemorrhage (see previous section) may also have a coagu-
found no difference in gastrin concentration compared with lopathy predisposing to their bleeding, they should be thor-
control dogs (Mazaki-Tovi et al., 2012). However, in the face oughly evaluated. However, the risk of hemorrhage increases