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

In a patient who died of complications of severe pulmonary hypertension, right ventricular failure, and sepsis, antemortem two-dimensional (2-D) echocardiography and magnetic resonance imaging (MRI) studies demonstrated a right ventricular mass which at autopsy proved to be thrombus. The diagnostic features of this mass as imaged by these two methods are compared. This case was complicated in that the patient had a history of right atrial myxoma that had been successfully removed three years previously, and a history of several prior pulmonary emboli. Gated MRI depicted the size, shape, and surface characteristics of the mass more clearly than 2-D echocardiography because MRI provided better contrast and spatial resolution. Both techniques were useful in localizing the mass and showing if it was fixed or mobile. Depiction of tumor attachment was unclear with echocardiography but very clear with MRI. MRI also showed a left pulmonary artery thrombus that was not visualized by 2-D echocardiography. Both techniques provided chamber dimension measurements showing enlargement of the right atrium and ventricle. This case demonstrates that gated MRI provides high-quality images of cardiac anatomy and masses. Gated cardiac MRI should be considered at least complementary and potentially superior to two-dimensional echocardiography in the evaluation of intracardiac masses in certain patients.
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PMID:Comparison of gated cardiac magnetic resonance imaging and two-dimensional echocardiography for the evaluation of right ventricular thrombi: a case report with autopsy correlation. 339 69

Thromboxane A2 has been implicated as a mediator of cardiorespiratory dysfunction in sepsis. This study evaluated whether or not thromboxane A2 was necessary or sufficient for these adverse effects to occur during bacteremia. Fourteen adult swine under barbiturate anesthesia and breathing room air were monitored with arterial and pulmonary artery catheters. Animals were studied for 4 hours in three groups: group I, graded infusion of 10(9)/ml Aeromonas hydrophila; group II, Aeromonas hydrophila infusion plus SQ 29,548 (thromboxane A2 antagonist); and group III, U46619 (thromboxane A2 agonist) infusion in normal swine to pulmonary artery pressures observed in group I. Hemodynamic parameters, arterial and mixed venous blood gases, and plasma thromboxane B2 and prostaglandin 6-keto-F1 were measured. At sacrifice after 4 hours, wet-to-dry lung weights were calculated. Results indicated that thromboxane A2 was necessary and sufficient for the development of pulmonary hypertension and impaired alveolar-capillary oxygen diffusion in graded bacteremia. It was necessary but not sufficient for increased lung water to occur and sufficient but not necessary for decreased cardiac index and stroke volume index. Thromboxane A2 was neither sufficient nor necessary to the pathophysiology of systemic hypotension during graded bacteremia. Plasma prostaglandin 6-keto-F1 levels were increased in hypotensive animals with sepsis, suggesting its involvement in hypotension during sepsis.
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PMID:Thromboxane A2 mediates hemodynamic and respiratory dysfunction in graded bacteremia. 352 3

The effects of intravenous phenylephrine (PE) on aortic blood pressure (AOP), pulmonary artery pressure (PAP), and cardiac output (CO) were evaluated in piglets with normal PAP and piglets with sepsis-induced pulmonary hypertension. Anesthetized, ventilated piglets (1-4 weeks; n = 22) were divided into four groups - group 1 (n = 5) received group B beta streptococci (GBS) followed by PE (300 micrograms/kg); group 2 (n = 6) received GBS alone; group 3 (n = 6) received placebo infusion; group 4 (n = 5) received PE alone (300 micrograms/kg). Infusion of GBS in piglets (groups 1 and 2) elevated PAP by 149 and 176%, reduced CO by 34 and 28%, and did not affect AOP. Administration of PE (groups 1 and 4) raised AOP by 30 and 27% without significantly affecting PAP. However, CO fell after PE by 31 and 39%, respectively. If selective elevation of systemic blood pressure is to become an effective strategy for human newborns with right-to-left shunts caused by sepsis-induced pulmonary hypertension, agents other than PE, with less associated reduction of CO, need to be identified.
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PMID:Effects of phenylephrine on systemic and pulmonary artery pressure during sepsis-induced pulmonary hypertension in piglets. 353 Jun 73

Infusions of group B streptococci cause pulmonary hypertension in several neonatal animal models. A continuous infusion of prostaglandin D2 reduced the magnitude of this pulmonary hypertensive response; indomethacin completely blocked the response. Prostaglandin D2 or cyclooxygenase inhibitors may be important therapeutic agents for infants with group B streptococcal sepsis who manifest pulmonary hypertension.
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PMID:Influence of prostaglandin D2 on hemodynamic effects of group B streptococcus in neonatal lambs. 353 Jun 74

An evaluation was made of 106 surgical patients with Gram-negative septic shock, both for clinical criteria as well as the biochemical mediators endotoxin, prostaglandin F2 alpha, prostaglandin I2 (prostacyclin), and thromboxane. These data were correlated to various defined shock phases, functional data of vital organs, and clinical outcome. Patients underwent invasive organ function monitoring and the usual laboratory tests of intensive care. Prostaglandins and thromboxane were measured radioimmunologically, endotoxin by the limulus amebocyte lysate test. Endotoxin proved to be a more accurate predictor of severe sepsis than did positive blood cultures. Endotoxin as well as prostaglandins and thromboxane are predominantly released in early shock phases, appearing in plasma concentrations, which correlate with the severity of organ failure. Sepsis-induced respiratory failure coincides with a deterioration of pulmonary prostaglandin inactivation, which contributes to the release mechanism. High systemic prostacyclin activity benefits the patients' organ functions and clinical outcomes, while a predominance of thromboxane seems to effect the opposite. Transpulmonary-thromboxane gradients correlate significantly with pulmonary hypertension in the early phases of septic shock.
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PMID:The clinical significance of prostaglandins and thromboxane as mediators of septic shock. 355 Feb 66

Eleven of 30 patients with MCTD, followed for a mean of 10 years, developed immune complex nephropathy (five membranous, two mesangial, one mixed, and one sclerosing) with NS in nine of 11. Another patient had membranous nephropathy at autopsy. Patients with renal disease tended to have more systemic manifestations than those without. NS was at times of abrupt onset, recurrent, and/or persistent. Anti-RNP and serum complement were not helpful in predicting nephritis. Seventy-two percent of nephropathy and 62% of NS episodes resolved or improved after corticosteroid therapy. Five patients became hypertensive, two developed chronic renal failure and required chronic dialysis, and one needed acute dialysis twice. One patient progressed to focal proliferative crescentic nephritis with necrotizing arteritis. Three patients with nephropathy died, two of pulmonary hypertension with acute cor pulmonale and one of overwhelming sepsis. Nephropathy is relatively common in MCTD, is associated with substantial morbidity, and with the risk of hypertension and chronic renal failure.
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PMID:Renal involvement in mixed connective tissue disease: a longitudinal clinicopathologic study. 356 25

The pathophysiology of the shock state includes a variety of hemodynamic changes such as systemic hypotension, pulmonary hypertension and increased vascular permeability leading to the extravasation of protein rich plasma. These changes can be initiated by different etiological factors, but many of them have been related to the stimulation of activation systems (complement, kinins, etc.) or to the generation of inflammatory mediators. The purpose of the present study has been to obtain evidence of the involvement of paf-acether in the pathogenesis of the shock state initiated in rat and mouse by Gram-negative bacteria and soluble aggregates of immunoglobulin G. The injection of 1-2 MDa aggregates of immunoglobulin G to normal Sprague-Dawley rats, induced a dose-dependent systemic hypotension which appeared about five minutes after completion of the intravenous challenge. Simultaneously, extravasation of protein-rich plasma occurred as judged from the finding of an increased clearance of 125I-BSA. In similar experiments in mice, a reduction of the vascular volume was observed using 51Cr-labelled homologous red blood cells. Under these conditions, a lipid compound analogous to paf-acether was obtained from the liver and the spleen of these animals. The generation of this compound preceded the development of blood volume depletion and could be suppressed by either quinacrine or depletion of mononuclear phagocytes by total irradiation with 700 rads. The previous treatment of the rats with the compound BN 52021 (a specific antagonist of the paf-acether receptor) at a dose of 5mg/kg, i.v., prevented the appearance of hypotension and extravasation in response to an i.v. challenge with soluble aggregates of immunoglobulin G. Interestingly, the reversal of hypotension was also observed when BN 52021 was infused after the immunoaggregates (5mg/kg). The possible involvement of paf-acether in the hemodynamic changes of Gram-negative sepsis was studied in rats which had received an intraperitoneal inoculation of E. coli. The animals inoculated with the doses of bacteria which produced mortality showed a time- and dose-dependent increase of vascular permeability as judged from the presence of abundant peritoneal exudate and the reduction of the circulating volume. Simultaneously, significant amounts of paf-acether could be obtained from the peritoneal exudate and from the spleen preceding to the development of the circulating volume depletion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Evidence of a role for PAF-acether in the pathophysiology of the shock state. 377 44

Although gram-negative sepsis is a major cause of neonatal morbidity and mortality, our understanding of endotoxemia in the neonate has been hampered by the lack of experimental models. Previous studies have suggested neonatal hyporesponsiveness to endotoxin. We studied unanesthetized neonatal lambs which had been exposed to the environment prior to study. These animals demonstrated the classic early phase changes of endotoxemia including pulmonary hypertension which was dependent upon prostanoid production. This model allows further studies of endotoxemia in the neonate.
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PMID:Endotoxemia in the neonatal lamb. 388 82

Our purpose was to determine whether peripheral soft tissues produce and release prostanoids in response to local sepsis, and whether this mediator release can produce pulmonary dysfunction. Escherichia coli endotoxin (2 micrograms/kg in 100 mL of saline) was injected below the hide of the flank in seven unanesthetized sheep. In three additional sheep, ibuprofen (12.5 mg/kg of body weight) was injected with the endotoxin. Thromboxane B2 and 6-keto-PGF1 alpha (prostacyclin) levels were measured in tissue lymph draining the flank, lung lymph, pulmonary artery (Ppa), and aortic plasma. One hour after endotoxin administration, mean PaO2 decreased from 90 to 74 mm Hg and Ppa increased from 22 to 35 mm Hg. Lung lymph flow (QL) increased only 50% with QL being protein poor. No increase in lung or peripheral soft-tissue vascular permeability was noted. Tissue lymph (TxB2) increased from 220 +/- 114 to greater than 10,000 pg/mL with levels in Ppa plasma increasing from 300 +/- 128 to 595 +/- 124 pg/mL and aortic plasma from 270 +/- 141 to 410 +/- 104 pg/mL. Lung lymph TxB2 paralleled aortic values. Peak levels of 6-keto-PGF1 alpha in systemic lymph exceeded 2,000 pg/mL while levels in lung lymph remained relatively constant. The pulmonary injury and the increase in TxB2 was prevented by ibuprofen. We conclude that the response of soft tissue to local endotoxin is to release thromboxane in quantities sufficient to raise plasma levels and to produce hypoxia and pulmonary hypertension. The lung dysfunction is not produced by an increase in lung water or vascular permeability.
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PMID:Pulmonary dysfunction secondary to soft-tissue endotoxin. 388 49

Myocardial performance in critically ill patients is primarily responsive to the need to supply O2 to the periphery. An increase in CO is the common finding in an acute illness characterized by an increase in systemic VO2 (for example, sepsis and trauma), since acute variations in flow are the most efficacious mode of augmenting systemic O2t to match the VO2. The lower systemic VO2 of a patient with an acute cardiac illness explains why the CO in this disease is not as elevated as that found in the acutely ill patient with sepsis or trauma. Endogenous compensatory mechanisms used to vary flow according to the need for O2t include heart rate, ventricular preload, contractility, and afterload. An increase in LV contractility and a reduction in afterload facilitate LV stroke volume, hence O2t. Conversely, pulmonary hypertension may result in a restriction of LV preload if RV pump failure ensues. Other factors relevant to the care of the critically ill that will decrease LV preload--and thus reduce the heart's left-sided adaptation to maintain O2t--include the presence of underlying cardiac disease, which will limit any necessary increase in contractility, and the use of PEEP, which will restrict venous return to the RV. Therapeutic intervention is required when O2t does not balance systemic VO2 and arterial lactate levels rise. The use of resuscitative fluid to improve flow by the Frank-Starling (preload) mechanism may be limited by the compliance properties of either ventricle, but it is a reasonable first choice, with guidelines for administration determined by the PCWP, which influences fluid flux across the pulmonary microvascular exchanging membrane. Vasodilators may be used to increase CO by reducing impedance to ventricular ejection; they may also improve LV compliance, thereby allowing the administration of more fluid (that is, increasing preload) without an untoward rise in the PCWP. If vasodilators are without effect or are potentially dangerous because of concomitant hypotension, inotropic support to increase O2t is required. A brief summary of interventional pharmacologic support in acute illness is depicted in Figure 8.
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PMID:Myocardial function in the critically ill: factors influencing left and right ventricular performance in patients with sepsis and trauma. 390 47


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