Splenorenal Shunt Research Articles

The influential factors of depressive symptom among children and adolescents with type 1 diabetes mellitus

Objective To describe the status of depressive symptom among children and adolescents with type 1 diabetes mellitus(T1DM) and explore the related factors. Methods This was a multi-plot cross-sectional survey. 136 cases in Hunan province were investigated by questionnaires. The questionnaires included General Information Questionnaire, Depression Self-Rating of Children(DSRS), Quality of Life Scale for Children and Adolescents. Results The DSRS score of all subjects was (9.51±5.19), 24 cases suffered from depressive symptom(17.6%). The multi-factor non-condition logistic regression analysis showed that age(OR=2.831), current education status(OR=9.822), parents' current marital status (OR=0.061), yearly household income(OR=0.415), hospitalization in the past 6 months(OR=8.797), peer relationship (OR=0.133), parent-child relationship(OR=0.182), FBS(OR=0.061) and sample source(OR=8.366) were factors which independently predicted depressive symptom in children and adolescents with T1DM. Conclusion The influential factors of depressive symptom among children and adolescents with T1DM include age, current education status, parents' current marital status , yearly household income, hospitalization in the past 6 months, peer relationship and parent-child relationship, FBS and sample source. Key words: Children; Adolescents; Diabetes mellitus, type 1; Depressive symptom; Cross-sectional survey

Perioperative Management of Spontaneous Splenorenal Shunts in Orthotopic Liver Transplant Patients

Spontaneous splenorenal shunts cause significant vascular steal from the liver. There is no accepted algorithm for treating spontaneous splenorenal shunts before, during, or after liver transplant, and evidence for efficacy of treatments remains limited. We reviewed the literature, and our institution's experience regarding spontaneous splenorenal shunts, including a case series of 6 patients with spontaneous splenorenal shunts undergoing transjugular intrahepatic porto-systemic shunts, a case of intraoperative ligation of a large spontaneous splenorenal shunts during transplant, and 1 patient requiring multiple endovascular interventions to embolize recurrent spontaneous splenorenal shunts after orthotopic liver transplant. Small spontaneous splenorenal shunts may not need intervention, as involution after liver transplant is well known. Transjugular intrahepatic porto-systemic shunts may decrease the porto-systemic gradient in patients with large spontaneous splenorenal shunts, as shown in our review of 6 patients with large spontaneous splenorenal shunts undergoing transjugular intrahepatic porto-systemic shunts. We have demonstrated re-establishment of physiologic flow after ligation of a large spontaneous splenorenal shunt at the time of transplant, supporting operative ligation may be justified if intraoperative compression of the spontaneous splenorenal shunts demonstrates significant improvement of allograft portal venous flow. Ligation of the left renal vein for large spontaneous splenorenal shunts is a safe and effective method of preventing portal venous steal. For concomitant spontaneous splenorenal shunts and portal vein thrombosis, renoportal anastomosis can be performed. We report transient success with endovascular embolization of large spontaneous splenorenal shunts in a patient posttransplant who required multiple interventions. Experience in the approach to and treatment of spontaneous splenorenal shunts in liver transplant recipients is limited. Further investigation into the best approach to treat spontaneous splenorenal shunts is warranted as the presence and persistence of spontaneous splenorenal shunts can lead to allograft dysfunction and possible allograft loss.

Microscopic hematuria and pelvic congestion syndrome in a patient with cirrhosis

This 53 year old white female presented with complaints of severe pelvic congestion syn-drome and hematuria. The patient gave a history of intermittent macro- and microscopic hematuria for the past 3 years. A recent urologic examina-tion with blue light cystoscopy had revealed some submucosal varices in the bladder, which were thought to be the source of bleeding. However, 2 cystoscopies, 1 and 2 years prior, had not shown any varices. The patient had a history of ethanol abuse and at 2 occasions experienced hematemesis which was controlled by application of a Black-more tube. A gynecologic examination comple-mented by ultrasound revealed a 3 cm submucosal fibroid. Laboratory finding were HB 12.8, HCT 38, RBC 4.2 mil, Platelets 180000, WBC 5800, BUN 28, Creatinine 1.3, estimate GFR 42, Na 136, K 5.6; Cl 98 mEq/lt, alk pts 18 KA U, Tot. Bil 0.6; Glucose 107, PT 10.0 , INR 1.3, Transaminase 500U. Urine-analysis revealed a spec grav 1022, 12 RBC/ hpf, 1.2 WBC/hpf, isolated clumps of bac-teria; culture showed no growth. Physical exami-nation noted pale complexion, distended abdomen with palotment suggesting the presence of ascitis; the spleen was markedly enlarged, BP 138/82, PR 78, Respiration 20 and regular. An enhanced angioCT demonstrated massive esophageal and gastric fundus varices (Figure-1). The spleen was markedly enlarged. There were spleeno-renal shunts resulting in mas-sive dilatation of the left renal vein (Figures 2,3). The left renal vein dilated to a degree, to be com-promised in its passage between aorta and supe-rior mesenteric artery (Figure-3). Dilated collateral veins to the umbilicus were present. In the pelvis one notes massive dilatation of parametrial veins; pelvic congestion syndrome (Figure 4).Renal failure in cirrhotic patients is usu-ally attributed to “hepato-renal syndrome” a con-sequence of albumen loss to ascitis. In our patients the massive spleno-renal shunt caused increased flow in the left renal vein and thereby increased left renal vein pressure (1). This was probably the cause for microscopic hemarturia that had been observed for 3 years (Figure-3). Moreover, the in-creased renal vein pressure caused parenchymal

Post operative chylous ascites after proximal splenorenal shunt

No abstract available. DOI: http://dx.doi.org/10.4038/sljs.v30i1.4509 The Sri Lanka Journal of Surgery 2012; 30(1):41-42

Portal hypertension from nodular regenerative hyperplasia of the liver treated with distal splenorenal shunt.

Portal hypertension (PH) is a devastating sequelae of several pathologic entities, with alcoholic cirrhosis being the most common cause in the western world and endemic schistosomiasis worldwide. A much less common aetiology of non-cirrhotic PH is nodular regenerative hyperplasia (NRH) of the liver. The hallmark of NRH is a benign remodeling of the hepatic parenchyma into regenerative nodules in the absence of fibrosis (1). A Warren-Zeppa Distal Splenorenal Shunt (DSRS) was performed in a young patient with NRH of the liver to alleviate PH. This procedure was chosen due to its low postoperative rates of hepatic insufficiency and high durability.

Surgical treatment for portosystemic encephalopathy in patients with liver cirrhosis: Occlusion of portosystemic shunt in combination with splenectomy

Operative ligation of the portosystemic shunt may control hepatic encephalopathy effectively, but the subsequent increase in portal vein pressure (PVP) leads to high mortality. Splenectomy can decrease inflow into the portal system, resulting in decreased portal pressure. We retrospectively examined the effect of splenectomy in combination with shunt closure on portosystemic encephalopathy. Clinical symptoms of encephalopathy disappeared in all six patients who underwent splenectomy in combination with portosystemic shunt ligation, with the exception of one patient who had relapsing encephalopathy after 6 months. Follow-up computed tomography showed complete obliteration of the portosystemic shunts, except in the one patient with relapsing encephalopathy who underwent balloon-occluded retrograde transvenous obliteration for the remaining splenorenal shunt 8 months after surgery. PVP significantly decreased after splenectomy. PVP did not increase to the baseline PVP value after ligation of the shunts, except in two patients who had elevated PVP after surgery: PVP increased from 18 to 19 mmHg after ligation in one patient and from 18 to 23 mmHg in one patient. Splenectomy followed by surgical ligation of the portosystemic shunt may be feasible and safe for cirrhotic patients with portosystemic shunts.

Cannabinoid receptor 2 agonist ameliorates mesenteric angiogenesis and portosystemic collaterals in cirrhotic rats

Angiogenesis in liver cirrhosis leads to splanchnic hyperemia, increased portal inflow, and portosystemic collaterals formation, which may induce lethal complications, such as gastroesophageal variceal hemorrhage and hepatic encephalopathy. Cannabinoids (CBs) inhibit angiogenesis, but the relevant influences in cirrhosis are unknown. In this study, Spraque-Dawley rats received common bile duct ligation (BDL) to induce cirrhosis. BDL rats received vehicle, arachidonyl-2-chloroethylamide (cannabinoid receptor type 1 [CB(1) ] agonist), JWH-015 (cannabinoid receptor type 2 [CB(2) ] agonist), and AM630 (CB(2) antagonist) from days 35 to 42 days after BDL. On the 43rd day, hemodynamics, presence of CB receptors, severity of portosystemic shunting, mesenteric vascular density, vascular endothelial growth factor (VEGF), VEGFR-1, VEGFR-2, phospho-VEGFR-2, cyclooxygenase (COX)-1, COX-2, and endothelial nitric oxide synthase (eNOS) expressions as well as plasma VEGF levels were evaluated. Results showed that CB(1) and CB(2) receptors were present in left adrenal veins of sham rats, splenorenal shunts (the most prominent intra-abdominal shunts) of BDL rats, and mesentery of sham and BDL rats. CB(2) receptor was up-regulated in splenorenal shunts of BDL rats. Both acute and chronic JWH-015 treatment reduced portal pressure and superior mesenteric arterial blood flow. Compared with vehicle, JWH-015 significantly alleviated portosystemic shunting and mesenteric vascular density in BDL rats, but not in sham rats. The concomitant use of JWH-015 and AM630 abolished JWH-015 effects. JWH-133, another CB(2) agonist, mimicked the JWH-015 effects. JWH-015 decreased mesenteric COX-1, COX-2 messenger RNA expressions, and COX-1, COX-2, eNOS protein expressions. Furthermore, JWH-015 decreased intrahepatic angiogenesis and fibrosis. CB(2) agonist alleviates portal hypertension (PH), severity of portosystemic collaterals and mesenteric angiogenesis, intrahepatic angiogenesis, and fibrosis in cirrhotic rats. The mechanism is, at least partly, through COX and NOS down-regulation. CBs may be targeted in the control of PH and portosystemic collaterals.

Management of splenic artery aneurysm associated with extrahepatic portal vein obstruction

Splenic artery aneurysms although rare are clinically significant in view of their propensity for spontaneous rupture and life-threatening bleeding. While portal hypertension is an important etiological factor, the majority of reported cases are secondary to cirrhosis of the liver. We report three cases of splenic artery aneurysms associated with extrahepatic portal vein obstruction and discuss their management. The records of three patients of splenic artery aneurysm associated with extrahepatic portal vein obstruction managed from 2003 to 2010 were reviewed retrospectively. The clinical presentation, surgical treatment and outcome were analyzed. The aneurysm was >3 cm in all patients. The clinical symptoms were secondary to extrahepatic portal vein obstruction (hematemesis in two, portal biliopathy in two) while the aneurysm was asymptomatic. Doppler ultrasound demonstrated aneurysms in all patients. A proximal splenorenal shunt was performed in two patients with excision of the aneurysm in one patient and ligation of the aneurysm in another one. The third patient had the splenic vein replaced by collaterals and hence underwent splenectomy with aneurysmectomy. All patients had an uneventful post-operative course. Splenic artery aneurysms are associated with extrahepatic portal vein obstruction. Surgery is the mainstay of treatment. Although technically difficult, it can be safely performed in an experienced center with minimal morbidity and good outcome.

Ascitis quilosa posquirúrgica en un adulto tratada con octreótida

Chylous ascites is infequent after abdominal surgery. We describe the case of a 43-year-old man with portal cavernomatosis who underwent surgery to insert a splenorenal shunt, which was not placed due to the absence of signs of portal hypertension. On postoperative day 20, the patient developed abdominal distension and mild dyspnea and was diagnosed with chylous ascites, which was related to the surgery. The patient was initially treated with diet and diuretics, with no clinical response, and consequently octreotide therapy was started. Four days later, the ascites was almost resolved and an ultrasound scan at 4 months showed its complete disappearance. This article demonstrates the effectiveness of octreotide in the treatment of postsurgical chylous ascites.

Selective surgical shunts for treating complications of portal hypertension: 10-year experience in a single institution in eastern Taiwan

ObjectiveSurgical portosystemic shunts are safe and effective for treating rebleeding gastric varices (GV) in portal hypertensive patients with well-preserved liver function. The aim of this study is to investigate the clinical outcomes of using selected surgical shunts for managing rebleeding GV at a single institution in eastern Taiwan. Materials and MethodsWe retrospectively recruited 12 patients who received distal splenorenal shunts (DSRS) following the indication of rebleeding GV or hypersplenism from January 2001 through December 2010. Their demographic data, etiology of portal hypertension, associated treatments, perioperative complications and clinical outcomes were reviewed. ResultsAll patients received DSRS, including 10 adults and two children, and were examined for a median follow-up period of 53 months. No postoperative encephalopathy, major complications, or surgical mortality occurred. Two of the patients were waiting for liver transplants. Late rebleeding in esophageal varices developed in two patients who were successfully managed using endoscopic treatment. The etiology of portal hypertension had no significant impact on the postoperative complications. ConclusionAlthough there were a limited number of cases in this series, our results indicate that the DSRS is an effective treatment for rebleeding GV, especially for patients with well-preserved liver function and taking into account the realities of organ shortages.

Management of hypersplenism in non-cirrhotic portal hypertension: a surgical series

Hypersplenism is commonly seen in patients with non-cirrhotic portal hypertension (NCPH). While a splenectomy alone can effectively relieve the hypersplenism, it does not address the underlying portal hypertension. The present study was undertaken to analyze the impact of shunt and non-shunt operations on the resolution of hypersplenism in patients with NCPH. The relationship of symptomatic hypersplenism, severe hypersplenism and number of peripheral cell line defects to the severity of portal hypertension and outcome was also assessed. A retrospective analysis of NCPH patients with hypersplenism managed surgically between 1999 and 2009 at our center was done. Of 252 patients with NCPH, 64 (45 with extrahepatic portal vein obstruction and 19 with non-cirrhotic portal fibrosis) had hypersplenism and constituted the study group. Statistical analysis was done using GraphPad InStat. Categorical and continuous variables were compared using the chi-square test, ANOVA, and Student's t test. The Mann-Whitney U test and Kruskal-Wallis test were used to compare non-parametric variables. The mean age of patients in the study group was 21.81+/-6.1 years. Hypersplenism was symptomatic in 70.3% with an incidence of spontaneous bleeding at 26.5%, recurrent anemia at 34.4%, and recurrent infection at 29.7%. The mean duration of surgery was 4.16+/-1.9 hours, intraoperative blood loss was 457+/-126 (50-2000) mL, and postoperative hospital stay 5.5+/-1.9 days. Following surgery, normalization of hypersplenism occurred in all patients. On long-term follow-up, none of the patients developed hepatic encephalopathy and 4 had a variceal re-bleeding (2 after a splenectomy alone, 1 each after an esophago-gastric devascularization and proximal splenorenal shunt). Patients with severe hypersplenism and those with defects in all three peripheral blood cell lineages were older, had a longer duration of symptoms, and a higher incidence of variceal bleeding and postoperative morbidity. In addition, patients with triple cell line defects had elevated portal pressure (P=0.001), portal biliopathy (P=0.02), portal gastropathy (P=0.005) and intraoperative blood loss (P=0.001). Hypersplenism is effectively relieved by both shunt and non-shunt operations. A proximal splenorenal shunt not only relieves hypersplenism but also effectively addresses the potential complications of underlying portal hypertension and can be safely performed with good long-term outcome. Patients with hypersplenism who have defects in all three blood cell lineages have significantly elevated portal pressures and are at increased risk of complications of variceal bleeding, portal biliopathy and gastropathy.

Multidetector CT-guided endovascular treatment of a splenic artery aneurysm in a child with split-liver transplant and surgically ligated splenic artery origin

We report the case of a child who underwent left lateral split-liver transplantation for biliary atresia and surgical ligation of the origin of the splenic artery at the time of the transplantation. Post-transplant portal vein thrombosis was initially treated with a meso-rex shunt. This shunt subsequently thrombosed and was replaced by a splenorenal shunt. Three months after splenorenal shunt placement, US showed a 3.7-cm pseudoaneurysm at the hilum of the spleen. Multidetector CT with 3-D reconstruction allowed precise identification of the pseudoaneurysm feeding artery and therefore helped in planning the interventional radiology procedure, avoiding explorative selective catheterisation. The pseudoaneurysm was successfully treated with endovascular coil embolisation.

Use of cine phase-contrast MRI in the assessment of distal splenorenal shunt function

Magnetic resonance imaging (MRI) features of a surgical splenorenal shunt in a 28-year-old girl are described. The woman underwent color doppler ultrasonography during follow up for the shunt, which was inconclusive. MR was used to investigate the function of the shunt. Velocity and flow direction in splanchnic vessels and in the shunt were evaluated using cine fast phase-contrast sequences. MR findings could be of help in the evaluation of patients undergoing surgical shunts during follow up.

The enlarged spleen – a blood bank

Splenomegaly may be the result of several diseases such as myeloproliferative disorders, portal hypertension etc. Sometimes the splenic size may assume massive proportions. A massive splenomegaly may lead to symptoms or changes in laboratory parameters over and above the original disease state. The predominant symptoms include pain due to the splenic infarcts, dragging sensation due to the sheer size, early satiety etc. It has been known for several decades that a large spleen is a massive pool of sequestered blood cells. It can be holding 30–90% of all platelets and 40% of all erythrocytes. The bone marrow is typically hypercellular to compensate for this sequestration. Splenectomy entails removal of the whole spleen along with the sequestered blood cells in the spleen. This seems like a terrible waste of the sequestered blood components. If one was able to harvest these components the potential benefits could include a rise in the hematocrit, possibly avoidance of blood transfusion, immediate rise in platelet count, with implications for hemostasis and a rise in leucocyte count. The potential secondary benefits may include easier handling of a smaller spleen, reduced blood loss and lesser operation time. While it is quite common practice to ligate the splenic artery first, during splenectomy for a massive splenomegaly, the objective benefits of this step have been studied by few. This step of the surgical procedure is commonly performed by surgeons to reduce the problems of handling a massive spleen and, possibly, reduce blood loss during peri-splenic dissection, particularly in patients with portal hypertension. The ‘auto-transfusion’ of sequestered components is but a side-effect of this step. One concern of such an auto-transfusion is the quality of blood cells being released into the blood stream. Other potential concerns are the risks of dissecting the large tortuous splenic artery, especially in patients with portal hypertension, in the face of unquantified benefits. The study by Madhavan et al in this issue of the journal studied the objective benefit of early ligation of the splenic artery during splenectomy for portal hypertension.They studied 30 patients with portal hypertension (NCPF 20, EHPVO 9, Cirrhosis 1) who underwent splenectomy and proximal spleno-renal shunt in their unit. They found that there is significant increase in the RBC and platelet counts, though there was no statistically significant increase in the total leucocyte count, differential leucocyte count and hemoglobin. Even though the study suffers from several methodologic flaws it does bring into focus the auto-transfusion benefits of early ligation of the splenic artery during splenectomy. However the study does not report the percentage changes in the cell counts and only the mean values have been used for analysis instead of paired analysis. Gazula et al had earlier studied a similar population and reported a significant increase in the hemoglobin, hematocrit, leucocyte, platelet and RBC counts after early ligation of the splenic artery. They had restricted intravenous fluid administration after splenic artery ligation and thus found that benefits extended to increased hemoglobin, hematocrit and leucocyte count also. Both the studies excluded patients requiring intravenous fluids or blood transfusion and did not include a control population. While this may have removed the confounding

Adams–Oliver syndrome and portal hypertension: Fortuitous association or common mechanism?

Adams-Oliver syndrome (AOS) is a rare condition defined by combination of cutis aplasia and transverse limb abnormalities. Some authors have described a possible association between this syndrome and portal hypertension (PH) due to hepatoportal sclerosis (HPS). We present a boy with AOS who developed a progressive splenomegaly and hypersplenism at the age of 2 months, and was admitted for acute gastrointestinal bleeding (GI) at the age of 9 months. Subsequently, we documented an extrahepatic portal vein obstruction and esophageal varices. After several episodes of cataclysmic upper GI bleeding a mesentero-portal shunt (MPS) was performed at 10 months. The shunt thrombosed, and after three failed attempts of thrombectomy, it was removed. One month later a splenorenal shunt was performed, and this closed spontaneously by 3 years. The patient suffered from ischemic stroke after placing the first shunt, and has spastic diplegia, left frontal lobe epilepsy, hyperactivity and attention deficit disorder, and severe psychomotor delay. At 11 years and he presented with chronic liver failure and hyperammonemia and coagulopathy. We hypothesize that there may be an early embryonic vascular abnormality (vascular disruption) that may explain these vascular phenomena.

The Roles of Angiotensin II Receptors in the Portosystemic Collaterals of Portal Hypertensive and Cirrhotic Rats

Background/Aims:In liver cirrhosis/portal hypertension, collaterals as varices may bleed and are influenced by vasoresponsiveness. An angiotensin blockade ameliorates portal hypertension but the influence on collaterals is unknown. Methods:Portal hypertension and cirrhosis were induced by portal vein (PVL) and common bile duct ligation (BDL). Hemodynamics, real-time PCR of angiotensin II receptors (AT₁R, AT₂R) in the left adrenal vein (LAV, sham) and splenorenal shunt derived from LAV (PVL, BDL) were performed. With an in situcollateral perfusion model, angiotensin II vasoresponsiveness with different preincubations was evaluated: (1) vehicle; (2) AT₁R blocker losartan; (3) losartan plus nonselective nitric oxide synthase (NOS) inhibitor (N^ω-nitro-L-arginine); (4) AT₂R blocker PD123319; (5) PD123319 plus N^ω-nitro-L-arginine; (6) N^ω-nitro-L-arginine, and (7) losartan plus inducible NOS inhibitor aminoguanidine. Results: LAV AT₁R and AT₂R expression decreased in PVL and BDL rats. Losartan attenuated angiotensin II-elicited vasoconstriction but PD123319 had no effect. N^ω-nitro-L-arginine but not aminoguanidine reversed the losartan effect. Conclusions:Angiotensin receptors are downregulated in the collateral vessel of portal hypertensive and cirrhotic rats. The AT₁R blockade attenuates the angiotensin II vasoconstrictive effect, suggesting AT₁R mediates collateral vasoconstriction and the influence of AT₂R is negligible. The lack of aminoguanidine influence indicates that endothelial NOS participates in the losartan effect.

Combined endoscopic-interventional radiologic approach for the treatment of bleeding gastric varices in the setting of a large splenorenal shunt

Endoscopic cyanoacrylate (glue) injection is an effective therapy for bleeding gastric varices (GV) but may result in life-threatening embolic complications. The risk of glue-related embolism is heightened if a large gastro/splenorenal shunt (SRS) is present.1 Techniques that minimize the risk of glue embolization via the SRS would significantly enhance the safety of the procedure.

Management of surgical splenorenal shunt-related hepatic myelopathy with endovascular interventional techniques

We present a case with hepatic myelopathy (HM) due to a surgical splenorenal shunt that was successfully treated by endovascular interventional techniques. A 39-year-old man presented with progressive spastic paraparesis of his lower limbs 14 mo after a splenorenal shunt. A portal venogram identified a widened patent splenorenal shunt. We used an occlusion balloon catheter initially to occlude the shunt. Further monitoring of the patient revealed a decrease in his serum ammonia level and an improvement in leg strength. We then used an Amplatzer vascular plug (AVP) to enable closure of the shunt. During the follow up period of 7 mo, the patient experienced significant clinical improvement and normalization of blood ammonia, without any complications. Occlusion of a surgically created splenorenal shunt with AVP represents an alternative therapy to surgery or coil embolization that can help to relieve shunt-induced HM symptoms.

Human thrombin for the treatment of gastric and ectopic varices

To evaluate the efficacy of human thrombin in the treatment of bleeding gastric and ectopic varices. Retrospective observational study in a Tertiary Referral Centre. Between January 1999-October 2005, we identified 37 patients who were endoscopically treated with human thrombin injection therapy for bleeding gastric and ectopic varices. Patient details including age, gender and aetiology of liver disease/segmental portal hypertension were documented. The thrombin was obtained from the Scottish National Blood Transfusion Service and prepared to give a solution of 250 IU/mL which was injected via a standard injection needle. All patient case notes were reviewed and the total dose of thrombin given along with the number of endoscopy sessions was recorded. Initial haemostasis rates, rebleeding rates and mortality were catalogued along with the incidence of any immediate complications which could be attributable to the thrombin therapy. The duration of follow up was also listed. The study was conducted according to the United Kingdom research ethics guidelines. Thirty-seven patients were included. 33 patients (89%) had thrombin (250 U/mL) for gastric varices, 2 (5.4%) for duodenal varices, 1 for rectal varices and 1 for gastric and rectal varices. (1) Gastric varices, an average of 15.2 mL of thrombin was used per patient. Re-bleeding occurred in 4 patients (10.8%), managed in 2 by a transjugular intrahepatic portosystemic shunt (TIPSS) (one unsuccessfully who died) and in other 2 by a distal splenorenal shunt; (2) Duodenal varices (or type 2 isolated gastric varices), an average of 12.5 mL was used per patient over 2-3 endoscopy sessions. Re-bleeding occurred in one patient, which was treated by TIPSS; and (3) Rectal varices, an average of 18.3 mL was used per patient over 3 endoscopy sessions. No re-bleeding occurred in this group. Human thrombin is a safe, easy to use and effective therapeutic option to control haemorrhage from gastric and ectopic varices.

Modulation of graft vascular inflow guided by flowmetry and manometry in liver transplantation

Survival of the partial graft after living donor liver transplantation owes much to its tremendous regenerative ability. With excellent venous outflow capacity, a graft within a wide range of graft-to-standard-liver-volume ratios can cope with portal hypertension that is common in liver transplant recipients. However, when the ratio range is exceeded, modulation of graft vascular inflow becomes necessary for graft survival. The interplay between graft-to-standard-liver-volume ratio and portal pressure, in the presence of portosystemic shunt or otherwise, requires individualized modulation of graft portal and arterial inflows. Boosting of portal inflow by shunt ligation can be guided by transonic flowmetry, whereas muting of portal inflow by splenic artery ligation can be monitored by portal electronic manometry. We describe four cases to illustrate the above. One patient had hepatic artery thrombosis resulting from splenic artery steal syndrome which was the sequela of small-for-size syndrome. Emergency splenic artery ligation and re-anastomosis of the hepatic artery successfully muted the portal inflow and boosted the hepatic arterial inflow. Another patient with portal vein thrombosis underwent thrombendvenectomy. Portal inflow was boosted with ligation of portosystemic shunt, which is often present in these patients with portal hypertension. The coexistence of splenic aneurysm and splenorenal shunt required ligation of both in the third patient. The fourth patient, with portal pressure and flow monitoring, avoided ligation of a coronary vein which became a main portal inflow after portal thrombendvenectomy. Management of graft inflow modulation guided selectively by transonic flowmetry or portal manometry was described.