Transhepatic fibrinolysis of mesenteric and portal vein thrombosis in a patient with uIterative colitis: A case report

AIM: To present a case of acute mesenteric and portal vein thrombosis treated with thrombolytic therapy in a patient with ulcerative colitis in acute phase and to review the literature on thrombolytic therapy of mesenteric-portal system. Treatment of acute portal vein thrombosis has ranged from conservative treatment with thrombolysis and anticoagulation therapy to surgical treatment with thrombectomy and/or intestinal resection. METHODS: We treated our patient with intraportal infusion of plasminogen activator and then heparin through a percutaneous transhepatic catheter. RESULTS: Thrombus resolved despite premature interruption of the thrombolytic treatment for neurological complications, which subsequently resolved. CONCLUSION: Conservative management with plasminogen activator, could be considered as a good treatment for patients with acute porto-mesenteric thrombosis.     

Cavernous mesenteric lymphangiomatosis mimicking metastasis in a patient with rectal cancer： A case report

Lymphangioma usually occurs in children and usually involves the skin. Mesenteric lymphangioma is extremely rare in adults. Typically, lymphangioma appears on computed tomography （CT） as a lower attenuation of a cystic mass, however, some cases appear to be a solid mass. We describe the CT and 18FFDG positron emission tomography/CT appearance in a case of jejunal and mesenteric cavernous lymphangiomatosis mimicking metastasis in an adult patient with rectal cancer.     

Portal venous gas and thrombosis in a Chinese patient with fulminant Crohn＇s colitis： A case report with literature review

Ever since its earliest reports, portal venous gas (PVG) has been associated with numerous intraabdominal catastrophes and has served as an indication for urgent surgical exploration. It is traditionally regarded to be an ominous finding of impending death, with highest mortality reported in patients with underlying bowel ischemia. Today, computed tomography has demonstrated a wider range of clinical conditions associated with PVG, some of which are "benign" and do not necessarily require surgery, unless when there are signs of intraabdominal catastrophe or systemic toxicity. One of these "benign" conditions is Crohn's disease. The present report describes a 19-year-old Chinese boy with Crohn's pancolitis who presented with septic shock associated with PVG and portal vein thrombosis, and was successfully managed surgically. To our knowledge, this is the first report of PVG and portal vein thrombosis associated with Crohn's disease in a Chinese patient. In addition, we have also reviewed the reports of another 18 Crohn's patients with PVG previously described in the English literature. Specific predisposing factors for PVG were identified in 8 patients, including barium enema, colonoscopy, blunt abdominal trauma, and enterovenous fistula. The patients who developed PVG following barium enema and blunt trauma were all asymptomatic and no specific treatment was necessary. Eleven patients (58%) who presented with signs of intraabdominal catastrophe or systemic toxicity required either immediate or eventual surgery. The overall mortality rate among the 19 patients was only 11%. The present literature review has shown that the finding of PVG associated with Crohn's disease does not always mandate surgical intervention. It is the clinical features and the related complications that ultimately determine the treatment approaches. The overall outcome of PVG associated with Crohn's disease has been favourable.     

Solitary colonic neurofibroma in a patient with transient segmental colitis： Case report

Neurofibromas of the large bowel are very rare and usually are part of the colonic involvement in neurofibromatosis type 1 (Nfl, von Recklinghausen's disease). Solitary neurofibromas of the colon are extremely rare. We describe a case of an isolated neurofibroma that was found in the large bowel of a patient who suffered from segmental colitis and presented with bloody diarrhea. A review of the literature is also included, concerning the disclosure of isolated neurofibromas in the gut and other body parts and the type of gastrointestinal involvement in von Recklinghausen's disease.     

Refractory ulcerative colitis accompanied with cytomegalovirus colitis and multiple liver abscesses： A case report

Various hepato-biliary complications are an increased incidence in patients with inflammatory bowel disease, and portal bacteremia is well documented in patients with ulcerative colitis (DC). However, few reports mention UC in association with liver abscesses. Recently, there are several reports describing cytomegalovirus (CMV) infection in association with disease exacerbation and steroid refractoriness in patients with UC. Here we present a case of refractory UC accompanied with multiple liver abscesses and CMV colitis. The patient, a 72-year-old male, with a five-year history of repeated admissions to our hospital for UC, presented with an exacerbation of his UC. Sigmoidoscopy performed on admission suggested that his UC was exacerbated, then he was given prednisolone and mesalazine orally, and betamethasone enemas. However, he had exacerbated symptoms. Repeat Sigmoidoscopy revealed multiple longitudinal ulcers and pseudopolyps in the rectosigmoid colon. Although immunohistochemical staining of biopsy specimens and the serum testing for antigenemia were negative on admission and after the repeat Sigmoidoscopy, they became histologically positive for CMV. Nonetheless, the patient developed spiking fevers, soon after ganciclovir was administered. Laboratory studies revealed an increased white cell count with left shift, and Enterococcus fecalis grew in blood cultures. An abdominal computed tomography (CT) scan was obtained and the diagnosis of liver abscesses associated with UC was made, based on CT results. The hepatic abscesses were successfully treated with intravenous meropenem for 6 wk, without further percutaneous drainage. To our knowledge, this is the first reported case of multiple liver abscesses that develop during UC exacerbation complicated by CMV colitis.     

Primary biliary cirrhosis and ulcerative colitis： A case report and review of literature

AIM: To summarize the characteristics of patients suffered from primary biliary cirrhosis associated with ulcerative colitis. METHODS: To report a new case and review the literature. RESULTS: There were 18 cases (including our case) of primary biliary cirrhosis complicated with ulcerative colitis reported in the literature. Compared with classical primary biliary cirrhosis, the patients were more often males and younger similar. The bowel lesions were usually mild with proctitis predominated. While ulcerative colitis was diagnosed before primary biliary cirrhosis in 13 cases, the presentation of primary biliary cirrhosis was earlier than that of ulcerative colitis in our new case reported here. The prevalence of primary biliary cirrhosis among patients of ulcerative colitis was almost 30 times higher than in general population. CONCLUSION: Association of primary biliary cirrhosis with ulcerative colitis is rare. It should be considered in the differential diagnosis of hepatobiliary disease in patients with ulcerative colitis, and vice versa.     

Pouchitis and pre-pouch ileitis developed after restorative proctocolectomy for ulcerative colitis： A case report

We report a case of pouchitis and pre-pouch ileitis, and inflammation in the neo-terminal ileum proximal to the pouch, developed after restorative proctocolectomy for ulcerative colitis. A 35-year old female presented with fever and abdominal pain five weeks after ileostomy closure following proctocolectomy. ComputEd tomography showed collection of feces in the pouch and proximal ileum. A drainage tube was placed in the pouch perianally, and purulent feces were discharged. With antibiotic treatment, her symptoms disappeared, but two weeks later, she repeatedly developed fever and abdominal pain along with anal bleeding. Pouchscopy showed mucosal inflammation in both the pouch and the pre-pouch ileum. The mucosal cytokine production was elevated in the pouch and pre-pouch ileum. With antibiotic and corticosteroid therapy, her symptoms were improved along with improvement of endoscopic inflammation and decrease of mucosal cytokine production. The fecal stasis with bacterial overgrowth is the major pathogenesis of pouchitis and pre-pouch ileitis in our case.     

Hypokalemic myopathy in a patient with gluten-sensitive enteropathy and dermatitis herpetiformis Duhring： A case report

The case of a 22-year-old patient with symptomatic hypokalemia caused by rhabdomyolysis is presented as a rarely reported complication of gluten-sensitive enteropathy (GSE) and dermatitis herpetiformis Duhring. The patient's myopathy ceased on potassium supplementation and her other complaints resolved while on gluten-free diet. Recovery was otherwise uneventful with a rapid decline in serum CPK level. At the time of her last follow-up a few months later, she was free of symptoms and CPK remained stable. Patients with GSE may present with hypokalemia in association with diarrhea and emesis, and if potassium loss is rapid, rhabdomyolysis may occur.     

Spontaneous liver rupture in a patient with peliosis hepatis： A case report

Peliosis hepatis is a rare pathological entity and may cause fatal hepatic hemorrhage and liver failure.Here, we present a young male patient with aplastic anemia, who had received long-term treatment with oxymetholone.The patient suffered from sudden onset of intra-abdominal hemorrhage with profuse hemoperitoneum.The patient was treated successfully with a right hemihepatectomy and is in good health after 13 postoperative months.We suggest that peliosis hepatis be considered in patients with hepatic parenchymal hematoma, especially in patients under prolonged synthetic anabolic steroid medication.The possibility of a potentially life-threatening complication of massive intra-abdominal bleeding should also be considered.     

Sclerosing encapsulating peritonitis in a liver transplant patient： A case report

We report a patient with HBV-related hepatocellular carcinoma (HCC) and refractory ascites who had received a peritoneal-venous shunt (PVS) 1 year before liver transplantation. Urgent surgical intervention following bowel obstruction and failure of immunosuppression therapy. No intestinal obstruction was found during an initial PVS. However, intestinal obstruction developed 2 wk after liver transplantation; and a cocoon abdomen was found upon exploration. This is the first reported case of cocoon abdomen caused by PVS and exacerbated by liver transplantation.     

原发性门静脉、肠系膜静脉广泛血栓伴发小肠梗阻1例治疗体会

肠系膜静脉血栓(mesenteric venous thrombosis,MVT)缺乏特异性的临床症状及体征,病情复杂,难于早期准确诊断,易误诊误治。对于有可疑诱发因素导致的无法用其他疾病解释的腹痛、腹胀、恶心、呕吐,需要考虑到MVT的可能,行腹部增强CT可明确诊断,给予积极的抗凝溶栓治疗,预防肠坏死、休克、多脏器功能衰竭等严重并发症,改善患者预后。及时跟踪患者病情,对于可能出现的并发症,应给予高度重视。     

Interventional treatment for symptomatic acute-subacute portal and superior mesenteric vein thrombosis

AIM: To summarize our methods and experience with interventional treatment for symptomatic acute-subacute portal vein and superior mesenteric vein thrombosis (PV-SMV) thrombosis. METHODS: Forty-six patients (30 males, 16 females,aged 17-68 years) with symptomatic acute-subacute portal and superior mesenteric vein thrombosis were accurately diagnosed with Doppler ultrasound scans, computed tomography and magnetic resonance imaging.They were treated with interventional therapy, including direct thrombolysis (26 cases through a transjugular intrahepatic portosystemic shunt; 6 through percutaneous transhepatic portal vein cannulation) and indirect thrombolysis (10 through the femoral artery to superior mesenteric artery catheterization; 4 through the radial artery to superior mesenteric artery catheterization).RESULTS: The blood reperfusion of PV-SMV was achieved completely or partially in 34 patients 3-13 d after thrombolysis. In 11 patients there was no PV-SMV blood reperfusion but the number of collateral vessels increased significantly. Symptoms in these 45 patients were improved dramatically without severe operational complications. In 1 patient, the thrombi did not respond to the interventional treatment and resulted in intestinal necrosis, which required surgical treatment.In 3 patients with interventional treatment, thrombi re-formed 1, 3 and 4 mo after treatment. In these 3 patients, indirect PV-SMV thrombolysis was performed again and was successful.CONCLUSION: Interventional treatment, including direct or indirect PV-SMV thrombolysis, is a safe and effective method for patients with symptomatic acutesubacute PV-SMV thrombosis.     

Hydatid disease of the liver with portal vein invasion mimicking portal vein thrombosis

Hydatid cyst disease is a zoonosis caused by the parasite Echinococcus. It may infest any organ of the body, but it most frequently involves the liver, lungs, and nervous system. Portal vein involvement by hydatid cyst disease is extremely rare with only five cases published in the English literature to our knowledge. We present the ultrasonography (US) and computed tomography (CT) findings of a 77-year-old male with hydatid disease of the liver with portal vein invasion mimicking portal vein thrombosis. Colour Doppler US confirmed the lack of blood flow within the portal vein and stigmata of cavernomatosis. CT clearly demonstrated a communication between the multiloculated lesion and the portal vein and the multiple daughter vesicles obstructing the portal vein. The consideration of this complication will make it possible to distinguish this entity from portal vein thrombosis and, thus, the management of the patients with hydatid cyst disease particulary in endemic regions.     

Acute portal vein thrombosis after liver transplant presenting with subtle ultrasound abnormalities:A case report and literature review

BACKGROUND Portal vein thrombosis(PVT) after liver transplantation(LT) is an uncommon complication with potential for significant morbidity and mortality that transplant providers should be cognizant of.Recognizing subtle changes in postoperative ultrasounds that could herald but do not definitively diagnose PVT is paramount.CASE SUMMARY A 30-year-old female with a history of alcohol-related cirrhosis presented with painless jaundice and received a deceased donor orthotopic liver transplant.On the first two days post-operatively,her liver Doppler ultrasounds showed a patent portal vein,increased hepatic arterial diastolic flows,and reduced hepatic arterial resistive indices.She was asymptomatic with improving labs.On postoperative day three,her resistive indices declined further,and computed tomography of the abdomen revealed a large extra-hepatic PVT.The patient then underwent emergent percutaneous venography with tissue plasminogen activator administration,angioplasty,and stent placement.Aspirin was started to prevent stent thrombosis.Follow-up ultrasounds showed a patent portal vein and improved hepatic arterial resistive indices.Her graft function improved to normal by discharge.Although decreased hepatic artery resistive indices and increased diastolic flows on ultrasound are often associated with hepatic arterial stenosis post-LT,PVT can also cause these findings.CONCLUSION Reduced hepatic arterial resistive indices on ultrasound can signify PVT post-LT,and thrombolysis,angioplasty,and stent placement are efficacious treatments.     

Extensive mesenteric vein and portal vein thrombosis successfully treated by thrombolysis and anticoagulation

Mesenteric vein thrombosis is generally difficult to diagnose and can be fatal. A case of extensive thrombosis of the mesenteric and portal veins was diagnosed early and successfully treated in a 26-year-old man with Down syndrome who was admitted to hospital because of abdominal pain, severe nausea and high fever. Ultrasonography revealed moderate ascites, and there was minimal flow in the portal vein (PV) on the Doppler examination. Computed tomography (CT) showed remarkable thickening of the walls of the small intestine and extensive thrombosis of the mesenteric, portal and splenic veins. Because neither intestinal infarction nor peritonitis was seen, combined thrombolysis and anticoagulation therapy without surgical treatment was chosen. Urokinase was administered intravenously and later through a catheter in the superior mesenteric artery. Heparin and antibiotics were given concomitantly. The patient's symptoms and clinical data improved gradually. After 10 days, CT revealed that collateral veins had developed and the thrombi in the distal portions of the mesenteric veins had dissolved, although the main trunk of the PV had not recanalized. The only risk factor of thrombosis that was detected was decreased protein S activity.     

Portal and mesenteric vein thrombosis after portal vein embolization in a patient with protein S deficiency

Portal vein embolization can be performed safely, and so far no major complications have been reported. We report an extremely rare complication of portal vein embolization, a case of portal and mesenteric thrombosis in a 65-year-old patient with protein S deficiency. Right portal vein embolization was carried out prior to extended right hepatectomy for advanced gallbladder carcinoma involving the hepatic hilus. Computed tomography 14 days after embolization revealed massive thrombosis of the portal and the superior mesenteric veins. A protein S deficiency was found by means of an extensive workup for hypercoagulable state. Portal vein embolization may have triggered a cascade of events that was expressed as portal and mesenteric vein thrombosis resulting from deficiency of protein S. It may be better to determine the concentrations of such coagulation regulators prior to portal vein embolization.     

Successful therapy with argatroban for superior mesenteric vein thrombosis in a patient with congenital antithrombin deficiency

A 38-year-old woman was admitted with superior mesenteric vein (SMV) thrombosis, which was refractory to anticoagulation therapy. The plasma antithrombin activity was decreased and hardly compensated by concentrated antithrombin preparation due to high consumption rate. However, successful anticoagulation was achieved by administration of direct thrombin inhibitor, argatroban. Family studies of antithrombin activity revealed that she had type I congenital antithrombin deficiency. A novel heterozygous mutation in the gene for antithrombin (single nucleotide T insertion at 7916 and 7917, Glu 272 to stop in exon 4) was identified. Argatroban administration would be effective in the treatment of congenital antithrombin deficiency with SMV thrombosis.