Symptoms of Disseminated Intravascular Coagulation (DIC)

Pathophysiology

Disseminated intravascular coagulation (DIC) is an acquired syndrome that occurs when a stimulus pathologically activates intravascular coagulation and fibrinolysis resulting in an unbalanced hemostasis (Cunningham, 1999; Huether & McCance, 2008; Wada, 2008). The initiation of DIC starts with the release of tissue factor (TF) by the endothelial cells or white blood cells (WBCs). TF are present on many different cell types including lungs, brain, and placenta. The release of TF is subsequent to a variety of causes including trauma, ischemia, excessive metabolic stress, tumors, infectious organisms, exposure to cytokines and endotoxins (Baglin, 1996; Vinay, Abul, Nelson, & Richard, 2007). The release of endotoxin is the means by which gram-negative sepsis triggers DIC (Vinay et al., 2007). These endotoxins are a structural component in gram-negative bacteria released when the bacteria are lysed. TF then reacts with coagulation factor VII leading to the common pathway and activation of coagulation factor X (Huether & McCance, 2008, p. 498). This complex pathway leads prothrombin to convert to thrombin, which transforms fibrinogen to fibrin (Huether & McCance, 2008, p. 542)

Excess activation of the coagulation pathway results in an overload of circulating thrombin leaving numerous fibrin clots in circulation (Cunningham, 1999). Fibrinolysis is also decreased during DIC. The main component of fibrinolysis is plasmin, a fibrin-eating enzyme that is activated by the clotting pathway to control the fibrin clots in the vessels (Huether & McCance, 2008). These micro-thrombi in the vasculature of organs cause tissue ischemia and dysfunction. Although fibrinolytic properties are present in the body, production is inadequate to control the systemic deposits of fibrin clots (Cunningham, 1999; Huether & McCance, 2008). DIC also places the patient at risk for hemorrhage due the rapid consumption of platelets and coagulation factors result in primary hemostasis failure (Bliss & Wallace-Jonathan, 2008; Huether & McCance, 2008). The failure and dysfunction of both the formation and stabilization pathways of clots bleeding from multiple sites are seen (Bliss & Wallace-Jonathan, 2008).

Relevant Signs and Symptoms

The signs and symptoms of disseminated intravascular coagulation present in a multitude of possibilities. In this specific patient with gram-negative sepsis leading to DIC may present with spontaneous bruising, prolonged bleeding from venipuncture sites, and bleeding from three different sites. There are also many other possible sites including the nose, gums, mucosa, eyes, arterial lines, or surgical wounds (Bliss & Wallace-Jonathan, 2008; Wada, 2008). Depending on where the fibrin clots have deposited, other symptoms may manifest as ischemia or organ failure occurs such as in the kidneys, heart, lungs, or in the brain. There is a possibility of hemorrhaging into a closed compartment, which may lead to shock (Huether & McCance, 2008).

Lab values during DIC are also of great importance. There is no specific test for DIC but a combination of PT (prothrombin time), aPTT (activated partial thromboplastin time), fibrinogen, platelet count and d-dimmer are used to assist in the diagnosis of DIC (Cunningham, 1999). Since many disorders can cause an increase of each of these lab values, it is important to use the whole picture to make the diagnosis.

Treatment

Treatments for DIC focus on elimination of the cause, controlling the coagulation and formation of clots, and maintain or return organ function (Huether & McCance, 2008). In this case study, the elimination of the gram-negative bacteria is one treatment. This essential treatment of antibiotic therapy has already started one hour ago. Another course of treatment is administration of blood products to resupply the body with the depleted clotting factor, platelets, thrombin, and plasmin in an attempt to reduce or eliminate the bleeding (Bliss & Wallace-Jonathan, 2008). Administration of fresh frozen plasma (FFP) along with cryoprecipitate and platelet concentrates replaces the clotting factors in patients with active bleeding (Bliss & Wallace-Jonathan, 2008).

Research on heparin use in DIC found successful in the treatment of DIC in some patients in an attempt to reduce the coagulation pathway activation though not recommended in septic DIC (Huether & McCance, 2008; Bliss & Wallace-Jonathan, 2008). Clinical trials have made a case for the specific treatment of septic DIC. Antithrombin III appears to be an effective treatment (Bliss & Wallace-Jonathan, 2008; Huether & McCance, 2008). Organ function requires fluid resuscitation for restoration of blood pressure as well as urine and cardiac output.

Outcomes

Prognosis varies depending on the underlying disorder. The outcome also depends on the magnitude of thrombi in the vascular system. The patient has a 10%-50% chance of dying with the diagnosis of DIC (Wada, 2008). The rate increases in patients with sepsis though there still is a possibility of a positive outcome. With rapid detection and treatment, DIC can be reversed.

Conclusion

Disseminated intravascular coagulation (DIC)

References

Baglin, T. (1996, March 16). Disseminated intravascular coagulation: diagnosis and treatment. British Medical Journal, 312, 683-688. Retrieved from www.galegroup.com

Bliss, T. T., & Wallace-Jonathan, J. (2008). Hematological and coagulation changes in sepsis. In Competency-based critical care (pp. 17-25). doi: 10.1007/978-1-84628-939-2

Cunningham, V. L. (1999, July). A review of disseminated intravascular coagulation: presentation, laboratory diagnosis, and treatment. Medical Laboratory Observer, 31(7), 42-50. Retrieved from www.generalonefile.com

Huether, S., & McCance, K. (2008). Understanding pathophysiology (4th ed.). St. Louis, MO: Mosby Elsevier.

Vinay, K., Abul, A. K., Nelson, F., & Richard, M. N. (2007). Robbins basic pathology (8th ed.). St. Louis, MO: Saunders Elsevier.

Wada, H. (2008). Disseminated intravascular coagulation. In Recent advances in thrombosis and hemostasis 2008. doi: 10.1007/978-4-431-78847-8