|Coagulopathies & Oral Surgery
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 &
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.
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
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.
Med Oral Patol Oral Cir Bucal 2008. Dental Management in Renal Failure - Patients on Dialysis
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 with Hæmophilia (Factors VIII & IX Deficiencies) & Von Willebrand's Disease
Hæmophilia is a group of hereditary genetic disorders that impair the body's ability to control coagulation (blood clotting).
Hæmophilia A (Clotting Factor VIII deficiency) is the most common form of the disorder (1 in 5,000 – 10,000 male births).
Hæmophilia B (Clotting Factor IX deficiency) is rarer than Hæmophilia A, occuring in around 1 in about 20,000 – 34,000 male
Hæmophilia lowers blood plasma clotting factor levels of the coagulation factors needed for normal coagulation. When a
blood vessel is injured, a clot does form but the missing coagulation factors prevent fibrin formation, which is necessary to
maintain the blood clot.
A hæmophiliac does not bleed more intensely than a person without it but can bleed for a much longer time. In severe cases,
even a minor injury can result in bleeding that can last days - weeks or there is incomplete healing. In areas such as the brain
or inside joints, this can be fatal or permanently debilitating.
Patients with Rare Clotting Factor Deficiencies
Clotting / Coagulation Factors are proteins in the blood that control bleeding.
If any of the clotting factors are deficient or defective, the coagulation cascade is blocked. When this happens, the blood clot
does not form & bleeding continues longer than it should.
Rare clotting factor deficiencies are bleeding disorders in where clotting factors other than those of Factors VIII & IX
(otherwise known as Hæmophilias) are deficient / defective. These are Factors I, II, V, VII, X, XI, XII & XIII.
Patients with Platelet Disorders & Deficiencies
Platelets are cell fragments that function in the clotting / coagulation system.
Platelets circulate for 7 - 10 days. About one third are always transiently sequestered in the spleen.
The platelet count is normally 140,000 - 440,000/μL. However, the count can vary slightly according to menstrual cycle
phase, decrease during near-term pregnancy (gestational thrombocytopænia) & increase in response to inflammatory
cytokines (secondary or reactive thrombocytosis).
Platelets are eventually destroyed, primarily by the spleen.
Platelet disorders include:
- Abnormal increase in platelets (thrombocythæmia)
- Decrease in platelets (thrombocytopænia)
- Platelet dysfunction
Any of these conditions, even those in which platelets are increased, may cause defective formation of hæmostatic plugs &
The risk of bleeding is inversely proportional to the platelet count.
When the platelet count is < 50,000/μL, minor bleeding occurs easily & the risk of major bleeding increases.
Counts between 20,000 - 50,000/μL predispose to bleeding with trauma, even minor trauma.
With counts < 20,000/μL, spontaneous bleeding may occur.
With counts < 5000/μL, severe spontaneous bleeding is more likely.
However, patients with counts < 10,000/μL may be asymptomatic for years.
Canadian Hæmophilia Society 2001. Glanzmann Thrombasthenia. An inherited bleeding disorder
J Oral Maxillofac Surg 2001. Management of the Oral and Maxillofacial Surgery Patient With Thrombocytopenia
Canadian Children's Platelet Study Group 2002. Disorders of Platelet Function
Treatment of Hæmophilia 2008. Platelet Function Disorders
Patients with Hæmatological Disorders
|Last Updated 20th May 2015
A careful history regarding bleeding problems is essential prior to surgery. Excessive bleeding may result from a variety of
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’.