Left-sided Portal Hypertension Research Articles

Significance of Simultaneous Splenic Artery Resection in Left-Sided Portal Hypertension After Pancreaticoduodenectomy with Combined Portal Vein Resection

BackgroundIn pancreaticoduodenectomy (PD) with resection of portal vein (PV)/superior mesenteric vein (SMV) confluence, the splenic vein (SV) division may cause left-sided portal hypertension (LPH).MethodsThe 88 pancreatic ductal adenocarcinoma patients who underwent PD with PV/SMV resection after chemoradiotherapy were classified into three groups: both SV and splenic artery (SA) were preserved in Group A (n = 16), SV was divided and SA was preserved in Group B (n = 58), and both SV and SA were divided in Group C (n = 14). We evaluated the influence of resection of SV and/or SA on LPH after PD with resection of PV/SMV confluence.ResultsThe incidence of postoperative varices in Groups A, B and C was 6.3, 67.2 and 38.5%, respectively (p < 0.001), and variceal bleeding occurred only in Group B (n = 4: 6.8%). In multivariate analysis, Group B was the only significant risk factor for the development of postoperative varices (Groups B vs. A: odds ratio = 39.6, p = 0.001, Groups C vs. A: odds ratio = 8.75, p = 0.066). The platelet count ratio at 6 months after operation comparing to preoperative value was 0.93, 0.73 and 1.09 in Groups A, B and C, respectively (Groups B vs. C: p < 0.05), and spleen volume ratio at 6 months was 1.00, 1.37 and 0.96 in Groups A, B and C, respectively (Groups B vs. A and C: p < 0.01 and p < 0.05).ConclusionIn PD with resection of PV–SMV confluence, the SV division causes LPH, but the concomitant division of SV and SA may attenuate it.

УСПЕШНАЯ ЭМБОЛИЗАЦИЯ СЕЛЕЗЕНОЧНОЙ АРТЕРИИ ПРИ ЛЕЧЕНИИ РЕЦИДИВИРУЮЩЕГО КРОВОТЕЧЕНИЯ ИЗ ВАРИКОЗНО РАСШИРЕННЫХ ВЕН ЖЕЛУДКА ПРИ ЛЕВОСТОРОННЕЙ ПОРТАЛЬНОЙ ГИПЕРТЕНЗИИ

Background. Left-sided portal hypertension (LSPH) is a rare cause of bleeding.Aim. To analyse the outcomes of roentgen-endovascular embolization of the splenic artery (RESA) in recurrent&nbsp;bleeding from fundal gastric varices (FGV) secondary to LSPH.Material and methods. RESA was performed in the patient with LSPH and recurrent bleeding from FGV who had&nbsp;been previously operated on for chronic pancreatitis.Results. The procedure contributed to a stable hemostasis in bleeding from FGV, as well as to the persistent&nbsp;absence of relapses during the eighteen months’ follow-up period.Conclusions. RESA in patients with LSPH and bleeding from FGV is a minimally invasive and highly effective tool.

Left-sided portal hypertension after pancreaticoduodenectomy with resection of superior mesenteric-portal vein confluence: Efficacy of concomitant splenic artery resection

Left-sided portal hypertension after pancreaticoduodenectomy with resection of superior mesenteric-portal vein confluence: Efficacy of concomitant splenic artery resection

Clinical features and treatment of rare etiologies of upper gastrointestinal bleeding

Objective To explore the clinical features and treatment of upper gastrointestinal bleeding with rare etiologies. Methods A total of 45 cases with rare etiologies was selected from a group of 1200 patients with upper gastrointestinal bleeding admitted from January 2012 to December 2015. Results The incidence of gastric stromal tumor (24.4%) and Dieulafoy's lesion (20.0%) was the highest. Among rare etiologies of upper gastrointestinal bleeding were Mallory-Weiss syndrome (17.8%) and stomal ulcer and hemorrhage of efferent loops after subtotal gastrectomy (17.8%), as well as left-side portal hypertension (6.7%), liver cirrhosis complicated with variceal bleeding in the descending part of the duodenum (2.1%), esophageal hematoma (2.1%), esophageal mucosa avulsion (2.1%), P-J syndrome (2.1%), duodenal adenocarcinoma (2.1%), and cutaneous malignant melanoma with duodenal metastasis (2.1%). Conclusions Gastroscopy in early stages played a role in etiologies identification, while etiological treatments could substantially reduce recurrent bleeding rate, thus enhanced cure rate. Analysis on rare etiologies promoted the medical understanding, with clinical diagnosis and treatment improved. Key words: Gastrointestinal hemorrhage/ET/TH

Refractory gastric variceal bleeding secondary to splenic vein occlusion associated with abdominal lymphadenopathy

Summary Splenic vein occlusion caused by abdominal lymphadenopathy is rare. We herein present the case of a 80-year-old man with refractory isolated gastric variceal bleeding in the absence of pancreatic or liver disease. Left-sided portal hypertension was confirmed by angiography, and para-aortic lymphadenopathy compressing the splenic vein was identified by serial abdominal computed tomography. Endoscopic sclerosing therapy failed to treat the recurring gastric variceal hemorrhage. Therefore, splenectomy was suggested and the patient was successfully treated. The patient had been variceal bleeding free for 12 months since the surgery. In patients with isolated gastric varices but without advanced liver disease, a variety of diagnostic techniques should be attempted to elucidate the nature of portal hypertension, and left-sided portal hypertension should be suspected. For those cases in which endoscopic treatment failed to treat refractory gastric variceal bleeding, splenectomy can be an effective option.

Laparoscopic distal pancreatosplenectomy for a large MCN with left portal hypertension

Aims: To demonstrate an operative video of a radical laparoscopic distal pancreatosplenectomy for a huge MCN with left portal hypertension in a young woman. Methods: A 35-year old woman presented with non specific upper abdominal pain, predominantly on the left. All relevant blood investigations were normal. An ultrasound scan detected a large upper left abdominal cyst over 15 cm in diameter. She then had a CT scan which suggested a large distal pancreatic cyst, extending to the spleen measuring 20 × 20 cm with no internal septations. The spleen was enlarged at 17 cm and the splenic vein was compressed. In preparation for surgery, she underwent an EUS to confirm the nature and content of the cyst. The fluid was confirmed to be mucinous and the aspirate was acellular. A laparoscopic distal pancreatosplenectomy was planned. Results: Surgery was undertaken in a supine partial lithotomy position with the surgeon standing between the legs. Four ports (12, 12, 5 and 5 mm) were used. An antegrade radical distal pancreatosplenectomy was performed. Intraoperatively, as expected, the patient was found to have significant left-sided portal hypertension due to compression of the splenic vein by the cyst. The procedure was completed laparoscopically in 95 minutes. The intraoperative blood loss was 350 ml. The patient developed a grade-A pancreatic fistula (as defined by ISGPF) for one day. She was discharged after drain removal on the fifth postoperative day with no other significant postoperative complications. Conclusions: It is feasable and safe to perform a laparoscopic distal pancreatosplenectomy for very large pancreatic cysts in presence of significant portal hypertension with minimal comorbidity and short postoperative stay.

Left-sided portal hypertension revisited

Background: Splenic vein obstruction can lead to left-sided portal hypertension, which is a rare segmental portal hypertension condition, often caused by inflammatory or neoplastic disease of the pancreas. Today, adequate study by cross-sectional imaging, e.g., ultrasound and computed tomography, allows the identification of particular features of the venous collateral pathways that favor the development of gastroesophageal varices. Methods: A retrospective study of 15 cases of left-sided portal hypertension secondary to complete thrombosis of the splenic vein was performed, with special attention to the morphodynamic conditions predicting the development of gastroesophageal varices. Results: In patients with left-sided portal hypertension, gastroesophageal varices were greatly favored by two conditions: collateral pathways directed to the gastric fundus and hypertension in the left gastric vein. This last condition typically occurs when the left gastric vein inflows into an already obstructed splenic trunk, or in the case of concomitant portal hypertension. On the contrary, patients with left-sided portal hypertension and collaterals connected with the left renal or adrenal veins have minor risk of gastroesophageal varices. Conclusions: In every case of left-sided portal hypertension, upper digestive endoscopy and close follow-up are recommended. Besides, computed tomography can demonstrate particular conditions directly favoring gastroesophageal varices, and aid in selection of the appropriate therapeutic decisions.

Look to the Left: A Rare Case of Recurrent Upper GI Bleeding

We present the case of a 63 year old male who developed recurrent massive gastric varicose vein bleedingepisodes years after necrotising pancreatitis. Endoscopy revealed extensive gastric but no esophageal varices. Ultrasonographic findings included an enlarged spleen, normal portal vein diameter and flow and a regular liver texture without signs of cirrhosis. CT scan demonstrated massive perigastric and splenic collateral veins due to chronic splenic vein occlusion. Left-sided portal hypertension was diagnosed and the patient treated with splenectomy. In an endoscopic 2-year follow-up, gastric varicose veins have completely regressed and the patient has remained free of recurrent GI bleeding complications.

Multiple Giant Splenic Artery Aneurysms Causing Sinistral (Left-Sided) Portal Hypertension

Background. Splenic artery aneurysm is the most common type of visceral aneurysms. They are usually asymptomatic and have a potential for rupture and therefore life-threatening hemorrhage. It is rare for them to cause sinistral portal hypertension. Case Report. A 23-year-old female patient presented to our clinic with gastric varices, splenomegaly, pancytopenia, and normal liver functions. She was thus diagnosed with left-sided portal hypertension. Radiologic evaluation showed splenomegaly, splenic vein obstruction, and multiple aneurysms along the splenic artery ranging from 2.5 cm to 7 cm. Splenic artery aneurysm was thought to be the cause of portal hypertension and hypersplenism. We decided splenectomy is the best course of treatment. Pancytopenia could not be corrected preoperatively despite the transfusion treatment. Surgical exploration revealed multiple aneurysms deeply embedded in pancreas. Thrombocyte and erythrocyte transfusion was performed after splenic artery ligation to correct pancytopenia before further intervention. Splenic artery, spleen, and distal pancreas were resected en bloc. Patient's blood parameters became normal within first postoperative day. Patient had an uneventful postoperative course and was discharged without incident. Conclusion. Splenic artery aneurysms are rare but potentially life-threatening incidents. Therefore, it is important to know the unusual presentations and prepare accordingly.

Spleen and splenic vessel preserving distal pancreatectomy for bifocal PNET in a young patient with MEN1

MEN1 patients requiring resection of neuroendocrine tumors (pNET) are frequently young, active patients in whom a minimal access approach minimizes perioperative morbidity and splenic preservation decreases the risk of post-splenectomy sepsis. Laparoscopic spleen preserving distal pancreatectomy can be performed with removal (Warshaw's technique) or preservation of the splenic vessels, the later having a higher rate of successful splenic preservation. This is an active, 16-year-old Jehovah's Witness with trifocal nonfunctioning neuroendocrine tumor in the proximal body and tail of the pancreas as part of MEN1 syndrome. A spleen preserving distal pancreatectomy was performed with the final pathology showing three pNET with low mitotic count and three lymph nodes free of cancer (final stage pT2pN0). This video demonstrates patient and trocar positioning as well as operative tactics for a laparoscopic distal pancreatectomy with preservation of splenic vessels. Intraoperative ultrasound is crucial in assessing pNETs' relation to critical vessels, pancreatic duct, and to exclude synchronous lesions. The video focuses on safe laparoscopic creation of the retropancreatic tunnel and dissecting the pancreas off the splenic vessels using novel energy devises to control direct splenic venous branches into the pancreas. Improvements in laparoscopic techniques and technology have enabled surgeons to preserve the major splenic vessels to avoid splenic infarcts, abscesses and re-operations, and minimize the risk of left-sided portal hypertension. Splenic preservation is particularly important in young MEN1 patients undergoing laparoscopic pancreatectomy for pNET due to the increased risk of overwhelming post-splenectomy sepsis.

Left-Sided Portal Hypertension: A Clinical Challenge

c i t i s i Left-sided portal hypertension (LSPH), also known as segmental, regional, localized, compartmental, lineal, splenoportal, or sinistral hypertension is a rare, but life threatening cause of upper gastrointestinal bleeding. It usually occurs as a result of isolated obstruction of the splenic vein. The incidence of LSPH has increased over the past three decades due to increased awareness of the entity and advances in diagnostic approaches. Since most patients are asymptomatic and experience no complications, its exact incidence is unknown. However, it accounts for less than 5% of all patients with portal hypertension.1 To date, less than 500 cases of LSPH have been reported in all. Most of the studies in the literature comprise a limited number of patients and are usually retrospective.2,3 Due to its low incidence, it is likely that most cases of sinistral hypertension are initially misdiagnosed as a generalized portal hypertension. Blood flow through the splenic vein may be blocked secondary to either thrombosis formation or neighboring mass effect.1 Following obstruction, splenic blood typically drains through the short gastric veins to the stomach. In the gastric wall veins of the fundus, blood flow and pressure increase and submucosal structures consequently dilate, producing gastric varices. Fortunately, due to several anatomic variations, obstruction of the splenic vein may not always result

A Rare Case of Gastric Variceal Hemorrhage Secondary to Infiltrative B-Cell Lymphoma: Presidential Poster

Portal hypertension commonly arises in the setting of advanced liver cirrhosis, and is the consequence of increased resistance within the portal vasculature. Less commonly, left-sided non-cirrhotic portal hypertension can develop in a patient secondary to isolated obstruction of the splenic vein. We present a rare case of left-sided portal hypertension and isolated gastric varices in a patient with large B-cell lymphoma, who was treated with splenic artery embolization. The patient is a 73-year-old male with no previous history of liver disease, who presented with coffee ground emesis and melena. On admission to an outside hospital, he was found to have a hemoglobin of 3.4 g/L. EGD showed isolated bleeding gastric varices (IGV1 by Sarin classification) in the fundus and cardia with subsequent APC injection. He was transferred to our tertiary center where work up revealed normal liver function tests, and abdominal ultrasound showed patent hepatic/portal vasculature without cirrhosis. MRI demonstrated a large heterogeneously enhancing mass in the pancreatic tail, with invasion into the spleen and associated splenic vein thrombosis. Surgery consultation was obtained, but urgent splenectomy was not recommended. He instead underwent splenic artery embolization to prevent future bleeding from his known gastric varices. Pathology from a CT guided biopsy was consistent with diffuse large B-cell lymphoma. PET imaging showed uptake in the splenic hilum/pancreatic tail region with no additional metastatic involvement. He was evaluated by Hematology to initiate R-CHOP chemotherapy. During his outpatient follow-up, he reported no further episodes of melena or hematemesis. To the best of our knowledge, there have only been two published case reports of large B cell lymphoma causing upper GI bleeding from isolated gastric varices. These cases were treated with splenectomy or chemotherapy alone. Thus far, splenectomy has been the standard treatment approach for splenic vein thrombosis with clinical complication such as gastric variceal bleeding. We present a case of successful treatment of bleeding isolated gastric varices using a less invasive and less morbid approach through splenic artery embolization. This case highlights the need for increased awareness of the diverse etiologies of left-sided portal hypertension and isolated gastric varices, as well as the consideration of minimally invasive management strategies.Figure 1Figure 2Figure 3

Left-sided portal hypertension with a patent splenic vein: An impossible or a not-so-uncommon scenario?

Introduction: Left-sided portal hypertension is usually thought to result from a mechanical obstruction of the splenic vein. However, a functional obstruction of a patent splenic vein due to high venous flow can also cause left-sided portal hypertension. Case Report: We report a case of left-sided portal hypertension with a patent splenic vein. Conclusion: The case illustrates that left-sided portal hypertension is a syndrome that results from the variable interactions of different mechanisms and highlights that the selection of suitable treatment is based on understanding the portal pathophysiology and portal venous anatomy in the patient.

Preoperatively diagnosed isolated hydatid cyst of pancreatic head with triad of obstructive jaundice, left-sided portal hypertension and chronic pancreatitis

We report a rare case of young female with isolated pancreatic head hydatid cyst causing obstructive jaundice, left-sided portal hypertension, and chronic pancreatitis.

脾摘が有用であったLeft-sided portal hypertentionの4例

脾摘が有用であったLeft-sided portal hypertentionの4例

Sinistral portal hypertension after pancreaticoduodenectomy with splenic vein ligation.

Splenic vein ligation may result in sinistral (left-sided) portal hypertension and gastrointestinal haemorrhage. The aim of this study was to analyse the pathogenesis of sinistral portal hypertension following splenic vein ligation in pancreaticoduodenectomy. Patients who underwent pancreaticoduodenectomy for pancreatic cancer between January 2005 and December 2012 were included in this retrospective study. The venous flow pattern from the spleen and splenic hypertrophy were examined after surgery. Of 103 patients who underwent pancreaticoduodenectomy with portal vein resection, 43 had splenic vein ligation. There were two predominant venous flow patterns from the spleen. In the varicose route (27 patients), flow from the spleen passed to colonic varices and/or other varicose veins. In the non-varicose route, flow from the spleen passed through a splenocolonic collateral (14 patients) or a spontaneous splenorenal shunt (2 patients). The varicose route was associated with significantly greater splenic hypertrophy than the non-varicose route (median splenic hypertrophy ratio 1·52 versus 0·94; P < 0·001). All patients with the varicose route had colonic varices, and none had a right colic marginal vein at the hepatic flexure. Pancreaticoduodenectomy with splenic vein ligation may lead to sinistral portal hypertension. To avoid the development of varices, it is important to preserve the right colic marginal vein. Reconstruction of the splenic vein should be considered if the right colic marginal vein is divided.

Sinistral Portal Hypertension and Anastamotic Varices Secondary to Splenic Vein Thrombosis After a Whipple Procedure

Introduction: A 70-year-old Pakistani woman with a past medical history of coronary artery disease status post recent bare metal stent x 3 (on aspirin and clopidogrel), with a remote history (1989) of a pancreaticoduodenectomy for a benign pancreatic mass that was complicated by splenic vein thrombosis, was admitted to the hospital for worsening anemia. On admission, she was noted to have a hemoglobin of 5 g per dL (9.7 grams per dL 1 month prior). Symptoms included increased fatigue and weakness, and she reported dark stools unchanged while taking oral iron. Of note she had a history of overt, obscure upper gastrointestinal bleeding with several admissions and extensive evaluations from 2001-2012, which were unsuccessful in identifying a source of bleeding. Her most recent endoscopic studies included a normal colonoscopy and an upper endoscopy that revealed post-Whipple anatomy with a widely patent gastrojejunostomy (GJ) and small type 2 gastro-esophageal varices (GOV2) without stigmata of recent bleeding. Push-enteroscopy was performed, which identified small, nonbleeding GOV2s along the fundus. The GJ anastomosis was characterized by friable mucosa and extensive vascular ectasia. The efferent jejunal limb was normal. During the procedure, active bleeding was induced by scope trauma to the GJ anastomosis requiring patient intubation and intra-procedural transfusions. A post-procedure CT angiogram revealed prominent submucosal vasculature localized to the GJ anastomosis diagnostic of anastomotic varices with additional short gastric varices between the spleen and stomach. Moreover, the spleen was enlarged (13 cm) and the splenic vein was not visualized secondary to chronic splenic vein thrombosis. There was no evidence of cirrhosis, suggesting isolated left-sided portal hypertension. Our patient was treated with splenectomy, and has not experienced recurrent bleeding during approximately 2 years of clinical follow-up. Sinistral portal hypertension, also known as left-sided portal hypertension, is hypertension confined to the gastrosplenic side of the portal venous system. To our knowledge, this is the first case of sinistral portal hypertension leading to varices at a GJ anastomosis. Sinistral portal hypertension accounts for less than 5% of all portal hypertension, and is most commonly caused by splenic vein occlusion related to pancreatic disorders. As most patients are asymptomatic, the exact incidence is unknown, but bleeding (variceal or nonvariceal) is the most common manifestation. Splenectomy decreases venous flow through collateral vessels and decompresses associated varices. Rebleeding is rare after splenectomy in various case series.

Effects of Secondary Left-sided Portal Hypertension on the Radical Operation Rate and Prognosis in Patients with Pancreatic Cancer

To investigate the effects of secondary left-sided portal hypertension (LSPH) on the radical operation rate of patients with pancreatic cancer and systemically evaluate the prognosis of patients with LSPH secondary to pancreatic cancer after radical surgery. The data of patients with pancreatic cancer who underwent laparotomy over a 15-year period in Department of Hepatobiliary Surgery of Chinese PLA Air Force General Hospital from Jan. 1, 1997, to Jun. 30, 2012 was retrospectively reviewed. A total of 362 patients with pancreatic cancer after laparotomy were selected, including 73 with LSPH and 289 without LSPH. Thirty-five patients with LSPH (47.9%) and 147 without non-LSPH (50.9%) respectively underwent radical operations. No significant difference was found between these two groups regarding the total resection rate and stratified radical resection rate according to different pathological types and cancer locations. The mean and median survival time of patients after radical operation in LSPH group were 13.9 ± 1.3 months and 14.8 months, respectively, while those in non-LSPH group were 22.6 ± 1.4 months and 18.4 months, respectively(P<0.05). Radical operations for pancreatic cancer and secondary LSPH are safe and effective. Because high-grade malignancy and poor prognosis are closely associated, the decision for radical surgery should be made more meticulously for the patients with pancreatic cancer.

Efficacy of partial splenic artery embolization for gastric varices with left-sided portal hypertension

We report the case of a 70-year-old man who was admitted to another hospital with a chief complaint of hematochezia. He had undergone total gastrectomy 15 years ago. Abdominal computed tomography (CT) showed complete obstruction of the splenic vein by a tumor in the head of the pancreas. He was then referred to our hospital for further management of anemia and the pancreatic tumor. Upper gastrointestinal endoscopy revealed isolated varices lacking the red color sign in the region of the gastric anastomosis. We made the diagnoses of pancreatic head cancer based on the findings on the cytological specimens obtained by endoscopic retrograde cholangiopancreatography, and left-sided portal hypertension due to splenic vein invasion of the tumor based on the CT findings. Because we could not conclude that the bleeding was caused by the varices, we started the patient on chemotherapy and kept her under observation. During the hospitalization, however, the hematochezia recurred repeatedly, and two blood transfusions were required. Upper gastrointestinal endoscopy performed a second time revealed enlarged and oozing varices, and we performed partial splenic artery embolization (PSE) to reduce the blood ooze from the site of bleeding. Well-developed collateral circulation was seen at the splenic hilum and we performed 80% embolization using Gelfoam and metallic coils. The PSE reduced the varices in the anastomosis, and nine months later, the varices had almost disappeared entirely. Left-sided portal hypertension complicated by pancreatic cancer is comparatively rare. In the present case, PSE was effective for stemming the bleeding from the gastric varices.

Idiopathic Splenic Vein Thrombosis Presenting as Splenic Infarction and Consequent Gastric Variceal Bleeding

Left-sided portal hypertension and consequent gastric varices can occur in patients with isolated splenic vein thrombosis. It is a rare but clinically significant and curable cause of gastrointestinal hemorrhage. Our patient, a 20-year-old woman, with left flank pain was diagnosed with having idiopathic splenic vein thrombosis with resultant splenic infarction. Thorough workups for the possible etiologies of splenic vein thrombosis were all negative. After six months of anticoagulation, follow-up computed tomography revealed formation of gastric varices; one month following the discovery, she developed gastrointestinal bleeding. Splenectomy was performed, resulting in the resolution of gastric varices.