How to treat a DIC diagnosis solved case study
CASE STUDY prompt: A 30-year-old male presents with acute trauma. The final diagnosis is DIC.
1. Discuss the clotting mechanism.
2. What do prolonged PT and aPTT tests indicate?
3. Fibrin degradation and split products are common to DIC patients. Why?
4. Identify two additional conditions that can initiate DIC and how?
Solution to case study prompts
Clotting mechanism
The clotting mechanism is categorised into two stages; primary and secondary hemostasis. Primary hemostasis is the formation of weak platelet plug in four phases: vasoconstriction, platelet adhesion, platelet activation, and platelet aggregation (Garmo et al., 2022).
Vasospasm is the initial response to injury of the vasculature. It stimulates vasoconstriction mediated by endothelin-1 synthesised by damaged endothelium. (Garmo et al., 2022). Damaged endothelium exposes von Willebrand factor and sub-endothelial collagen and releases inflammatory mediators and ATP initiating the second stage phase, platelet adhesion. The Platelet adhesion phase is a process by which platelet adhere to exposed subendothelial collagen and von Willebrand factor aided by G protein receptors in platelet membranes.
Platelet activation is mediated via thrombin through two mechanisms. In the first mechanism, “thrombin directly activates platelets via proteolytic cleavage by binding the protease-activated receptor” (Garmo et al., 2022). Also, thrombin stimulates platelet granules to release Adenosine Diphosphate (ADP), serotonin and platelet-activating factor. ADP binds to P2Y1 and P2Y12, inducing pseudopod shape change aiding in platelet aggregation and formation of the weak plug.
Secondary hemostasis stabilises weak platelet plugs through one of the two pathways, i.e. intrinsic and extrinsic pathways (Garmo et al., 2022). The process is achieved by completing three tasks, including activating clotting factors, converting prothrombin to thrombin, and fibrinogen to fibrin.
Prolonged PT indicates an individual has a condition like liver disease or deficiency of vitamin k or factor VII (Garmo et al., 2022), whereas prolonged aPTT suggests a deficiency of intrinsic factors, for example, VII, IX, XI and XII. Also, it can be due to von Willebrand disease, vitamin K deficiency, hypofibrinogenemia etc.
Fibrin degradation and split products are common in DIC due to the excessive presence of coagulation factors and the consumption of platelets (Moake, 2022). Conditions like cancer and shock mimic the DIC because they express and release excess tissue factors.
References
Garmo, C., Bajwa, T. and Burns, B., 2022. Physiology, Clotting Mechanism. [online] Ncbi.nlm.nih.gov. Available at: <https://www.ncbi.nlm.nih.gov/books/NBK507795/> [Accessed 31 May 2022].
Moake, J., 2022. Disseminated Intravascular Coagulation (DIC) – Hematology and Oncology – MSD Manual Professional Edition. [online] MSD Manual Professional Edition. Available at: <https://www.merckmanuals.com/professional/hematology-and-oncology/coagulation-disorders/disseminated-intravascular-coagulation-dic> [Accessed 31 May 2022].
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