Search

Background Distal gastrectomy with lymph node dissection, a standard operative technique for gastric cancer treatment, is safely performed because the stomach has a rich vascular supply. Gastric remnant necrosis caused by cholesterol crystal embolization following distal gastrectomy has not been described previously. We report a case of gastric remnant necrosis in a patient with cholesterol crystal embolization. Case presentation A 70-year-old man with a history of cholesterol crystal embolization presented to our surgery department with complaints of anorexia and dysphasia. He was diagnosed with gastric cancer invading the pyloric antrum and underwent distal gastrectomy with Billroth 2 reconstruction. On postoperative day 11, he developed abdominal pain without fever. Emergency laparotomy revealed that most parts of the remnant stomach were necrosed. Total gastrectomy with Roux-en-Y reconstruction and abscess drainage were performed. After surgery, anastomotic leakage occurred and was treated conservatively. However, the superior pancreaticoduodenal artery aneurysm suddenly ruptured and he expired. Conclusions Gastric remnant necrosis after distal gastrectomy can be a gastrointestinal presentation of cholesterol crystal embolization. Perioperative/intraoperative risk assessments such as preventive total gastrectomy or intraoperative assessment with indocyanine green fluorescence angiography may be desirable to avoid this complication.

BACKGROUND: The liver has unique anatomy in that most blood flow to normal hepatocytes is derived from the portal venous system, while liver tumors obtain their nutrient blood supply exclusively from the hepatic artery. The focused arterial delivery of anticancer agents to liver tumors has been performed for decades; however, preclinical models to standardize drug regimens and examine novel agents have been lacking. The purpose of this study was to establish preclinical hepatic artery infusion (HAI) models in a mouse, and to evaluate the safety and delivery capability of the models. MATERIAL AND METHODS: Female C57BL/6 and BALB/c mice aged 8–12 wk were used to develop models of HAI via the hepatic artery (HA), superior pancreaticoduodenal artery (SPDA), or lienogastric artery (LGA). Success rates, distribution of perfusion, and associated morbidity and mortality were analyzed between groups. RESULTS: All three models were feasible and reproducible in mice, and there was no statistical difference on body weight change between models. The HA model had a 13.3% mortality from acute liver failure, and the SPDA model demonstrated significant duodenal and pancreatic toxicity. SPDA and LGA routes had the highest success rates (96.7% and 91.4%, respectively) with low mortality, better drug delivery, and preserved physiologic liver function compared to the HA model. CONCLUSIONS: The optimal route of HAI was mouse breed-specific; SPDA access in BALB/c mice, and the LGA access in C57BL/6 mice. The described techniques serve as a reproducible platform for the identification and characterization of therapeutics for diverse metastatic liver tumors.

Background Neurofibromatosis type 1 (NF-1) is an autosomal dominant disease and arteriovenous abnormalities are a well-recognized complication. There are several case reports of ruptured aneurysms; however, among them, reports of superior pancreaticoduodenal artery (PDA) and superior mesenteric artery (SMA) aneurysms are rare. We experienced the case of ruptured PDA and SMA aneurysms in a patient of neurofibromatosis type I successfully treated by endovascular treatment. Case presentation A 55-year-old woman with NF-1 came to our hospital with abdominal pain and vomiting. Enhanced abdominal computed tomography revealed a hematoma in the retroperitoneum and an aneurysm in the head of the pancreas. Angiography was performed, and a ruptured aneurysm was suspected the periphery of the PDA, and we embolized it using coils. However, on postoperative day 2, the hemoglobin level decreased, and a branch of the SMA was ruptured. She underwent embolization using coils again and discharged on postoperative day 27 without any further hemorrhage. Conclusions To our knowledge, this is the first successfully treated case of ruptured SMA and PDA aneurysms in a patient with NF-1.

AIM: This study was designed as a preliminary investigation of safety and efficacy of LifePearl, polyethylene glycol microspheres loaded with doxorubicin for treatment of locally untreatable (i.e., unresectable and not suitable for local thermal ablation) hepatocellular carcinoma (HCC). MATERIAL AND METHODS: Patients with locally untreatable HCC (mono- or bilobar disease, ECOG performance status 0-1, Chilg-Pugh score < 11) were analysed for this single arm Unicenter retrospective study. All the information were acquired through our local hospital information system. DEB-TACE was performed with 100-200 microns LifePearl loaded with 75-150 mg of doxorubicin depending on tumour size. One interventional radiologist with experience of more than 350 TACE procedures and one fellow in radiology performed all embolisations. RESULTS: Twenty subjects with 29 tumours were treated (mean age 66.2 years). Child-Pugh status was A for 12 pts. (60%), B for 6 pts. (30%) and C for 2 pts. (10%). Three patients had insignificant ascites. Most patients (70%) underwent < 3 DEB-TACE procedures. Average doxorubicin dose was 71.1 mg per procedure. One patient had procedure-related SAE (acute pancreatitis) within the postembolization period which was induced due to non-target embolisation of the superior pancreaticoduodenal artery. Six-month freedom from procedure-related SAE or death was 95% (one necrotizing pancreatitis). Tumor response or stable disease was achieved in 95% (19/20) of subjects. Freedom from tumor progression or death at 6 months was 95%. One-year survival rate was 90% overall. CONCLUSION: The results from this investigation suggest that LifePearl microspheres, Terumo loaded with doxorubicin can provide an excellent local tumour control with very few side effects in a relatively homogeneous group of patients with locally untreatable HCC.

Introduction Large tumors in the head of the pancreas pose technical challenges during resection in minimally invasive pancreatoduodenectomy (PD). The precise and systematic vascular control of the pancreaticoduodenal branches of the superior mesenteric artery and vein during robotic PD for a large solid pseudopapillary tumor of the pancreas is described in this video. Methods A 16-year-old female presented with a lump in the abdomen, early satiety, and epigastric pain of 3 months duration. Contrast-enhanced computed tomography abdomen revealed 7.1 × 6.2 cm solid mass with cystic areas in the head of the pancreas. The tumor was compressing the portal vein with dilated pancreaticoduodenal veins. In the present technique, the anterosuperior pancreaticoduodenal vein is controlled first, followed by the superior pancreaticoduodenal artery (by ligating Gastroduodenal artery). This is followed by the control of inferior pancreaticoduodenal veins and arteries. The posterosuperior pancreaticoduodenal vein is ligated at the end to prevent vascular congestion of the uncinate region. Results The duration of surgery and intraoperative blood loss were 440 minutes and 200 mL, respectively. The patient had an uneventful postoperative course and discharged on the sixth postoperative day. Histopathological examination confirmed the diagnosis of the solid pseudopapillary tumor. At nine months follow-up, the patient remains asymptomatic with no recurrence. Conclusions A stepwise precise vascular control described in this report could minimize intraoperative bleeding during robotic PD for large tumors in the head of the pancreas.

Visceral artery aneurysms are uncommon, especially in the pediatric population. We report a rare case of a ruptured saccular aneurysm of the superior pancreaticoduodenal artery (PDA) in a 7-month-old girl presenting with hematemesis. Esophagogastroduodenoscopy showed a constriction of the duodenum and MRI demonstrated a saccular aneurysm of the superior PDA. The infant was taken to the operating room and resection of the ruptured aneurysm was performed. Histologic examination confirmed the diagnosis of an aneurysm, but could not clarify the underlying etiology. This is a rare case report about a female infant presenting with hematemesis due to a ruptured aneurysm of the superior PDA. Ruptured visceral artery aneurysms are a very unusual but serious cause of upper intestinal bleeding, even in infants.

A rare variation was seen in the arterial supply of liver and gall bladder during dissection of an adult female cadaver. The right hepatic artery was having a tortuous course with double loops and cystic artery was arising from the distal loop within the hepatobiliary triangle. There was an accessory cystic artery arising from the superior pancreaticoduodenal artery outside the hepatobiliary triangle which ascended anterior to the common bile duct and cystic duct towards the gall bladder. The knowledge of these vascular variations is very much essential owing to increase in surgical interventions involving the biliary tract. Recognition of such vascular variations is essential for laparoscopic surgeons to reduce complications like uncontrolled intraoperative bleeding, iatrogenic extrahepatic biliary injuries and conversion to open cholecystectomy. This report emphasizes the necessity of all surgeons being well aware of vascular variations and anomalies to be able to accomplish safe and uneventful hepatobiliary surgeries.

/10.10 16 A mmo ence: outh, nielco One common reasons that many surgeons do not perform a duodenal switch (DS) is lack of experience with the dissection over the head of the pancreas [1]. We have developed a more tolerable and simpler technique for this dissection that allows any surgeon who has the skills to perform a gastric bypass to perform this dissection easily. One of the most common fears with this dissection is injury to the portal triad [2]. This can result in serious injuries. Our technique offers the surgeon complete exposure so that injury to the portal triad is rare. The second most common fear is a duodenal stump leak [3,4]. In the past, papers have reported duodenal leak rates after DS of 1.5% [3,5]. We believe this occurs when there are injuries to the supraduodenal artery and vein or the superior pancreaticoduodenal artery and vein, leading to ischemia [1,6]. These injuries can be avoided using our technique, preserving the blood supply to the duodenal stump. Briefly, the technique involves taking down all the perforating gastroepiploic vessels from 4 cm proximal to the pylorus, thus raising the antrum and providing exposure of the pancreas and portal triad. When the dissection is carried down to the head of the pancreas, the superior pancreaticoduodenal artery branches are seen rising from the body of the pancreas onto the posterior duodenal surface. These vessels are always 2–4 cm beyond the pylorus and afford a safe and vascularized spot to perform the duodenal transection. This is also safely above the

We report this case of a 74-year-old man with altered anatomy secondary to Billroth-II surgery who underwent endoscopic retrograde cholangiopancreatography (ERCP) for choledocholithiasis and subsequently developed severe diffuse abdominal pain with drop in hemoglobin. Patient was found to have hemorrhagic shock requiring aggressive resuscitative measures. Patient was found to have large peripancreatic hematoma secondary to bleeding from gastroduodenal and superior pancreaticoduodenal artery pseudoaneurysms. Gastroduodenal artery aneurysm is the rarest of all the splanchnic artery aneurysms, and to our knowledge this is the only reported case of a gastroduodenal artery pseudoaneurysm complicating ERCP.

OHNEDA, A., OHNEDA, K. and KOIZUMI, F. Insulin Releasing Action of N-Terminal Peptides of Glucagon in Dogs. Tohoku J. Exp. Med., 1992, 167 (4), 287-295-The relationship between the molecular structure and insulin releasing action of glucagon remains unknown. In order to investigate the direct action of N-terminal peptides of glucagon, glucagon (1-14), and glucagon (1-21) were studied using an in situ local circulation of the canine pancreas. These glucagon fragments as well as glucagon (1-29) were infused into the superior pancreaticoduodenal artery in a dose of 400pmol for 10min during the glucose or arginine infusion, and plasma insulin and glucagon in the superior pancreaticoduodenal vein were determined by radioimmunoassay. During the glucose infusion, glucagon (1-14) elicited a slight increase in plasma insulin, whereas glucagon (1-21) and (1-29) revealed significant changes in plasma insulin. In these experiments plasma glucagon did not change significantly following the administration of glucagon (1-14) or (1-21). During the arginine infusion all of the glucagon fragments studied enhanced insulin secretion markedly, whereas glucagon secretion was not affected. Furthermore, graded doses of glucagon (1- 14) (50, 150, and 400pmol) elicited an increase in plasma insulin in a dose-related manner. It is concluded from the present study that the N-terminal peptides of glucagon stimulate insulin release especially during the arginine infusion.- glucagon fragments; canine pancreas; arginine; glucose; insulin

The superior pancreaticoduodenal artery typically arises as the first branch of gastroduodenal artery, above the upper border of the head of the pancrease, and passes either above or behind the first part of duodenum. During the routine dissection in the department of Anatomy, This rare variation of superior pancreaticoduodenal artery was noticed in a male cadaver of approximately 50 years of age. In this case the superior pancreaticoduodenal artery showed variation in its branching pattern. The artery appeared more tortuous, wide and long. More details in this regard and clinical aspects will be discussed.

Introduction: Minimal access surgery has revolutionized surgery and is considered the gold standard of management for most surgical pathologies of the abdomen. We present a case which to our best knowledge is the first ever report of the non­surgical management of a pancreaticoduodenal artery (PDA) pseudo­ aneurysm following laparoscopy assisted Frey’s procedure (LAFP). Case Report: A 38­year­old male patient was transferred to our hospital due to persistent gastrointestinal bleeding following LAFP. He underwent LAFP for chronic calcific pancreatitis (CCP) two weeks prior to his transfer. Computed tomography angiogram showed the source of bleeding to be a branch of superior pancreaticoduodenal artery (SPDA). The patient was taken to interventional radiology where successful superselective microcoil embolization was performed. We present this rare case of pancreaticoduodenal pseudoaneurysm along with a review of medical literature. Conclusion: A prudent selection of the operative candidate for laparoscopic pancreatic surgery and a high degree of vigilance is imperative to circumvent avoidable morbidity and mortality.

Although low molecular weight (LMW) dextran has been said to decrease the lethality of experimental acute pancreatitis (AP) by reversing stasis in the pancreatic microcirculation, the actual mechanism(s) of action is unknown. This investigation was designed to measure the effects of low molecular weight dextran on pancreatic capillary flow (QCAP) and arteriovenous shunt flow (QAVS), and on pancreatic oxygen consumption (O2CP) following bile-trypsin-induced AP in dogs. Total pancreatic blood flow (QT) was measured with an electromagnetic flow probe on the superior pancreaticoduodenal artery (SPDA). QAVS was measured by liver trapping of 99mTc-albumin microspheres after SPDA injection. QCAP was calculated as QT minus QAVS. Seventeen dogs were treated with lactated Ringer's (LR) solution at 6.5 ml/kg/hr; 10 dogs were treated with LMW dextran 10% in normal saline at 1.5 ml/kg/hr plus LR at 5.0 ml/kg/hr. Mean arterial and central venous pressures remained constant throughout the 4-hr experiment. In the dogs receiving LR only, QT decreased from 42.7 to 24.4 ml/min (P less than 0.001); QAVS remained constant at 1.35 +/- 0.04 ml/min. During the first 30 min O2CP decreased from 1.17 to 0.76 ml O2/min (P less than 0.05) and remained constant thereafter. LMW dextran treatment altered none of these hemodynamic or metabolic parameters significantly.bile trypsin AP in the dog causes significant decreases in QT and QCAP without altering QAVS. The decrease in O2CP in association with a constant QAVS suggests a metabolic block to oxygen uptake at the cellular level. Continuous infusion of LMW dextran at a dose of 1.5 ml/kg/hr in the dog does not reverse these abnormalities.

A case of leiomyosarcoma of the duodenum accompanied with nonrotation was reported. The patient was a 39-year-old man who complained of a mass the size of a child's head in the epigastrium. The upper gastrointestinal series demonstrated moderate lateral displacement of the discending duodenum, and a vertical duodenum that did not cross the midline. Barium enema showed a left-sided colon and entirely right-sided small bowel, indicating nonrotation. On selective celiac angiogram, it was noted that the tumor was nourished by the superior pancreaticoduodenal artery. The tumor showed mottled staining with contrast medium, indicating hypervascularity. Ultrasonography revealed a large mass with a thick echogenic wall and sonolucent center. Operation was performed under the diagnosis of submucosal tumor of the duodenum. At surgery, a large tumor involving the first portion of the duodenum with peritoneal dissemination was identified. To remove the lesion, subtotal gastrectomy was performed. The histologic examination revealed that the tumor was leiomyosarcoma.

Tolbutamide was administered into the superior pancreaticoduodenal artery of anesthetized dogs. A prompt hyperinsulinemia was induced but the plasma gastrin increased gradually in the right gastroepiploic vein; acutely secreted endogenous insulin did not result in gastrin secretion. These findings suggest that gastrin is not released by insulin per se, but by decreased blood glucose.By infusion of somatostatin into the superior pancreaticoduodenal artery, plasma gastrin in the antral vein and plasma insulin in the pancreatic vein decreased promptly, and the tolbutamide-and arginine-induced gastrin and insulin secretions were impaired. These inhibitory effects of somatostatin on the plasma gastrin and insulin secretion were quite clearly demonstrated in the right gastroepiploic vein and superior pancreaticoduodenal vein. The inhibitory effect of somatostatin was more pronounced on gastrin release than on insulin release.It appears likely that the inhibitions of gastrin and insulin secretion by somatostatin were caused by direct action on the gastrin secretory cell and on the pancreatic beta cell. Somatostatin may play an important role in the entero-insular axis.

The direct inhibitory action of somatostatin (cyclized SRIF) on the pancreatic endocrine function was investigated by a technique using pancreaticoduodenal arteriovenous system in vivo. Somatostatin was infused for 20 minutes at a speed of 2.5 mug/minute into the superior pancreaticoduodenal vein and femoral artery were measured before and every 5 minutes throughout the experiment for 30 minutes. The results were compared with those obtained from the control experiment which was carried out in the same time schedule under infusion of physiologic saline solution instead of somatostatin. Next, the effect of somatostatin on the glucose-induced insulin release from the pancreas was also evaluated. The following findings were obtained. (1) Somatostatin infused at a speed of 2.5 mug/minute into the superior pancreaticoduodenal artery caused a statistically significant inhibition of plasma levels of IRI and IRG and also pancreatic output of these hormones. With the sessation of somatostatin infusion an abrupt rise of the hormones were seen. This "rebound" phenomenon was more pronounced in insulin secretion than in glucagon. No significant changes in the plasma glucose levels in either the pancreaticoduodenal vein or the femoral artery throughout the experiment were found. (2)During infusion of somatostatin at a speed of 1.25 mug/minute, insulin response to glucose injected into the pancreaticoduodenal artery in a small dose, as well as having no effect on the plasma glucose level in systemic circulation, was also significantly inhibited. From these findings obtained by direct experiment using the pancreaticoduodenal arterio-venous system, it was confirmed that somatostatin exhibits a direct inhibitory action on pancreas endocrine in a very low concentration in vivo, and it was suggested that this action might be partly due to a reduction in pancreatic circulation.

Experimental evidence suggests that in acute haemorrhagic pancreatitis in the dog the percentage of the cardiac output distributed to the pancreas falls. Histological evidence indicates arteriovenous shunt flow, but this has not been confirmed by flow measurements. It has recently been reported that in experimental preparations in which pancreatic blood flow is measured through the superior pancreaticoduodenal artery after ligation of other (accessory) vessels, perfusion is reduced in distal regions of the gland. There are no data regarding regional perfusion measurements in acute pancreatitis or the effect of ligating accessory vessels. This study therefore evaluates blood flow and regional perfusion in haemorrhagic pancreatitis in various preparations of the canine pancreas. Perfusion was assessed by measuring the clearance of Krypton-85 after injection into the arterial blood supply of the pancreas. Arterial blood flow was measured by the electromagnetic flow technique. The results show that perfusion in different regions of the gland is similar both before and during disease. If accessory vessels are ligated, however, only perfusion in the head of the gland is maintained. No arteriovenous shunt flow was shown. The percentage of the cardiac output being distributed to the gland did not change in any of the experiments; this contradiction to previous reports may arise from the effective control of acid base balance in this study.

The effect of infusion of small doses of xylitol into the pancreatic artery upon insulin release was studied in anaesthetized dogs, in order to decide whether the strong insulin-releasing effect of xylitol in dogs is mediated by a direct action of xylitol upon the islets or indirectly by some of its metabolites. Xylitol or glucose was infused at 0.5–1.0 mg/kg · min either into the femoral vein or into the superior pancreaticoduodenal artery, and the changes in plasma insulin were measured in the superior pancreaticoduodenal vein. Infusion into the pancreatic artery always resulted in a sharp increase in insulin release, whereas intravenous infusion caused no or little increase. Infusion of xylitol into the superior pancreaticoduodenal artery produced a prompt increase in plasma insulin in the superior pancreaticoduodenal vein but not in the splenic vein. These data suggest that xylitol has a direct stimulatory effect upon islet cells. — During intravenous infusion of epinephrine (1.0 μg/kg. min), plasma insulin did not increase despite intravenous administration of glucose or xylitol (0.4 g/kg). There was a rebound rise of plasma insulin after cessation of epinephrine infusion. Plasma insulin responses to intravenous injection of glucose or xylitol (0.4 g/kg) were inhibited also by the intravenous infusion of diazoxide (0.2 mg/kg · min), but this was somewhat variable among individual dogs. The suppression by epinephrine or diazoxide of both glucose and xylitol-induced hyperinsulinaemia may suggest that there is some common mechanism between the insulin-releasing effects of glucose and xylitol.

We describe the clinical experience of application of an aortic anastomotic device for aortoceliac artery bypass with a saphenous vein graft from the supraceliac aorta. A 53-year-old female with celiac artery occlusion and multiple superior pancreaticoduodenal artery aneurysms had an aortoceliac artery bypass surgery using the aortic anastomosis device. Coil embolization of the aneurysms was performed via the superior mesenteric artery. The postoperative angiogram revealed good graft patency and complete aneurysm embolization. This device can be considered for application in various anastomotic situations.

Dogs with an electromagnetic flowprobe implanted around the superior pancreaticoduodenal artery and with an hydraulic occluder implanted upstream from the flowprobe were examined between the 3rd and the 8th postoperative day. During an oral glucose load, blood flow increased from the beginning of administration to about 25 minutes, but not when blood glucose and plasma IRI exhibit their maxima. The rise of pancreatic blood flow is assumed to be produced by reflexes similar to those stimulating insulin secretion and exocrine pancreatic function during the early phase of an oral glucose load.

The superselective transcatheter arterial embolization has currently become an accepted treatment of hepatic tumors. We have developed an experimental model for the evaluation of this therapy in the rat liver. Using the retrograde catheterization of the superior pancreaticoduodenal artery, only the peripheral intrahepatic arterial branches and sinusoids of the median and left lobes of the liver were embolized with 1.2 and 1.5 mg of Gelfoam powder. This method resembles the clinical practice because the superselective embolization could be performed adequately and allows the comparative evaluation of the responses of the embolized and non-embolized lobes.

Two cases of tuberculous mesenteric lymphadenitis with emphasis on the angiographic findings are reported.In one the celiac axis was stenosed and became less so with antituberculous therapy. The other had enlargement and bowing of a superior pancreaticoduodenal artery and staining around the duodenum and head of the pancreas thought to have been secondary to hypervascularity of the inflamed lymph nodes.This disease may be successfully treated either medically or surgically.