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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Little attention has been paid to the function of lipoproteins as part of a nonspecific immune defense system that binds and inactivates microbes and their toxins effectively by complex formation. Because of high extra-capillary tissue pressure, aggregates of such complexes may be trapped in vasa vasorum of the major arteries. This complex formation and aggregation may be enhanced by hyperhomocysteinemia, because homocysteine thiolactone reacts with the free amino groups of apo-B to form homocysteinylated low-density lipoprotein (LDL), which is subject to spontaneous precipitation in vitro. Obstruction of the circulation in vasa vasorum, caused by the aggregated complexes, may result in local ischemia in the arterial wall, intramural cell death, bursting of the capillary, and escape of microorganisms into the intima, all of which lead to inflammation and creation of vulnerable plaques. The presence of homocysteinylated LDL and oxidized LDL stimulates production of LDL autoantibodies, which may start a vicious circle by increasing the complex formation and aggregation of lipoproteins. The content of necrotic debris and leukocytes and the higher temperature than its surroundings give the vulnerable plaque some characteristics of a micro-abscess that by rupturing may initiate an occluding thrombosis. This suggested chain of events explains why many of the clinical symptoms and laboratory findings in acute myocardial infarction are similar to those seen in infectious diseases. It explains the presence of microorganisms in atherosclerotic plaques and why bacteriemia and sepsis are often seen in myocardial infarction complicated with cardiogenic shock. It explains the many associations between infections and cardiovascular disease. And it explains why cholesterol accumulates in the arterial wall. Some risk factors may not cause vascular disease directly, but they may impair the immune system, promote microbial growth, or cause hyperhomocysteinemia, leading to vulnerable plaques.
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PMID:Review and Hypothesis: Vulnerable plaque formation from obstruction of Vasa vasorum by homocysteinylated and oxidized lipoprotein aggregates complexed with microbial remnants and LDL autoantibodies. 1920 35

Critical limb ischemia (CLI) is the term used to designate the condition in which peripheral artery disease has resulted in resting leg or foot pain or in a breakdown of the skin of the leg or foot, causing ulcers or tissue loss. If not revascularized, CLI patients are at risk for limb loss and for potentially fatal complications from the progression of gangrene and the development of sepsis. The management of CLI requires a multidisciplinary team of experts in different areas of vascular disease, from atherosclerotic risk factor management to imaging, from intervention to wound care and physical therapy. In the past decade, the most significant change in the treatment of CLI has been the increasing tendency to shift from bypass surgery to less invasive endovascular procedures as first-choice revascularization techniques, with bypass surgery then reserved as backup if appropriate. The goals of intervention for CLI include the restoration of pulsatile, inline flow to the foot to assist wound healing, the relief of rest pain, the avoidance of major amputation, preservation of mobility, and improvement of patient function and quality of life. The evaluating physician should be fully aware of all revascularization options in order to select the most appropriate intervention or combination of interventions, while taking into consideration the goals of therapy, risk-benefit ratios, patient comorbidities, and life expectancy. We discuss the incidence, risk factors, and prognosis of CLI and the clinical presentation, diagnosis, available imaging modalities, and medical management (including pain and ulcer care, pharmaceutical options, and molecular therapies targeting angiogenesis). The endovascular approaches that we review include percutaneous transluminal angioplasty (with or without adjunctive stenting); subintimal angioplasty; primary femoropopliteal and infrapopliteal deployment of bare nitinol, covered, drug-eluting, or bioabsorbable stents; cryoplasty; excimer laser-assisted angioplasty; excisional atherectomy; and cutting balloon angioplasty.
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PMID:Medical and endovascular management of critical limb ischemia. 1962 74

Atherosclerosis with its complications like heart attack and stroke, is the most frequent cause of death in the industrialized countries. Oxidized low-density lipoproteins (LDL) play a major role in the pathogenesis of atherosclerosis. Inhibition of cholesterol synthesis by statins has several protective effects but is not sufficient to prevent the uptake of oxidized LDL and the development of atherosclerotic plaques. For this reason a selective pharmacological inhibition of the uptake of oxidized LDL (oxLDL) in endothelial cells is an interesting therapeutic approach. An important novel target molecule is the endothelial lectin-like oxLDL receptor LOX-1. This receptor is able to take up both minimally and highly oxidized LDL. In addition it mediates endothelial phagocytosis of aged and apoptotic cells and plays a role in thrombocyte adhesion and in the interaction between bacterial proteins and endothelial cells in sepsis. LOX-1 is induced by proinflammatory cytokines, oxLDL, angiotensin II, endothelin-1 and arterial hypertension. LOX-1 increases endothelial dysfunction and atherosclerosis by endothelial uptake of oxLDL. This is the reason why LOX-1 has been considered as a novel link between hypertension and atherosclerosis. Transgenic overexpression of the LOX-1 receptor and high-fat diet induces intramyocardial vascular disease and endothelial dysfunction in resistance arteries. In contrast, genetic deletion of the LOX-1 gene reduces the development of atherosclerotic plaques. In the clinical context LOX-1 has been detected in the early phase of endothelial dysfunction and atherosclerosis in arteries of patients with coronary heart disease. Several novel data support a role of LOX-1 in the endothelial dysfunction in diabetic vascular and renal disease, hypercholesterolemia, obesity and preeclampsia. This makes the LOX-1 receptor a novel and interesting target molecule in endothelial dysfunction and atherosclerosis.
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PMID:[LOX-1 receptor as a novel target in endothelial dysfunction and atherosclerosis]. 2014 62

Internal jugular vein thrombosis (IJVT) is an elusive vascular disease that is rarely seen, with potentially lethal complications such as sepsis and pulmonary embolism. Spontaneous IJVT is considered when no apparent predisposing cause of thrombosis is present. A previously healthy, 31-year-old woman presented to the university-based emergency department because of painless swelling in the right anterior side of her neck. Physical examination revealed a painless, soft and immobile mass in the right anterior side of her neck beneath the sternocleidomastoid muscle, without hyperemia or local heat. On ultrasonographic examination, a hyperechogenic mass was visualized around the thoracic entrance of the right internal jugular vein, which was suggestive of a thrombus. The patient was administered intravenous antibiotic and low-molecular-weight heparin followed by oral coumadin as anticoagulant therapy. Her complaints were relieved within 5 days. She was completely well after 6 months. Venous thrombosis generally results from impaired blood flow locally or systemically that leads to activation of coagulation. Primary care physicians should sustain a high index of suspicion in patients who present with undiagnosed swelling in the neck, or other signs and symptoms attributed to IJVT.
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PMID:Spontaneous internal jugular vein thrombosis: a case report. 2118 18

The evolution of techniques in plastic surgery and orthopedic surgery over the past few decades has enabled a great level of success in limb salvage. Limb salvage can now be achieved when faced with trauma, tumor, sepsis, or vascular disease. In fact, "What can be salvaged?" is now a less common debate among clinicians than "What should be salvaged?" Often discussions among surgeons from various subspecialties, including orthopedics, plastics, trauma, and vascular surgery, are characterized by how each of them can perform their respective part of the salvage operation, be it bony fixation, revascularization, or soft-tissue coverage, but none of them is certain whether it should be attempted. What is needed in these clinical situations is an interdisciplinary team approach led by individual or groups of clinicians who are familiar not only with their own subspecialized skills but also with those of their colleagues and the outcomes associated with integrated efforts at limb salvage. The concept of orthoplastic surgery is based on such an idea, where the combined skills and techniques of the orthopedic surgeon and reconstructive microsurgeon are used in concert to direct efforts toward limb salvage or decide against it when it is not indicated. This article presents a review of the roles of the two subspecialties and how an orthoplastic team can function with the current techniques to improve outcomes in limb salvage surgery.
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PMID:The respective roles of plastic and orthopedic surgery in limb salvage. 2120 Feb 94

Vascular integrity or the maintenance of blood vessel continuity is a fundamental process regulated, in part, by the endothelial glycocalyx and cell-cell junctions. Defects in endothelial barrier function are an initiating factor in several disease processes including atherosclerosis, ischemia/reperfusion, tumor angiogenesis, cancer metastasis, diabetes, sepsis and acute lung injury. The glycosaminoglycan, hyaluronan (HA), maintains vascular integrity through endothelial glycocalyx modulation, caveolin-enriched microdomain regulation and interaction with endothelial HA binding proteins. Certain disease states increase hyaluronidase activity and reactive oxygen species (ROS) generation which break down high molecular weight HA to low molecular weight fragments causing damage to the endothelial glycocalyx. Further, these HA fragments can activate specific HA binding proteins upregulated in vascular disease to promote actin cytoskeletal reorganization and inhibition of endothelial cell-cell contacts. This review focuses on the crucial role of HA in vascular integrity and how HA degradation promotes vascular barrier disruption.
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PMID:Hyaluronan regulation of vascular integrity. 2225 99

We present a case of a 60-year old patient hospitalized at the Department of Infectious Diseases and Travel Medicine, Medical faculty of UPJS and L. Pasteurs University Hospital in Kosice with suspected gastroenteritis. The patient was admitted to an intensive care unit because of the signs of septic shock. Within one hour from admission, the patient was administered early goal directed therapy for septic shock. Subsequently, infectious endocarditis of stimulation electrodes and tricuspid valve was identified as the origin of the infection. The stimulation system was then explanted from a stabilized and afebrile patient at the Department of cardiac Surgery of Eastern Slovak Institute of Cardiac and Vascular Diseases in Kosice. This case should emphasise frequently atypical course of this serious disease and the need for early identification of severe sepsis to enable timely management to affect mortality.
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PMID:[Septic shock due to infective endocarditis of stimulation system of implantable cardioverter-defibrillator]. 2244 94

The transpulmonary pressure gradient (TPG), defined by the difference between mean pulmonary arterial pressure (P(pa)) and left atrial pressure (P(la); commonly estimated by pulmonary capillary wedge pressure: P(pcw)) has been recommended for the detection of intrinsic pulmonary vascular disease in left-heart conditions associated with increased pulmonary venous pressure. In these patients, a TPG of >12 mmHg would result in a diagnosis of "out of proportion" pulmonary hypertension. This value is arbitrary, because the gradient is sensitive to changes in cardiac output and both recruitment and distension of the pulmonary vessels, which decrease the upstream transmission of P(la). Furthermore, pulmonary blood flow is pulsatile, with systolic P(pa) and mean P(pa) determined by stroke volume and arterial compliance. It may, therefore, be preferable to rely on a gradient between diastolic P(pa) and P(pcw). The measurement of a diastolic P(pa)/P(pcw) gradient (DPG) combined with systemic blood pressure and cardiac output allows for a step-by-step differential diagnosis between pulmonary vascular disease, high output or high left-heart filling pressure state, and sepsis. The DPG is superior to the TPG for the diagnosis of "out of proportion" pulmonary hypertension.
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PMID:The transpulmonary pressure gradient for the diagnosis of pulmonary vascular disease. 2327 16

The mean age of the ESRD population continues to increase, with the 2011 USRDS Annual Data report noting it to be 62.6 years among a prevalent chronic dialysis population (both hemo- and peritoneal dialyses) of approximately 399,000. As with previous reports, the greatest growth rate per million population in the ESRD cohort occurs in age range >75 years. Entering the ESRD pool >75 years of age are about 5,000 patients/million population; in contrast, the number is about 2,100/million population that falls in the age range 45-65 years. Baseline comorbid conditions, especially complications associated with diabetes and cardiovascular disease (CVD), accelerate with duration of ESRD, and compound the already high morbidity and mortality. With aging comes progressive vascular disease, making it more likely that the elderly will have a central venous catheter (CVC) access, rather than a fistula, for starting and continuing dialysis, hence, increased hospitalization and death rates associated with access clotting and infection (sepsis). The scenario in the elderly patient on dialysis is often a poor quality of life with repeated hospitalizations and eventual nursing home placement. For those patients who survive such a disabled state leads to the question whether chronic dialysis therapy is the best option. Our goal as committed nephrologists is to deliver compassionate, quality care. In the sick, older patient let us rethink what is the best option as they enter ESRD.
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PMID:The older patient with end-stage renal disease: is chronic dialysis the best option? 2317 89

Hemolysis occurs in many hematologic and nonhematologic diseases. Extracellular hemoglobin (Hb) has been found to trigger specific pathophysiologies that are associated with adverse clinical outcomes in patients with hemolysis, such as acute and chronic vascular disease, inflammation, thrombosis, and renal impairment. Among the molecular characteristics of extracellular Hb, translocation of the molecule into the extravascular space, oxidative and nitric oxide reactions, hemin release, and molecular signaling effects of hemin appear to be the most critical. Limited clinical experience with a plasma-derived haptoglobin (Hp) product in Japan and more recent preclinical animal studies suggest that the natural Hb and the hemin-scavenger proteins Hp and hemopexin have a strong potential to neutralize the adverse physiologic effects of Hb and hemin. This includes conditions that are as diverse as RBC transfusion, sickle cell disease, sepsis, and extracorporeal circulation. This perspective reviews the principal mechanisms of Hb and hemin toxicity in different disease states, updates how the natural scavengers efficiently control these toxic moieties, and explores critical issues in the development of human plasma-derived Hp and hemopexin as therapeutics for patients with excessive intravascular hemolysis.
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PMID:Hemolysis and free hemoglobin revisited: exploring hemoglobin and hemin scavengers as a novel class of therapeutic proteins. 2326 91


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