Understanding Haemostasis and Blood Loss

• Haemostasis is the process by which bleeding stops.
• It involves overlapping processes that occur when a blood vessel is damaged, stopping the bleeding.
• Blood is an important connective tissue that nourishes all organs, and haemostasis ensures that blood loss is stopped quickly after injury.

Consequences of Rapid Blood Loss

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

Stages of Haemostasis:

• Vasoconstriction: First stage; initial bleeding is stopped by constriction of blood vessels.
• Platelet Plug Formation: Second stage; platelets clump together around exposed collagen fibres to form a plug.
• Coagulation: Third stage; the platelet plug gets stabilised by insoluble fibrin strands forming a mesh.

Primary Haemostasis: Vasoconstriction

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

Primary Haemostasis: Platelet Plug

• Platelets clump together around exposed collagen fibres.
• A glycoprotein in blood plasma called von Willebrand factor assists the process as it stabilises the platelet plug.
• Platelets release chemicals, such as adenosine diphosphate (ADP), attracting other platelets to the site, leading to platelet plug formation.

Bleeding time

• Bleeding time is the time it takes for primary haemostasis (blood vessel constriction and platelet plug formation) to happen, normally 2-7 minutes.
• Bleeding time may be prolonged by Thrombocytopaenia, severe anaemia, collagen disorders such as Ehlers Danlos syndrome, Von Willebrand's disease, and anti-platelet drugs e.g. aspirin or clopidogrel.

Secondary Haemostasis: Coagulation

• This is a complex process stabilizing the platelet plug by forming a mesh of insoluble fibrin strands
• Fibrin created from soluble fibrinogen through the clotting cascade.

Clotting Cascade

• A series of steps responding to bleeding caused by tissue injury and each step activates the next, ultimately creating a blood clot, also known as secondary haemostasis

Extrinsic Pathway (Tissue Factor Pathway)

• The main pathway triggered by tissue factor (factor III) which is released by damaged endothelial cells.
• Tissue factor converts factor VII to factor VIIa, which goes on to activate factor X into factor Xa, and proceeds to the common pathway.
• Extrinsic pathway is measured by Prothrombin Time (PT) with a normal value of 11-16 seconds.

Intrinsic Pathway (Contact Pathway)

• Triggered by blood coming into contact with collagen fibres in the broken wall of a blood vessel. Initiated by a factor inside the blood vessel
• Activation of factor XII (serine protease) initiates this pathway, becoming factor XIIa after exposure to endothelial collagen post damage.
• Ends with common pathway
• Intrinsic pathway is measured by Activated Partial Thromboplastin Time (aPTT) where Normal value = 23-35 seconds.

Common Pathway

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

Coagulation Factors

• Most coagulation factors synthesised in the liver.
• Factor VII is created by the vascular endothelium.
• Vitamin K is essential for formation of clotting factors in the liver.
• Liver pathology might cause issues in clotting factors forming.
• Inherited disorders such as Haemophilia A, B, and C cause a lack of factor VIII, IX, and XI respectively

Effects of Anticoagulants on the Clotting Cascade

• Anticoagulants are drugs which are designed to help prevent blood from clotting.
• Drugs include Warfarin, Heparin, and Rivaroxaban which block different parts of the clotting cascade.
• Atrial fibrillation, deep vein thrombosis and stroke are main indications for anticoagulants.

Clot Retraction

• Contraction of approximately 90% of initial clot volume happens within a 24 hour period.
• Actin and myosin proteins within activated platelets pull clot tight and fibrin threads draw more closely together.
• Serum exudes with Clot shrinkage pulling the edges of the damaged vessel together, reducing blood loss

Clot Breakdown – Fibrinolysis

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

Fibrinolysis Abnormalities:

• Fibrinolysis may be enhanced by Disseminated intravascular coagulation and Metastatic prostate cancer.
• Fibrinolysis may be depressed by Alcoholic liver disease, Antiphospholipid syndrome, Hypothyroidism, Chronic renal disease, and Pregnancy.

Thrombosis

• Thrombosis is often a result of over-activity of coagulation, under-activity of fibrinolysis, or start because of vascular endothelial damage.

Dental Relevance

• Dental procedures cause haemorrhage, which should stop 4-10 min depending on the wound.

Haemorrhage in Dentistry

• Haemorrage is controlled in dentistry by pressure, sutures, and packing with haemostatic agents, like Surgicel.
• Less commonly, Electrosurgery unit or Lasers may control heamorraging

Explore haemostasis, the body's process for stopping bleeding, and the consequences of blood loss. Learn about vasoconstriction and platelet plug formation stages. Understand how the body maintains blood volume following injury.