Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary edema is common cause of acute respiratory failure and can be seen in not only cardiac but also noncardiac diseases. The pathophysiologic mechanism for the development of acute pulmonary edema in any clinical situation can usually be explained alterations in the forces governing the transvascular flux of fluid in the pulmonary microvasculature, according to the Starling equation. "Cardiac" pulmonary edema is primarily due to an increase in the capillary hydrostatic pressure of sufficient magnitude to overcome the forces maintaining fluid within the vessel and the ability of the lymphatics to drain the transudated fluid. On the other hand, pulmonary edema occurring in association with noncardiac disease (e.g., sepsis, aspiration or shock) is secondary to an increase in the permeability of the pulmonary microvasculature and is referred to as noncardiogenic pulmonary edema or the adult respiratory distress syndrome. This article examines the mechanisms for the development of pulmonary edema and discusses the differences between the cardiac and noncardiac types.
 ...
PMID:Pathogenesis of pulmonary edema associated with the adult respiratory distress syndrome. 37 80

Twenty-six cases of hemorrhagic fever with renal syndrome from 1981 to 1986 were retrospectively reviewed to determine the scope of clinical presentation and the unique complications of the illness. The diagnosis was confirmed by detection of Hantaan virus antibody in 25 cases and by characteristic autopsy findings in 1 case. The illness could be classified into three distinct clinical subgroups. Fever was universally present. Two patients presented with intractable shock and diffuse hemorrhage and died within 6 days from multi-organ system failure, mimicking the clinical picture of overwhelming sepsis. Eighteen patients presented with acute renal failure with an illness lasting a mean of 21 days (range, 10 to 36 days). Resolution of thrombocytopenia heralded recovery of renal function. At discharge, the serum creatinine level was normal in 13 patients; 5 patients had evidence of minimal renal dysfunction. Acute pulmonary edema requiring hemodialysis and retroperitoneal hemorrhage were the major complications in this subgroup. Six patients had an undifferentiated febrile illness with normal renal function. Fever, thrombocytopenia, abnormal urinalysis, hypertransaminasemia, and a benign clinical course characterized the third clinical pattern. The recent availability of serodiagnostic methods to detect Hantavirus group antibody facilitates the diagnosis of hemorrhagic fever with renal syndrome. Application of this test in the described clinical settings will identify unsuspected cases, broaden the knowledge of the geographic distribution of Hantavirus infection, and increase physician awareness of its protean manifestations.
 ...
PMID:The protean manifestations of hemorrhagic fever with renal syndrome. A retrospective review of 26 cases from Korea. 197 4

This article reports a case of leaflet embolization of a mitral Edwards-Duromedics prosthesis. The patient had abrupt onset of acute pulmonary edema and was initially treated medically for 3 days. Fluoroscopy showed only one freely moving leaflet and the other was (incorrectly) assumed to be blocked in the closed position. The patient received IV thrombolysis for another 3 days and was finally operated. He died 8 days later from sepsis and the leaflet was recovered at autopsy in the abdominal aorta. Leaflet escape of a mitral Edwards-Duromedics prosthesis is a rare, potentially curable mode of valve failure. Correct interpretation of clinical signs and symptoms and of fluoroscopy should allow early diagnosis and surgical therapy.
 ...
PMID:Leaflet escape of a mitral Duromedics prosthesis. Case report. 271 82

Acute pulmonary oedema can be induced by intraperitoneal injection of Escherichia coli endotoxin in the mouse. A fall in serum angiotensin converting enzyme activity is found in mice given endotoxin and in patients with septic adult respiratory distress syndrome, and has been proposed as an indicator of lung microvascular injury. Protein concentration and angiotensin converting enzyme activity in serum, lung, and bronchoalveolar lavage fluid were determined in male mice up to eight hours after injection of endotoxin. By six hours the serum protein concentration had increased and the bronchoalveolar lavage fluid protein concentration had fallen, suggesting fluid shift into the lung. Angiotensin converting enzyme activity fell in serum and lung but increased in bronchoalveolar lavage fluid. As these changes in enzyme activity were not paralleled by changes in protein concentration they are unlikely to be a result of fluid shift or protein leak, and may indicate an active role of the enzyme in the response to sepsis.
 ...
PMID:Angiotensin converting enzyme and endotoxin induced lung damage in the mouse. 299 46

Five patients with nonoliguric adult respiratory distress syndrome (ARDS) secondary to severe sepsis showed improved blood oxygenation after up to 36 h of conventional therapy and mechanical ventilation with optimal positive end-expiratory pressure. However, metabolic acidosis was unchanged, and blood urea had increased. Some patients showed hemodynamic signs of incipient heart failure. After sequential hemofiltration, the altered physiologic shunt and blood pH returned to normal. Chest x-rays showed clearing of interstitial pulmonary edema. Patients recovered from ARDS in spite of fluid accumulation. Mechanical ventilation was stopped up to 8.5 h after the last hemofiltration. We postulate that convective ultrafiltration clears the blood of circulating low- and middle-weight vasoactive molecules implicated in the development of high microvascular permeability acute pulmonary edema secondary to sepsis.
 ...
PMID:Sequential hemofiltration in nonoliguric high capillary permeability pulmonary edema of severe sepsis: preliminary report. 638 9

We evaluated the efficacy of noninvasive mechanical ventilation (NIMV) in alleviating distress and avoiding intubation in patients with de novo acute respiratory failure complicating primary medical disorders. Eleven consecutive patients with severe respiratory distress were entered. In all patients a decision to intubate on an urgent basis had been made, but NIMV could be initiated within minutes. The patients suffered from acute pulmonary edema (five), sepsis/ARDS (two), status asthmaticus (two), and severe pneumonia (two). Dyspnea score (max=10) was (+/- SD) 8.4 +.- 1.6, scale for accessory muscle use (max=5) was 4.2 +/- 0.7, and respiratory rate was 37.6 +/- 3.8 min -1. Pa CO2, pH, and base excess (BE) were 48 +/- 18 mm Hg, 7.27 +/- 0.13, and -5.5 +/- 7.4, respectively, with five patients showing severe metabolic acidosis (BE < - 10). NIMV was applied using proportional assist ventilation. There were three early failures. These included the two patients with sepsis/ARDS who did not tolerate the mask. One patient failed because Pa CO2 and pH deteriorated despite subjective improvement. The remaining eight patients demonstrated progressive improvement, and none required intubation. The duration of NIMV was 3 h to 2 d. We conclude that when NIMV is made available on a "few minutes" basis, selected patients with severe de novo respiratory distress/failure caused by reversible medical disorders, who would otherwise have been intubated, can be given substantial relief and be spared intubation.
 ...
PMID:Noninvasive positive-pressure ventilation in acute respiratory distress without prior chronic respiratory failure. 863 May 38

The authors report two cases of pulmonary valve endocarditis which required emergency surgical treatment. A 74 year old patient with trivalvular endocarditis (pulmonary, aortic, mitral), due to Sptreptococcus D bovis, developed cardiogenic shock with acute pulmonary oedema and underwent double aortic and pulmonary valve replacement with Carpentier-Edwards prostheses and simple resection of a mitral valve vegetation. Another 36 year old drug addict developed isolated pulmonary valve endocarditis due to Staphylococcus aureus infection complicated by pulmonary regurgitation with right ventricular failure and by septic pulmonary embolism with persistent sepsis: he underwent pulmonary valve replacement with a Bravo 300 bioprosthesis. The postoperative course was uncomplicated in both cases, with interruption of the infection and normalisation of the haemodynamic status. The insidious and severe nature of pulmonary valve endocarditis is demonstrated by these two cases, confirming previous reports which have underlined the poor prognosis of this condition. Surgery has been shown to be effective and well tolerated and should be integrated early in the therapeutic strategy, the results being all the better when an aggressive attitude is taken.
 ...
PMID:[Pulmonary valve replacement for endocarditis. Apropos of 2 cases]. 876 8

Acute respiratory distress syndrome (ARDS) is the result of severe injuries of different etiologies of the capillary system in patients with previously healthy lungs, resulting in noncardiogenic pulmonary edema. The authors studied 42 infants in whom the histopathologic aspects were suggestive for ARDS. The etiologic factors of this syndrome were: severe gastroenteritis with hypovolemic or endotoxic shock (13 cases), sepsis (9 cases), fulminans purpura (2 cases), severe neurological disorders (13 cases), pulmonary infections (5 cases). In such conditions, if the infant presents hyperpnea followed by generalised cyanosis, refractory to oxygen therapy, and if there are clinical and radiologic signs of acute pulmonary edema, the diagnosis of ARDS must be considered and a complete intensive care therapy is compulsory in order to alleviate the severe prognosis of this syndrome.
 ...
PMID:Etiological, clinical and pathomorphological aspects of acute respiratory distress syndrome in children. 1075 53

1. The present study was undertaken to determine the locus of nitric oxide (NO) production that is toxic to the lung and produces acute pulmonary oedema in endotoxin shock, to examine and compare the effects of changes in lung perfusate on endotoxin-induced pulmonary oedema (EPE) and to evaluate the involvement of constitutive and inducible NO synthase (cNOS and iNOS, respectively). 2. Experiments were designed to induce septic shock in anaesthetized rats with the administration of Escherichia coli lipopolysaccharide (LPS). Exhaled NO, lung weight (LW)/bodyweight (BW) ratio, LW gain (LWG) and lung histology were measured and observed to determine the degree of EPE 4 h following LPS. The EPE was compared between groups in which LPS had been injected either into the systemic circulation or into the isolated perfused lung. The lung perfusate was altered from whole blood to physiological saline solution (PSS) with 6% albumin to test whether different lung perfusions affected EPE. Pretreatment with various NOS inhibitors was undertaken 10 min before LPS to investigate the contribution of cNOS and iNOS to the observed effects. 3. Endotoxin caused profound systemic hypotension, but little change in pulmonary arterial pressure. The extent of EPE was not different between that induced by systemic injection and that following administration to isolated lungs preparations. Replacement of whole blood with PSS greatly attenuated (P < 0.05) EPE. In blood-perfused lungs, pretreatment with NOS inhibitors, such as Nomega-nitro-L-arginine methyl ester, aminoguanidine and dexamethasone, significantly prevented EPE (P < 0.05). 4. The major site of NO production through the whole blood is in the lung. The NO production mediated by the iNOS system is toxic to the endothelium in the pulmonary microvasculature. Inhalation of NO for patients with sepsis may be used with clinical caution. Therapeutic consideration of lung extracorporeal perfusion with PSS and pharmacological pretreatment with iNOS inhibitors may be warranted.
 ...
PMID:The lung is the major site that produces nitric oxide to induce acute pulmonary oedema in endotoxin shock. 1125 47

Acute lung injury (ALI) and its more severe form, the acute respiratory distress syndrome (ARDS), are syndromes of acute respiratory failure that result from acute pulmonary edema and inflammation. The development of ALI/ARDS is associated with several clinical disorders including direct pulmonary injury from pneumonia and aspiration as well as indirect pulmonary injury from trauma, sepsis, and other disorders such as acute pancreatitis and drug overdose. Although mortality from ALI/ARDS has decreased in the last decade, it remains high. Despite two major advances in treatment, low VT ventilation for ALI/ARDS and activated protein C for severe sepsis (the leading cause of ALI/ARDS), additional research is needed to develop specific treatments and improve understanding of the pathogenesis of these syndromes. The NHLBI convened a working group to develop specific recommendations for future ALI/ARDS research. Improved understanding of disease heterogeneity through use of evolving biologic, genomic, and genetic approaches should provide major new insights into pathogenesis of ALI. Cellular and molecular methods combined with animal and clinical studies should lead to further progress in the detection and treatment of this complex disease.
 ...
PMID:Future research directions in acute lung injury: summary of a National Heart, Lung, and Blood Institute working group. 1266 42


1 2 3 Next >>