Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of severe pulmonary embolism in a 37 years old man admitted to the intensive care unit for severe acute respiratory failure. The presenting signs and symptoms were typical for severe pulmonary oedema. Chest radiograph shortly after admission showed local alveolar shadows. In the absence of sepsis, haemodynamic evidence of left ventricular failure on catheterization of the right heart and because of the history of the recent illness, a tentative diagnosis of pulmonary embolism was made. The diagnosis was confirmed by selective pulmonary angiography. The latter demonstrated that pulmonary oedema had been localized only in areas with patent pulmonary arteries and, in addition, confirmed that left ventricular function was normal. Such a pattern of local pulmonary oedema is uncommon in patients and is reminiscent of that observed in animal experiments with severe pulmonary arterial obstruction and overperfusion of unblocked territories. Possible mechanisms of overperfusion oedema are discussed and the hypothesis that humoral factors may increase the permeability of pulmonary microvasculature in cases of severe pulmonary embolism is put forward.
 ...
PMID:[Pulmonary edema in pulmonary embolism]. 670 66

Blockade of the arachidonic acid cascade has been shown to improve survival and hemodynamic alterations in animal models of sepsis and acute respiratory failure (ARF). The effects of intravenous ibuprofen, a cyclooxygenase inhibitor, were observed in 20-30 kg pigs with ARF induced by a continuous LD100 infusion of live Pseudomonas aeruginosa (2 X 10(8)/20 kg/min). Cardiopulmonary parameters were monitored in animals intubated, paralyzed, and ventilated at a 250-ml tidal volume and 0.5 FiO2. Pigs were randomly assigned to three groups: Group I received 2 bolus infusions of ibuprofen (12.5 mg/kg) at 20 and 210 min after baseline; Group II had Ps. aeruginosa (2 X 10(8) CFU/20 kg/min) only; Group III received Ps. aeruginosa and 12.5 mg/kg of ibuprofen at 20 and 210 min of ARF. Ibuprofen alone caused no significant changes in cardiorespiratory parameters. With Ps. aeruginosa infusion, significant pulmonary hypertension, hypoxemia, increased intrapulmonary shunt fraction, and systemic hypotension occurred. In the septic animals treated with ibuprofen, oxygenation was improved by a significant decrease in shunt, pulmonary edema, and pulmonary hypertension.
 ...
PMID:Effects of ibuprofen on a porcine model of acute respiratory failure. 670 94

Clinical and autopsy studies have shown an association between pulmonary microembolism and acute respiratory failure after trauma or sepsis. Prophylaxis and treatment with the aim of decreasing the fibrin deposition in the lungs were associated with a decrease in the incidence and death rate of this syndrome. Small fibrin degradation products (peptides) are accumulated in the lungs and are only slowly cleared from this organ, especially during states of fibrinolysis inhibition. These peptides may contribute to the pulmonary damage in several ways. They act by interfering with other vasoactive substances as bradykinin, histamine and products of the arachidonic acid cascade. Products of the cyclooxygenase pathways as thromboxane A2 play a major role in early microembolism whereas lipoxygenase products seem to be involved in delayed microembolism. Pulmonary microembolism thus seems to be one important, but certainly not the only pathogenetic factor in acute "idiopathic" respiratory failure. Other factors such as pulmonary contusion, aspiration of gastric contents or blood, or oxygen toxicity, might well be contributory in some cases. Pulmonary microemboli containing fibrin and leukocytes are probably also involved as contributory agents in some cases in the large group of acute respiratory failure due to "known factors".
 ...
PMID:Pulmonary microembolism as a cause of acute respiratory failure. 696 76

A group of 19 patients with acute respiratory failure (ARF) of diverse etiology received as a part of their treatment positive and expiratory pressure (PEEP). All of them were evaluated clinically and with several respiratory parameters. The response to treatment, complications and mortality rates are analyzed. The addition of PEEP in the management of this patients was accompanied by a significant increase of the PAO2 (p < 0.001) and a simultaneous decrease in the following parameters: FiO2/PaO2 index, Alveolo-arterial oxygen gradient (A-aDO2) and the pulmonary shunt (Qs/Qt). No hemodynamic deterioration was observed. None of the clinical parameters such as: blood pressure, heart rate and diuresis was significantly modified; neither a significant change in the arterious-venous oxygen gradient (a-vDO2) was detected. Pneumothorax as a complication of the use of PEEP was present in the 10.4% of the patients. The course of the ARF was toward the improvement in most of them at the end of the evolution. The high mortality rate in this study was considered to be secondary to uncontrollable sepsis and also to the presence of multiple organ failure. In none of the cases the poor outcome was secondary to refractory acute hypoxemia. PEEP which is one of the varieties of continuous positive pressure ventilation (CPPV) represents one of the most importants therapeutic advances in the last decade in the management of patients with acute respiratory failure.
 ...
PMID:[Use of final positive expiratory pressure (FPEEP) in the management of acute respiratory insufficiency]. 700 26

Acute respiratory failure, particularly if associated with sepsis, results in diffuse changes in pulmonary vascular geometry and the afterload characteristics against which the right ventricle must perform. Therapy in these patients frequently requires replacement of intravascular volume which, if pulmonary vascular resistance is abnormally elevated, may cause a substantial enlargement in right ventricular (RV) end-diastolic volume. The low compliance characteristics of the RV invalidate the use of filling pressure (CVP) as a guide to RV size. We have examined RV volume in critically ill patients by means of the gated 99TAc scan and noted a substantial increase in RV volume despite filling pressure in the upper normal range. This enlargement appears to encroach upon LV function because the ejection fraction of the LV remained high despite elevation of pulmonary capillary wedge pressure (PCWP). Older patients with "silent" right coronary artery disease may become hemodynamically limited during therapy for acute respiratory failure and sepsis due to RV enlargement, increased wall tension and RV ischemia, a condition not readily diagnosed at the bedside with the usual monitoring techniques.
 ...
PMID:[Hemodynamic changes in acute respiratory insufficiency: the role of the right ventricle]. 731 51

Acute respiratory failure is a common complication in patients with disseminated intravascular coagulation associated with sepsis. To elucidate the role of coagulation abnormalities in acute lung injury in sepsis, we investigated the effect of anticoagulants on the pulmonary vascular injury in rat induced by lipopolysaccharide (LPS). When administered intravenously, LPS (5 mg/kg body weight) significantly increased the accumulation of 111indium-labeled neutrophils in lung 30 min after administration. Subsequently, the pulmonary vascular permeability and the serum level of fibrin and fibrinogen degradation products (E) [FDP (E)] increased and remained elevated for several hours. Neither heparin alone, heparin plus antithrombin III, or dansyl-Glu-Gly-Arg-chloromethyl ketone-treated factor Xa, a selective inhibitor of thrombin generation, prevented LPS-induced vascular injury 6 hours after LPS administration, whereas these substances significantly inhibited the increase in serum FDP (E) at that time. LPS-induced pulmonary vascular injury was significantly attenuated in rats with methotrexate-induced leukocytopenia or treated with ONO-5046, a potent granulocyte elastase inhibitor, although ONO-5046 did not inhibit the LPS-induced increase in serum FDP (E). Thus, activated leukocytes play a more important role than coagulation abnormalities in the pathogenesis of LPS-induced pulmonary vascular injury in an experimental rat model of endotoxemia.
 ...
PMID:Endotoxin-induced pulmonary vascular injury is mainly mediated by activated neutrophils in rats. 748 29

Previous studies of experimental sepsis suggested that excessive systemic vasodilatation might be the stimulus to renal hypofiltration and fluid retention in sepsis. Successful therapy for this syndrome requires agents that either act to improve systemic haemodynamics without adverse renal effects, or that act directly on the kidney without impairing circulatory homeostasis. The plasma kallikrein-kinin system is a potent vasodilator pathway, activated by endotoxin. We studied the effect of aprotinin (Trasylol), which inhibits plasma kallikrein, in an ovine model of surgically-induced intra-abdominal sepsis. Given either as an early or late intervention, aprotinin was associated with increased mean arterial pressure and systemic vascular resistance, improved glomerular filtration rate, and increased urinary sodium excretion. In further studies, treatment with the thromboxane synthetase inhibitor, U63,557A (Upjohn), either before or after the surgical induction of peritonitis, was associated with increased glomerular filtration rate and sodium excretion, without any effect on systemic haemodynamics. Logical use of specific antagonists, based on an understanding of the pathophysiology of the septic ARF syndrome, is a desirable strategy.
 ...
PMID:Acute renal failure and sepsis: therapeutic approaches. 752 64

An international, multicenter, prospective survey has been conducted to determine the hospital survival rates of patients with potentially reversible acute respiratory failure (ARF) who are managed in sophisticated intensive care units by leading critical care specialists, using current (1991 to 1992) support and treatment techniques and protocols. Twenty-five clinical centers participated in the survey, 11 in the United States and 14 in Europe. A total of 1,426 patients with ARF were studied, all of whom had been receiving closed system positive pressure mechanical ventilation at an FIo2 of at least 0.50 for at least 24 h at the time of entry into the survey. Of the survey patients, 793 (55.6%) survived their hospitalization, while 633 (44.4%) died in the hospital. The 1,426 patients with ARF were prospectively divided into two groups: group A, containing 375 patients, who at the time of entry into the study were hypoxemic or hypercarbic while receiving mechanical ventilator assistance; and group B, containing 1,051 patients, who at the time of entry into the study were neither hypoxemic nor hypercarbic while receiving mechanical ventilator support at an FIo2 of 0.50 or greater. Hospital survival rate for group A patients was 33.3% and for group B patients it was 63.6%. Survival rates were higher in patients with ARF caused by pneumonia (63%) or post shock lung injury (67%) and lower in patients with ARF caused by sepsis (46%). Severity of lung injury at the time of entry into the survey was a major prognostic factor, varying from an 18% hospital survival rate for patients with ARF with far advanced lung injury to a survival rate of 67% for patients with ARF with less severe lung injury. Low survival rates (< 20%) were seen if mechanical ventilator FIo2 was 0.80 to 1.0, while 50% of the patients with ARF survived hospitalization whose FIo2 at entry was 0.50. Peak inspiratory pressure (PIP) > 50 cm H2O at entry into the survey was associated with survival rate of less than 20%, while PIP < 30 cm H2O was associated with survival rate of 60%. Shorter periods of mechanical ventilation (< 48 h) of group A patients before entering the survey were associated with higher survival rates (38%) than patients requiring mechanical ventilation for more than 2 weeks (30%). Patients with ARF with multiorgan failure had lower survival rates (10%) than those with pulmonary dysfunction alone (45%).(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Hospital survival rates of patients with acute respiratory failure in modern respiratory intensive care units. An international, multicenter, prospective survey. 770 20

Multiple organ failure is the most common cause of death in critically ill patients in the United States. Acute respiratory failure is the most important single component of this clinical scenario, with a mortality risk > 50%. Key pathophysiologic events occur in the pulmonary microvasculature at the interface between circulating elements and the external environment. In particular, the response of the alveolar capillary endothelial cell is of fundamental importance in this injury process. A variety of clinical stimuli initiate a systemic inflammatory response that contributes to acute microvascular lung injury. Sepsis, trauma, thermal injury, acute pancreatitis, and ischemia-reperfusion injury are among these stimuli. The particular emphasis of this review is on events associated with intestinal ischemia-reperfusion, a common and important clinical event. The pathogenic mechanisms that lead to acute lung injury in this setting are not completely understood, although it is clear that neutrophil-endothelial interactions regulated by both humoral and local mediators are crucial. Oxygen-derived free radicals, proteases, cytokines, eicosanoids, endotoxin, complement activation products, and probably platelet activating factor and nitric oxide are involved as either signalling or effector molecules. The key cellular participants during the acute phase of injury are the polymorphonuclear neutrophil (PMN) and the microvascular endothelial cell. Each of these participants is considered with regard to phlogistic behavior and the potential for therapeutic intervention. Adherence of the neutrophil to the endothelium creates a microenvironment in which PMN-derived oxidants, proteases, and cationic proteins are discharged under conditions that lead to cellular injury. Loss of microvascular integrity results and pulmonary dysfunction follows. At present, we offer only nonspecific supportive care for patients with this problem. However, investigations into relevant molecular and cellular regulatory events offer important opportunities for directed therapy. We are now approaching the threshold for utilization of several new and specific approaches. While no single pharmacologic therapy is likely to be curative for this complex problem, it is probable that certain approaches will be of clinical benefit in the near future. This review is designed to provide a basis for understanding this evolution.
 ...
PMID:Pulmonary microvascular injury following intestinal reperfusion. 780 96

In this paper the authors have evaluated the incidence and the clinical implications of sick euthyroid syndrome (SES) in a group of 144 patients in a department of internal medicine. SES is an alteration of thyroid hormone values in the absence of a thyroid disease, which is seen in patients suffering from serious diseases. Having classified SES into 3 subgroups according to the different alterations seen in the values of T3, T4, FT3, FT4, TSH, rT3 and TBG, they show the hypotheses that explain the biochemical mechanisms which are at the basis of these hormonal alterations. Fourteen of the 144 patients under observation were excluded as they were suffering from ascertained or subclinical thyroid disease. Thirty (23% of cases) of the remaining 130 patients had alterations of the thyroid hormones in accordance with SES diagnosis. Of these 30 patients, 19 had hormone values found in SES type I (63%), 2 in SES type II (6.5%) and 9 in SES type III (30.5%). In SES type I the diseases seen, in order of frequency, were: obstructive chronic bronchopneumopathy with acute respiratory failure, diabetic ketoacidosis, neoplasms, ischemic heart disease, cardiac failure, chronic renal failure, liver diseases, acute cerebral vasculopathies, sepsis and collagenopathies. The disease seen in the 2 cases of SES type II was obstructive chronic bronchopneumopathy with acute respiratory failure. In SES type III the diseases seen were, in order of frequency: diabetic ketoacidosis, lung diseases, ischemic heart disease, cardiac failure, peripheral arteriopathies, acute cerebral vasculopathies, neoplasms, liver diseases, acute renal failure. The incidence of SES in 23% of the admitted to hospital patients was found to be slightly higher than in other studies; this could be explained by a stricter selection of inpatients: in fact self-sufficient patients or those not needing urgent admission, were sent to an efficient out patient clinic where necessary examinations were quickly carried out, hospitalization being reserved for patients with more serious illnesses. We would like to underline how the incidence of SES is much greater than that of what is known as thyroid disease (23% compared to 5%), thereby confirming that it is the most frequent cause of alterations of thyroid hormones. With regard to the pathogenetical hypotheses, it is confirmed that in SES, the reduction of T3 values is accompanied by an increase in the values of rT3 as for reduced activity of 5-desiodinasis enzyme. In SES type III the increase of T4 values is due to the increase of TBG resulting in an increase in the link for T4 and therefore a reduced peripheral hormone activity.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[The euthyroid sick syndrome. Its incidence and clinical significance in an internal medicine department]. 802 42


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>