Acute Pancreatitis Complicated by Massive Inferior Vena Cava and Right Atrial Thrombosis: A Case Report Kangeui Lee, Jung-In Ko, and Taejin Park, Seoul, Korea
Venous thrombosis is a relatively common complication of acute pancreatitis. A 58-year-old man came to our emergency department with abdominal pain. Pancreatitis complicated with a huge thrombosis through inferior vena cava (IVC) to right atrium and left renal vein was diagnosed. Gabexate and enoxaparin were administered for pancreatitis and thrombosis. Surgical removal of thrombosis was considered but was not possible because of poor general condition. Despite conservative management, the patient expired. We believe this is the first case of pancreatitis complicated by right atrial thrombosis.
Venous thrombosis is a relatively common complication of acute pancreatitis, which mainly involves the splenic, portal, and superior mesenteric vein. We experienced a very rare case of a 58-year-old male patient with acute pancreatitis complicated by a huge thrombosis through inferior vena cava (IVC) to right atrium and left renal vein; hence, we report the case.
CASE REPORT A 58-year-old man presented to the emergency department with mental change and right-upper-quadrant (RUQ) abdominal pain. He was a heavy alcoholic, with alcohol consumption of about 150 mL/day. He had a past medical history of chronic pancreatitis and duodenal ulcer. His initial blood pressure was 160/ 86 mm Hg with heart rate of 114 beats/min, respiratory rate was 20 breaths/min, body temperature via
Conflicts of Interest: The authors declare that they have no conflicts of interest and financial disclosures to report. Department of Emergency Medicine, National Medical Center, Seoul, Korea. Correspondence to: Taejin Park, MD, Department of Emergency Medicine, National Medical Center, 18-79, 6-ka, Ulchiro, Choong-ku, Seoul 100-799, Korea; E-mail: [email protected]
Ann Vasc Surg 2015; 29: 1020.e7–1020.e10 http://dx.doi.org/10.1016/j.avsg.2015.01.019 Ó 2015 Elsevier Inc. All rights reserved. Manuscript received: August 4, 2014; manuscript accepted: January 16, 2015; published online: March 9, 2015.
tympanic membrane was 34.0 C, and O2 saturation via pulse oximeter was 99%. In physical examination, there was no specific finding except RUQ abdominal tenderness. In laboratory data, amylase (>2,400 U/L) and lipase (>400 U/L) were elevated, consistent with acute pancreatitis. The liver function tests were nonspecific with slightly elevated aspartate transaminase of 65 U/L, alanine transaminase of 13 U/L, and total bilirubin of 1.1 mg/dL. Albumin level was decreased by 2.5 g/dL. His initial glucose level was 10 mg/dL. A full evaluation for clotting disorders was done, which showed positive results for coagulopathy and disseminated intravascular coagulation. There was no thrombocytopenia (156 103/mL), but both prothrombin time and activated partial thromboplastin time were prolongated (2.41 international normalized ratio and 68.4 seconds, respectively). The antithrombin III, protein C, and protein S levels were low (38%, 45%, and 9%, respectively). The fibrinogen level was low (60 mg/dL), but FDP and D-dimer levels were very high (120 and >20 mg/mL, respectively). In abdominopelvic contrast-enhanced computed tomography (CT), massive thrombosis in left renal vein and from IVC up to right atrium with perisplenic and hepatoduodenal pseudocyst, acute fluid collection in aortocaval space, and pancreatic calcification consistent with acute pancreatitis on chronic pancreatitis were seen (Fig. 1). His mentality was recovered after infusion of 50% dextrose solution. Passive rewarming was done via blanket, and fever of 38.8 C was checked after 4 hours. Empiric antibiotics were given because of fever. He was admitted to the intensive care unit. Gabexate and
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Fig. 1. CT findings at admission. (A) Axial image at right atrium level, (B) axial image at pancreas level, (C) coronal image at atrium level, (D) coronal image at IVC and renal vein level. Perisplenic and hepatoduodenal
pseudocyst, acute fluid collection in aortocaval space, and pancreatic calcification were seen (arrow). Massive thrombosis in left renal vein and IVC extending to right atrium was seen (arrowhead ).
enoxaparin were administered to manage acute pancreatitis and huge thrombus. Surgical removal of thrombus was considered to prevent life-threatening thromboembolic complications but was not possible because of poor general condition. A follow-up CT was taken on the 19th hospital day, which showed partial resolution of the thrombus (Fig. 2). Despite intensive care, the patient’s condition worsened and expired on the 55th hospital day.
previously reported cases, and thrombosis extending to the right atrium has not been reported. The pathogenesis of venous thrombosis involves stasis, spasm, and mass effect from the surrounding inflamed pancreas and direct damage of the venous wall by liberated pancreatic enzymes.4 And, thrombosis is most commonly associated with chronic pancreatitis, but a single event of acute pancreatitis is also able to cause thrombotic complications.5,6 In this case, we think direct venous wall injury by pancreatic enzymes was the cause of thrombus formation. No correlation between the severity of pancreatitis and complicated thrombosis is proven,4 so clinicians should be highly suspicious even in asymptomatic pancreatitis. There are various ways for treating pancreatitisassociated thrombosis, depending on the involved vessel and patient’s conditions: surgical management, radiologic interventions, thrombolysis, systemic anticoagulation, and management of underlying pancreatitis alone. There is no
DISCUSSION Vascular complication of pancreatitis includes venous thrombosis, arterial hemorrhage, and pseudoaneurysm formation.1 Among which, venous thrombosis is the most common with an incidence of 1.8e15%.2,3 Splenic vein is most commonly involved with an incidence of 11e19%, followed by portal and superior mesenteric vein (7e13% and 2e14%, respectively).2,4 Involvement of the IVC is relatively rare with 7 reported cases and involvement of the renal vein is rarer with 3
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Fig. 2. Comparison between CT findings at admission [(A) atrium, (C) IVC] and 19th hospital day [(B) atrium, (D) IVC]. Follow-up CT scan revealed partial resolution of the thrombus (arrowheads).
established guideline regarding the treatment of thrombosis complicated by pancreatitis, but anticoagulation using heparin with subsequent warfarin is the most commonly used treatment,7 whereas some reports suggest that there is not any significant difference in recanalization rate after anticoagulation.2,3,8 Still, it is certain that the earlier the treatment is given, the better the outcome.7,8 Enoxaparin was used for anticoagulation in this case because subcutaneous enoxaparin was proven as effective and as safe as dose-adjusted, unfractionated heparin, in many reports.9 Medications regulating coagulation, such as antithrombin and thrombomodulin, might have been an option because antithrombin III and protein C and S levels were low but was not used because of insurance and cost problems.10,11 Regarding the treatment of IVC thrombosis itself, vena caval filters may be an option, when anticoagulation is an absolute contraindication, when adverse effects of anticoagulation occurred, so that the need for discontinuation of anticoagulation arises, when thrombosis propagates or recurred despite adequate anticoagulation, or when pulmonary embolism could not be
tolerated because of reduced cardiopulmonary function.12 Thrombolysis or mechanical thrombectomy may be indicated in patients with occlusive symptoms.13 In this case, anticoagulation combined with mechanical thrombectomy of the thrombus would have been a favorable treatment strategy, but mechanical thrombectomy was not undertaken because the patient’s general condition did not support the surgery and the patient showed no lifethreatening occlusive symptoms. We think the patient died from septic complications because the patient showed persistent fever and low blood pressure, in spite of aggressive antibiotic treatment. REFERENCES 1. Mallick IH, Winslet MC. Vascular complications of pancreatitis. JOP 2004;5:328e37. 2. Gonzelez HJ, Sahay SJ, Samadi B, et al. Splanchnic vein thrombosis in severe acute pancreatitis: a 2-year, singleinstitution experience. HPB (Oxford) 2011;13:860e4. 3. Harris S, Nadkarni NA, Naina HV, et al. Splanchnic vein thrombosis in acute pancreatitis: a single-center experience. Pancreas 2013;42:1251e4.
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4. Mortel e KJ, Mergo PJ, Taylor HM, et al. Peripancreatic vascular abnormalities complicating acute pancreatitis: contrast-enhanced helical CT findings. Eur J Radiol 2004;52:67e72. 5. Lillemoe KD, Yeo CJ. Management of complications of pancreatitis. Curr Probl Surg 1998;35:1e98. 6. Johnston FR, Myers RT. Etiologic factors and consequences of splenic vein obstruction. Ann Surg 1973;177: 736e9. 7. Ponziani FR, Zocco MA, Campanale C, et al. Portal vein thrombosis: insight into physiopathology, diagnosis, and treatment. World J Gastroenterol 2010;16:143e55. 8. Plessier A, Darwish-Murad S, Hernandez-Guerra M, et al. Acute portal vein thrombosis unrelated to cirrhosis: a prospective multicenter follow-up study. Hepatology 2010;51: 210e8.
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9. Merli G, Spiro TE, Olsson CG, et al. Subcutaneous enoxaparin once or twice daily compared with intravenous unfractionated heparin for treatment of venous thromboembolic disease. Ann Intern Med 2001;134:191e202. 10. Maclean PS, Tait RC. Hereditary and acquired antithrombin deficiency: epidemiology, pathogenesis and treatment options. Drugs 2007;67:1429e40. 11. Schwartz RS, Bauer KA, Rosenberg RD, et al. Clinical experience with antithrombin III concentrate in treatment of congenital and acquired deficiency of antithrombin. The Antithrombin III Study Group. Am J Med 1989;87:53se60s. 12. Rutherford RB. Prophylactic indications for vena cava filters: critical appraisal. Semin Vasc Surg 2005;18: 158e65. 13. Vedantham S. Interventional approaches to deep vein thrombosis. Am J Hematol 2012;87(Suppl 1):S113e8.