The sepsis syndrome:
Saved in:
| Format: | Book |
|---|---|
| Language: | English |
| Published: |
Philadelphia [u.a.]
Saunders
1996
|
| Series: | Clinics in chest medicine
17,2 |
| Subjects: | |
| Online Access: | Inhaltsverzeichnis |
| Physical Description: | IX S., S. 175 - 353 Ill., graph. Darst. |
Staff View
MARC
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| 245 | 1 | 0 | |a The sepsis syndrome |c Paul M. Dorinsky guest ed. |
| 264 | 1 | |a Philadelphia [u.a.] |b Saunders |c 1996 | |
| 300 | |a IX S., S. 175 - 353 |b Ill., graph. Darst. | ||
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| 490 | 1 | |a Clinics in chest medicine |v 17,2 | |
| 650 | 7 | |a Septikemie |2 gtt | |
| 650 | 2 | |a Syndrome de réponse inflammatoire systémique | |
| 650 | 4 | |a Sepsis Syndrome | |
| 650 | 4 | |a Septicemia | |
| 650 | 0 | 7 | |a Sepsis |0 (DE-588)4181014-4 |2 gnd |9 rswk-swf |
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Record in the Search Index
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| adam_text | THE SEPSIS SYNDROME
CONTENTS
Preface xi
Paul M. Dorinsky
The Sepsis Syndrome: Definition and General Approach
to Management 175
Roger C. Bone
Sepsis is the systemic response to severe infection in critically ill patients.
Sepsis, sepsis syndrome, and septic shock represent the increasingly severe
stages of the same disease. Severe sepsis and septic shock occur in persons
with preexisting illness or trauma. If sepsis is not diagnosed and treated
early, it can become self perpetuating, and elderly persons, in particular,
are at a greater risk of death from sepsis.
The Pathogenesis of Sepsis: Factors That Modulate the Response to
Gram Negative Bacterial Infection 183
Clay B. Marsh and Mark D. Wewers
Gram negative bacteria gain access to the bloodstream by evading host
defenses. Once in circulation, lipopolysaccharide interacts with the host
receptor CD14 and initiates the host s immune response. Lipolysaccharide
stimulates the host to produce a cascade of mediators that activate and
target leukocytes, opsonize the bacteria, and induce fever to defend against
the invading bacteria. Unregulated release of these mediators, however,
leads to the production of vasoactive substances, activation of the clotting
cascade, and diminution of cardiac performance, which leads to the sepsis
syndrome. This article discusses the pathogenic events that lead to sepsis
syndrome and reviews critical steps in regulating these inflammatory
mediators to allow the host to recover from gram negative bacteremia.
Early Detection and Markers of Sepsis 199
Polly E. Parsons and Marc Moss
Numerous potential markers identified in in vitro and animal models of
sepsis have been studied in patients at risk for and with sepsis. No
single marker or combination of markers convincingly identifies sepsis or
predicts the development of sepsis or complications, including mortality.
CLINICS IN CHEST MEDICINE VOLUME 17 • NUMBER 2 • JUNE 19% vii
As new mediators and modulators of inflammation are identified, it will
be important to study their role as markers in sepsis, individually and in
combination.
Current Concepts of Sepsis and Acute Lung Injury 213
Curtis N. Sessler, Geoffrey L. Bloomfield, and Alpha A. Fowler III
Acute respiratory distress syndrome continues to be a vexing clinical
problem with no specific therapy. Epidemiologic and basic sciences have
advanced our understanding of the clinical syndrome and have brought
us to the brink of effective intervention strategies. This article carefully
examines the current state of knowledge, with reference to acute lung
injury and current efforts, to arrive at effective pharmacologic approaches.
Cardiac Dysfunction During Septic Shock 237
Eugene Bunnell and Joseph E. Parrillo
Cardiac dysfunction is common in sepsis and septic shock. An understand¬
ing of this pathophysiology is crucial in treatment of this disorder. This
article reviews the numerous studies of septic shock in humans that focus
on cardiovascular physiology, briefly addresses the possible etiology, and
concludes with therapeutic implications.
Metabolic Consequences of Sepsis: Correlation With
Altered Intracellular Calcium Homeostasis 249
Elliott D. Crouser and Paul M. Dorinsky
The sepsis syndrome is associated with well characterized circulatory and
inflammatory abnormalities; however, sepsis also results in widespread
metabolic alterations. In this article, the authors review the effects of severe
infection and sepsis on oxygen, glucose, protein, and lipid metabolism. In
addition, the authors show the link between the inflammatory and meta¬
bolic consequences of sepsis by examining the effects of severe infection
on calcium homeostasis.
Oxygen Delivery and Consumption During Sepsis 263
Dean R. Chittock and James A. Russell
This article discusses the oxygen consumption (Vo2) and delivery (Do2)
relationship as it pertains to animal models of sepsis and human sepsis
syndrome and septic shock. Pathologic dependence of Vo2 on Do2 is not
present in resuscitated patients who have sepsis syndrome and septic
shock. Defects in oxygen extraction and use at the individual organ level
with maldistribution of blood flow probably do occur in sepsis; however,
there is no clinical evidence that augmenting Do2 to supernormal levels
decreases organ dysfunction or mortality in sepsis. We need improved
techniques to assess tissue hypoxia at the organ level, and we need to test
therapies directed at correcting the maldistribution of blood flow and O2
use defects of sepsis.
Hemodynamic Support During Sepsis 279
Frederick P. Ognibene
Hemodynamic support during sepsis should focus on aggressive resuscita¬
tion coupled with vasopressors aimed at restoration of blood pressure and
end organ perfusion and preservation. The choice of vasopressors should
be based on the degree and persistence of peripheral vasodilatation as
well as the degree of cardiac stimulation required. Norepinephrine can
and should be used when dopamine fails to improve blood pressure
and perfusion after adequate volume resuscitation. Dopamine s role of
viii CONTENTS
renovascular preservation remains controversial. Therapeutic strategies
aimed at supranormal improvements in cardiac index or oxygen delivery
have no documented effect in septic patients and should not be part of
their therapy.
Pharmacotherapy of Sepsis 289
Laura F. Weikert and Gordon R. Bernard
The pharmacotherapy of sepsis has been the focus of intense research
during the past decade. This article is a broad overview of the majority of
the recently proposed pharamcotherapeutic strategies to combat sepsis.
The authors review cyclooxygenase inhibitors, platelet activating factor
antagonists, pentoxifylline, antioxidants including N acetylcysteine, nalox
one, and bradykinin antagonists. The authors summarize the results of the
major animal human studies that have been conducted with these agents.
Immunotherapy for Sepsis 307
David R. Ralston and Roy C. St. John
In recent years, an improved understanding of the pathogenesis of sepsis,
along with an explosion in the biotechnology industry, has led to the
development of a variety of agents with potential to interdict the patho¬
genesis of sepsis at many points. This article reviews the rationale, efficacy,
and shortcomings of these immunotherapeutic agents as they relate to the
management of human septic shock.
Granulocyte Colony Stimulating Factor and Modulation of
Inflammatory Cells in Sepsis 319
Steve Nelson and Gregory J. Bagby
Although antimicrobial therapy has been the central clinical strategy for
patients with sepsis and multiple organ failure, the survival rate in these
patients remains low because their host defense mechanisms usually are
compromised. Various inflammatory cytokines recently have been shown
to play important roles in normal host defense mechanisms and in sepsis
and its sequelae. Cytokine modulation therapies, which have focused on
the downregulation of the inflammatory response, have not been shown
to benefit these patients. This article examines the role of granulocyte
colony stimulating factor as a proinflammatory mediator and a potential
adjuvant treatment in patients with severe infection.
Nitric Oxide in Sepsis 333
Didier Payen, Catherine Bernard, and Sadek Beloucif
The synthesis of nitric oxide (NO) and its targets are reviewed physiologi¬
cally during sepsis and wound healing, a self limiting process in which
mechanisms are still identified incompletely. NO also plays an active and
direct role during infection, aimed at protecting the host and destroying
the microbe. During septic shock, an overproduction of NO has been
described experimentally and clinically that might be responsible for the
systemic vasodilatation with hyporesponsiveness to exogenous vasocon
strictive agents. The different manipulations of NO pathway during sepsis
are described (transcription and post transcription of iNOS, enzymatic
function, substrate availability, NO concentration, and NO effector mole¬
cules), although their clinical benefit remains controversial.
Index 351
Subscription Information Inside back cover
CONTENTS ix
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| physical | IX S., S. 175 - 353 Ill., graph. Darst. |
| publishDate | 1996 |
| publishDateSearch | 1996 |
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| publisher | Saunders |
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| series | Clinics in chest medicine |
| series2 | Clinics in chest medicine |
| spelling | The sepsis syndrome Paul M. Dorinsky guest ed. Philadelphia [u.a.] Saunders 1996 IX S., S. 175 - 353 Ill., graph. Darst. txt rdacontent n rdamedia nc rdacarrier Clinics in chest medicine 17,2 Septikemie gtt Syndrome de réponse inflammatoire systémique Sepsis Syndrome Septicemia Sepsis (DE-588)4181014-4 gnd rswk-swf (DE-588)4143413-4 Aufsatzsammlung gnd-content Sepsis (DE-588)4181014-4 s DE-604 Dorinsky, Paul M. Sonstige oth Clinics in chest medicine 17,2 (DE-604)BV000001084 17,2 HBZ Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=007260493&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
| spellingShingle | The sepsis syndrome Clinics in chest medicine Septikemie gtt Syndrome de réponse inflammatoire systémique Sepsis Syndrome Septicemia Sepsis (DE-588)4181014-4 gnd |
| subject_GND | (DE-588)4181014-4 (DE-588)4143413-4 |
| title | The sepsis syndrome |
| title_auth | The sepsis syndrome |
| title_exact_search | The sepsis syndrome |
| title_full | The sepsis syndrome Paul M. Dorinsky guest ed. |
| title_fullStr | The sepsis syndrome Paul M. Dorinsky guest ed. |
| title_full_unstemmed | The sepsis syndrome Paul M. Dorinsky guest ed. |
| title_short | The sepsis syndrome |
| title_sort | the sepsis syndrome |
| topic | Septikemie gtt Syndrome de réponse inflammatoire systémique Sepsis Syndrome Septicemia Sepsis (DE-588)4181014-4 gnd |
| topic_facet | Septikemie Syndrome de réponse inflammatoire systémique Sepsis Syndrome Septicemia Sepsis Aufsatzsammlung |
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