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FRANK J. MILNE STATE-OF-THE-ART LECTURE


very high (up to 300 umol/L) in some PSS foals without evidence of encephalopathic signs. The chronicity of the hyperammonemia and, in some cases, its gradual development may somehow allow the brain to adapt to the elevated ammonia levels. PSS can be confirmed by liver ultrasonography, by ultrasound-guided, percutaneous trans-splenic in- jection of 10 mL agitated saline into the spleen with simultaneous echocardiography of the right heart (“bubblegram”) or by transrectal hepatic scintigra- phy.201,205 The bubblegram may have higher sen- sitivity because air bubbles will appear in the right heart almost immediately after splenic injection if PSS is present.201 Theoretically, if portal circula- tion is normal the liver will filter the bubbles and the bubbles will not reach the heart. Trans-rectal scin- tigraphy for the diagnosis of PSS is performed by placing a soft rubber catheter as far into the rectum as safely possible and administering 30 mC of tech- netium pertechnetate followed immediately by ra- dioisotope scanning of both the heart and liver. If the majority of technetium is detected first in the liver then PSS can be ruled out. Conversely, if most of the radioactivity appears in the heart first then the foal either has a PSS or the technetium was not administered “high” enough in the distal bowel (substances absorbed from the distal rectum enter the caudal vena cava, not the portal circulation).205 If a liver biopsy is performed (usually unnecessary), lobular atrophy characterized by decreased distance between the central veins and portal areas and ar- teriolar proliferation in the portal tract with mild proliferation of interlobular arteries are usually seen.201 The number and size of portal veins may be subjectively less than normal. These findings may vary depending upon location of the shunt (ex- tra- vs. intrahepatic), but all of the changes develop as a result of decreased oxygen supply to the liver caused by the PSS (recall that the majority of oxygen to the liver is delivered via the portal vein, not the hepatic arteries). Positive-contrast portography following anesthesia and catheterization of a mes- enteric (usually jejunal) vein or computed tomo- graphic angiography (Fig. 9) with contrast and ultra-sonography may all be required to determine the shunt location prior to considering surgical re- pair. Shunts may occur as either intrahepatic or extrahepatic and be single or multiple shunts.198 Shunts may occur due to aberrant connections be- tween the systemic circulation (often the caudal vena cava or azygous vein) and virtually any gastric, splenic or mesenteric vessel.198 Surgical repair has been successful using suture ligation, cellophane bands, or casein–stainless steel rings (ameroid rings) placed around the shunt.198,201 Immediate, total surgical ligation of the shunt vessel can cause life-threatening portal hypertension with increased mesenteric venous pressures and congestion of the bowel. As opposed to suture ligation, cellophane bands or casein rings can be fitted around the shunt vessel, modestly occluding blood flow initially; over


Fig. 9. Computed tomographic slice through the liver of a foal with a portosystemic shunt. Three vascular structures are seen aorta (A), caudal vena cava (C) and portal vein (P). At this point, well within the hepatic parenchyma, the portal vein should have branched indicating an intrahepatic shunt.


the following weeks gradual attenuation of the shunt occurs due to either vascular constriction as- sociated with the inflammation caused by cello- phane banding or because of gradual casein swelling in the ameroid rings.201 Placement of transvenous coils or umbrellas into shunts could also result in slow embolization and progressive closure of the shunt, but experience has shown that the umbrellas made for children are too small to cause a sufficient thrombus in the vessel in neonatal large animals.204 While preparing for diagnostics and surgery, treat- ments for foals with HE secondary to PSS are sim- ilar to HE treatment caused by intrinsic liver disease and failure (page 92). Enemas are often used on foals with HE if the manure becomes abnor- mally firm. One foal with a PSS and a blood am- monia as high as 300 umol/L was maintained on lactulose and minocycline per os, in addition to en- emas, until surgery could be attempted.


Hyperammonemia Syndrome in Morgan Foals


An acute onset of clinical signs such as coma, blind- ness, and seizures has been associated with the hy- perammonemia syndrome seen in Morgan foals, usually 4–7 months of age.199,206 The onset of clin- ical signs often occurs soon after weaning. Liver enzymes may be mildly elevated and variable de- grees of liver pathology can be seen on microscopic examination but the degree of microscopic disease is modest and other liver function tests are not abnor- mal in affected foals. The cause of the disease is unknown but it seems to be a disorder of metabolism of ammonia and possibly other amino acids. The blood ammonia is extremely high in affected foals (300–500 umol/L), indicating that they have likely developed some compensatory or protective mecha- nism against the persistent elevation in ammonia to


AAEP PROCEEDINGS  Vol. 61  2015 89


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