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CNE
NURSING
EDUCATION
Disseminated Intravascular
Coagulation and Implications
For Medical-Surgical Nurses
Fees
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Regular: $20
Objectives
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
(DIC).
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.
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
Conditions
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
Infections
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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Table 2.
ISTH Diagnostic Scoring System for DIC
Risk assessment Does the patient have an underlying disorder (sepsis, trauma,
obstetric emergency) compatible with DIC?
Laboratory
Platelet count
coagulation tests D-dimer and Fibrin degradation products (FDPs)
Fibrinogen
PT and aPTT
Scoring
Calculate score
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-
Figure 1.
Pathophysiology of Sepsis-Induced DIC
Accumulation of
micro thrombi
Hemorrhage
Platelet aggregation
Vascular Occlusion
Microvasculature
necrosis
Fibrinolysis inhibited
Accumulation of
neutrophils
Endothelial injury
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Table 3.
Treatment Approaches
Basic Treatment
Advanced Treatment
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
10
Table 4.
Clinical Manifestations of DIC
Spontaneous bruising
Petechiae
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.
Conclusion
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.
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References
Becker, J.U., Kumar, A., Shaaban, H.S., & Wira, C.R. (2009). Disseminated
intravascularcoagulation in emergency medicine. Retrieved from
http://emedicine.medscape.com/article/779097-overview
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 http://emedicine.medscape.com/article/199627
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.
doi:10.4103/0971-9261.44767
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.
doi:10.1182/blood-2009-04-210021
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
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.
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