EUROMEDICA  Hanover 3-4  Juni 2010	Advanced methods of diagnosis, treatment and prophylactics
	European Academy of Natural Sciences, Hanover European Scientific Society, Hanover Berliner Medizinischen Gesellschaft, Berlin

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Research objective: to define the importance of caval hypertensia and intracaval crossflows in the progress of portal hypertensia.

The research conducted includes gradually performed experiments on cadavers, animals, and clinical observations: cavagraphy, and osteoiliacography, - for studying the importance of caval hypertensia and intracaval crossflows in the progress of portal hypertensia.

Osteoiliacovenography is performed with the compliance of aseptics, under local anesthesia. The puncture of crista iliaca, left or right to spina iliaca posterior superior is performed with the Kassirskiy needle. In order to do this, the patient is laid on his/her side, and after the needle is administered, is moved on the back. After that 40-60ml of contrast agent solution was administered during 5-7 seconds; serial angiography was being conducted when administration of contrast agent started.

After the end of the research the needle was taken out(RF License #2194447). Osteoiliacography was performed on 35 patients – 18 of them were from the main group: 2 with ascites and no gradient between vena cava superior and vena cava inferior (VCS, VCI), 2 with Budd-Chiari syndrome, 14 with VCI dilatation; and 17 patients of control group. In 18 patients with VCI circulation disorder (out of main group: 2 with Budd-Chiari syndrome; in control group: in 2 patients with tumor obstruction of VCI suprarenal section) cava-caval crossflow through dilated pelvic, lumbar, paravertebral vein and further into VCS was marked. In the rest 17.

17 patients (2 with ascites and no gradient between VCS, VCI, 7 with liver cirrhosis without ascites, with also no gradient, and 8 patients with Leriche’s syndrome) contrast agent went right to iliac veins and VCI, cava-caval crossflows were not revealed in these patients.

Conclusion. In this morphologic experiment, the model of caval hypertensia with cava-portal and cavocaval crossflows had shown, that in liver cirrhosis the number of collateral anastamoses between azygous and VCI increase in iliac, lumbar, and paravertebral area. This requires more fluid for filling vasculature, but at the same time less time required for moving the fluid up to the mouth of azygous vein. The data of this research allows to claim that the development of porto-caval circulation through retroperitoneal, mesenterico-hemorrhoidal, umbilical and paraumbilical collaterals taking the blood of portal vein into VCI, leads to caval hypertensia, stimulates blood crossflow through pelvic and lumbar veins to azygous vein. On the one hand, it unloads VCI, since the vast portion of blood from lover extremities go to VCS system, but this might be the cause of pressure increase in it, as well as the degradation of collateral outflow through gastro-oesofageal pathway, which can lead to oesophageal an cardial veins’ rupture and hemorrhage. The modeling of portal hypertensia in experiment with animal had shown that the prassure in caudal vena cava increases together with the portal pressure inrease, as the result of developing porto-caval shunts, thus retrohepatic postsinusoidal block, - it leads to the termination of transhepatic bloodflow in 19.3% of cases.

Cavocaval crossflows in portal hypertensia are revealed when performing cavagraphy and osteoiliacography in patients with liver cirrhosis, subcompensated ascitis, VCI dilatation, and Budd-Chiari syndrome.