Chapter 146 Portosystemic Shunt Management
Portosystemic shunts (PSSs) are vascular anomalies that connect the portal circulation with the systemic circulation, diverting portal blood away from the liver. These vascular anomalies are categorized most commonly as extrahepatic or intrahepatic shunts. Extrahepatic PSSs can be further categorized as congenital or acquired and often are described based on the supplying and draining vessels, such as portocaval or portoazygos shunts. Intrahepatic PSSs usually are classified based on the branch of the portal vein supplying the shunt and divide intrahepatic PSSs into left-divisional, central-divisional, and right-divisional categories.
Single extrahepatic PSSs are the most commonly reported type in dogs and cats; they are congenital and seen primarily in small breed dogs.1-3 Clinical signs are related to hepatic dysfunction, including gastrointestinal (GI) signs, central nervous system (CNS) disturbances, and urolithiasis. Some patients will require intensive therapy to stabilize them before surgical correction of the PSS. Postoperative complications can occur in an unpredictable and precipitous manner and can range in severity from ascites to life-threatening hemodynamic and neurologic abnormalities, making these patients extremely challenging to treat after surgery.
Animals with PSS commonly will have neurologic abnormalities, GI signs, urinary signs, and other signs such as prolonged recovery from a previous anesthesia.3 Preoperative stabilization depends on the animal’s status on arrival and often includes fluid therapy and anticonvulsant medications to stop the progression of neurologic signs. If a patient has mild clinical signs of hepatic encephalopathy and is stable, medical treatment may be initiated (i.e., low-protein diet, anticonvulsants, antibiotics, and cathartics).
On the other hand, if a patient has moderate to severe signs of hepatic encephalopathy, more aggressive therapy is indicated. A major contributing factor to worsening hepatic encephalopathy is hemorrhage into the GI tract, which acts as a large protein source for further ammonia production. To reduce signs of hepatic encephalopathy, immediate removal of any protein source within the GI tract with lactulose enemas is a priority. Ongoing ammonia production and absorption should be prevented with oral antibiotics and cathartics (see Chapter 103, Hepatoencephalopathy).
GI signs in patients with PSS often include vomiting and diarrhea, which can lead to fluid and electrolyte imbalances. These imbalances should be addressed before surgical correction of the PSS. Pica is reported frequently in PSS patients, and as a result the patient may be vomiting secondary to a GI foreign body.
Occasionally animals can have a urinary emergency secondary to PSS, such as a urethral obstruction. Initial treatment may include correcting fluid and electrolyte abnormalities followed by relief of the obstruction.
As long as portal blood flow is being shunted away from the liver, hepatic function will continue to decline. Surgery offers the opportunity to redirect portal blood back to the liver. Medical management should be initiated before surgical correction of the PSS in animals with signs of hepatic encephalopathy, and anticonvulsant therapy may be beneficial in PSS patients preoperatively. The benefit of preoperative anticonvulsant therapy was evaluated by Tisdall and others4 and showed that prophylactic anticonvulsants did not significantly reduce the risk of postoperative neurologic signs, but may have reduced their severity. Therefore routine use of prophylactic anticonvulsant therapy in all dogs with PSS may be warranted. There are several protocols for preoperative anticonvulsant therapy and the authors’ recommendation in dogs is potassium bromide at a loading dosage for 24 hours (100 mg/kg PO q6h) or a maintenance dosage for a minimum of 2 weeks (40 mg/kg PO q24h) (Table 146-1).
|Drug||Canine and Feline Dosage||Therapeutic Blood Levels|
|Phenobarbital||1 to 2 mg/kg PO q12h||15 to 45 μg/ml|
|Potassium bromide||Loading dosage*:|
100 mg/kg PO q6h × 4 doses (total dosage of 400 mg/kg in 24 hr)
60 to 100 (canine) mg/kg once a day
|2 to 3 mg/ml when used as a sole agent|
1 to 2 mg/ml when used in conjunction with phenobarbital
*A loading dose is recommended if therapeutic levels are required quickly. This is one of several protocols for potassium bromide loading. A maintenance dose given longer than 15 days in dogs will provide adequate blood levels as an alternative to giving the loading dose.22 These drugs can be associated with neurologic and respiratory depression and patients should be monitored accordingly. Loading doses of potassium bromide can cause gastrointestinal disturbances.
PO, Per os, PSSs, portosystemic shunts.
From Plumb DC. Plumb’s veterinary drug handbook, ed 5, Stockholm, 2005. PharmaVet Inc.
Feline patients with PSS have a high incidence of neurologic complications after surgery,5,6 so preoperative anticonvulsant therapy is often instituted. Potassium bromide has been associated with allergic airway disease in cats; consequently the author uses phenobarbital (1 to 2 mg/kg PO q12h) and recommends confirming that the serum concentrations reach therapeutic levels before surgery (see Table 146-1). Because phenobarbital is metabolized in the liver, animals with liver insufficiency may require lower dosages to achieve therapeutic levels.
The goal of medical therapy is to decrease production and absorption of ammonia, and management includes dietary modification, antibiotic therapy, and cathartics. Typically, a diet high in carbohydrates and low in protein will decrease the building blocks for ammonia production. Dairy and vegetable protein sources are less likely to cause signs of hepatic encephalopathy than are meat proteins. Antibiotics that concentrate in the GI tract, such as amoxicillin, neomycin, and metronidazole, will reduce the number of bacteria responsible for ammonia production. Cathartics, such as lactulose, will shorten the transit time in the GI tract and trap ammonium ions in the lumen, reducing its absorption. Acid-base imbalances, electrolyte abnormalities, and hypoglycemia should be identified and corrected before surgery.
Hypoalbuminemia is a consistent finding in patients with PSSs. Because their hypoalbuminemia is chronic, it generally is not associated with signs in the stable patient and as such it does not warrant therapy. It will, however, be a concern in the patient that requires significant fluid resuscitation, a common requirement of the preoperative PSS patient. Large volumes of crystalloid fluid will cause hemodilution and worsen the hypoalbuminemia, making maintenance of intravascular volume very difficult.
Hemodynamically compromised hypoproteinemic patients generally require support of serum colloid osmotic pressure (COP). Although synthetic colloids such as hetastarch are very effective at increasing COP, they interfere with coagulation. Because patients with PSSs tend to have coagulation deficits,7 synthetic colloids should be avoided or minimized. Plasma transfusions will support intravascular volume, help maintain COP, and provide coagulation factors. For this reason plasma can be an invaluable therapy in the perioperative stabilization of the patient with a PSS.