Haemostatic Failure in Critically Ill Patients

Abstract

Summary H aemostasis is the process of forming clots in the walls of damaged blood vessels and preventing blood loss while maintaining blood in a fluid state within the vascular system. The main components of normal haemostasis are palatelets and coagulation factors. Human platelets are small and discoid in shapeand are produced from megakaryocytes under the effect of thrombopoietin. They are the second most numerous corpuscles in the blood normally circulating between 150 and 450x109/L. Platelets have many functional characteristics of whole cells, even though they do not have nuclei and cannot reproduce. In their cytoplasm are such active factors as (1) actin and myosin molecules; (2) residuals of both the endoplasmic reticulum and the Golgi; (3) mitochondria and enzyme systems that are capable of forming adenosine triphosphate (ATP) and adenosine diphosphate (ADP); (4) enzyme systems that synthesize prostaglandins; (5) an important protein called fibrin-stabilizing factor; and (6) a growth factor that causes vascular endothelial cells to multiply and grow. The liver is the primary site of synthesis of most of the clotting factors and the proteins involved in the fibrinolytic system. These include all the vitamin K-dependent coagulation proteins (factors II, VII, IX, X, protein C, protein S and protein Z), as well as factor V, XIII and fibrinogen. Failure of haemostasis is common in critically ill patients and may be complex and multifactorial in pathogenesis. As haemostatic failure may complicate a wide range of medical, surgical and obstetric disorders, definitive diagnosis and specific therapy can significantly impact on outcome. Haemostatic failure in critically ill patients is caused mainly due to: I-Thrombocytopenia. II-Coagulation factors defect. Thrombocytopenia is the most common coagulation problem in the intensive care unit with an incidence of 15 to 60%. The cause of thrombocytopenia in most ICU patients is multifactorial, involving some combination of the following four mechanisms: increased destruction or consumption; decreased production; dilution; and sequestration. The most common causes of thrombocytopenia in ICU are: 1. HIT 2. Drug induced thrombocytopenia 3. DIC 4. Massive transfusion The most common causes of acquired coagulation disorders: 1. DIC 2. Trauma 3. Liver disease 4. Vitamin K deficiency 5. Exposure to anticoagulants In general, there may be clinical features suggesting local or generalized failure of the haemostatic system .Clinical history is important, especially with respect to previous bleeding problems, family history, comorbid medical conditions and medications. The nature of surgery or an invasive intervention may have haemostatic issues that need specific consideration. A full blood count, PT, APTT, fibrinogen level, D-Dimer, provide a broad screen for most clinically significant haemostatic disorders. The laboratory investigation of a patient with a potential haemostatic defect depends on the degree of urgency. It may be necessary to administer blood component therapy without a definitive haemostatic defect being established. Transfusion therapy in patients with haemostatic failure has specific indications and precautions to avoid complications. Types of transfusions include platelets concentrate , FFP and cryoprecipitate plus the pharmaceutical agents as DDAVP and vitamin K. Platelets transfusion indications may be therapeutic as in the presence of thrombocytopenia (platelets < 100,000/μ L) or functional defects (including iatrogenic ones) of platelets, depends on the nature and the site of the bleeding, on the presence or absence of coagulation disorders, ongoing treatments, as well as the clinical condition of the patient, or prophylactic which refers to maintenance of the platelet count above a certain threshold in patients who are neither bleeding nor actively consuming platelets because of immune destruction or infection.