Mr D is a 32yearold white male admitted last week following

Mr. D is a 32-year-old white male admitted last week following a motor vehicle accident in which he sustained a massive head injury, multiple fractured ribs, a pneumothorax, and a spinal cord injury. He has been unresponsive since admission and is completely ventilator dependent. This morning his white blood cell (WBC) count is 25,000/µL, and his temperature is 102°F. His blood pressure (BP) is now 98/50, which is a significant drop from his BP on admission, and his heart rate is 102.

1.) Based on his lab results and vital signs, what does the nurse suspect?

You notice oozing of serosanguineous fluid from previous IV sites. The nurse alerts the health care provider (HCP) about her concern that Mr. D may be developing disseminated intravascular coagulation (DIC).

1.) Based on your assessments, what labs do you anticipate to order and what findings do you anticipate?

2.) What other manifestations are typically associated with DIC?

3.) Discuss the pathophysiology associated with DIC.

Solution

Ans:

1)      Based on his lab results and vital signs, what does the nurse suspect?

Based on the lab results the nurse suspect that Me. D suffering with Disseminated intravascular coagulation due to multiple organ injury or severe trauma.

2)      Based on your assessments, what labs do you anticipate to order and what findings do you anticipate?

Based on signs and symptoms of blood clots and bleeding. Mr. D will undergo a physical exam to look for signs and symptoms of blood clots and internal and external bleeding. For example, doctor may look for bleeding from your gums. He may suggest the following tests to be performed in the laboratory.

Diagnostic Tests: To diagnose DIC, your doctor may recommend blood tests to look at your blood cells and the clotting process. For these tests, a small amount of blood is drawn from a blood vessel, usually in your arm.

Complete Blood Count and Blood Smear:A complete blood count (CBC) measures the number of red blood cells, white blood cells, and platelets in your blood.

Platelets are blood cell fragments that help with blood clotting. Abnormal platelet numbers may be a sign of a bleeding disorder (not enough clotting) or a thrombotic disorder (too much clotting).

A blood smear is a test that may reveal whether your red blood cells are damaged.

Tests for Clotting Factors and Clotting Time:

The following tests examine the proteins active in the blood clotting process and how long it takes them to form a blood clot.

3) What other manifestations are typically associated with DIC?

Disseminated intravascular coagulation (DIC), also known as disseminated intravascular coagulopathy is a pathological process characterized by the widespread activation of the clotting cascade that results in the formation of blood clots in the small blood vessels throughout the body. This leads to compromise of tissue blood flow and can ultimately lead to multiple organ damage. In addition, as the coagulation process consumes clotting factors and platelets, normal clotting is disrupted and severe bleeding can occur from various sites. The combination of widespread loss of tissue blood flow and simultaneous bleeding leads to an increased risk of death in addition to that posed by the underlying disease.

4) Discuss the pathophysiology associated with DIC.

The studies have demonstrated that the systemic formation of fibrin observed in this setting is the result of the simultaneous coexistence of four different mechanisms: increased thrombin generation, a suppression of the physiologic anticoagulant pathways, impaired fibrinolysis and activation of the inflammatory pathway. The systemic generation of thrombin has been shown to be mediated predominantlyby the extrinsic (factor VIIa) pathway. In fact, while the abrogation of the tissue factor/factor VIIa pathway resulted in complete inhibition of thrombin generation in experimental animal models of endotoxemia, the inhibition of the contact system did not prevent systemic activation of coagulation.

Impaired function of physiological anticoagulant pathways may amplify thrombin generation and contribute to fibrin formation. Plasma levels of antithrombin are markedly reduced in septic patients as a result of a combination of increased consumption by the ongoing formation of thrombin, enzyme degradation by elastase released from activated neutrophils, impaired synthesis due to liver failure and vascular capillary leakage. Likewise, there may be significant depression of the protein C system, caused by enhanced consumption, impaired liver synthesis, vascular leakage and a down-regulation of thrombomodulin expression on endothelial cells by pro-inflammatory cytokines, such as tumor necrosis factor (TNF)- and interleukin(IL)-1. Moreover, the evidence that administration of recombinant tissue factor pathway inhibitor (TFPI) results in complete inhibition of endotoxin-induced thrombin generation suggests that tissue factor is involved in the pathogenesis of DIC. Although no acquired or deficiency or functional defect of TFPI has been identified in patients with DIC, there is evidence that the inhibitor does not regulate tissue factor activity sufficiently in such patients.

As regards impaired fibrinolysis, experimental models of bacteremia and endotoxemia are characterized by rapidly increasing fibrinolytic activity, most probably due to the release of plasminogen activators from endothelial cells. However, this initialhyperfibrinolytic response is followed by an equally rapid suppression of fibrinolytic activity, due to the increase in plasma levels of plasminogen activator inhibitor type 1 (PAI-1). The importance of PAI-1 in the pathogenesis of DIC is further demonstrated by the fact that a functional mutation in the PAI-1 gene, the 4G/5G polymorphism, which causes increased plasma levels of PAI-1, was linked to a worse clinical outcome in patients with meningococcal septicemia.

Finally, another important mechanism in the pathogenesis of DIC is the parallel and concomitant activation of the inflammatory cascade mediated by activated coagulation proteins, which in turn can stimulate endothelial cells to synthesize pro-inflammatory cytokines. In fact, while cytokines and inflammatory mediators can induce coagulation, thrombin and other serine proteasesinteract with protease-activated receptors on cell surfaces to promote further activation and additional inflammation. Since activated protein C has an anti-inflammatory effect through its inhibition of endotoxin-induced production of TNF-, IL-1, IL-6 and IL-8 by cultured monocytes/macrophages, depression of the protein C system may result in a pro-inflammatory state. Thus, inflammatory and coagulation pathways interact with each other in a vicious circle which amplifies the response further and leads to dysregulated activation of systemic coagulation.