Background: Sinistral, or left-sided, portal hypertension (SPH) is a rare cause of upper gastrointestinal (GI) hemorrhage resulting from obstruction of the splenic vein. Venous drainage from the spleen via collaterals can result in venous hemorrhage into both the retroperitoneal and intra-abdominal spaces due to increased venous blood pressure in peripancreatic and gastroduodenal vasculature. SPH can occur secondary to pancreatitis with thrombosis of the splenic vein. Another possible cause is the surgical ligation of the splenic vein as part of pancreaticoduodenectomy (PD). Although splenectomy has been traditionally considered as the treatment of choice to relieve venous hypertension, individual concepts for each patient have to be developed. Considering the venous collateral drainage pathways, a comprehensive approach involving surgical, endoscopic, and interventional radiology interventions may be necessary to address the underlying cause of variceal bleeding. Among these approaches, splenic artery embolization (SAE) has demonstrated efficacy in mitigating the adverse effects associated with elevated venous outflow pressure. Summary: This review summarizes key imaging findings in SPH patients after PD and highlights the potential of minimally invasive embolization for curative treatment of variceal hemorrhage. Key Messages: (i) SPH is a potential consequence after major pancreas surgery. (ii) Collateral flow can lead to life-threatening abdominal bleeding. (iii) Depending on the origin and localization of the bleeding, a dedicated management is required, frequently involving interventional radiology techniques.

Variceal bleeding secondary to sinistral portal hypertension (SPH) is a rare condition [1]. It is characterized by localized portal hypertension, most commonly due to obstruction of the splenic vein (SV) by a pancreatic pathology (acute or chronic pancreatitis, pancreatic pseudocysts, and malignancies) and/or subsequent surgery resulting in venous hypertension [2‒4]. This may lead to peripancreatic as well as gastric varices formation, which eventually can cause life-threatening upper gastrointestinal (GI) hemorrhage. While the association between SV ligation in pancreaticoduodenectomy (PD) and SPH is recognized, the incidence of clinically relevant SPH remains undetermined. The management of SPH has frequently been performed surgically by splenectomy to decompress the left portal venous system [3, 5, 6]. Previous studies also displayed good feasibility and outcomes for endovascular treatment of symptomatic SPH [7, 8]. The role of splenic artery embolization (SAE) in SPH cases after PD is not well known, as patients with pancreatic cancer mostly do not survive long enough to develop this complication. The continuous improvement of care leads to increased numbers of long-term survivors from pancreatic cancer. Ligation of the SV as part of PD has shown to be a common cause for SPH, which in long-term cancer survivors may lead to an increased incidence of SPH [9, 10].

Pathophysiology of SPH

SPH is distinguished by the presence of segmental portal venous hypertension, commonly attributed to the occurrence of SV thrombosis (SVT) [11]. Since the SV runs in proximity to the pancreas (shown in Fig. 1a), pathologies affecting the pancreas can compromise the SV and its flow [12]. In pancreatic cancer affecting the pancreatic head, the superior mesenteric vein (SMV) and/or portal vein (PV) are the most frequently involved vascular structures due to anatomical proximity to the pancreas [13]. In the case of tumor infiltration of the PV-SMV confluence, the SV is frequently ligated during PD to achieve a margin-negative resection (shown in Fig. 1a). The occlusion of the SV through surgical ligation causes an elevation in blood pressure within the collateral vessels, resulting in diversion of blood from the portal venous system to the short gastric, gastroepiploic, coronary veins, and the veins running along the gastric fundus (shown in Fig. 1b). In patients after PD with vascular resection of the SV, higher incidence of SPH was displayed compared to cases where the SV was preserved [10].

Fig. 1.

Formation of pancreatic and gastric varices after PD and ligation of the SV. a Anatomy after the PD procedure with resection of the pancreas head, pylorus, and ligation of the SV in the case of tumor infiltration of the splenic-mesenteric confluence as in the presented case. Dashed arrows illustrate the direction of blood flow. b The formation of pancreatic and gastric varices if sufficient outflow is not preserved. c, d Venous flow pattern from the spleen after PV-SMV confluence resection with preserved outflow. c When the inferior mesenteric vein (IMV) is not divided, the flow from the spleen passes through the IMV or arc of Barkow to the colonic marginal vein and through the PV. d If the middle colic vein (MCV) was preserved, the flow from the spleen passed through the arc of Barkow and drained into the SMV via the MCV. If the left gastric vein (LGV) is not divided, blood flow from the spleen passes through the short gastric veins and drained into the PV via the LGV. Created with BioRender.com.

Fig. 1.

Formation of pancreatic and gastric varices after PD and ligation of the SV. a Anatomy after the PD procedure with resection of the pancreas head, pylorus, and ligation of the SV in the case of tumor infiltration of the splenic-mesenteric confluence as in the presented case. Dashed arrows illustrate the direction of blood flow. b The formation of pancreatic and gastric varices if sufficient outflow is not preserved. c, d Venous flow pattern from the spleen after PV-SMV confluence resection with preserved outflow. c When the inferior mesenteric vein (IMV) is not divided, the flow from the spleen passes through the IMV or arc of Barkow to the colonic marginal vein and through the PV. d If the middle colic vein (MCV) was preserved, the flow from the spleen passed through the arc of Barkow and drained into the SMV via the MCV. If the left gastric vein (LGV) is not divided, blood flow from the spleen passes through the short gastric veins and drained into the PV via the LGV. Created with BioRender.com.

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Diagnosis

SPH patients remain mostly asymptomatic. Most common symptoms include chronic postprandial fullness and upper GI hemorrhage in the case of gastric varices [4]. Diagnosis is mostly incidental in routine evaluation or in an acute setting with upper GI hemorrhage.

Upper GI endoscopy is the initial diagnostic procedure, which reveals distinctive fundal gastric varices that commonly spare the esophagus and the remainder of the stomach. This distinct characteristic is attributed to two factors: (1) the diversion of splenic venous blood into the gastric fundal veins via the short gastric vessels and (2) the decompression of blood through the coronary and epiploic veins into the portal system, typically directed toward the main PV. The endoscopic presentation varies from microscopic capillaries to enlarged submucosal veins (varices) within the gastric mucosa of the fundus region [14]. As an exemplary SPH case, a patient presented to the emergency room 8 months after PD for the resection of a pancreatic head carcinoma with fatigue and drop of hemoglobin (Hb) value to 5.7 g/dL (initial Hb value 10.6 g/dL). A gastroscopy was performed that showed no evidence of gastric and esophageal varices as a possible cause of GI bleeding (shown in Fig. 2a–c). In principle, the complete exclusion of the stomach, esophagus, and colon as the site of varices as in our case is rare, since gastric or gastrojejunostomy varices are usually detected in the majority of patients [9]. Data from a systematic review identified 14 patients with upper GI bleeding due to SPH after PD and venous resection (resection of the PV-SMV confluence and SV ligation), with gastric varices detected in only 5 of the 14 patients [15]. In the case presented herein, the first GI bleeding event (Hb drop from 10.6 g/dL to 5.7 g/dL within 4 weeks) occurred 8 months after PD for respectable pancreatic ductal adenocarcinoma. This appears relatively early compared to previous data where patients had GI bleeding events at a mean of 28 months after pancreatoduodenectomy [15]. An anastomotic ulcer in the area of the gastroenterostomy was identified and eliminated by clip application. Furthermore, multiple angiectasias were found in the area of the gastrojejunostomy site. Peripancreatic hematoma detected on contrast-enhanced computed tomography (CECT) is suggestive of a bleeding originating from the extensive pancreatic varices (shown in Fig. 3). Whether the likelihood of GI bleeding events in SPH patients actually correlates strictly with the presence of varices alone cannot be answered unequivocally in view of the literature and is presumably subject to multiple hemodynamic factors, such as anatomy of the collaterals or pressure changes in the splenic collaterals [16].

Fig. 2.

Absence of (macroscopic) gastric or esophageal varices in SPH. In some SPH patients, esophageal and gastric varices are completely excised. In our case, the stomach (a) and esophagus (b) are presented free of varices 8 months after the PD operation. An anastomotic ulcer (c) in the area of the gastrojejunostomy is seen and is treated with two metal clips. In addition, angiectasias are localized anatomically close to the ulcer (white arrow).

Fig. 2.

Absence of (macroscopic) gastric or esophageal varices in SPH. In some SPH patients, esophageal and gastric varices are completely excised. In our case, the stomach (a) and esophagus (b) are presented free of varices 8 months after the PD operation. An anastomotic ulcer (c) in the area of the gastrojejunostomy is seen and is treated with two metal clips. In addition, angiectasias are localized anatomically close to the ulcer (white arrow).

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Fig. 3.

Multiphase CECT images. The upper images are arterial phase CT scans, and the lower images were acquired in the venous phase. a Axial thin slice (0.63 mm slice thickness) in the arterial phase. b Coronal maximum intensity projection image (MIP, 7 mm slice thickness) of the pancreatic varices showing early arterial filling. Image (c) is equivalent to image (a) in venous phase. The white arrows in (a) and (b) show the main collateral branch of the SV feeding the varicose formation at the area of the pancreas head. d MIP displaying filling of the varicose pancreatic vessels in the venous phase.

Fig. 3.

Multiphase CECT images. The upper images are arterial phase CT scans, and the lower images were acquired in the venous phase. a Axial thin slice (0.63 mm slice thickness) in the arterial phase. b Coronal maximum intensity projection image (MIP, 7 mm slice thickness) of the pancreatic varices showing early arterial filling. Image (c) is equivalent to image (a) in venous phase. The white arrows in (a) and (b) show the main collateral branch of the SV feeding the varicose formation at the area of the pancreas head. d MIP displaying filling of the varicose pancreatic vessels in the venous phase.

Close modal

Imaging modalities play a pivotal role in the accurate diagnosis of SPH. Due to the rarity of this disease, it is crucial to differentiate its etiology from varices caused by general portal hypertension, as the management strategies differ significantly [17]. Transabdominal ultrasonography (US) is a more useful diagnostic tool for exclusion of systemic portal hypertension by excluding hepatic cirrhosis [18]. Endoscopic US is compared to US the superior imaging modality in evaluating the SV [11]. Multiphase CECT plays a major role in the detection of SV thrombosis and pancreatic pathologies [19]. The arterial phase is essential in detecting pancreatic pathologies, and the portal phase for the detection of secondary complications like thrombosis of the SV. In the presented case, multiphase CECT revealed early enhancement of the pancreatic varices (shown in Fig. 3a, b) including a prominent splenic collateral being the main feeding vessel of the peripancreatic varices (white arrows), with increasing attenuation in the venous phase (shown in Fig. 3c, d). Therefore, in cases with suspected GI hemorrhage after PD, a multiphase CT comprising a non-CECT, arterial phase of the upper abdomen (pancreas protocol), and portal phase should always be performed.

Magnetic resonance imaging (MRI) can also be used as a diagnostic tool for the detection of pancreas pathologies and complication such as portal or SVT. At spin-echo MRI, a thrombus located in the portal or SV exhibits an isointense to hyperintense signal on T1-weighted images, typically demonstrating a higher signal intensity on T2-weighted images. In contrast, older thrombi predominantly display hyperintensity solely on T2-weighted images [20]. Contrast-enhanced MR angiography has been proven more effective in detecting splenic venous collaterals compared to Doppler ultrasound [21].

Therapeutic Management

In acute upper GI hemorrhage, measures to stabilize the patient include endoscopic procedures and vasoconstrictive agents. The endoscopic therapy of choice for the treatment of gastric variceal bleeding is cyanoacrylate injection (bleeding control by cyanoacrylate injection in 93.9% of cases compared to 79.5% by use of band ligation; p = 0.03), but this does not resolve the underlying cause of bleeding [22, 23]. In contrary to systemic portal hypertension, refractory variceal hemorrhage mostly due to SPH cannot be controlled by endoscopic banding or proximal portal decompressive procedures, such as splenorenal shunt [8]. Management of SPH requires interdisciplinary consensus of a board of specialists in surgery, GI endoscopy, and both diagnostic and interventional radiology. Both surgical and endovascular treatments are based on the reduction of the arterial supply to the collateral draining veins and gastric fundal varices. This targeted approach effectively mitigates venous hypertension resulting in a concomitant decrease in venous hypertension and susceptibility to hemorrhage.

Due to rarity of this entity, the management of asymptomatic patients is subject to greater controversy when compared to symptomatic patients. Some studies propose splenectomy as a prophylactic intervention, while others have not demonstrated a substantial survival benefit associated with this procedure [4, 24]. However, some evidence suggests that watchful waiting is an acceptable course of management in asymptomatic patients [19]. The data in these studies were generated in the setting of SVT and do not necessarily reflect the complexity of post-surgical SPH. To our knowledge, there are no large cohort studies on the efficacy of interventional SAE in asymptomatic patients.

Surgical Treatment

Splenectomy has been frequently regarded as the treatment of choice for symptomatic SPH patients with recurrent variceal bleeding [25]; however, the role of surgical treatment of asymptomatic patients remains controversial [4]. First, while splenectomy effectively resolves bleeding from gastric varices, venous collaterals passing along the biliodigestive anastomosis may not be adequately treated. Second, splenectomy may not be a safe option for patients who have had a history of complex abdominal surgery such as PD. And third, the complete loss of the splenic function nowadays can be avoided. As shown in Figure 1, preservation of the inferior mesenteric vein (IMV) despite ligation of the middle colic vein (MCV) can allow sufficient venous drainage through the IMV or arc of Barkow to the colonic marginal veins and into the PV. If the IMV is not preserved, it is recommended to preserve the MCV and/or the left gastric vein to ensure sufficient venous drainage to the PV, thus preventing formation of pancreatic and gastric varices due to insufficient outflow [9]. If not surgically feasible, some studies have recommended different vascular surgical approaches to provide sufficient venous drainage of the splenic and gastric veins, such as SV reimplantation and SV-SMV anastomosis [26, 27]. Other studies have suggested that an SV-IMV anastomosis or surgical as well as percutaneous creation of a splenorenal shunt can also be effective [28‒30].

Endovascular Treatment

SAE is an established endovascular treatment option with multiple indications [18, 31]. Partial splenic embolization (PSE) is the treatment of choice for the treatment of SPH. The most important advantage of PSE over splenectomy is the preservation of the splenic function. SAE can be performed in a selective or non-selective matter. A recent study by Liu et al. [7] highlighted the safety and feasibility of a two-step complete SAE approach for the management of symptomatic SPH cases. Another endovascular therapeutic option is the creation of a percutaneous retroperitoneal splenorenal shunt [32]. This technique carries inherent risks as it involves the puncturing of the splenic parenchyma and subsequent manipulation of the SV through retroperitoneal tissue to establish the splenorenal shunt. Large cohort studies are lacking in regards to the efficacy of percutaneous retroperitoneal splenorenal shunt in the treatment of SPH as few case reports in liver-transplanted patients reporting successful outcomes [29].

Coil embolization of the splenic artery can be beneficial in the setting of traumatic splenic bleeding [18]. However, it can result in recurrence of symptoms and failure of treatment in the case of SPH [18]. Polyvinyl alcohol (PVA) or spherical particles also in combination with coils are the most commonly used embolization agents for SAE. Embolization with non-selective PVA particles (300–500 µm) effectively blocks the splenic blood supply at the level of the red pulp, leading to dry infarction of the functional splenic parenchyma, even in the presence of collateralization. A disadvantage of embolization with particles is possible early and more severe post-embolization pain than coil embolization. A possible explanation is the distal embolization using particles and peripheral infarction leading to the accumulation of exudates and subcapsular fluid, which in turn causes stretching of the splenic capsule [18].

Vascular plugs can also be used at the distal splenic artery proximal to branching of hilar vessels [33]. Agents like lipiodol and absolute alcohol offer cheaper and readily available alternatives [31].

Infarction of spleen parenchyma happens immediately following embolization resulting in rapid decrease of venous blood flow and associated SPH. Following embolization ultrasound examination of the spleen is recommended within the first 10 days to screen for potential abscess formation. In this case, control angiogram performed directly after embolization shows substantially reduced forward flow (shown in Fig. 4, left image) and contrast-enhanced ultrasound of the spleen 2 days after treatment displayed 50–60% embolized (non-enhancing) spleen parenchyma (shown in Fig. 4, right image).

Fig. 4.

SAE. The left image displays an angiogram of the coeliac trunk after partial embolization of the splenic artery (asterisk) with 300–500-µm PVA particles and some pushable coils. The right image displays contrast-enhanced ultrasound (CEUS) of the spleen 2 days after treatment displayed 50–60% embolized (non-enhancing) spleen parenchyma.

Fig. 4.

SAE. The left image displays an angiogram of the coeliac trunk after partial embolization of the splenic artery (asterisk) with 300–500-µm PVA particles and some pushable coils. The right image displays contrast-enhanced ultrasound (CEUS) of the spleen 2 days after treatment displayed 50–60% embolized (non-enhancing) spleen parenchyma.

Close modal

SPH is a rare clinical syndrome that occurs as a result of isolated obstruction of blood flow of the SV due to various etiologies, mainly pancreatic diseases. In rare cases, SPH develops after PV-SMV confluence resection in extended PD for the surgical treatment of infiltrative pancreatic head cancer. This complication can occur especially when the major draining venous vessels are also ligated (left gastric vein, gastrocolic trunk of Henle, right gastric vein, and the MCV) [9].

Immediate intervention is necessary to control bleeding in cases of gastric hemorrhage secondary to SPH [4]. Endoscopic hemostasis in the case of gastric variceal bleeding using cyanoacrylate injection is an important pillar in the therapy management of SPH-related bleeding [23, 34]. However, it is important to note that endoscopic treatment alone does not address the underlying cause of SPH. It is primarily recommended as a rescue treatment for acute gastric variceal bleeding [35]. In the case of SPH after SV ligation, upper GI endoscopy displays characteristic fundal gastric varices typically with sparing the esophagus and the rest of stomach. This characteristic feature is due to the redirection of splenic outflow into the gastric fundal veins via short gastric vessels and decompression via the coronary and epiploic veins toward the portal system. The presented case examples highlight the difficulties of endoscopic treatment of SPH as no treatable gastric varices were detected in endoscopy. The main outflow of the ligated SV resulted in the formation of pancreatic/gastrojejunal varices, which could only be detected through multiphase CECT imaging.

For definitive treatment of SPH, both open surgical and endovascular procedures have been established and are being evaluated recently. Patients with SPH typically exhibit elevated venous pressure primarily on the left side of the portal circulation due to interrupted drainage to the PV. Consequently, the use of transjugular intrahepatic portosystemic shunt is not considered effective in these cases [36]. Transjugular intrahepatic portosystemic shunt leads to direct decompression of the portal pressure (right-sided portal hypertension), which is usually not elevated in cases with isolated SPH [37].

Of note, there is “no-size-fits-all” approach. While splenectomy reduces arterial inflow and venous outflow into gastric and esophageal varices, e.g., having developed following SVT in pancreatitis, it is of little benefit in cases of pancreas head resection with the variceal bleeding occurring along the pancreaticojejunostomy. Therefore, individual treatment concepts have to be tailored from the large toolbox of surgical and endovascular techniques, accompanying endoscopic approaches as the first-line technique in the setting of acute variceal bleeding.

SAE is an effective technique that achieves a non-surgical reduction of the splenic parenchyma, therefore leading to a decrease in blood flow to the spleen. Current data suggest PSE or complete embolization in a two-step approach to be safe and effective endovascular treatments of choice [7, 18].

As surgery in pancreatic cancer has seen great advances in recent years, increasing incidences of long-term survivors with variceal bleeding as a complication of SPH after ligation of the SV may be observed. Interventional radiology plays a leading role in the management and curative treatment of this rare but life-threatening entity. Further investigation involving a larger sample size and long-term follow-up is necessary to establish the efficacy of SAE in cases of SPH following pancreatic surgery. However, physicians dealing with symptomatic SPH should be knowledgeable about the advantages and role of SAE over splenectomy in SPH management.

The authors have no conflicts of interest to declare.

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

All authors contributed to the study conception and design. Material preparation, data collection, and analysis were performed by Nabeel Mansour and Moritz Wildgruber. The first draft of the manuscript was written by Nabeel Mansour, and Simon Sirtl, Martin K. Angele, and Moritz Wildgruber revised the manuscript. All authors read and approved the final manuscript.

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