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      Acute pancreatitis complicated with deep vein thrombosis and pulmonary embolism: a case report

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          Abstract

          Background

          Acute pancreatitis is an acute inflammatory process of the pancreas that can trigger a systemic inflammatory response. Pulmonary embolism refers to obstruction of the pulmonary artery or one of its branches by material (usually a thrombus) that originated elsewhere in the body. Extensive lower limb deep vein thrombosis with pulmonary embolism is a rare complication of acute pancreatitis that has been described in a few case reports. Deep vein thrombosis and hypercoagulable states in pancreatitis are thought to be due to release of pancreatic proteolytic enzymes from a cyst that is connected to the pancreatic duct and penetrates into a vessel. Proteolytic damage or inflammation of the vessels may also play a significant part. Acute pancreatitis also causes a systemic inflammatory response that has effects on an endothelium-dependent relaxing response for acetylcholine.

          Case presentation

          A 38-year-old Sri Lankan man presented with acute pancreatitis and later he developed progressive abdominal distention with bilateral ankle edema. A contrast-enhanced computed tomographic scan showed two pancreatic pseudocysts and deep vein thrombosis in both lower limbs, as well as a pulmonary embolism involving the right lower lobe pulmonary artery and the left segmental pulmonary arteries. One of the pseudocysts in the head of the pancreas was compressing the inferior vena cava without direct communication. The patient’s thrombophilia screen result was negative. He was started on subcutaneous enoxaparin 1 mg/kg twice daily and warfarin to achieve a target international normalized ratio of 2–3.

          Conclusions

          Deep vein thrombosis with pulmonary embolism is a rare but life-threatening complication of acute pancreatitis. Once diagnosed, early treatment with intravenous heparin or thrombolysis is effective. Patients with severe acute pancreatitis may be at risk of deep vein thrombosis due to immobilization and other mechanisms, but anticoagulation as prophylaxis is often not used. However, it may be considered on a case-by-case basis in patients with pancreatitis who are acutely ill and immobilized, need intensive care unit admission, and have multiple risk factors for deep vein thromboembolism. Further studies must be undertaken to determine guidelines for deep vein thromboembolism prophylaxis in these patients.

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          Most cited references9

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          Prevention of venous thromboembolism: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition).

          This article discusses the prevention of venous thromboembolism (VTE) and is part of the Antithrombotic and Thrombolytic Therapy: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Grade 1 recommendations are strong and indicate that the benefits do or do not outweigh risks, burden, and costs. Grade 2 suggestions imply that individual patient values may lead to different choices (for a full discussion of the grading, see the "Grades of Recommendation" chapter by Guyatt et al). Among the key recommendations in this chapter are the following: we recommend that every hospital develop a formal strategy that addresses the prevention of VTE (Grade 1A). We recommend against the use of aspirin alone as thromboprophylaxis for any patient group (Grade 1A), and we recommend that mechanical methods of thromboprophylaxis be used primarily for patients at high bleeding risk (Grade 1A) or possibly as an adjunct to anticoagulant thromboprophylaxis (Grade 2A). For patients undergoing major general surgery, we recommend thromboprophylaxis with a low-molecular-weight heparin (LMWH), low-dose unfractionated heparin (LDUH), or fondaparinux (each Grade 1A). We recommend routine thromboprophylaxis for all patients undergoing major gynecologic surgery or major, open urologic procedures (Grade 1A for both groups), with LMWH, LDUH, fondaparinux, or intermittent pneumatic compression (IPC). For patients undergoing elective hip or knee arthroplasty, we recommend one of the following three anticoagulant agents: LMWH, fondaparinux, or a vitamin K antagonist (VKA); international normalized ratio (INR) target, 2.5; range, 2.0 to 3.0 (each Grade 1A). For patients undergoing hip fracture surgery (HFS), we recommend the routine use of fondaparinux (Grade 1A), LMWH (Grade 1B), a VKA (target INR, 2.5; range, 2.0 to 3.0) [Grade 1B], or LDUH (Grade 1B). We recommend that patients undergoing hip or knee arthroplasty or HFS receive thromboprophylaxis for a minimum of 10 days (Grade 1A); for hip arthroplasty and HFS, we recommend continuing thromboprophylaxis > 10 days and up to 35 days (Grade 1A). We recommend that all major trauma and all spinal cord injury (SCI) patients receive thromboprophylaxis (Grade 1A). In patients admitted to hospital with an acute medical illness, we recommend thromboprophylaxis with LMWH, LDUH, or fondaparinux (each Grade 1A). We recommend that, on admission to the ICU, all patients be assessed for their risk of VTE, and that most receive thromboprophylaxis (Grade 1A).
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            Vascular complications of pancreatitis.

            Vascular complications of pancreatitis are a major cause of morbidity and mortality. Arterial complications include haemorrhage from direct arterial erosion or pseudoaneurysm formation, and visceral ischaemia. Venous complications predominantly are related to splanchnic vein thrombosis. This review, with illustrative cases, describes the main manifestations of these complications and emphasizes the importance of early radiological diagnosis and intervention.
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              Pulmonary vascular injury in pancreatitis: evidence for a major role played by pancreatic elastase.

              Using an experimental model of pancreatitis in the rat, the role of trypsin and elastase in mediating lung vascular injury in this condition was examined. The induction of pancreatitis by injection of sodium cholate in the pancreas resulted in a significant decrease in serum trypsin inhibitory capacity, and in a complete saturation of serum elastase inhibitory capacity matched by the appearance of endothelial injury of pulmonary capillaries and edema formation. The complete lack of serum elastase inhibitory capacity was associated with the presence of elastase activity in serum and bronchoalveolar lavage (BAL) fluids. The pretreatment of animals with N-furoyl saccharin (a potent inhibitor of many serine proteinases) prevented lung capillary injury and the imbalance of serum proteinase-anti-proteinase activities as well as the appearance of any elastolytic activity in serum and BAL fluids. These findings which clearly demonstrate the protease dependence of the pulmonary vascular injury in our experimental model, strongly suggested a major role for elastase(s). The suppression, in the experimental model, of the serum elastase inhibitory capacity by using chloramine-T resulted in an earlier onset of lung vascular damage, a marked worsening of pulmonary lesions, and an increase of elastolytic levels in serum and BAL fluids. Furthermore the physical properties of the protein molecule with enzyme activity detected in BAL fluids were consistent with those of rat pancreatic elastase. The reported data strongly support the hypothesis that pancreatic elastase plays a major role in the development of pulmonary vascular injury after acute pancreatitis.
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                Author and article information

                Contributors
                tharukaherath11@gmail.com
                Journal
                J Med Case Rep
                J Med Case Rep
                Journal of Medical Case Reports
                BioMed Central (London )
                1752-1947
                23 June 2016
                23 June 2016
                2016
                : 10
                : 182
                Affiliations
                National Hospital Of Sri Lanka, Colombo, Sri Lanka
                Article
                968
                10.1186/s13256-016-0968-6
                4917977
                27339635
                181f427c-8665-4d9f-89b5-8ab694932a26
                © The Author(s). 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 6 March 2016
                : 2 June 2016
                Categories
                Case Report
                Custom metadata
                © The Author(s) 2016

                Medicine
                acute pancreatitis,deep vein thrombosis,pulmonary embolism,case report
                Medicine
                acute pancreatitis, deep vein thrombosis, pulmonary embolism, case report

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