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The developmental dynamics of cloned Mexican bighorn sheep ( Ovis canadensis mexicana ) embryos were evaluated based on morphological quality standards. Categories determined by standards were correlated with the embryonic development stage, number of nuclei and viability. The results showed no differences in the blastocyst rate between the experimental (cloned Mexican bighorn sheep embryos) and control (parthenogenetic domestic sheep embryos) groups ( p > .05), while type IV fragmentation was higher in clones ( p < .05). The standards allowed for the identification of embryos that divided at least once or fragmented after 24 hr of culture. The highest percentage of morulae appeared at 96 hr, the final stages of development: nonsegmented, blocked, fragmented and blastocysts appeared at 192 hr. Embryonic quality decreased over time, making 96 hr the ideal time point to predict the final morphological quality of embryos. Nuclear staining of the morulae and blastocysts showed that higher embryo quality was associated with a higher percentage of normal and viable blastomeres. The evaluated criteria allowed for descriptions of the dynamics, stage and quality of cloned Mexican bighorn sheep embryos with a high degree of reliability. In addition, developmental anomalies, including fragmentation, multinucleation and blocking, were identified.

INTRODUCTION: Congenital portosystemic shunts or Abernethy malformations are rare anatomical abnormalities shunting blood from the portal venous system to the systemic venous system, thereby bypassing passage through the hepatic acinus. The presentation may range from incidental finding on imaging to hepatic encephalopathy and liver failure depending on the degree and type of shunt. Here, we describe an interesting case of unexplained encephalopathy in a patient without liver cirrhosis found to have congenital intrahepatic Type II Abernethy malformation. CASE DESCRIPTION/METHODS: A 73-year-old female with a past medical history of Rheumatoid arthritis and Gilbert syndrome was admitted to hospital with clinical evidence of encephalopathy. Vitals were stable and physical examination was unremarkable except for encephalopathy. Laboratory investigations were unremarkable except for elevated ammonia levels (165 µmol/L). Computed tomography (CT) of the brain was unremarkable. Abdominal ultrasonography revealed the normal size and echotexture of the liver. Abdominal CT angiography showed the presence of dilated portal vein measuring up to 1.8 cm at the porta-hepatis along with dilated superior mesenteric and splenic veins. Multiple dilated vascular channels were seen within the right hepatic lobe. An intrahepatic portosystemic shunt between an enlarged middle hepatic vein and 2 separate branches of the right portal vein was visualized. Pressure gradients were measured and were normal. She received conservative management with lactulose and rifaximin and discharged on day 6 after the resolution of encephalopathy. DISCUSSION: Encephalopathy associated with portal-systemic bypass and no intrinsic hepatocellular disease is often referred to as Type B hepatic encephalopathy as was in our patient. Ammonia which is the culprit for the neuropsychiatric manifestation is usually metabolized by the liver in normal conditions, however in cases of portosystemic shunting, whether congenital or not, ammonia bypasses the liver and enters the systemic circulation and directly reaches the brain. The degree of symptomatology associated with these venous shunts depends on the shunt ratio and patient age. Treatment options include medical management including use of lactulose and non-absorbable antibiotics or endovascular shunt closure. Our patient was managed medically with the plan to refer her for shunt closure if she continues to have recurrent episodes.