Update in sepsis:
Saved in:
| Other Authors: | |
|---|---|
| Format: | Book |
| Language: | English |
| Published: |
Philadelphia, Pa.
Saunders
2008
|
| Series: | Clinics in chest medicine
29,4 |
| Subjects: | |
| Online Access: | Inhaltsverzeichnis |
| Physical Description: | XIII S., S. 585 - 754 Ill., graph. Darst. |
| ISBN: | 9781416062806 1416062807 |
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| 245 | 1 | 0 | |a Update in sepsis |c guest ed. Mitchell M. Levy |
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Contents
Preface xiii
Mitchell M. Levy
Defining Sepsis 585
Jean-Louis Vincent and Hakan Atalan Korkut
Definitions have been considered important in all fields of medicine, both at a patient
level to facilitate accurate diagnosis and treatment, and at a research level to clarify
patient inclusion criteria and interpretation of study results. Although there is agree¬
ment that sepsis refers to the host response to infection, the complexity of this re¬
sponse and of the patient groups affected, however, has meant that establishing
accepted definitions of sepsis has been difficult. Recent consensus has provided
global definitions of sepsis and infection, but further work is necessary to provide
a means of more completely characterizing the sepsis response in individual pa¬
tients, such that new interventions can be targeted better as physicians strive to de¬
crease the still high mortality rates associated with this condition.
Biomarkers: Diagnosis and Risk Assessment in Sepsis 591
Corey E.Ventetuolo and Mitchell M. Levy
Prompt diagnosis, intervention, and risk assessment are critical in caring for septic
patient but remain difficult with currently available methods. Biomarkers may be¬
come useful adjuncts to clinicians and ultimately serve as targets for future thera¬
peutic trials in sepsis. The most relevant markers are reviewed in this article,
including interleukin-6, C-reactive protein, procalcitonin, triggering receptor ex¬
pressed on myeloid cells-1, and biomarker panels.
The Immune System in Critical Illness 605
John C Marshall, Emmanuel Charbonney, and Patricia Duque Gonzalez
The mammalian immune system comprises a complex network of physical and
molecular elements that protect the individual from danger in the environment. An
evolutionary ancient innate immune system recognizes danger through pattern-
recognition receptors that are encoded in the genome and mobilizes a rapid and
potent but nonspecific response. This response is responsible for the clinical syn¬
dromes of sepsis and the multiple organ dysfunction syndrome. The adaptive im¬
mune system is highly selective in its targets and is endowed with memory but is
slow in initial activation. Critical illness results in derangements of all components
of the immune response, but the very complexity of the process has frustrated at¬
tempts to correct these derangements and to affect significantly the clinical course
of sepsis.
Contents
The Compensatory Anti-inflammatory Response Syndrome (CARS) in Critically III Patients 617
Nicholas S.Ward, Brian Casserly, and Alfred Ayala
Like the systemic inflammatory response syndrome (SIRS), the compensatory anti-
inflammatory response syndrome (CARS) is a complex pattern of immunologic
responses to severe infection or injury. The difference is that while SIRS is a proin-
flammatory response tasked with killing infectious organisms through activation of
the immune system, CARS is a global deactivation of the immune system tasked
with restoring homeostasis. Much research now suggests that the timing and
relative magnitude of this response have a profound impact on patient outcomes.
The Coagulant Response in Sepsis 627
Marcel Levi
Sepsis is often associated with systemic intravascular activation of coagulation, po¬
tentially leading to widespread microvascular deposits of fibrin, and thereby contrib¬
uting to multiple organ dysfunction. A complex interaction exists between activation
of inflammatory systems and the initiating and regulating pathways of coagulation. A
diagnosis of sepsis-associated disseminated intravascular coagulation can be
made by a combination of routinely available laboratory tests, for which simple diag¬
nostic algorithms have become available. Strategies to inhibit coagulation activation
may theoretically be justified and are being evaluated in clinical studies.
The Heterogeneity of the Microcirculation in Critical Illness 643
Eva Klijn, C.A. Den Uil, Jan Bakker, and Can Ince
Microcirculation, a complex and specialized facet of organ architecture, has charac¬
teristics that vary according to the function of the tissue it supplies. Bedside technol¬
ogy that can directly observe microcirculation in patients, such as orthogonal
polarization spectral imaging and sidestream dark field imaging, has opened the
way to investigating this network and its components, especially in critical illness
and surgery. These investigations have underscored the central role of microcircu¬
lation in perioperative disease states. They have also highlighted variations in the na¬
ture of microcirculation, both among organ systems and within specific organs.
Supported by experimental studies, current investigations are better defining the
nature of microcirculatory alterations in critical illness and how these alterations
respond to therapy. This review focuses on studies conducted to date on the micro-
circulatory beds of critically ill patients. The functional anatomy of microcirculation
networks and the role of these networks in the pathogenesis of critical illness are dis¬
cussed. The morphology of microvascular beds that have been visualized during
surgery and intensive care at the bedside are also described, including those of
the brain, sublingual region, skin, intestine, and eyes.
Cellular Dysfunction in Sepsis 655
Mervyn Singer
Cellular dysfunction is a commonplace sequelum of sepsis and other systemic
inflammatory conditions. Impaired energy production (related to mitochondrial inhi¬
bition, damage, and reduced protein turnover) appears to be a core mechanism un¬
derlying the development of organ dysfunction. The reduction in energy availability
Contents
appears to trigger a metabolic shutdown that impairs normal functioning of the cell.
This may well represent an adaptive mechanism analogous to hibernation that pre¬
vents a massive degree of cell death and thus enables eventual recovery in
survivors.
The Right Ventricle in Sepsis 661
CheeM. Chan and James R. Klinger
Right ventricular dysfunction is common in sepsis and septic shock because of
decreased myocardial contractility and elevated pulmonary vascular resistance
despite a concomitant decrease in systemic vascular resistance. The mainstay of
treatment for acute right heart failure includes treating the underlying cause of sepsis
and reversing circulatory shock to maintain tissue perfusion and oxygen delivery.
Decreasing pulmonary vascular resistance with selective pulmonary vasodilators
is a reasonable approach to improving cardiac output in septic patients with right
ventricular dysfunction. Treatment for right ventricular dysfunction in the setting of
sepsis should concentrate on fluid repletion, monitoring for signs of RV overload,
and correction of reversible causes of elevated pulmonary vascular resistance,
such as hypoxia, acidosis, and lung hyperinflation.
Antimicrobial Management of Sepsis and Septic Shock 677
Sat Sharma and Anand Kumar
Every patient who has sepsis and septic shock must be evaluated appropriately at
presentation before the initiation of antibiotic therapy. However, in most situations,
an abridged initial assessment focusing on critical diagnostic and management
planning elements is sufficient. Intravenous antibiotics should be administered as
early as possible, and always within the first hour of recognizing severe sepsis
and septic shock. Broad-spectrum antibiotics must be selected with one or more
agents active against likely bacterial or fungal pathogens and with good penetration
into the presumed source. Antimicrobial therapy should be reevaluated daily to op¬
timize efficacy, prevent resistance, avoid toxicity, and minimize costs. Consider
combination therapy in septic shock Pseudomonas infections in neutropenic pa¬
tients. Combination therapy should be continued for no more than 3 to 5 days and
de-escalation should occur following availability of susceptibilities. The duration of
antibiotic therapy typically is limited to 7 to 10 days. Longer duration is considered
if response is slow, if there is inadequate surgical source control, or if immunologic
deficiencies are evident. Antimicrobial therapy should be stopped if infection is not
considered the etiologic factor for a shock state.
Management of Sepsis: Early Resuscitation 689
Emanuel P. Rivers.Victor Coba, AlvaroVisbal, MelissaWhitmill, and David Amponsah
Key links in the chain of survival for the management of severe sepsis and septic
shock are early identification and comprehensive resuscitation of high-risk patients.
Multiple studies have shown that the first 6 hours of early sepsis management are
especially important from a diagnostic, pathogenic, and therapeutic perspective,
and that steps taken during this period can have a significant impact on outcome.
The recognition of this critical time period and the robust outcome benefit realized
in previous studies provides the rationale for adopting early resuscitation as a distinct
Contents
intervention. Sepsis joins trauma, stroke, and acute myocardial infarction in having
golden hours, representing a critical opportunity early on in the course of disease
for actions that offer the most benefit.
Corticosteroids and Human Recombinant Activated Protein C for Septic Shock 705
Gwenhael Colin and Djillali Annane
This article summarizes the current knowledge on the benefit/risk profile from the
use of low-dose corticosteroids and activated protein C in treating septic shock.
Physicians should consider using low-dose corticosteroids and drotrecogin alpha
activated in the treatment of patients who have vasopressor-dependent septic
shock with persistent signs of hypoperfusion, organ dysfunction, or hypotension.
The optimal timing for initiating these treatments is from 6 to 24 hours from onset
of shock. When patients are receiving these drugs, physicians should systematically
screen for superinfection and serious bleeding events.
Glucose Control in Sepsis 713
B.Taylor Thompson
Hyperglycemia is common during the course of critical illness and is associated with
adverse clinical outcomes. Randomized controlled trials and large observational tri¬
als of insulin therapy titrated to achieve glucose values approximating the normal
range (80 to 110 mg/dL) demonstrate improved morbidity and mortality in heteroge¬
neous populations and have led to recommendations for improved glucose control.
Patients who have septic shock, however, appear to be at higher risk for hypoglyce-
mia, and a recent randomized trial focusing exclusively on patients who had severe
sepsis did not show benefit. The recent Surviving Sepsis consensus statement rec¬
ommends insulin therapy using validated protocols to lower glucose (less than 150
mg/dL) pending the results of adequately powered trials to determine if normaliza¬
tion (less than 110 mg/dL) of glucose is needed to optimize outcomes in patients
who have severe sepsis.
Reducing Mortality in Severe SepsisrThe Surviving Sepsis Campaign 721
Sean R.Townsend, Christa Schorr, Mitchell M. Levy, and R. Phillip Dellinger
This article traces the history and evolution of the Surviving Sepsis Campaign as
a public health initiative through its several stages of development. The literature
that has characterized clinical experiences with interventions related to the cam¬
paign is reviewed and conclusions discussed.
Sepsis Strategies in Development 735
Steven P. LaRosaand Steven M. Opal
Severe sepsis, defined as inflammation and organ failure due to infection, continues
to result in a mortality of approximately 30% despite advances in critical care. Cur¬
rent therapy includes timely administration of antibiotics, source control of infection,
aggressive fluid resuscitation, support of failing organs, and use of activated protein
C where clinically indicated. Bacterial mediators, including endotoxin and
Contents
superantigens, as well endogenous proinflammatory cytokines are considered im¬
portant to the pathogenesis of sepsis-induced organ failure and are being targeted
with numerous molecules and removal devices. Additional therapeutic strategies are
aimed at restoring the natural anticoagulant levels, blocking deleterious effects of
the complement cascade, reversing cytopathic hypoxia, and inhibiting excessive
lymphocyte apoptosis. Molecules with pluripotent activity, such as interalpha inhib¬
itor proteins and estrogen-receptor ligands, are also being investigated.
Index 749
|
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| author_facet | Levy, Mitchell M. 1950- |
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| callnumber-search | RC182.S4 |
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| callnumber-subject | RC - Internal Medicine |
| ctrlnum | (OCoLC)263427197 (DE-599)HBZHT015776820 |
| dewey-full | 616.944 |
| dewey-hundreds | 600 - Technology (Applied sciences) |
| dewey-ones | 616 - Diseases |
| dewey-raw | 616.944 |
| dewey-search | 616.944 |
| dewey-sort | 3616.944 |
| dewey-tens | 610 - Medicine and health |
| discipline | Medizin |
| format | Book |
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| spelling | Update in sepsis guest ed. Mitchell M. Levy Philadelphia, Pa. Saunders 2008 XIII S., S. 585 - 754 Ill., graph. Darst. txt rdacontent n rdamedia nc rdacarrier Clinics in chest medicine 29,4 Critical Care Sepsis Septicemia Levy, Mitchell M. 1950- (DE-588)13691411X edt Clinics in chest medicine 29,4 (DE-604)BV000001084 29,4 HBZ Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=017045511&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
| spellingShingle | Update in sepsis Clinics in chest medicine Critical Care Sepsis Septicemia |
| title | Update in sepsis |
| title_auth | Update in sepsis |
| title_exact_search | Update in sepsis |
| title_full | Update in sepsis guest ed. Mitchell M. Levy |
| title_fullStr | Update in sepsis guest ed. Mitchell M. Levy |
| title_full_unstemmed | Update in sepsis guest ed. Mitchell M. Levy |
| title_short | Update in sepsis |
| title_sort | update in sepsis |
| topic | Critical Care Sepsis Septicemia |
| topic_facet | Critical Care Sepsis Septicemia |
| url | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=017045511&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |
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