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Biomedical subjects

T Emerson

Publications and source records attributed to T Emerson.

8 recordsLinked to original sources
PubMed1998

Therapeutic use of antithrombin concentrate in sepsis.

Sepsis and its associated complications of disseminated intravascular coagulation (DIC) and multiple organ dysfunction syndrome (MODS) continue to be a major cause of morbidity and mortality. Improved detection of all forms of DIC is essential to assure earlier diagnosis. Studies already indicate that the therapeutic use of antithrombin (AT) concentrate may produce a more positive outcome for sepsis-associated DIC. If DIC could be identified earlier and AT concentrate could then be given earlier in the sepsis continuum, study results for the use of AT concentrate in humans might reveal a statistically significant difference versus placebo, and the efficacy of AT concentrate for this syndrome is more likely to be proved. Fixed-bolus doses of AT concentrate based on body weight are currently preferred, but improved, user-friendly assays for plasma AT levels would permit more rapid turnaround time for AT results and could help fine-tune the use of AT concentrate to the specific needs of each patient. Clinical trials involving the therapeutic use of AT concentrate in sepsis should continue, and it can be hoped that their design will reflect the concepts and conclusions offered by this panel of investigators.

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PubMed1996

Group A streptococcal bacteremia: the role of tumor necrosis factor in shock and organ failure.

Severe group A streptococcal infections associated with early onset shock and multiorgan failure define the streptococcal toxic shock syndrome. In the United States, group A streptococcal strains most commonly isolated are M types 1 and 3, which produce pyrogenic exotoxin type A. The role of tumor necrosis factor (TNF)-alpha and the dynamics of cardiovascular and laboratory abnormalities were investigated in a baboon model of group A Streptococcal bacteremia that mimics human Streptococcal toxic shock syndrome. Profound hypotension, leukopenia, metabolic acidosis, renal impairment, thrombocytopenia, and disseminated coagulopathy developed within 3 h after intravenous infusion of M type 3, pyrogenic exotoxin A-producing group A streptococci. Serum TNF-alpha peaked at 3 h and returned to baseline by 10 h. Mortality was 100%. Anti-TNF-alpha monoclonal antibody treatment markedly improved mean arterial blood pressure, tissue perfusion, and survival, suggesting that TNF-alpha plays an important role in the induction of shock and organ failure in group A streptococcal bacteremia.

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PubMed1994

A resource guide to VR in medicine.

This guide provides a bibliography of many of the most noteworthy contributions to the emerging literature about virtual reality in medicine, along with listings of the most relevant conferences and resources for researchers. This is an abridged version of a continuously updated comprehensive document which is available on-line to the research community.

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PubMed1994

Retrospective description and experimental reconstitution of three different responses of the baboon to lethal E. coli.

This paper is divided into a retrospective descriptive section in which we report on three distinctly different and spontaneous responses of the baboon to LD100 Eschericia coli observed over the last 6 years. This section is followed by an experimental section in which we reproduce the immediate and delayed responses based on hypothetical mechanisms. In the descriptive section, we arbitrarily divided all the non-survivor animals on which we had sufficient data into three groups based on duration of survival (i.e., 12 hr or less, immediate, 12 to 30 hr, intermediate, and 30 hr or more, delayed). The natural history and pathophysiology of the 12 hr or less group matched that of capillary leak syndrome with a rapid fall in blood pressure, rise in hematocrit, massive edema, and congestion with leukocyte sequestration in both lung and liver, with only limited adrenal cortical hemorrhage. The 12 to 30 hr group matched the natural history of a consumptive hemorrhagic diatheses with a biophasic blood pressure response, limited change in hematocrit, a severe consumptive coagulopathy, severe adrenal cortical hemorrhage, and a moderate renal cortical tubular necrosis, but limited renal cortical thrombosis. The greater than 30 hr group matched the natural history of a microvascular thrombotic (hemolytic uremic) syndrome with a stable blood pressure, a fall in hematocrit associated with a massive renal cortical thrombosis with a severe medullary, and cortical tubular necrosis. We did not analyze these groups further (i.e., type of intervention etc.) once we found that time of survival correlated with a unique clinical syndrome, because based on these observations, we hypothesized that we could reproduce the immediate capillary leak and pulmonary failure, and the delayed microvascular thrombosis and renal failure syndromes experimentally. We reproduced the immediate (< 12 hr) and delayed (> 30 hr) responses by infusion of either tumor necrosis factor or C4b binding protein with sublethal E. coli. This provides models of the immediate and delayed as well as the intermediate responses to E. coli for study of mechanism and the efficacy of therapeutic interventions.

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PubMed1993

Retrospective study comparing the pathophysiology of antibiotic-treated and untreated Escherichia coli- and Staphylococcus aureus-infused baboons.

Escherichia coli and Staphylococcus aureus are the most common pathogens encountered in septic shock. This is a descriptive study in which the pathophysiologic response to infusions of LD100 concentrations of E. coli and S. aureus are staged and compared. Equivalent concentrations of both organisms were infused over a 2 hr period into antibiotic-treated and untreated animals with the following results: 1) The apparent clearance of E. coli was less than that of S. aureus over the 2-hr infusion period, but far greater during the next 8 hr in both antibiotic-treated and untreated animals. Thus the clearance of E. coli fits a one-compartment (intravascular), and that of S. aureus fits a two-compartment (intra- and extravascular) model. 2) The intensity of the cardiovascular, temperature, and metabolic response to E. coli was greater, whereas that of the disseminated intravascular coagulant (DIC) response to S. aureus was greater. We conclude, therefore, that the response to E. coli consists of four stages with no invasion and colonization of tissues, whereas the response to S. aureus consists of two stages with invasion and colonization of tissues.

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PubMed1992

Efficacy of monoclonal antibody against human recombinant tumor necrosis factor in E. coli-challenged swine.

Monoclonal antibody against human tumor necrosis factor alpha (TNF MAb) prevents death induced by intravenous gram-negative bacteria or lipopolysaccharide (LPS) in primates. Although these studies have demonstrated that TNF plays a prominent role in the development of lethal septic shock, exploration of dose-response relationships and possible mechanisms of protection have been limited. We addressed these questions in a series of experiments conducted in E. coli-challenged pigs. First, we determined that TNF MAb neutralized the cytotoxic activity found in septic pig plasma and in culture media from pig monocytes incubated with LPS. Second, we demonstrated that pretreatment with TNF MAb promotes survival, in a dose-dependent fashion, in an otherwise lethal E. coli bacteremic pig model. The results of the survival study highly correlate (r = 0.96, P < 0.01) the presence of TNF in the circulation with mortality. In an additional series of physiologic monitoring experiments designed to delineate possible mechanisms of protection, the authors demonstrate that TNF MAb pretreatment abrogates the prolonged leukopenia, thrombocytopenia, and microvascular leakiness resulting from intravenous bacterial challenge and maintains arterial blood pressure while diminishing pulmonary edema. These findings may provide a mechanism whereby neutralization of TNF systemically affords protection against the lethal sequelae of bacteremia.

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