Understanding Haemostasis

• Haemostasis is the process by which bleeding stops.
• Damage to a blood vessel initiates a series of overlapping processes to halt bleeding.

Importance of Haemostasis

• Blood is a crucial connective tissue.
• It nourishes all organs.
• It is vital to stop blood loss as quickly as possible after injury.

Consequences of Rapid Blood Loss

• Minor blood loss: The body's homeostatic mechanisms maintain blood volume and cells.
• Moderate blood loss: Symptoms include headache, fatigue, nausea, sweating, and dizziness.
• Severe blood loss: Symptoms include clammy, cold, pale skin, rapid shallow breathing, rapid heart rate, little or no urine output, confusion, weakness, weak pulse, blue lips and fingernails, light-headedness, loss of consciousness, and death.

Stages of Haemostasis

• There are three stages of haemostasis:
  • Vasoconstriction
  • Platelet plug formation
  • Coagulation

Primary Haemostasis: Vasoconstriction

• Initial bleeding is stopped by constriction of blood vessels.
• Platelets adhere to the damaged vessel wall.
• Platelets release serotonin (5-HT) and thromboxanes.
• Smooth muscle in the vessel wall contracts.
• Other vasoconstrictors, such as endothelins, are released by the damaged vessel.

Primary Haemostasis: Platelet Plug

• Platelets clump together around exposed collagen fibers.
• The process is assisted by a glycoprotein in the blood plasma called von Willebrand factor, which stabilizes the platelet plug.
• Platelets release chemicals such as adenosine diphosphate (ADP), which attracts other platelets to the site.
• A platelet plug forms.

Bleeding Time

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

Secondary Haemostasis: Coagulation

• This is a complex process resulting in the platelet plug being stabilized by insoluble fibrin strands forming a mesh.

• Fibrin is formed from the soluble fibrinogen through the clotting cascade.

• The fibrin mesh stabilizes the platelet plug.

Clotting Cascade

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

Extrinsic Pathway

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

Intrinsic Pathway

• The intrinsic pathway is triggered by blood coming into contact with collagen fibres in the broken wall of a blood vessel.
• It is called "intrinsic" because it's initiated by a factor inside the blood vessel.
• The pathway starts with the activation of factor XII (serine protease), which becomes factor XIIa after exposure to endothelial collagen after damage.
• It culminates in the common pathway.
• The intrinsic pathway is measured by Activated Partial Thromboplastin Time (aPTT), with a normal value of 23-35 seconds.

Common Pathway

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

Coagulation Factors

• The majority of coagulation factors are synthesised in the liver.

• Factor VII is created by the vascular endothelium.

• Vitamin K is essential for the formation of clotting factors in the liver.

• Liver pathology can cause problems with the formation of clotting factors.

• Inherited disorders such as Haemophilia A, B, and C lead to a deficiency of factors VIII, IX, and XI respectively.

Effects of Anticoagulants on the Clotting Cascade

• Anticoagulants are drugs that help prevent blood from clotting.

• Drugs such as Warfarin, Heparin, and Rivaroxaban block different parts of the clotting cascade.

• Indications for anticoagulants include atrial fibrillation, deep vein thrombosis, and stroke.

• Summary of coagulation cascade consists of, vessel injury, vasoconstriction, platelet plug formation, and coagulation.

Clot Retraction

• The clot contracts to approximately 90% of its initial volume within 24 hours.
• Actin and myosin proteins within activated platelets pull the clot tight.
• Fibrin threads draw more closely together.
• Serum exudes.
• 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) helps stabilises clots.

Fibrinolysis Abnormalities

• Fibrinolysis is enhanced in conditions like disseminated intravascular coagulation and metastatic prostate cancer.
• Fibrinolysis is depressed in conditions like alcoholic liver disease, antiphospholipid syndrome, hypothyroidism, chronic renal disease, and pregnancy.

Thrombosis

• Thrombosis is caused by over-activity of coagulation or under-activity of fibrinolysis.
• It most often starts at an area of vascular endothelial damage to which platelets adhere.

Dental Relevance

• Dental procedures can cause hemorrhaging.
• Bleeding should typically stop naturally within 4-10 minutes, varying based on the wound.
• A separate lecture will cover the causes of prolonged bleeding and how to manage them.

Haemorrhage in Dentistry

• Methods used to control haemorrhage in dentistry include Pressure and Sutures.
• Packing with haemostatic agents such as Surgicel can be used.
• Less common methods are Electrosurgery unit-coagulation wavelength, and lasers.