Haemostasis

Haemostasis Overview

• Haemostasis is the process that stops bleeding.
• When a blood vessel is damaged, overlapping processes occur to halt bleeding.
• Blood loss must be stopped quickly following injury.

GDC Learning Outcomes

• Explain general and systemic diseases, relating them to oral health.
• Describe relevant and appropriate physiology, showing how it applies to patient management.
• Describe medicine properties and therapeutic agents, discussing their impact on patient management.
• Describe haemostasis and clot formation.
• Describe the clotting cascade and the significance of clotting factors
• Outline the significance of haemostasis to dental hygienists/therapists.

What is Haemostasis?

• Bleeding stops through haemostasis.
• When a blood vessel is damaged, multiple overlapping processes halt the blood loss.

Why Haemostasis is Important

• Blood is important connective tissue.
• Blood nourishes all organs.
• It's vital to stop blood loss quickly in case of injury.

Consequences of Rapid Blood Loss

• Minor loss: Body's homeostatic mechanisms preserve blood volume and cells.
• Moderate loss: Headache, fatigue, nausea, sweating, dizziness.
• Severe loss: Clammy skin, rapid shallow breathing, rapid heart rate, little or no urination, confusion, weakness, weak pulse, blue lips/fingernails, lightheadedness, loss of consciousness, and death.

Stages of Haemostasis

• 1. Vasoconstriction: Initial bleeding halted by blood vessel constriction. Platelets adhere to damaged vessel walls.
• 2. Platelet plug formation: Platelets clump around exposed collagen fibers. Von Willebrand factor assists in stabilizing the platelet plug. Platelets release chemicals like ADP to draw in more platelets
• 3. Coagulation (Secondary Haemostasis): Complex process where a stable fibrin clot is formed from liquid fibrinogen through the cascade.

Stages of Primary Haemostasis - 1. Vasoconstriction

• Initial bleeding is stopped by the constriction of blood vessels.
• Platelets stick to damaged vessel walls.
• Platelets release serotonin and thromboxanes, which lead to smooth muscle contraction in the vessel walls.
• Other vasoconstrictors, like endothelins, are released by damaged vessels.

Stages of Primary Haemostasis - 2. Platelet Plug

• Platelets clump at the site of exposed collagen fibres.
• Platelets release substances like adenosine diphosphate (ADP), which draws in more platelets to form a plug.
• Von Willebrand factor stabilizes the platelet plug.

Bleeding Time

• Time taken for primary haemostasis (vessel constriction and platelet plug formation).
• Normal range: 2-7 minutes. Factors that may cause prolonged bleeding times: thrombocytopaenia, severe anaemia, collagen disorders (e.g., Ehlers-Danlos syndrome), Von Willebrand's disease, as well as anti-platelet drugs.

Secondary Haemostasis - 3. Coagulation

• Platelet plug is stabilized through insoluble fibrin strands to form a mesh.
• Fibrin is generated from soluble fibrinogen through the clotting cascade.

Fibrin Mesh

• Fibrin forms a mesh-like structure that entraps blood cells, platelets, and other components, reinforcing the clot.

Clotting Cascade

• A series of steps resulting in the formation of a blood clot in response to bleeding following injury.
• The cascade involves activation of various clotting factors.

Extrinsic Pathway (Tissue Factor Pathway)

• Tissue factor (factor III) in damaged endothelial cells activates factor VII.
• Factor VIIa triggers a cascade of reactions leading to the formation of factor Xa.
• Factor Xa along with Va and calcium activate prothrombin.

Intrinsic Pathway (Contact Pathway)

• Triggered by blood coming into contact with collagen fibers in a damaged blood vessel wall.
• Factor XII (serine protease) is the first key activation step, which is converted to factor XIIa.
• Factor XIIa activation triggers a cascade of reactions ultimately leading to activation of factor X.

Common Pathway

• Prothrombin is converted to thrombin, which converts soluble fibrinogen into fibrin strands.
• Factor XIII acts on the fibrin strands to form a fibrin mesh, stabilizing the clot.

Coagulation Factors

• Synthesized primarily in the liver.
• Vitamin K is essential for the synthesis of several clotting factors.
• Liver disease can impair coagulation factor production.

Inherited Disorders

• Deficiencies in clotting factors (e.g., haemophilia A, B, and C) can occur, impacting the blood's ability to clot appropriately.

Effects of Anticoagulants on the Clotting Cascade

• Anticoagulants block different parts of the clotting cascade, thus preventing blood clotting.
• Examples of anticoagulants include Warfarin, Heparin, and Rivaroxaban.

Clot Retraction

• Clot shrinks and draws the damaged blood vessel edges together, reducing further blood loss.
• Proteins actin and myosin contract within activated platelets.
• Fibrin threads draw more tightly together.
• Serum exudes.

Clot Breakdown (Fibrinolysis)

• Plasminogen is trapped within the clot and converts to plasmin.
• Plasmin breaks down fibrin within the clot.
• Thrombin-activated fibrinolysis inhibitor (TAFI) stabilizes clots.

Fibrinolysis Abnormalities

• Excessive fibrinolysis can lead to bleeding problems.
• Suppressed or impaired fibrinolysis can cause blood clots.
• Example conditions: DVT (deep vein thrombosis), PE (pulmonary embolism)).

Thrombosis

• Caused by either over-activity of coagulation or under-activity of fibrinolysis.
• Often begins in areas of vascular endothelial damage where platelets adhere.
• Formation of clots in blood vessels.

Dental Relevance

• Dental procedures cause bleeding.
• Natural stoppage of bleeding is typically within 4-10 minutes.
• Prolonged bleeding may be caused by various factors, and requires specific management strategies.

Haemorrhage in Dentistry

• Dentistry employs methods like pressure, sutures, and hemostatic agents (e.g., Surgicel) to effectively manage bleeding.
• Electrosurgery units and lasers are less common techniques.

Summary of the Coagulation Cascade

• The presentation details the step-by-step process of clot formation, starting from vascular injury through vasoconstriction, platelet plug formation, coagulation, clot retraction, and lastly fibrinolysis.