Vous êtes sur la page 1sur 6

Running head: DISSEMINATED INTRAVASCULAR COAGULATION

Disseminated Intravascular Coagulation


Alyssa Cardinal
California State University, Stanislaus

DISSEMINATED INTRAVASCULAR COAGULATION

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 fibrindegrading 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.,

DISSEMINATED INTRAVASCULAR COAGULATION

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

DISSEMINATED INTRAVASCULAR COAGULATION

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 lifethreatening 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 2030 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;

DISSEMINATED INTRAVASCULAR COAGULATION

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.

DISSEMINATED INTRAVASCULAR COAGULATION

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

Vous aimerez peut-être aussi