Splenic Venous Thrombosis Research Articles

Association between acute peripancreatic fluid collections and early readmission in acute pancreatitis: A propensity-matched analysis.

Patients with acute pancreatitis (AP) frequently experience hospital readmissions, posing a significant burden to healthcare systems. Acute peripancreatic fluid collection (APFC) may negatively impact the clinical course of AP. It could worsen symptoms and potentially lead to additional complications. However, clinical evidence regarding the specific association between APFC and early readmission in AP remains scarce. Understanding the link between APFC and readmission may help improve clinical care for AP patients and reduce healthcare costs. To evaluate the association between APFC and 30-day readmission in patients with AP. This retrospective cohort study is based on the Nationwide Readmission Database for 2016-2019. Patients with a primary diagnosis of AP were identified. Participants were categorized into those with and without APFC. A 1:1 propensity score matching for age, gender, and Elixhauser comorbidities was performed. The primary outcome was early readmission rates. Secondary outcomes included the incidence of inpatient complications and healthcare utilization. Unadjusted analyses used Mann-Whitney U and χ 2 tests, while Cox regression models assessed 30-day readmission risks and reported them as adjusted hazard ratios (aHR). Kaplan-Meier curves and log-rank tests verified readmission risks. A total of 673059 patients with the principal diagnosis of AP were included. Of these, 5.1% had APFC on initial admission. After propensity score matching, each cohort consisted of 33914 patients. Those with APFC showed a higher incidence of inpatient complications, including septic shock (3.1% vs 1.3%, P < 0.001), portal venous thrombosis (4.4% vs 0.8%, P < 0.001), and mechanical ventilation (1.8% vs 0.9%, P < 0.001). The length of stay (LOS) was longer for APFC patients [4 (3-7) vs 3 (2-5) days, P < 0.001], as were hospital charges ($29451 vs $24418, P < 0.001). For 30-day readmissions, APFC patients had a higher rate (15.7% vs 6.5%, P < 0.001) and a longer median readmission LOS (4 vs 3 days, P < 0.001). The APFC group also had higher readmission charges ($28282 vs $22865, P < 0.001). The presence of APFC increased the risk of readmission twofold (aHR 2.52, 95% confidence interval: 2.40-2.65, P < 0.001). The independent risk factors for 30-day readmission included female gender, Elixhauser Comorbidity Index ≥ 3, chronic pulmonary diseases, chronic renal disease, protein-calorie malnutrition, substance use disorder, depression, portal and splenic venous thrombosis, and certain endoscopic procedures. Developing APFC during index hospitalization for AP is linked to higher readmission rates, more inpatient complications, longer LOS, and increased healthcare costs. Knowing predictors of readmission can help target high-risk patients, reducing healthcare burdens.

English

It is difficult to diagnose pancreatic cysts in children. Any previous history of acute pancreatitis is very important because it can lead to a wide set of complications like pseudocyst, pancreatic necrosis, splenic venous thrombosis etc. The most known and common cause of pancreatic pseudocyst in children is trauma. The characteristic features of pancreatitis include abdominal pain, serum lipase or amylase values three times more than that of the normal range and characteristic radiological features. Pancreatic pseudocyst may occur in 15 % of children with acute pancreatitis as a complication.1 Pancreatic juice collection enclosed by a wall of granulation or fibrous tissue, is defined as a pseudocyst. As the resulting cyst has no true endothelial lining, it is classified as a pseudocyst.2 The pseudocyst contains inflammatory pancreatic fluid, mainly the lipase enzyme or semisolid matter. The incidence of pseudocyst is relatively low 1.6 % - 4.5 %, or 0.5 - 1 per 100 000 adults per year.2 Very few cases of pancreatic pseudocyst have been reported in world literature. Commonly, it develops as a sequel of acute or chronic pancreatitis. It develops around 4 weeks after the episode of acute pancreatitis.3 It is characterized by pancreatic inflammation, abdominal pain and raised levels of serum digestive enzymes.4 Here we discuss a case report of pancreatic pseudocyst in a 10-year-old male child presenting with history of abdominal pain and decreased appetite.

Treatment of gastric body variceal bleeding caused by splenic vein thrombosis using color Doppler endoscopic ultrasonography.

Watch a video of this article. A 58-year-old man with a history of alcoholic liver cirrhosis and pancreatitis was admitted for the treatment of gastric body varices (Lg-b)1 on the greater curvature caused by left-sided portal hypertension (LSPH) with splenic venous thrombosis. The supplying vein was the short gastric vein, and drainage veins were the left gastric vein and gastrorenal shunt (Fig. 1a,b, Video S1). We performed balloon-occluded retrograde transvenous obliteration (BRTO), but the Lg-b did not disappear. Seven days after BRTO, Lg-b bleeding occurred. Temporary hemostasis was obtained by endoscopic variceal ligation and 75% N-butyl-2-cyanoacrylate (NBCA) injection. However, the remaining Lg-b were indistinguishable from the gastric mucosal folds (Fig. 1c,d). We hence performed color Doppler endoscopic ultrasonography (CDEUS; GF-UCT260, Olympus Medical Systems, Tokyo, Japan) with water supplied. This enabled visualization of the bloodstream of the Lg-b and gastric-antrum varices (Lg-a) and distinguished risky Lg-b from the gastric folds (and the thrombotic Lg-b) (Fig. 2a). We changed the endoscope (GIF-H290) and succeeded in intravariceal injection of 5% ethanolamine oleate (EO; 17 mL) using a 21-gauge needle on endoscopic injection sclerotherapy. After a 5% glucose solution flush, 2 mL of 75% NBCA was injected, and the needle was flushed with 5% glucose solution again (glucose sandwich method) to avoid NBCA polymerization in the needle. Bleeding did not occur even after needle removal. One month after the treatment, we additionally performed scheduled intravariceal injection (13 mL of EO and 2 mL of 75% NBCA) by glucose sandwich method (Fig. 2b,c). The Lg-b and Lg-a completely disappeared, and part of the varices was replaced by NBCA without any liver dysfunction or complications on computed tomography (Fig. 2d). LSPH is a rare type of portal hypertension.2-5 This is the first report showing the usefulness of endoscopic treatment for Lg-b using CDEUS and combination injection of EO plus NBCA. Authors declare no conflict of interest for this article. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

Efficacy and Safety of Early Systemic Anticoagulation for Preventing Splanchnic Thrombosis in Acute Necrotizing Pancreatitis.

Splanchnic venous thrombosis (SVT) is a relevant complication in patients with acute necrotizing pancreatitis. So far, no specific treatment for preventing development of SVT exists, and the effect of systemic anticoagulation (SAC) is unclear. Patients with acute necrotizing pancreatitis admitted to our center within 7 days from onset of abdominal pain were screened. In the historic group, during which period, most patients received no SAC. Patients in the study group received SAC therapy considering the risk of deep vein thrombosis and SVT. The primary outcome measure was the incidence of SVT. Splenic vein was involved in 71% of all 84 SVT patients. Compared with the historic cohort, patients who received SAC experienced lower incidence of SVT (P < 0.001), especially for splenic venous thrombosis (P = 0.002). Patients in the study group also showed lower mortality (P = 0.04) and incidence of new-onset organ failure (P = 0.03). The incidence of bleeding shows no statistical significance between 2 groups. Application of SAC seems to reduce the incidence of SVT and improve clinical outcomes without increasing the risk of bleeding. Randomized clinical trials are needed to confirm our findings.

Massive Gastric Variceal Hemorrhage Due to Splenic Vein Thrombosis: A Rare Initial Presentation of Asymptomatic Metastatic Pancreatic Adenocarcinoma

Isolated sinistral portal hypertension (SPH) is extremely rare, representing less than 5% of all portal hypertension cases [1]. Rare cases of gastric varices can cases occur due to non-cirrhotic splenic venous thrombosis causing SPH. Here, we present massive gastric variceal bleeding from splenic vein thrombosis as the initial presentation of pancreatic adenocarcinoma. A 71-year old man presented to the emergency department with acute onset massive hematemesis and epigastric pain. He had tenderness in the epigastric and left upper quadrant without peritoneal signs. Hemoglobin was decreased at 8.3 g/d from baseline 12. Total bilirubin and liver function tests were within normal limits. Contrast enhanced CT showed splenic vein thrombosis (Figure 1A), gastric varices (Figure 1B) with active hemorrhage noted, and a 5 cm mass in the pancreatic tail (Figure 1C). No changes of cirrhosis were noted in the liver. The patient underwent successful splenic artery embolization (Figure 2). Diagnosis of metastatic pancreatic adenocarcinoma was confirmed with peritoneal biopsy. Gastric variceal bleeding as the initial presentation of pancreatic adenocarcinoma is incredibly unusual. Splenic vein thrombosis causes SPH and formation of collateral pathways to shunt blood around the occluded splenic vein, increasing pressure within the submucosal veins of the gastric fundus forming varices. Splenic vein thrombosis arising from pancreatic cancer carcinoma represents a rare occurrence. One study showed only 49% of 209 patients were correctly diagnosed with SPH after the first episode of bleeding with a median delay of 11 months[2]. Splenectomy is the standard treatment for splenic vein thrombosis, with splenic artery embolization reserved for patients who are poor surgical candidates with metastatic disease. Massive gastricvariceal hemorrhage due to non-cirrhotic portal hypertension from splenic vein thrombosis as the initial presentation of pancreatic adenocarcinoma is a rare occurrence. Recognizing rare causes of gastric varices such as SPH due to splenic vein thrombosis is important for early diagnosis of possible pancreatic adenocarcinoma.1357.tif Figure 1: Figures for Case Report

Coronary Renal Shunt with Splenectomy (CRSS) for Selective Variceal Decompression

Distal splenorenal shunt and coronary caval shunt are commonly used for selective decompression of esophagogastric varices, but they may not solve severe hypersplenism and their application may be hampered by the presence of splenic venous thrombosis or a left gastric vein (LGV) situated deeply behind the pancreas. On the other hand, some patients have an LGV entering the splenic vein (SV). We tried to work out a new selective shunt for this group of patients. Sixteen patients with severe hypersplenism and esophagogastric varices received coronary renal shunt using the SV following splenectomy. After splenectomy, the proximal portion of the SV and the LGV was isolated from the pancreas. The isolated SV was divided at a point 3-5cm left to its junction with the LGV. The proximal orifice was anastomosed to the left renal vein, and the distal orifice was ligated. A clip was applied to the SV for occlusion between the portal vein and LGV. The right gastric and gastroepiploic vessels were divided to block backflow from the portal vein and to reduce the arterial inflow of the varices. No operative mortality or procedure-related complications occurred. Postoperative computed tomography and endoscopy showed that all the shunts were patent and that the varices had been obliterated or markedly alleviated. In the 6-36months' follow-up period, no recurrent variceal hemorrhage or encephalopathy occurred. Coronary renal shunt combined with splenectomy can achieve the goal of selective decompression of esophagogastric varices. It would become an alternative means of selective variceal decompression for patients whose LGV enters the SV.

Bowel Block in Pancreatitis

Acute pancreatitis is a multisystem disorder which can result in a variety of complications. Vascular complications can occur commonly in acute pancreatitis. Splenic artery rupture, aneurysms; gastro duodenal artery aneurysms; splenic venous thrombosis; portal venous thrombosis and rarely, superior mesenteric venous thrombosis, are the vascular complications of pancreatitis. Ischaemic stricture of the small bowel can occur secondary to pancreatitis, but it is extremely rare. Hence, we are reporting this case of a proximal jejunal stricture which occurred secondary to the pancreatitis which was caused by a superior mesenteric thrombosis.

Splenic irradiation-induced gastric variceal bleeding in a primary splenic diffuse large B-cell lymphoma patient: a rare complication successfully treated by splenectomy with short gastric vein ligation

Primary splenic diffuse large B-cell lymphoma (DLBCL) is a rare clinical condition, which is generally treated by six to eight cycles of chemotherapy involving a combination of rituximab and the cyclophosphamide, adriamycin, vincristine, and prednisolone (CHOP) regimen. However, the treatment for chemorefractory primary splenic DLBCL remains controversial. Therapeutic splenic irradiation (SI) might be a reasonable and possibly the only treatment option with curative intention for patients with chemorefractory primary splenic DLBCL. However, the efficacy and safety of therapeutic SI are unclear. Herein, we present the case of a primary splenic DLBCL patient who was refractory to multiple chemotherapy regimens but achieved complete remission after administration of therapeutic SI. However, his condition was complicated with severe gastric variceal bleeding due to splenic venous thrombosis, which was successfully treated via splenectomy and short gastric vein ligation. On the basis of our findings, we concluded that the splenic venous thrombosis-induced gastric variceal bleeding was a rare but life-threatening adverse effect of the therapeutic SI administered for primary splenic DLBCL. Surgical intervention involving splenectomy and short gastric vein ligation is mandatory and should be performed as soon as possible for such patients.

Splanchnic vein thrombosis complicating severe acute pancreatitis

Splanchnic vein thrombosis complicating severe acute pancreatitis

Concurrent Diseases and Conditions in Dogs with Splenic Vein Thrombosis

Splenic venous thrombosis (SVT) is usually considered an incidental finding on abdominal ultrasound examination but can indicate the presence of underlying disease. Concurrent disease processes and conditions in dogs with SVT have not been identified previously. To identify concurrent diseases and conditions in dogs with SVT. Eighty dogs with SVT. Retrospective review. Medical records from 1994 through 2008 were searched for dogs with SVT identified by ultrasound examination. These records were then reviewed for signalment, medical history, clinicopathologic testing, diagnostic imaging, and clinical diagnosis. The most common concurrent conditions were neoplasia (54%), exogenous corticosteroid administration (43%), systemic inflammatory response syndrome (26%), disseminated intravascular coagulation (20%), pancreatitis (18%), and immune-mediated disease (16%). The most common neoplastic disease was lymphoma, and the most common immune-mediated disease was immune-mediated hemolytic anemia. Protein-losing nephropathy and naturally occurring hyperadrenocorticism were identified in <10% of the dogs. Concurrent splenic infarcts were identified in 33% of dogs, and concurrent portal vein thrombi were found in 18% of dogs. SVT is a sonographic finding of clinical importance, and dogs with SVT can have 1 or more coexisting diseases.

Co-Existance of JAKV617F and PIG-A mutations in Primary Budd-Chiari Syndrome.

Abstract 3193Poster Board III-130Paroxysmal nocturnal hemogloginuria (PNH) is a clonal genetic disorder associated with multiple mutations in the X-linked phosphatidylinositol glycan class A (PIG-A) gene that causes glycosyl phosphatidylinositol (GPI) anchor protein (AP) deficiency in patients with PNH. Conditional PIG-A gene inactivation (PIG-A (-/-)) in hematopoietic cells of mice does not induce overt proliferative advantage to the HPC compartment. In humans, the molecular basis of clonal expansion of GPI-AP deficient cells is unknown but may relate to selective pressure from the bone marrow microenvironment conducive to GPI-AP survival. Alternatively, coexistence of additional genetic anomalies that confer growth potential has been speculated. A single mutation in the Janus Kinase (JAK)-2 gene has been reported to be the underlying molecular mechanism for myeloproliferative diseases including polycythemia vera (PV), essential thrombocythemia, and myelofibrosis. Substitution of a valine for phenylalanine destabilizes the auto-inhibitory activation domain of JAK2 leading to myeloproliferation. Genetic evidence and in vitro functional studies indicate that V617F gives hematopoietic precursors proliferative and survival advantages. A high proportion of patients with myeloproliferative disorders and myelodysplastic syndrome (MDS) carry this dominant gain-of-function mutation of JAKV617F. The clinical syndromes of PNH and JAKV617F mutations often present as overlapping clinical syndromes raising the possibility that acquired JAKV617F mutations confer growth and survival potential to PNH clones in at least a subset of patients. To address this possibility, 21 PNH patients were screened for the presence of JAKV617F mutations. We show here that the features of Budd-Chiari syndrome (BCS) as well as a predisposition to myelodysplastic syndrome can be caused by an acquired co-existing PIGA and JAKV617F activating mutation. Of the 21 cases examined, PNH with JAK2V617F mutations co-existed in three cases (14.3%). Thus far, two patients have been well characterized. Both cases were male, ages 51 (case 1) and 65 year-old (case 2) with normal cytogenetics and de novo classic PNH manifested by Budd-Chiari syndrome. Flow cytometry assay using CD55, CD59, and CD48 (GPI-APs) and FLAER to detect PNH type cells showed that 90% of granulocytes (case 1) and almost 100% of granulocytes (case 2) were GPI-AP deficient cells. Interestingly, T-cells in both cases displayed a normal phenotype suggesting that the PIGA gene mutation was selectively acquired in a common myeloid progenitor (CMP). From sorted populations of PNH+ and normal type granulocytes (case 1 only) or T cells (case 2), the JAK2V617F mutant clone was found to co-exist with the PIGA mutation using allele-specific polymerase chain reaction (PCR). Real-time quantitative PCR using primers and probe to the junction of exon 5-6 coding region demonstrated drastically low to absent mRNA transcript expression of PIGA only in PNH-type granulocytes in both cases. Individual RT-PCR of the coding region of each exon (2-6) confirmed that transcription was absent in case 1 but limited to regions encoded by exons 2,4, and 6 in case 2. These results suggest that case 2 possesses a splicing mutation involving exon 5 to 6. In conclusion, JAK2V617F mutation is known to cause the constitutive activation of the JAK-STAT signaling pathway, and leads to autonomous cell growth in a cytokine-independent expansion of HPCs. While it has been reported that JAK2V617F mutation occurs in roughly 50% of primary Budd-Chiari syndrome and in 15 patients of 163 (9.2%) (Hoekstra et al, Journal of Hepatology, 6:19, 2009) of patients with PNH, these findings implicate co-existing JAK2V617F /PIG-A mutations may contribute clinically to specific manifestations of splenic venous thrombosis or hepatic vein thrombosis in association with intravascular coagulation and myelodysplasia. DisclosuresNo relevant conflicts of interest to declare.

Splenic and portal vein thrombosis following laparoscopic splenectomy in a pediatric patient with chronic myeloid leukemia

Splenic or portal vein thrombosis is a rare complication following splenectomy. We report a case of splenic and portal venous thrombosis in a 10-year-old girl with chronic myeloid leukemia who underwent laparoscopic splenectomy prior to bone marrow transplant. Clinical suspicion of such thrombosis should be high for patients who have had splenectomy. The diagnosis is confirmed by Doppler ultrasound or contrast-enhanced computed tomography; magnetic resonance imaging magnetic resonance angiography or arteriography can also be used. Proposals for postoperative screening protocols are discussed. Patients with primary myeloproliferative disorders are at increased risk of portal vein thrombosis, independent of surgical intervention, perhaps due to platelet dysfunction resulting from abnormalities of pluripotent stem cells. Marked splenomegaly (with larger draining veins) is thought to increase the risk of thrombosis.

INTESTINAL AND MULTIVISCERAL TRANSPLANTATION FOR PORTOMESENTERIC VENOUS THROMBOSIS: TECHNICAL CONSIDERATIONS AND THERAPEUTIC EFFICACY

P607 Aims: Splanchnic arterial and venous thrombosis is second most common indication for visceral transplantation. The underlying etiology, disease gravity and extent of thrombosis should guide the decision-making process and influence post-transplant outcome. This study is the first to address the different causes of splanchnic thrombosis, indications for each type of the visceral allograft, and survival outcomes. Methods: Between May 1990 and March 2004, 135 consecutive adult patients received 148 intestinal allografts at the University of Pittsburgh. Of these, 48(36%) were transplanted due to splanchnic thrombosis that was limited to the portomesenteric venous system in 20. Diagnosis was with abdominal imaging studies including visceral angiography. Age ranged from 23 to 65 years with a median of 45. Twelve patients suffered from short gut syndrome prior to transplantation and the remaining 8 required full visceral replacement because of variceal bleeding and hepatic failure. Results: Visceral venous thrombosis was due to protein C, S and anti-thrombin III deficiency in 3, Factor V/II mutation in 2, antiphospholipid antibodies in 3, myeloproliferative disorder in 3 and unknown etiology in the remaining 9 patients. The required intestinal allograft was tailored to intestine alone in 6(30%), combined liver-intestine in 4(20%) and multivisceral in 10(50%) patients. The median operative time (hr) was 12 for intestinal 18 for liver-intestinal, and 15 for multivisceral transplantation with an average blood loss of 4, 14 and 23 units, respectively. The pre-transplant liver functions were preserved in all of isolated intestinal recipients and the allograft venous outflow was drained into the recipient vena cava. In two of these, a splenorenal shunt was performed one year prior to transplant for treatment of gastric varcies in presence of chronic anticoagulation therapy. In 3 out of the 4 combined liver-intestinal recipients, systemic venous drainage of the retained left upper abdominal organs was via non-conventional portosystemic shunts. All of multivisceral recipients had combined extensive portomesenteric and splenic venous thrombosis with diffuse minute collaterals combined with Budd-Chiari(3), diabetes(2), renal failure(2) and hepatocellular carcinoma(1). All recipients were anticoagulated despite hepatic replacement. With a mean follow-up of 23±27 months, 14 recipients were alive with a cumulative survival rate of 79% at 6 months and 67% at 5 years. Causes of patient death were graft failure(1), upper gastrointestinal hemorrhage(1), enteric leak(1) and opportunistic infections(3). All of 14 survivors were free of TPN enjoying unrestricted oral diet 6 months to 8 years after transplantation. Conclusions: Despite disease gravity, inherent technical complexity and associated morbidity, intestinal and multivisceral transplantation are effective therapeutic modalities for patients with symptomatic splanchnic venous thrombosis. Thorough pretransplant evaluation with proper tailoring of the required allograft is mandatory for successful outcomes.

Vascular complications of pancreas transplantation.

The purpose of our study was to focus on the early diagnosis and treatment of vascular complications after simultaneous pancreas-kidney (SPK) transplantation. Description of the technique for salvage of the graft after venous thrombosis (VT) is also provided. From July 1994 to December 2002, 14 patients of 206 SPK transplant recipients had partial VT. Partial splenic VT (PSVT) was documented in 10 patients (4.8%), two had complete thrombosis of the splenic vein, one partial superior mesenteric thrombosis, and one developed partial thrombosis of the splenic and superior mesenteric vein. Four patients developed complete VT of the pancreas allograft and one superior mesenteric artery thrombosis. Our experience with four arteriovenous fistulae is also reported. The immunosuppression included tacrolimus, steroids, and monoclonal antibody to the IL-2 receptor. Thymoglobulin was introduced in June 2000 in our protocol combined with rapamycin or mycophenolate mofetil. These cases were identified following the intravenous (iv) use of tacrolimus with or without anti-IL-2R therapy. One case of complete VT is also reported one month following transplantation in a recipient with high rapamycin levels. Diagnosis was established during routine color Doppler ultrasonography. Partial VT was effectively treated with anticoagulation. Complete VT required surgical thrombectomy. In our series, the pancreas was salvaged successfully in all patients with the technique described here. Early diagnosis of vascular complications after pancreas transplantation is of paramount importance for the appropriate treatment with organ salvage. Based on our experience, we suggest that VT can be effectively treated with anticoagulation. Aspirin is sufficient for PSVT.

Partial venous thrombosis of the pancreatic allografts after simultaneous pancreas-kidney transplantation.

Despite new advances in transplantation, complete venous thrombosis (VT) of the pancreas after simultaneous pancreas kidney (SPK) transplantation usually results in graft loss. Data are limited regarding the outcome and treatment of partial VT of the pancreas allograft. From July 1994 to December 1999, 126 patients with IDDM/end-stage renal disease underwent SPK with systemic bladder drainage at the University of Miami. We retrospectively reviewed our experience regarding the outcome and treatment options of partial VT of the pancreas allografts. From July 1994 to April 1997, partial VT was not seen in the first 66 SPK patients induced with anti-CD3 rnAb and oral or intravenous (i.v.) tacrolimus (TAC) in the operating room. From May 1997 to June 1999, 14 (29%) out of 48 patients had VT. These cases were identified following the i.v. use of TAC with anti-IL-2R antibody-induction therapy (7/15) or without (7/33). Partial thrombosis of the splenic vein (PTSV) was documented in 10 patients, 2 had complete thrombosis of the splenic vein (CTSV), 1 had partial thrombosis of the superior mesenteric vein (PTSMV), and 1 patient had PTSV and PTSMV. These were identified incidentally during routine color Doppler ultrasonography (CDU). None of these SPK recipients demonstrates a change in clinical parameters. The first 8 patients were systemically heparinized, followed by oral anticoagulation, except 1 patient with CTSV. He progressed to complete thrombosis of the pancreas allograft and was treated with percutaneous thrombectomy and urokinase infusion, followed by heparinization and oral anticoagulation. One patient required exploration for bleeding. In an attempt to reduce the morbidity of heparinization, we treated the next 6 patients with PTSV with aspirin followed by serial CDU. All 14 patients had preservation of the endocrine and exocrine pancreatic functions. CDU showed resolution with recanalization of the thrombosed vein(s). From July 1999 to December 1999, 12 SPK recipients were administered TAC orally with or without induction therapy with anti-IL-2R antibody. So far, in this group, VT has not been identified. In summary, a total of 14 out of 126 patients (11%) had isolated VT with a mean follow-up of 36.4 months. Based on our experience, we suggest that extensive VT after pancreas transplantation, including splenic and superior mesenteric VT, be treated with heparin and subsequent oral anticoagulation for 3 months. For more limited, partial splenic VT, aspirin may be sufficient. Follow-up CDU is critical for a successful outcome. The i.v. use of TAC appears to be a risk factor for the increased incidence of VT. Currently, using IL-2rmAb as induction, TAC is started orally on postoperative days 3 or 4 and aspirin on postoperative day 2.

Occlusions vasculaires spléniques au cours du cancer du pancréas

Pancreatic cancer is responsible for 6,000 deaths per year in France. During the course of the disease, venous thrombosis is common. Conversely, arterial thrombosis is rarely described. We report the case of a 59-year-old patient with pancreatic adenocarcinoma. Treatment by gemcitabine allowed rapid and persistent improvement of the body weight and a prolonged survival (18 months). Sudden complication, i.e. splenic arterial thrombosis, reversed the favorable outcome. Splenic venous thrombosis is a frequent complication occurring in the course of pancreatic cancer. It is easily diagnosed using abdominal computerized tomography. Arterial thrombosis is rarely observed. It might be due to either sporadic, unexpected, occurrence of cases related to the evolution of underlying pathological mechanisms, or to omitted treatment of vascular complications, as until the introduction of new anticancer drugs this disease was considered to be of very poor prognosis.

Preliminary clinical application of contrast-enhanced MR portography.

The clinical application of contrast enhanced (CE) MR was evaluated. A total of 66 CE MR portograms were obtained by performing fast imaging with steady procession (FISP) technique on a 1.5-T Siemens magnetom vision. A maximum intensity projection algorithm was also employed to include all vessels in a single image. The patency of portal venous system, the presence and extent of varices were also evaluated. The results showed that all images had diagnostic quality. Main portal vein (MPV) and its 4th-6th level intrahepatic branches were visualized in 10 normal persons serving as control. The diameter of MPV, splenic vein and superior mesenteric vein was 1.02 +/- 0.21, 0.8 +/- 0.15, 0.8 +/- 0.26 cm respectively, which were significantly lower than that in portal hypertension patients (1.38 +/- 0.27, 1.26 +/- 0.18, 1.24 +/- 0.18 cm, respectively). In 23 preoperative cases of portal hypertension, dilated portal vein and tortuous enlarged splenic vein were found in 23 cases; esophageal and coronary varices in 12 and 19 cases, respectively. In 7 postoperative re-examined cases with portal hypertension, the flow velocity and flow of MPV were decreased in all cases and esophageal varices could still be observed in 3 cases. New vessels appeared in the great curvature of stomach in 2 cases. In 20 cases of liver carcinoma, occlusion of MPV or its intrahepatic branches were showed in 14, compression and dislocation of intrahepatic portal vein were found in 6. In other 6 cases, 2 were splenic venous thrombosis and 4 were tumors in the intestine or retro-peritoneum. It is concluded that three-dimensional CE MR portography is an accurate technique for evaluating the portal venous system. It is a reliable and noninvasive technique that can provide important information for the evaluation of patients' condition before TIPSS and liver transplantation.

Functional Deficiency of Protein C Associated with Mesenteric Venous Thrombosis and Splenic Infarction

A 16-year-old girl had abdominal pain, hematemesis, and fever. Radiographic evaluation showed her to have an infarcted spleen and jejunum. Pathologic description revealed thrombi involving the vessels of both organs. A hypercoagulation evaluation of the patient and her family resulted in the diagnosis of hereditary protein C activity deficiency. She is unusual both in the diagnosis of protein C activity deficiency and in her appearance with mesenteric and splenic venous thrombosis. This appearance has not been previously reported in the literature and should be considered in the differential diagnosis of any thrombotic event, even in the face of a negative family history.

Portal, Mesenteric, and Splenic Venous Thrombosis after Endoscopic Injection Sclerotherapy

Portal, Mesenteric, and Splenic Venous Thrombosis after Endoscopic Injection Sclerotherapy

Splenic and portal venous thrombosis: A vascular complication of pancreatic disease demonstrated on computed tomography

Portal and splenic venous thrombosis is a rare but well recognised complication of pancreatic carcinoma and pancreatitis. We report a series of five patients with pancreatic disease in whom CT detected this complication. The appearances on CT are of an enlarged vein with a centre of lower attenuation which does not enhance following intravenous contrast injection, ring enhancement and opacification of collateral veins. Splenic vein thrombosis following pancreatitis should be considered in all patients with pancreatic disease as this complication is increasingly recognised as a cause of upper gastrointestinal haemorrhage from varices.