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Superior Mesenteric Vein Thrombosis and Duodenal Diverticulum
Superior Mesenteric Vein Thrombosis and Duodenal Diverticulum Joel Smith, Teresa L. Carman, MD, Bernardo B. Fernandez, Jr., MD, Marc E. Sesto, MD, and Regina Portnova, MD, Fort Lauderdale, Florida
We report a case of superior mesenteric vein thrombosis resulting from an inflamed duodenal diverticulum with associated inflammation of the uncinate process of the pancreas. (Ann Vasc Surg 2000;14:278-282.) DOI: 10.1007/s100169910048
Superior mesenteric vein thrombosis (SMVT) is an uncommon but potentially lethal cause of mesenteric ischemia. There are numerous predisposing conditions that may result in SMVT, including abdominal inflammation (pancreatitis, abscesses, postoperative states), hypercoagulable states (cancer, Protein C and S deficiencies, polycythemia vera), trauma, and portal hypertension.1-5 Because symptoms are often nonspecific, more common causes of abdominal pain are first considered. In fact, SMVT is often discovered at the time of surgery. We report a case of SMVT resulting from an inflamed duodenal diverticulum with associated inflammation of the uncinate process of the pancreas. Although thrombosis of the inferior mesenteric vein has been associated with diverticulitis of the sigmoid colon,3,4 to our knowledge, no case of venous thrombosis due to a duodenal diverticulum has been reported.
CASE REPORT A 65-year-old male presented to the emergency department with a 3-day history of lower abdominal pain, nauFrom Hanahman University, Philadelphia, PA (J.S.); Department of Vascular Medicine (T.L.C., B.B.F., R.P.); and Department of General and Vascular Surgery (M.E.S.), and Cleveland Clinic Florida, Fort Lauderdale, FL. Correspondence to: B.B. Fernandez, Jr., MD, Section Head of Vascular Medicine, Cleveland Clinic Florida, 3000 W. Cypress Creek Road, Fort Lauderdale, FL 33309, USA. 278
sea, and vomiting. The pain was described as continuous, with radiation to the back, and without identifiable exacerbating or relieving factors. Past medical history was significant for radical prostatectomy for Gleason’s stage 6 adenocarcinoma. The patient also had a history of bilateral deep vein thrombosis with a small pulmonary embolus that developed during treatment for urolithiais. This occurred 10 years prior to admission and required only medical therapy. The patient denied a history of smoking and imbibed 4-6 ounces of hard liquor per day. He had no known drug allergies and was not currently on any medications. Family history was significant for a half-brother with prostate cancer. He denied personal or family history of coagulopathy. On examination, the patient appeared well and was not in acute distress. His blood pressure was 153/92, with a pulse of 83 and a temperature of 99.7°F. Cardiopulmonary exam was normal. The prostatectomy incision was clean and intact and his abdomen did not appear distended. Bowel sounds were diminished in all quadrants. There was tenderness to palpation in the lower quadrants but no rebound or guarding. Stool was heme negative. Abnormal laboratory results included a slightly elevated white blood cell count of 11.6 and a lipase of 311 (32-203 U/L). Amylase, liver enzymes, and the remainder of the complete blood count were normal. An abdominal series did not demonstrate gas-fluid levels or dilated loops of bowel. The patient was admitted for observation and intravenous hydration. Esophagogastroduodenoscopy was performed to rule out peptic ulcer disease and showed only gastritis. A computed tomography (CT) scan of his abdomen and pelvis without contrast revealed mesenteric inflammation and free fluid in the
Vol. 14, No. 3, 2000
Case reports 279
section about the second portion of the duodenum demonstrated a 2 × 2 cm diverticulum on the medial wall adjacent to the head and uncinate process of the pancreas. The diverticulum was not perforated and located in such a manner as to not permit a simple diverticuloplasty or excision. Since the entire bowel was viable, no further surgical intervention was attempted nor necessary. The patient did well following surgery and was restarted on intravenous heparin, and subsequently placed on warfarin prior to discharge. Laboratory results including amylase, lipase, and a hypercoagulable profile were normal. The patient was discharged 5 days after surgery on warfarin therapy and remained well at 5-month follow-up.
DISCUSSION
Fig. 1. CT scan demonstrating thrombus within the SMV (arrow) and the adjacent uncinate process mass (arrowhead).
peritoneal cavity, most consistent with appendicitis, colonic diverticulitis, or ischemic bowel. Based on the clinical findings, colonic diverticulitis was considered the most likely diagnosis and intravenous antibiotics were initiated with ampicillin/sulbactam 1.5 g every 6 hr. Continuing abdominal pain led to a follow-up contrast-enhanced CT scan of the abdomen and pelvis, which demonstrated a 2 × 2 cm hypodense mass in the uncinate process of the pancreas with adjacent thrombosis of the SMV (Fig. 1). The portal and splenic veins were not thrombosed. Thickened loops of ileum and jejunum, likely secondary to venous congestion, were also seen. The pelvis demonstrated increasing ascites. The patient was anticoagulated with intravenous heparin for SMVT. The association of thrombosis with a pancreatic mass was of concern for carcinoma of the uncinate process with SMV invasion. Because of his age and good health, surgical intervention with the hope of resection of the mass and cure was planned. Initial diagnostic laparoscopy revealed no obvious carcinomatosis and the procedure was converted to open laparotomy. Examination of the base of the mesentery, duodenum, and head of the pancreas revealed edema and induration. The pancreas, however, felt normal. There was some edema and induration of the uncinate process without evidence of carcinoma. A transduodenal true-cut needle biopsy of a suspicious area in the uncinate process was performed, revealing normal pancreatic acinar tissue. The intestine was viable and normal, although 1 foot of distal jejunum was edematous and slightly hyperemic. Further dissection showed the area of the SMV to be quite vascular with collateral circulation and considerable edema, consistent with a freshly thrombosed vessel. Dis-
The patient in this case presented with nonspecific abdominal symptoms without clinical signs of peritonitis. Three weeks prior he had undergone a radical prostatectomy for Gleason’s stage 6 adenocarcinoma. It is likely that he had an adynamic postoperative ileus following the surgical procedure that caused distention of the previously acquired duodenal diverticulum. We propose that distention resulted in local inflammation of the diverticulum (diverticulitis). The inflammation of contiguous tissues, including the head and uncinate process of the pancreas, caused acute thrombosis of the juxtaposed SMV. The patient’s symptoms were caused by all of these in addition to the resulting small bowel edema and venous congestion. SMVT is rare but potentially lethal when associated with intestinal ischemia and infarction. In fact, the mortality rate may be as high as 27%.6 SMVT is implicated in only 5-15% of cases of intestinal ischemia.6,7 Factors that determine the presence of ischemia in association with SMVT include the degree of venous occlusion, thrombosis of associated vessels, and the degree of venous collateralization.3 Mesenteric vein thrombosis can be categorized as primary or secondary. Approximately 15-45% of cases are considered primary, or idiopathic.1,4-6,8 Recognized secondary causes of SMVT are included in Table I.1,2,4-7 Often these conditions are not associated with isolated SMVT but also involve the splenic or portal veins. Of course, as more causes of thrombosis are discovered, the percentage of cases considered secondary will increase. The clinical presentation of SMVT is variable and depends on the degree of intestinal ischemia, local pain of the thrombus, and associated conditions. The patient’s history may include such nonspecific complaints such as nausea, vomiting, diarrhea, hematemesis, and anorexia.6,7 Generalized abdominal discomfort is often present and may be prolonged in
280
Case reports
Annals of Vascular Surgery
Table I. Secondary causes of SMVT Abdominal inflammatory processes Abscess Appendicitis Inflammatory bowel disease Pancreatitis Peritonitis Postoperative state Hypercoagulable states Antithrombin III deficiency Malignancy Protein S deficiency Protein C deficiency Myeloproliferative disorders Polycythemia vera Thrombocytosis Portal hypertension Cirrhosis Other Oral contraceptives Postsplenectomy Pregnancy Trauma
cases of chronic SMVT. Physical findings can include pain out of proportion to physical findings and a low-grade fever. Peritoneal signs are present in cases of bowel infarction. Approximately 29 to 50% of patients will be heme positive and about half will have leukocytosis.5,6 Since it is rare and symptoms are nonspecific, SMVT is often not considered in the differential diagnosis. In fact, more common causes of abdominal symptoms should be explored first. About 80% of cases are discovered during a diagnostic or curative surgical procedure.1 Plain radiographs and barium exams are generally nonspecific and not helpful in the diagnosis of SMVT.4 If SMVT is suspected on the basis of history and clinical presentation, a CT scan with intravenous contrast should be performed and has a sensitivity as high as 90-100%.5 Typical findings include a central filling defect with a highdensity venous wall, anterior and to the right of the superior mesenteric artery, and bowel wall or mesenteric edema, as in Figure 2.1,3 Ultrasound may also be helpful in making the diagnosis. Visualization of the thrombus or absence of flow in the vessel may be seen in up to 80% of patients.4,6 The treatment for SMVT varies with the symptoms and predisposing condition. Chronic isolated SMVT is often associated with the presence of large collaterals and is asymptomatic; therefore it may not require therapy.8 Anticoagulation is recommended for acute, symptomatic SMVT.4,5 Rhee et
Fig. 2. CT scan demonstrating the central filling defect of the SMV (arrow) with associated perivascular and mesenteric inflammatory changes.
al.6 proposed an algorithm in which all patients with peritoneal signs be anticoagulated and undergo laparotomy with resection of nonviable bowel and undergo a second-look procedure at 24 hr if necessary. Other series do not recommend second-look procedures secondary to increased mortality.1 If no peritoneal signs are present, then CT and/or angiography can be performed with anticoagulation following a positive study.6 Duration of treatment varies, with recommendations from 6 months to lifelong anticoagulation.5,6 Certainly, patients with known coagulopathy or recurrent SMVT may require longer treatment. Other proposed methods of treatment include surgical thrombectomy and thrombolysis. 5,9 Thrombolysis is suggested in cases of thrombosis without or prior to the development of bowel ischemia.9 Thrombolytic therapy has also been used to reduce the length and duration of ischemic bowel prior to surgical resection.5 The patient in this case had no peritoneal signs, but surgery was indicated for suspicion of pancreatic cancer. Intraoperatively, an inflamed duodenal diverticulum causing inflammation of the contiguous head and uncinate process of the pancreas was found and thought to be the logical cause of the SMVT. The appearance of the pancreatic tissue was consistent with inflammation and not with carcinoma and this was confirmed by biopsy. Because of the chronicity of the event (days) and the fact that
Vol. 14, No. 3, 2000
the small bowel was clearly viable and not obstructed, no resection was performed, nor was any attempt made to recanalize the SMV. The duodenum ranks second to the colon as the most common site for development of diverticula in the alimentary tract.10 The incidence at autopsy/ endoscopy ranges from 2.2 to 23%.11,12 However, only 1-5% are seen on plain film or barium studies.13,14 There is a rare congenital form of duodenal diverticulum that is intraluminal and a more common acquired extraluminal form. Extraluminal diverticula are asymptomatic in over 90% of cases.14 Often they are detected incidentally during evaluation for other gastrointestinal disorders. They are asymptomatic in part because inflammation of duodenal diverticula is uncommon. When compared to colonic diverticula, those in the duodenum are larger in size and have increased intraluminal flow, so that food particles are less likely to be trapped; in addition, the environment is relatively sterile.10,11 When duodenal diverticula are symptomatic, complaints are usually nonspecific and mild,14 unless a serious complication has occurred. Complications include ulceration, bile or pancreatic duct obstruction, duodenal obstruction, perforation, or abscess.12,13 Bile or pancreatic duct obstruction occurs with diverticula adjacent to the ampulla of Vater and can lead to pancreatitis or choledocolithiases.12,14 If duodenal diverticula are suspected, the diagnosis may be made by CT scan. Generally, CT findings will include thickening of the diverticular wall and deformity of its lumen, but complications resulting from the diverticulum may alter these findings.11 As they are generally asymptomatic, only about 1-12% of duodenal diverticula require intervention.11,14,15 If serious complications are not present, conservative treatment with fasting followed by frequent small meals with high-fiber content can be attempted.14 More invasive intervention may be indicated in cases of ulceration, duodenal obstruction, perforation, or abscess.12,13 There are several operative procedures depending on location and severity of symptoms, from sphincteroplasty with diverticuloplasty or simple diverticulectomy to more complex excisional procedures.10-11,14 Excision is the treatment of choice for extraluminal diverticula,10,13 but may be difficult depending on the location relative to the pancreas and pancreatic and biliary ducts. The patient in this case demonstrated no clinical evidence of biliary or pancreatic duct obstruction. Because of the size and location of the diverticulum and lack of direct complications, (ulceration, bleed-
Case reports 281
ing, obstruction, perforation, or abscess), no attempt was made to resect it. Pancreatic duct obstruction from a periampullary duodenal diverticulum can lead to pancreatitis that in turn can cause SMVT usually in association with splenic vein thrombosis.2-4 The etiology includes spasm of the vein, stasis, mass effect, perivascular extension of inflammation, and thrombogenic factor release from the inflamed pancreas. While our patient had more of a local phenomenon with a mildly elevated serum lipase rather than pancreatitis per se, some of these factors probably contributed to the SMVT. Hypercoagulable states, myeloproliferative disorders, and malignancy are common and important causes of SMVT. Our patient had a history of previous thrombosis, so these possibilities were explored. As stated previously, the hypercoagulable profile and blood count provided no evidence for a predisposition to thrombosis or a myeloproliferative disorder. Although prostate cancer specifically has not been reported as a cause of SMVT, it cannot be ruled out as a contributing factor in this case.
SUMMARY Although rare, SMVT is important to consider in cases of abdominal discomfort and mesenteric ischemia. Diagnosis is aided by the use of a CT scan and evidence can also be seen on ultrasound. If the patient has SMVT and peritoneal signs, surgical intervention is warranted and nonviable bowel should be resected. Concomitant existence of a duodenal diverticulum, discovered radiographically or at the time of surgery, should not necessarily be removed unless is implicated in a separate pathologic process.14 If there is no obvious cause of the thrombosis, one should look for a predisposing hypercoagulable state.7 When discovered, lifelong anticoagulation may be indicated. Otherwise, a patient with acute and/or symptomatic SMVT should remain on oral anticoagulation for a minimum of 6 months.
REFERENCES 1. Al-Hilaly MA, Abu-Zidan FM. Mesenteric vein thrombosis: is it one disease? Eur J Vasc Endovasc Surg 1995;9:103-106. 2. Cornu-labat G, Kasirajan K, Simon R, et al. Acute mesenteric vein thrombosis and pancreatitis. Int J Pancreatol 1997; 21:249-251. 3. Crowe PM, Sagar G. Reversible superior mesenteric vein thrombosis in acute pancreatitis. The CT appearances. Clin Radiol 1995;50:628-633. 4. Font VE, Hermann RE, Longworth DL. Chronic mesenteric venous thrombosis: difficult diagnosis and therapy. Cleve Clin J Med 1989;56:823-828. 5. Rijs J, Depreiter B, Beckers A, et al. Mesenteric vein throm-
282
6.
7.
8.
9.
10.
Case reports
bosis: diagnostic and therapeutic approach. Acta Chir Belg 1997;97:247-249. Rhee RY, Gloviczki P, Mendonca CT, et al. Mesenteric venous thrombosis: still a lethal disease in the 1990s. J Vasc Surg 1994;29:688-697. Crespo I, Murphy J, Wong RKH. Superior mesenteric venous thrombosis masquerading as Crohn’s disease. Am J Gastroenterol 1994;89:116-118. Rattner DW, Warshaw AL. Venous, biliary, and duodenal obstruction in chronic pancreatitis. Hepatogastroenterology 1990;37:301-306. Poplausky MR, Kaufman JA, Geller SC, et al. Mesenteric venous thrombosis treated with urokinase via the superior mesenteric artery. Gastroenterology 1996;110:1633-1635. Gore RM, Ghahremani GG, Kirsch MD, et al. Diverticulitis of the duodenum: clinical and radiological manifestations of seven cases. Am J Gastroenterol 1991;86:981-985.
Annals of Vascular Surgery
11. Trondsen E, Rosseland AR, Bakka AO. Surgical management of duodenal diverticula. Acta Chir Scand 1990;156: 383-386. 12. Uomo G, Manes G, Ragozzinio A, et al. Periampullary extraluminal duodenal diverticula and acute pancreatitis: an underestimated etiologic association. Am J Gastroenterol 1996;91:1186-1188. 13. Medhi A, Closset J, Houben JJ, et al. Duodenal diverticula: diagnosis and management of complicated forms: report of two clinical cases and review of the literature. Acta Chir Belg 1994;94:311-313. 14. Psathakis D, Utschakowski A, Muller B, et al. Clinical significance of duodenal diverticula. J Am Coll Surg 1994;178: 257-260. 15. Akhrass R, Yaffe MB, Fischer C, et al. Small bowel diverticulosis: perceptions and reality. J Am Coll Surg 1997;184: 383-388.
We report a case of superior mesenteric vein thrombosis resulting from an inflamed duodenal diverticulum with associated inflammation of the uncinate process of the pancreas. (Ann Vasc Surg 2000;14:278-282.) DOI: 10.1007/s100169910048
Superior mesenteric vein thrombosis (SMVT) is an uncommon but potentially lethal cause of mesenteric ischemia. There are numerous predisposing conditions that may result in SMVT, including abdominal inflammation (pancreatitis, abscesses, postoperative states), hypercoagulable states (cancer, Protein C and S deficiencies, polycythemia vera), trauma, and portal hypertension.1-5 Because symptoms are often nonspecific, more common causes of abdominal pain are first considered. In fact, SMVT is often discovered at the time of surgery. We report a case of SMVT resulting from an inflamed duodenal diverticulum with associated inflammation of the uncinate process of the pancreas. Although thrombosis of the inferior mesenteric vein has been associated with diverticulitis of the sigmoid colon,3,4 to our knowledge, no case of venous thrombosis due to a duodenal diverticulum has been reported.
CASE REPORT A 65-year-old male presented to the emergency department with a 3-day history of lower abdominal pain, nauFrom Hanahman University, Philadelphia, PA (J.S.); Department of Vascular Medicine (T.L.C., B.B.F., R.P.); and Department of General and Vascular Surgery (M.E.S.), and Cleveland Clinic Florida, Fort Lauderdale, FL. Correspondence to: B.B. Fernandez, Jr., MD, Section Head of Vascular Medicine, Cleveland Clinic Florida, 3000 W. Cypress Creek Road, Fort Lauderdale, FL 33309, USA. 278
sea, and vomiting. The pain was described as continuous, with radiation to the back, and without identifiable exacerbating or relieving factors. Past medical history was significant for radical prostatectomy for Gleason’s stage 6 adenocarcinoma. The patient also had a history of bilateral deep vein thrombosis with a small pulmonary embolus that developed during treatment for urolithiais. This occurred 10 years prior to admission and required only medical therapy. The patient denied a history of smoking and imbibed 4-6 ounces of hard liquor per day. He had no known drug allergies and was not currently on any medications. Family history was significant for a half-brother with prostate cancer. He denied personal or family history of coagulopathy. On examination, the patient appeared well and was not in acute distress. His blood pressure was 153/92, with a pulse of 83 and a temperature of 99.7°F. Cardiopulmonary exam was normal. The prostatectomy incision was clean and intact and his abdomen did not appear distended. Bowel sounds were diminished in all quadrants. There was tenderness to palpation in the lower quadrants but no rebound or guarding. Stool was heme negative. Abnormal laboratory results included a slightly elevated white blood cell count of 11.6 and a lipase of 311 (32-203 U/L). Amylase, liver enzymes, and the remainder of the complete blood count were normal. An abdominal series did not demonstrate gas-fluid levels or dilated loops of bowel. The patient was admitted for observation and intravenous hydration. Esophagogastroduodenoscopy was performed to rule out peptic ulcer disease and showed only gastritis. A computed tomography (CT) scan of his abdomen and pelvis without contrast revealed mesenteric inflammation and free fluid in the
Vol. 14, No. 3, 2000
Case reports 279
section about the second portion of the duodenum demonstrated a 2 × 2 cm diverticulum on the medial wall adjacent to the head and uncinate process of the pancreas. The diverticulum was not perforated and located in such a manner as to not permit a simple diverticuloplasty or excision. Since the entire bowel was viable, no further surgical intervention was attempted nor necessary. The patient did well following surgery and was restarted on intravenous heparin, and subsequently placed on warfarin prior to discharge. Laboratory results including amylase, lipase, and a hypercoagulable profile were normal. The patient was discharged 5 days after surgery on warfarin therapy and remained well at 5-month follow-up.
DISCUSSION
Fig. 1. CT scan demonstrating thrombus within the SMV (arrow) and the adjacent uncinate process mass (arrowhead).
peritoneal cavity, most consistent with appendicitis, colonic diverticulitis, or ischemic bowel. Based on the clinical findings, colonic diverticulitis was considered the most likely diagnosis and intravenous antibiotics were initiated with ampicillin/sulbactam 1.5 g every 6 hr. Continuing abdominal pain led to a follow-up contrast-enhanced CT scan of the abdomen and pelvis, which demonstrated a 2 × 2 cm hypodense mass in the uncinate process of the pancreas with adjacent thrombosis of the SMV (Fig. 1). The portal and splenic veins were not thrombosed. Thickened loops of ileum and jejunum, likely secondary to venous congestion, were also seen. The pelvis demonstrated increasing ascites. The patient was anticoagulated with intravenous heparin for SMVT. The association of thrombosis with a pancreatic mass was of concern for carcinoma of the uncinate process with SMV invasion. Because of his age and good health, surgical intervention with the hope of resection of the mass and cure was planned. Initial diagnostic laparoscopy revealed no obvious carcinomatosis and the procedure was converted to open laparotomy. Examination of the base of the mesentery, duodenum, and head of the pancreas revealed edema and induration. The pancreas, however, felt normal. There was some edema and induration of the uncinate process without evidence of carcinoma. A transduodenal true-cut needle biopsy of a suspicious area in the uncinate process was performed, revealing normal pancreatic acinar tissue. The intestine was viable and normal, although 1 foot of distal jejunum was edematous and slightly hyperemic. Further dissection showed the area of the SMV to be quite vascular with collateral circulation and considerable edema, consistent with a freshly thrombosed vessel. Dis-
The patient in this case presented with nonspecific abdominal symptoms without clinical signs of peritonitis. Three weeks prior he had undergone a radical prostatectomy for Gleason’s stage 6 adenocarcinoma. It is likely that he had an adynamic postoperative ileus following the surgical procedure that caused distention of the previously acquired duodenal diverticulum. We propose that distention resulted in local inflammation of the diverticulum (diverticulitis). The inflammation of contiguous tissues, including the head and uncinate process of the pancreas, caused acute thrombosis of the juxtaposed SMV. The patient’s symptoms were caused by all of these in addition to the resulting small bowel edema and venous congestion. SMVT is rare but potentially lethal when associated with intestinal ischemia and infarction. In fact, the mortality rate may be as high as 27%.6 SMVT is implicated in only 5-15% of cases of intestinal ischemia.6,7 Factors that determine the presence of ischemia in association with SMVT include the degree of venous occlusion, thrombosis of associated vessels, and the degree of venous collateralization.3 Mesenteric vein thrombosis can be categorized as primary or secondary. Approximately 15-45% of cases are considered primary, or idiopathic.1,4-6,8 Recognized secondary causes of SMVT are included in Table I.1,2,4-7 Often these conditions are not associated with isolated SMVT but also involve the splenic or portal veins. Of course, as more causes of thrombosis are discovered, the percentage of cases considered secondary will increase. The clinical presentation of SMVT is variable and depends on the degree of intestinal ischemia, local pain of the thrombus, and associated conditions. The patient’s history may include such nonspecific complaints such as nausea, vomiting, diarrhea, hematemesis, and anorexia.6,7 Generalized abdominal discomfort is often present and may be prolonged in
280
Case reports
Annals of Vascular Surgery
Table I. Secondary causes of SMVT Abdominal inflammatory processes Abscess Appendicitis Inflammatory bowel disease Pancreatitis Peritonitis Postoperative state Hypercoagulable states Antithrombin III deficiency Malignancy Protein S deficiency Protein C deficiency Myeloproliferative disorders Polycythemia vera Thrombocytosis Portal hypertension Cirrhosis Other Oral contraceptives Postsplenectomy Pregnancy Trauma
cases of chronic SMVT. Physical findings can include pain out of proportion to physical findings and a low-grade fever. Peritoneal signs are present in cases of bowel infarction. Approximately 29 to 50% of patients will be heme positive and about half will have leukocytosis.5,6 Since it is rare and symptoms are nonspecific, SMVT is often not considered in the differential diagnosis. In fact, more common causes of abdominal symptoms should be explored first. About 80% of cases are discovered during a diagnostic or curative surgical procedure.1 Plain radiographs and barium exams are generally nonspecific and not helpful in the diagnosis of SMVT.4 If SMVT is suspected on the basis of history and clinical presentation, a CT scan with intravenous contrast should be performed and has a sensitivity as high as 90-100%.5 Typical findings include a central filling defect with a highdensity venous wall, anterior and to the right of the superior mesenteric artery, and bowel wall or mesenteric edema, as in Figure 2.1,3 Ultrasound may also be helpful in making the diagnosis. Visualization of the thrombus or absence of flow in the vessel may be seen in up to 80% of patients.4,6 The treatment for SMVT varies with the symptoms and predisposing condition. Chronic isolated SMVT is often associated with the presence of large collaterals and is asymptomatic; therefore it may not require therapy.8 Anticoagulation is recommended for acute, symptomatic SMVT.4,5 Rhee et
Fig. 2. CT scan demonstrating the central filling defect of the SMV (arrow) with associated perivascular and mesenteric inflammatory changes.
al.6 proposed an algorithm in which all patients with peritoneal signs be anticoagulated and undergo laparotomy with resection of nonviable bowel and undergo a second-look procedure at 24 hr if necessary. Other series do not recommend second-look procedures secondary to increased mortality.1 If no peritoneal signs are present, then CT and/or angiography can be performed with anticoagulation following a positive study.6 Duration of treatment varies, with recommendations from 6 months to lifelong anticoagulation.5,6 Certainly, patients with known coagulopathy or recurrent SMVT may require longer treatment. Other proposed methods of treatment include surgical thrombectomy and thrombolysis. 5,9 Thrombolysis is suggested in cases of thrombosis without or prior to the development of bowel ischemia.9 Thrombolytic therapy has also been used to reduce the length and duration of ischemic bowel prior to surgical resection.5 The patient in this case had no peritoneal signs, but surgery was indicated for suspicion of pancreatic cancer. Intraoperatively, an inflamed duodenal diverticulum causing inflammation of the contiguous head and uncinate process of the pancreas was found and thought to be the logical cause of the SMVT. The appearance of the pancreatic tissue was consistent with inflammation and not with carcinoma and this was confirmed by biopsy. Because of the chronicity of the event (days) and the fact that
Vol. 14, No. 3, 2000
the small bowel was clearly viable and not obstructed, no resection was performed, nor was any attempt made to recanalize the SMV. The duodenum ranks second to the colon as the most common site for development of diverticula in the alimentary tract.10 The incidence at autopsy/ endoscopy ranges from 2.2 to 23%.11,12 However, only 1-5% are seen on plain film or barium studies.13,14 There is a rare congenital form of duodenal diverticulum that is intraluminal and a more common acquired extraluminal form. Extraluminal diverticula are asymptomatic in over 90% of cases.14 Often they are detected incidentally during evaluation for other gastrointestinal disorders. They are asymptomatic in part because inflammation of duodenal diverticula is uncommon. When compared to colonic diverticula, those in the duodenum are larger in size and have increased intraluminal flow, so that food particles are less likely to be trapped; in addition, the environment is relatively sterile.10,11 When duodenal diverticula are symptomatic, complaints are usually nonspecific and mild,14 unless a serious complication has occurred. Complications include ulceration, bile or pancreatic duct obstruction, duodenal obstruction, perforation, or abscess.12,13 Bile or pancreatic duct obstruction occurs with diverticula adjacent to the ampulla of Vater and can lead to pancreatitis or choledocolithiases.12,14 If duodenal diverticula are suspected, the diagnosis may be made by CT scan. Generally, CT findings will include thickening of the diverticular wall and deformity of its lumen, but complications resulting from the diverticulum may alter these findings.11 As they are generally asymptomatic, only about 1-12% of duodenal diverticula require intervention.11,14,15 If serious complications are not present, conservative treatment with fasting followed by frequent small meals with high-fiber content can be attempted.14 More invasive intervention may be indicated in cases of ulceration, duodenal obstruction, perforation, or abscess.12,13 There are several operative procedures depending on location and severity of symptoms, from sphincteroplasty with diverticuloplasty or simple diverticulectomy to more complex excisional procedures.10-11,14 Excision is the treatment of choice for extraluminal diverticula,10,13 but may be difficult depending on the location relative to the pancreas and pancreatic and biliary ducts. The patient in this case demonstrated no clinical evidence of biliary or pancreatic duct obstruction. Because of the size and location of the diverticulum and lack of direct complications, (ulceration, bleed-
Case reports 281
ing, obstruction, perforation, or abscess), no attempt was made to resect it. Pancreatic duct obstruction from a periampullary duodenal diverticulum can lead to pancreatitis that in turn can cause SMVT usually in association with splenic vein thrombosis.2-4 The etiology includes spasm of the vein, stasis, mass effect, perivascular extension of inflammation, and thrombogenic factor release from the inflamed pancreas. While our patient had more of a local phenomenon with a mildly elevated serum lipase rather than pancreatitis per se, some of these factors probably contributed to the SMVT. Hypercoagulable states, myeloproliferative disorders, and malignancy are common and important causes of SMVT. Our patient had a history of previous thrombosis, so these possibilities were explored. As stated previously, the hypercoagulable profile and blood count provided no evidence for a predisposition to thrombosis or a myeloproliferative disorder. Although prostate cancer specifically has not been reported as a cause of SMVT, it cannot be ruled out as a contributing factor in this case.
SUMMARY Although rare, SMVT is important to consider in cases of abdominal discomfort and mesenteric ischemia. Diagnosis is aided by the use of a CT scan and evidence can also be seen on ultrasound. If the patient has SMVT and peritoneal signs, surgical intervention is warranted and nonviable bowel should be resected. Concomitant existence of a duodenal diverticulum, discovered radiographically or at the time of surgery, should not necessarily be removed unless is implicated in a separate pathologic process.14 If there is no obvious cause of the thrombosis, one should look for a predisposing hypercoagulable state.7 When discovered, lifelong anticoagulation may be indicated. Otherwise, a patient with acute and/or symptomatic SMVT should remain on oral anticoagulation for a minimum of 6 months.
REFERENCES 1. Al-Hilaly MA, Abu-Zidan FM. Mesenteric vein thrombosis: is it one disease? Eur J Vasc Endovasc Surg 1995;9:103-106. 2. Cornu-labat G, Kasirajan K, Simon R, et al. Acute mesenteric vein thrombosis and pancreatitis. Int J Pancreatol 1997; 21:249-251. 3. Crowe PM, Sagar G. Reversible superior mesenteric vein thrombosis in acute pancreatitis. The CT appearances. Clin Radiol 1995;50:628-633. 4. Font VE, Hermann RE, Longworth DL. Chronic mesenteric venous thrombosis: difficult diagnosis and therapy. Cleve Clin J Med 1989;56:823-828. 5. Rijs J, Depreiter B, Beckers A, et al. Mesenteric vein throm-
282
6.
7.
8.
9.
10.
Case reports
bosis: diagnostic and therapeutic approach. Acta Chir Belg 1997;97:247-249. Rhee RY, Gloviczki P, Mendonca CT, et al. Mesenteric venous thrombosis: still a lethal disease in the 1990s. J Vasc Surg 1994;29:688-697. Crespo I, Murphy J, Wong RKH. Superior mesenteric venous thrombosis masquerading as Crohn’s disease. Am J Gastroenterol 1994;89:116-118. Rattner DW, Warshaw AL. Venous, biliary, and duodenal obstruction in chronic pancreatitis. Hepatogastroenterology 1990;37:301-306. Poplausky MR, Kaufman JA, Geller SC, et al. Mesenteric venous thrombosis treated with urokinase via the superior mesenteric artery. Gastroenterology 1996;110:1633-1635. Gore RM, Ghahremani GG, Kirsch MD, et al. Diverticulitis of the duodenum: clinical and radiological manifestations of seven cases. Am J Gastroenterol 1991;86:981-985.
Annals of Vascular Surgery
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