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)

Sepsis syndrome frequently results in endothelial injury in many organ systems. To evaluate neutrophil-pulmonary endothelial cell interaction in the sepsis syndrome, we studied 39 critically ill patients prospectively and 20 normal volunteers. Thirteen patients with sepsis (mean age, 71.4 years), 14 patients in an intensive care unit control group (mean age 65.4 years), and 12 patients admitted with acute myocardial infarction (mean age, 66.8 years) were evaluated. Blood samples were drawn from septic patients within 24 hours and from ICU and MI patients within 72 hours of admission. All sepsis patients were culture positive, 6 of 13 from the blood. Both renal failure and ARDS developed in 54 percent of septic patients. 51Cr-labelled neutrophils were prepared and added to bovine pulmonary endothelial cell monolayers with and without added phorbol myristate acetate. Endothelial cells with adherent PMA and nonadherent PMN's, were harvested and radioactivity in each fraction measured with a gamma scintillation counter. Baseline and maximally stimulated (PMA, 3.0 ng/ml) neutrophil adherence to endothelial cells were similar in all patients groups. However, in septic patients, PMA-stimulated PMN adherence was reduced at lower doses, most significantly in those who developed ARDS within 24 to 48 hours of admission (p less than 0.05). Seventy-one percent of patients who developed ARDS had reduced stimulated adherence (PMA 1.0 ng/ml) compared to 22 percent of critically ill patients who did not. We conclude that diminished adherence of neutrophils to endothelium in response to low-level PMA stimulation is significantly more common in patients with sepsis who develop ARDS. Our findings suggest that PMN-endothelial cell interaction is altered by the time sepsis is clinically recognized but before the development of ARDS. We speculate that the observed reduction in adherence of the PMN to endothelial cells may be a consequence of down-regulation by mediators generated in the inflammatory response to sepsis and/or the need for active participation of septic endothelium in this interaction.
 ...
PMID:Neutrophil-endothelial cell interaction in critical illness. 203 31

With advances in critical care, multisystem organ failure (MSOF) has replaced single organ failure as the major cause of death in adult patients. The purpose of this report is to characterize neonatal MSOF (NMSOF) in the surgical newborn. The records of 84 infants who died during a 5-year period in the surgical neonatal intensive care unit were reviewed. There was sufficient information available in 10 newborns to characterize the NMSOF syndrome. Criteria for renal, hepatic, microvascular, pulmonary, cardiac, and hematologic failure were developed. The sequence of organ failure was determined by calculating the number of days prior to death when these criteria were first noted. Systemic infections were recorded. The sequence of organ failure was as follows: microvascular (edema) 17 +/- 10 days, renal 14 +/- 7 days, hepatic 13 +/- 5 days, hematologic 8 +/- 4 days, pulmonary 5 +/- 2 days, and cardiac 3 +/- 2 days. Adult respiratory distress syndrome (ARDS) was absent. The 10 infants showed both culture-positive sepsis (8) and culture-negative sepsis (2). This is the first report to characterize NMSOF in newborn surgical patients. The earliest findings were edema, followed by renal and hepatic failure. In contrast to adult MSOF, anasarca is a prominent early finding, pulmonary failure develops late, and classic ARDS is absent.
 ...
PMID:Characterization of neonatal multisystem organ failure in the surgical newborn. 205 14

Physicians and surgeons have long recognized that septic illness may be accompanied by abnormal brain functions; however, no systematic, comprehensive study has been done to define the clinical and laboratory features of the syndrome of sepsis-associated encephalopathy. We undertook such a prospective study in a tertiary care hospital and found that of 69 patients with fever and microbial cultures, 32 had marked brain dysfunction, 17 showed mild encephalopathy, and 20 were clinically nonencephalopathic. Severe cases showed obtundation and paratonic rigidity while milder cases showed confusion, inappropriate behavior, inattention, disorientation, and writing errors. There were no focal neurological deficits. The following factors correlated with the severity of brain dysfunction: adult respiratory distress syndrome; fatal outcome; certain types of EEG abnormality; axonal peripheral neuropathy; elevated peripheral white blood cell count; elevated serum levels of alkaline phosphatase, bilirubin, creatinine, phosphate, potassium, and urea; reduced blood pressure and reduced serum albumin level. Our data suggest that brain functions fail with dysfunction of other organs in septic illness. Pathogenetic mechanisms are discussed. The brain dysfunction should be regarded as potentially reversible, even in severely encephalopathic cases. Prompt control of the infection is the most important measure in controlling the encephalopathy and in preventing the increased mortality found with severely encephalopathic patients.
 ...
PMID:The encephalopathy associated with septic illness. 207 9

A review of the mechanism of ischemic-reperfusion injury, proposed interventions to prevent injury, and future directions have been presented to enhance the practitioner's knowledge of this new, exciting concept in myocardial injury. There is increasing evidence in the literature that reperfusion injury may occur in other organ systems and is responsible for some of the more prevalent pathologies seen in critically ill patients. Investigators have indicated that the tissue damage in sepsis, the development of adult respiratory distress syndrome (ARDS), delayed organ recovery in transplanted organs, and delayed ventricular recovery after cardiopulmonary bypass may be attributed to reperfusion injury. The next few years will prove to be exciting as this concept is further investigated and refined. Critical care nurses need to understand the concept of reperfusion injury and may soon begin to apply the results of ongoing research studies to patients undergoing reperfusion.
 ...
PMID:Myocardial reperfusion injury. 209 70

The patients with acute respiratory failure of different etiology are presented. The results of hemodynamic measurements together with those of oxygen transport and tissue oxygenation are given. The results reveal that in hypovolemic shock the transport system of oxygen and tissue oxygenation have been soon normalized by adequate therapy. However, more complicated is the condition of patients with sepsis and adult respiratory distress syndrome (ARDS) with disturbances in microcirculation. In them the oxygen uptake (VO2) is directly dependent upon the oxygen transport (DO2) i.e. much higher values of DO2 should be maintained by therapeutic measures than in conditions with intact microcirculation. According to their own experiences and data from the literature the authors consider that in patients with ARF in whom by the conventional methods the condition cannot be improved an invasive monitoring for following the hemodynamic measurements of oxygen transport and tissue oxygenation should be indicated for successful treatment.
 ...
PMID:[Importance of measurement of systemic oxygen transport and tissue oxygenation in the treatment of acute respiratory insufficiency]. 210 53

Mechanically ventilated, nonsurgical, critically ill patients represent a group not rigorously studied by energy expenditure measurements for formulating nutritional support guidelines. Most strategies for predicting caloric requirements in this group are based on studies of spontaneously breathing surgical patients. It is unclear whether "severity of disease" or "stress" factors employed in this group are justifiable in medical patients with compromised pulmonary function, who may be particularly prone to the complications of overfeeding. We therefore measured the energy expenditures of 73 consecutive ventilator-supported patients with various primary diagnoses in a medical ICU. These results are compared to estimates of caloric requirements based on the Harris-Benedict equations, without modification for severity of disease or other factors. These comparisons are (kcal/day +/- SE, measured vs predicted): sepsis, 1,982 +/- 97 vs 1,534 +/- 56 (p less than 0.0001); cardiogenic shock, 1,452 +/- 119 vs 1,339 +/- 62; cardiogenic pulmonary edema, 1,427 +/- 87 vs 1,338 +/- 93; ARDS, 1,732 +/- 203 vs 1,550 +/- 125; pneumonia, 1,508 +/- 148 vs 1,259 +/- 55; and "other" 1,585 +/- 104 vs 1,419 +/- 55. These data reveal that in mechanically ventilated nonsurgical patients without sepsis, no modifications of the Harris-Benedict equations are necessary; in those with sepsis an increase of approximately 20 percent over these predictions is appropriate.
 ...
PMID:Energy expenditures of mechanically ventilated nonsurgical patients. 211 45

To determine the magnitude, duration, and associated factors of perioperative changes in pulmonary function, we retrospectively reviewed the medical records of 145 patients who required preoperative mechanical ventilation for acute respiratory failure before undergoing 200 surgical procedures. Patients were grouped into five pulmonary diagnostic categories: (1) adult respiratory distress syndrome (ARDS) (n = 49); (2) pneumonia (n = 20); (3) atelectasis (n = 65); (4) congestive heart failure (n = 11); and (5) acute ventilatory failure (n = 55). Sixty patients underwent intra-abdominal surgery, 135 patients required surgery on the periphery, and five patients had a thoracotomy. For all patients, PaO2/FIO2 declined significantly from 321 mm Hg (mean) preoperatively to 258 mm Hg intraoperatively, and shunt fraction (Qs/QT) increased from 0.16 to 0.23 without a significant change in PaCO2. The magnitude of the increase in Qs/QT did not differ among pulmonary diagnostic groups. Preoperatively, patients undergoing laparotomy had lower PaO2/FIO2 (278 vs 340) and higher Qs/QT (0.19 vs 0.14) than patients requiring surgery on the periphery. Intraoperatively, Qs/QT increased more during abdominal procedures than during peripheral procedures. Intraoperative hypoxemia (PaO2/FIO2 less than 80 mm Hg) occurred during 13 procedures. Hypoxemic patients had a mean increase in Qs/QT of 0.20 (0.25 preoperatively to 0.45 intraoperatively), and a significant increase in PaCO2 from 38 mm Hg to 45 mm Hg intraoperatively). In general, these patients had ARDS (n = 10), sepsis (n = 10), a laparotomy (n = 9), and intraoperative mechanical ventilation via the Ohio Anesthesia ventilator (n = 8), a commonly used operating room ventilator. Their preoperative peak airway pressure (54 cm H2O) and minute ventilation (20 L/min) requirements exceeded the capabilities of the Ohio Anesthesia ventilator and likely contributed to impaired gas exchange intraoperatively. Within the first several hours postoperatively, PaO2/FIO2 recovered to preoperative levels in all patients, even in those who had severe intraoperative hypoxemia develop and who underwent laparotomy. We conclude that most patients with acute respiratory failure receiving preoperative mechanical ventilation experienced mild-to-moderate deterioration in intraoperative pulmonary oxygen exchange that rapidly returned to preoperative levels after surgery. We recommend that necessary surgery not be postponed by concern that pulmonary function will be worsened by surgery and anesthesia.
 ...
PMID:Factors affecting perioperative pulmonary function in acute respiratory failure. 212 51

Despite significant advances in intensive care unit technology and mechanical ventilatory support, mortality due to adult respiratory distress syndrome (ARDS) or multiorgan failure (MOF) has not changed significantly within the past two decades. The key to improving survival requires understanding and modifying (or eliminating) factors that may initiate (or modulate) these syndromes. Infection, and the host responses to infection, are major etiological factors responsible for the induction and perpetuation of the injury to the lung and microvasculature in ARDS and MOF, and contribute to late mortality. While the pathogenesis of ARDS and MOF-complicating sepsis remains to be elucidated, bacterially derived (eg, endotoxin or lipopolysaccharides [LPS]) and host-derived humoral and cellular mediators are of importance in both disease states. In fact, the host response to infection (or injurious stimuli) may be a more critical determinant of the outcome of sepsis and ARDS than the original inciting stimulus. The pleiotropic effects of LPS are largely indirect, and are orchestrated via its ability to trigger the release of an array of host-derived mediators of inflammation. Several potential mechanisms of injury in ARDS, sepsis, and MOF have been suggested and include a variety of inflammatory cells (neutrophils, mononuclear phagocytes, platelets), activated complement and coagulation components, vasoactive mediators (kinins, arachidonic acid metabolites, lipids, peptides), reactive oxygen radicals, and diverse cytokines. Interactions between these humoral and cellular mediators appear to set in motion an amplified cascade of events culminating in cellular and tissue injury. In this article, several of these putative inflammatory mediators are discussed in detail, and the importance of cytokine networking and the possible role of nonimmune cells in the orchestration of the inflammatory response associated with ARDS and MOF are explained. Finally, future therapeutic strategies aimed at blocking or suppressing the release or effects of endogenous mediators may be the key to improving the outcome of these disorders.
 ...
PMID:Host responses in mediating sepsis and adult respiratory distress syndrome. 212 91

Trauma causes more years of lost life than any other cause of death. Traumatic shock and sepsis are the most common late causes of death following trauma. Traumatic shock and sepsis cause multiple organ failure. The most common organ to fail is the lung, which develops Adult Respiratory Distress Syndrome (ARDS). ARDS can be caused by Disseminated Intravascular Coagulation (DIC) with microscopic clots in the lungs. Trauma causes hemolysis and the red cell stroma may initiate DIC. Plasminogen activators, which causes lysis of blood clot, can lyse pulmonary microthrombi and prevent the onset of ARDS even when given several hours after the trauma.
 ...
PMID:A new treatment for traumatic shock and ARDS. 215 24

Our laboratory has previously shown that the administration of tumor necrosis factor (TNF), a cytokine produced by activated mononuclear cells, to guinea pigs produces a syndrome similar to gram-negative sepsis or ARDS. Pentoxifylline (PTX), a methylxanthine, protects against TNF-induced and sepsis-induced acute lung injury in vivo. We now report on in vitro cellular studies of PMN-mediated cellular injury and its attenuation. We studied TNF-induced bovine pulmonary artery endothelial cell (EC) cytotoxicity both with and without PMN. A 51Cr release assay was used to measure EC damage. Further, we investigated PMN function in response to TNF by measuring chemiluminescence. Agents that attenuate EC damage and PMN activation were evaluated in the above assays. Results revealed that TNF causes EC injury (p less than 0.05) and PMN increase TNF-induced EC injury. Furthermore, PTX, aminophylline (AMPH), caffeine, and forskolin attenuate TNF-induced EC cytotoxicity only in the presence of PMN (p less than 0.05). Of interest, dibutyryl cAMP (DBcAMP) protects EC from TNF-induced injury both with and without PMN. Agents that may increase cAMP levels in PMN (PTX, DBcAMP, forskolin, isobutyl methylxanthine, and terbutaline) significantly attenuate TNF-induced PMN chemiluminescence (p less than 0.05). We conclude that TNF causes EC damage and PMN increase this damage. Furthermore, PTX, AMPH, caffeine, and forskolin can attenuate TNF-induced EC injury in the presence of PMN, whereas DBcAMP attenuates TNF-induced EC injury with and without PMN. In addition, agents that may increase intracellular cAMP levels in PMN can attenuate TNF-induced PMN chemiluminescence. Thus, these agents likely attenuate TNF-induced PMN-mediated EC injury through their inhibitory effects on PMN.
 ...
PMID:Attenuation of tumor necrosis factor-induced endothelial cell cytotoxicity and neutrophil chemiluminescence. 217 54


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