Coagulopathies & Oral Surgery
Introduction
Dental procedures, such as dental extractions & periodontal surgery (treatment of ‘gum’ disease / pyorrhoea), are among the most common ‘invasive’ (surgical) procedures carried out worldwide.
Many oral surgical / dental procedures are associated with post-operative bleeding, which, in most cases, is self-limiting & non-problematic.
However, a small but significant segment of the population has an increased risk of bleeding due to inherited bleeding disorders (such as hæmophila), hæmatological conditions (such as leukæmia or thrombocytopænia) or various drug-induced coagulopathies (such as with warfarin or aspirin), in which even relatively minor invasive procedures can precipitate a prolonged bleeding episode.
Excessive bleeding in these patients is not only distressing for the patient but also hinders the completion of the procedure (e.g. suturing) & can compromise wound healing. More common are patients with hæmostatic defects secondary to underlying disease or medication.
The dental management of such patients can present a significant challenge; however, the onus is very much on the dentist / oral surgeon to maintain clear & frequent communication with the patient’s primary doctor, hæmatologist or both to assess the risk & plan appropriate management.
Clinical Assessment
A careful history regarding bleeding problems is essential prior to surgery. Excessive bleeding may result from a variety of causes.
For instance, drugs such as acetyl-salicylic acid (Aspirin) & other non-selective Non-Steroidal Anti-Inflammatory (NSAID’s such as Ibuprofen) analgesics may inhibit platelet function.
Liver disease may decrease the production of clotting factors.
To help uncover previously unrecognised bleeding disorders prior to major oral surgery, it has been recommended that pre-operative laboratory assessment of hæmostasis be carried out. However, a large number of studies concluded that routine hæmostatic testing of asymptomatic patients does not significantly alter treatment & is not cost effective for its low ‘yield’.
When a bleeding disorder is suspected, the usual screening tests include the PT or INR to test the activity of the extrinsic & final common pathways & the activated partial thromboplastin time to test the intrinsic & final common pathways.
Platelet counts may be important when thrombocytopenia is suspected and bleeding time is prolonged.
If a factor deficiency is known of or suspected, the factor levels will need to be measured and if needs be, augmented.
Patients with multiple or more severe single coagulopathies are best managed by oral surgeons familiar with these disorders & in settings where blood products are available, should they become necessary.
What follows are principles of patient management that relate to the underlying disease process, & which have varying scientific support.
Dialysis Patients
The degree to which kidney, liver & bone marrow disease interfere with coagulation following oral surgical procedures is not well understood. Although there are no randomised, prospective studies, it is unlikely that individuals whose kidney failure is well managed with dialysis would be at increased risk for clinically significant bleeding, even from multiple dental extractions.
In the case of dialysis for Chronic Renal Failure, patients are heparinised for the time they are receiving dialysis, & they could be anti-coagulated to some degree for several hours thereafter.
Heparinisation, along with chronic anti-coagulation (eg aspirin, warfarin), creates a multi-factorial coagulopathy that puts a patient at higher risk for bleeding from oral surgical procedures immediately following dialysis. Although the half-life of heparin is approximately 4 hours, dialysis is a long & fatiguing procedure, & for this reason patients are better able to tolerate dental care on a non-dialysis day. On the other hand, the longer a patient is from their last dialysis, the more likely they are to have a coagulopathy from uræmia.
Patients on Anti-Coagulation & Anti-Thrombotic Medications
An increasing number of patients are taking “blood thinners” for various medical conditions.
These drugs interfere with the body’s normal clotting mechanism. There are 2 main processes by which the body normally forms a blood clot at the site of tissue injury.
The 1st involves small blood cells called platelets which clump together at the wound to form a mechanical plug. This plug slows the flow of blood through the vessel and forms a matrix for the next phase of coagulation. During coagulation, chemicals in the blood interact with each other to fill in the spaces between the platelets, stabilise the clot, & make it more solid until the process stops the bleeding.
Anti-platelet drugs such as aspirin, ticlopidine & clopidogrel target this phase of clot formation by preventing platelets from sticking together and adhering to blood vessels. These drugs do this by creating permanent changes in the platelets which last for the lifetime of the platelet (7 – 10 days). These effects can only be countered as the body produces new platelets that have not been exposed to the drug.
Anti-coagulant agents such as warfarin inhibit the 2nd phase of clotting by blocking production of proteins that stabilise the clot. Warfarin can only affect these blood proteins when they are being made.
Patients on Anti-Coagulation & Anti-Thrombotic Medications
An increasing number of patients are taking “blood thinners” for various medical conditions.
These drugs interfere with the body’s normal clotting mechanism. There are 2 main processes by which the body normally forms a blood clot at the site of tissue injury.
The 1st involves small blood cells called platelets which clump together at the wound to form a mechanical plug. This plug slows the flow of blood through the vessel and forms a matrix for the next phase of coagulation. During coagulation, chemicals in the blood interact with each other to fill in the spaces between the platelets, stabilise the clot, & make it more solid until the process stops the bleeding.
Anti-platelet drugs such as aspirin, ticlopidine & clopidogrel target this phase of clot formation by preventing platelets from sticking together and adhering to blood vessels. These drugs do this by creating permanent changes in the platelets which last for the lifetime of the platelet (7 – 10 days). These effects can only be countered as the body produces new platelets that have not been exposed to the drug.
Anti-coagulant agents such as warfarin inhibit the 2nd phase of clotting by blocking production of proteins that stabilise the clot. Warfarin can only affect these blood proteins when they are being made.