Symptoms of Disseminated Intravascular Coagulation (DIC)

Symptoms of Disseminated Intravascular Coagulation (DIC)PathophysiologyDisseminated intravascular coagulation (DIC) is an acquired syndrome that occurs when a stimulus pathologically activates intravascular coagulation and fibrinolysis payoffing 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 turn in on many different cell types including lungs, brain, and placenta. The release of TF is subsequent to a variety of causes including trauma, ischemia, unreasonable 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 bacterium released when the bacteria are lysed. TF then reacts wi th 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 in any case decreased during DIC. The chief(prenominal) 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 impart 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 con sumption 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 discharge from multiple sites are seen (Bliss Wallace-Jonathan, 2008).Relevant Signs and SymptomsThe 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 troika 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 limpid 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 unappealing 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 cabal 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 for each one of these lab values, it is important to use the whole picture to make the diagnosis.TreatmentTreatments 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 arcminute 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). harmonium function requires fluid resuscitation for restoration of blood pressure as well as urine and cardiac output.OutcomesPrognosis 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 d ying with the diagnosis of DIC (Wada, 2008). The rate increases in patients with sepsis though there mum is a possibility of a positive outcome. With rapid detection and treatment, DIC can be reversed.ConclusionDisseminated intravascular coagulation (DIC)ReferencesBaglin, T. (1996, March 16). Disseminated intravascular coagulation diagnosis and treatment. British medical checkup Journal, 312, 683-688. Retrieved from www.galegroup.comBliss, T. T., Wallace-Jonathan, J. (2008). Hematological and coagulation changes in sepsis. In Competency-based critical care (pp. 17-25). doi 10.1007/978-1-84628-939-2Cunningham, 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.comHuether, 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 bas ic 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