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

Evidence for a major participatory role of the myocardium in the hemodynamic response to endotoxemia and sepsis has been controversial. Early interpretations about in situ changes in cardiac performance during shock were confounded by the concomitant influence of uncontrolled pathophysiologic adjustments in cardioactive variables such as preload, afterload, sympathoadrenal discharge, left ventricular diastolic compliance (stiffness), and in some studies myocardial hypoperfusion/ischemia. Despite such complexities, many recent studies with intact subjects and isolated preparations consistently point toward a relatively early involvement of myocardial dysfunction in circulatory shock syndromes associated with gram-negative bacteria and sepsis. The cardiac dysfunction cannot be accounted for by a direct toxic effect of the endotoxin molecule itself on cardiac myocytes. Rather, evidence is compelling that endotoxin interacts first with other types of cellular or tissue elements. The latter evoke biologic reactions through some unknown pathway culminating in deleterious effects in the heart. Discovery of the casual mechanism(s) responsible for myocardial sequelae of endotoxemia and sepsis remains a key objective in experimental and clinical research in circulatory shock pathogenesis.
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PMID:Does the heart fail in endotoxin shock? 240 36

The catastrophe theory evolved by Thom and Zeeman proposes a mathematical definition for the abrupt or 'catastrophic' changes that can suddenly occur in normally well-ordered and smooth-running systems. We have integrated this theory with our own PAF/cytokine feedback network hypothesis to explain the control and dysfunction of the inflammatory response. This process involves the activation of cells and factors such as proteases, and is coordinated by mediators such as PAF, cytokines and growth factors, minute amounts of which can prime cells to respond in an enhanced manner to subsequent agonistic stimuli. PAF and certain cytokines also possess the unique property of being able to induce the release of each other and their own generation in vivo. This 'singularity' may enable a self-generating feedback network to become established. The priming ability of these mediators indicates the extreme sensitivity of the inflammatory process and importance of a homeostatic equilibrium between the vectors involved in the priming and feedback processes and internal suppressive mechanisms. In pathological conditions, one can consider the phenomenon of PAF and cytokine autogeneration as a 'fold' in the feedback network and an expression of the singularity characteristic of the catastrophe hypothesis. This may lead to systemic toxicity and microcirculatory collapse, a characteristic feature of shock, sepsis, asthma, ischemia and graft rejection. A combination of drugs antagonizing the various feedback components may inhibit this catastrophic process and thus provide more successful therapy of these conditions.
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PMID:PAF/cytokine auto-generated feedback networks in microvascular immune injury: consequences in shock, ischemia and graft rejection. 251 89

A young woman presented with a 4-month history of retinal and vertebrobasilar ischemia. Angiography demonstrated narrowing of major branches of the aortic arch. Intractable, severe retroorbital pain of the right eye developed after a middle cerebral artery stroke. During 4 weeks of aggressive immunosuppressive therapy including IV high dose bolus corticosteroids and pulse cyclophosphamide, her neurologic deficit improved transiently, but her retroorbital pain persisted. She died of staphylococcal sepsis and pneumonia. An autopsy demonstrated thrombotic or fibrous occlusion, with minimal inflammation, of extracranial arteries.
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PMID:Takayasu arteritis presenting as retinal and vertebrobasilar ischemia. 257 Jan 49

Patients suffering blunt leg trauma resulting in below-knee fracture, tibial artery injury, and soft-tissue damage are at major risk for amputation. In an attempt to identify the factors which may forecast limb loss despite vascular surgical repair, all patients with tibial fractures admitted between 1980-1988 were reviewed. Forty-four of 366 (12%) patients presented with clinical evidence of tibial artery injury. Twenty-seven of these 44 patients had angiographic evidence of at least one patent tibial vessel providing adequate distal flow. The remaining 17 patients required operative repair of injured tibial arteries because of persistent distal ischemia. The amputation rate was 35% (6/17--4 BKA, 2 AKA), three of these having patent vascular repairs at the time of the amputation. Operative indications for amputation were ischemic nonviable muscle in three patients, and severe soft-tissue wound infection in three. Patients who required amputation had a significantly greater incidence (Fisher's exact test) of three or more fascial compartments involved in muscular injury (p = 0.005), two or more injured tibial vessels (p = 0.01), failed vascular reconstruction (p = 0.03), a cadaveric foot at initial exam (p = 0.03), and severe muscle crush injury or muscle tissue loss (p = 0.03). No extremity was salvaged when more than two of these factors was present, and a failed vascular reconstruction led to limb amputation in all cases. These factors will predict an irretrievable extremity following blunt tibial artery trauma, allowing amputation before life-threatening wound sepsis develops.
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PMID:Blunt tibial artery trauma: predicting the irretrievable extremity. 259 89

We retrospectively evaluated the clinical features and therapeutic outcomes in 13 consecutive patients with the diagnosis of fusiform aneurysm of the vertebrobasilar system. Four patients (31%) presented with compressive symptoms and 10 (77%) with ischemic symptoms; one patient presented with both types of symptoms. No patient presented with rupture of the fusiform aneurysm. Based on the attending physician's choice, treatment included antiplatelet therapy in five patients, anticoagulation in seven, and no medication in one. Five patients died, four treated with antiplatelet agents and one not treated with any medication. The cause of death was progressive brainstem ischemia in three, sepsis in one, and gastrointestinal bleeding in one patient. All seven patients who received anticoagulants were alive, with no recurrence of symptoms or hemorrhagic complications after a mean follow-up period of 18 months. Based on previous and current series, we conclude that rupture of fusiform aneurysms is rare. Our results suggest a more favorable outcome in the management of these aneurysms with anticoagulation therapy to prevent progressive thrombosis and embolization.
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PMID:Fusiform aneurysm of the vertebrobasilar arterial system. 259 37

Inflammation is usually a tightly controlled process which confines tissue damage, prevents infection, and assists in cellular regeneration. However, if the inflammatory response becomes unregulated, this normally beneficial local event may escalate into a wider malignant activity, characterized by endothelial injury, excessive cell infiltration, and vascular leakage. Due to the ability of platelet-activating factor and tumor necrosis factor to elicit the release of each other, 'prime' cell responses, and influence the activity of other cytokines, we propose that these two mediators play a pivotal role in the formation of deleterious feedback cycles leading to the above endothelial damage which may underlie pathologies such as shock, sepsis, ischemia, and asthma. Platelet-activating factor antagonists such as BN 52021 inhibit the priming and other effects induced by platelet-activating factor and thus may be of therapeutic value in such conditions.
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PMID:Role of cytokines and platelet-activating factor in microvascular immune injury. 265 21

Fifty-five cases of primary (that is, without urinary tract abnormalities), acute pyelonephritis (PN) were studied by computed tomodensitometry (CT). There were 48 women and 7 men. All were febrile and 16 had positive blood cultures. In 7 cases, (4 diabetics and 3 malnourished alcoholics) PN was painless, diagnosis was delayed and lesions were severe. Two diabetics underwent emergency nephrectomy for sepsis. Conventional radiological techniques (IVP and ultrasonography) were poorly informative. In contrast, initial CT abnormalities were visible in 44 patients. They consisted of triangular or round hypodense images, diffuse hypodensity in a grossly swollen kidney, and/or abscesses. Hypodense images were presumably due to acute focal ischemia. Renal histology was available in five patients. It showed acute interstitial nephritis with leukocyte infiltrates, edema and hemorrhagic streaks. Pyelonephritis was due to E. coli in 48 cases (87.5%). In 27 cases E. coli isolates were studied by genotypic assays which detect the three most frequent (pap, afa and sfa) of the four operons known to encode adhesin. In all cases, at least one of these genotypic markers of uropathogenicity was found. In 27 cases, repeat CT was done shortly after treatment. It showed healing in only 12. Early cortical scar formation was visible in 2. Final evaluation in 27 cases with adequate follow-up showed that (in addition to the 2 patients who had been nephrectomized), in only 17 of 27 (63%) had the kidneys recovered a normal appearance. In two cases one kidney had undergone atrophy; renal biopsy showed subacute-chronic interstitial nephritis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Frequency of development of early cortical scarring in acute primary pyelonephritis. 265 59

Patients who acquire sepsis, ARDS, ARF, or MSOF subsequent to multiple trauma have a high mortality rate. The pathophysiology of these complications is complex and is thought to involve ischemia, the generation of mediators, alterations in regional perfusion, and cellular oxygen use. Because of the critical nature of the patient with these complications, nursing care requires indepth knowledge as well as competent nursing management, necessitating use of both the art and science of nursing.
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PMID:Complications of multiple trauma. 267 90

Renal vein thrombosis in early infancy is a complication of dehydration and prolonged hypotension. The onset is usually acute and the most common clinical signs are uni- or bilateral frank masses, hematuria, proteinuria and thrombocytopenia. In most cases, with conservative management, the late outcome is favorable. In the adult, renal vein thrombosis is often a silent complication of the nephrotic syndrome, the hypercoagulability of which may be an important factor in the pathogenesis of the thrombosis. Clinically, the presentation of a sudden complete occlusion is that of severe abdominal and lumbar pain with hematuria and loss of function of the kidney that suffers hemorrhagic infarction. Physical examination often reveals an enlarged kidney. With gradual occlusion, renal function is preserved. The initial diagnostic approach is with ultrasound studies and computed tomography; definitive diagnosis is established by renal venography or by selective renal arteriography. In general, a conservative approach including the use of anticoagulant treatment is preferred to surgical intervention. Priapism is a persistent painful penile erection due to ischemic or non-ischemic causes; therapeutic intracavernosal injection of papaverine is becoming the most common cause. In early and mild stages, aspiration of blood from the corpora cavernosa supplemented with intracavernosal irrigation with alpha-stimulating agents is the procedure of first choice; in late and severe ischemia, a shunt procedure may become necessary. Hepatic vein thrombosis occurs in association with a number of conditions considered predisposing factors including the use of oral contraceptives. The clinical picture may be that of an acute illness with abdominal pain, hepatomegaly, ascites and hepatic failure as well as early death. More often, the onset is insidious with slowly developing ascites and wasting. For the diagnosis, hepatic scintigraphy may be helpful but, at present, ultrasonography, computed tomography and magnetic resonance scanning are procedures of choice. There is, as yet, no adequate treatment. A fatal outcome may be prevented by surgical decompression of the congested liver and, in recent years, liver transplantation has been employed. Portal vein thrombosis, in children, is usually considered a complication of umbilical sepsis or a result of a congenital abnormality of the portal vein. In adults, the most frequent causes are hepatic cirrhosis and neoplasia. Clinically, there may be a sudden appearance of ascites with resolution in a symptom-free interval until the onset of other features of portal hypertension occur. Currently, ultrasound real-time imaging supplemented with Doppler capability, computed tomography and magnetic resonance scanning provide the necessary diagnostic information. Variceal hemorrhage is often the first major complication requiring treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Thrombosis in particular organ veins. 268 Aug 53

A case of pyogenic liver abscess following successful mesenteric artery revascularization is described in a patient with acute mesenteric ischemia. Prior to revascularization, arteriography confirmed celiac and superior mesenteric artery occlusion. Occurrence of liver abscess is explained on the basis of ischemia impairing the barrier function of the intestinal mucosa, contributing to portal bacteremia that seeds ischemic or necrotic liver. In patients with acute mesenteric ischemia, sequential sonographic examination of the liver following mesenteric revascularization is advocated for early diagnosis of liver abscess if there is clinical evidence of the sepsis.
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PMID:Liver abscess following superior mesenteric artery revascularization for acute mesenteric ischemia. 277 41


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