[Portacaval anastomosis over an open ductus venosus Arantii in portal-vein-splenic-vein thrombosis].
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Vascular characteristics of the splenic vein are entirely different from the portal vein in the dog. We compared the responsiveness of the splenic capsule, which contains abundant smooth muscle with the portal and splenic veins. With respect to potentiation of acetylcholine-induced contraction by neostigmine, the relaxation response to isoproterenol and the contractile response to 5-hydroxytryptamine, the splenic capsule differed from the splenic vein, but was rather similar to the portal vein. A site of morphological and pharmacological discontinuity between the portal vein and the splenic vein occurred at the junction of the splenic vein and the left gastric vein to form the gastrosplenic vein. This junction may coincide with the site of connection of the embryonic splenic vein, a newly formed efferent vein of the spleen, with the portal vein, which was reported by Miki [cf. Bevan et al.: 4th Int. Symp. on Vascular Neuroeffector Mechanisms; Raven Press, New York 1983]. On the splenic side, histological examination revealed that smooth muscle of the splenic capsule and trabeculae are interconnected, but did not extend to the splenic vein. At openings of the trabecular veins into the 'intrasplenic' portion of the splenic vein the trabecular smooth muscle continued to the extended capsule. The site of change in pharmacological responses was also found to be located between the trabeculae and the intrasplenic portion of the splenic vein. Thus the splenic vein can be regarded as a distinct segment of vessel inserted between the portal vein and the spleen. This may reflect differences in embryogenesis of their smooth muscle.
To elucidate the possible implication of hepatic blood supply to the occurrence of hepatolithiasis, the rat superior mesenteric vein, which drains blood from the intestine, or the splenic vein, which drains from the spleen, was occluded for 30 minutes. Changes in the hepatic oxygen saturation index, intrahepatic uridine diphosphate-glucuronic acid concentration, bile flow, and the excretion of bilirubin as well as its fraction, along with bile acid in bile before and after the procedure, were observed. In association with superior mesenteric vein occlusion, oxygen saturation index, hepatic uridine diphosphate-glucuronic acid concentration, bile flow, bile acid concentration in bile, and percentage of biliary bilirubin diglucuronide were all decreased. Incubation of bile under sterile conditions from rats with occluded superior mesenteric veins resulted in precipitation of mainly calcium salt of fatty acid. In contrast, splenic vein occlusion caused no changes except for a decrease in biliary bilirubin concentration. Incubation of bile from rats with occluded splenic veins did not induce precipitation. From these findings it can be concluded that blood flow in the superior mesenteric vein is the primary source of oxygen supply to the rat liver and that this vein plays an important role in maintaining bile flow, bile acid excretion, and bilirubin conjugation and in preventing the precipitation of bile (possibly preventing hepatolithiasis).
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Bovine splenic vein has an abundant sympathetic innervation. Isolated strips were used to examine whether autoinhibition of norepinephrine release from the noradrenergic nerve terminals could be demonstrated under various experimental conditions and whether additional local regulatory modulators of transmitter release could also be implicated. In particular, the possibility of a histamine interaction with presynaptic inhibitory receptors was examined because ultrastructural evidence disclosed a close spatial relationship between mast cells and noradrenergic nerve terminals in the vessel wall. To investigate the presence of presynaptic alpha-receptors the competitive blocking agent phentolamine was included in the superfusion medium at concentrations ranging from 1 to 50 microM during electrical field stimulation at frequencies between 1 and 10 Hz. Transmitter outflow was measured as fractional tritium release. Low frequency stimulation (1 Hz) with 1 microM phentolamine resulted in the typical increase in norepinephrine release characteristics for presynaptic alpha-receptor inhibition. In contrast, high frequency (10 Hz) stimulation in the presence of 50 microM phentolamine caused an unexpected decrease in norepinephrine outflow. This unusual result can be explained by additional pharmacological actions of phentolamine unrelated to alpha-receptor blockade, e.g. histamine release from the mast cells which subsequently can act on presynaptic inhibitory histamine receptors. This effect, manifested at higher phentolamine concentrations, would overcome the alpha-receptor blockade. The presence of histamine receptors was supported by the results from electrical stimulation in the presence of exogenous histamine. Histamine decreased norepinephrine outflow while increasing basal tension and the contractile response of the vein strip. Unexpectedly, these effects appeared to be mediated by histamine receptors of the H1-type because they were reduced after pyrilamine but unaffected by agonists and antagonists to receptors of the H2-type. It is speculated that interactions between mast cells and noradrenergic nerve terminals may serve to maintain homeostasis in the bovine splenic vein.
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To re-establish the portal circulation following extensive resection of the portal vein, we interposed an autograft of the splenic vein between the portal and superior mesenteric veins during total pancreatectomy in three patients with cancer of the pancreas. The postoperative course in two patients was uneventful, and patency of the graft was demonstrated angiographically on the 41st and 78th postoperative days, respectively. In the remaining patient an episode of postoperative peritonitis occurred with leakage of the gastrointestinal anastomosis. The patient died on the 78th postoperative day from a massive metastasis to the liver. Autopsy revealed a narrowing of the graft due to technical failure and inflammatory changes, but there was no evidence of cancer invasion. Thus, the autograft of the splenic vein proved useful to bridge the portal vein system.
Splenic vein thrombosis is a complication of pancreatic carcinoma or pancreatitis. It may lead to gastric varices which are difficult to treat and splenectomy may be required to stop variceal bleeding. A case of bleeding gastric varices secondary to splenic vein thrombosis and successfully treated by splenic artery embolization is reported. Embolization was performed by transcatheter deposition of four Gianturco coils into the splenic artery. This resulted in reduced blood flow through the spleen with partial splenic infarction and cessation of variceal bleeding. There has been no recurrence of bleeding in the 6 months since the procedure. Literature review confirms that experience of using this treatment is very limited and it should therefore be restricted to patients at high risk from surgery.
BACKGROUND: Previous reports have described the computed tomographic (CT) appearance of collateral veins following splenic vein occlusion (SVO). This retrospective study was performed to determine the etiology, clinical manifestations, and accuracy of CT diagnosis in patients with this entity. METHODS: A computer search of radiology reports for a 1-year period found 52 patients with SVO diagnosed by absence of visualization of the splenic vein accompanied by the formation of the expected perigastric collateral veins. Clinical data were reviewed for sequela of SVO and clinical impact of the diagnosis. RESULTS: In 12 cases, other studies confirmed the CT diagnosis of SVO. In no case was the CT diagnosis proved to be incorrect by other imaging studies. Angiographic records found five additional cases with SVO not diagnosed by CT, but two of five had convincing CT evidence of SVO noted upon reevaluation by the authors. Review of clinical data showed heme-positive stool in six, of which three had significant gastrointestinal hemorrhage. Splenic infarction occurred in two cases. CONCLUSIONS: Our data indicate that SVO is more common than previously suspected and usually remains clinically silent, but CT appears to be highly specific and fairly sensitive for its diagnosis.
Isolated splenic vein thrombosis may lead to a specific clinical presentation, namely, bleeding from isolated gastric varices (which are difficult to diagnose), splenomegaly, and normal liver function. The most common cause is pancreatic disease. To exclude associated portal venous thrombosis, angiography is essential prior to a splenectomy, which is curative of the variceal hemorrhage. Splenic vein thrombosis may also be noted as an incidental finding during angiography. Although the natural history is uncertain, a splenectomy is probably not indicated until a hemorrhage occurs.
The splenic vein was ligated in ten dogs in order to evaluate the time course of changes in splenic size and to relate them to splenic arterial flow, splenic pressure and development of venous collaterals. Following ligation of the splenic vein, splenic size and venous pressure immediately rose in all dogs. Arterial flow to the spleen simultaneously fell in roughly inverse proportion to the elevation of venous pressure. During the following weeks, the splenic parenchymal pressure decreased to basline levels in all but one dog, as collateral veins developed through the gastric venous network to the portal vein. Splenic size gradually decreased toward normal in eight of the ten dogs. At the time of sacrifice, 8-16 weeks after splenic vein ligation, pathologic examination demonstrated fibrosis from healed infarction. Recent hemorrhage, indicating persistence of the congestive process, we also present, although difficult to explain in view of normal splenic parenchymal pressure.
We report a case of splenic vein aneurysm (SVA) that was enlarged during a 17-month follow-up. A 62-yr-old female with liver cirrhosis was followed up in our hospital. Real-time ultrasonography initially detected aechoic space at the middle part of the splenic vein, confirmed as SVA by contrast-enhanced computed tomography, magnetic resonance imaging and angiography. Magnetic resonance imaging showed the stagnation of blood flow in SVA, which suggests the presence of hypertension in the portal venous system. Moreover, SVA enlarged in parallel with the development of esophageal varices. These observations suggest that the persistent stagnation of blood flow in the portal venous system may have played a major role in the increase in size of the SVA in this case.
A 27-year old female patient, born and living in Morocco, suffered from severe variceal bleeding and weight loss. Eventually a diagnosis of gastric fundus varices was made supposedly resulting from partial obstruction of the splenic vein and collateral blood flow via the short gastric veins. Splenectomy was proposed. Peroperatively it became apparent that a solitary ecchinococcal cyst in the hilus of the spleen obstructed the blood flow in the splenic vein. The cyst, the spleen, and part of the pancreatic tail were removed. After splenectomy bleeding did not recur.
A model of heterotopic liver transplantation had been studied. The graft was laid under the recipient liver and the portal blood flow was supplied by anastomosis with the distal part of the splenic vein. Both liver can then receive portal blood through two parallel portal circulation. Liver function of transplant was satisfactory at three months after transplantation. Their had been no alteration of the recipient liver during the same period.
A case of splenic vein obstruction due to infiltration by Hodgkin's lymphoma of the colon is reported. The patient presented with massive upper gastrointestinal hemorrhage and a lump in the abdomen. Laparotomy revealed a colonic tumor infiltrating the splenic vein, causing left sided portal hypertension.
The presence of splenic vein thrombosis is sometimes very difficult to diagnose. We present a patient in whom the splenic vein was thought to be patent by ultrasound and conventional celiac angiography. Because of high clinical suspicion and continued bleeding, he underwent a selective intra-arterial digital splenic angiogram. The venous phase clearly showed proximal (hilar) splenic vein occlusion with filling via collaterals in real time. Splenectomy confirmed the diagnosis. We believe that a selective intra-arterial digital splenic angiogram is the radiographic study of choice for suspected splenic vein thrombosis.