Inflammation, hemostasis, and blood conservation strategies:
Gespeichert in:
| Format: | Buch |
|---|---|
| Sprache: | English |
| Veröffentlicht: |
Philadelphia, Pa. [u.a.]
Saunders
2007
|
| Schriftenreihe: | Hematology, oncology clinics of North America
21,1 |
| Schlagworte: | |
| Online-Zugang: | Inhaltsverzeichnis |
| Beschreibung: | XVII, 206 S. Ill., graph. Darst. |
| ISBN: | 9781416043225 1416043225 |
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| 245 | 1 | 0 | |a Inflammation, hemostasis, and blood conservation strategies |c guest ed. Jerrold H. Levy |
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| adam_text | Inflammation, Hemostasis, and Blood
Conservation Strategies
CONTENTS VOLUME 21 » NUMBER 1 « FEBRUARY 2007
Preface xv
Jerrold H. Levy
Coagulation 2006: A Modern View of Hemostasis 1
Maureane Hoffman and Dougald M. Monroe
The authors propose that hemostasis occurs in a stepwisc process, reg¬
ulated by cellular components in vivo. The effectiveness of hemostasis
in vivo depends not only on the procoagulant reactions but also on the
fibrinolytic process. Causes of coagulopathic bleeding include consump¬
tion of coagulation factors and platelets, excessive fibrinolysis, hypo¬
thermia, and acidosis. Generation of the right amount of thrombin
during the coagulation process not only may be essential for effective
hemostasis but also may set the stage for effective wound healing.
The Balance of Thrombosis and Hemorrhage
in Surgery 13
George L. Adams, Roberto J. Manson, Immanuel Turner,
David Sindram, and Jeffrey H. Lawson
Postoperative hemorrhage and thrombosis is a significant problem dur¬
ing the perioperative period. Understanding the complex and dynamic
interplay of factors, proteins, and enzymes during coagulation is imper¬
ative to maintain balance between hemostasis and thrombosis. To im¬
prove patient outcome, each patient should be risk stratified for
bleeding or thrombosis during the preoperative examination. Addi¬
tional research focused on improvement in screening tools, monitoring,
and therapeutic regimens for surgical patients with a coagulopathy art
warranted.
Clot Stabilization for the Prevention of Bleeding 25
Lisa Payne Rojkjaer and Rasmus Rojkjaer
Coagulation is a finely tuned sequence of reactions beginning with the
interaction between tissue factor (TF) and its substrate, factor VII
(FVII), and resulting in the formation of a fibrin clot localized to the
site of vascular endothelial disruption. While important for fibrin clot
formation, thrombin also plays a role in stabilizing the clot against pre¬
mature fibrinolysis by activating thrombin activatable fibrinolysis in¬
hibitor (TAPT) and factor XEI (FXIH). the terminal enzyme in the
vii
CONTENTS continued
coagulation cascade. Despite use of antifibrinolytic agents in various
types of surgery to inhibit clot lysis, thereby limiting blood loss and pa¬
tient exposure to allogeneic blood products, numerous patients still re¬
quire transfusions for nonsurgical bleeding. This article describes new
concepts of localized hemostasis, a potential role for clot stabilization,
and inhibition of fibrinolysis for control of bleeding.
Regulation of Thrombin Activity—Pharmacologic
and Structural Aspects 33
Kenichi A. Tanaka and Jerrold H. Levy
Thrombin is an essential serine protease for survival. Since the discov¬
ery of heparin in the early twentieth century, significant advances have
been made in the understanding of thrombin structure and function in
coagulation system. Endogenous anticoagulant proteins in blood tightly
regulate thrombin generation, but additional anticoagulant agents may
be necessary to suppress excessive thrombin formation or defective an¬
ticoagulant proteins. Despite the availability of an array of anticoagulant
agents based on chemical and biological engineering technologies, anti
coagulation therapy remains a challenge for clinicians in terms of bal¬
ancing bleeding and thrombosis. The aim of this article is to review
endogenous serine protease inhibitors and novel antithrombotic agents
in relation to pharmacologic regulation of thrombin.
Platelet Inhibitors and Monitoring Platelet Function:
Implications for Bleeding 51
Linda Shore Lesserson
Cardiovascular disease is prevalent in our medical and surgical patient
population. Patients who have atherosclerotic heart disease suffer from
endothelial disorders that predispose them to plaque and thrombus for¬
mation in diseased arteries. As our knowledge of platelet physiology im¬
proves, we can understand the contribution of platelet activation to
arterial disease and we can specifically inhibit that activation with plate¬
let inhibitory drugs. The recent increase in the number of coronary in
terventional procedures performed has spawned the increasing use of
antiplatelet medication as prophylaxis against thrombus formation in
the instrumented artery.
Heparin induced Thrombocytopenia,
a Prothrombotic Disease 65
Jerrold H. Levy and Marcie J. Hursting
Heparin induced thrombocytopenia (HIT) is a serious, yet treatable pro¬
thrombotic disease that develops in approximately 0.5% to 5°/o of hepa
rin treated patients and dramatically increases their risk of thrombosis
(odds ratio, 37). The antibodies that mediate HIT (ie, heparin platelet
Will
CONTENTS continued
factor 4 antibodies) occur more frequently than the overt disease itself,
and, even in the absence of thrombocytopenia, are associated with
increased thrombotic morbidity and mortality. HIT should be sus¬
pected whenever the platelet count drops more than 50% from baseline
(or to 150 x 109/L) beginning 5 to 14 days after starting heparin (or
sooner if there was prior heparin exposure) or new thrombosis occurs
during, or soon after heparin treatment, with other causes excluded.
When HIT is strongly suspected, with or without complicating throm¬
bosis, heparins should be discontinued, and a fast acting, nonheparin
alternative anticoagulant such as argatroban should be initiated immedi¬
ately. With prompt recognition, diagnosis, and treatment of HIT, the
clinical outcomes and health economic burdens of this prothrombotic
disease are improved significantly.
Anti inflammatory Strategies and Hemostatic
Agents: Old Drugs, New Ideas 89
Jerrold H. Levy
Hemostatic abnormalities occur following injury associated with both
cardiac and noncardiac surgery. These changes are part of inflam¬
matory pathways with signaling mechanisms that link these diverse
pathways. The inflammatory response to surgery is exacerbated by al
logeneic blood transfusion by enhancing intrinsic inflammatory activity
and directly increasing plasma levels of inflammatory mediators. Surgi¬
cal patients can be preventively treated with pharmacologic agents to
modulate inflammatory responses. Multiple studies have reported pre¬
ventive pharmacologic therapies to reduce bleeding and the need for
allogeneic transfusions in surgery. Strategies for cardiac surgical patients
during cardiopulmonary bypass include administration of either lysine
analogs, such as epsilon aminocaproic acid and tranexamic acid, or the
serine protease inhibitor aprotinin.
Protease Activated Receptors: Clinical Relevance
to Hemostasis and Inflammation 103
R. Clive Landis
The protease activated receptors (PARs) are a unique family of vascular
receptors that confer on cells an ability to sense, and respond to, local
changes in the proteolytic environment. They are activated by serine
proteases of the blood coagulation cascade, notably thrombin, and are
linked to thrombotic and inflammatory effector pathways. In surgery
with cardiopulmonary bypass (CPB), thrombin is generated in large
quantities in the extracorporeal circuit and can exert systemic effects
by way of platelet and endothelial PAR1. Aprotinin (Trasylol). a serine
protease inhibitor used in cardiac surgery, preserves platelet function,
and attenuates the inflammatory response by protecting the PAR 1 re¬
ceptor on platelets and endothelium.
ix
CONTENTS continued
Platelets as Mediators of Inflammation 115
Steven R. Steinhubl
An expanding body of evidence continues to build on the central role of
inflammation in the progression and clinical manifestations of athero¬
sclerosis. Platelets, long thought to play only a reactionary role at the
time of endothelial disruption, are now recognized as important media¬
tors of the inflammatory process. Platelet activation, which is modulated
by both inflammatory and hemostatic factors, can lead to the release of
hundreds of proteins—many with known proinflammatory functions.
Although compelling evidence is lacking that antiplatelet therapies di¬
rectly lower markers of inflammation, there are intriguing, aldiough
preliminary, data suggesting that markers of inflammation predict the
clinical benefit of antiplatelet therapies.
Inflammation, Proinflammatory Mediators
and Myocardial Ischemia reperfusion Injury 123
Jakob Vintenjohansen, Rong Jiang, James G. Reeves,
James Mykytenko, Jeremiah Deneve, and LynettaJ. Jobe
Ischemic myocardium must be reperfused to terminate the ischemic
event; otherwise the entire myocardium involved in the area at risk
will not survive. However, there is a cost to reperfusion that may offset
the intended clinical benefits of minimizing infarct size, postischemic en¬
dothelial and microvascular damage, blood flow defects, and contractile
dysfunction. There are many contributors to this reperfusion injury.
Targeting only one factor in the complex web of reperfusion
injury may not be effective because the untargeted mechanisms induce
injury. An integrated strategy of reducing reperfusion injury in the cath
eterization laboratory involves controlling both die conditions and die
composition of the reperfusate to target the broadest array of mecha¬
nisms of injury. Mechanical interventions such as gradually restoring
blood flow or applying postconditioning may be used independently in
or conjunction with various cardioprotective pharmaceuticals in an inte¬
grated strategy of reperfusion therapeutics to reduce postischemic injury.
Transfusion Risks and Transfusion related
Pro inflammatory Responses 147
George John Despotis, Lini Zhang, and Douglas M. Lublin
Despite improvements in blood screening and administration tech¬
niques, serious adverse events related to transfusion continue to occur,
albeit at a much lower incidence. Li addition to the development and im¬
plementation of new screening and blood purification/modification tech¬
niques and implementation of an optimal blood management program,
the incidence and consequences of transfusion reactions can be reduced
by a basic understanding of transfusion related complications. Although
CONTENTS continued
acute hemolytic transfusion reactions, transfusion associated anaphy
laxis and sepsis, and transfusion associated acute lung injury occur infre¬
quently, diligence in administration of blood and monitoring for
development of respective signs/symptoms can minimize the severity
of these potentially life threatening complications. In addition, emerging
blood banking techniques such as psoralen UV inactivation of patho¬
gens and use of patient identification systems may attenuate the inci¬
dence of adverse events related to transfusion. With respect to
optimizing blood management by means of an effective blood manage¬
ment program involving pharmacologic and nonpharmacologic strate¬
gies, the ability to reduce use of blood products and to decrease
operative time or re exploration rates has important implications for dis¬
ease prevention, blood inventory and costs, and overall health care costs.
Transfusion related Acute Lung Injury 163
Chelsea A. Sheppard, Lennart E. Logdberg, James C. Zimring,
and Christopher D. Hillyer
With the success of reducing the risk of transfusion transmitted infec¬
tious diseases, noninfectious serious hazards of transfusion have come
to the forefront with respect to transfusion safety. Transfusion related
acute lung injury has emerged as a dominant noninfectious serious haz¬
ard of transfusion. Improved understanding of its pathophysiology is
needed to improve clinical strategies to deal with the risk. Such under¬
standing, in turn, will depend on the continued progress in development
of good model systems, in vitro and in vivo, for experimental studies.
As the pathologic mechanisms are elucidated, a universal definition
and strategies for the prevention and/or mitigation may become more
tangible. This article reviews the clinical manifestations, evolving defini¬
tion, incidence, pathophysiology, animal modeling, donor screening,
and deferral algorithms as they relate to transfusion related acute lung
injury.
Transfusion Algorithms and How They Apply
to Blood Conservation: The High risk Cardiac
Surgical Patient 177
Marie E. Steiner and George John Despotis
Considerable blood product support is administered to the cardiac sur
gery population. Due to the multifactorial etiology of bleeding in the
cardiac bypass patient, blood products frequently and empirically are
infused to correct bleeding, with varying success. Several studies have
demonstrated the benefit of algorithm guided transfusion in reducing
blood loss, transfusion exposure, or rate of surgical re exploration for
bleeding. Some transfusion algorithms also incorporate laboratory
based decision points in their guidelines. Despite published success
with standardized transfusion practices, generalized change in blood use
has not been realized, and it is evident that current laboratory guided
xi
CONTENTS continued
hemostasis measures are inadequate to define and address the bleeding
etiology in these patients.
Red Cell Transfusions and Guidelines:
A Work in Progress 185
Bruce D. Spiess
Blood transfusion utilization continues to rise, yet it has never under¬
gone prospective safety and efficacy testing. Recent data regarding ox¬
ygen delivery, microcirculation, and inflammation all point toward
potential problems with allogeneic transfusion. Outcome data from ret¬
rospective data bases are sobering, calling to question the present prac¬
tices of red cell transfusion.
Index 201
|
| adam_txt |
Inflammation, Hemostasis, and Blood
Conservation Strategies
CONTENTS VOLUME 21 » NUMBER 1 « FEBRUARY 2007
Preface xv
Jerrold H. Levy
Coagulation 2006: A Modern View of Hemostasis 1
Maureane Hoffman and Dougald M. Monroe
The authors propose that hemostasis occurs in a stepwisc process, reg¬
ulated by cellular components in vivo. The effectiveness of hemostasis
in vivo depends not only on the procoagulant reactions but also on the
fibrinolytic process. Causes of coagulopathic bleeding include consump¬
tion of coagulation factors and platelets, excessive fibrinolysis, hypo¬
thermia, and acidosis. Generation of the right amount of thrombin
during the coagulation process not only may be essential for effective
hemostasis but also may set the stage for effective wound healing.
The Balance of Thrombosis and Hemorrhage
in Surgery 13
George L. Adams, Roberto J. Manson, Immanuel Turner,
David Sindram, and Jeffrey H. Lawson
Postoperative hemorrhage and thrombosis is a significant problem dur¬
ing the perioperative period. Understanding the complex and dynamic
interplay of factors, proteins, and enzymes during coagulation is imper¬
ative to maintain balance between hemostasis and thrombosis. To im¬
prove patient outcome, each patient should be risk stratified for
bleeding or thrombosis during the preoperative examination. Addi¬
tional research focused on improvement in screening tools, monitoring,
and therapeutic regimens for surgical patients with a coagulopathy art
warranted.
Clot Stabilization for the Prevention of Bleeding 25
Lisa Payne Rojkjaer and Rasmus Rojkjaer
Coagulation is a finely tuned sequence of reactions beginning with the
interaction between tissue factor (TF) and its substrate, factor VII
(FVII), and resulting in the formation of a fibrin clot localized to the
site of vascular endothelial disruption. While important for fibrin clot
formation, thrombin also plays a role in stabilizing the clot against pre¬
mature fibrinolysis by activating thrombin activatable fibrinolysis in¬
hibitor (TAPT) and factor XEI (FXIH). the terminal enzyme in the
vii
CONTENTS continued
coagulation cascade. Despite use of antifibrinolytic agents in various
types of surgery to inhibit clot lysis, thereby limiting blood loss and pa¬
tient exposure to allogeneic blood products, numerous patients still re¬
quire transfusions for nonsurgical bleeding. This article describes new
concepts of localized hemostasis, a potential role for clot stabilization,
and inhibition of fibrinolysis for control of bleeding.
Regulation of Thrombin Activity—Pharmacologic
and Structural Aspects 33
Kenichi A. Tanaka and Jerrold H. Levy
Thrombin is an essential serine protease for survival. Since the discov¬
ery of heparin in the early twentieth century, significant advances have
been made in the understanding of thrombin structure and function in
coagulation system. Endogenous anticoagulant proteins in blood tightly
regulate thrombin generation, but additional anticoagulant agents may
be necessary to suppress excessive thrombin formation or defective an¬
ticoagulant proteins. Despite the availability of an array of anticoagulant
agents based on chemical and biological engineering technologies, anti
coagulation therapy remains a challenge for clinicians in terms of bal¬
ancing bleeding and thrombosis. The aim of this article is to review
endogenous serine protease inhibitors and novel antithrombotic agents
in relation to pharmacologic regulation of thrombin.
Platelet Inhibitors and Monitoring Platelet Function:
Implications for Bleeding 51
Linda Shore Lesserson
Cardiovascular disease is prevalent in our medical and surgical patient
population. Patients who have atherosclerotic heart disease suffer from
endothelial disorders that predispose them to plaque and thrombus for¬
mation in diseased arteries. As our knowledge of platelet physiology im¬
proves, we can understand the contribution of platelet activation to
arterial disease and we can specifically inhibit that activation with plate¬
let inhibitory drugs. The recent increase in the number of coronary in
terventional procedures performed has spawned the increasing use of
antiplatelet medication as prophylaxis against thrombus formation in
the instrumented artery.
Heparin induced Thrombocytopenia,
a Prothrombotic Disease 65
Jerrold H. Levy and Marcie J. Hursting
Heparin induced thrombocytopenia (HIT) is a serious, yet treatable pro¬
thrombotic disease that develops in approximately 0.5% to 5°/o of hepa
rin treated patients and dramatically increases their risk of thrombosis
(odds ratio, 37). The antibodies that mediate HIT (ie, heparin platelet
Will
CONTENTS continued
factor 4 antibodies) occur more frequently than the overt disease itself,
and, even in the absence of thrombocytopenia, are associated with
increased thrombotic morbidity and mortality. HIT should be sus¬
pected whenever the platelet count drops more than 50% from baseline
(or to 150 x 109/L) beginning 5 to 14 days after starting heparin (or
sooner if there was prior heparin exposure) or new thrombosis occurs
during, or soon after heparin treatment, with other causes excluded.
When HIT is strongly suspected, with or without complicating throm¬
bosis, heparins should be discontinued, and a fast acting, nonheparin
alternative anticoagulant such as argatroban should be initiated immedi¬
ately. With prompt recognition, diagnosis, and treatment of HIT, the
clinical outcomes and health economic burdens of this prothrombotic
disease are improved significantly.
Anti inflammatory Strategies and Hemostatic
Agents: Old Drugs, New Ideas 89
Jerrold H. Levy
Hemostatic abnormalities occur following injury associated with both
cardiac and noncardiac surgery. These changes are part of inflam¬
matory pathways with signaling mechanisms that link these diverse
pathways. The inflammatory response to surgery is exacerbated by al
logeneic blood transfusion by enhancing intrinsic inflammatory activity
and directly increasing plasma levels of inflammatory mediators. Surgi¬
cal patients can be preventively treated with pharmacologic agents to
modulate inflammatory responses. Multiple studies have reported pre¬
ventive pharmacologic therapies to reduce bleeding and the need for
allogeneic transfusions in surgery. Strategies for cardiac surgical patients
during cardiopulmonary bypass include administration of either lysine
analogs, such as epsilon aminocaproic acid and tranexamic acid, or the
serine protease inhibitor aprotinin.
Protease Activated Receptors: Clinical Relevance
to Hemostasis and Inflammation 103
R. Clive Landis
The protease activated receptors (PARs) are a unique family of vascular
receptors that confer on cells an ability to sense, and respond to, local
changes in the proteolytic environment. They are activated by serine
proteases of the blood coagulation cascade, notably thrombin, and are
linked to thrombotic and inflammatory effector pathways. In surgery
with cardiopulmonary bypass (CPB), thrombin is generated in large
quantities in the extracorporeal circuit and can exert systemic effects
by way of platelet and endothelial PAR1. Aprotinin (Trasylol). a serine
protease inhibitor used in cardiac surgery, preserves platelet function,
and attenuates the inflammatory response by protecting the PAR 1 re¬
ceptor on platelets and endothelium.
ix
CONTENTS continued
Platelets as Mediators of Inflammation 115
Steven R. Steinhubl
An expanding body of evidence continues to build on the central role of
inflammation in the progression and clinical manifestations of athero¬
sclerosis. Platelets, long thought to play only a reactionary role at the
time of endothelial disruption, are now recognized as important media¬
tors of the inflammatory process. Platelet activation, which is modulated
by both inflammatory and hemostatic factors, can lead to the release of
hundreds of proteins—many with known proinflammatory functions.
Although compelling evidence is lacking that antiplatelet therapies di¬
rectly lower markers of inflammation, there are intriguing, aldiough
preliminary, data suggesting that markers of inflammation predict the
clinical benefit of antiplatelet therapies.
Inflammation, Proinflammatory Mediators
and Myocardial Ischemia reperfusion Injury 123
Jakob Vintenjohansen, Rong Jiang, James G. Reeves,
James Mykytenko, Jeremiah Deneve, and LynettaJ. Jobe
Ischemic myocardium must be reperfused to terminate the ischemic
event; otherwise the entire myocardium involved in the area at risk
will not survive. However, there is a cost to reperfusion that may offset
the intended clinical benefits of minimizing infarct size, postischemic en¬
dothelial and microvascular damage, blood flow defects, and contractile
dysfunction. There are many contributors to this reperfusion injury.
Targeting only one factor in the complex web of reperfusion
injury may not be effective because the untargeted mechanisms induce
injury. An integrated strategy of reducing reperfusion injury in the cath
eterization laboratory involves controlling both die conditions and die
composition of the reperfusate to target the broadest array of mecha¬
nisms of injury. Mechanical interventions such as gradually restoring
blood flow or applying postconditioning may be used independently in
or conjunction with various cardioprotective pharmaceuticals in an inte¬
grated strategy of reperfusion therapeutics to reduce postischemic injury.
Transfusion Risks and Transfusion related
Pro inflammatory Responses 147
George John Despotis, Lini Zhang, and Douglas M. Lublin
Despite improvements in blood screening and administration tech¬
niques, serious adverse events related to transfusion continue to occur,
albeit at a much lower incidence. Li addition to the development and im¬
plementation of new screening and blood purification/modification tech¬
niques and implementation of an optimal blood management program,
the incidence and consequences of transfusion reactions can be reduced
by a basic understanding of transfusion related complications. Although
CONTENTS continued
acute hemolytic transfusion reactions, transfusion associated anaphy
laxis and sepsis, and transfusion associated acute lung injury occur infre¬
quently, diligence in administration of blood and monitoring for
development of respective signs/symptoms can minimize the severity
of these potentially life threatening complications. In addition, emerging
blood banking techniques such as psoralen UV inactivation of patho¬
gens and use of patient identification systems may attenuate the inci¬
dence of adverse events related to transfusion. With respect to
optimizing blood management by means of an effective blood manage¬
ment program involving pharmacologic and nonpharmacologic strate¬
gies, the ability to reduce use of blood products and to decrease
operative time or re exploration rates has important implications for dis¬
ease prevention, blood inventory and costs, and overall health care costs.
Transfusion related Acute Lung Injury 163
Chelsea A. Sheppard, Lennart E. Logdberg, James C. Zimring,
and Christopher D. Hillyer
With the success of reducing the risk of transfusion transmitted infec¬
tious diseases, noninfectious serious hazards of transfusion have come
to the forefront with respect to transfusion safety. Transfusion related
acute lung injury has emerged as a dominant noninfectious serious haz¬
ard of transfusion. Improved understanding of its pathophysiology is
needed to improve clinical strategies to deal with the risk. Such under¬
standing, in turn, will depend on the continued progress in development
of good model systems, in vitro and in vivo, for experimental studies.
As the pathologic mechanisms are elucidated, a universal definition
and strategies for the prevention and/or mitigation may become more
tangible. This article reviews the clinical manifestations, evolving defini¬
tion, incidence, pathophysiology, animal modeling, donor screening,
and deferral algorithms as they relate to transfusion related acute lung
injury.
Transfusion Algorithms and How They Apply
to Blood Conservation: The High risk Cardiac
Surgical Patient 177
Marie E. Steiner and George John Despotis
Considerable blood product support is administered to the cardiac sur
gery population. Due to the multifactorial etiology of bleeding in the
cardiac bypass patient, blood products frequently and empirically are
infused to correct bleeding, with varying success. Several studies have
demonstrated the benefit of algorithm guided transfusion in reducing
blood loss, transfusion exposure, or rate of surgical re exploration for
bleeding. Some transfusion algorithms also incorporate laboratory
based decision points in their guidelines. Despite published success
with standardized transfusion practices, generalized change in blood use
has not been realized, and it is evident that current laboratory guided
xi
CONTENTS continued
hemostasis measures are inadequate to define and address the bleeding
etiology in these patients.
Red Cell Transfusions and Guidelines:
A Work in Progress 185
Bruce D. Spiess
Blood transfusion utilization continues to rise, yet it has never under¬
gone prospective safety and efficacy testing. Recent data regarding ox¬
ygen delivery, microcirculation, and inflammation all point toward
potential problems with allogeneic transfusion. Outcome data from ret¬
rospective data bases are sobering, calling to question the present prac¬
tices of red cell transfusion.
Index 201 |
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| genre | (DE-588)4143413-4 Aufsatzsammlung gnd-content |
| genre_facet | Aufsatzsammlung |
| id | DE-604.BV022308983 |
| illustrated | Illustrated |
| index_date | 2024-07-02T16:57:45Z |
| indexdate | 2024-07-09T20:54:40Z |
| institution | BVB |
| isbn | 9781416043225 1416043225 |
| language | English |
| oai_aleph_id | oai:aleph.bib-bvb.de:BVB01-015518834 |
| oclc_num | 150507279 |
| open_access_boolean | |
| owner | DE-19 DE-BY-UBM DE-355 DE-BY-UBR |
| owner_facet | DE-19 DE-BY-UBM DE-355 DE-BY-UBR |
| physical | XVII, 206 S. Ill., graph. Darst. |
| publishDate | 2007 |
| publishDateSearch | 2007 |
| publishDateSort | 2007 |
| publisher | Saunders |
| record_format | marc |
| series | Hematology, oncology clinics of North America |
| series2 | Hematology, oncology clinics of North America |
| spelling | Inflammation, hemostasis, and blood conservation strategies guest ed. Jerrold H. Levy Philadelphia, Pa. [u.a.] Saunders 2007 XVII, 206 S. Ill., graph. Darst. txt rdacontent n rdamedia nc rdacarrier Hematology, oncology clinics of North America 21,1 Blutkonserve (DE-588)4146080-7 gnd rswk-swf Entzündung (DE-588)4014975-4 gnd rswk-swf Blutstillung (DE-588)4069555-4 gnd rswk-swf (DE-588)4143413-4 Aufsatzsammlung gnd-content Entzündung (DE-588)4014975-4 s Blutstillung (DE-588)4069555-4 s Blutkonserve (DE-588)4146080-7 s b DE-604 Levy, Jerrold H. Sonstige oth Hematology, oncology clinics of North America 21,1 (DE-604)BV000625446 21,1 HBZ Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=015518834&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
| spellingShingle | Inflammation, hemostasis, and blood conservation strategies Hematology, oncology clinics of North America Blutkonserve (DE-588)4146080-7 gnd Entzündung (DE-588)4014975-4 gnd Blutstillung (DE-588)4069555-4 gnd |
| subject_GND | (DE-588)4146080-7 (DE-588)4014975-4 (DE-588)4069555-4 (DE-588)4143413-4 |
| title | Inflammation, hemostasis, and blood conservation strategies |
| title_auth | Inflammation, hemostasis, and blood conservation strategies |
| title_exact_search | Inflammation, hemostasis, and blood conservation strategies |
| title_exact_search_txtP | Inflammation, hemostasis, and blood conservation strategies |
| title_full | Inflammation, hemostasis, and blood conservation strategies guest ed. Jerrold H. Levy |
| title_fullStr | Inflammation, hemostasis, and blood conservation strategies guest ed. Jerrold H. Levy |
| title_full_unstemmed | Inflammation, hemostasis, and blood conservation strategies guest ed. Jerrold H. Levy |
| title_short | Inflammation, hemostasis, and blood conservation strategies |
| title_sort | inflammation hemostasis and blood conservation strategies |
| topic | Blutkonserve (DE-588)4146080-7 gnd Entzündung (DE-588)4014975-4 gnd Blutstillung (DE-588)4069555-4 gnd |
| topic_facet | Blutkonserve Entzündung Blutstillung Aufsatzsammlung |
| url | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=015518834&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |
| volume_link | (DE-604)BV000625446 |
| work_keys_str_mv | AT levyjerroldh inflammationhemostasisandbloodconservationstrategies |