Superior Mesenteric Vasculature Research Articles

1920 Superior Mesenteric Arteriovenous Fistula Mimicking Hepatic Cirrhosis With Spontaneous Bacterial Peritonitis

INTRODUCTION: Arteriovenous fistula of the superior mesenteric vasculature is a rare entity that was reported for this first time by Movitz and Finne in 1960. The majority of these cases are iatrogenic after surgical bowel resection. We present a 52-year-old male patient who had a spontaneous AFV of the superior mesenteric vasculature that presented as a chronic portal vein thrombosis. CASE DESCRIPTION/METHODS: A 52-year-old male patient with a past medical history significant for active hepatitis C infection. The patient presented to our institution complaining of progressive abdominal distention and chronic abdominal pain for 3 months. He had been diagnosed with cirrhosis two months prior to admission and was started on furosemide and spironolactone for ascites and underwent multiple therapeutic paracentesis. At presentation, the patient was found to have a normal platelet count and INR which were not consistent with cirrhosis calling the diagnosis into question. Further workup with ultrasound examination of the liver revealed portal vein thrombosis with extension to the proximal part of the splenic vein. This was followed by CT of the abdomen and pelvis with IV contrast which showed smooth liver surface, enlarged portal, superior and inferior mesenteric veins with clot seen in the left portal vein extending into the main portal vein (Figure 1).it also showed a fistula of the mid superior mesenteric artery with the superior mesenteric vein (Figure 2) which explained the prominence and the enlargement of the portal venous system. Upon diagnosis, the patient was transferred to a tertiary center for endovascular closure of the fistula. DISCUSSION: Arteriovenous fistula of the superior mesenteric vasculature is a rare entity. Most cases are iatrogenic in origin occurring after bowel resection. The most common presentation is gastrointestinal bleeding due to portal hypertension and resulting variceal changes. Treatment with endovascular with coil embolization is often preferred over surgical repair. In summary, we discuss an unusual presentation of idiopathic arteriovenous fistula of the superior mesenteric vasculature with portal vein thrombosis, abdominal pain and ascites mimicking hepatic cirrhosis with spontaneous bacterial peritonitis.

Fortuitous Splenic Rupture: An Unusual Presentation of Pancreatic Cancer

Early diagnosis of pancreatic ductal adenocarcinoma (PDAC) is difficult. Multifocal pancreatic masses are not common when it comes to PDAC. This especially holds true for cancer of the pancreatic body and tail that do not manifest with jaundice. We present a case of pancreatic cancer involving the head and tail A 52-year-old Caucasian male with past history of hypertension, gout and osteoarthritis presented to the hospital with acute left upper quadrant pain radiating to the back after sustaining a fall. Examination revealed severe tenderness to palpation of the left upper quadrant. Initial laboratory data showed hemoglobin of 10.4 g/dl, AST of 166 U/L, ALT of 352 U/L, ALP of 368 U/L and serum lipase level of 869 U/L. CT abdomen showed splenic laceration with hemoperitoneum. The patient was vigorously resuscitated, and subsequently underwent emergency laparotomy. Operative findings revealed splenic laceration with hemoperitoneum. Intraoperatively, the pancreatic tail was hard and abutted the mesocolon and omentum. Short gastric vessels were engorged suggestive of splenic vein thrombosis. Irregular masses were noticed in the head of the pancreas without involvement of superior mesenteric vasculature. Histopathology of the mass revealed PDAC. The patient underwent Whipple surgery with adjuvant FOLFIRINOX therapy. Post-operative pathology showed T3N1 disease with perineural and lymphovascular invasion. The patient is currently undergoing surveillance for recurrence. Splenic rupture is extremely rare presenting feature of pancreatic cancer. Only ten prior cases have been reported in literature. Most of those cases reported rupture of splenic artery aneurysm secondary to direct vascular invasion of PDAC. Cancer of the pancreatic tail can invade the splenic hilum causing splenic ischemia and vein occlusion which may culminate in splenic rupture. Another rare finding in our case was the multifocal nature of pancreatic cancer. Only around 50 cases have been reported so far as per our literature review. Most of the cases that have been reported in literature present as contiguous masses. Surgical removal is recommended in the absence of distant metastatic disease and local vascular invasion. Overall prognosis continues to remain grim for all stages.Figure: Splenic rupture is a rare presenting feature of pancreatic cancer. It can however present an opportunity for early stage discovery that may lead to improvement in prognosis by earlier initiation of treatment.

Whipple’s pancreaticoduodenectomy: Surgical technique and perioperative clinical outcomes in a single center

IntroductionPancreatic cancer is the fourth cause of death from cancer in Western countries. The radical surgical resection is the only curative option for this pathology. The prevalence of this disease increases with age in population. The causes of pancreatic cancer are unknown, but we consider risk factors like smoke and tobacco usage, alcohol consumption coffee, history of diabetes or chronic pancreatitis. In this study we report our experience in the treatment of resectable pancreatic cancer and periampullary neoplasms with particular attention to evaluate the evolution of surgical technique and the clinical postoperative outcomes. MethodsIn our Department between January 2010 and December 2014 we performed a total of 97 pancreaticoduodenectomy. We considered only resectable pancreatic cancer and periampullary neoplasms defined by absence of distant metastases, absence of local tumor extension to the celiac axis and hepatic artery as the lack of involvement of the superior mesenteric vasculature. None of these patients received neoadjuvant chemotherapy. ResultsThe mean age of these patients was 64.5 years. Jaundice was the commonest presenting symptom associated to anorexia and weight loss. The mean operative time was 295 min (±55 min). The mean blood loss was 450 ml and median blood transfusion was 1 units. 12.1% of patients had an intra-abdominal complication. The commonest complication was Delayed Gastric Emptying responsable of increased length of hospital stay and readmission rate. Postoperative pancreatic fistula of grade C occurred in 4 patients. 2 patients developed a postpancreatectomy hemorrhage. Perioperative mortality was 4.1%. ConclusionPancreaticoduodenectomy is a complex surgical technique and the associated high morbidity and mortality resulted in initial reluctance to adopt this surgery for the management of pancreatic and periampullary tumors. Surgical outcomes of pancreatic surgery are better at high-volume experienced center reporting mortality rates below 5%. We perform an end-to-side duct-to-mucosa pancreaticojejunostomy with routinely use of internal pancreatic stent. However no one technique has been shown to definitely be the solution to the problem of postoperative pancreatic fistula. At our center we have a reasonable volume and our data are comparable to literature data.

Superior Mesenteric Arteriovenous Fistula Presenting with Massive Lethal Upper Gastrointestinal Bleeding 14 Years after Small Bowel Resection.

Arteriovenous fistulas (AVFs) of the superior mesenteric vasculature are rarely encountered. We present a case of an iatrogenic superior mesenteric AVF in a patient who had undergone a small bowel resection 14 years previously. The 45-year-old male was admitted with bloody diarrhea, fatigue, weight loss and moderate ascites. On the fifth hospital day, while being evaluated for suspected liver cirrhosis, the patient developed severe gastrointestinal (GI) bleeding. An upper GI endoscopy revealed bleeding, esophago-gastric varices. A thorough clinical examination pointed to a paraumbilical murmur and thrill, while a contrast enhanced computerized tomography (CT) scan of the abdomen revealed the presence of cystic dilatation of the superior mesenteric vein (SMV), hepatomegaly and ascites. Duplex ultrasonography and 3D-computed tomography angiography (3D-CTA) confirmed the existence of AVF between the superior mesenteric artery (SMA) and SMV, which was the cause of portal hypertension and variceal bleeding. Despite the fact that AVF was ultimately recognized, uncontrollable hypovolemic shock caused by hematemesis, precluded the probable efficiency of further therapeutic attempts. Successful management of mesenteric blood vessel AVFs involves timely and the accurate diagnosis and early treatment in order to prevent the development of life threatening complications.

Superior Mesenteric Arteriovenous Fistula

Arteriovenous fistulae (AVF) of the superior mesenteric vasculature are rarely encountered. We present a case of an iatrogenic superior mesenteric AVF following subtotal colectomy, which was successfully treated with coil embolization. Cross-sectional imaging and angiographic findings are reviewed along with the options for endovascular therapy.

Two Zebras in a Corral

Abstract: Pediatric hypertension is rare, and an underlying cardiac, renal, or endocrine etiology should be considered. We report an adopted 26-year-old white man with asymptomatic hypertension identified at age 14 during a sports examination. His medical history was notable for ulcerative colitis. The physical examination revealed hypertension despite a body mass index of 20.3 kg/m2. A left adrenal mass enhanced on T2-weighted magnetic resonance imaging. The presumptive diagnosis was pheochromocytoma. A 7.0 × 6.0 × 3.5-cm lesion was resected without complication, and the hypertension resolved. Over the next 3 years, he developed thyroid nodules, a presumptive osteochondroma, and benign fibrous lesions. By age 15, his colitis symptoms worsened and multiple polyps were observed. Polyps were identified later in the duodenum and stomach as well. A desmoid tumor involved the superior mesenteric vasculature. Sequential surgical resections left only residual small bowel. Review of adrenal gland histology revealed sheets and nests of lipid-poor epithelioid cells with vesicular nuclei and variably prominent nucleoli. Pseudoglandular architecture and degenerative hemorrhagic “angiomatoid” change was present. Findings were diagnostic of adrenal cortical adenoma, but not pheochromocytoma. The clinical presentation is consistent with Gardner syndrome. The location and nature of mutations in the adenomatous polyposis coli tumor-suppressor gene often determine the presence of extraintestinal disease and disease severity. Seven percent to 13% of patients with Gardner syndrome have adrenal lesions. Most are nonfunctional. Functional lesions typically secrete cortisol. Although such lesions may not come to the attention of endocrinologists because of their nonsecretory status, endocrinologists should be aware of the syndrome and its diverse manifestations.

Role of the heme oxygenases in abnormalities of the mesenteric circulation in cirrhotic rats.

Carbon monoxide (CO), a product of heme metabolism by heme-oxygenase (HO), has biological actions similar to those of nitric oxide (NO). The role of CO in decreasing vascular responses to constrictor agents produced by experimental cirrhosis induced by carbon tetrachloride was evaluated before and after inhibition of HO with tin-mesoporphyrin (SnMP) in the perfused superior mesenteric vasculature (SMV) of cirrhotic and normal rats and in normal rats transfected with the human HO-1 (HHO-1) gene. Perfusion pressure and vasoconstrictor responses of the SMV to KCl, phenylephrine (PE), and endothelin-1 (ET-1) were decreased in cirrhotic rats. SnMP increased SMV perfusion pressure and restored the constrictor responses of the SMV to KCl, PE, and ET-1 in cirrhotic rats. The relative roles of NO and CO in producing hyporeactivity of the SMV to PE in cirrhotic rats were examined. Vasoconstrictor responses to PE were successively augmented by stepwise inhibition of CO and NO production, suggesting a complementary role for these gases in the regulation of reactivity of the SMV. Expression of constitutive but not of inducible HO (HO-1) was increased in the SMV of cirrhotic rats as was HO activity. Administration of adenovirus containing HHO-1 gene produced detection of HHO-1 RNA and increased HO activity in the SMV within 7 days. Rats transfected with HO-1 demonstrated reduction in both perfusion pressure and vasoconstrictor responses to PE in the SMV. We propose that HO is an essential component in mechanisms that modulate reactivity of the mesenteric circulation in experimental hepatic cirrhosis in rats.

Effects of endothelin-1 on vasoactivity and its synthesis, storage, and acting sites in the rat superior mesenteric vasculature: an ultrastructural and immunocytochemical study.

Vasoactivity after treatment with endothelin (ET)-1 and immunoreactivity for ET-1 and its receptors were investigated in the rat superior mesenteric vasculature (SMV). By measurements of corrosion cast images of the SMVs, it was seen that ET-1 induces remarkable vasocontraction of the distal arterial branches, consisting of small arteries and arterioles, and localized vasoconstriction throughout the venous branches which possess localized medial thickenings. Immunoreactivity for ET-1 was preferentially seen along the endothelia of the proximal arterial branches. Cisterns of the rough endoplasmic reticulum and Weibel-Palade (WP) bodies of the endothelial cells were immunoreacted. Immunoreactivity for the ETa receptor was preferentially seen on the media of the distal arterial branches. These findings indicate that endothelial cells of the proximal arterial branches synthesize ET-1 and store it in the WP bodies. Because WP bodies are involved in the release of ET-1, this suggests that this endogenous ET-1, which is released from the proximal arterial branches, may be involved in the regulation of blood flow through the distal arterial branches by mediation of the ETa receptor. In addition, it seems likely that ET-1-induced vasoconstriction of the venous branches may act to impel the portal blood flow.

Regional Blood Flow Dynamics in Response to Insulin and IGF-1 in Diabetic Animals

Vascular changes in diabetes characterized by increased contractile or decreased dilator responses have been demonstrated in isolated blood vessels as well as in vivosystems. Previous studies in our laboratory have demonstrated that insulin and insulin like growth factor-1 (IGF-1) can decrease mean arterial pressure (MAP) and increase blood flow in vascular beds. In this study we evaluated the regional hemodynamic responses to insulin and IGF-1 in normal and diabetic rats. Normal male rats were made diabetic with streptozotocin (55 mg/kg) i.v. and maintained 60 to 70 days. On the day of the study the rats were anesthetized with urethane/chloralose, the femoral artery and vein cannulated for blood pressure monitoring and blood sampling or infusion, respectively. Pulsed-Doppler flow probes were placed around the iliac artery, renal artery and superior mesenteric artery to monitor blood flow. Insulin (16 nmol/kg) was infused as a bolus via the femoral vein and it decreased the MAP approximately 17% in both normal and diabetic rats. Insulin enhanced vascular flow (expressed as conductance) in the iliac and renal vascular bed but not the superior mesenteric vascular bed in normals. In diabetic rats the flow response to insulin compared to normals was attenuated in the iliac and renal vascular beds and increased in the superior mesenteric vascular bed. A bolus infusion of IGF-1 (16 nmol/kg) also decreased the MAP in normals and diabetics. IGF-1 increased vascular flow in all three vascular beds in normals but in the diabetics the response to IGF-1 was artenuated in the iiiac, increased in h e renal vascular bed and suppressed in the superior mesenteric vascularure. From these studies we conciude that diabetes is associated with an anenllared vascular response to insulin and IGF-1 in the iliac and renal vessels while insulin augments and IGF-1 decreases blood flow in the superior mesenteric vasculature

The origin and distribution of 5-hydroxytryptamine-like immunoreactive nerve fibres to major mesenteric blood vessels of the rat

5-Hydroxytryptamine-like immunoreactive nerve plexuses were demonstrated by indirect immunofluorescence histochemistry in whole-mount preparations and cryostat sections of blood vessels from the mesenteric vasculature of the adult rat. The major veins showed a density of innervation greater than that of the accompanying arteries. Removal of the coeliac-superior mesenteric ganglion complex resulted in almost total loss of 5-hydroxytryptamine-like immunoreactive nerves from superior mesenteric blood vessels. The results of crush lesions applied to distal vessels of the superior mesentery indicate that there were no 5-hydroxytryptamine-like immunoreactive nerve fibres extending from the enteric nervous system to these vessels. The administration of 6-hydroxydopamine resulted in a large reduction in the noradrenergic innervation, accompanied by a similar fall in the number of 5-hydroxytryptamine-like immunoreactive nerve fibres. It is suggested that the cell bodies of the 5-hydroxytryptamine-like immunoreactive nerve fibres demonstrated in the superior mesenteric vasculature are located within the sympathetic ganglia which supply the noradrenergic innervation to the same region and that the 5-hydroxytryptamine-like immuno-reactivity may be co-localized with noradrenaline within sympathetic nerve fibres.

Circulatory effects of VIP in anesthetized man

VIP was given intravenously over 1 min at the doses 0.1 and 0.2 μg·kg·min −1 to twentyone anesthetized patients undergoing abdominal surgery. Intra-arterial blood pressure was monitored and various blood flows were measured simultaneously by electromagnetic technique. Following VIP, intra-arterial blood pressure was decreased. The blood flows were increased in the gastroduodenal-, and the left gastric arteries. The flow in the hepatic artery proper was increased only following the 0.2 μg dose. The flow in the superior mesenteric artery varied considerably inter-individually. In branches supplying only the small intestine, it seemed to be unaffected. The flow in the splenic artery was decreased in normal-sized spleens, but unaffected in enlarged spleens. The flow in the external iliac artery initially decreased and thereafter increased. Changes in vascular resistances showed that VIP acted as a vasodilator in the splanchnic region except in the superior mesenteric vasculature, where it was ineffective. In normal spleens it was a vasoconstrictor. In the external iliac artery, an initial insignificant vasoconstriction was followed by vasodilation. It seemed that VIP acts directly on the vessels and has a specific pattern of vasoactivity of probable physiological significance.

Digoxin induced intestinal vasoconstriction. The effects of proximal arterial stenosis and glucagon administration.

Previous studies have been shown that intravenous cardiac glycosides produce mesenteric vasoconstriction (MVC). The possibility that this might critically compromise blood flow in patients with mesenteric vascular disease was suggested. To evaluate whether MVC occurs with intravenous cardiac glycosides in the presence of proximal mesenteric artery stenosis, blood flow in the superior mesenteric artery (SMA) of thirteen dogs was measured with a Doppler flowmeter. The SMA was constricted and pressures were measured in the aorta, SMA, and superior mesenteric vein. Superior mesenteric vascular resistance (SMVR) was calculated by dividing the pressure difference between the SMA and superior mesenteric vein by the total blood flow to the superior mesenteric vasculature and was reported as mm Hg/cc-min. Blood flow was measured simultaneously by a drop rate meter in the vein of a surgically isolated intestinal segment supplied by a single arterial arcade. Venous outflow pressure from this segment was also monitored, which allowed calculation of isolated gut segment resistance (IGSR) in mm Hg/cc-min per 100 g gut. Stenosis of the SMA produced pressure gradients of 10 to 75 mm Hg and decreased resting blood flow by as much as 82%. Digoxin produced an increase in both SMVR and IGSR throughout the 30 to 120 minute period of the study in thirteen dogs despite the presence of severe grades of SMA stenosis. There was no relationship between the degree of proximal SMA stenosis and the magnitude of resistance change due to digoxin. To determine if this MVC was reversible, glucagon was administered to eleven dogs 30 to 60 minutes after digoxin and completely overcame the constriction. Thus, digoxin produced MVC in the presence of proximal SMA stenosis. This MVC was pharmacologically reversible. These data suggest that intravenous digoxin might contribute to intestinal ischemia in patients with preexisting vascular disease.