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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prior studies of vascular rejection in transplanted human hearts have stressed the importance of accelerated coronary arteriosclerosis (chronic vascular rejection). We, however, have had four patients with sudden onset of acute heart failure within 90 days of transplantation who have died without significant myocardial interstitial rejection or the concentric intimal thickening with dense collagen that is typical of chronic vascular rejection. In contrast, the coronary arteries in our patients had a prominent lymphocytic infiltrate, a loosely organized intimal thickening composed of smooth muscle cells, and extensive endothelial injury. We believe that these changes define acute vascular rejection of the coronary artery. In 14 transplanted hearts obtained consecutively, at autopsy or at a second transplant procedure, graft failure was caused by acute coronary vascular rejection in six cases and by chronic coronary vascular rejection in one case. The remaining seven patients showed no evidence of vascular rejection and died primarily of sepsis. Cytomegalovirus (CMV) disease was present in 6 of 7 patients with vascular rejection, of which 43% were CMV-negative recipients of hearts from CMV-positive donors. The adoption of a triple-drug protocol, in which azathioprine was added to cyclosporine and prednisone, reduced the incidence of acute vascular rejection from 27% to 8%. We conclude that acute coronary vascular rejection may be initially seen as global cardiac ischemia in the absence of significant interstitial myocardial rejection. Further, acute vascular rejection should be pathologically distinguished from chronic vascular rejection, although both are probably stages in the natural history of immune-mediated vascular injury.
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PMID:Acute vascular rejection of the coronary arteries in human heart transplantation: pathology and correlations with immunosuppression and cytomegalovirus infection. 165 3

The paper is a unique pathological description of a bilateral, symmetric, anterior, temporal ischemic optic neuropathy with the morphological characteristics of cavernous optic atrophy initially described by Schnabel in glaucomatous eyes. The 80-year-old woman had suffered from cardiac insufficiency and diabetes mellitus for many years. She died from sepsis and circulatory collapse due to ischemic colitis, intestinal perforation, and peritonitis. There was widespread arteriosclerosis but no evidence of giant-cell arteritis. Cell loss was demonstrated in both retinas, the chiasm, and in the central lateral geniculate body. These represent a retrograde, descending and ascending optic atrophy, with transsynaptic degeneration in the LGB. A small craniopharyngioma was found by chance in the infundibulum. Neither clinically nor morphologically were there any signs of glaucoma.
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PMID:[Histopathology of the retina, optic fascicle and lateral geniculate body in chronic, bilateral symmetric ischemic Schnabel's cavernous optic atrophy]. 224 78

The pathophysiology and pathologic appearances of adult osteomyelitis are discussed, without reference to childhood hematogenous (metaphyseal) osteomyelitis or chronic osteomyelitis secondary to vascular phenomena such as diabetes or arteriosclerosis. Osteomyelitis as a feature of generalized sepsis in the immunocompromised patient is also excluded. The focus is on infection of the adult skeleton that occasionally arises spontaneously but more commonly presents as a complication of an open fracture or an operative procedure. The special features of adult osteomyelitis that are the result of the infection developing within the confined and rigid structure of the skeleton are highlighted. Lastly, the histopathology of osteomyelitis is examined in an effort to demonstrate the host bone's response to this injury.
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PMID:The pathogenesis of adult osteomyelitis. 265 95

Two new cases of primary aortoduodenal fistula (ADF), one associated with an arteriosclerotic aneurysm and the other without, are presented and 4 cases of primary ADF without aneurysm published between 1972 and 1985 are reviewed. The anatomic relationship of the distal part of the duodenum to the infrarenal segment of the aorta, arteriosclerosis, mechanical trauma, infection and sepsis are prominent factors in the pathogenesis of ADF irrespective of its type. Intermittent haematemesis and/or melaena are the main presenting symptoms in all variants of ADF and awareness of the existence of this condition is essential for its early detection. Upper gastrointestinal endoscopy including examination of the distal part of the duodenum and explorative laparotomy are important tools in the preoperative diagnostic workup specially in primary ADF without previous knowledge of the presence of an aneurysm.
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PMID:Aortoduodenal fistula revisited. 269 33

This is a report about 4 patients with aneurysms of the superior mesenteric artery of arteriosclerotic, mycotic and probably congenital etiology together with a review of the literature as to the etiology, diagnostic possibilities and therapy. Arteriography is the method of choice even though a diagnosis may be possible by sonography or CT in special cases. Even though an aneurysm of the superior mesenteric artery is rare, it has to be considered in the differential diagnosis of persisting abdominal problems of unknown origin. This is especially true for patients with a predisposing history such as previous or existing endocarditis, sepsis, arteriosclerosis and hypertension. Because of the possibility of rupture followed by life threatening bleeding an adequate diagnostic step such as arteriography has to be considered finally.
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PMID:[Aneurysm of the superior mesenteric artery. Its diagnosis and clinical significance]. 643 18

In spite of a systemically increased clotting tendency in progredient arteriosclerosis there are locally restricted haemorrhagic sequelae following arterial vasoreconstruction. Because of the fact that each bleeding simultaneously includes the risk of wound infection with subsequent sepsis the formation of a haematoma is to be avoided in the surgical procedure. The development of disseminated intravascular coagulation caused by sepsis and that caused by massive haemorrhage are represented as to their clinical importance. Finally, an internationally accepted substitution concept for severe bleeding sequelae, e.g. in case of the rupture of an aortic aneurysm, is submitted.
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PMID:[Disorders of blood coagulation during and after arterial vascular reconstruction]. 663 15

The objective in this paper is to describe the severity and outcome of arterial occlusion complicating treatment of women with gynecologic cancer. A series of six patients who underwent amputation were identified. Acute arterial occlusions were seen in three patients. One patient suffered extensive thrombosis of the hand and wrist resulting in amputation 3 weeks after cytoreductive surgery and chemotherapy for Fallopian tube cancer. She had a history of pulmonary embolism and deep-vein thrombosis. This patient was thought to have thrombophilia. One elderly patient with known arteriosclerosis developed sepsis following radical deep excision and groin dissection for vulvar cancer and lost two digits presumably due to microemboli. One patient developed thrombosis of the femoral artery on the second day following cytoreductive surgery for ovarian cancer. She responded to anticoagulation therapy; however, necrosis remained in portions of the heel and toes. Three patients underwent amputation of a lower extremity when they developed chronic arterial insufficiency after pelvic radiotherapy. The patients were irradiated at the ages of 28, 30, and 35 years for cervix cancer in two patients and a low-grade retroperitoneal sarcoma in one patient. Two received neutron beam therapy and one received conventional photon beam therapy. All three had extensive late radiation morbidity to the bladder and rectum and had multiple prior surgeries. The amputations occurred at the ages of 48, 48, and 55 due to accelerated arteriosclerosis. Two patients died as a result of this complication. Acute and chronic arterial occlusions are rare yet dramatic complications of therapy for gynecologic cancer. This series illustrates the predisposing factors, presentation, and management of these unusual events.
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PMID:Arterial occlusion complicating treatment of gynecologic cancer: a case series. 889 66

The development of acute acalculous cholecystitis (AAC) after cardiovascular surgery is an infrequent but devastating complication, the etiology and management of which remains controversial. To evaluate the etiology, treatment, and outcome of patients with AAC, the cases of six patients encountered within an 8-year period who developed AAC after cardiovascular surgery requiring cardiopulmonary bypass (CPB) were reviewed. Atherosclerotic risk factors including diabetes, hyperlipidemia, and smoking were evident in five patients, three of whom had a history of stroke or arteriosclerosis obliterans, while low cardiac output was recognized in three. Percutaneous transhepatic cholecystostomy was performed in five patients, and another required cholecystectomy for peritonitis due to gangrene of the gallbladder. Two patients died of respiratory failure and sepsis after 15 and 82 days of percutaneous drainage, respectively; however, the four survivors had an excellent outcome without any biliary tract disease during a mean follow-up period of 5.3 years. In conclusion, AAC after cardiovascular surgery may result from hypoperfusion of the gallbladder due to various factors including CPB, visceral atherosclerosis, and low cardiac output. We advocate early percutaneous cholecystostomy for patients without peritonitis, while early cholecystectomy is indicated for those with peritonitis.
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PMID:Acute acalculous cholecystitis after cardiovascular surgery. 1087 May 75

The clinical presentation of mesenteric ischemia depends on the site, grade, and cause of vascular obstruction; the degree of collateralization; and the stage of disease. Patients in the early stages of ischemia typically have abdominal pain out of context with an unimpressive abdominal examination. It is during this stage that medical and endovascular techniques can be most effective. After signs of peritonitis are present (signaling bowel infarction), surgical exploration and bowel resection are necessary. Chronic mesenteric ischemia induced by stenotic arteriosclerosis should be treated with percutaneous transluminal angioplasty and stenting (PTAS). Chronic mesenteric arterial occlusions are better handled with bypass surgery. Acute embolic or thrombotic ischemia is surgically treated after medical resuscitation. Endovascular techniques may be applicable in selected patients (usually in those with subacute symptoms), but thrombolytic therapy should be avoided if intestinal infarction is suspected. Non-occlusive mesenteric ischemia requires a rapid correction of the predisposing hypotension or sepsis followed by papaverine infusion into the superior mesenteric artery. Celiac artery compression syndrome requiring treatment is best treated with surgical release of the median arcuate ligament; PTAS should not be performed. Mesenteric venous occlusion should be treated with anticoagulation. Surgical exploration and bowel resection is necessary in patients presenting with acute signs and symptoms, reserving thrombolytic therapy for early, mildly symptomatic, thromboses in whom there is no contraindication to thrombolysis.
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PMID:Mesenteric Vascular Disease. 1134 65

Plasminogen activator inhibitor-1 (PAI-1) is the major inhibitor of plasminogen activation and likely plays important roles in coronary thrombosis and arteriosclerosis. Tumor necrosis factor-alpha (TNFalpha) is one of many recognized physiological regulators of PAI-1 expression and may contribute to elevated plasma PAI-1 levels in sepsis and obesity. Although TNFalpha is a potent inducer of PAI-1 expression in vitro and in vivo, the precise location of the TNFalpha response site in the PAI-1 promoter has yet to be determined. Transient transfection studies using luciferase reporter constructs containing PAI-1 promoter sequence up to 6.4 kb failed to detect a response to TNFalpha. Moreover, TNFalpha failed to induce expression of enhanced green fluorescent protein under the control of a 2.9-kb human PAI-1 promoter in transgenic mice, although endogenous murine PAI-1 was strongly induced. These data suggested that the TNFalpha response element in the PAI-1 gene is remote from the proximal promoter region. In this study, seven candidate regulatory regions were identified using cross-species sequence homology analysis as well as DNase I-hypersensitive site analysis. We identified a 5' distal TNFalpha-responsive enhancer of the PAI-1 gene located 15 kb upstream of the transcription start site containing a conserved NFkappaB-binding site that mediates the response to TNFalpha. This newly recognized site is fully capable of binding NFkappaB subunits p50 and p65, whereas overexpression of the NFkappaB inhibitor IkappaB prevents TNFalpha-induced activation of this enhancer element.
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PMID:Tumor necrosis factor alpha activates the human plasminogen activator inhibitor-1 gene through a distal nuclear factor kappaB site. 1496 43


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