Treatment of Superior Mesenteric Vein Thrombus by Catheter-Directed Thrombolysis.

Contrast-enhanced computed tomography (CT) greatly improves the diagnosis of superior mesenteric vein (SMV) thrombosis, which presents as the unspecific symptom of abdominal pain. Prothrombotic states or thrombophilia and local intra-abdominal infections are major causes of SMV thrombosis. A 37-year-old Chinese woman was diagnosed with SMV and portal vein thrombosis. The patient was initially given 40 mg of heparin sodium every 12 hr and 80,0000 U/day of urokinase using superior mesenteric artery angiography. The abdominal pain was not relieved after treatment. The patient then underwent open surgery, where an ileal branch of the SMV was punctured, a 4F sheath was introduced into the vein toward the portal vein, and a 20-cm Unifuse catheter was placed inside the thrombus for further thrombolysis. Both heparin sodium and urokinase were infused through catheter-directed thrombolysis. The patient's symptoms then gradually resolved.

Successful intravenous administration of argatroban in the management of heparin-resistant and surgery-resistant mesenteric vein thrombosis.

A 78-year-old woman visited the emergency department with complaints of progressively worsening abdominal pain for a week. Nausea and vomiting started at the time of the visit. An abdominal contrast-enhanced CT (CECT) revealed a filling defect of portal vein, splenic vein and superior mesenteric vein (SMV) which was diagnosed as portal vein and mesenteric venous thrombosis (MVT). Intravenous administration of unfractionated heparin was initiated. However, her symptoms did not improve, and she underwent surgical thrombectomy on the second day of hospitalisation. On the sixth day, CECT revealed the recurrence of thrombi in the portal vein, SMV and along the central venous catheters. We switched heparin to argatroban on the eighth day. After administering argatroban, CECT revealed that the thrombi had almost disappeared by the 40th day. In this case, argatroban was considered effective for heparin-resistant and surgery-resistant portal vein and MVT.

Primary Nonbacterial Thrombotic Endocarditis Presenting with Bowel Infarction Secondary to Superior Mesenteric Artery Embolism.

Nonbacterial thrombotic endocarditis (NBTE) is a rare antemortem diagnosis that is commonly associated with hypercoagulable states such as advanced malignancies, disseminated intravascular coagulation, and autoimmune diseases such as antiphospholipid syndrome and systemic lupus erythematosus. We present a case of a previously healthy 42-year-old man who presented with small bowel infarction caused by embolic occlusion of the superior mesenteric artery and was subsequently diagnosed with NBTE. Despite thorough investigation, efforts to find an underlying cause failed to reveal any associated systemic illnesses. This case report emphasizes the importance of further investigation into the possible underlying causes of NBTE, as it can manifest without any apparent systemic factors.

[A case of superior mesenteric artery occlusion with ischemic enteritis after transcatheter therapy].

An 84-year-old female was admitted with sudden-onset upper abdominal pain. Contrast-enhanced computed tomography (CECT) revealed complete occlusion of the superior mesenteric artery (SMA). After transcatheter infusion of urokinase, embolic occlusion resolved. However, the pain recurred when she started eating. CECT revealed a lesion with thickening of the intestinal wall; therefore, laparoscopy-assisted surgery was undertaken. Histological examination yielded a definitive diagnosis of ischemic enteritis caused by SMA occlusion. Rapid diagnosis and treatment are important in SMA occlusion, and careful observation of the clinical course is recommended after transcatheter therapy.

Protective effects of osthole on intestinal ischemia-reperfusion injury in mice.

OBJECTIVES: The purpose of this study was to evaluate the effect of intravenous injection of osthole on intestinal ischemia-reperfusion injury and parameters of oxidative stress. MATERIALS AND METHODS: In 45 Kunming male mice, treatment included sham surgery (15 mice); intestinal ischemia-reperfusion injury (clamping of the superior mesenteric artery, 2 h; clamp release, 1 h; 15 mice); or osthole treatment before and after ischemia-reperfusion injury (15 mice). Evaluation included histopathology, determination of intestinal wet/dry weight ratio, and measurement of levels of diamine oxidase, superoxide dismutase, malondialdehyde, interleukin 1ß, tumor necrosis factor α, and interleukin 2. Intestinal barrier permeability was evaluated with Evans blue test. RESULTS: The mean wet-to-dry weight ratio, Evans blue content, and Chiu score were significantly greater in the ischemia-reperfusion than in the sham group and lower in the osthole-treated than the ischemia-reperfusion group. The mean serum diamine oxidase, malondialdehyde, interleukin 1ß, and tumor necrosis factor α levels were significantly greater in the ischemia-reperfusion than in the sham group and lower in the osthole-treated than in the ischemia-reperfusion group. The mean superoxide dismutase activity and interleukin 2 levels were lower in the ischemia-reperfusion than in the sham group and greater in the osthole-treated than in the ischemia-reperfusion group. CONCLUSIONS: Treatment with osthole may protect against oxidative stress and tissue damage from intestinal ischemia-reperfusion injury.

Beneficial effects of intra-arterial and intravenous prostaglandin E1 in intestinal ischaemia-reperfusion injury.

OBJECTIVES: Ischaemia-reperfusion (I/R) injury is encountered in conditions that diminish intestinal blood flow. There is no clinically feasible technique available for mucosal preservation. METHODS: One hundred Wistar rats were subjected to intestinal ischaemia for 15 and 60 min (I15', I60'), followed by 1 and 7 days of reperfusion (R1d, R7d). Rats were subjected to ischaemia by clamping the superior mesenteric artery. Prostaglandin E1 (PGE1) (2.500 ng/kg intra-arterial bolus or 20 ng/kg intravenous infusion) was administered immediately prior to the commencement of the experimental period. Animals were divided into 20 groups: sham (laparotomy alone), sacrificed at 1 or 7 days; saline administration, 15 or 60 min of ischaemia, 1 or 7 days of reperfusion; prostaglandin E1 administration, 15 or 60 min of ischaemia, 1 or 7 days of reperfusion, each one for intra-arterial or intravenous administration. Ileal segments were excised and assessed for histopathological score, polymorphonuclear (PMN) leucocytes encountered and myeloperoxidase (MPO) activity measurement. RESULTS: I/R caused deterioration of histological characteristics. Prophylactic administration of PGE1 resulted in a significant decrease in the histological score compared with the respective saline group (analysis of variance, P < 0.005). In groups treated with PGE1, PMN leucocyte infiltration was lower for the 60 min of ischaemia group (I60'/R1d *P = 0.026; I60'/R7d P = 0.015). I15'/R7d did not lead to a significant reduction in PMN infiltration (P = 0.061). Pretreatment with PGE1 attenuates MPO levels after intestinal I/R injury (P < 0.05). No differences were encountered between types of administration. CONCLUSIONS: Results of this study showed that administration of prostaglandin E1 prevents I/R injury by diminishing histological damage parameters, inhibiting PMN leucocyte infiltration and attenuating MPO activity.

Modern treatment of acute mesenteric ischaemia.

BACKGROUND: Diagnosis of acute mesenteric ischaemia in the early stages is now possible with modern computed tomography (CT), using intravenous contrast enhancement and imaging in the arterial and/or portal venous phase. The availability of CT around the clock means that more patients with acute mesenteric ischaemia may be treated with urgent intestinal revascularization. METHODS: This was a review of modern treatment strategies for acute mesenteric ischaemia. RESULTS: Endovascular therapy has become an important alternative, especially in patients with acute thrombotic superior mesenteric artery (SMA) occlusion, where the occlusive lesion can be recanalized either antegradely from the femoral or brachial artery, or retrogradely from an exposed SMA after laparotomy, and stented. Aspiration embolectomy, thrombolysis and open surgical embolectomy, followed by on-table angiography, are the treatment options for embolic SMA occlusion. Endovascular therapy may be an option in the few patients with mesenteric venous thrombosis who do not respond to anticoagulation therapy. Laparotomy is needed to evaluate the extent and severity of visceral organ ischaemia, which is treated according to the principles of damage control surgery. CONCLUSION: Modern treatment of acute mesenteric ischaemia involves a specialized approach that considers surgical and, increasingly, endovascular options for best outcomes.

Clinical and radiologic course of symptomatic spontaneous isolated dissection of the superior mesenteric artery treated with conservative management.

OBJECTIVE: To determine the clinical and radiological outcomes of patients with symptomatic spontaneous isolated dissection of the superior mesenteric artery (SIDSMA) who were treated with conservative management. METHODS: This retrospective study included 27 consecutive patients who were diagnosed with symptomatic SIDSMA and managed conservatively from April 2007 to April 2013. Twenty-six patients were treated using anticoagulation therapy, and one patient with chronic liver disease underwent observation only. For evaluation, patients were divided into two groups, those with a patent false lumen with both entry and re-entry (group I), and those with partial or complete thrombosis of the false lumen (group II). In general, the patients underwent follow-up computed tomography angiography (CTA) 1 week, 1 month, and 6 months after admission. Thereafter, they underwent annual CTAs. RESULTS: There were five group I and 22 group II patients. During hospitalization, none of the patients needed additional endovascular or surgical intervention, and after conservative management, every patient was asymptomatic upon discharge. The mean duration of clinical follow-up was 27.3 months. There was no recurrent abdominal pain associated with SIDSMA, and no invasive procedures due to SIDSMA were needed. During a mean of 17.1 months of CTA follow-up in group I patients, serial CTAs found sustained patent false lumen and no angiographic changes in all patients. Among 22 group II patients, despite anticoagulation and symptomatic relief, CTA 1 week after admission revealed increased stenosis of the true lumen in 84.2% (16/19) of patients including six cases of progressive SMA occlusion. Five patients, including the three patients initially presenting with SMA occlusion, had no interval changes, and only one patient had improved compression of the true lumen. During a mean of 18.0 months of CTA follow-up in group II patients, serial CTAs revealed improvement in the occlusion or stenosis of the true lumen in 89% (16/18) of patients and progressive resolution of false lumen thrombosis in all patients. Aneurysmal dilatation greater than 2 cm was not detected in either group of patients during follow-up. CONCLUSIONS: During the acute stage of SIDSMA, we found a discrepancy between the clinical and angiographic findings. The therapeutic regimen should be based on clinical symptoms, and conservative management is feasible in most cases. SMA stenosis could not be an indication for invasive treatment, because stenosis of the true lumen has been seen to improve after the acute stage of dissection.

Superior mesenteric vein thrombosis after laparoscopic sleeve gastrectomy.

Laparoscopic procedures for morbid obesity are becoming standard of care which, in experienced hands, has a very low mortality and morbidity. Superior mesenteric vein thrombosis has been reported in the literature after different bariatric and nonbariatric laparoscopic procedures. Laparoscopic sleeve gastrectomy is a relatively new procedure in the treatment of morbid obesity; its complications being well-known including staple line leak, bleeding, and stricture among others. We present a case of superior mesenteric vein thrombosis after laparoscopic sleeve gastrectomy successfully managed conservatively with therapeutic anticoagulation, and propose a different hypothesis for the development of such a complication.

Effects of exogenous vasoactive intestinal peptide on mesenteric lymph pathway during early intestinal ischemia-reperfusion injury in rats.

Mesenteric lymph pathway serves as the primary route by which gut injury leads to systemic inflammation and distant organ injury. The inflammation of the intestinal tract is partially mediated by vasoactive intestinal peptide (VIP). Therefore, the aim of this study was to test whether exogenous VIP affects mesenteric lymph pathway during early intestinal ischemia-reperfusion (IIR) injury. Rats were randomized into control, control+VIP, IIR and IIR+VIP groups. The observation of mesenteric lymph flow was carried out by cannulation of mesenteric lymphatics. The distribution of in vivo lymphocyte trafficking was performed by (51)Cr labeled lymphocytes and was measured by γ-counter. Endotoxin concentration was assayed using the limulus test kit and TNF-α level was detected by ELISA. When IIR injury treated with VIP, the volumes of lymph flow increased by 80%, which caused the number of lymphocytes exiting in mesenteric lymphatic increased by 50% while the proportion of (51)Cr-lymphocytes in Peyer's patches, intestinal effector tissues, mesenteric nodes, large intestine, stomach decreased by 58%, 51%, 58%, 63%, 64% respectively at the 6th h after reperfusion following intestinal ischemia. Meanwhile, endotoxin and TNF-α levels in intestinal lymph decreased by 51% and 83%. These results suggest that exogenous VIP ameliorates IIR induced splanchnic organ damage via inhibition of toxic mediators reaching systemic circulation and reinforcement of the effective immune responses in gut-associated lymphoid tissues (GALT).

Preconditioning with soluble guanylate cyclase activation prevents postischemic inflammation and reduces nitrate tolerance in heme oxygenase-1 knockout mice.

Previously we have shown that, unlike wild-type mice (WT), heme oxygenase-1 knockout (HO-1-/-) mice developed nitrate tolerance and were not protected from inflammation caused by ischemia-reperfusion (I/R) when preconditioned with a H2S donor. We hypothesized that stimulation (with BAY 41-2272) or activation (with BAY 60-2770) of soluble guanylate cyclase (sGC) would precondition HO-1-/- mice against an inflammatory effect of I/R and increase arterial nitrate responses. Intravital fluorescence microscopy was used to visualize leukocyte rolling and adhesion to postcapillary venules of the small intestine in anesthetized mice. Relaxation to ACh and BAY compounds was measured on superior mesenteric arteries isolated after I/R protocols. Preconditioning with either BAY compound 10 min (early phase) or 24 h (late phase) before I/R reduced postischemic leukocyte rolling and adhesion to sham control levels and increased superior mesenteric artery responses to ACh, sodium nitroprusside, and BAY 41-2272 in WT and HO-1-/- mice. Late-phase preconditioning with BAY 60-2770 was maintained in HO-1-/- and endothelial nitric oxide synthase knockout mice pretreated with an inhibitor (dl-propargylglycine) of enzymatically produced H2S. Pretreatment with BAY compounds also prevented the I/R increase in small intestinal TNF-α. We speculate that increasing sGC activity and related PKG acts downstream to H2S and disrupts signaling processes triggered by I/R in part by maintaining low cellular Ca²âº. In addition, BAY preconditioning did not increase sGC levels, yet increased the response to agents that act on reduced heme-containing sGC. Collectively these actions would contribute to increased nitrate sensitivity and vascular function.

Pentoxifylline protects the small intestine after severe ischemia and reperfusion.

OBJECTIVES: Pentoxifylline, a methylxanthine derivative with significant hemorheologic properties, is used for claudication in patients with peripheral vascular disease, and experimentally for ischemic injury to organs because of its antioxidant and antiinflammatory effects. We used a rat model of severe small intestinal ischemia and reperfusion to determine the ability of pentoxifylline in improving survival, molecular response, and pathological protection. MATERIALS AND METHODS: We used 6 groups of male Wistar rats (n=25 each). The superior mesenteric artery was occluded for 120 minutes. Laboratory and tissue studies were done on 5 animals, 1 hour after reperfusion, and animal survival was assessed at 7 days. There were 2 control groups that received normal saline, either before ischemia or during reperfusion. The 4 treated groups received pentoxifylline 1 or 10 mg/kg at the same times mentioned above. Laboratory studies included measuring serum lactic acid dehydrogenase, tumor necrosis factor-α, interleukin-1ß, and interleukin-6.Intestinal tissue malondialdehyde and myeloperoxidase in small intestine tissue also were measured. Histology and laser vascular blood flow at baseline and reperfusion were obtained, and survival was determined 7 days after ischemia. RESULTS: A significant survival benefit in the animals treated with 10 mg/kg of pentoxifylline at reperfusion was noted. This coincided with a reduction in biochemical markers of cell damage - specifically, serum lactic acid dehydrogenase, and tissue malondialdehyde, ischemia, and reperfusion. Additionally, we saw decreased levels of tumor necrosis factor-α, interleukin-1ß, and interleukin-6. Improved postreperfusion blood flow shown by laser Doppler technology also was seen in the treated groups. Histologically, we observed less neutrophil infiltration in the intestine of ischemic-treated rats. Also seen in the control animals were increased necrotic lesions in the microvilli with a higher presence of lysozyme in the Paneth cells. Survival was significantly better at 7 days (70% vs 40%) when we compared the pentoxifylline group treated at reperfusion (10 mg/kg) to the ischemic controls. CONCLUSIONS: Pentoxifylline had a significant protective effect on severely ischemic bowel when administered during reperfusion at a dosage of 10 mg/kg. Better survival, improved histology, and molecular response should urge consideration of the consideration of applying these findings in some general surgery and transplant conditions.

Portomesenteric vein thrombosis in patients with inflammatory bowel disease.

BACKGROUND: Inflammatory bowel disease (IBD) is associated with a high risk of deep venous thromboembolism. However, few data are available so far on portomesenteric vein thrombosis (PMVT). The aim of this study was to describe the characteristics of PMVT in patients with IBD. METHODS: A retrospective study was conducted at 13 GETAID (Groupe d'Etude Thérapeutique des Affections Inflammatoires du Tube Digestif) centers from January 1995 to June 2010. The following data were collected, using a standardized questionnaire: characteristics of IBD, disease status at the time of PMVT, PMVT characteristics and mode of discovery, concomitant prothrombotic disorders, anticoagulant therapy, and evolution of PMVT. RESULTS: Fifty cases (29 men and 21 women; median age, 41 years) were identified, including 14 patients with ulcerative colitis and 36 with Crohn's disease. Thirty-one patients (62%) presented with acute PMVT. Twenty-four patients had previously undergone surgical treatment, and IBD was active in 23 cases (77%) of acute thrombosis. The discovery of PMVT was fortuitous in 40% of our cases. Among the 43 patients screened for a prothrombotic disorder, abnormalities were observed in 17 patients (40%) (mainly hyperhomocysteinemia, n = 12). Forty-four patients (88%) were treated with anticoagulants. Recanalization of the vein was significantly more successful in patients with acute thrombosis (65% versus 37%, P = 0.05). CONCLUSIONS: PMVT can occur when IBD is inactive, and its diagnosis was fortuitous in 40% of our cases. Screening for prothrombotic disorders is essential because it is positive in more than one third of cases.

Protective effect of ginsenoside Rb1 against lung injury induced by intestinal ischemia-reperfusion in rats.

Intestinal ischemia-reperfusion (I/R) is a critical event in the pathogenesis of multiple organ dysfunction syndromes (MODS). The lungs are some of the most vulnerable organs that are impacted by intestinal I/R. The aim of this study is to investigate whether ginsenoside Rb1 can ameliorate remote lung injury induced by intestinal I/R. Adult male Wistar rats were randomly divided into four groups: (1) a control, sham-operated group (sham group); (2) an intestinal I/R group subjected to 1 h intestinal ischemia and 2 h reperfusion (I/R group); (3) a group treated with 20 mg/kg ginsenoside Rb1 before reperfusion (Rb1-20 group); and (4) a group treated with 40 mg/kg ginsenoside Rb1 before reperfusion (Rb1-40 group). Intestinal and lung histology was observed. The malondialdehyde (MDA) levels in intestinal tissues were measured. Myeloperoxidase (MPO), TNF-α, MDA levels, wet/dry weight ratio and immunohistochemical expression of intracellular adhesion molecule-1 (ICAM-1) in lung tissues were assayed. In addition, a western blot of lung NF-kB was performed. Results indicated that intestinal I/R induced intestinal and lung injury, which was characterized by increase of MDA levels and pathological scores in intestinal tissues and MPO, TNF-α , MDA levels, wet/dry weight ratio and ICAM-1, NF-kB expression in the lung tissues. Ginsenoside Rb1 (20, 40 mg/kg) ameliorated intestinal and lung injury, decreased MPO, TNF-α, MDA levels, wet/dry weight ratio, ICAM-1 and NF-kB expression in lung tissues. In conclusion, ginsenoside Rb1 ameliorated the lung injuries by decreasing the NF-kB activation-induced inflammatory response.

Management of acute portomesenteric venous thrombosis induced by protein S deficiency: report of a case.

Hereditary protein S deficiency is a risk factor which may predispose patients to venous thrombosis. Deep venous thrombosis of the lower extremities can result in painful congestion, while the presence of mesenteric venous thrombosis (MVT) can cause abdominal emergencies. We herein report a protein S-deficient patient presenting with acute portomesenteric venous thrombosis. Early management using anticoagulant therapy was initially successful. However, the subsequent bowel stricture resulting from the ischemic insult was further managed with a surgical bypass. The patient was kept on long-term thrombophylaxis. The treatment strategy for MVT with bowel ischemia has evolved from aggressive portomesenteric thrombectomy with resection of the involved bowel, to conservative anticoagulation to recanalize thrombotic mesenteric veins with bowel preservation. Surgical intervention is reserved for transmural necrosis or bowel perforation. The perioperative thrombophylaxis of inherited thrombophilic patients is also important for preventing further thromboembolic events.

Infusion of recombinant human tissue plasminogen activator through the superior mesenteric artery in the treatment of acute mesenteric venous thrombosis.

Acute mesenteric venous thrombosis is an uncommon condition that is usually treated with systemic anticoagulation. Catheter-directed thrombolysis through the superior mesenteric artery may be a viable adjunct to treat this morbid condition. In the present article, we have described a case of superior mesenteric venous thrombosis treated with catheter-directed infusion of tissue plasminogen activator through the superior mesenteric artery.