Disseminated Intravascular Coagulation

Running head: DISSEMINATED INTRAVASCULAR COAGULATION 1

Disseminated Intravascular Coagulation

Alyssa Cardinal

California State University, Stanislaus

DISSEMINATED INTRAVASCULAR COAGULATION 2

Disseminated Intravascular Coagulation

Disseminated intravascular coagulation (DIC) is a serious thrombotic and hemorrhagic

disorder, characterized by an overwhelming consumption of clotting factors, thereby resulting in

widespread, and often uncontrollable, hemorrhage (Lewis, Dirksen, Heitkemper, & Bucher,

2014). The following literature encapsulates the etiology, clinical manifestations, pathogenesis,

diagnostic criteria, and medical management of DIC, while suggesting appropriate nursing

diagnoses and patient teaching for the disorder.

Etiology and Clinical Manifestations

DIC is the intense manifestation of hemostatic activation that occurs secondary to various

diseases and disorders (Lewis et al., 2014). Risk factors for DIC include shock, septicemia,

mismatched blood transfusions, various obstetric complications, malignancies, tissue damage,

liver disease, and chronic disorders such as systemic lupus erythematosus (Lewis et al., 2014).

Levi (2014) claims that the “activation of coagulation in the systemic circulation, inefficiently

counteracted by coagulation inhibitors and amplified by decreased physiological fibrin-

degrading potential, may result in fibrin formation in small and midsize vessels and

microvascular thrombotic microangiopathy” (p. 228). Consequently, depletion of coagulation

factors and platelets leads to the classic manifestation of systemic hemorrhage (Levi, 2014).

DIC may present with bleeding and/or thrombotic manifestations (Lewis et al., 2014).

Bleeding manifestations consist of “pallor, petechiae, purpura, oozing blood, venipuncture site

bleeding, hematomas, and occult hemorrhage” (Lewis et al., 2014, p. 659). Additional bleeding

manifestations include tachypnea, orthopnea, hemoptysis, hypotension, tachycardia, upper and

lower gastrointestinal bleeding, abdominal distention, bloody stools, hematuria, vision changes,

dizziness, headache, irritability, changes in mental status, and bone and joint pain (Lewis et al.,


2014). Thrombotic manifestations include cyanosis, ischemic tissue necrosis, hemorrhagic

necrosis, pulmonary emboli, acute respiratory distress syndrome, electrocardiogram changes,

venous distension, abdominal pain, paralytic ileus, kidney damage, and oliguria. Quickly

recognizing that these symptoms are attributed to DIC aids in diagnosing the disorder, while

allowing for immediate initiation of the appropriate therapeutic interventions (Lewis et al.,

2014).

Pathogenesis

DIC is grossly identified as a major bleeding disorder, and therefore involves the

functional pathways of blood components and clotting factors. DIC initially activates thrombin,

leading to “(1) conversion of fibrinogen to fibrin, (2) activation of platelets (and their

consumption), (3) activation of factors V and VIII, (4) activation of protein C (and degradation

of factors Va and VIIIa), (5) activation of endothelial cells, and (6) activation of fibrinolysis”

(DeLoughery, 2015, p. 39). As clots are increasingly formed throughout the body, more

byproducts of fibrin and fibrinogen are also formed (Lewis et al., 2014). These byproducts are

termed fibrin split products (FSPs), and they interfere with blood coagulation by (1)

coating the platelets and interfering with platelet function; (2) interfering with thrombin

and thus disrupting coagulation; and (3) attaching to fibrinogen, which interferes with

the polymerization process necessary to form a stable clot (Lewis et al., 2014).

This process leads to abnormal serum laboratory findings.

Diagnostics and Medical Management

As DIC stems from the degradation of clotting factors, diagnostics heavily rely on serum

laboratory testing. Upon examination of coagulation parameters, a patient with DIC will present

with elevated fibrin-split products and D-dimer levels; prolonged prothrombin time (PT), partial


thromboplastin time (PTT), activated partial thromboplastin time (aPTT), and thrombin time;

and lastly, reduced fibrinogen and platelet levels (Lewis et al., 2014).

Treatment for DIC is primarily aimed at targeting the primary cause (Lewis et al., 2014).

If the patient is not actively bleeding, no therapy is required. However, if the patient is actively

bleeding, and efforts have been made to treat the primary cause, therapy becomes focused on

providing support with the necessary blood products. Providing blood products such as platelets,

cryoprecipitate, and fresh frozen plasma (FFP), is typically reserved for patients with life-

threatening hemorrhage. Platelets are given to treat thrombocytopenia in patients with platelet

levels less than 20,000 or greater than 50,000 with bleeding, and cryoprecipitate is given for

patients with fibrinogen levels less than 100 mg/dL (Lewis et al., 2014). Patients receiving

platelets “for low platelet counts usually consist of 1 or 2 units of platelet concentrate (five

donors/unit) aiming to increase the platelet count to at least 20–30 x 109/L and in patients with

active hemorrhage or scheduled for a high-risk intervention to at least 50 x 109/L (Levi, 2014).

Additional research provides evidence that anticoagulant therapy is beneficial for treating

thrombosis in acute DIC. According to Perry, Lazar, Quillen, and Sloan (2012), “several case

reports have shown successful management of DIC with subcutaneous unfractionated heparin or

[low molecular weight heparin], with reported durations of successful treatment as long as 30

months” (p. 734). Lewis et al. (2014) add that “antithrombin III (ATnativ) may be useful in

fulminant DIC, although it increases the risk of bleeding” (p. 659). Anticoagulation therapy,

however, should only be used when the benefits outweigh the risks (Lewis et al., 2014).

Nursing Diagnoses

Four appropriate nursing diagnoses related to DIC include “ineffective peripheral tissue

perfusion related to bleeding and sluggish or diminished blood flow secondary to thrombosis;


acute pain related to bleeding into tissues and diagnostic procedures; decreased cardiac output

related to fluid volume deficit; [and] anxiety related to fear of the unknown, disease process,

diagnostic procedures, and therapy” (Lewis et al., 2014, p. 659). Ineffective peripheral tissue

perfusion will present as cyanosis, and can be treated with anticoagulation therapy and oxygen

(Lewis et al., 2014). Pain can be treated with analgesics, while decreased cardiac output can be

treated with fluid and blood product administration. Treating anxiety requires the nurse to

provide patient teaching, empathy, and anxiolytics if necessary.

Patient teaching for the medical diagnosis of DIC should include both pathophysiological

and emotionally therapeutic components. According to Lewis et al. (2014), patients with any

form of thrombocytopenia should be educated on the importance of reporting bleeding

manifestations, including black, tarry, or bloody stools; black or bloody vomit, sputum, or urine;

bruising or small red or purple spots on the skin; bleeding from the mouth or anywhere in the

body; headache or vision changes; muscle weakness; and lastly confusion (Lewis et al., 2014).

DIC is a thrombotic and hemorrhagic disorder, diagnosed secondary to a multitude of

conditions. After the vast consumption of clotting factors, patients with DIC present with

systemic hemorrhage. Diagnosing the disorder relies on serum laboratory testing, and may be

treated with anticoagulants. However, the treatment of DIC is primarily focused on pinpointing

and reversing the underlying cause. It is important to educate patients on the symptomatology of

DIC, as well as the importance of reporting these clinical manifestations to their providers, due

to the rapid deterioration of patients with the disorder.


References

DeLoughery, T. G. (2015). Disseminated intravascular coagulation. Hemostasis and Thrombosis,

39-42. doi:10.1007/978-3-319-09312-3_8

Levi, M. (2014). Diagnosis and treatment of disseminated intravascular coagulation.

International Journal of Laboratory Hematology, 36(3), 228-236. doi:10.1111/ijlh.12221

Lewis, S. L, Dirksen, S. R., Heitkemper, M. M., & Bucher, L. (2014). Medical-surgical

nursing: Assessment and management of clinical problems (9th ed.). St. Louis, MO:

Elsevier Mosby.

Perry, J., Lazar, H., Quillen, K., & Sloan, J. (2012). Successful long-term management of

aneurysm-associated chronic disseminated intravascular coagulation with low molecular

weight heparin. Journal Of Cardiac Surgery, 27(6), 730-735. doi:10.1111/jocs.12010

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Disseminated Intravascular Coagulation