CONTINUING EDUCATION
How Hemostatic Agents
Interact With the Coagulation
Cascade
DOUGLAS M. OVERBEY, MD; EDWARD L. JONES, MD, MS;
THOMAS N. ROBINSON, MD
1.7
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Purpose/Goal
To provide the learner with knowledge specific to surgical
hemostasis and the coagulation cascade.
Objectives
1. Discuss surgical hemostasis.
2. Describe the normal coagulation cascade.
3. Identify blood products for intraoperative blood loss
resuscitation.
4. Discuss hemostatic agents.
Conflict of Interest Disclosures
Douglas M. Overbey, MD, and Edward L. Jones, MD, MS,
have no declared affiliations that could be perceived as posing
potential conflicts of interest in the publication of this article.
As a consultant for Covidien and ConMed and as a recipient of grant money paid to his institution by Medtronics and
Storz, Thomas N. Robinson, MD, has declared affiliations that
could be perceived as posing potential conflicts of interest in
the publication of this article.
The behavioral objectives for this program were created by
Helen Starbuck Pashley, MA, BSN, CNOR, clinical editor,
with consultation from Rebecca Holm, MSN, RN, CNOR,
clinical editor, and Susan Bakewell, MS, RN-BC, director,
Perioperative Education. Ms Starbuck Pashley, Ms Holm,
and Ms Bakewell have no declared affiliations that could be
perceived as posing potential conflicts of interest in the publication of this article.
Sponsorship or Commercial Support
No sponsorship or commercial support was received for this
article.
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Commission on Accreditation.
AORN recognizes these activities as CE for RNs. This recognition does not imply that AORN or the American Nurses
Credentialing Center approves or endorses products mentioned
in the activity.
http://dx.doi.org/10.1016/j.aorn.2013.12.012
148 j AORN Journal August 2014
Vol 100 No 2
Ó AORN, Inc, 2014
How Hemostatic Agents
Interact With the Coagulation
Cascade
1.7
DOUGLAS M. OVERBEY, MD; EDWARD L. JONES, MD, MS;
THOMAS N. ROBINSON, MD
www.aorn.org/CE
ABSTRACT
Hemostasis is a critical component of the preservation of hemodynamic stability and
operative visibility during surgery. Initially, hemostasis is achieved via the careful
application of direct pressure to allow time for the coagulation cascade to create a
fibrin and platelet plug. Other first-line methods of hemostasis in surgery include
repair or ligation of the bleeding vessel with sutures, clips, or staples and coagulation
of the bleeding site with a thermal energy-based device. When these methods are
insufficient to provide adequate hemostasis, topical hemostatic agents can be used to
augment the creation of a clot during surgery. A basic understanding of how and
where these products interact with the coagulation cascade is essential to achieving
optimal hemostasis outcomes. AORN J 100 (August 2014) 149-156. Ó AORN, Inc,
2014. http://dx.doi.org/10.1016/j.aorn.2013.12.012
Key words: hemostasis, clotting cascade, hemodynamic stability, coagulation,
hemostatic agents.
T
he goals of surgical hemostasis are to preserve the patient’s hemodynamic stability
and provide operative field visibility by
limiting blood loss. The surgeon can begin hemostasis by mechanically applying careful pressure on
the bleeding site using a single digit. He or she can
repair or ligate large and medium vessels using
sutures, clips, or staples or coagulate the bleeding
site with thermal energy-based devices (eg, electrosurgery). Hemostasis of smaller vessels relies on
the body’s innate ability to coagulate bleeding sites.
This complex process is known as the coagulation
cascade, which culminates in fibrin plug formation.
The coagulation cascade can be augmented by a
variety of surgical hemostatic agents that assist in
either thrombin or fibrin formation or that provide
additional scaffolding to which platelets and a clot
can adhere.
COAGULATION CASCADE
The classic end point of the coagulation cascaded
otherwise known as the clotting cascadedis fibrin
formation, which is achieved via two distinct
mechanisms: extrinsic and intrinsic pathways. Both
pathways involve a series of enzymatic reactions
that coalesce in thrombin formation, which cleaves
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Ó AORN, Inc, 2014
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No 2 AORN Journal j 149
OVERBEYeJONESeROBINSON
August 2014 Vol 100 No 2
fibrinogen into its active form of fibrin. Table 1 lists
the key components of the clotting process. A
blood “clot” forms in the blood vessel at the site of
an injury by the deposition of fibrin intermixed with
platelets that rush to “plug the hole” or repair the
damaged area in the vessel. A basic understanding
of fibrin creation will assist clinicians in selecting
and using the appropriate hemostatic agents in
the OR.
Intrinsic Pathway
The intrinsic pathway of the coagulation cascade
involves factors that are present in normal plasma
and thus does not require a vascular surface to form
fibrin. This pathway is labeled “intrinsic” because it
does not require a damaged surface to begin and is
therefore balanced by constant fibrinolysis in vivo.
This process begins with factor XII, which starts a
cascade of reactions when it is activated to become
factor XIIa. Factor XIIa converts factor XI into
XIa, which converts factor IX into IXa, which in
turn is responsible for cleaving factor X into Xa at
the junction with the extrinsic pathway (Figure 1).1
Factor VIII is bound to von Willebrand factor in the
circulation. It is inactive and only participates in
the conversion of factor X to Xa as a cofactor to the
enzyme IXa.
Extrinsic Pathway
The extrinsic pathway begins when a vascular
injury exposes platelet tissue factor (ie, thromboplastin) on the damaged subendothelial surface of
the blood vessel. Platelet tissue factor then activates
factor VII into VIIa, which directly activates factor
X to Xa to join the common pathway to fibrin
formation.1
Common Pathway
Factor Xa is created on the phospholipid surface of
activated platelets and, along with factor Va and
calcium, forms the prothrombinase complex that
cleaves prethrombin (ie, factor II) into the active
form of thrombin (ie, factor IIa). Thrombin then
cleaves the fibrinogen that is present within the
circulating blood to create fibrin. Fibrin then links
together with platelets to form a clot.1 Factor Va
is a cofactor to factor Xa. Factor V must be first
converted to Va before it can be applied as a
cofactor; that sequence has been left out of the
pathway for simplification purposes because it involves both negative and positive feedback loops,
culminating in thrombin activating factor V to Va.
Although the coagulation cascade can be simplified into a series of proenzyme cleavages, it is
important to recognize that these reactions can take
TABLE 1. Key Components of the Coagulation Process and Their Activation and Function
Name
Factor Iaa
Factor IIaa
Factor Xa
Factor VIIb
Tissue factorb
a
b
Component
Activation
Function
Protein formed from fibrinogen (factor I) in the
Polymerized to form a hemostatic mesh
presence of thrombin
and then cross-linked
Thrombin
Proteolytically cleaved from prothrombin (factor II) Serine protease that converts the soluble
fibrinogen strands to fibrin mesh
Stuart-Prower
Directly activated by tissue factorefactor VIIa
Cleaves prothrombin to yield active
factor
complex for the principal route of thrombin
thrombin in the common pathway
generation
Proconvertin
Activated to factor VIIa after contact with tissue
Once activated, binds and activates X,
factor in the extrinsic pathway
which converts to Xa
Thromboplastin Protein present in subendothelial tissue
High affinity receptor for coagulation
factor VII
Fibrin
Factors involved in the common pathway.
Factors that reside explicitly in the extrinsic pathway.
150 j AORN Journal
HEMOSTATIC AGENTS AND THE COAGULATION CASCADE
www.aornjournal.org
Figure 1. The coagulation cascade.
Figure 2. Augmentation of the coagulation cascade by biologic and nonbiologic topical agents.
AORN Journal j 151
August 2014 Vol 100 No 2
place in a number of places and likely involve both
known and unknown elements that may alter the
behavior of these enzymes. Additionally, the body
can express tissue factor during times of significant
stress or inflammatory conditions (eg, sepsis), resulting in intravascular coagulation (eg, disseminated intravascular coagulation).2 In short, these
coagulation pathways are much more complex in
vivo than depicted here. This basic understanding
of the coagulation cascade, however, has allowed
for significant manipulation of hemostasis both
intraoperatively and in nonsurgical settings. A
basic understanding of procoagulant agents can
help the surgical team best manage intraoperative
bleeding.
HEMOSTASIS
Mechanical pressure is the most effective method
of achieving hemostasis, and the rapid use of a digit
to control bleeding in the OR should not be underestimated. Often the surgeon then obtains proximal
OVERBEYeJONESeROBINSON
and distal control of the injured vessel and repairs
or ligates it with sutures, clips, or staples or coagulates the bleeding site with a thermal energye
based device. Although mechanical pressure is the
first-line treatment for bleeding, small vessels often
cannot be seen adequately enough to apply direct
pressure, and supplementation of the innate coagulation cascade is necessary. When needed, the
surgical team can replace missing or nonfunctioning factors with blood products. In addition,
normalization of the patient’s core temperature
promotes coagulation factor function.
Systemic Products
Various factors within the coagulation cascade are
lost when bleeding occurs (Figure 2), making replenishment necessary. Blood products remain at
the forefront for blood loss resuscitation in the
surgical setting (Figure 3). Fresh frozen plasma
replaces the majority of the factors, including all
of the vitamin Kedependent factors. It is also a
Figure 3. Augmentation of the coagulation cascade by common blood products.
152 j AORN Journal
HEMOSTATIC AGENTS AND THE COAGULATION CASCADE
Biologically active agents include thrombin or fibrin replacements, which can be used alone or in combination with nonbiologically active agents for hemostasis.
EVITHROM, SURGIFLO, and EVICEL are registered trademarks of Ethicon, Johnson & Johnson, Inc, Somerville, NJ. Thrombin-JMI is a registered trademark of Pfizer, New York, NY. GELFOAM PLUS and FLOSEAL
are registered trademarks and Artiss and TISSEEL are trademarks of Baxter Corporation, Deerfield, IL.
n
n
n
n
n
GELFOAM
PLUSÒ
FLOSEALÒ
SURGIFLOÒ
TISSEELTM
EVICELÒ
ArtissTM
n
a
n
n
n
Frozen, must
be thawed
n
Potential exposure to bloodborne viruses
Contraindicated in patients with certain
anaphylactic tendencies (immunoglobulin A deficiency)
n
n
Must be reconstituted and mixed before application
n
Foam
Gelatin sponge þ
thrombin
Gelatin þ thrombin
in a flowable source
Fibrin sealant
Liquid
n
Frozen but can remain thawed for 24 hours
n
n
Liquid
Thrombin
EVITHROMÒ
Thrombin-JMIÒ
n
n
Available forms
Class
FLOSEAL includes bovine gelatin
SURGIFLO is porcine gelatin
Two tubes: fibrinogen/factor XII and
thrombin/calcium
Fibrin is from human pooled plasma
EVITHROM includes human pooled
plasma thrombin with porcine gelatin
Thrombin-JMI includes bovine thrombin
n
Intravascular application can lead to thrombosis
Contraindications
a
Name
Nonbiologic Topical Hemostatic Agents
Other topical agents are available that do not
include specific coagulation factors but instead
create an inert scaffold that exerts direct pressure
on vessels and provides a surface for fibrin deposition and platelet adherence. These include products such as GELFOAMÒ and SURGIFOAMÒ,
among others (Table 3). These products are created
from porcine, bovine, or polysaccharide sources
and have been proposed to offer the added benefit
of activating platelets as a result of their xenographic
TABLE 2. Biologically Active Topical Hemostatic Agents
Biologic Hemostatic Agents
The active topical hemostatic agents are thrombin
derivatives. These products include thrombinimpregnated matrices such as Gelfoam PlusÒ and
flowable thrombin products such as FLOSEALÒ.
The purified thrombin directly activates native
fibrinogen to convert to fibrin. Fibrin also has been
purified and can be directly applied in several
different forms (Table 2). These products have both
fibrinogen and prothrombin to obviate the need for
any plasma-derived factors, thus directly creating a
fibrin meshwork and promoting further fibrin clot
formation. Further details on specific fibrin and
thrombin agents and their mechanisms can be
found in the articles by Burks and Spotnitz5 and
Camp6 in this issue of AORN Journal.
Comments
significant source of factor V, which is required for
thrombin formation and the initiation of the common
pathway. Cryoprecipitate offers replacement of
fibrinogen in addition to factor VIII, factor XIII,
and von Willebrand factor, which is required for
normal platelet function. Platelets also can be replaced, and this should be considered whenever
thrombocytopenia or platelet malfunction is suspected (eg, renal failure, genetic platelet disorders).
Additionally, bioengineered replacements of factors VII, VIII, and IX are an option and are most
commonly used for patients with hemophilia.
Activated factor VII is also available, but its use
remains controversial because of an increased risk
of arterial thrombosis.3,4
www.aornjournal.org
AORN Journal j 153
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August 2014 Vol 100 No 2
TABLE 3. Biologically Inactive Topical Hemostatic Agents
Name
n
n
GELFOAMÒ
SURGIFOAMÒ
Class
Available
forms
Matrixa
Mechanical
Gelatin
Sponge or
powder
Matrixa
Mechanical
Collagen
Sheets, foam,
or powder
Contraindications
n
Infection, abscess,
granuloma formation
Comments
n
n
n
n
INSTATÒ
n
n
Granuloma formation
Allergenic
n
n
n
n
n
n
n
n
n
n
n
n
n
SURGICELÒ
SURGICEL
NU-KNITÒ
AristaTM
Hemostase
MPHÒ
CoSealTM
DuraSealTM
ProgelÒ
Matrixa
Mesh
Mechanical
Oxidized
regenerated
cellulose
Matrixa
Powder
Mechanical
Polysaccharide
spheres
Hydrogel
Sealantb
Polyethylene glycol
(PEG) polymer
DERMABONDÒ Adhesiveb
Tissue adhesive
BioGlueÒ
Adhesiveb
Albumin adhesive
Applicator
adhesive
Liquid
n
n
b
n
Can cause hyperglycemia
n
n
n
n
CoSeal swells to 4 times
its initial volume
n
n
n
n
Unintentional application
n
n
Potential for glutaraldehyde
exposure
Antibodies can form against
bovine thrombin
n
n
a
Can lead to a foreign body
reaction or adhesions
Absorbs blood or fluid up to
40 times its weight
Absorption time of 4 to 6 weeks
Porcine source
Absorption time of 8 weeks
or more
More costly than the other
dry matrix alternatives
May be more efficacious
Bovine source
Absorption time of 1 to 2 weeks
Plant source
Synthetic
Absorbs quickly, < 2 days
CoSeal is completely synthetic
DuraSeal also has trilysine amine
Progel includes human serum
albumin
Glue
Includes bovine serum albumin
and glutaraldehyde
Biologically inactive scaffolding and/or matrix agents are available in numerous forms, from powders to liquids and mesh.
Tissues sealants and adhesives are nonbiologically active agents that approximate tissues without reliance on the coagulation cascade (ie, BioGlue,
CoSeal, DERMABOND, DuraSeal, Progel).
GELFOAM is a registered trademark and CoSeal is a trademark of Baxter Corporation, Deerfield, IL. SURGIFOAM, INSTAT, SURGICEL, SURGICEL NUKNIT, and DERMABOND are registered trademarks of Ethicon, Inc, Somerville, NJ. Arista is a trademark of Medafor, Minneapolis, MN. Hemostase MPH and
BioGlue are registered trademarks of CryoLife, Kennesaw, GA. DuraSeal is a trademark of Covidien, Boulder, CO. Progel is a registered trademark of
Neomend Inc, Irvine, CA.
nature.7 Additionally, these agents are storable at
room temperature and typically have a longer shelf
life than the biologically active agents, making
them cheaper and theoretically safer to use because
of their inert nature. Some of these products have
porcine or bovine origin; therefore, whenever
possible, health care providers must advise the
patient of this to allow him or her to voice any
religious or personal objections to their use.
154 j AORN Journal
Lastly, multiple tissue adhesives are available
that do not affect the coagulation cascade or
provide scaffolding and instead simply “glue”
opposing tissues together. Commonly used examples include DERMABONDÒ and BioGlueÒ.
These agents are unique in their strong adhesive
properties to native tissues without the direct
need for clot formation and have widespread
applications.8-10
HEMOSTATIC AGENTS AND THE COAGULATION CASCADE
www.aornjournal.org
Figure 4. Suggested algorithm for topical hemostatic agent use. FLOSEAL, GELFOAM, and GELFOAM PLUS
are registered trademarks and CoSeal and TISSEEL are trademarks of Baxter Corporation, Deerfield, IL.
SURGICEL is a registered trademark and OMNEX is a trademark of Ethicon, Johnson & Johnson, Inc, Somerville,
NJ. BioGlue is a registered trademark of CryoLife, Kennesaw, GA. Progel is a registered trademark of Neomend
Inc, Irvine, CA. Arista is a trademark of Medafor, Minneapolis, MN. DuraSeal is a trademark of Covidien, Boulder,
CO. Helistat is a registered trademark of Integra Life Sciences Corporation, Plainsboro, NJ.
CONCLUSION
Selecting the appropriate hemostatic agent depends
on numerous variables, and generalized approaches
have been outlined extensively elsewhere.11-17 In
general, localized bleeding is best treated mechanically with careful application of pressure;
repair or ligation of the bleeding vessel with sutures, clips, or staples; or coagulation of the bleeding
site with a thermal energyebased device followed
by augmentation of the coagulation cascade with
scaffolding/nonbiologically active agents (Figure 4).
In the case of diffuse bleeding, the surgeon should
direct his or her attention first to normalization of
body temperature, treatment of acidosis, and replacement of blood products as needed to avoid the
“bloody vicious cycle” that results in persistent
bleeding.18,19 With these issues resolved, the surgeon can use spray and flowable agents alone or
in conjunction with scaffolding agents to achieve
hemostasis.
Editor’s notes: GELFOAM, GELFOAM PLUS, and
FLOSEAL are registered trademarks of Baxter
Corporation, Deerfield, IL. SURGIFOAM and
DERMABOND are registered trademarks of Ethicon,
Inc, Somerville, NJ. BioGlue is a registered
trademark of CryoLife, Kennesaw, GA.
AORN does not endorse any commercial company’s products or services. Although any commercial products that may be referenced in this
material are expected to conform to professional medical/nursing standards, inclusion
of this material does not constitute a guarantee
or endorsement by AORN of the quality or value
of such product or of the claims made by its
manufacturer.
AORN Journal j 155
August 2014 Vol 100 No 2
References
1. Gonzalez EA, Jastrow KM, Holcomb JB, Kozar RA.
Hemostasis, surgical bleeding, and transfusion. In:
Brunicardi F, Andersen D, Billiar T, et al, eds. Schwartz’s
Principles of Surgery. 9th ed. McGraw-Hill Companies
Inc: New York, NY; 2010:67-85.
2. Levi M, van der Poll T. Hemostasis and coagulation. In:
Norton JA, Barie PS, Bollinger RR, et al, eds. Surgery:
Basic Science and Clinical Evidence. 2nd ed. Springer
ScienceþBusiness Media, LLC: New York, NY; 2008:
149-165.
3. Peyvandi F, Garagiola I, Seregni S. Future of coagulation
factor replacement therapy. J Thromb Haemost. 2013;
11(Suppl 1):84-98.
4. Simpson E, Lin Y, Stanworth S, Birchall J, Doree C,
Hyde C. Recombinant factor VIIa for the prevention and
treatment of bleeding in patients without haemophilia.
Cochrane Database Syst Rev. 2012;3:CD005011.
5. Burks S, Spotnitz WD. Hemostats, sealants, and adhesives: a guide to safety and use. AORN J. 2014;100(2):
160-176.
6. Camp MA. Hemostatic agents: a guide to safe practice
for perioperative nurses. AORN J. 2014;100(2):131-147.
7. Schonauer C, Tessitore E, Barbagallo G, Albanese V,
Moraci A. The use of local agents: bone wax, gelatin,
collagen, oxidized cellulose. Eur Spine J. 2004;13
(Suppl 1):S89-S96.
8. Hallock GG. Expanded applications for octyl-2cyanoacrylate as a tissue adhesive. Ann Plast Surg.
2001;46(2):185-189.
9. Luk A, David TE, Butany J. Complications of Bioglue
postsurgery for aortic dissections and aortic valve replacement. J Clin Pathol. 2012;65(11):1008-1012.
10. Jones EL, Burlew CC, Moore EE. BioGlue hemostasis
of penetrating cardiac wounds in proximity to the left
anterior descending coronary artery. J Trauma Acute
Care Surg. 2012;72(3):796-798.
11. Spotnitz WD. Hemostats, sealants, and adhesives: a practical
guide for the surgeon. Am Surg. 2012;78(12):1305-1321.
12. Spotnitz WD, Burks S. Hemostats, sealants, and adhesives III: a new update as well as cost and regulatory
considerations for components of the surgical toolbox.
Transfusion. 2012;52(10):2243-2255.
13. Achneck HE, Sileshi B, Jamiolkowski RM, Albala DM,
Shapiro ML, Lawson JH. A comprehensive review of
topical hemostatic agents: efficacy and recommendations
for use. Ann Surg. 2010;251(2):217-228.
14. Sileshi B, Achneck H, Ma L, Lawson JH. Application of
energy based technologies and topical hemostatic agents
in the management of surgical hemostasis. Vascular.
2010;18(4):197-204.
156 j AORN Journal
OVERBEYeJONESeROBINSON
15. Emilia M, Luca S, Francesca B, et al. Topical hemostatic
agents in surgical practice. Transfus Apher Sci. 2011;
45(3):305-311.
16. Gabay M, Boucher BA. An essential primer for understanding the role of topical hemostats, surgical sealants,
and adhesives for maintaining hemostasis. Pharmacotherapy. 2013;33(9):935-955.
17. Schreiber MA, Neveleff DJ. Achieving hemostasis with
topical hemostats: making clinically and economically
appropriate decisions in the surgical and trauma settings.
AORN J. 2011;94(5):S1-S20.
18. Scalea TM. Hemostatic resuscitation for acute traumatic
coagulopathy. Scand J Trauma Resusc Emerg Med. 2011;
19:2.
19. Kashuk JL, Moore EE, Millikan JS, Moore JB. Major
abdominal vascular traumada unified approach. J Trauma.
1982;22(8):672-679.
Douglas M. Overbey, MD, is a surgical resident
PGY2 at the University of Colorado Department
of Surgery, Aurora, CO. Dr Overbey has no
declared affiliation that could be perceived as
posing a potential conflict of interest in the
publication of this article.
Edward L. Jones, MD, MS, is a surgery resident PGY5 at the University of Colorado Department of Surgery, Aurora, CO. Dr Jones has no
declared affiliation that could be perceived as
posing a potential conflict of interest in the
publication of this article.
Thomas N. Robinson, MD, is an associate professor of surgery at the University of Colorado
Department of Surgery, Aurora, CO. As a consultant for Covidien and ConMed and as a
recipient of grant money paid to his institution
by Medtronics and Storz, Dr Robinson has declared affiliations that could be perceived as
posing potential conflicts of interest in the publication of this article.
EXAMINATION
1.7
CONTINUING EDUCATION
How Hemostatic Agents Interact
With the Coagulation Cascade
www.aorn.org/CE
PURPOSE/GOAL
To provide the learner with knowledge specific to surgical hemostasis and the
coagulation cascade.
OBJECTIVES
1.
2.
3.
4.
Discuss surgical hemostasis.
Describe the normal coagulation cascade.
Identify blood products for intraoperative blood loss resuscitation.
Discuss hemostatic agents.
The Examination and Learner Evaluation are printed here for your convenience. To receive continuing education credit, you must complete the online
Examination and Learner Evaluation at http://www.aorn.org/CE.
QUESTIONS
1.
2.
3.
The goals of surgical hemostasis are to
1. limit blood loss.
2. preserve the patient’s hemodynamic stability.
3. provide operative field visibility.
a. 1 and 2
b. 1 and 3
c. 2 and 3
d. 1, 2, and 3
Coagulation, which culminates in fibrin plug formation, occurs as a result of a complex process
known as
a. hemostasis.
b. the coagulation cascade.
c. the bleeding cascade.
d. homeostasis.
A variety of surgical hemostatic agents are available that assist in either thrombin formation or
fibrin formation or that provide additional scaffolding to which platelets and a clot can adhere.
a. true
b. false
Ó AORN, Inc, 2014
4.
The intrinsic pathway of the coagulation cascade
involves factors that are present in normal plasma
and thus does not require a vascular surface to
form fibrin.
a. true
b. false
5.
The extrinsic pathway begins when a vascular
injury ___________________on the damaged
subendothelial surface of the blood vessel.
a. creates a rough surface
b. activates a neural message in the brain
c. exposes platelet tissue factor
6.
Mechanical methods that can be used to achieve
hemostasis include
1. using a digit to apply pressure and control
bleeding.
2. repairing or ligating bleeding vessels using
sutures, clips, or staples.
3. coagulating the bleeding site with thermal
energyebased devices.
August 2014
Vol 100
No 2 AORN Journal j 157
CE EXAMINATION
August 2014 Vol 100 No 2
4.
injecting a variety of hemostatic agents.
a. 3 and 4
b. 1, 2, and 3
c. 2, 3, and 4
d. 1, 2, 3, and 4
7.
When supplementation of the innate coagulation
cascade is necessary, the surgical team ________
1. can replace missing factors with blood
products.
2. can replace nonfunctioning factors with
blood products.
3. should ensure normalization of the patient’s
core temperature.
a. 1 and 3
b. 1 and 2
c. 1, 2, and 3
8.
The majority of the coagulation factors, including
all of the vitamin Kedependent factors and factor
V, can be replaced by infusion of
a. bioengineered replacement factors.
b. fresh frozen plasma.
c. cryoprecipitate.
d. platelets.
9.
10.
158 j AORN Journal
Topical agents that create an inert scaffold, which
exerts direct pressure on vessels and provides a
surface for fibrin deposition and platelet adherence, are created from ____________________
sources.
1. porcine
2. human
3. polysaccharide
4. equine
5. feline
6. bovine
a. 1, 3, and 6
b. 2, 4, and 6
c. 2, 3, 5, and 6
d. 1, 2, 3, 4, 5, and 6
Multiple ______________ are available that do
not affect the coagulation cascade or provide
scaffolding and instead simply “glue” opposing
tissues together.
a. tissue pastes
b. fibrin plugs
c. common pathway activators
d. tissue adhesives
LEARNER EVALUATION
1.7
CONTINUING EDUCATION PROGRAM
How Hemostatic Agents Interact
With the Coagulation Cascade
T
his evaluation is used to determine the extent to
which this continuing education program met
your learning needs. The evaluation is printed
here for your convenience. To receive continuing
education credit, you must complete the online
Examination and Learner Evaluation at http://www
.aorn.org/CE. Rate the items as described below.
OBJECTIVES
To what extent were the following objectives of this
continuing education program achieved?
1. Discuss surgical hemostasis.
Low 1. 2. 3. 4. 5. High
2. Describe the normal coagulation cascade.
Low 1. 2. 3. 4. 5. High
3. Identify blood products for intraoperative blood loss
resuscitation.
Low 1. 2. 3. 4. 5. High
4. Discuss hemostatic agents.
Low 1. 2. 3. 4. 5. High
CONTENT
5. To what extent did this article increase your
knowledge of the subject matter?
Low 1. 2. 3. 4. 5. High
6. To what extent were your individual objectives
met? Low 1. 2. 3. 4. 5. High
7. Will you be able to use the information from this
article in your work setting? 1. Yes 2. No
Ó AORN, Inc, 2014
www.aorn.org/CE
8. Will you change your practice as a result of reading
this article? (If yes, answer question #8A. If no,
answer question #8B.)
8A. How will you change your practice? (Select all that
apply)
1. I will provide education to my team regarding
why change is needed.
2. I will work with management to change/
implement a policy and procedure.
3. I will plan an informational meeting with
physicians to seek their input and acceptance
of the need for change.
4. I will implement change and evaluate the
effect of the change at regular intervals until
the change is incorporated as best practice.
5. Other: ________________________________
8B. If you will not change your practice as a result of
reading this article, why? (Select all that apply)
1. The content of the article is not relevant to my
practice.
2. I do not have enough time to teach others
about the purpose of the needed change.
3. I do not have management support to make a
change.
4. Other: ________________________________
9. Our accrediting body requires that we verify
the time you needed to complete the 1.7 continuing education contact hour (102-minute)
program: _______________________________
August 2014
Vol 100
No 2 AORN Journal j 159