[Advances in nephrology. Kidneys in systemic diseases].
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A 46-year-old female patient was supported for 185 days with a total artificial heart, underwent successful transplantation, and survived for over 1 year with no clinical residual findings suggestive of embolic events. Daily observation, analysis of a large battery of coagulation tests, and eight serial computed tomographic scans suggest that she had 12 embolic events while receiving mechanical support. Furthermore, it appears that the events were associated temporally with several mild infections and that coagulation was stimulated several days to 1 week before we detected the events.
We report a case of splenic volvulus caused by a mobile spleen. Preoperative ultrasonography and CT-scan did not provide the diagnosis. Splenectomy was performed at laparotomy, the only possible treatment in this exceptional case.
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The sonographic appearances of benign and malignant splenic lesions in 154 patients are illustrated. Sixty-six of the 154 patients had malignant splenic lesions; 55 of these had malignant lymphoma and 11 had splenic metastatic lesions. The lesions were hypoechoic in 64 cases (97%), including all cases of malignant lymphoma, and were hyperechoic in two. Eighty-eight patients had benign splenic lesions; findings included cysts, infarcts, abscesses, hemangiomas, and calcifications.
OBJECTIVE: To investigate the effects of splenic artery and vein ligation and the influence of hyperbaric oxygen after the double vascular ligation on the viability of spleen tissue. METHODS: Sixty nine adult male Wistar rats (285-375 g) were randomly separated in three groups: group 1, four rats, sham operated, group 2, 34 rats, submitted to simultaneous splenic artery and vein ligation and group 3, 31 rats, submitted to hyperbaric oxygen during 11 days, after double vascular ligation. All animals were killed on day 12 after surgery. The spleen was removed and paraffin embedded for microscopic examination. RESULTS: In the groups submitted to vascular ligation, the spleen was normal in 8.82% of rats not treated with hyperbaric oxygen and in 45.16% of rats that received hyperbaric oxygen after vascular ligation (p=0.01). In the spleens with white infarct, the mass of preserved splenic tissue in relation to the total body mass did not differ between the groups treated or not with hyperbaric oxygen. The preserved splenic tissue had normal histology in both groups. The healing process was more accelerated in the group of rats treated with hyperbaric oxygen. CONCLUSION: Results demonstrate that exposure to hyperbaric oxygen increased the frequency of total spleen mass preservation after simultaneous ligation of the splenic artery and vein but did not alter the percentage of the spleen's viable area, however the healing process in necrotic areas was accelerated.
We have developed an embolizing material consisting of Y-shaped silicone particles for partial splenic embolization. Wide spaces for blood flow are left around the particles when these are lodged in arterial branches. We embolized one kidney in each of 3 dogs with the particles and observed a slowly induced occlusion of renal arterial branches during one month. The particles were also used for partial splenic embolization in 14 patients. The average portion of infarcted spleen tissue 7 days after embolization was 51% calculated from CT images. In 6 patients who had CT both 2 and 7 days after embolization, the average rate of splenic infarction increased from 29% at 2 days to 60% at 7 days. Our patients required analgesics for only 2.3 days on average. The Y-shaped silicone particles by slowly occluding splenic arterial branches produce ischemia in a gradual fashion which may minimize the pain after embolization.
Splenic complications of chronic pancreatitis appear to be less exceptional than is usually accepted, particularly since preoperative diagnosis has been facilitated by ultrasound and abdominal scan imaging. Complications noted in 37 cases were: infarcts (2 cases), hematoma or false blood cysts (26 cases) and rupture (9 cases). The splenic infarcts were revealed by digestive hemorrhage, the false blood cysts of spleen by a painful mass in left hypochondrium associated with pleural effusion and rupture of spleen by an acute hemoperitoneum. Treatment included splenectomy in 19 cases, splenectomy caudal pancreatectomy in 17 cases and drainage of a splenic hematoma in one patient. Operative mortality was 16.2% and the long-term prognosis was poor and related to underlying condition. Data from an experimental study suggest that the effect of an episode of acute pancreatitis on the splenic pedicle is the most important physiopathologic factor. A hemorrhagic infarct or infarction of splenic parenchyma are common starting points for all clinicopathologic forms described.
PURPOSE: To determine the abdominal computed tomographic (CT) findings in patients with antiphospholipid antibody syndrome (APS). MATERIALS AND METHODS: Retrospective review of medical records from two university medical centers from 1994 through 1997 revealed 215 patients who had a hypercoagulable state attributed to primary or secondary APS. Abdominal CT findings in these patients were reviewed for evidence of large-vessel occlusion or visceral ischemia. RESULTS: In 42 (19.5%) of 215 patients with APS (age range, 32-65 years; mean age, 42 years), abdominal thromboses or ischemic events were detected at CT. Twenty-two (52%) had major vascular thromboses, including those in the inferior vena cava (n = 10), portal and superior mesenteric veins (n = 7), splenic vein (n = 4), and aorta (n = 1). Thirty-six (86%) patients had abdominal visceral ischemia resulting in renal infarction (n = 22), bowel ischemia (n = 13), splenic infarction (n = 6), pancreatitis (n = 3), hepatic infarction (n = 1), and/or hepatic dysfunction with portal hypertension (n = 1). In some patients, more than one abdominal organ and/or vessel was involved. CONCLUSION: Patients who have circulating antiphospholipid antibodies are at risk for major abdominal vascular thromboses and organ infarction. Radiologists must be familiar with this syndrome; they may be the first physicians to suggest the diagnosis on the basis of findings of unusual or recurrent sites of thrombosis, especially in young patients.
The splenic vein was ligated in ten dogs in order to evaluate the time course of changes in splenic size and to relate them to splenic arterial flow, splenic pressure and development of venous collaterals. Following ligation of the splenic vein, splenic size and venous pressure immediately rose in all dogs. Arterial flow to the spleen simultaneously fell in roughly inverse proportion to the elevation of venous pressure. During the following weeks, the splenic parenchymal pressure decreased to basline levels in all but one dog, as collateral veins developed through the gastric venous network to the portal vein. Splenic size gradually decreased toward normal in eight of the ten dogs. At the time of sacrifice, 8-16 weeks after splenic vein ligation, pathologic examination demonstrated fibrosis from healed infarction. Recent hemorrhage, indicating persistence of the congestive process, we also present, although difficult to explain in view of normal splenic parenchymal pressure.
Congenital deficiency or acquired laxity of the suspensory ligaments, that usually hold the spleen in place in its compartment, may result in extreme splenic mobility. Consequently, this mobility predisposes to torsion of the elongated splenic vascular pedicle creating a situation of acute abdomen due to haemorrhagic infarction. Various imaging modalities for diagnosing the wandering spleen such as ultrasonography, CT scan, MR-angiography, nuclear scan and arteriography are of great value both in the asymptomatic condition and in acute abdomen. We report on an unusual case of wandering spleen with torsion of the pedicle in a middle-aged woman which we casually diagnosed intraoperatively. It was not possible to preserve the wandering spleen by means of splenopexy because the splenic infarction required a splenectomy. Though the condition was not diagnosed prior to surgery, prompt intervention enabled the prognosis to remain unvaried. We review the cases reported in the literature and discuss the diagnostic and therapeutic problems raised by this rare condition.
A 26-year-old female was on continuous ambulatory peritoneal dialysis (CAPD) because of diabetic end-stage renal failure. She developed an acute peritonitis that relapsed repeatedly despite appropriate antibiotic treatment. Investigations showed the presence of a splenic abscess, and splenectomy and peritoneal cannula removal were required. The patient died of myocardial infarction two weeks postoperatively. This is the first recorded case of peritonitis secondary to splenic abscess in a CAPD patient. Autopsy findings suggest that the abscess developed from infection of a splenic infarct.
Forty-nine dogs were made diabetic by total pancreatectomy. Fifteen untreated pancreatectomized animals survived a mean (+/-S.E.) of 7.0 +/- 1.1 days with a mean (+/-S.E.) plasma glucose level of 402 +/- 26 mg/100 ml before death. The pancreata of 32 dogs were distended with cold (4 degrees ) Hanks' solution, minced, digested with collagenase (600 U/ml tissue) for 15-25 minutes, and autotransplanted either into the splenic artery (three dogs), directly into the splenic pulp (21 dogs), or into the portal vein (ten dogs). Tissue infusion into the splenic artery resulted in infarction and persistent hyperglycemia. Direct implantation into the splenic pulp of tissue digested for 15, 20 and 25 minutes resulted in permanent normoglycemia (fasting plasma glucose < 150 mg/100 ml) in 7 of 8, 7 of 7, and 6 of 6 dogs respectively. Glucose tolerance test mean (+/-S.E.) K values (% decline of plasma glucose concentration/minute) in these groups two weeks after transplantation were 1.20 +/- 0.20%, 1.60 +/- 0.25 and 0.70 0.08% respectively, indicating that 20 minutes digestion was best for intrasplenic transplantation. Tissue prepared in the optimal manner (20 minutes digestion) and embolized into the liver resulted in normoglycemia in three of eight dogs, and a mean (+/-S.E.) K value of 0.77 +/- 0.10%. Both dogs receiving tissue dispersed for 25 minutes into the portal vein remained hyperglycemic. In the dogs subjected to intraportal transplantation, portal pressure rose from a mean (+/-S.E.) of 6.5 +/- 0.6 cm H(2)O before to 21.9 +/- 2.2 cm H(2)O immediately after tissue embolization, but declined to 6.5 +/- 1.0 cm H(2)O by ten weeks in animals becoming normoglycemic. We conclude that in dogs direct implantation of pancreatic tissue into the splenic pulp is superior to embolization into the portal vein or splenic artery because the splenic circulation is not compromized, portal hypertension is obviated, and glucose metabolism is best controlled as judged by glucose tolerance test K values.
PURPOSE: To evaluate the effects of reducing the volume of spleen infarcted during partial splenic embolization (PSE) for treatment of hypersplenism in children. MATERIALS AND METHODS: Five children with hypersplenism underwent embolization of 30%-40% of the splenic volume. The results were compared with those of a previous study of 70%-80% PSE performed in 17 children. RESULTS: The hospital stay after the procedure was reduced from 16.0 days +/- 8.0 to 6.6 days +/- 5.6. The febrile period decreased from 15.0 days +/- 8.1 to 5.0 days +/- 6.6. The peak white blood cell count was 8,300/mm3 +/- 4,600 (8.3 x 10(9)/L +/- 4.6) versus 19,400/mm3 +/- 7,800 (19.4 x 10(9)/L +/- 7.8) in the earlier study. The peak platelet count was 153,000/mm3 +/- 65,000 (153 x 10(9)/L +/- 65) versus 636,000/mm3 +/- 406,000 (636 x 10(9)/L +/- 406). The platelet count after a mean follow-up of 14 months was 70,000/mm3 +/- 7,000 (70 x 10(9)/L +/- 7) versus 230,000/mm3 +/- 62,000 (230 x 10(9)/L +/- 62) after a mean follow-up of 45 months. The frequency of variceal hemorrhage decreased from 3.5 to 0.5 episodes per year. The frequency of epistaxis decreased from 30 to 15 episodes per month. CONCLUSION: Reduced-volume embolization decreased morbidity. All patients maintained a platelet count above baseline, and no patient required repeat embolization.
The use of splenic embolization for nonoperative management has increased. With increased use of this adjunct, a new and frequent finding has been air within the areas of infarction in patients with or without clinical signs of infection. The purpose of this study was to determine if air within areas of splenic infarction is pathologic of infection or rather an incidental finding. A retrospective review over the past 3 years of inpatients undergoing splenic embolization and having pre- and postembolization abdominal computed tomography scans were reviewed for the findings of free air as well as any clinical signs of infection. A total of 96 consecutive patients were included. Of these, 12 had evidence of infarction with air. Six of these patients had undergone distal embolization with intraparenchymal air, but no symptoms. These were successfully observed. Two patients demonstrated subcapsular air/fluid levels, which underwent drainage with splenic preservation. Cultures were negative for infection. The remaining 4 underwent splenectomy. Of these, all had large collections of air. Two of these 4 spleens were infected: 1 with alpha-hemolytic Streptococcus and one with Clostridia perfringens. The remainder was sterile. This gave an overall infection rate of 17 per cent of patients with evidence of air. This yield increased to 33 per cent if the patient had symptoms and 50 per cent in those with large amounts of air and symptoms. Overall, we feel that air following embolization is a concern, but does not constitute infection. Patients with large amounts of air and signs and symptoms of infection will have a far higher infectious rate, 50 per cent in this limited series. In these patients, evaluation for infection is indicated; that being percutaneous sampling versus splenectomy.