Effect of hepatic collateral hemodynamics on gastric mucosal blood flow in patients with liver cirrhosis

The dependence of the gastric mucosal change in liver cirrhosis on the extrahepatic collaterals is still unknown. Therefore we studied the influence of these collateral hemodynamics on gastric mucosal blood flow and gastric mucosal lesions. The subjects were 23 cirrhotic patients and were divided into two groups by the findings of percutaneous transhepatic portography. The first group consisted of 14 cases whose extrahepatic collaterals were via esophageal varices (group I). The second group included 9 cases having collaterals other than esophageal varices (group II). Multiple red spots were observed in 13 of 14 cases in group I, and two of nine cases in group II. Gastric mucosal blood flow was 2.0±0.9 volts (mean±sd) in group I, 4.0±1.2 in group II. A statistically significant difference was observed between groups I and II. Gastric mucosal blood flow was not significantly correlated with portal venous pressure in group I. It is concluded that, in liver cirrhosis, gastric mucosal blood flow is changeable according to the types of the extrahepatic collaterals.     

Portal hemodynamics in patients with gastric varices. A study in 230 patients with esophageal and/or gastric varices using portal vein catheterization

The hemodynamic features of gastric varices are not well documented. The purpose of this study was to investigate the nature of hepatofugal collateral veins, their origins, the direction of blood flow in the major veins and collateral veins, and portal venous pressure. To this end, 230 patients, mostly cirrhotic, who had esophageal or gastric varices, or both, demonstrated by endoscopy were investigated by portal vein catheterization. The findings were correlated with endoscopically assessed degrees of varices. Gastric varices were seen in 57% of the patients with varices due to portal hypertension. In most of the patients with advanced gastric varices, esophageal varices were minimal or absent. When patients with gastric varices were compared with those having predominantly esophageal varices, it was found that advanced gastric varices were more frequently supplied by the short and posterior gastric veins, they were almost always associated with large gastrorenal shunts, and portal venous pressure in patients with large gastric varices was lower. Chronic portal systemic encephalopathy was more common in patients with large gastric varices due to hepatofugal flow of superior mesenteric venous blood in the splenic vein than in patients with predominantly esophageal varices. Thus, the hemodynamics in patients with large gastric varices are distinctly different from those in patients with mainly esophageal varices, and such differences seem to account for the differing incidence of chronic encephalopathy and variceal bleeding.     

Endoscopic Evaluation of Rectal Mucosal Reddening in Patients with Liver Cirrhosis

Background: Colonic mucosal lesions observed in patients with portal hypertension have been reported as portal hypertensive colopathy. We studied the rectal mucosa in patients with liver cirrhosis to evaluate the prevalence of mucosal reddening which looks like gastric red spots in the portal hypertensive gastropathy and to determine whether there is a correlation between this lesion and portal hypertension or the severity of liver disease. Methods: Seventy‐two patients with liver cirrhosis and 50 control subjects were examined. Colonoscopy was performed to evaluate the presence of mucosal reddening in the rectum. We investigated the relations between rectal mucosal reddening and esophageal varices, portal hypertensive gastropathy and the severity of liver cirrhosis. Results: Rectal mucosal reddening was observed in eight of 72 patients with liver cirrhosis but in none of the 50 control subjects; its prevalence in cirrhosis patients was significantly higher than that in the control subjects (P < 0.05). Cirrhosis patients with esophageal varices were more likely to have rectal mucosal reddening than cirrhosis patients without esophageal varices (P < 0.05). In addition, the occurrence of rectal mucosal reddening correlated with the severity of cirrhosis, based on Child–Pugh's classification (P < 0.05). Conclusion: We have shown that rectal mucosal reddening develops in patients with liver cirrhosis and is associated with the existence of esophageal varices and the severity of liver cirrhosis. These results suggest the possibility that portal hypertension and impaired liver function may play an important role in the pathogenesis of rectal mucosal reddening in patients with cirrhosis.     

Effect of transjugular intrahepatic portosystemic shunt formation on portal hypertensive gastropathy and gastric circulation

OBJECTIVES: The aim of this study was to investigate the effect of a transjugular intrahepatic portosystemic shunt (TIPS) on portal hypertensive gastropathy (PHG) and gastric hemodynamics. METHODS: A total of 16 patients with cirrhosis and portal hypertensive gastropathy were prospectively studied. Of these, 12 patients underwent TIPS for esophageal varices and four for refractory ascites. Gastric mucosal blood flow (GMBF) was assessed by laser Doppler flowmeter, and total blood flow (TBF) in submucosa and mucosa by near-infrared endoscopy. Portal venous pressure was obtained by a transducer during the TIPS procedure. The severity of portal hypertensive gastropathy was classified as none, mild, or severe. The examinations were performed before and 2 wk after the procedure. RESULTS: TIPS significantly reduced portal venous pressure. PHG improved in all four patients with severe PHG and in five of 12 patients with mild PHG after treatment. Gastric mucosal blood flow increased from 49.0 to 55.6 ml/min/100 g after TIPS. In contrast, TBF decreased from 0.35/s to 0.27/s after treatment. Liver function tests showed no significant changes before and after the procedure. CONCLUSIONS: It is considered that TIPS may have a beneficial effect on PHG at least for a short time. The mechanism by which PHG improves may be closely related to the improvement of the injured gastric perfusion in cirrhotic patients with PHG.     

Gastric mucosal hexosamine content in various liver diseases.

Since gastric mucosal lesions are frequently encountered in patients with liver disease, we measured the levels of gastric mucosal hexosamine. In chronic hepatitis patients, hexosamine levels were reduced in both the antrum and corpus as compared with those in normal controls, while values in the advanced liver cirrhosis group (total bilirubin greater than 5 mg/dl) were lower than in the less advanced group. Although the presence or absence of esophageal varices had no influence on hexosamine, higher concentrations were found in patients with the red color sign (+) in comparison with those with negative red color sign (-). One month after endoscopic injection sclerotherapy of esophageal varices, hexosamine did not change, but decreases were seen in both the antrum and corpus at 3 months. We observed an increase in gastric mucosal blood flow after treatment with teprenone, a new antiulcerative agent, in normal controls. Gastric mucosal hexosamine increased significantly after teprenone treatment in both chronic hepatitis and liver cirrhosis groups. From these results, we conclude that hexosamine has a defensive action against gastric lesions in various liver diseases.     

Classification of gastric lesions associated with portal hypertension

Abstract There are two gastric mucosal lesions which commonly occur in patients with portal hypertension; one is portal hypertensive gastropathy and the other is gastric varices. These lesions occasionally cause fatal haemorrhage. Several classifications for these lesions have been proposed, but none of them have been evaluated prospectively. We consider it better to classify portal hypertensive gastropathy into three stages including non-specific redness, specific mosaic pattern and red spots. Gastric varices may be classified according to form, location and mucosal lesions. Prospective trials are needed to obtain more practical evidence for the accurate classification of these gastric lesions.     

Balloon-occluded retrograde transvenous obliteration of high risk gastric fundal varices

OBJECTIVE: Balloon-occluded retrograde transvenous obliteration is an effective new method for treating gastric fundal varices, but subsequent occurrence of esophageal varices creates a problem. The relationship between portal hemodynamics and the occurrence of esophageal varices after prophylactic balloon-occluded retrograde transvenous obliteration was investigated. METHODS: Ten cirrhotic patients considered to have high risk gastric fundal varices underwent angiography. Six patients showed a communication between blood flow in gastric wall vessels and that in the gastrorenal shunt (type I), whereas the others (type II) did not. Depending on the flow direction in the left gastric vein, the two groups were further divided into hepatopetal (a) and hepatofugal (b) subgroups. The therapeutic effect on portal hemodynamics and the relationship between pretreatment portal hemodynamics and posttreatment occurrence of esophageal varices were investigated. RESULTS: Fundal varices disappeared endoscopically in all 10 patients and the gastrorenal shunt was also occluded after the procedure. No patient showed worsening of liver function or systemic complications during follow-up. The increase in portal blood flow was more significant in type Ib patients than in the others. Esophageal varices occurred in all type I patients, and as to those in type Ib, high risk varices developed within 6 months after treatment. On the other hand, esophageal varices did not occur in type II patients. CONCLUSIONS: This procedure was effective for treating gastric fundal varices. However, type Ib patients are likely to develop high risk esophageal varices after occlusion of the gastrorenal shunt.     

卡维地洛治疗老年乙肝肝硬化门静脉高压症疗效分析

目的探讨卡维地洛对老年乙肝肝硬化门静脉高压症患者的治疗效果。 方法选取2014年8月至2018年1月山东省泰安市中心医院收治的60例老年乙肝肝硬化门静脉高压症患者,其中采用常规治疗30例（对照组）,在常规治疗基础上加用卡维地洛治疗30例（观察组）。对照组进行常规保肝、抗病毒、抗肝纤维化治疗,治疗组在对照组的基础上给予卡维地洛口服治疗（12.5 mg,1次/d）。6个月后观察门静脉血流动力学、食管胃底静脉曲张程度、肝纤维化指标、凝血指标的变化。 结果观察组患者治疗后门静脉主干内径（DPV）、脾静脉内径（DSV）、静脉主干血流量（QPV）、脾静脉血流量（QSV）、透明质酸（HA)、Ⅲ型前胶原N端肽（PCⅢ）、层粘连蛋白（LN）、Ⅳ型胶原（CⅣ）、凝血酶原时间（PT）、活化部分PT（APTT）、PT活动度（PTA）均较治疗前均明显改善（P<0.05或0.01）,而对照组治疗后各指标并无明显改善（均P>0.05）。治疗前,两组患者DPV、DSV、QPV、QSV、HA、PCⅢ、LN、CⅣ、PT、APTT、PTA的差异均无统计学意义（均P>0.05）;治疗后,观察组DPV、DSV、QPV、QSV、HA、PCⅢ、LN、CⅣ、PT、APTT、PTA均较对照组明显改善（P<0.05或0.01）。治疗前,两组患者食管-胃底静脉曲张程度的差异无统计学意义（z=-0.319,P>0.05）;治疗后,观察组轻度曲张患者明显增多、重度曲张患者明显减少,明显优于对照组（z=-2.277,P<0.05）。 结论在常规治疗基础上口服卡维地洛治疗,能显著提高老年乙肝肝硬化门静脉高压症患者的治疗效果。     

Endoscopic, portographic, and hemodynamic evaluation of prolonged propranolol administration in pigs with experimental portal hypertension and esophageal varices

The effect of long-term propranolol administration on esophageal varices, portocollateral shunting, portal pressure, hepatosplanchnic hemodynamics, and liver function was studied in a pig model with experimentally induced prehepatic portal hypertension and esophageal varices. Five pigs were treated with 160 mg propranolol daily from week 5 to week 24 after portal-vein banding, and five pigs served as nontreated controls. Administration of propranolol caused an initial, significant reduction (20%) of portal venous pressure, followed by a gradual increase to levels not different from control pressures. In contrast, a marked reduction of the caliber of the coronary vein and size of the esophageal varices was noticed. Twenty weeks of propranolol treatment did not change liver blood flow or liver function. We conclude that the size of the varices rather than portal venous pressure depicts the effect of propranolol treatment and suggest that the beneficial effect of propranolol on variceal bleeding can be explained by a reduction in the wall tension of the varices, initiated and maintained by a diminution of splanchnic blood flow.     

Transjugular intrahepatic portosystemic shunting improves splanchnic hemodynamics and renal Na excretion in cirrhosis with refractory ascites

To clarify the pathogenesis of ascites in patients with liver cirrhosis, we explored the effects of transjugular intrahepatic portosystemic shunting in six cirrhotic patients with refractory ascites. The portal pressure decreased from 39 ± 7 cmH₂O before treatment to 32 ± 5 cmH₂O immediately after the procedure. Liver function transiently deteriorated after the procedure, but recovered within 1 week. Urinary Na excretion increased 1 week after treatment. In five patients, ascites improved within 3 weeks. Along with the decrease of portal congestion, there was an improvement of esophageal varices, and an increase of gastric mucosal blood flow, and an inhibition of the renin-angiotensin-aldosterone system in all of the patients after 2–4 weeks. Manageable shunt encephalopathy occurred in three patients. These findings strongly suggest the pivotal role of increased portal pressure in the formation of ascites in patients with liver cirrhosis.     

门静脉高压患者胃静脉曲张的内镜识别和分类

背景：肝硬化门静脉高压的出血原因中，食管和（或）胃静脉曲张破裂出血最为常见。胃静脉曲张的发生率较食管静脉曲张低，但再出血率高，出血量大，死亡率亦较高。尽管如此，胃静脉曲张在临床诊治过程中未受到应有的重视。目的：根据内镜下对食管和胃静脉曲张的识别和分类，了解食管和胃静脉曲张的比例。方法：根据Sarin分类，在内镜直视下将114例门静脉高压患者分为单纯食管静脉曲张、胃食管静脉曲张1型（GOV1型）、胃食管静脉曲张2型（GOV2型）、孤立性胃静脉曲张1型（IGV1型）和孤立性胃静脉曲张2型（IGV2型）五种类型。结果：本组患者中单纯食管静脉曲张42例（36．8％），GOV1型40例（35．1％），GOV2型20例（17．5％），IGV1型12例（10．5％），未见IGV2型。结论：半数门静脉高压患者存在胃静脉曲张，临床工作中仅处理食管静脉曲张是很片面的。须努力开展组织黏合剂、球囊闭塞下逆行经静脉栓塞术（B．RTO）或外科分流等治疗：对有条件的患者应鼓励开展肝移植治疗。     

Portal venous system after endoscopic sclerotherapy of esophageal varices in patients with liver cirrhosis--prospective study with Doppler sonography

BACKGROUND/AIMS: The aim of this prospective, clinical study was an ultrasonographic color Doppler evaluation of morphological and hemodynamic changes in the portal system prior to and after repeated, endoscopic injection sclerotherapy in patients with liver cirrhosis and hemorrhage from esophageal varices. METHODOLOGY: Twenty-six patients before and after complete eradication of esophageal varices by repeated sclerotherapy with 5% ethanolamine oleate as obliterating agent were examined. The diameter of the portal and splenic veins, the patency of the veins, the direction of the blood flow, the mean and maximal velocity of blood flow, spleen size and presence and number of collateral circulation pathways were determined. Hemodynamic examinations of the portal system were performed with duplex Doppler method with color imaging of blood flow. RESULTS: The study revealed no statistically significant differences between diameters of the portal and the splenic vein or between the size of the spleen prior to and after sclerotherapy. The blood flow was intrahepatic and portal vein thrombosis was not detected in any of the patients. The mean velocity blood flow in the portal vein prior to and after sclerotherapy did not reveal any changes. The maximal velocity of blood flow in the portal vein increased from 23.7 +/- 2.5 cm/s to 27.2 +/- 2.8 cm/s, but it was not statistically significant. Prior to the commencement of sclerotherapy collateral portal-systemic circulation was detected in 17 out of 26 patients (65%), with a total of 25 collateral circulation pathways. After completion of sclerotherapy collaterals were detected in 19 out of 26 patients (73%) and number of pathways was increased by 7. CONCLUSIONS: Endoscopic sclerotherapy of esophageal varices does not affect the direction of blood flow in the portal vein and causes no thrombosis of the portal system. Effective sclerotherapy and complete eradication of esophageal varices results in closure of collateral circulation pathways through submucosal esophageal varices as well as development of new pathways of collateral circulation.     

经皮经肝曲张静脉栓塞治疗断流术后食管胃底静脉破裂出血的疗效

目的 研究以组织胶为主要栓塞材料,采用经皮经肝曲张静脉栓塞术(PTVE)治疗和预防门奇静脉断流术后食管胃底静脉曲张破裂出血的临床疗效.方法 2006年11月至2008年9月,对22例曾行断流术再发食管胃底静脉曲张破裂出血的患者行PTVE组织胶栓塞(n=10)或内镜下硬化剂(EIS,n=12)治疗,随访两组患者治疗后再出血率、死亡率、治疗前后静脉曲张和肝功能以及PTVE治疗组患者在曲张侧支静脉栓塞前后门静脉压力的变化.结果 ①在平均12.5个月的随访期内,PTVE治疗组患者再出血率和死亡率分别为1/10和0;EIS治疗组随访13.4个月,患者再出血率和死亡率分别为7/12和3/12,两组问差异有统计学意义(P<0.05).②PTVE和EIS治疗均可显著减轻食管和胃底静脉曲张程度.③对有门静脉血栓患者,PTVE联合门静脉球囊成形术,可以改善肝脏门静脉血供.④PTVE和EIS治疗均未加重肝功能损伤.结论 对门奇静脉断流术后食管胃底静脉破裂出血的患者,采用以组织胶为主要栓塞材料的PTVE治疗的疗效优于EIS治疗.     

Role of mucosal microcirculation in gastric lesions induced by lateral hypothalamic lesions in rats

To evaluate the pathophysiology underlying gastric mucosal lesions induced by lateral hypothalamic (LH) lesions, we investigated the changes in acid secretion, gastric mucosal blood flow, gastric mucus and mucosal integrity in the corpus during the 4 h period and 48 h after the production of bilateral electrolytic LH lesions in male Sprague-Dawley rats. Gastric mucosal lesions were macroscopically produced 24 h (63%) and 48 h (83%) after LH lesions, although there were no visible lesions at 7 h. Gastric acid secretion was significantly increased 48 h after LH lesions, compared with that in the control group. Gastric mucosal blood flow and transmucosal potential difference (PD) in the LH lesion group immediately decreased after LH lesions and did not recover during 4 h and at 48 h. On the contrary, in the control group, gastric mucosal blood flow decreased after the brain surgery but soon recovered, and there was no significant change in PD. LH lesions resulted in the reduction of intramucosal mucus to 50% 3 h after LH lesions. Moreover, we exposed the stomach to 10 mmol/L taurocholic acid (TCA) 3 h after LH lesions to examine the disruption in gastric mucosal defensive function in rats with LH lesions. The recovery of the reduced PD by TCA was slow and gastric mucosal lesions were easily formed in the LH lesion group. These results suggest that gastric mucosal ischaemia after lesioning of LH immediately results in the disruption of mucosal defensive function before the formation of visible gastric lesions, and predisposes to the formation of gastric mucosal lesions by a delayed increase in acid secretion.     

Beneficial long term effect of a phosphodiesterase-5-inhibitor in cirrhotic portal hypertension: A case report with 8 years follow-up

Non-selective beta-blockers are the mainstay of medical therapy for portal hypertension in liver cirrhosis. Inhibitors of phosphodiesterase-5(PDE-5-inhibitors) reduce portal pressure in the acute setting by 10% which may suggest a long-term beneficial effect. Currently, there is no available data on long-term treatment of portal hypertension with PDE-5-inhibitors. This case of a patient with liver cirrhosis secondary to autoimmune liver disease with episodes of bleeding from esophageal varices is the first documented case in which a treatment with a PDE-5-inhibitor for eight years was monitored. In the acute setting, the PDE-5-inhibitor Vardenafil lowered portal pressure by 13%. The portal blood flow increased by 28% based onDoppler sonography and by 16% using MRI technique. As maintenance medication the PDE-5-inhibitor Tadalafil was used for eight consecutive years with comparable effects on portal pressure and portal blood flow. There were no recurrence of bleeding and no formation of new varices. Influencing the NO-pathway by the use of PDE-5 inhibitors may have long-term beneficial effects in compensated cirrhosis.     

The long-term outcome of patients with bleeding gastric varices after balloon-occluded retrograde transvenous obliteration

Background The purpose of our study was to evaluate the long-term outcome and complications of balloon-occluded retrograde transvenous obliteration (B-RTO) in patients with hemorrhage from gastric fundal varices. Methods Thirty-four consecutive patients with bleeding from gastric varices who were treated with B-RTO were enrolled in this study between December 1994 and September 2005 (urgent cases, n = 12; elective cases, n = 22). The long-term outcome, complications, and various liver functions were evaluated. Results Complete obliteration was achieved in 31 of 34 (91%) patients with an acute bleeding episode. In one of the remaining patients, there was a technical failure, and the other two had only partial obliteration. The two patients with partial obliteration did not obtain hemostasis. Thus, the rate of hemostasis was 94% (31/33). Gastric varices disappeared in all patients with complete obliteration during the treatment. The rate of gastric variceal eradication was 91%. Variceal rebleeding from esophageal varices occurred in three patients. The rate of rebleeding was 10% (3/31). Rebleeding from gastric varices was not observed after complete obliteration. None of the patients showed worsening of their Child-Pugh score. Although the 5-year cumulative worsening rate of esophageal varices was 52%, neither portal hypertensive gastropathy nor ectopic varices were observed. The patients with worsening esophageal varices were successfully treated with an endoscopic procedure. The 5-year survival rate was 68%. Conclusions B-RTO is useful for treatment of bleeding gastric varices, achieving high eradication of gastric varices, a low rebleeding rate, and a fairly good prognosis with improved hepatic function.     

Congestive Gastropathy: Factors Influencing Development, Endoscopic Features, Helicobacter pylori Infection, and Microvessel Changes

Objectives: To study 1 ) the factors influencing the development of congestive gastropathy (CG) in patients with portal hypertension (PHT). 2 ) the changes in gastric microvessels in patients with PHT with and without CG. and 3 ) determine whether Helicobacter pylori plays any role in the pathogenesis of CG. Methods: One hundred eighteen patients with PHT (102 cirrhosis, 16 noncirrhotic portal fibrosis) were evaluated by videogastroscopic examination. Antral biopsy tissue was examined for microvessel changes, histological gastritis, and H. pylori infection in 85 of 118 patients and 45 controls. Portal venous pressure (PVP) was determined by hepatic venous pressure gradient in 17 patients with CG. Results: CG was present in 71 (60%) patients with PHT, of whom 41 (58%) had mild and 30 (42%) had severe CG. CG was observed with equal frequency in cirrhosis (63%) and noncirrhotic portal fibrosis (44%). The incidence of CG was higher in patients with severe liver disease, a past history of hemetemesis, in those with esophageal varices, and in those with gastric varices. Severe CG was commonly observed in patients with large size esophageal varices and in those with gastric varices. There was significant dilation of gastric mucosal vessels in patients with PHT, but in this regard there was no significant difference between patients with and without CG. The presence of H. pyiori , histological gastritis, degree of PVP, or degree of capillary dilation did not influence the severity of CG. Conclusions: CG occurs commonly in patients with PHT, especially those with severe liver disease, past history of hemetemesis, and esophagogastric varices. Patients with PHT have significant gastric micro-vessel changes. The severity of CG appears to be independent of PVP, capillary dilation, H. pylori infection, or histological gastritis.     

Effects of metoclopramide and domperidone on azygos venous blood flow in patients with cirrhosis and portal hypertension

The effects of pharmacological manipulation of the lower esophageal sphincter pressure on the esophageal circulation in patients with cirrhosis and portal hypertension were investigated in 33 patients by measuring the azygos venous blood flow, which is an index of blood flow through esophageal varices and periesophageal collaterals draining into the azygos venous system. Measurements were performed in baseline conditions and after the blind administration of metoclopramide (20 mg i.v.) (12 patients), domperidone (10 mg i.v.) (12 patients) and placebo (9 patients). Both metoclopramide and domperidone caused a significant reduction of azygos blood flow, that decreased by 11.5% (p less than 0.01) and 15.6% (p less than 0.02) respectively, while no change was observed in patients receiving placebo (+1.4%, not statistically significant). Reduction of azygos blood flow represents a selective effect of metoclopramide and domperidone on the esophageal circulation, since portal pressure, hepatic blood flow, cardiac output, heart rate and arterial blood pressure were unchanged by the administration of metoclopramide, domperidone or placebo. These results indicate that the administration of drugs that increase the lower esophageal sphincter pressure may reduce the inflow of blood into the esophageal varices in cirrhotic patients with portal hypertension.     

Nodules in antrum after variceal eradication a new finding in patients with portal hypertension

Portal hypertension is known to cause esophageal varices, gastric varices and portal hypertensive gastropathy (PHG). The prevalence of gastric varices and PHG is known to increase after eradication of esophageal varices. PHG includes the presence of a mucosal mosaic pattern, cherry red spots, and/or black-brown spots and gastric vascular ectasia (GAVE). Patients with portal hypertension in whom esophageal varices were eradicated were on follow up endoscopy for detection of recurrence of esophageal varices. Their status of PHG was assessed and patients antral nodules were enrolled. Twenty patients with antral nodules were identified over one year. Fifteen out of 20 patients had cirrhosis as etiology of portal hypertension, three had non-cirrhotic portal hypertension and two had extra-hepatic portal vein thrombosis. GAVE was seen more commonly (n=8, 40%) in patients with PHG with nodules. PHG with antral nodules is a novel endoscopic finding present both in cirrhotic and non-cirrhotic portal hypertension with unknown pathogenesis, and is seen more commonly in patients with eradicated varices who are on long-term follow up.     

食管胃底静脉曲张血供与侧支的研究

目的通过多层螺旋CT(multi—detecter row computed tomography，MDCT)了解食管胃底静脉曲张及与之相关的侧支循环，为食管胃底静脉曲张破裂出血治疗方案的选择和预后的判断提供客观依据。方法选择51例临床证实的肝硬化门静脉高压患者，其中胃镜显示食管静脉曲张51例，伴胃底静脉曲张31例。对所有患者进行MDCT血管成像，重点观察食管胃底静脉曲张及相关侧支循环。结果MDCT血管成像能清晰地显示肝硬化门体侧支血管，并显示所有食管静脉曲张。MDCT显示胃底静脉曲张32例(62．7％)，与胃镜检查结果(31／51，60．8％)比较，两者具有高度一致性，Kappa值为0．876。食管曲张静脉几乎全部由胃左静脉供血，30例(58．8％)单纯由胃左静脉前支供血，21例(41．2％)伴有食管旁静脉；24例(75％)胃底曲张静脉为单纯胃左静脉供血，3例(9．4％)由胃短(胃后)静脉供血，5例(15．6％)为胃短(胃后)和胃左静脉双重供血，双重供血者因胃底静脉曲张和食管静脉曲张常相互交通，所以这些病例胃短(胃后)静脉也同时参与食管静脉曲张的形成。结论MDCT能较清晰地显示食管胃底静脉曲张侧支循环。食管静脉曲张主要由胃左静脉供血，大部分由前支经贲门进入曲张静脉，部分伴有食管旁静脉。胃底静脉曲张大部分由胃左静脉供血，但小部分则由胃短系统供血。