Shunt porto-sistémico congénito en hígado no cirrótico como causante de síndrome confusional agudo reiterado: report of one case / Portosystemic shunt in a normal liver causing confusional states

Portosystemic shunts are rare vascularization disorders, and an uncommon cause of confusional states. We report an 87-year-old male with a previously normal cognitive status who was repeatedly admitted for sudden symptoms of disorientation and functional limitation. The patient had high ammonium levels which lead to the suspicion of the presence a portosystemic shunt, even in the absence of pre-existing liver disease. A contrast enhanced computed tomography of the abdomen confirmed the presence an abnormal communication of the right portal vein with the suprahepatic veins. The communication was embolized and the confusional states of the patient subsided.

Non invasive prediction of varices in Egyptian cirrhotic patients

Cirrhotic patients frequently undergo screening endoscopy for the presence of varices. In the future, this social and medical burden will increase due to the greater number of patients with chronic liver disease and their improved survival. In this study, our aim was to develop a predictive model using independent risk factors for the presence of varices in the enrolled patients. 200 patients with liver cirrhosis with no history of variceal haemorrhage were subjected to clinical examination; laboratory investigations [CBC, Liver biochemical profile, serum urea and creatinine], modified Child-Pugh score and MELD score were calculated. Abdominal ultrasonography and Doppler study of the portal and splenic veins studying the liver size, the presence of periportal thickening, hepatic veins flow pattern, the splenic longest axis and volume, the presence of ascites and collaterals. Portal vein and splenic vein diameter, patency, cross sectional area, mean flow velocity, blood flow volume congestion index and direction of flow of portal vein were calculated. Platelets count/Splenic diameter ratio and Right liver lobe diameter/ albumin ratio were calculated for all patients. Upper endoscopy was done where oesophageal varices were graded according to modified Thakeb classification. This study revealed that 83% of patients had oesophageal varices; 52% had small sized oesophageal varices and 31% had large sized oesophageal varices. In patients with varices; 12% had biphasic and 22.9% had monophasic hepatic veins flow pattern, with p value of 0.002. Portal vein direction of flow was bidirectional in 22.9% and Hepatofugal in 9.6% with a p value of 0.004. The portal vein velocity of 9.3 +/- 2.3cm/ sec with a p value of <0.001 and the ascites was present in 77% of patients with a p value of 0.005. In patients with large sized varices; shrunken liver was present in 83.1% of patients with a p value of 0.005 and serum albumin <2.5gm/dl with a p value of 0.008. Hepatic veins flow pattern [biphasic and monophasic], portal vein direction of flow [hepatofugal and bidirectional], decreased portal vein velocity and the presence of ascites [moderate and marked] were the significant variables for prediction of presence of varices. Shrunken liver and the low serum albumin were the significant variables for prediction of large varices

Significance of elevated aanticardiolipin antibodies in children with protal vein thrombosis

Portal vein thrombosis [PVT] is characterized by obscure obstruction of the portal vein somewhere along its course between the hilum of spleen and portahepatis though hypercoagulable states are implicated in the causation of PVT, the etiology remains unknown in most cases. Anticardioitpin antibodies [a CL] are autoantibodies, whose presence is a known cause of hypercoagulable state. In view of the strong association of aCL with thrombosis, we estimated the levels of aCL-JgG and 1gM in 25 children suffering from PVT with age ranged from 3.5 to 12.0 years with the mean +/- SD 6.9 +/- 2.7 to evaluate the role of aCL in the pathogenesis and causation of PVT. An indirect ELISA technique was used for the assay. Values exceeding the mean+2SD [cut-off value] of healthy controls were taken as abnormal. The study revealed that the levels of aCL, specially the IgG were significantly elevated [p<0.01] in patients with PVT in comparison to the control group [the mean values +/- SD were 12.94 +/- 6.56 versus 6.75 +/- 2.19 GPLU/ml] while there was a mild non-sigi4flcanr increase of aCL-IgM than the control [the mean values +/- SD were 1.60 +/- 2.25 versus 1.05 +/- 0.66 MPL U/ml] [p> 0.05]. Also the levels of aCL-lgG were above the cut-off value of the normal control in 13 patients [52%]. We found significant thrombocytopenia in children with PVT, the mean value +/- SD was 114.36 +/- 89.39 thousand/cmm, while that of the control was 240.1 +/- 45.47 thousand/cmm. In conclusion, aCL may have a role in the pathogenesis and causation of PVT, and it should be included in the investigation list of causes of PVT in children, as these patients may get benefit from the long-term use of anticoagulants

Ultrasonographic and splenoportographic evaluation of patients with portal hypertension

Different ultrasonographic [US] and splenoportographic findings and their relation to splenic pulp pressure [SPP] were evaluated in 50 patients with portal hypertension [PH] secondary to liver cirrhosis and/or schistosomal hepatic fibrosis [SHF]. The mean SPP was 35.77 +/- 7.14 ml saline and portal vein diameter [PVD] by US and 16.74 +/- 4.28 mm. There was a weak positive correlation between SPP and PVD = 0.1. Twenty one [42%] had history of hematemsis. The mean grade of esophgeal varices [2.19 +/- 1.66 VS 1.07 +/- 1.62], SPP [36.43 +/- 7.59 VS 31.76 +/- 4.77 ml saline] were significantly more in patients who had history or hematemesis than those without [P < 0.05 and < 0.05 respectively]. The mean PVD [17.6 +/- 4.1 VS 13.8 +/- 2.2 mm] and SPP [33.7 +/- 3.8 VS 29.6 +/- 6.8 ml saline] were significantly more in patients who had shrunken liver than those with enlarged liver P < 0.05. The means of PVD, SPP and grade of esophageal varices were significantly more in patients who had past history of schistosomiasis and US evidence of periportal thickening suggestive of SHF. Thirty four [68%] cases did not have changes in the caliber of splenic vein [SV] or superior mesenteric vein [SMV] with respiration. Patients without caliber variation had a significantly higher means of grade of esophageal varices, SPP and number of collaterals as seen by splenoportography and US. Splenoportography had more success rate in demonstration of coronary, short gastric veins and esophageal varices. While US had more success rate in demonstration of the umblical and splenorenal collaterals. In conclusion inspite of some limitations of US, it has several advantages that justifies its wide spread use in screening pf patients with portal hypertension