Disseminated Intravascular Coagulation

Nurses can facilitate improved outcomes by understanding factors and anticipating changes in patients.

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Learning Scope #434
1 contact hour
Expires May 16, 2015

You can earn 1 contact hour of continuing education credit in three ways: 1) Grade and certificate are available immediately after taking the online test. 2) Send the answer sheet (or a photocopy) to ADVANCE for Nurses, Learning Scope, 2900 Horizon Dr., King of Prussia, PA 19406. 3) Fax the answer sheet to 610-278-1426. If faxing or mailing, allow 30 days to receive certificate or notice of failure. A certificate of credit will be awarded to participants who achieve a passing grade of 70% or better.

Merion Matters is an approved provider of continuing nursing education by the Pennsylvania State Nurses Association (No. 221-3-O-09), an accredited approver by the American Nurses Credentialing Center's Commission on Accreditation.

Merion Matters is also approved as a provider by the California Board of Registered Nursing (No. 13230) and by the Florida Board of Nursing (No. 3298).

The goal of this continuing education offering is to provide the latest information to nurses about disseminated intravascular coagulation (DIC). After reading this article, you will be able to:

1. List specific blood factors related to the development of DIC.
2. Identify risk factors, disease processes and signs and symptoms associated with the development of DIC.
3. Discuss available treatment options and nursing implications for care of the patient with DIC.

  • The author has completed a disclosure form and reports no relationships relevant to the content of this article.

The human body is a masterpiece of interactive feedback mechanisms that serve to maintain homeostasis amid chaos in both internal and external environments. Among defense mechanisms that function to maintain stability are the blood factor components involved with coagulation and fibrinolysis in the process of hemostasis. The complex processes of protein-clotting factors, platelets, electrolyte reactions and thrombin formation are normally activated and down-regulated based on the interaction of tissue and cellular structures unique to the human body. And, while the normal localized action of clot formation to protect the individual from cuts and scrapes occurs in a seemingly effortless fashion, widespread activation of the coagulation process can have devastating outcomes when the course goes awry.

Inflammation and coagulation are interrelated functions that protect the individual from infectious organisms and massive hemorrhage. Pro-inflammatory mediators can activate the clotting cascade. Activated protein C and protein S interact in the process to inhibit thrombin, thus halting excessive clot formation. In the disease states where these mechanisms are activated and become uncontrolled, systemic intravascular coagulation can occur, leading to microvascular clot formation, organ dysfunction and tissue death.

This disease state, known as disseminated intravascular coagulation (DIC), is an acquired condition often associated with severe illnesses such as sepsis, trauma, malignancies and obstetrical complications. Also known as consumptive coagulopathy, defibrination syndrome or acute intravascular coagulation, DIC is an emergent condition associated with high mortality rates due to acute organ dysfunction and bleeding.1 While it has a poorly documented incidence associated with many disease presentations, it is estimated to be the cause of up to 27% of all bleeding disorders.2 DIC affects approximately 1% of hospitalized individuals with an incidence of up to 50% in patients with sepsis.3

Intrinsic & Extrinsic Pathways

To understand the pathology of DIC, normal clotting mechanisms must first be considered. Clotting factors circulate in normal blood flow in the inactivated state. The intact endothelial cell layer that lines blood vessels usually lacks the activated form of clotting factors and those that promote formation of thrombin. Blood clots as a result of activation of these factors through the intrinsic and extrinsic pathways. Activation of either course leads to a common pathway with the final step being the deposition of the fibrin mesh to form a stable clot.

The intrinsic pathway can be activated through mechanisms of injury to blood vessels and endothelial cell layer exposure to activated serum clotting factors. Components involved in the clotting mechanism such as factor XII are attracted to the area and begin a cascade of events leading to activated platelet aggregation, thrombin formation, fibrinogen conversion and a fibrin mesh deposition, trapping platelets to form a more stable clot.

Currently thought to be of greater importance and observed more frequently in disease states, the extrinsic pathway is activated via tissue factor release from interactions at the endothelial level and entry of activated thromboxane into the circulation, promoting thrombin generation through direct and indirect mechanisms. This process, also mediated in sepsis via the inflammatory response, is a complex mechanism that serves to place thrombin generation at the center of the coagulation cascade. Both intrinsic and extrinsic mechanisms merge at the common pathway where the interaction of calcium, phospholipids and factor X support thrombin generation and a further cascade of events leading to fibrin deposition and a cohesive, stable clot.

Fibrinolysis

Integral to the process of healing and clot dissolution is fibrinolysis, which is involved in vessel wall repair and resumption of normal blood flow. When a vessel is damaged, a localized vessel wall contraction occurs at the site of injury to help limit bleeding. This is a protective mechanism. As the precise mechanism of healing with coagulation evolves, fibrinolysis through the conversion of plasminogen to plasmin occurs and the clot is dissolved to restore the normal blood flow through the vessel.

This precise interaction of plasma proteins, blood cell types, activated factors, platelets, thrombin, clot formation and the ensuing breakdown contribute to the unique hemostatic process. Endogenous tissue plasminogen activator (tPA) is activated in the normal coagulation pathway from substances in the formed blood clot, which subsequently leads to total clot dissolution. Fibrin regulates its own clot degradation by allowing both TPA and plasmin to bind at its surface, which promotes further breakdown.

An Uncontrolled Process

In DIC, the process of clot formation and degradation is an accelerated and uncontrolled process leading to consumption of circulating clotting factors and an increase in fibrin degradation products. This systemic and simultaneously occurring viscous circle of events leads to excessive bleeding despite clot formation.

As fibrin degradation products (FDPs) circulate, an anticoagulant effect occurs, which serves to limit more clot formation. As more clotting factors are consumed, there are limited sources available for clot formation, leading to excessive bleeding, which can be both external and internal. Occurring simultaneously with clot accumulation at capillary levels, tissue oxygenation decreases, leading to organ damage and cellular death if the process remains uncontrolled. Microvascular clot formation plugs essential conduits for blood transportation to tissues and organs, causing ischemia from a decrease in oxygen delivery to cells, which limits their normal function.

The organs most commonly affected by this process are lungs and kidneys, followed by the brain, heart, liver, spleen, adrenals, pancreas and gut.4 As a result, organ function declines and overt signs and symptoms of deterioration may become apparent.

Causes of DIC

DIC does not occur in isolation and is a pathologic process associated with other disease states, most common of which are noted in Table 1. These conditions have the ability to induce the coagulation cascade, setting the process of clot formation and degradation in motion and necessitating treatment interventions to halt a complicated course.

Sepsis, triggered by an infection from bacterial, viral, fungal or parasitic organisms, results in the circulation of pro-inflammatory mediators, which can stimulate tissue factor release and activation of the extrinsic coagulation pathway. DIC as a result of severe sepsis has an incidence as high as 50%.5,6

Complications of pregnancy, such as retained fetal parts, amniotic fluid embolism, preeclampsia, placenta previa and placenta abruption, have been associated with DIC. In developed countries, up to 5% of obstetric patients with DIC have a precipitating peripartum emergency that activates the process.7,8

Other factors associated with the development of DIC may be direct trauma from an insult to the vessel wall or the result of the activated inflammatory process related to burn injuries or toxic exposure that may trigger the clotting cascade.

Release of pro-inflammatory mediators, such as tissue necrosis factor in patients with cancer, may lead to DIC. Patients with various forms of leukemia often have a higher incidence of DIC, which is a major complicating factor in treating the underlying disease. The overall clotting process is a result of the enhanced production of thrombin.9 Assessment of therapies, including over-the-counter use of medications such herbals or NSAIDs for pain, with the oncology patient should alert the nurse to additional bleeding risks.10

Ultimately, treating the underlying disease condition should be the first priority to avoid the complications of DIC.9 Successful treatment of the underlying condition, such as with sepsis, often is all that is required to stem the tide of a coagulation catastrophe.

Signs & Symptoms

The most obvious sign of a coagulation disorder is overt bleeding, which can be from old puncture sites or trauma.6 But often bleeding is not so overt and may be internal, forming hematomas, causing intense pain or exhibited as areas of ecchymosis or petechiae.

Overt bleeding can cause acute changes in hemodynamics as a result of hypovolemia, which further decreases tissue perfusion, leading to an increase in hydrogen ion production, lactic acid accumulation and depletion of the vital energy components needed for cellular function.

Concern should be raised when invasive puncture sites, which have been dry and intact, start to ooze blood or pulmonary function changes occur with a need for increased oxygen demands.

Arterial blood gases may signal a compensatory respiratory alkalosis and an increased respiratory rate (tachypnea) in an attempt to decrease hydrogen ion concentration from hypoxia striking at the tissue level.

Tachycardia can signal intravascular volume changes and serve as a compensatory measure to increase oxygen delivery to tissues.

Decreased urine output may signal a decreased perfusion to the kidneys as a result of tissue injury and clotted capillary beds.

Neurologic changes with somulence or a decreased level of consciousness can be precipitated by hemorrhagic changes or lack of oxygen delivery to the brain.

Results of a thorough nursing assessment, looking for trends in hemodynamics, respiratory requirements for oxygenation and neurologic function as well as evidence of overt bleeding or skin abnormalities, can be signals to initiate early interventions to halt the process.

Laboratory Tests

While there is not one specific test to identify DIC, the overall clinical picture must be considered with supportive lab values when determining a diagnosis. Changes in the underlying condition often are dynamic and treatment should be based on the clinical assessment picture and review of lab value trends. Lab tests associated with DIC must reflect the hemostatic function as well as the overall dynamic clinical picture.9 See Table 2.

Platelet Count

A clear downward trend in the platelet count is a signal for a number of conditions, including DIC. While not the only measure to consider, it has been associated with up to 98% of all cases.9 Decreasing platelet values are a result of excess thrombin production, which induces platelet aggregation and consumption in an effort to form a clot.

Fibrin Degradation Products

Enhanced fibrinolytic activity as measured with FDPs or D-dimers are additional markers of clot degradation. High values in association with a clinical picture may indicate DIC. Although not specific to DIC, D-dimers also can be elevated in conditions such as trauma, surgery or venous thrombotic events.9 FDPs are remnants of free fibrin or fibrinogen breakdown while D-dimers are clot remnants with multiple fibrin strands.11

PT, INR & aPTT

Generally speaking, prothrombin time (PT), international normalization ratio (INR) and activated partial thromboplastin time (aPTT) often are prolonged in DIC, with more than 50% of all cases showing elevated levels at some point in the disease.9 This may result from many factors, including liver function abnormalities, vitamin K deficiency or massive bleeding. These lab values must be monitored and considered with the overall clinical disease process.

Fibrinogen

Levels of fibrinogen can vary throughout the disease course and often are not clear markers for DIC. One study demonstrated low fibrinogen levels in only 28% of patients with DIC.9 Because fibrinogen acts as an acute phase reactant, circulating levels may remain within normal ranges during the active disease process.

Additional lab values to consider are those diagnostic tests appropriate for the underlying condition. It cannot be overemphasized that the dynamic disease process warrants ongoing assessment and consideration in relation to lab and diagnostic test results.

ISTH Overt DIC Scale

To alleviate confusion and define a precise method to identify DIC, the International Society on Thrombosis and Hemostasis (ISTH) and the Japanese Association for Acute Medicine developed a scoring system using interpretation of lab results with a clinical correlation. This method for identifying "overt" DIC suggests an algorithmic approach toward the diagnosis.

To use the scoring system, a disease entity known to be associated with the development of DIC must be present. Scores of 5 or greater are suggestive of DIC (see Table 3). This tool has been validated for use in identifying "overt" DIC only and does not confirm less overt disease presentations.4,12 Additionally, while the scoring system for overt DIC has been validated for infective and non-infective causes, it remains controversial, specifically when attempting to identify DIC within the first 24 hours of trauma.13

Treatment

Ongoing assessment and treatment of DIC focuses on monitoring and treating the underlying condition and changing trends. For instance, patients with an underlying sepsis have a high incidence of DIC and source control should be a primary consideration for treatment.14 Trending of data and correlation with the overall clinical condition may help to guide appropriate interventions. While no specific treatment for DIC has been fully endorsed, a number of therapies focusing on anticoagulation and blood component replacement have been used.

Blood Component Therapy

Decreased levels of platelets and blood coagulation factors may not necessitate replacement unless associated with overt bleeding or complications of an invasive procedure that may precipitate an acute hemorrhagic event. While blood component therapy has been controversial in earlier research, trends suggest this may not be relevant based on current concentrates used.9

Red blood cells and component transfusion guidelines recently have endorsed a more conservative approach with "less being more" in improving outcomes.15 However, active bleeding, acute decline in coagulation and component factors and the patient's clinical condition are all considerations that should be taken into account when deciding in favor of blood transfusion therapy.

Heparin

Heparin therapy for anticoagulation has been in use for more than half a century and remains a widely prescribed drug therapy today. Heparin and low-molecular-weight heparin derivatives act as an indirect thrombin inhibitor, which interacts with antithrombin (heparin cofactor) to inactivate factor X and the subsequent conversion of prothrombin to thrombin. It also prevents activation of fibrin stabilizing factor, which is responsible for clot stabilization and therapeutically alters the ability to form and maintain a stable blood clot. While heparin therapy for treatment of DIC remains controversial, some research has shown improvement in abnormal lab values but no significant improvement in clinical outcomes.4,9

Nursing Implications

Close observation of patients with conditions associated with the development of DIC is important in nursing assessments. Focusing on trends in vital signs and alterations in the clinical condition during physical assessment can alert the nurse to developing problems. Integumentary changes such as ecchymosis or petechiae should raise suspicions of a coagulation abnormality. Treatment of an underlying condition such as an abscess or infection often can halt progression of the coagulopathic event. Understanding important lab values to assess and monitor while considering trends in association with the clinical picture are important functions for nursing staff.

Additional Study Needed

Research examining the intricate cellular functions associated with DIC may support future interventions and treatments for care, but until that point, much will remain controversial as the process is multifactorial and complicated. Recently, a study showed recombinant thrombomodulin improved outcomes in a small cohort of patients with DIC.16 Additional randomized controlled studies need to identify intervention strategies.

Nurses can facilitate improved outcomes by understanding the factors associated with DIC and anticipating the changes occurring in their patient's condition that signal the onset. Understanding the processes occurring at the cellular level, then anticipating and assessing clinical signs is an important intervention necessary to halt the damage at the tissue level and provide appropriate individualized care.

References

1. Martí-Carvajal A, Simancas D, Cardona A. Treatment for disseminated intravascular coagulation in patients with acute and chronic leukemia. Cochrane Database Syst Rev. 2011;15(6).
2. Asthana B, Sharma P, Ranjan R, et al. Patterns of acquired bleeding disorders in a tertiary care hospital. Clin Appl Thromb Hemost. 2009;15(4):448-453.
3. Frazier T. Disseminated intravascular coagulation and implications for medical-surgical nurses. Med-Surg Matters. 2012; 21(3-4):8-11.
4. Levi M. Disseminated intravascular coagulation. In: Hoffman R, et al., eds. Hematology: Basic Principles and Practice. 6th ed. St. Louis: W.B. Saunders; 2012.
5. Wada H, Hatada T. Pathophysiology and diagnostic criteria for disseminated intravascular coagulation associated with sepsis. Crit Care Med. 2008;36(1):348-349.
6. Dressler D. Coagulopathy in the intensive care unit. Crit Care Nurse. 2012;32(5):48-59.
7. Martí-Carvajal A, Comunián-Carrasco G, Peña-Martí G. Haematological interventions for treating disseminated intravascular coagulation during pregnancy and postpartum. Cochrane Database Syst Rev. 2011;16(3).
8. Association of Anaesthetists of Great Britain and Ireland Membership of the Working Party, et al. Blood transfusion and the anaesthetist: management of massive haemorrhage. Anaesthesia. 2010;65(11):1153-1161.
9. Levi M, Toh CH, Thachil J, et al. Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology. Br J Haematol. 2009;145(1):24-33.
10. Demshar R, Vanek R, Mazanec P. Oncologic emergencies: new decade, new perspectives. AACN Adv Crit Care. 2011;(22)4:337-348.
11. Geiter H. Disseminated intravascular coagulation. Dimens Crit Care Nurs. 2003;(22)3:108-114.
12. Taylor F, Toh C, Hoots W, et al. Towards definition, clinical and laboratory criteria, and a scoring system for disseminated intravascular coagulation. Thrombosis Haemost. 2001;86(5):1327-1330.
13. Rizoli S, Nascimento B, Key N, et al. Disseminated intravascular coagulopathy in the first 24 hours after trauma: the association between ISTH score and anatomopathologic evidence. J Trauma. 2011;71(5 Suppl 1):S441-S447.
14. Dellinger RP, Levy M, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock. Crit Care Med. 2013;41(2):580-637.
15. Retter A, Wyncoll D, Pearse R, et al. Guidelines on the management of anaemia and red cell transfusion in adult critically ill patients. Br J Haematol. 2013;160(4):445-464.
16. Kawano N, Kuriyama T, Yoshida S, et al. Clinical features and treatment outcomes of six patients with disseminated intravascular coagulation resulting from acute promyelocytic leukemia and treated with recombinant human soluble thrombomodulin at a single institution. Intern Med. 2013;52(1):55-62.

Sue E. Durkin is an advanced practice nurse and clinical nurse specialist at Advocate Good Samaritan Hospital, Downers Grove, IL.




 
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