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Omental Vein Catheter Thrombolysis for Acute Porto-Mesenteric Vein Thrombosis
Case Reports Omental Vein Catheter Thrombolysis for Acute Porto-Mesenteric Vein Thrombosis Annabelle L. Fonseca,1 Muriel A. Cleary,1 Walter Cholewczynski,2 Bauer E. Sumpio,1 and Nabil A. Atweh,2 New Haven and Bridgeport, Connecticut
Mesenteric venous thrombosis (MVT) is an uncommon clinical condition with potential high morbidity. We report here a patient who presented with acute-onset MVT and bowel infarction, which was successfully ameliorated with intramesenteric vein thrombolytic therapy.
CASE REPORT A 34-year-old woman presented with a 2-week history of episodic abdominal pain, nausea, and emesis that had worsened in the preceding 48 hours. She had no significant relevant medical or surgical history. She had recently started taking oral contraceptive pills. She was afebrile and hemodynamically stable. Her examination was significant for a soft, diffusely tender abdomen. Peritoneal signs were absent. There was no evidence of gastrointestinal (GI) bleeding; recent history of fever, weight loss, or early satiety; or significant family history. She had no history of deep vein thrombosis (DVT), pulmonary embolus (PE), or hypercoagulable state. Her admitting laboratory values were unremarkable with normal white blood cell count, platelets, coagulation panel, and hematocrit. Abdominal computed tomography (CT) revealed nonspecific mid-mesenteric inflammation, periportal edema, and concern for right portal vein nonoccluding thrombus (Fig. 1). She was admitted to a medical service and maintained on bowel rest and intravenous fluid hydration. A surgical consultation was obtained. Upper endoscopy revealed a normal esophagus
1 Department of Surgery, Yale University School of Medicine, New Haven, CT. 2 Department of Surgery, Bridgeport Hospital, Yale New Haven Health, Bridgeport, CT.
Correspondence to: Annabelle L. Fonseca, MD, Department of Surgery, Yale University School of Medicine, FMB 107, 333 Cedar Street, New Haven, CT 06511, USA; E-mail: [email protected] Ann Vasc Surg 2013; 27: 497.e1e497.e4 http://dx.doi.org/10.1016/j.avsg.2012.09.009 Ó 2013 Elsevier Inc. All rights reserved. Manuscript received: August 21, 2012; manuscript accepted: September 25, 2012; published online: April 8, 2013.
and duodenum and no evidence of upper GI bleeding. A work-up for hypercoagulable state was initiated. Two days later her hematocrit dropped to 16% from 34%. A repeat CT scan revealed complete thrombosis of the portal and mesenteric system, including the tributaries from the inferior mesenteric and splenic veins, new ascites, and bowel wall thickening (Fig. 2). Her examination now showed worsening abdominal tenderness that progressed to an acute abdomen. She was taken urgently to the operating room for an exploratory celiotomy. Intraoperative findings demonstrated serous ascitic fluid and a 75-cm segment of congested ischemic small bowel that was subsequently resected (Fig. 3). The liver appeared normal with no evidence of congestion or cirrhosis. A mesenteric portogram was obtained via a 6F catheter inserted into an omental vein and demonstrated no outflow from the thrombosed portomesenteric vein (Fig. 4A). Alteplase (2-mg doses) was injected with heparinized saline via the catheter, after which a follow-up portogram demonstrated improved visualization of the venous structures (Fig. 4B), but the portal structures were still not well defined. A decision was made to perform continuous thrombolytic therapy at 1 mg/hr and systemic heparinization, and therefore the catheter was secured in the omental vein. The patient’s abdomen was left open, and a temporary abdominal closure (TAC) was placed. She was started on total parenteral nutrition (TPN). On postoperative day 1 (POD 1) the patient underwent repeat portal venography through the indwelling catheter, which now showed some antegrade flow in the superior mesenteric vein but persistent residual thrombus. The portal vein was now visualized along with the right and left hepatic portal vein branches (Fig. 4C) with residual thrombus. It was decided to continue low-dose thrombolytic therapy at 0.5 mg/hr in the surgical intensive care unit. The patient remained hemodynamically stable
497.e1
497.e2 Case reports
Annals of Vascular Surgery
Fig. 1. Initial presenting CT revealed (A) stranding within the mid-abdominal mesentery, periportal edema, and (B) concern for right portal vein thrombosis versus contrast delay.
Fig. 2. (AeC) Repeat CT obtained on hospital day 3 revealed extensive portal vein thrombus involving the right and left portal vein, the main portal vein (A), and extending into the superior mesenteric vein (B). Also
seen was new, diffuse thickening of jejunal loops (C) with concern for ischemia versus congestion and new moderate ascites.
throughout and was returned to the operating room (OR) on POD 2 for reexploration and resection of any nonviable bowel. Two areas of ischemic small bowel, 20 cm at the proximal end and 10 cm distally, were resected. The patient’s intestines were left in discontinuity and a TAC was performed. On POD 4, she returned to the OR where all remaining bowel appeared viable. A completion small bowel anastomosis was performed, the mesenteric omental vein catheter was removed, thrombolytic therapy was ceased, and the abdominal wall was closed. She was continued on systemic anticoagulation with heparin. On POD 7, an intraabdominal collection was detected and percutaneously drained. On POD 16 fondaparinux was started, and systemic heparinization was discontinued. Her diet was slowly advanced without incident and she was cycled off TPN. She underwent layered closure of her abdominal wound on POD 24 and was subsequently discharged on POD 28 with a therapeutic international normalized ratio (INR). Six-month outpatient follow-up
revealed a healthy, asymptomatic patient who was tolerating her diet, gaining weight, and back to full employment. The pathologic examination of the resected bowel showed transmural hemorrhage, inflammation, and necrosisdall changes compatible with ischemia. Interestingly, her coagulation work-up revealed a low protein C level of 27% (normal 70e140%).
DISCUSSION Mesenteric venous thrombosis is a relatively rare disorder. It is estimated that about 2e6% of all cases of acute mesenteric ischemia are related to MVT.1,2 It can occur in acute, subacute, or chronic forms. Acute MVT is defined as new-onset symptomatic thrombosis of the superior mesenteric vein (SMV) or its branches, without evidence of collateralization.3
Vol. 27, No. 4, May 2013
Case reports 497.e3
Fig. 3. Intraoperative images of ischemic small bowel demonstrating (A) smaller segment of infarcted bowel (arrow) (B) surrounding large segments of edematous ischemic bowel.
Fig. 4. (A) Initial intraoperative mesenteric portogram demonstrating absence of mesenteric and portal vein flow. (B) Repeat intraoperative mesenteric portogram after thrombolytic therapy demonstrating improved
portal vein filling. (C) POD 1 repeat portal venogram demonstrating visualization of the portal vein and right and left hepatic veins.
This typically presents with sudden-onset abdominal pain, nausea, vomiting, and diarrhea. It is associated with a definite risk of bowel infarction. Subacute and chronic MVT, on the other hand, usually present more insidiously, and have a low risk of bowel infarction due to the development of venous collaterals.
MVT may be classified as either primary or secondary. Secondary MVT occurs in the presence of a predisposing risk factor. Protein C or S deficiency, antithrombin III deficiency, and polycythemia vera have been implicated as causes of MVT.4 Other causes, such as pregnancy,
497.e4 Case reports
contraceptive use, and malignancy, are also associated with hypercoagulable conditions that may predispose to MVT.4 The patient described here had an underlying protein C deficiency and had recently started contraceptive use, two conditions that may have predisposed her to the development of MVT. The treatment of MVT has not changed significantly since it was first described as a cause of intestinal infarction in 1895. Treatment consisted of bowel resection and delayed re-anastomosis.5 The more frequent use of CT scanning in patients with abdominal pain has significantly decreased the time from presentation to diagnosis.6 This early diagnosis presents a brief window of opportunity to treat patients with ischemic bowel, prior to the development of bowel infarction. The aim of treatment is to reestablish flow through the portomesenteric vein and conserve as much bowel as possible. Immediate heparinization is the first line of treatment. This approach has been shown to clearly increase survival, and is currently accepted standard therapy.3,7 Anticoagulation has been demonstrated to prevent recurrence of thrombosis after intestinal resection, and also to be associated with lower mortality if recurrence does occur.7 It has been suggested that anticoagulation with warfarin should be continued for 3e6 months in patients with a temporary risk factor, and should be administered lifelong for patients whose thrombosis is considered to be idiopathic or due to irreversible systemic conditions.3 Systemic thrombolysis with intravenous streptokinase and tissue plasminogen activator (tPA)8,9 or mechanical thrombectomy10 have been used successfully, especially with fresh thrombus localized to the SMV. Selective thrombolysis has been described utilizing the transjugular or transhepatic routes.11e13 More recently, Ozdogan et al. reported a case of acute MVT successfully treated by a limited bowel resection and thrombolytic infusion via an operatively placed mesenteric vein catheter. A central venous catheter was inserted through a peripheral jejunal vein and positioned at the junction of the superior mesenteric vein and splenic vein under fluoroscopic guidance. Thrombolysis through this catheter with streptokinase resulted in complete resolution of the SMV thrombosis, although not the portal vein thrombosis, within 36 hr.14 Unlike our group, Ozgodan and colleagues were able to advance the catheter placed through the peripheral jejunal vein fairly proximally under fluoroscopic guidance. Nevertheless, despite our inability to similarly advance the catheter proximally due to the
Annals of Vascular Surgery
significant burden of clot in the omental veins, we were able to obtain excellent results. In our case, thrombus extended through the entire portomesenteric venous system, with most of the patient’s bowel appearing edematous, and a significant segment of bowel was necrotic. We resected short segments of the bowel and, in an attempt to salvage additional bowel, intraportal thrombolytic therapy was used. We therefore combined surgical resection of nonviable bowel with direct infusion of thrombolytic into the site of thrombosis, with excellent results. Although thrombolytic therapy has its own risks, we believe that in certain life-threatening situations, such as portomesenteric thrombosis, the benefits associated with selective thrombolysis far outweigh potential risks. This therapeutic intervention was life-saving in our patient, and should be considered in similar cases. REFERENCES 1. Schoots IG, et al. Systematic review of survival after acute mesenteric ischaemia according to disease aetiology. Br J Surg 2004;91:17e27. 2. Abu-Daff S, Abu-Daff N, Al-Shahed M. Mesenteric venous thrombosis and factors associated with mortality: a statistical analysis with five-year follow-up. J Gastrointest Surg 2009;13:1245e50. 3. Harnik IG, Brandt LJ. Mesenteric venous thrombosis. Vasc Med 2010;15:407e18. 4. Kumar S, Sarr MG, Kamath PS. Mesenteric venous thrombosis. N Engl J Med 2001;345:1683e8. 5. Elliot JW II. The operative relief of gangrene of intestine due to occlusion of the mesenteric vessels. Ann Surg 1895;21:9e23. 6. Zhang J, et al. Acute mesenteric venous thrombosis: a better outcome achieved through improved imaging techniques and a changed policy of clinical management. Eur J Vasc Endovasc Surg 2004;28:329e34. 7. Abdu RA, Zakhour BJ, Dallis DJ. Mesenteric venous thrombosisd1911 to 1984. Surgery 1987;101:383e8. 8. al Karawi MA, et al. Mesenteric vein thrombosis, noninvasive diagnosis and follow-up (US + MRI), and noninvasive therapy by streptokinase and anticoagulants. Hepatogastroenterology 1990;37:507e9. 9. Robin P, et al. Complete thrombolysis of mesenteric vein occlusion with recombinant tissue-type plasminogen activator. Lancet 1988;1:1391. 10. Inahara T. Acute superior mesenteric venous thrombosis: treatment by thrombectomy. Ann Surg 1971;174:956e61. 11. Rivitz SM, et al. Treatment of acute mesenteric venous thrombosis with transjugular intramesenteric urokinase infusion. J Vasc Interv Radiol 1995;6:219e23. 12. Lopera JE, et al. Percutaneous transhepatic treatment of symptomatic mesenteric venous thrombosis. J Vasc Surg 2002;36:1058e61. 13. Nakayama S, Murashima N, Isobe Y. Superior mesenteric venous thrombosis treated by direct aspiration thrombectomy. Hepatogastroenterology 2008;55:367e70. 14. Ozdogan M, et al. Thrombolysis via an operatively placed mesenteric catheter for portal and superior mesenteric vein thrombosis: report of a case. Surg Today 2006;36:846e8.
Mesenteric venous thrombosis (MVT) is an uncommon clinical condition with potential high morbidity. We report here a patient who presented with acute-onset MVT and bowel infarction, which was successfully ameliorated with intramesenteric vein thrombolytic therapy.
CASE REPORT A 34-year-old woman presented with a 2-week history of episodic abdominal pain, nausea, and emesis that had worsened in the preceding 48 hours. She had no significant relevant medical or surgical history. She had recently started taking oral contraceptive pills. She was afebrile and hemodynamically stable. Her examination was significant for a soft, diffusely tender abdomen. Peritoneal signs were absent. There was no evidence of gastrointestinal (GI) bleeding; recent history of fever, weight loss, or early satiety; or significant family history. She had no history of deep vein thrombosis (DVT), pulmonary embolus (PE), or hypercoagulable state. Her admitting laboratory values were unremarkable with normal white blood cell count, platelets, coagulation panel, and hematocrit. Abdominal computed tomography (CT) revealed nonspecific mid-mesenteric inflammation, periportal edema, and concern for right portal vein nonoccluding thrombus (Fig. 1). She was admitted to a medical service and maintained on bowel rest and intravenous fluid hydration. A surgical consultation was obtained. Upper endoscopy revealed a normal esophagus
1 Department of Surgery, Yale University School of Medicine, New Haven, CT. 2 Department of Surgery, Bridgeport Hospital, Yale New Haven Health, Bridgeport, CT.
Correspondence to: Annabelle L. Fonseca, MD, Department of Surgery, Yale University School of Medicine, FMB 107, 333 Cedar Street, New Haven, CT 06511, USA; E-mail: [email protected] Ann Vasc Surg 2013; 27: 497.e1e497.e4 http://dx.doi.org/10.1016/j.avsg.2012.09.009 Ó 2013 Elsevier Inc. All rights reserved. Manuscript received: August 21, 2012; manuscript accepted: September 25, 2012; published online: April 8, 2013.
and duodenum and no evidence of upper GI bleeding. A work-up for hypercoagulable state was initiated. Two days later her hematocrit dropped to 16% from 34%. A repeat CT scan revealed complete thrombosis of the portal and mesenteric system, including the tributaries from the inferior mesenteric and splenic veins, new ascites, and bowel wall thickening (Fig. 2). Her examination now showed worsening abdominal tenderness that progressed to an acute abdomen. She was taken urgently to the operating room for an exploratory celiotomy. Intraoperative findings demonstrated serous ascitic fluid and a 75-cm segment of congested ischemic small bowel that was subsequently resected (Fig. 3). The liver appeared normal with no evidence of congestion or cirrhosis. A mesenteric portogram was obtained via a 6F catheter inserted into an omental vein and demonstrated no outflow from the thrombosed portomesenteric vein (Fig. 4A). Alteplase (2-mg doses) was injected with heparinized saline via the catheter, after which a follow-up portogram demonstrated improved visualization of the venous structures (Fig. 4B), but the portal structures were still not well defined. A decision was made to perform continuous thrombolytic therapy at 1 mg/hr and systemic heparinization, and therefore the catheter was secured in the omental vein. The patient’s abdomen was left open, and a temporary abdominal closure (TAC) was placed. She was started on total parenteral nutrition (TPN). On postoperative day 1 (POD 1) the patient underwent repeat portal venography through the indwelling catheter, which now showed some antegrade flow in the superior mesenteric vein but persistent residual thrombus. The portal vein was now visualized along with the right and left hepatic portal vein branches (Fig. 4C) with residual thrombus. It was decided to continue low-dose thrombolytic therapy at 0.5 mg/hr in the surgical intensive care unit. The patient remained hemodynamically stable
497.e1
497.e2 Case reports
Annals of Vascular Surgery
Fig. 1. Initial presenting CT revealed (A) stranding within the mid-abdominal mesentery, periportal edema, and (B) concern for right portal vein thrombosis versus contrast delay.
Fig. 2. (AeC) Repeat CT obtained on hospital day 3 revealed extensive portal vein thrombus involving the right and left portal vein, the main portal vein (A), and extending into the superior mesenteric vein (B). Also
seen was new, diffuse thickening of jejunal loops (C) with concern for ischemia versus congestion and new moderate ascites.
throughout and was returned to the operating room (OR) on POD 2 for reexploration and resection of any nonviable bowel. Two areas of ischemic small bowel, 20 cm at the proximal end and 10 cm distally, were resected. The patient’s intestines were left in discontinuity and a TAC was performed. On POD 4, she returned to the OR where all remaining bowel appeared viable. A completion small bowel anastomosis was performed, the mesenteric omental vein catheter was removed, thrombolytic therapy was ceased, and the abdominal wall was closed. She was continued on systemic anticoagulation with heparin. On POD 7, an intraabdominal collection was detected and percutaneously drained. On POD 16 fondaparinux was started, and systemic heparinization was discontinued. Her diet was slowly advanced without incident and she was cycled off TPN. She underwent layered closure of her abdominal wound on POD 24 and was subsequently discharged on POD 28 with a therapeutic international normalized ratio (INR). Six-month outpatient follow-up
revealed a healthy, asymptomatic patient who was tolerating her diet, gaining weight, and back to full employment. The pathologic examination of the resected bowel showed transmural hemorrhage, inflammation, and necrosisdall changes compatible with ischemia. Interestingly, her coagulation work-up revealed a low protein C level of 27% (normal 70e140%).
DISCUSSION Mesenteric venous thrombosis is a relatively rare disorder. It is estimated that about 2e6% of all cases of acute mesenteric ischemia are related to MVT.1,2 It can occur in acute, subacute, or chronic forms. Acute MVT is defined as new-onset symptomatic thrombosis of the superior mesenteric vein (SMV) or its branches, without evidence of collateralization.3
Vol. 27, No. 4, May 2013
Case reports 497.e3
Fig. 3. Intraoperative images of ischemic small bowel demonstrating (A) smaller segment of infarcted bowel (arrow) (B) surrounding large segments of edematous ischemic bowel.
Fig. 4. (A) Initial intraoperative mesenteric portogram demonstrating absence of mesenteric and portal vein flow. (B) Repeat intraoperative mesenteric portogram after thrombolytic therapy demonstrating improved
portal vein filling. (C) POD 1 repeat portal venogram demonstrating visualization of the portal vein and right and left hepatic veins.
This typically presents with sudden-onset abdominal pain, nausea, vomiting, and diarrhea. It is associated with a definite risk of bowel infarction. Subacute and chronic MVT, on the other hand, usually present more insidiously, and have a low risk of bowel infarction due to the development of venous collaterals.
MVT may be classified as either primary or secondary. Secondary MVT occurs in the presence of a predisposing risk factor. Protein C or S deficiency, antithrombin III deficiency, and polycythemia vera have been implicated as causes of MVT.4 Other causes, such as pregnancy,
497.e4 Case reports
contraceptive use, and malignancy, are also associated with hypercoagulable conditions that may predispose to MVT.4 The patient described here had an underlying protein C deficiency and had recently started contraceptive use, two conditions that may have predisposed her to the development of MVT. The treatment of MVT has not changed significantly since it was first described as a cause of intestinal infarction in 1895. Treatment consisted of bowel resection and delayed re-anastomosis.5 The more frequent use of CT scanning in patients with abdominal pain has significantly decreased the time from presentation to diagnosis.6 This early diagnosis presents a brief window of opportunity to treat patients with ischemic bowel, prior to the development of bowel infarction. The aim of treatment is to reestablish flow through the portomesenteric vein and conserve as much bowel as possible. Immediate heparinization is the first line of treatment. This approach has been shown to clearly increase survival, and is currently accepted standard therapy.3,7 Anticoagulation has been demonstrated to prevent recurrence of thrombosis after intestinal resection, and also to be associated with lower mortality if recurrence does occur.7 It has been suggested that anticoagulation with warfarin should be continued for 3e6 months in patients with a temporary risk factor, and should be administered lifelong for patients whose thrombosis is considered to be idiopathic or due to irreversible systemic conditions.3 Systemic thrombolysis with intravenous streptokinase and tissue plasminogen activator (tPA)8,9 or mechanical thrombectomy10 have been used successfully, especially with fresh thrombus localized to the SMV. Selective thrombolysis has been described utilizing the transjugular or transhepatic routes.11e13 More recently, Ozdogan et al. reported a case of acute MVT successfully treated by a limited bowel resection and thrombolytic infusion via an operatively placed mesenteric vein catheter. A central venous catheter was inserted through a peripheral jejunal vein and positioned at the junction of the superior mesenteric vein and splenic vein under fluoroscopic guidance. Thrombolysis through this catheter with streptokinase resulted in complete resolution of the SMV thrombosis, although not the portal vein thrombosis, within 36 hr.14 Unlike our group, Ozgodan and colleagues were able to advance the catheter placed through the peripheral jejunal vein fairly proximally under fluoroscopic guidance. Nevertheless, despite our inability to similarly advance the catheter proximally due to the
Annals of Vascular Surgery
significant burden of clot in the omental veins, we were able to obtain excellent results. In our case, thrombus extended through the entire portomesenteric venous system, with most of the patient’s bowel appearing edematous, and a significant segment of bowel was necrotic. We resected short segments of the bowel and, in an attempt to salvage additional bowel, intraportal thrombolytic therapy was used. We therefore combined surgical resection of nonviable bowel with direct infusion of thrombolytic into the site of thrombosis, with excellent results. Although thrombolytic therapy has its own risks, we believe that in certain life-threatening situations, such as portomesenteric thrombosis, the benefits associated with selective thrombolysis far outweigh potential risks. This therapeutic intervention was life-saving in our patient, and should be considered in similar cases. REFERENCES 1. Schoots IG, et al. Systematic review of survival after acute mesenteric ischaemia according to disease aetiology. Br J Surg 2004;91:17e27. 2. Abu-Daff S, Abu-Daff N, Al-Shahed M. Mesenteric venous thrombosis and factors associated with mortality: a statistical analysis with five-year follow-up. J Gastrointest Surg 2009;13:1245e50. 3. Harnik IG, Brandt LJ. Mesenteric venous thrombosis. Vasc Med 2010;15:407e18. 4. Kumar S, Sarr MG, Kamath PS. Mesenteric venous thrombosis. N Engl J Med 2001;345:1683e8. 5. Elliot JW II. The operative relief of gangrene of intestine due to occlusion of the mesenteric vessels. Ann Surg 1895;21:9e23. 6. Zhang J, et al. Acute mesenteric venous thrombosis: a better outcome achieved through improved imaging techniques and a changed policy of clinical management. Eur J Vasc Endovasc Surg 2004;28:329e34. 7. Abdu RA, Zakhour BJ, Dallis DJ. Mesenteric venous thrombosisd1911 to 1984. Surgery 1987;101:383e8. 8. al Karawi MA, et al. Mesenteric vein thrombosis, noninvasive diagnosis and follow-up (US + MRI), and noninvasive therapy by streptokinase and anticoagulants. Hepatogastroenterology 1990;37:507e9. 9. Robin P, et al. Complete thrombolysis of mesenteric vein occlusion with recombinant tissue-type plasminogen activator. Lancet 1988;1:1391. 10. Inahara T. Acute superior mesenteric venous thrombosis: treatment by thrombectomy. Ann Surg 1971;174:956e61. 11. Rivitz SM, et al. Treatment of acute mesenteric venous thrombosis with transjugular intramesenteric urokinase infusion. J Vasc Interv Radiol 1995;6:219e23. 12. Lopera JE, et al. Percutaneous transhepatic treatment of symptomatic mesenteric venous thrombosis. J Vasc Surg 2002;36:1058e61. 13. Nakayama S, Murashima N, Isobe Y. Superior mesenteric venous thrombosis treated by direct aspiration thrombectomy. Hepatogastroenterology 2008;55:367e70. 14. Ozdogan M, et al. Thrombolysis via an operatively placed mesenteric catheter for portal and superior mesenteric vein thrombosis: report of a case. Surg Today 2006;36:846e8.