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newsletter 6/21/12 12:02 PM Page 8


Instructions For
Continuing Nursing
Education Contact Hours



Disseminated Intravascular
Coagulation and Implications
For Medical-Surgical Nurses

DIC and Implications for

Medical-Surgical Nurses
Deadline for Submission:
August 31, 2014

To Obtain CNE Contact Hours

1. For those wishing to obtain CNE contact
hours, you must read the article and complete the evaluation through AMSNs
Online Library. Complete your evaluation
online and print your CNE certificate
immediately, or later. Simply go to
2. Evaluations must be completed online by
August 31, 2014. Upon completion of the
evaluation, a certificate for 1.0 contact
hour(s) may be printed.

Member: FREE

Regular: $20

The purpose of this continuing nursing education
article is to increase the awareness of disseminated
intravascular coagulation (DIC) in nurses and other
health care professionals. After studying the information presented in this article, you will be able to:
1. Define disseminated intravascular coagulation
2. Discuss symptoms and diagnosis of the patient
with DIC.
3. Identify the medical-surgical nurses role in the
care of the patient with DIC.

Note: The author, editor, and education director

reported no actual or potential conflict of interest in relation to this continuing nursing education article.
This educational activity has been co-provided by
AMSN and Anthony J. Jannetti, Inc.
Anthony J. Jannetti, Inc. is a provider approved by
the California Board of Registered Nursing, provider
number CEP 5387. Licensees in the state of CA must
retain this certificate for four years after the CNE
activity is completed.
Anthony J. Jannetti, Inc. is accredited as a
provider of continuing nursing education by the
American Nurses Credentialing Centers Commission
on Accreditation.
This article was reviewed and formatted for contact hour credit by Rosemarie Marmion, MSN, RN-BC,
NE-BC, AMSN Education Director. Accreditation status
does not imply endorsement by the provider or ANCC
of any commercial product.

Tammeshin Frazier
The patients platelets are 50,000, and
were giving heparin. Something seems
amiss, and I do not understand what is
happening with this patient.
Although this scenario may sound
absurd, a logical and plausible explanation
exists. Disseminated intravascular coagulation (DIC) is the explanation, which
affects approximately 1% of hospitalized
patients and 30% to 50% of patients with
sepsis (Becker, Kumar, Shaaban, & Wira,
2009). DIC is not a new or rare phenomenon but a syndrome that has been
around for some time. At first discovery,
the pathophysiology was elusive and hard
to understand; however, with recent
advances in medicine and diagnostic technologies, hematologists are not only
understanding the condition, but they can
effectively diagnose and treat it.

What Is DIC?
DIC, also known as consumptive
coagulopathy and defibrination syndrome, is an acquired syndrome secondary to tissue damage, vessel damage, or
infections (LeMone, Burke, & Bauldoff,
2010). Table I lists common conditions
that precipitate the development of DIC.

Table 1.
Conditions that Trigger the DIC Process

Physiological Results
of Conditions
Tissue damage

Trauma: Burns, gunshot wounds, motor vehicle
accidents, head injuries
Obstetric complications: HELLP, abruption placenta,
amniotic fluid embolus
Cancer: Acute leukemia, adenocarcinoma
Fat emboli

Vessel damage

Aortic aneurysm, acute glomerulonephritis, hemolytic

uremic syndrome


Severe bacterial, viral, parasite, or rickettsial infection


Source: Adapted from LeMone et al., 2010.

Present in the syndrome is an inappropriate activation of the clotting cascade, leading to hypercoagulation and then bleeding
once the clotting factors are consumed.
Unless the disorder is detected early and
the initiating cause is corrected, multiple
system organ failure due to microembolie
will result (Becker et al., 2009).
DIC is classifiable as either overt or
non-overt. Overt DIC is a noncompensatory syndrome with a high rate
of mortality and organ failure. Overt DIC
is associated with sepsis, severe infections,
HELLP (hemolysis, increased liver
enzymes, and decreased platelet count),
liver failure, and obstetrical complications.
The overt form of DIC is recognizable by
obvious bleeding and a symptomatic
patient. Non-overt DIC is compensatory
or chronic and is associated with blood
dyscrasias, such as anemias, leukemias, and
malignancies (Somashekhar, Kadamba, &
Wakodkar, 2008). In compensatory (nonovert) DIC, the patients hematological
system is continously or intermittently
exposed to small amounts of tissue factors. The patient may be asymptomatic,
and the syndrome may only be noticeable
in laboratory studies (Becker et al., 2009).

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Volume 21 Number 3/4

Table 2.
ISTH Diagnostic Scoring System for DIC

Risk assessment Does the patient have an underlying disorder (sepsis, trauma,
obstetric emergency) compatible with DIC?
Platelet count
coagulation tests D-dimer and Fibrin degradation products (FDPs)
PT and aPTT

Platelet count: Greater than 100 = 0 points, less than 100 = 1

point, less than 50 = 2 points
Elevated fibrin marker: No elevation = 0 points, moderate increase
= 2 points, strong increase = 3 points
Prolonged PT: Less than 3 seconds = 0 points, greater than 3 but
less than 6 seconds = 1 point, greater than 6 seconds = 2 points
Fibrinogen level: Greater than 1 g/L = 0 points, less than 1 g/L = 1

Calculate score

Greater than or equal to 5 = compatible with overt DIC, repeat

scoring daily
Less than 5 = suggestive of non-overt DIC

Source: Levi et al., 2009.

The Pathogenesis of DIC

vating the clotting cascade. The inflammation reduces the plasma levels of
antithrombin III, a serine protease
inhibitor, causing an increase in fibrin clot
formation within the intravascular system
(Wei, Yan, Carrell, & Zhou, 2009).
Normally, the body is able to break down
fibrin clots by a process known as fibrinolysis, but in DIC, the process is impaired
due to high levels of the principle inhibitor
of the fibrinolytic system: plasminogenactivator inhibitor type 1 (PAI-1). As a
result, fibrin continues to be deposited in
the intravascular system and thrombosis
form within small and midsize blood ves-

The pathogenesis of DIC can be easily stated as impaired coagulation, suppressed fibrinolysis, and inflammation that
occur prior to the onset of manifestations. The defining pathophysiological
process is the amplification of procoagulation factors, which overwhelms the anticoagulant mechanisms. In essence, the
bodys coagulation system is overworked
in response to a triggering factor that has
activated the clotting cascade (LeMone et
al., 2010).
The systemic response to an injury,
infection, or condition triggers inflammation in the intravascular system, thus acti-

sels, leading to decreased blood flow to

vital organs, such as the kidneys.
The process of thrombosis occurrence is mediated by key proinflammatory
cytokines, interleukin-6 (IL-6), and tumor
necrosis factor- (TNF-). As deposits of
fibrin in the intravascular system continue
to occur, platelets and coagulation factors
are consumed, leading to a global deficiency of clotting factors and predisposing
the body to bleeding. In essence, clotting
is stimulated, and when clotting factors
are consumed, bleeding starts (Levi &
Schmaier, 2009; Somashekhar et al., 2008).
The occurrence of either oozing or frank
bleeding is often the first sign that DIC
has developed. Figure 1 shows the
Generalized Schwartzman Reaction
(GSR) progression of sepsis-induced DIC.

Diagnosis and Treatment

A definitive test for DIC does not
exist; diagnosis is made after careful analysis of laboratory studies, objective scoring, and repeat assessment of coagulation
factors. The International Society for
Thrombosis and Haemostasis (ISTH)
developed a DIC scoring system to aid in
the diagnosing and confirmation of the
syndrome (Levi, Toh, Thachil, & Watson,
2009). The tool provides an objective
measurement with 91% sensitivity and
97% specificity of diagnosing DIC. The
ISTH system should be used throughout
the care of the patient (see Table 2).
Specific laboratory assays to diagnose
DIC include prothrombin time (PT), activated partial thromboplastin time (aPTT),
platelet count, fibrinogen measurement,
and fibrin D-dimer (FDP). PT and aPTT
are prolonged in approximately half of

Figure 1.
Pathophysiology of Sepsis-Induced DIC

Accumulation of
micro thrombi

Platelet aggregation

Vascular Occlusion

Apoptosis (regulated cell

death) varies in degree


Fibrinolysis inhibited
Accumulation of
Endothelial injury

Source: Adapted from Slofstra, Cate, & Spek, 2006.

Matters_Summer_12_Matters! newsletter 6/21/12 12:02 PM Page 10

Academy of Medical-Surgical Nurses

Table 3.
Treatment Approaches

Basic Treatment

Advanced Treatment

Monitor vital signs

Monitor lab work and anticoagulation factors
Determine presence of risk factors and patients DIC score
per ISTH
Assess for signs of bleeding or possible thrombi formation
Correct hypovolemia if present
Identify primary factor and ensure proper treatment is in
Advocate for patient care, hematology should be consulted
and possible transfer to ICU if patient is critical (overt DIC)
Antibiotics for infections and sepsis
Routine platelet and coagulation factor replacement is not
indicated in acute DIC

Administration of unfractionated heparin (UFH) weightbased

Lovenox (Enoxaparin) or other low molecular weight
Fresh frozen plasma if the PT or aPTT is prolonged and clinically relevant
Platelet transfusion, if count is less than 50,000 and active
bleeding noted, or prior to an invasive procedure
Recombinant activated human protein C
Continue treatment of the primary disorder
Severe bleeding can be treated with lysine analogues (such
as tranexamic acid)

Source: Adapted from Becker et al., 2009; Levi et al., 2009.

DIC cases. Prolonged coagulation factors

reflect the consumption and depletion of
various coagulation agents, which lead to
the measurement of Factors V and VII.
FDP measures the breakdown and lysis of
fibrinogen. Laboratory assays are done
frequently in the attempt to capture and
understand the dynamic environment of
the DIC.
Diagnosis and treatment of DIC
occur with the collaboration of clinical
and laboratory information. ISTH consistently states that the key to DIC treatment is specific and vigorous treatment of
the underlying disorder; not treating the
primary condition leads to increased
mortality. Most cases of DIC syndrome
resolve spontaneously once the underlying condition is managed (Levi &
Schmaier, 2009).
The patients plan of care is individualized depending on the initiating factor
that caused the DIC, whether it is acute
(overt) or chronic (non-overt) DIC;
therefore, no single course of action
exists (see Table 3). Platelets may or may
not be given depending on the clinical
condition and laboratory results of the
patient. Heparin or low molecular heparin
is ordered when thrombosis is apparent
and dominating.

Medical-Surgical Nurses
Response to DIC
DIC is a dynamic condition that
changes rapidly and contributes to
increased patient mortality and morbidity.
The medical-surgical nurse must be

Table 4.
Clinical Manifestations of DIC

Spontaneous bruising
Decline in organ function
Low blood pressure
Bleeding from more than one site (gastrointestinal, mucous membranes, urinary,
and venipuncture sites)
Bleeding ranges from minimal to severe hemorrhaging
Source: Adapted from Smeltzer, Bare, Hinkle, & Cheever, 2009.

knowledgeable of the risk factors, how

the risk factors trigger DIC, and the
pathophysiological processes involved in
DIC. The medical-surgical nurse responds
first by identifying patients at risk and
then being alert for the subtle changes in
the patients condition that could signal
the development of DIC (Levi & Schmaier,
2009). Medical-surgical nurses should be
vigilant about identifying manifestations in
patients at risk for DIC (see Table 4) and
should also monitor laboratory values,
such as a complete blood count (CBC)
for decreases in red blood cells, hemoglobin, hematocrit, and platelets.
Medical-surgical nurses must practice
aseptic care and advocate for patients and
themselves. A transfer to a critical care unit
is needed for a critical, unstable patient with

overt DIC. In developing the plan of care

for the patient, it is important not to focus
on curing or alleviating DIC, but eliminating
the underlying causative factor. Successful
treatment or management of the initiating
factor will eradicate or control DIC syndrome. Nursing interventions are directed
at the primary illness and DIC collectively.

DIC is relevant to the medicalsurgical specialty because it is the one
specialty outside of critical care that cares
for patients with multiple diagnoses, susceptibilities, and co-morbidities. A patient
can present with and/or develop DIC at
any time, and medical-surgical nurses
need to assess patients at risk for this lifethreatening condition and be prepared to
advocate for the appropriate level of care.

Matters_Summer_12_Matters! newsletter 6/21/12 12:02 PM Page 11

Becker, J.U., Kumar, A., Shaaban, H.S., & Wira, C.R. (2009). Disseminated
intravascularcoagulation in emergency medicine. Retrieved from
LeMone, P., Burke, K.M., & Bauldoff, G. (2010). Medical-surgical nursing: Critical
thinking in patient care (5th ed.). Upper Saddle River, NJ: Pearson.
Levi, M., & Schmaier, A. (2009). Disseminated intravascular coagulation.
Retrieved from
Levi, M.,Toh, C.H.,Thachil, J., & Watson, H.G. (2009). Guidelines for the diagnosis and management of disseminated intravascular coagulation.
British Journal of Haemotology, 145(1), 24-33. doi:10.1111/j.13652141.2009.07600.x
Slofstra, S.H., Cate, H., & Spek, C.A. (2006). Low dose endotoxin priming is
accountable for coagulation abnormalities and organ damage
observed in the Shwartzman reaction. A comparison between a single dose endotoxemia model and a double hit endotoxin induced
Shwartzman reaction. Thrombosis Journal, 4(13), 1-7. doi:10.1186/14779560-4-13
Smeltzer, S.C., Bare, B.G., Hinkle, J.L., & Cheever, K.H. (2009). Brunner &
Suddarths textbook of medical-surgical nursing (12th ed.). Philadelphia;
Lippincott Williams & Wilkins.
Somashekhar, M., Kadamba, P.S., & Wakodkar, M. (2008). Chronic disseminated intravascular coagulation presenting as a renal mass. Journal of
Indian Association of Pediatric Surgeons, 13(4), 144-146.
Wei, Z.,Yan,Y., Carrell, R.W., & Zhou, A. (2009). Crystal structure of protein
Zdependent inhibitor complex shows how protein Z functions as a
cofactor in the membrane inhibition of factor X. Journal of the
American Hematological Society: Blood, 114(17), 3662-3667.
Additional Reading
Levi, M. (2010). Disseminated intravascular coagulation or extended
intravascular coagulation in massive pulmonary embolism. Journal of
Thrombosis and Haemostasis, 8(7), 1475-1476. doi:10.1111/j.15387836.2010.03891.x

Tammeshin Frazier, RN, BSN, CMSRN, is a Travel Nurse,

Randstad HealthCare, Baltimore, MD. She is a member of the
MedSurg Matters! Editorial Committee.

Volume 21 Number 3/4

Defining a Healthy Work Environment

continued from page 1

Working with Clinically Competent Nurses

Clinically competent nurses will have degrees, national specialty certifications, and peer reinforcement. When a nurse lacks
competent co-workers, it hurts both quality patient care and job

Positive Nurse/Physician Relationships

A good relationship between nurses and physicians is essential for improving patient care.The work of nurses and physicians
overlaps more and more, and these professionals must recognize
the other is bringing an important facet of care to the table.

Autonomous Nursing Practice

A nurse must have the freedom to act on what he or she
knows to provide the best patient care. Inherent in this is the
need for the nurse to be knowledgeable to know what best
practice is through evidence-based practice and continuing education.

Control Over Nursing Practice

When nurses have control over their practice, they are
asked for and provide feedback and input in decision-making,
policies, and personnel issues. The enabling structure must be
visible, viable, and supported (Kramer et al., 2008).

Supportive Nurse Managers

Nurse-managers are very involved in many levels, working
with budgets, managing staff, placing patients, and more. Because
of this, their role is pivotal in creating (or hindering) a HWE
through each of these essentials. The nurse-manager must support his or her nurses.

Adequacy of Staffing
Kramer and colleagues (2008) reported that the perception
of adequate staffing is the measurable factor in creating a HWE.
Nurses must perceive that they have the support of adequate
staffing to help them better perform their duties. Thus administration should confer with nurses on staffing standards.

A Culture of Concern for Patients

One Value of Membership:

Contact Hours
Membership in AMSN is $84 per year. AMSN
members get free contact hours from journal and
newsletter articles. Contact hours often total over 20
per year. To receive all the contact hours provided in
2011 without an AMSN membership, you would spend
approximately $285. If you have an AMSN membership,
youd have an extra $201 in your pocket. This does
cause one problem what are you going to do with all
your savings?
Just another way AMSN is supporting you!

Shared values and beliefs must be reflected in behaviors.

Each employee plays a role in communicating and reinforcing the
culture.The concern is for both the patients and the nurses who
care for them.
Inserted in this copy of MedSurg Matters! is a removable
poster explaining the characteristics of a healthy work environment. Please use it to engage conversation in your workplace by
displaying it on your unit, in your break room, rest room, or in
your cafeteria.
Be sure to visit to learn more about
how you can help create a healthy work environment in your
workplace. You have the support of AMSN with you!
Kramer, M., Schmalenberg, C., & Maguire, P. (2008). Essentials of a magnetic
work environment. Nursing2008, 38(1), 23-27.

Melissa Patterson is Customer Service Coordinator, Academy

of Medical-Surgical Nurses (AMSN), Pitman, NJ.

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.