|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 & 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
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.
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
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
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
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
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 births.
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 & bleeding.
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
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
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 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’.