Akira Mitsuyoshi

Survival in Nonocclusive Mesenteric Ischemia: Early Diagnosis by Multidetector Row Computed Tomography and Early Treatment With Continuous Intravenous High-dose Prostaglandin E1

Objectives:The aim of the study was to establish a procedure for early diagnosis and treatment of nonocclusive mesenteric ischemia (NOMI). Background:NOMI has a high mortality rate, and early diagnosis and treatment are important for improving survival in patients with this condition. Methods:The subjects were 22 patients treated at our hospital over 13 years. Diagnostic criteria for NOMI were established based on the first 13 cases. In the 9 more recent cases, we performed abdominal contrast multidetector row computed tomography (MDCT) upon suspicion of NOMI based on these criteria. Imaging allowed definite diagnosis of NOMI, and continuous intravenous high-dose PGE1 administration was initiated immediately after diagnosis (dose, 0.01–0.03 μg/kg per min; mean administration period, 4.8 days). Results:Nine of the first 13 patients died of multiple organ failure associated with multiple intestinal necrosis. These cases suggested that NOMI may develop when 3 of the following 4 criteria are met after cardiovascular surgery or maintenance dialysis in elderly patients: symptoms of the ileus develop slowly from abdominal symptoms, such as an unpleasant abdominal feeling or pain; a requirement for catecholamine treatment; an episode of hypotension; and slow elevation of the serum transaminase level. In the 9 recent cases, definite diagnosis was made from spasm of the principal arteries in arterial volume rendering and curved planar reformation MDCT images. Early treatment with PGE1 prevented acute-stage NOMI in 8 of the 9 cases. Conclusions:Early diagnosis of NOMI is possible using the above criteria and MDCT, and initiation of PGE1 treatment may increase survival in patients with NOMI.

Hemodynamics and Hepatic Energy Metabolism in Canine Model of Acute Hepatic Venous Occlusion with Mesocaval Shunt

The relationship between portal hemodynamics and the energy metabolism of the liver with acute hepatic venous occlusion (HVO) was investigated by assessing the changes in the hepatic blood flow, arterial blood ketone body ratio (AKBR) and adenylate energy charge potential (ECP) of the liver tissue in canine model. Acute HVO was induced by the ligation of both the supra- and infrahepatic inferior vena cava (IVC) over the protruding ends of a heparin-coated polyethylene cannula inserted into the IVC. All dogs with only HVO (n = 5) died within 30 min. HVO dogs with additional mesocaval (MC) shunt (n = 10) survived longer than 7 days, during which time their AKBR were maintained in the normal range (over 1.0). ECP was also maintained above the normal level (over 0.850) during the 28-day period. Along with increasing portal pressure caused by the narrowing of the shunt anastomosis, the hepatic blood flow decrease gradually, resulting in a sudden decrease in AKBR and ECP when the portal pressure increased over 11 mm Hg. It is suggested that the normalization of portal pressure is one of the most important factors for maintaining the hepatic energy metabolism and that MC shunt is an effective therapy for maintaining the function of the liver with HVO, as long as portal pressure can be kept within normal range.

Distal gastrectomy with reconstruction of the right gastroepiploic artery for gastric cancer after coronary artery bypass grafting: Report of a case

A 61-year-old man was found to have anemia 3 years after an aortic valve replacement (AVR) and coronary artery bypass grafting (CABG) of the left intrathoracic artery to the left anterior descending artery and the right gastroepiploic artery (RGEA) to the right coronary artery (RCA) for aortic insufficiency and angina pectoris. A IIc gastric cancer in the antrum was subsequently diagnosed. Computed tomography (CT) and coronary angiography showed lymph node metastasis at the root of the RGEA, which perfused a large area of the inferoposterior wall of the heart. To prevent cardiac ischemia and perform complete #6 lymph node dissection, percutaneous intervention was carried out on the RCA before distal gastrectomy with D2 lymph node dissection, and the RGEA was reconstructed as a free graft to the left gastric artery. This procedure may be a surgical option for gastric cancer in patients who have undergone CABG using the RGEA.

A new strategy for management of retroperitoneal tumors with supradiaphragmatic vena caval thrombi

A new surgical technique to treat retroperitoneal tumors with supradiaphragmatic vena caval invasion is described. In this technique, hepatic warm ischemia can be avoided with reversed hepatic outflow through the portal vein and neither hypothermic circulatory arrest nor cardiopulmonary bypass is necessary using centrifugal blood pump-driven bypass.

Evaluation of the Protective Effect of a Novel Prostacyclin Analog on Mesenteric Circulation following Warm Ischemia

The protective effect of a novel prostacyclin (PGI2) analog, OP-2507, on mesenteric circulation was investigated in a canine warm ischemia model. In 20 mongrel dogs, the entire portion of the intestine supplied by the superior mesenteric artery (SMA) and drained by the superior mesenteric vein (SMV) was completely isolated, maintaining the blood and lymph vessels intact. Sixty or 120 min of complete warm ischemia (WI) of the intestine was induced by clamping SMA and SMV, followed by reperfusion for 120 min. Animals were divided into five groups (each n = 4): group 1, sham operation; group 2, 60 min WI; group 3, 120 min WI; group 4, 60 min WI with PGI2 analog administration; group 5, 120 min WI with PGI2 analog administration. The analog was administered at a rate of 6 micrograms.kg-1.h-1 immediately after laparotomy until the end of the observation period. Mean arterial pressure, SMA blood flow (SMABF), SMV pressure were monitored and total mesenteric vascular resistance (TMVR) was calculated. To evaluate the endothelial activation, endothelin, which is secreted from the endothelium under hypoxic stress, was assayed from blood samples of SMV. None of the animals showed significant changes in mean arterial pressure. In groups 2 and 3, SMABF decreased significantly to less than 60% of preoperative value (15 ml.kg-1.min-1) and TMVR significantly increased from 8.1 and 7.3 mm Hg.ml-1.kg.min before WI to 14.0 and 16.4 mm Hg.ml-1.kg.min after 120 min reperfusion, respectively, resulting in delayed hypoperfusion. In contrast, in groups 4 and 5, SMABF increased to over 100% of preoperative level, while TMVR declined from 7.8 and 8.4 mm Hg.ml-1.kg.min before WI to 6.2 and 6.3 mm Hg.ml-1.kg.min after 120 min reperfusion. After 60 min reperfusion, SMABF and TMVR showed a significant difference between the treated and nontreated groups. Only in group 3, high endothelin concentrations (over 20 pg/ml) were observed even after 120 min reperfusion. It was concluded that the PGI2 analog was able to suppress the endothelial activation and the disturbance of mesenteric circulation caused by WI and reperfusion.

Pathogenic mechanisms of intestinal pneumatosis and portal venous gas: should patients with these conditions be operated immediately?

We aimed to histologically observe portal venous gas (PVG)-causing intestinal pneumatosis (IP) and evaluate pathogenic mechanisms and therapeutic strategies, including decisions on whether emergency surgery should be performed. Autopsy was performed in two cases of nonocclusive mesenteric ischemia (NOMI). We directly histologically observed the pathogenic mechanisms of IP caused by gas-producing bacteria and IP considered to be caused by mechanical damage to the intestinal mucosa. IP can be classified hypothetically into the following types according to pathogenesis: (1) infection, (2) rupture (damage) of the intestinal mucosa + increased intestinal intraluminal pressure, and (3) mixed type. In cases of IP caused by gas-producing bacteria or IP associated with intestinal wall damage extending beyond the mucosa to the deep muscular layer, emergency surgery should be considered. However, it is highly possible that patients who test negative for infection with gas-producing bacteria whose intestinal wall damage remains only in the mucosa can be conservatively treated.

Preserved mitochondrial function by allopurinol despite deteriorated hemodynamics in warm ischemia-damaged canine liver

SummaryTo investigate the pathophysiology of warm ischemia (WI) of the liver, the changes in hemodynamics and energy metabolism were studied during and after 60-min complete WI induced by total hepatic vascular exclusion (HVE) in the canine model. Hepatic arterial blood flow after WI was maintained at 76% of the pre-ischemic level, while portal blood flow was only 27% of the pre-ischemic level associated with increased portal vein pressure, which was twice the pre-ischemic level, resulting in a decrease of total hepatic blood flow to 46% of the pre-ischemic level. Concentration of tissue lipid peroxide increased after WI. Arterial blood ketone body ratio (AKBR), which reflects the hepatic mitochondrial redox state, could not recover to the pre-ischemic level after termination of WI. However, when 100 mg/kg of allopurinol (xanthine oxidase inhibitor) was administered intravenously 10 min prior to initiating WI, AKBR was restored to the pre-ischemic level at 30 min after WI in spite of the fact that allopurinol administration to one group produced no remarkable changes in the hepatic hemodynamics compared with the group without allopurinol treatment. Concentration of adenine nucleotides was significantly higher for the treated group at the end of and after WI than for the group without allopurinol treatment and was maintained at a higher level even after WI. Lipid peroxide production was suppressed. Electron microscopic examination revealed that allopurinol treatment could not prevent mitochondrial swelling. It is suggested that WI causes injury primarily to the portal sinusoidal circulation, resulting in portal congestion concomitant with high portal pressure after the release of WI. Allopurinol could prevent the deterioration of mitochondrial ATP metabolism, and was able to inhibit lipid peroxide production, resulting in the rapid recovery of mitochondrial redox state in spite of the fact that it produced no amelioration of hepatic hemodynamics and morphological alterations.

What We Can Learn from Cases of Synchronous Acute Mesenteric Obstruction and Nonocclusive Mesenteric Ischemia: How to Reduce the Acute Mesenteric Ischemia-Related Mortality Rate.

Although the survival rate of patients with ischemic heart disease has recently increased, it remains unknown why the mortality rate of acute mesenteric ischemia (AMI) remains high. Here, we report a possible method of improving the survival rate of patients with AMI obtained through 2 cases of simultaneous acute mesenteric obstruction (AMO) and nonocclusive mesenteric ischemia (NOMI). Case 1 was a 74-year-old woman with atrial fibrillation, hypertension, and dyslipidemia as underlying diseases who developed NOMI immediately after undergoing SMA thrombolysis. Case 2 was a 69-year-old man with atrial fibrillation, hypertension, chronic heart failure, chronic renal failure, and old myocardial infarction who was diagnosed with SMA occlusion complicated by NOMI on the basis of abdominal angiography findings during the first visit. Cure was achieved by thrombolytic therapy, resection of the necrotic intestine, and continuous intra-arterial and/or intravenous injection of prostaglandin E1 (PGE1) in case 1 and by resection of the necrotic intestine and continuous intra-arterial and/or intravenous injection of PGE1 in case 2. AMO and NOMI have many background similarities (e.g., atherosclerosis, hypertension, and ischemic heart disease), making their coexistence very likely. However, no case of AMO plus NOMI has been reported until now. It is highly probable that concomitant NOMI is overlooked in cases of AMO. When managing AMO, NOMI should be considered as a complication, which may lower the patients potential risk of developing NOMI and contribute to improved prognosis of both AMO and AMI.

Advantageous effect of low-molecular-weight heparin administration on hepatic mitochondrial redox state

The effect of low-molecular-weight heparin (LMWH) on hepatic mitochondrial metabolism was compared with that of unfractionated heparin (UH) after the intravenous administration of these two kinds of heparin to normal rabbits. The magnitude of decrease in blood triglyceride levels 5 min after administration of UH (200 U/kg) was significantly greater than after LMWH (200 U/kg). Free fatty acid levels in the blood were significantly higher after this dose of UH than after LMWH. Blood total ketone body levels (acetoacetate+3-hydroxybutyrate) 15 min after injection of 50 U/kg of UH were significantly higher than those after a dose of 50 U/kg of LMWH, and levels after 200 U/kg of UH were significantly higher than those after 200 U/kg of LMWH at 15, 30, 45 and 60 min. Enhanced ketogenesis was not noted after LMWH at any of the doses, or after UH at 3 U/kg. Arterial ketone body ratio (AKBR; acetoacetate/3-hydroxybutyrate), which reflects the hepatic mitochondrial oxidation-reduction state (NAD+/NADH), was maintained above 1.0 in all groups except in the U-200 group, while AKBR in that group was significantly decreased to 0.99±0.14 at 30 min, and further decreased to 0.80±0.08 at 60 min. These results indicate that LMWH has less effect on lipolysis than UH and does not enhance ketogenesis, resulting in less deterioration of mitochondrial redox state.

Proposal for a Safe and Functional Pancreaticojejunostomy Technique from a Histopathological Perspective

AbstractBackgroundTo prevent leakage of pancreatic juice from the main pancreatic duct (MPD), complete external drainage appears to be the most effective technique. However, because this requires a pancreatic stent tube to be ligated with MPD, duct-to-mucosa pancreaticojejunostomy (PJ) is difficult. From our histopathological examination, a large amount of pancreatic juice is drained from the ducts other than MPD. This study aimed to evaluate our new conceptual technique of PJ after pancreaticoduodenectomy (PD).MethodsWe considered it important to drain pancreatic juice from the branch pancreatic ducts to the intestinal tract and to perform duct-to-mucosa PJ, while pancreatic juice from MPD is completely drained out of the body. We designed a technique that could simultaneously achieve these points. In our technique, which is based on conventional “two-row” anastomosis, a stent tube is fixed with MPD and its surrounding tissue by purse-string suture at the cut surface of the pancreas, and duct-to-mucosa PJ is concomitantly performed.ResultsOf 45 patients undergoing PD, 12 of soft pancreas underwent surgery with this technique. According to the classification of the International Study Group on Pancreatic Fistula, a Grade A PF was observed in four patients, whereas no patient had a Grade B or C PF.ConclusionsWe propose our anastomotic technique that could simultaneously prevent PF and keep the pancreatic duct patent.