- Email: [email protected]
Transhepatic Catheter-directed Thrombectomy and Thrombolysis of Acute Superior Mesenteric Venous Thrombosis
Transhepatic Catheter-directed Thrombectomy and Thrombolysis of Acute Superior Mesenteric Venous Thrombosis Hyun S. Kim, MD, Ajanta Patra, MD, Jawad Khan, MD, Aravind Arepally, MD, and Michael B. Streiff, MD
PURPOSE: To evaluate clinical outcomes after percutaneous treatment of superior mesenteric vein (SMV) thrombosis. MATERIALS AND METHODS: A retrospective chart review was conducted of all patients with SMV thrombosis treated with percutaneous catheter-directed thrombectomy/thrombolysis. The demographics of the study population, potential causative factors contributing to SMV thrombosis, and morbidity and mortality associated with therapy were assessed. RESULTS: Eleven patients (mean age, 44.3 years ⴞ 12.8) with SMV thrombosis were treated with percutaneous transhepatic catheter-directed thrombectomy/thrombolysis. Potential causative factors included recent major abdominal surgery, thrombophilic conditions, pancreatitis, and repetitive abdominal trauma. The mean duration between the onset of symptoms and percutaneous treatment was 8.6 days ⴞ 6.5. Computed tomography confirmed the clinical diagnosis in nine patients (81.8%). One patient (9.1%) had a bleeding complication, which was treated by chest tube drainage without long-term sequelae. One patient (9.1%) with refractory SMV thrombosis died of sepsis and multiple organ failure. No recurrent episode of SMV thrombosis or mortality was documented during a mean follow-up of 42 months ⴞ 22.5. CONCLUSIONS: Percutaneous transhepatic catheter-directed thrombectomy/thrombolysis for SMV thrombosis is associated with a rapid improvement in symptoms and low incidences of long-term morbidity and mortality. Percutaneous thrombectomy and thrombolysis should be considered in all patients with acute SMV thrombosis without evidence of bowel necrosis. J Vasc Interv Radiol 2005; 16:1685–1691 Abbreviation:
SMV ⫽ superior mesenteric vein
ACUTE superior mesenteric vein (SMV) thrombosis is an uncommon and insidious disease that is potentially lethal because its presenting symptoms overlap with those of many other diseases, leading to significant delays in diagnosis and therapy.
From the Division of Vascular and Interventional Radiology, Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Blalock 545, Baltimore, Maryland 21205. Received May 31, 2005; accepted August 3. Address correspondence to H.S.K.; E-mail: [email protected] None of the authors have identified a conflict of interest. © SIR, 2005 DOI: 10.1097/01.RVI.0000182156.71059.B7
Among all mesenteric ischemic events, mesenteric venous thrombosis accounts for 5%–15% (1,2). The exact mechanism and natural history of SMV thrombosis remain unclear. An identifiable etiology may be found in approximately 75% of patients (3), with as many as 56% of patients having identifiable coagulopathy (4). Most commonly, SMV thrombosis is a manifestation of a hypercoagulable state resulting from or exacerbated by an event such as pancreatitis or abdominal surgery (3). Thrombophilic conditions associated with SMV thrombosis include deficiencies of antithrombin III, protein C, and protein S; factor V Leiden and prothrombin gene mutation; and the antiphospholipid antibody syndrome.
Other clinical conditions associated with SMV thrombosis include myeloproliferative disorders, paroxysmal nocturnal hemoglobinuria, abdominal trauma, infection or inflammation, portal hypertension, malignancies, and use of estrogen-containing compounds (5,6). Historically, the identification of SMV thrombosis has frequently been delayed because symptoms were often insidious and nonspecific, such that definitive diagnosis in some cases was made only during surgery or at autopsy (3). More recently, the availability of noninvasive imaging studies such as contrast material– enhanced high-resolution computed tomography (CT), which can establish the diagnosis of SMV thrombosis with a sen-
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Figure. (a) Direct venography with the catheter in the splenic vein demonstrates thrombus extending from the SMV into the portal vein. (b) Three-dimensional coronal reconstructed CT image demonstrates complete SMV thrombosis. Note SMV thrombus (arrow) as it joins the portal vein. (c) Venogram after percutaneous treatment shows restoration of flow in the SMV.
sitivity of 90%, has greatly facilitated early diagnosis and treatment (7). Even with correct diagnosis, SMV thrombosis remains potentially lethal, with 30-day mortality rates ranging from 13%–50% with traditional anticoagulation and bowel resection (8,9). In
early series, recurrence rates as high as 60% at the site of the bowel anastomosis were reported (10,11). Rhee et al (2) reported an overall 3-year mortality rate of 36% in patients with acute SMV thrombosis. Among those patients who do not die of SMV thrombosis
within 30 days, an overall survival rate as high as 88% at a mean of 57.7 months of follow-up has been reported (7). Therefore, an improved 30day survival rate has important implications for long-term outcomes in patients with acute SMV thrombosis.
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Table 1 Patient Demographics, Presenting Symptoms, and Etiologies Pt. Age No. (y) Sex
Presenting Symptoms
Etiologies
1
37
M
2 3 4
39 58 50
F F M
5
64
M
6
32
M
Abdominal pain, fever, rigor, nausea, vomiting Abdominal pain Abdominal pain, nausea Spontaneous bacterial peritonitis, Abdominal pain, fever, distension Abdominal pain, chills, distension Abdominal pain, jaundice
7
24
F
Abdominal pain, jaundice
8
57
M
9 10 11
52 32 42
M F M
Abdominal pain, nausea, vomiting, diarrhea Abdominal pain Abdominal pain, distension Abdominal pain
Interval from Surgery Interval from Symptom Onset to to Acute SMV Hospitalization (days) Thrombosis (days)
Splenectomy
2
1
Trauma Hemicolectomy for malignancy Splenectomy and idiopathic myelofibrosis
NA 10 10
9 2 1
Hemicolectomy for malignancy
6
4
NA
1
NA
7
NA
7
14 19 NA
2 1 5
Hypercoagulable state with antiphospholipid antibody Hypercoagulable state with activated protein C deficiency Hypercoagulable state and malignancy Splenectomy TAH/BSO for malignancy Chronic pancreatitis
Note.—All patients had total SMV occlusion. BSO ⫽ bilateral salpingo-oophorectomy; NA ⫽ not available; TAH ⫽ total abdominal hysterectomy.
More recently, catheter-directed thrombolysis has been proposed as a minimally invasive treatment option for patients with acute SMV thrombosis (5,12–16). The objective of the present study is to report the clinical outcomes in 11 patients with acute SMV thrombosis who were treated with percutaneous transhepatic thrombectomy/thrombolysis at our institution.
was collected for each subject by retrospective chart review: demographic data, presenting symptoms, date of onset of symptoms, hospitalization and diagnosis, potential associated clinical conditions and risk factors for SMV thrombosis, therapy and response to therapy, duration of hospitalization, and clinical status at 30 days and at last follow-up. Laboratory Testing
MATERIALS AND METHODS Patient Group After institutional review board approval was obtained, we conducted a retrospective search of our clinical database to identify patients with radiologically documented acute SMV thrombosis treated with percutaneous transhepatic thrombolysis/thrombectomy between March 1999 (when the clinical database was established) and December 2003. Among patents admitted for mesenteric ischemia (with midabdominal colicky pain that is not explained by physical findings), only patients with acute/subacute SMV thrombosis (duration of symptoms ⬍14 days) were included in the study population. The following information
All patients underwent laboratory testing for thrombophilic states. Activated partial thromboplastin times were measured on a BCS automated coagulometer (Dade Behring, Newark, DE) with use of the Actin FSL reagent (Dade Behring). Thrombin times and fibrinogen, antithrombin III, protein C, and protein S levels were assessed with standard activity and antigen assays. Anticardiolipin and 2 glycoprotein I antibodies were measured with use of the Quanta Lite enzyme-linked immunosorbent assay system (INOVA Diagnostics, San Diego, CA). A low phospholipid activated partial thromboplastin time and the dilute Russell viper venom time with a Confirm procedure (LA1 screening reagent/LA2 confirmation reagent; Dade Behring)
were used to detect lupus inhibitors. Homocysteine levels were measured by high-performance liquid chromatography. Factor V Leiden screening was performed with use of a modified activated protein C resistance assay (Coatest APC resistance kit; Chromagenix, Molndal, Sweden). Genetic confirmation of factor V Leiden and prothrombin gene mutation was performed with use of previously described polymerase chain reaction– based assays (17,18) or Invader assay technology (Third Wave Technologies, Madison, WI). Thrombolytic Technique All patients were treated initially with bowel rest and nasogastric suction, intravenous fluid administration, broad-spectrum prophylactic antibiotics (including ampicillin, gentamycin, and metronidazole), and intravenous unfractionated heparin adjusted to maintain the activated partial thromboplastin time ratio between 2.0 and 2.5 times control. Before the initiation of catheter-directed therapy, informed consent was obtained from each patient after a discussion of the risks of bleeding complications and benefits of nonsurgical treatment with catheter-
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Table 2 Percutaneous Thrombectomy/Thrombolysis and Clinical Outcome Pt. No.
Interval from Symptom Onset to Percutaneous Treatment (d)
1 2 3 4 5 6 7 8 9 10 11
2 13 3 7 5 22 8 11 4 3 17
Thrombectomy
Thrombolytic Agent
Lytic Agent Dose
Lytic Agent Duration (h)
Results
Length of Hospital Stay (d)
Amplatz No AngioJet AngioJet Amplatz No No AngioJet AngioJet AngioJet No
None UK tPA tPA tPA rt-PA rt-PA rt-PA UK UK UK
NA 8.5 million U 11.9 mg 50 mg 10 mg 14.5 U 24 U 30 U 3.8 million U 250,000 U 125,000 U
NA 40 7 45 0.33 29 24 45 35 1 0.33
Successful Successful Successful Unsuccessful Successful Successful Successful Successful Successful Successful Successful
11 15 11 14 15 36 11 10 11 7 22
Note.—NA ⫽ not available; rt-PA ⫽ recombinant tissue plasminogen activator; tPA ⫽ tissue plasminogen activator; UK ⫽ urokinase.
directed thrombectomy and thrombolysis for acute SMV thrombosis. Contraindications to percutaneous thrombolysis included previous stroke, primary or metastatic central nervous system malignancies, an active bleeding diathesis, and recent gastrointestinal bleeding. Mesenteric infarction was also a contraindication to thrombolysis, but this contraindication was waived in one patient who was considered a poor candidate for surgical treatment. Percutaneous transhepatic access to the portal vein was achieved with a 21-gauge trocar needle (Cook, Bloomington, IN). Transhepatic access was achieved according to a technique similar to percutaneous transhepatic cholangiography aiming for the right portal vein via the right midaxillary line subcostally under fluoroscopic guidance. With transhepatic access secured with a 6-F vascular sheath (Cordis, Miami, FL), we performed direct mesenteric and portal venography (Figure, part a). The SMV thrombosis was recanalized with use of a hockey stick–shaped Glide catheter (Terumo, Somerset, NJ) and a 0.035-inch Glide wire (Terumo). Percutaneous thrombectomy was performed with the 6-F AngioJet rheolytic thrombectomy device (Possis Medical, Minneapolis, MN) or the Helix Clot Buster thrombectomy device (ev3, Plymouth, MN). We performed percutaneous thrombectomy in patients who were at risk of bleeding complications as a result of recent sur-
geries or malignancy in an attempt to decrease duration of thrombolytic agent administration. Percutaneous thrombectomy was performed from distal to proximal clot in two cycles with the AngioJet device and in one cycle with the Helix Clot Buster device, both for less than 1 minute of activation time. Percutaneous thrombectomy activation time was minimized to decrease the risk of hemolysis and tachycardia. Residual thromboses were treated with catheter-directed thrombolysis. Catheter-directed thrombolysis was initiated via a multiple–side hole infusion catheter (Angiodynamics, Queensbury, NY) securely placed within the thrombosed SMV. Pulsespray thrombolysis was performed with urokinase (Abbott Laboratories, North Chicago, IL) or recombinant human tissue plasminogen activator (alteplase; Genentech, South San Francisco, CA). Catheter-directed thrombolysis without the pulse-spray technique was performed with recombinant plasminogen activator (reteplase; Centocor), recombinant human tissue plasminogen activator (alteplase; Genentech) or urokinase. Selection of thrombolytic agent was at the discretion of the individual attending physicians and was based on the operator’s experience. Any stenosis after thrombolysis was treated with balloon venoplasty. No stents were used. At the completion of catheter-directed therapy, intravenous unfractionated heparin administration was
reinitiated to maintain the activated partial thromboplastin time ratio at 2.0 –2.5 times control, followed by chronic anticoagulation with warfarin adjusted to maintain an International Normalized Ratio of 2–3. Study Endpoints and Definitions The endpoint of the study was the measurement of clinical outcomes and complications. Short-term technical success was assessed venographically at the conclusion of the therapy by full restoration of flow in the main SMV with filling of SMV branches. Other short-term outcome measures were patient survival at 30 days, improvement of abdominal pain, need for exploratory surgery, and ability to resume oral intake during hospitalization. Long-term outcome was assessed by survival rate and recurrence of abdominal pain or SMV thrombosis in subsequent outpatient visits or hospitalizations. Minor complications were defined as temporary and self-limiting symptoms without any clinical sequelae and major complications were defined as those requiring further intervention or hospitalization or causing permanent sequelae.
RESULTS We treated 11 patients with acute SMV thrombosis with percutane-
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Complications at 30 Days
Length of Follow-up (months)
Long-term Follow-up
None None None Death None Hemothorax None None None None None
71 70 67 NA 46 43 41 35 17 16 12
No recurrence No recurrence No recurrence NA No recurrence No recurrence No recurrence No recurrence No recurrence No recurrence No recurrence
ous catheter-directed thrombectomy/ thrombolysis between March 1999 and December 2003 (Table 1). The study population consists of four female patients and seven male patients with a mean age of 44.3 years ⫾ 12.8 (range, 24 – 64 years). The presenting symptoms of the cohort are presented in Table 1. The most common symptom was abdominal pain, which was present in all patients. Less common presenting symptoms included abdominal distension (n ⫽ 3), nausea and vomiting (n ⫽ 3), fevers or chills (n ⫽ 3), and jaundice (n ⫽ 2). CT was performed in all patients for further evaluation of SMV thrombosis (Figure, part b). SMV thrombosis was seen on preprocedural CT in nine of 11 patients (81.8%). Because the clinical suspicion for SMV thrombosis was high, all patients were referred for mesenteric venography and percutaneous treatment. Potential etiologies and associated conditions in our cohort of patients with SMV thrombosis included recent major abdominal surgeries in six patients (54.5%), underlying hypercoagulable states in five patients (45.5%), chronic pancreatitis in one patient (9.1%), spontaneous bacterial peritonitis in one patient (9.1%), and repetitive abdominal trauma (from martial arts) in one patient (9.1%). Associated surgical procedures included three splenectomies, two partial colectomies, and one total abdominal hysterectomy. The mean duration between previous surgery and the onset of
SMV thrombosis was 10.2 days ⫾ 6.0 (range, 2–19 d). Thrombophilic conditions included antiphospholipid antibody syndrome in two patients, heterozygous factor V Leiden in one patient, heterozygous prothrombin gene G20210A mutation in one patient, and malignancy-associated hypercoagulability in one patient. One patient with idiopathic myelofibrosis had an SMV thrombosis associated with postsplenectomy thrombocytosis. Percutaneous therapy was attempted in all 11 patients (Table 2). The mean duration between the onset of symptoms and percutaneous therapy was 8.6 days ⫾ 6.5. We performed percutaneous thrombectomy with the 6-F AngioJet device (Possis Medical) in five patients and the Helix Clot Buster device (ev3) in two patients. Percutaneous mechanical thrombectomy was employed in patients deemed to be at higher risk of bleeding because of recent surgeries or malignancy in an attempt to decrease duration of thrombolytic agent administration. Ten patients (90.9%) were treated with catheter-directed thrombolysis. One patient did not receive thrombolytic therapy because SMV thrombosis occurred 2 days after a splenectomy and the patient was referred for percutaneous treatment 2 days after the onset of SMV thrombosis. Pulse-spray thrombolysis was employed in three patients. Urokinase was used in two patients; one received 250,000 U of
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urokinase over a period of 1 hour and the second patient was treated with 125,000 U of urokinase over a period of 20 minutes. The third patient was treated with 10 mg of recombinant human tissue plasminogen activator (alteplase; Genentech) over 20 minutes. Seven patients received catheter-directed thrombolytic infusions without the pulse-spray technique. Three patients were treated with recombinant tissue plasminogen activator (Reteplase; Centocor) in the dose range of 14.5–30 U over 24 – 45 hours. Two patients received recombinant human tissue plasminogen activator at doses ranging from 11.9 mg to 50 mg over periods of 7– 45 hours. The remaining two patients received 3.8 million to 8.5 million U of urokinase over periods of 35– 40 hours. The mean duration of thrombolytic therapy was 22.7 hours ⫾ 18.9. Restoration of flow in the main SMV was documented on immediate follow-up direct portal venography in 90.9% of patients after percutaneous treatment (Figure, part c). Clinical symptoms rapidly improved after the procedure in all patients treated with successful thrombolysis. One patient (9.1%) had a small right hemothorax after successful thrombolysis. Percutaneous access was achieved below the level of the 10th rib, but the patient had unusually low pleural reflection; therefore, the percutaneous access to the portal vein caused blood accumulation from the portal vein into the right pleural space during percutaneous treatment. This patient was successfully treated with chest tube drainage, which extended the hospital stay by 13 days but was not associated with any long-term sequelae. The mean hospital stay for the study cohort was 14.8 days ⫾ 8.0. There was a single mortality (9.1%) at 30-day follow-up, which resulted from sepsis and multiple organ failure. This patient initially presented with a SMV thrombosis in the setting of bacterial peritonitis, sepsis, and multiple organ failure. His critically ill clinical condition precluded emergent surgical exploration, so percutaneous treatment was attempted. An initial 24-hour infusion of tissue plasminogen activator via the SMA was unsuccessful. Subsequent direct thromboly-
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sis in the SMV was also unsuccessful and no surgical procedure could be attempted before the patient’s death. The remaining 10 patients (90.9%) were discharged from the hospital in stable condition. No thrombotic, hemorrhagic, or infectious complications were noted during the remainder of the hospitalization. The mean duration of follow-up after hospital discharge was 42 months ⫾ 22.5. All patients with successfully recanalized SMVs are alive, and no recurrent episodes of SMV thrombosis have developed during oral anticoagulation therapy.
DISCUSSION This cohort study of 11 patients with acute SMV thrombosis treated with percutaneous transhepatic thrombectomy/thrombolysis demonstrates the feasibility of this nonoperative approach to the management of this challenging illness. Treatment was associated with rapid recanalization of the SMV, resolution of symptoms, and resumption of oral nutrition intake. No responder developed recurrent symptoms or required subsequent operative intervention, attesting to the potential of this approach in achieving reperfusion of the intestinal mucosa and preventing bowel infarction. Percutaneous treatment in our series led to a 30-day and long-term survival rate of 90.9% with a mean follow-up time of 42 months. The mean duration of hospitalization was 14 days. These results compare favorably with those of other contemporary series of SMV thrombosis. The mixed series of patients with SMV thrombosis managed operatively and nonoperatively by Morasch et al (7) included a 30-day survival rate of 77%. At 58 months of follow-up, the long-term survival rate was 68%. Brunaud et al (19) reported a retrospective series of 26 patients, half of whom were treated operatively and half of whom received anticoagulation alone. The mean duration of symptoms at presentation was 4.7 days ⫾ 0.8. The 2-year survival rates were 78.6% for surgically treated patients and 75% for patients receiving anticoagulation alone. The mean duration of hospitalization was 52 days ⫾ 15 among surgically treated patients and 23 days ⫾ 8 for patients receiving anticoagulation alone (19).
Several case reports or small case series of percutaneous treatment of SMV thrombosis have been published and have demonstrated its utility (12– 15). Recently, Hollingshead et al (16) reported a series of 20 patients with acute/subacute SMV thrombosis or portal vein thrombosis treated with percutaneous thrombolysis with use of a variety of approaches and thrombolytic agents. Three of their patients had complete thrombus resolution and 12 exhibited partial lysis. Five derived no benefit. Eighty-five percent had resolution of symptoms but 60% of patients had a complication of therapy. In four patients, therapy had to be interrupted. The mean time from symptom onset to presentation was 14.4 days. The mean duration of therapy was 44 hours (16). Several factors may account for the favorable results we obtained with percutaneous transhepatic thrombolysis/thrombectomy for SMV thrombosis. In contrast to some cases reported in the literature, we performed percutaneous thrombectomy and thrombolysis via a transhepatic route, which affords access to the portal/SMV system at a favorable angle for thrombectomy and instillation of thrombolytic agents directly into the clots, reducing the need for greater lytic agent doses and longer durations of infusion therapy. The advantages of direct instillation of thrombolytic agents into venous clots has been previously reported (20). In addition, direct access also made additional therapies such as venoplasty for stenosis or stent placement for elastic recoil or persistent stenosis possible. Another added advantage of transhepatic access is its relative ease technically compared with transjugular intrahepatic access. Rapid access and initiation of direct therapy is of paramount importance for critically ill patients with SMV thrombosis. Indirect thrombolytic therapy via the SMA has been described for its potential benefits in infusing thrombolytic agents into small mesenteric venous branches (12). However, this approach may result in lytic agents diverting through patent branches and collaterals, thereby bypassing clotted branches, which could limit the utility of lytic agent infusion and prolong therapy. In addition, the potential risk of thrombosis or embolization in the
SMA and SMA branches or in the common femoral artery near the arteriotomy site is increased during prolonged catheterization (21,22). Percutaneous thrombectomy devices have been proposed to assist in thrombolytic therapy in lower-extremity deep vein thrombosis (23,24). We performed thrombectomy in seven of 11 patients, so percutaneous thrombectomy is feasible and may assist in restoration of mesenteric venous circulation. The goal of its use is rapid removal of the SMV clots to restore flow promptly, thereby preventing propagation of clots. As demonstrated in one of our patients who had complete clot removal by thrombectomy without thrombolysis, thrombectomy alone may help patients with contraindications to thrombolytic therapy. In addition, mechanical thrombectomy likely reduces the duration of thrombolysis required to clear the thrombus burden and therefore may have contributed to our acceptable major bleeding rate. Our study has several limitations that deserve mention. Similar to previously published reports of SMV thrombosis, our study is a small retrospective cohort study. Therefore, our results, although promising, must be considered preliminary. Although it is plausible that our favorable results reflect, at least in part, the treatment approach employed, differences in patient populations may clearly also be contributory. Although the percutaneous treatment approach was uniform during the study period, the choice of thrombolytic agent and mechanical thrombectomy device was left to the investigators’ discretion. Nevertheless, because SMV thrombosis is a rare illness, it is unlikely that large randomized controlled studies of sufficient power will be conducted to assess the relative efficacy of different management approaches. We reported the long-term clinical outcomes of 11 patients who underwent percutaneous catheter-directed thrombectomy/thrombolysis for acute SMV thrombosis. Our results indicate that percutaneous catheter-directed thrombectomy/thrombolysis should be considered in patients with acute SMV thrombosis without signs of bowel necrosis.
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CONCLUSION Percutaneous transhepatic catheterdirected thrombectomy/thrombolysis for acute mesenteric ischemia with SMV thrombosis is feasible and appears to be an effective therapy. Our study demonstrates a 91.7% 30-day and long-term survival rate after a mean follow-up of 42 months. Percutaneous thrombectomy and thrombolysis followed by anticoagulation appears effective therapy for improvement in acute symptoms and longterm prognosis with a low complication rate. References 1. Grendell J, Ockner R. Mesenteric venous thrombosis. Gastroenterology 1982; 82:358–372. 2. Rhee RY, Gloviczki P, Mendonca CT, et al. Mesenteric venous thrombosis: still a lethal disease in the 1990s. J Vasc Surg 1994; 20:688–697. 3. Kumar S, Sarr MG, Kamath PS. Mesenteric venous thrombosis. N Engl J Med 2001; 345:1683–1688. 4. Harward T, Green D, Bergan J, et al. Mesenteric venous thrombosis. J Vasc Surg 1989; 9:328–333. 5. Lopera JE, Correa G, Brazzini A, et al. Percutaneous transhepatic treatment of symptomatic mesenteric venous thrombosis. J Vascular Surgery 2002; 36:1058–1061. 6. Divino CM, Park IS, Angel LP, et al. A retrospective study of diagnosis and management of mesenteric vein thrombosis. Am J Surgery 2001; 181:20–23. 7. Morasch MD, Ebaugh JL, Chiou AC, et al. Mesenteric venous thrombosis: a
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10. 11. 12.
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17.
changing clinical entity. J Vasc Surg 2001; 34:680–684. Wilson C, Walker ID, Davidson JF, et al. Mesenteric venous thrombosis and antithrombin III deficiency. J Clin Pathol 1987; 40:906–908. Grieshop RJ, Dalsing MC, Cikrit DF, et al. Acute mesenteric venous thrombosis: revisited in a time of diagnostic clarity. Am Surg 1991; 57:573–577. Jona J, Cummins GJ, Head H, et al. Recurrent primary mesenteric venous thrombosis. JAMA 1974; 227:1033–1035. Naitove A, Weismann R. Primary mesenteric venous thrombosis. Ann Surg 1965; 161:516–523. Poplausky MR, Kaufman JA, Geller SC, et al. Mesenteric venous thrombosis treated with urokinase via the superior mesenteric artery. Gastroenterology 1996; 110:1633–1635. Goldberg MF, Kim HS. Treatment of acute superior mesenteric vein thrombosis with percutaneous techniques. AJR Am J Roentgenol 2003; 181:1305– 1307. Sze DY, O’Sullivan GJ, Johnson DL, et al. Mesenteric and portal venous thrombosis treated by transjugular mechanical thrombolysis. AJR Am J Roentgenol 2000; 175:732–734. Sehgal M, Haskal ZJ. Use of transjugular intrahepatic portosystemic shunts during lytic therapy of extensive portal splenic and mesenteric venous thrombosis: long-term follow-up. J Vasc Interv Radiol 2000; 11:61–65. Hollingshead M, Burke CT, Mauro MA, et al. Transcatheter thrombolytic therapy for acute mesenteric and portal vein thrombosis. J Vasc Interv Radiol 2005; 16:651–661. Bertina R, Koeleman B, Koster T, et al. Mutation in blood coagulation factor V
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associated with resistance to activated protein C. Nature 1994; 369:64–67. Poort SR, Rosendaal FR, Reitsma PH, et al. A common genetic variation in the 3=-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis. Blood 1996; 88:3698–3703. Brunaud L, Antunes L, Collinet-Adler S, et al. Acute mesenteric venous thrombosis: case for nonoperative management. J Vasc Surg 2001; 34:673– 679. Mewissen MW, Seabrook GR, Meissner MH, et al. Catheter-directed thrombolysis for lower extremity deep venous thrombosis: report of a national multicenter registry. Radiology 1999; 211:39–49. Koenigsberg RA, Wysokia M, Weissa J, et al. Risk of clot formation in femoral arterial sheaths maintained overnight for neuroangiographic procedures. AJNR Am J Neuroradiol 1999; 20:297– 299. Tsetis DK, Kochiadakis GE, Hatzidakis AA, et al. Transcatheter thrombolysis with high-dose bolus tissue plasminogen activator in iatrogenic arterial occlusion after femoral arterial catheterization. Cardiovasc Intervent Radiol 2002; 25:36–41. Kasirajan K, Gray B, Ouriel K. Percutaneous AngioJet thrombectomy in the management of extensive deep venous Thrombosis. J Vasc Interv Radiol 2001; 12:179–185. Delomex M, Beregi J, Willoteaux S, et al. Mechanical thrombectomy in patients with deep venous thrombosis. Cardiovasc Intervent Radiol 2001; 24: 42–48.
PURPOSE: To evaluate clinical outcomes after percutaneous treatment of superior mesenteric vein (SMV) thrombosis. MATERIALS AND METHODS: A retrospective chart review was conducted of all patients with SMV thrombosis treated with percutaneous catheter-directed thrombectomy/thrombolysis. The demographics of the study population, potential causative factors contributing to SMV thrombosis, and morbidity and mortality associated with therapy were assessed. RESULTS: Eleven patients (mean age, 44.3 years ⴞ 12.8) with SMV thrombosis were treated with percutaneous transhepatic catheter-directed thrombectomy/thrombolysis. Potential causative factors included recent major abdominal surgery, thrombophilic conditions, pancreatitis, and repetitive abdominal trauma. The mean duration between the onset of symptoms and percutaneous treatment was 8.6 days ⴞ 6.5. Computed tomography confirmed the clinical diagnosis in nine patients (81.8%). One patient (9.1%) had a bleeding complication, which was treated by chest tube drainage without long-term sequelae. One patient (9.1%) with refractory SMV thrombosis died of sepsis and multiple organ failure. No recurrent episode of SMV thrombosis or mortality was documented during a mean follow-up of 42 months ⴞ 22.5. CONCLUSIONS: Percutaneous transhepatic catheter-directed thrombectomy/thrombolysis for SMV thrombosis is associated with a rapid improvement in symptoms and low incidences of long-term morbidity and mortality. Percutaneous thrombectomy and thrombolysis should be considered in all patients with acute SMV thrombosis without evidence of bowel necrosis. J Vasc Interv Radiol 2005; 16:1685–1691 Abbreviation:
SMV ⫽ superior mesenteric vein
ACUTE superior mesenteric vein (SMV) thrombosis is an uncommon and insidious disease that is potentially lethal because its presenting symptoms overlap with those of many other diseases, leading to significant delays in diagnosis and therapy.
From the Division of Vascular and Interventional Radiology, Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Blalock 545, Baltimore, Maryland 21205. Received May 31, 2005; accepted August 3. Address correspondence to H.S.K.; E-mail: [email protected] None of the authors have identified a conflict of interest. © SIR, 2005 DOI: 10.1097/01.RVI.0000182156.71059.B7
Among all mesenteric ischemic events, mesenteric venous thrombosis accounts for 5%–15% (1,2). The exact mechanism and natural history of SMV thrombosis remain unclear. An identifiable etiology may be found in approximately 75% of patients (3), with as many as 56% of patients having identifiable coagulopathy (4). Most commonly, SMV thrombosis is a manifestation of a hypercoagulable state resulting from or exacerbated by an event such as pancreatitis or abdominal surgery (3). Thrombophilic conditions associated with SMV thrombosis include deficiencies of antithrombin III, protein C, and protein S; factor V Leiden and prothrombin gene mutation; and the antiphospholipid antibody syndrome.
Other clinical conditions associated with SMV thrombosis include myeloproliferative disorders, paroxysmal nocturnal hemoglobinuria, abdominal trauma, infection or inflammation, portal hypertension, malignancies, and use of estrogen-containing compounds (5,6). Historically, the identification of SMV thrombosis has frequently been delayed because symptoms were often insidious and nonspecific, such that definitive diagnosis in some cases was made only during surgery or at autopsy (3). More recently, the availability of noninvasive imaging studies such as contrast material– enhanced high-resolution computed tomography (CT), which can establish the diagnosis of SMV thrombosis with a sen-
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Figure. (a) Direct venography with the catheter in the splenic vein demonstrates thrombus extending from the SMV into the portal vein. (b) Three-dimensional coronal reconstructed CT image demonstrates complete SMV thrombosis. Note SMV thrombus (arrow) as it joins the portal vein. (c) Venogram after percutaneous treatment shows restoration of flow in the SMV.
sitivity of 90%, has greatly facilitated early diagnosis and treatment (7). Even with correct diagnosis, SMV thrombosis remains potentially lethal, with 30-day mortality rates ranging from 13%–50% with traditional anticoagulation and bowel resection (8,9). In
early series, recurrence rates as high as 60% at the site of the bowel anastomosis were reported (10,11). Rhee et al (2) reported an overall 3-year mortality rate of 36% in patients with acute SMV thrombosis. Among those patients who do not die of SMV thrombosis
within 30 days, an overall survival rate as high as 88% at a mean of 57.7 months of follow-up has been reported (7). Therefore, an improved 30day survival rate has important implications for long-term outcomes in patients with acute SMV thrombosis.
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Table 1 Patient Demographics, Presenting Symptoms, and Etiologies Pt. Age No. (y) Sex
Presenting Symptoms
Etiologies
1
37
M
2 3 4
39 58 50
F F M
5
64
M
6
32
M
Abdominal pain, fever, rigor, nausea, vomiting Abdominal pain Abdominal pain, nausea Spontaneous bacterial peritonitis, Abdominal pain, fever, distension Abdominal pain, chills, distension Abdominal pain, jaundice
7
24
F
Abdominal pain, jaundice
8
57
M
9 10 11
52 32 42
M F M
Abdominal pain, nausea, vomiting, diarrhea Abdominal pain Abdominal pain, distension Abdominal pain
Interval from Surgery Interval from Symptom Onset to to Acute SMV Hospitalization (days) Thrombosis (days)
Splenectomy
2
1
Trauma Hemicolectomy for malignancy Splenectomy and idiopathic myelofibrosis
NA 10 10
9 2 1
Hemicolectomy for malignancy
6
4
NA
1
NA
7
NA
7
14 19 NA
2 1 5
Hypercoagulable state with antiphospholipid antibody Hypercoagulable state with activated protein C deficiency Hypercoagulable state and malignancy Splenectomy TAH/BSO for malignancy Chronic pancreatitis
Note.—All patients had total SMV occlusion. BSO ⫽ bilateral salpingo-oophorectomy; NA ⫽ not available; TAH ⫽ total abdominal hysterectomy.
More recently, catheter-directed thrombolysis has been proposed as a minimally invasive treatment option for patients with acute SMV thrombosis (5,12–16). The objective of the present study is to report the clinical outcomes in 11 patients with acute SMV thrombosis who were treated with percutaneous transhepatic thrombectomy/thrombolysis at our institution.
was collected for each subject by retrospective chart review: demographic data, presenting symptoms, date of onset of symptoms, hospitalization and diagnosis, potential associated clinical conditions and risk factors for SMV thrombosis, therapy and response to therapy, duration of hospitalization, and clinical status at 30 days and at last follow-up. Laboratory Testing
MATERIALS AND METHODS Patient Group After institutional review board approval was obtained, we conducted a retrospective search of our clinical database to identify patients with radiologically documented acute SMV thrombosis treated with percutaneous transhepatic thrombolysis/thrombectomy between March 1999 (when the clinical database was established) and December 2003. Among patents admitted for mesenteric ischemia (with midabdominal colicky pain that is not explained by physical findings), only patients with acute/subacute SMV thrombosis (duration of symptoms ⬍14 days) were included in the study population. The following information
All patients underwent laboratory testing for thrombophilic states. Activated partial thromboplastin times were measured on a BCS automated coagulometer (Dade Behring, Newark, DE) with use of the Actin FSL reagent (Dade Behring). Thrombin times and fibrinogen, antithrombin III, protein C, and protein S levels were assessed with standard activity and antigen assays. Anticardiolipin and 2 glycoprotein I antibodies were measured with use of the Quanta Lite enzyme-linked immunosorbent assay system (INOVA Diagnostics, San Diego, CA). A low phospholipid activated partial thromboplastin time and the dilute Russell viper venom time with a Confirm procedure (LA1 screening reagent/LA2 confirmation reagent; Dade Behring)
were used to detect lupus inhibitors. Homocysteine levels were measured by high-performance liquid chromatography. Factor V Leiden screening was performed with use of a modified activated protein C resistance assay (Coatest APC resistance kit; Chromagenix, Molndal, Sweden). Genetic confirmation of factor V Leiden and prothrombin gene mutation was performed with use of previously described polymerase chain reaction– based assays (17,18) or Invader assay technology (Third Wave Technologies, Madison, WI). Thrombolytic Technique All patients were treated initially with bowel rest and nasogastric suction, intravenous fluid administration, broad-spectrum prophylactic antibiotics (including ampicillin, gentamycin, and metronidazole), and intravenous unfractionated heparin adjusted to maintain the activated partial thromboplastin time ratio between 2.0 and 2.5 times control. Before the initiation of catheter-directed therapy, informed consent was obtained from each patient after a discussion of the risks of bleeding complications and benefits of nonsurgical treatment with catheter-
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Table 2 Percutaneous Thrombectomy/Thrombolysis and Clinical Outcome Pt. No.
Interval from Symptom Onset to Percutaneous Treatment (d)
1 2 3 4 5 6 7 8 9 10 11
2 13 3 7 5 22 8 11 4 3 17
Thrombectomy
Thrombolytic Agent
Lytic Agent Dose
Lytic Agent Duration (h)
Results
Length of Hospital Stay (d)
Amplatz No AngioJet AngioJet Amplatz No No AngioJet AngioJet AngioJet No
None UK tPA tPA tPA rt-PA rt-PA rt-PA UK UK UK
NA 8.5 million U 11.9 mg 50 mg 10 mg 14.5 U 24 U 30 U 3.8 million U 250,000 U 125,000 U
NA 40 7 45 0.33 29 24 45 35 1 0.33
Successful Successful Successful Unsuccessful Successful Successful Successful Successful Successful Successful Successful
11 15 11 14 15 36 11 10 11 7 22
Note.—NA ⫽ not available; rt-PA ⫽ recombinant tissue plasminogen activator; tPA ⫽ tissue plasminogen activator; UK ⫽ urokinase.
directed thrombectomy and thrombolysis for acute SMV thrombosis. Contraindications to percutaneous thrombolysis included previous stroke, primary or metastatic central nervous system malignancies, an active bleeding diathesis, and recent gastrointestinal bleeding. Mesenteric infarction was also a contraindication to thrombolysis, but this contraindication was waived in one patient who was considered a poor candidate for surgical treatment. Percutaneous transhepatic access to the portal vein was achieved with a 21-gauge trocar needle (Cook, Bloomington, IN). Transhepatic access was achieved according to a technique similar to percutaneous transhepatic cholangiography aiming for the right portal vein via the right midaxillary line subcostally under fluoroscopic guidance. With transhepatic access secured with a 6-F vascular sheath (Cordis, Miami, FL), we performed direct mesenteric and portal venography (Figure, part a). The SMV thrombosis was recanalized with use of a hockey stick–shaped Glide catheter (Terumo, Somerset, NJ) and a 0.035-inch Glide wire (Terumo). Percutaneous thrombectomy was performed with the 6-F AngioJet rheolytic thrombectomy device (Possis Medical, Minneapolis, MN) or the Helix Clot Buster thrombectomy device (ev3, Plymouth, MN). We performed percutaneous thrombectomy in patients who were at risk of bleeding complications as a result of recent sur-
geries or malignancy in an attempt to decrease duration of thrombolytic agent administration. Percutaneous thrombectomy was performed from distal to proximal clot in two cycles with the AngioJet device and in one cycle with the Helix Clot Buster device, both for less than 1 minute of activation time. Percutaneous thrombectomy activation time was minimized to decrease the risk of hemolysis and tachycardia. Residual thromboses were treated with catheter-directed thrombolysis. Catheter-directed thrombolysis was initiated via a multiple–side hole infusion catheter (Angiodynamics, Queensbury, NY) securely placed within the thrombosed SMV. Pulsespray thrombolysis was performed with urokinase (Abbott Laboratories, North Chicago, IL) or recombinant human tissue plasminogen activator (alteplase; Genentech, South San Francisco, CA). Catheter-directed thrombolysis without the pulse-spray technique was performed with recombinant plasminogen activator (reteplase; Centocor), recombinant human tissue plasminogen activator (alteplase; Genentech) or urokinase. Selection of thrombolytic agent was at the discretion of the individual attending physicians and was based on the operator’s experience. Any stenosis after thrombolysis was treated with balloon venoplasty. No stents were used. At the completion of catheter-directed therapy, intravenous unfractionated heparin administration was
reinitiated to maintain the activated partial thromboplastin time ratio at 2.0 –2.5 times control, followed by chronic anticoagulation with warfarin adjusted to maintain an International Normalized Ratio of 2–3. Study Endpoints and Definitions The endpoint of the study was the measurement of clinical outcomes and complications. Short-term technical success was assessed venographically at the conclusion of the therapy by full restoration of flow in the main SMV with filling of SMV branches. Other short-term outcome measures were patient survival at 30 days, improvement of abdominal pain, need for exploratory surgery, and ability to resume oral intake during hospitalization. Long-term outcome was assessed by survival rate and recurrence of abdominal pain or SMV thrombosis in subsequent outpatient visits or hospitalizations. Minor complications were defined as temporary and self-limiting symptoms without any clinical sequelae and major complications were defined as those requiring further intervention or hospitalization or causing permanent sequelae.
RESULTS We treated 11 patients with acute SMV thrombosis with percutane-
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Complications at 30 Days
Length of Follow-up (months)
Long-term Follow-up
None None None Death None Hemothorax None None None None None
71 70 67 NA 46 43 41 35 17 16 12
No recurrence No recurrence No recurrence NA No recurrence No recurrence No recurrence No recurrence No recurrence No recurrence No recurrence
ous catheter-directed thrombectomy/ thrombolysis between March 1999 and December 2003 (Table 1). The study population consists of four female patients and seven male patients with a mean age of 44.3 years ⫾ 12.8 (range, 24 – 64 years). The presenting symptoms of the cohort are presented in Table 1. The most common symptom was abdominal pain, which was present in all patients. Less common presenting symptoms included abdominal distension (n ⫽ 3), nausea and vomiting (n ⫽ 3), fevers or chills (n ⫽ 3), and jaundice (n ⫽ 2). CT was performed in all patients for further evaluation of SMV thrombosis (Figure, part b). SMV thrombosis was seen on preprocedural CT in nine of 11 patients (81.8%). Because the clinical suspicion for SMV thrombosis was high, all patients were referred for mesenteric venography and percutaneous treatment. Potential etiologies and associated conditions in our cohort of patients with SMV thrombosis included recent major abdominal surgeries in six patients (54.5%), underlying hypercoagulable states in five patients (45.5%), chronic pancreatitis in one patient (9.1%), spontaneous bacterial peritonitis in one patient (9.1%), and repetitive abdominal trauma (from martial arts) in one patient (9.1%). Associated surgical procedures included three splenectomies, two partial colectomies, and one total abdominal hysterectomy. The mean duration between previous surgery and the onset of
SMV thrombosis was 10.2 days ⫾ 6.0 (range, 2–19 d). Thrombophilic conditions included antiphospholipid antibody syndrome in two patients, heterozygous factor V Leiden in one patient, heterozygous prothrombin gene G20210A mutation in one patient, and malignancy-associated hypercoagulability in one patient. One patient with idiopathic myelofibrosis had an SMV thrombosis associated with postsplenectomy thrombocytosis. Percutaneous therapy was attempted in all 11 patients (Table 2). The mean duration between the onset of symptoms and percutaneous therapy was 8.6 days ⫾ 6.5. We performed percutaneous thrombectomy with the 6-F AngioJet device (Possis Medical) in five patients and the Helix Clot Buster device (ev3) in two patients. Percutaneous mechanical thrombectomy was employed in patients deemed to be at higher risk of bleeding because of recent surgeries or malignancy in an attempt to decrease duration of thrombolytic agent administration. Ten patients (90.9%) were treated with catheter-directed thrombolysis. One patient did not receive thrombolytic therapy because SMV thrombosis occurred 2 days after a splenectomy and the patient was referred for percutaneous treatment 2 days after the onset of SMV thrombosis. Pulse-spray thrombolysis was employed in three patients. Urokinase was used in two patients; one received 250,000 U of
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urokinase over a period of 1 hour and the second patient was treated with 125,000 U of urokinase over a period of 20 minutes. The third patient was treated with 10 mg of recombinant human tissue plasminogen activator (alteplase; Genentech) over 20 minutes. Seven patients received catheter-directed thrombolytic infusions without the pulse-spray technique. Three patients were treated with recombinant tissue plasminogen activator (Reteplase; Centocor) in the dose range of 14.5–30 U over 24 – 45 hours. Two patients received recombinant human tissue plasminogen activator at doses ranging from 11.9 mg to 50 mg over periods of 7– 45 hours. The remaining two patients received 3.8 million to 8.5 million U of urokinase over periods of 35– 40 hours. The mean duration of thrombolytic therapy was 22.7 hours ⫾ 18.9. Restoration of flow in the main SMV was documented on immediate follow-up direct portal venography in 90.9% of patients after percutaneous treatment (Figure, part c). Clinical symptoms rapidly improved after the procedure in all patients treated with successful thrombolysis. One patient (9.1%) had a small right hemothorax after successful thrombolysis. Percutaneous access was achieved below the level of the 10th rib, but the patient had unusually low pleural reflection; therefore, the percutaneous access to the portal vein caused blood accumulation from the portal vein into the right pleural space during percutaneous treatment. This patient was successfully treated with chest tube drainage, which extended the hospital stay by 13 days but was not associated with any long-term sequelae. The mean hospital stay for the study cohort was 14.8 days ⫾ 8.0. There was a single mortality (9.1%) at 30-day follow-up, which resulted from sepsis and multiple organ failure. This patient initially presented with a SMV thrombosis in the setting of bacterial peritonitis, sepsis, and multiple organ failure. His critically ill clinical condition precluded emergent surgical exploration, so percutaneous treatment was attempted. An initial 24-hour infusion of tissue plasminogen activator via the SMA was unsuccessful. Subsequent direct thromboly-
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sis in the SMV was also unsuccessful and no surgical procedure could be attempted before the patient’s death. The remaining 10 patients (90.9%) were discharged from the hospital in stable condition. No thrombotic, hemorrhagic, or infectious complications were noted during the remainder of the hospitalization. The mean duration of follow-up after hospital discharge was 42 months ⫾ 22.5. All patients with successfully recanalized SMVs are alive, and no recurrent episodes of SMV thrombosis have developed during oral anticoagulation therapy.
DISCUSSION This cohort study of 11 patients with acute SMV thrombosis treated with percutaneous transhepatic thrombectomy/thrombolysis demonstrates the feasibility of this nonoperative approach to the management of this challenging illness. Treatment was associated with rapid recanalization of the SMV, resolution of symptoms, and resumption of oral nutrition intake. No responder developed recurrent symptoms or required subsequent operative intervention, attesting to the potential of this approach in achieving reperfusion of the intestinal mucosa and preventing bowel infarction. Percutaneous treatment in our series led to a 30-day and long-term survival rate of 90.9% with a mean follow-up time of 42 months. The mean duration of hospitalization was 14 days. These results compare favorably with those of other contemporary series of SMV thrombosis. The mixed series of patients with SMV thrombosis managed operatively and nonoperatively by Morasch et al (7) included a 30-day survival rate of 77%. At 58 months of follow-up, the long-term survival rate was 68%. Brunaud et al (19) reported a retrospective series of 26 patients, half of whom were treated operatively and half of whom received anticoagulation alone. The mean duration of symptoms at presentation was 4.7 days ⫾ 0.8. The 2-year survival rates were 78.6% for surgically treated patients and 75% for patients receiving anticoagulation alone. The mean duration of hospitalization was 52 days ⫾ 15 among surgically treated patients and 23 days ⫾ 8 for patients receiving anticoagulation alone (19).
Several case reports or small case series of percutaneous treatment of SMV thrombosis have been published and have demonstrated its utility (12– 15). Recently, Hollingshead et al (16) reported a series of 20 patients with acute/subacute SMV thrombosis or portal vein thrombosis treated with percutaneous thrombolysis with use of a variety of approaches and thrombolytic agents. Three of their patients had complete thrombus resolution and 12 exhibited partial lysis. Five derived no benefit. Eighty-five percent had resolution of symptoms but 60% of patients had a complication of therapy. In four patients, therapy had to be interrupted. The mean time from symptom onset to presentation was 14.4 days. The mean duration of therapy was 44 hours (16). Several factors may account for the favorable results we obtained with percutaneous transhepatic thrombolysis/thrombectomy for SMV thrombosis. In contrast to some cases reported in the literature, we performed percutaneous thrombectomy and thrombolysis via a transhepatic route, which affords access to the portal/SMV system at a favorable angle for thrombectomy and instillation of thrombolytic agents directly into the clots, reducing the need for greater lytic agent doses and longer durations of infusion therapy. The advantages of direct instillation of thrombolytic agents into venous clots has been previously reported (20). In addition, direct access also made additional therapies such as venoplasty for stenosis or stent placement for elastic recoil or persistent stenosis possible. Another added advantage of transhepatic access is its relative ease technically compared with transjugular intrahepatic access. Rapid access and initiation of direct therapy is of paramount importance for critically ill patients with SMV thrombosis. Indirect thrombolytic therapy via the SMA has been described for its potential benefits in infusing thrombolytic agents into small mesenteric venous branches (12). However, this approach may result in lytic agents diverting through patent branches and collaterals, thereby bypassing clotted branches, which could limit the utility of lytic agent infusion and prolong therapy. In addition, the potential risk of thrombosis or embolization in the
SMA and SMA branches or in the common femoral artery near the arteriotomy site is increased during prolonged catheterization (21,22). Percutaneous thrombectomy devices have been proposed to assist in thrombolytic therapy in lower-extremity deep vein thrombosis (23,24). We performed thrombectomy in seven of 11 patients, so percutaneous thrombectomy is feasible and may assist in restoration of mesenteric venous circulation. The goal of its use is rapid removal of the SMV clots to restore flow promptly, thereby preventing propagation of clots. As demonstrated in one of our patients who had complete clot removal by thrombectomy without thrombolysis, thrombectomy alone may help patients with contraindications to thrombolytic therapy. In addition, mechanical thrombectomy likely reduces the duration of thrombolysis required to clear the thrombus burden and therefore may have contributed to our acceptable major bleeding rate. Our study has several limitations that deserve mention. Similar to previously published reports of SMV thrombosis, our study is a small retrospective cohort study. Therefore, our results, although promising, must be considered preliminary. Although it is plausible that our favorable results reflect, at least in part, the treatment approach employed, differences in patient populations may clearly also be contributory. Although the percutaneous treatment approach was uniform during the study period, the choice of thrombolytic agent and mechanical thrombectomy device was left to the investigators’ discretion. Nevertheless, because SMV thrombosis is a rare illness, it is unlikely that large randomized controlled studies of sufficient power will be conducted to assess the relative efficacy of different management approaches. We reported the long-term clinical outcomes of 11 patients who underwent percutaneous catheter-directed thrombectomy/thrombolysis for acute SMV thrombosis. Our results indicate that percutaneous catheter-directed thrombectomy/thrombolysis should be considered in patients with acute SMV thrombosis without signs of bowel necrosis.
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CONCLUSION Percutaneous transhepatic catheterdirected thrombectomy/thrombolysis for acute mesenteric ischemia with SMV thrombosis is feasible and appears to be an effective therapy. Our study demonstrates a 91.7% 30-day and long-term survival rate after a mean follow-up of 42 months. Percutaneous thrombectomy and thrombolysis followed by anticoagulation appears effective therapy for improvement in acute symptoms and longterm prognosis with a low complication rate. References 1. Grendell J, Ockner R. Mesenteric venous thrombosis. Gastroenterology 1982; 82:358–372. 2. Rhee RY, Gloviczki P, Mendonca CT, et al. Mesenteric venous thrombosis: still a lethal disease in the 1990s. J Vasc Surg 1994; 20:688–697. 3. Kumar S, Sarr MG, Kamath PS. Mesenteric venous thrombosis. N Engl J Med 2001; 345:1683–1688. 4. Harward T, Green D, Bergan J, et al. Mesenteric venous thrombosis. J Vasc Surg 1989; 9:328–333. 5. Lopera JE, Correa G, Brazzini A, et al. Percutaneous transhepatic treatment of symptomatic mesenteric venous thrombosis. J Vascular Surgery 2002; 36:1058–1061. 6. Divino CM, Park IS, Angel LP, et al. A retrospective study of diagnosis and management of mesenteric vein thrombosis. Am J Surgery 2001; 181:20–23. 7. Morasch MD, Ebaugh JL, Chiou AC, et al. Mesenteric venous thrombosis: a
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associated with resistance to activated protein C. Nature 1994; 369:64–67. Poort SR, Rosendaal FR, Reitsma PH, et al. A common genetic variation in the 3=-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis. Blood 1996; 88:3698–3703. Brunaud L, Antunes L, Collinet-Adler S, et al. Acute mesenteric venous thrombosis: case for nonoperative management. J Vasc Surg 2001; 34:673– 679. Mewissen MW, Seabrook GR, Meissner MH, et al. Catheter-directed thrombolysis for lower extremity deep venous thrombosis: report of a national multicenter registry. Radiology 1999; 211:39–49. Koenigsberg RA, Wysokia M, Weissa J, et al. Risk of clot formation in femoral arterial sheaths maintained overnight for neuroangiographic procedures. AJNR Am J Neuroradiol 1999; 20:297– 299. Tsetis DK, Kochiadakis GE, Hatzidakis AA, et al. Transcatheter thrombolysis with high-dose bolus tissue plasminogen activator in iatrogenic arterial occlusion after femoral arterial catheterization. Cardiovasc Intervent Radiol 2002; 25:36–41. Kasirajan K, Gray B, Ouriel K. Percutaneous AngioJet thrombectomy in the management of extensive deep venous Thrombosis. J Vasc Interv Radiol 2001; 12:179–185. Delomex M, Beregi J, Willoteaux S, et al. Mechanical thrombectomy in patients with deep venous thrombosis. Cardiovasc Intervent Radiol 2001; 24: 42–48.