Hemostasis

MULTI-STEPPED PROCESS OF CONTROLLED BLOOD HEMOSTASIS AND CLOTTING

OBJECTIVES

  • Students will be able to define and describe the concept of blood hemostasis and clotting.

  • Students will be able to identify risk factors for ineffective clotting, including bleeding and excessive clotting.

  • Students will be able to recognize signs of compromised clotting in individuals.

  • Students will be able to describe appropriate nursing and collaborative interventions to prevent complications associated with clotting problems.

ANATOMY & PHYSIOLOGY REVIEW

Blood Components

  • White Blood Cells (WBC): Part of the immune system, they detect and fight viruses and bacteria, comprising less than 1% of blood.

  • Platelets: Important for blood clotting, they form clots to stop bleeding, making up less than 1% of blood.

  • Red Blood Cells (RBC): Carry oxygen to the body and remove carbon dioxide, constituting about 40% to 45% of blood volume.

  • Plasma: The yellow liquid component of blood that transports nutrients, hormones, and proteins; makes up about 55% of the total blood volume.

Accessory Organs

  • Spleen and Liver: These organs help regulate the growth of blood cells and produce factors essential for proper blood clotting.

CLOTTING CONCEPT

  • Excessive Clotting: Can occur locally or systemically, and can be either expected/efficient or inefficient (leading to bleeding).

RISK FACTORS FOR IMPAIRED CLOTTING

  • Age: Older adults are at increased risk due to physiological changes, notably increased platelet adhesiveness which promotes blood stasis.

  • Genetics: Inherited diseases such as hemophilia and thrombocytopenia contribute to ineffective clotting.

  • Immobility: Contributes to the formation of blood clots, particularly venous clots.

  • Smoking: Leads to hypercoagulability of blood, increasing the risk of clot formation.

NORMAL CLOTTING PROCESS

Pathways

  • Intrinsic Pathway: Begins with activation after contact with a damaged vessel surface.

  • Extrinsic Pathway: Initiated by damaged tissues that expose tissue factors.

  • Common Pathway: Involves prothrombin, tissue thromboplastin, and ultimately leads to the conversion of fibrinogen into fibrin, forming a stable clot.

Key Components

  • Activated Factors and Enzymes: Factors such as XII, XIa, IXa, and VIII work together to catalyze the conversion of prothrombin to thrombin, which then splits fibrinogen into fibrin monomers.

  • Fibrin Stabilization: Stabilized by factor XIII.

KEY TERMS

  • Thrombus: A blood clot that forms within a blood vessel.

  • Embolus: A thrombus that has detached and travels through the bloodstream.

VIRCHOW'S TRIAD

Components

  • Stasis: Reduced blood flow can lead to clot formation.

  • Vessel Wall Injury: Damage to blood vessels prompts the release of clotting factors, leading to thrombosis.

  • Hypercoagulability: An imbalance in the clotting mechanism, where the body has an increased tendency to form clots.

Causes of Venous Stasis

  • Dysfunctional vein valves.

  • Inactive extremity muscles.

  • Changes in unidirectional blood flow.

BLOOD HYPERCOAGULABILITY

Definition

  • A condition (either acquired or inherited) that increases the likelihood of developing blood clots, often marked by an increase in fibrin production.

CONDITIONS THAT AFFECT CLOTTING

  • Thrombocytopenia: A reduction in platelet count, increasing the risk of bleeding.

  • Hemophilia: A genetic disorder associated with defective or deficient clotting factors.

  • Polycythemia: An increase in red blood cells, elevating the risk for thrombus formation.

  • Atrial Fibrillation: Leads to blood stasis in the atrium, heightening the risk of stroke, myocardial infarction, and pulmonary embolism.

ANTI-CLOTTING FORCES

Mechanisms of Prevention

  • Fibrinolysis: The dissolution of blood clots.

  • Plasmin: An enzyme that degrades fibrin in blood clots.

  • Protein C and Protein S: Proteins that prevent excessive clotting by regulating clotting factors.

  • Antithrombin III: A protein that inhibits clotting and helps maintain the balance between bleeding and clotting.

LABORATORY TESTS

  • Prothrombin Time (PT): Measures how long it takes blood to clot.

  • International Normalized Ratio (INR): Standardized measure of PT.

  • Partial Thromboplastin Time (PTT): Assesses the intrinsic pathway of coagulation.

  • Fibrinogen: Measures the level of fibrinogen in the blood.

  • Platelet Count: A count of the number of platelets in the blood, normal range is 150,000-450,000.

  • D-Dimer: A test that measures clot breakdown products.

  • Red Blood Count (RBC), Hemoglobin, Hematocrit: Tests that evaluate overall blood health.

RADIOLOGIC TESTS

  • Ultrasound: A non-invasive method for detecting venous thrombosis.

  • Arteriograms: Visualization of arteries using contrast medium.

  • Venograms: Visualization of veins using contrast medium.

CONDITIONS LEADING TO EXCESSIVE BLEEDING

  • Hemophilia: Genetic disorder leading to severe bleeding issues.

  • Thrombocytopenia: Uncontrolled bleeding due to low platelet counts.

  • Idiopathic Thrombocytopenic Purpura (ITP): An autoimmune disorder leading to low platelet levels; involves teaching patients to manage bruises with ice.

  • Liver Damage: Affected liver function impairs coagulation factor production.

  • Polycythemia Vera: Rare blood cancer with an overproduction of blood cells which may lead to complications like thrombi.

  • COPD Patients: Tend to have increased red blood cell production as a response to hypoxia, leading to potential blood clot-related complications.

IDIOPATHIC THROMBOCYTOPENIA (ITP)

  • Demographics: Usually acute in children post-viral infection, more common in women (2-3 times).

  • Symptoms of ITP:

    • Easy or excessive bruising.

    • Petechial rash (tiny reddish-purple spots on skin due to bleeding under the skin).

    • Long healing time for cuts or minor wounds.

    • Blood in urine or stools.

    • Heavy menstrual flow in women.

    • Unexplained bleeding from nose or gums.

HEMOPHILIA

Overview

  • An inherited blood disorder leading to ineffective clotting due to deficiency in clotting factors (classically factors VIII or IX).

  • Symptoms include prolonged nosebleeds, easy bruising, and swollen joints.

  • No cure; management includes regular injections of clotting factors and preventative care.

Types of Hemophilia

  1. Hemophilia A: Deficiency in factor VIII (more common).

  2. Hemophilia B: Deficiency in factor IX.

  3. Acquired Hemophilia: Develops later in life unrelated to prior hereditary conditions.

Incidence in U.S.

  • Approximately 500 babies born yearly with hemophilia, predominantly males due to X-linked inheritance.

DIAGNOSIS OF HEMOPHILIA

  • Testing is often requested for newborn boys, especially if there is a family history.

  • Diagnostic blood tests assess overall clotting ability and specific factor assays to identify which type of hemophilia is present.

TREATMENTS

  • Clotting Factor Injections: Mainstay of management to prevent bleeding episodes.

  • Treatment of complications related to aging and hemophilia includes regular medical review for risks like intracranial hemorrhages.

CLINICAL MANAGEMENT: CONTROL OF BLEEDING

  • Immediate Care: Direct pressure on the bleeding site, ice application, and use of topical agents like Gel-foam or fibrin foam.

  • Critical Care: For suspected hemorrhage leading to shock, volume replacement is necessary.

PHARMACOLOGIC AGENTS TO CONTROL BLEEDING

  • Desmopressin Acetate: Stimulates the release of clotting factors.

  • Platelet transfusions: May be required in the case of significant bleeding or very low platelet counts.

  • Fresh Frozen Plasma (FFP): Use in emergencies to replenish clotting factors and blood volume in patients who have experienced acute blood loss.

HEMOPHILIA MANAGEMENT: PHARMACOTHERAPY

  • Anticoagulant Agents: Warfarin/Coumadin, Heparin, Low-Molecular-Weight Heparin (LMWH).

  • Antiplatelet Agents: Includes Aspirin, Plavix.

  • Thrombolytic Agents: Essential agents such as alteplase for clot dissolution.

HEPARIN: DETAILS

  • Mechanism: Anticoagulant that prevents clot enlargement by interrupting clotting steps.

  • Administration: Administered subcutaneously or intravenously; does not dissolve existing clots.

Heparin Antidote

  • Protamine Sulfate: Effectively neutralizes the effects of heparin; dosage is 1 mg of protamine per 100 IU of heparin received.

COUMADIN (WARFARIN) MANAGEMENT

  • Indications: Used in treatment of both arterial and venous thrombosis.

  • Mechanism: Inhibits vitamin K-dependent coagulation factors.

  • Dosing & Monitoring: Requires careful monitoring of PT/INR; can take several days to achieve therapeutic levels.

Antidote for Coumadin

  • Vitamin K: Administration will take time to reverse effects.

MANAGING WARFARIN OVERDOSE

  • Monitoring for bleeding is critical; action taken depends on INR levels:

    • INR 3.5-5: Reduce dose, do not stop.

    • INR 5-8: High bleeding risk, give oral or subcutaneous Vitamin K.

    • INR > 8: Stop the drug, administer Vitamin K, and consider FFP for severe cases.