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Vascular Complications in Patients with Chronic Pancreatitis

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Vascular Complications in Patients with Chronic Pancreatitis Journal of Clinical Medicine Article Vascular Complications in Patients with Chronic Pancreatitis Miroslav Vujasinovic 1,2,* , Ana Dugic 2 , Amar Nouri 2, Torkel B Brismar 3 , Francisco Baldaque-Silva 1,2, Ebba Asplund 2, Wiktor Rutkowski 1,2, Poya Ghorbani 1,4 , Ernesto Sparrelid 1,4, Hannes Hagström 1,2,5 and J.-Matthias Löhr 1,4 1 Department of Upper Abdominal Diseases, Karolinska University Hospital, 141 86 Stockholm, Sweden; [email protected] (F.B.-S.); [email protected] (W.R.); [email protected] (P.G.); [email protected] (E.S.); [email protected] (H.H.); [email protected] (J.-M.L.) 2 Department of Medicine, Huddinge, Karolinska Institutet, 141 86 Stockholm, Sweden; [email protected] (A.D.); [email protected] (A.N.); [email protected] (E.A.) 3 Department of Radiology, Karolinska University Hospital, 141 86 Stockholm, Sweden; [email protected] 4 Department of Clinical Science, Intervention, and Technology (CLINTEC), Karolinska Institutet, 141 86 Stockholm, Sweden 5 Clinical Epidemiology Unit, Department of Medicine, Solna, Karolinska Institutet, 171 77 Stockholm, Sweden * Correspondence: [email protected]; Tel.: +46-(0)-72-469-49-38; Fax: +46-(0)-8-5858-2335 Abstract: Introduction: Chronic pancreatitis (CP) is a long-standing progressive inflammation of the pancreas, which can lead to a variety of vascular complications, such as splanchnic venous thrombosis (VT) and arterial pseudoaneurysm (PA). There is a lack of studies on vascular complications in Citation: Vujasinovic, M.; Dugic, A.; Scandinavian countries. Methods: We performed a retrospective analysis of medical records of Nouri, A.; Brismar, T.B.; patients with CP identified from the Karolinska University Hospital database between 2003 and 2018. Baldaque-Silva, F.; Asplund, E.; A total of 394 patients with definite CP were included in the study. Results: There were 33 patients Rutkowski, W.; Ghorbani, P.; with vascular complications, with a median age of 62 (IQR 55–72) years. The cumulative incidence of Sparrelid, E.; Hagström, H.; et al. vascular events was 3.2% at 5 years. Thirty patients had isolated VT, whereas three patients had PA Vascular Complications in Patients (7.6% and 0.8%, respectively). Isolated splenic vein thrombosis was most common (53.3%), followed with Chronic Pancreatitis. J. Clin. by a combination with other splanchnic veins. PA was found in the splenic artery in two patients Med. 2021, 10, 3720. https://doi.org/ 10.3390/jcm10163720 and in the left gastric artery in one patient. Varices were present in three (10%) patients; variceal bleeding was not recorded. All patients had asymptomatic splanchnic VT, most with chronic VT with Academic Editors: Andrea Mancuso, developed collaterals (83.3% had abdominal collateral vessels). Nearly two-thirds of patients with Giovanni Perricone, Xingshun Qi and VT (63.3%) received no treatment, whereas 11 (36.6%) were treated with anticoagulants. Pseudocysts Dominique Valla and alcoholic etiology of CP are risk factors for vascular complications. Conclusions: The cumulative incidence of vascular complications was 3.2% at 5 years. Splanchnic VT is more common than PA. Received: 19 July 2021 Patients were asymptomatic with no variceal bleeding, explained by well-developed collateral vessels Accepted: 20 August 2021 and strong study inclusion criteria. Published: 21 August 2021 Keywords: chronic pancreatitis; splanchnic circulation; hepatic vein thrombosis; pseudoaneurysm; Publisher’s Note: MDPI stays neutral vascular complications with regard to jurisdictional claims in published maps and institutional affil- iations. 1. Introduction Chronic pancreatitis (CP) is characterized by the progressive inflammation of the pancreas, which can lead to a variety of life-threatening long-term complications [1]. Copyright: © 2021 by the authors. Vascular sequelae of CP include splanchnic venous thrombosis (VT) and arterial pseudoa- Licensee MDPI, Basel, Switzerland. neurysm (PA). This article is an open access article distributed under the terms and Consequences of pancreatitis-associated splanchnic VT are manifested in a pathophys- conditions of the Creative Commons iological pathway starting with a localized form of portal hypertension, venous hyperten- Attribution (CC BY) license (https:// sion in the splenoportal and/or gastroepiploic systems ultimately leading to oesophageal, creativecommons.org/licenses/by/ gastric or colonic varices [2]. A systematic review and meta-analysis of observational 4.0/). studies showed a pooled prevalence of splanchnic VT of 13.6% in all types of pancreatitis, J. Clin. Med. 2021, 10, 3720. https://doi.org/10.3390/jcm10163720 https://www.mdpi.com/journal/jcm J. Clin. Med. 2021, 10, 3720 2 of 9 with a pooled prevalence of splanchnic VT of 16.6% and 11.6% in patients with acute and chronic pancreatitis, respectively [2]. Risk factors for splanchnic VT include persistent acquired risk factors (liver cirrhosis, cancers, inflammatory bowel disease, antiphospho- lipid syndrome, autoimmune diseases), transient acquired risk factors (abdominal surgery, hormonal therapy, pregnancy, puerperium, abdominal infections) and inherited risk fac- tors (factor V Leiden mutation, protein C deficiency, protein S deficiency, antithrombin deficiency, JAK2V617F mutation, prothrombin G20210A mutation) [3]. The prevalence of splanchnic VT in acute and chronic pancreatitis was higher (16.9%) in Europe, compared to studies from America (11.5%) and Asia (8.5%) [2]. There is significant variability in the reported risk for arterial PA in pancreatitis. A recently published meta-analysis showed the pooled incidence rates of PA in acute and chronic pancreatitis were 0.05% and 0.03%, respectively [4]. Angiographic embolization is the method of choice for the treatment of PA [1] and shows a high technical and clinical success rate [4]. There is a lack of studies on vascular complications in Scandinavian countries. We aim to fill the knowledge gap on VT and PA through a retrospective analysis of patients with CP in a high-volume tertiary center. 2. Methods 2.1. Patients We performed a retrospective analysis of medical records of patients presented with CP at the Department of Upper Abdominal Diseases at Karolinska University Hospital. Patients with ICD codes for CP (K86.0 and K86.1) were identified in our database between 2003 and 2018. The definite diagnosis of CP was determined according to M-ANNHEIM criteria [5]. We excluded patients <18 years at the time of data analysis, patients with cancers in the abdominal cavity, patients with cirrhosis of the liver, patients without a Swedish personal identity number, patients with probable CP according to M-ANNHEIM criteria, patients diagnosed with vascular complications before or at the time of CP diagnosis, and patients who have previously undergone pancreatic surgery or splenectomy. We initially identified 954 patients with CP, and after application of the above-mentioned exclusion criteria, 394 patients were included in the final analysis (Figure1). 2.2. Definitions Definite CP was diagnosed by imaging (computed tomography (CT), magnetic res- onance imaging (MRI) or both, with one or more of the following criteria: (a) pancreatic calcifications, (b) moderate or marked ductal lesions, (c) marked and persistent exocrine insufficiency defined as pancreatic steatorrhea markedly reduced by enzyme supplementa- tion or (d) typical histology of an adequate histological specimen). Vascular complications (VT and PA) were detected by contrast enhanced CT, MRI or both. We used the data from institutional imaging reports performed and signed by two independent radiologists according to routines at our hospital. J. Clin. Med. 2021, 10, x FOR PEER REVIEW 3 of 10 J. Clin. Med. 2021, 10, 3720 3 of 9 Patients with ICD codes for chronic pancreatitis (K 86.0 and K86.1) identified in the database between 2003-2018 Excluded patients with: (N = 954) • Missing data or wrong diagnosis (N = 150) • probable CP (N = 209) •PDAC (N = 20) • Liver cirrhosis (N = 12) • History of HPB surgery or splenectomy (N = 154) • VC before or at the time of CP diagnosis (N = 15) Patients with definite chronic pancreatitis (N = 394) Patients without vascular events Patients with vascular events (N = 33) (N = 361) • Venous thrombosis (N = 30) • Pseudoaneurysm (N = 3) Figure 1. Flow chart of patient selection. CP—chronic pancreatitis; PDAC—pancreatic ductal Figure 1. Flow chart of patient selection. CP—chronic pancreatitis; PDAC—pancreatic ductal ade- adenocarcinoma; HPB—hepato-pancreatico-biliary. nocarcinoma; HPB—hepato-pancreatico-biliary. 2.3. Follow Up 2.2. Definitions Follow-up began on the date of CP diagnosis. Data were censored at the time of the lastDefinite clinical CP contact was diagnosed with the patient by imaging or death. (computed tomography (CT), magnetic reso- nance imaging (MRI) or both, with one or more of the following criteria: (a) pancreatic calcifications,2.4. Antithrombotic (b) moderate Treatment or marked ductal lesions, (c) marked and persistent exocrine insufficiencyPatients defined weretreated as pancreatic with anticoagulant steatorrhea therapymarkedly according reduced to by local enzyme clinical supplemen- practice. The tationstandard or (d) initial typical treatment histology was of weight-adaptedan adequate histological subcutaneous specimen). application (200 IE/kg/day) of low-molecular-weightVascular complications heparin (VT and (LMWH) PA) were until de occurrencetected by ofcontrast collateral enhanced vessels. CT, The MRI duration or both.of therapyWe
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