Haemostasis

• Haemostasis is the process that stops bleeding.
• Multiple overlapping processes occur when a blood vessel is damaged.

Importance of Haemostasis

• Blood is an important connective tissue that keeps all organs nourished.
• Stopping blood loss quickly is important when tissue is injured.

Consequences of Rapid Blood Loss

• Minor blood loss is managed by the body's homeostatic mechanisms to maintain blood volume and cells.
• Moderate blood loss can result in headache, fatigue, nausea, sweating, and dizziness.
• Severe blood loss S/S include clammy, cold, pale skin, rapid/shallow breathing, rapid heart rate, low/no urine output, confusion, weakness, weak pulse, blue lips/fingernails, light-headedness, loss of consciousness, and death.

Stages of Haemostasis

• Vasoconstriction is the first stage, considered primary haemostasis.
• Platelet plug formation is the 2nd stage, considered primary haemostasis.
• Coagulation is the third stage and is considered secondary haemostasis.

Primary Haemostasis: Vasoconstriction

• The constriction of blood vessels stops the initial bleeding
• Platelets adhere to the damaged vessel wall.
• Platelets release serotonin (5-HT) and thromboxanes.
• Smooth muscle in the vessel wall contracts.
• Endothelins are released by the damaged vessel, leading to vasoconstriction.

Primary Haemostasis: Platelet Plug

• Platelets clump together around exposed collagen fibres.
• Von Willebrand factor (a glycoprotein in blood plasma) assists and stabilizes the platelet plug.
• Platelets release adenosine diphosphate (ADP), attracting more platelets.
• Platelet plug formation occurs.

Bleeding Time

• Bleeding time is the time it takes for primary haemostasis, including blood vessel constriction and platelet plug formation, to occur.
• Normal bleeding time is 2-7 minutes.
• Bleeding time is prolonged in conditions like thrombocytopaenia, severe anaemia, collagen disorders such as Ehlers Danlos syndrome, and Von Willebrand's disease.
• Anti-platelet drugs, such as aspirin and clopidogrel, can prolong bleeding time.

Secondary Haemostasis: Coagulation

• A complex process results in stabilization of the platelet plug by insoluble fibrin strands that form a mesh.
• Fibrin is formed from soluble fibrinogen through the clotting cascade.

Clotting Cascade

• It is a series of steps in response to bleeding caused by tissue injury.
• Each step activates the next and ultimately produces a blood clot, also known as secondary haemostasis.

Extrinsic Pathway (Tissue Factor Pathway)

• It is the main pathway in the clotting cascade.
• Tissue factor (factor III) released by damaged endothelial cells triggers it.
• Tissue factor converts factor VII to factor VIIa.
• Factor VIIa activates factor X into factor Xa.
• The common pathway then begins after this.
• Prothrombin Time (PT) measures the extrinsic pathway, with a normal value of 11-16 seconds.

Intrinsic Pathway (Contact Pathway)

• Blood coming into contact with collagen fibres in the broken wall of a blood vessel triggers it.
• It is "intrinsic" because a factor inside the blood vessel starts it.
• Activation of factor XII (serine protease) begins the process; it becomes factor XIIa after exposure to endothelial collagen after damage.
• The common pathway ends the process.
• Activated Partial Thromboplastin Time (aPTT) measures the intrinsic pathway, with a normal value of 23-35 seconds.

Common Pathway

• Prothrombin is converted to thrombin (serine protease).
• Thrombin converts soluble fibrinogen into fibrin strands.
• Factor XIII acts on fibrin strands to form a fibrin mesh.

Coagulation Factors

• Majority of coagulation factors are synthesized in the liver.
• Factor VII is created by the vascular endothelium.
• Vitamin K is essential for forming clotting factors in the liver.
• Liver pathology can cause problems with forming clotting factors.
• Inherited disorders such as Haemophilia A, B, and C result in a lack of factors VIII, IX, and XI, respectively.

Effects of Anticoagulants

• Anticoagulants are drugs that help prevent blood from clotting.
• Warfarin, Heparin, and Rivaroxaban can block different parts of the clotting cascade.
• Anticoagulants indications: Atrial fibrillation, Deep vein thrombosis and Stroke.

Clot Retraction

• The clot volume contracts by ~ 90% within 24 hours.
• Actin and myosin proteins within activated platelets pull the clot tight.
• Fibrin threads draw more closely together.
• Serum exudes during this process.
• Clot shrinkage pulls the edges of the damaged vessel together, reducing blood loss.

Clot Breakdown - Fibrinolysis

• Plasminogen, trapped within the clot, is converted to plasmin.
• Plasmin breaks down fibrin.
• Thrombin activated fibrinolysis inhibitor (TAFI) is a fibrinolysis inhibitor that stabilizes clots.

Fibrinolysis Abnormalities

• Disseminated intravascular coagulation and metastatic prostate cancer enhance fibrinolysis.
• Alcoholic liver disease, antiphospholipid syndrome, hypothyroidism, chronic renal disease, and pregnancy depress fibrinolysis.

Thrombosis

• Over-activity of coagulation or under-activity of fibrinolysis can cause it.
• Frequently, it starts where vascular endothelial damage allows platelets to adhere.

Dental Relevance

• Dental procedures can cause haemorrhage.
• Bleeding should stop naturally after 4-10 minutes.

Haemorrhage Control in Dentistry

• Pressure and sutures control haemorrhage.
• Packing with haemostatic agents like Surgicel can help.
• Electrosurgery units and lasers (less commonly) can be used if needed.