Canadian Pharmacists Journal - May/June 2019 - 173

PRACTiCeTOOL
invasive measures to manage bleeding.11,51-55
The major difference in managing these patients
lies in the consideration of modifying the antithrombotic regimen when the antithrombotic
drug is thought to be a major contributor to the
nosebleed. Of note, consultation with or referral to the clinician most responsible for managing a patient's antithrombotic therapy should be
sought prior to recommending a modification in
therapy to the patient.
Three key factors must be evaluated when
determining whether or not an antithrombotic
agent is a major contributor to the epistaxis and
subsequently if modification in therapy should
be considered. They are the severity of bleeding,
the degree of anticoagulation/platelet inhibition
at the time of bleeding and the patient's thrombotic risk. First, the severity of bleeding must be
assessed. Though there is no validated tool to
stratify epistaxis severity, community-based clinicians may use objective parameters to estimate
severity such as duration and history of epistaxis,
volume of blood loss, whether a patient is symptomatic for blood loss (e.g., dizziness, hypotension, tachycardia, lightheadedness or syncope)
and, for patients with recurrent epistaxis, assessment of hemoglobin for a downward trend over
time may be helpful.
Second, anticoagulation status or degree of
platelet inhibition at the time of bleeding should
be estimated. It should be noted that therapeutic anticoagulation (e.g., patients on warfarin
with an INR within target range or appropriately
dosed direct oral anticoagulants [DOACs] for
renal function) should not cause overt bleeding but rather might uncover preexisting tendencies or anomalies for bleeding. For platelet
inhibition, one would infer a greater degree of
inhibition with larger doses of antiplatelets or
dual antiplatelet therapy (DAPT). Therefore,
excessive anticoagulation or platelet inhibition
should be ruled out as a contributor for epistaxis,
including an assessment of factors that may contribute to an enhanced inability to clot.
* For patients taking warfarin: INR should be
assessed, including an assessment of factors
known to increase INR, such as the presence of a drug interaction, deterioration
in health status or changes in lifestyle (e.g.,
reduction in vitamin K intake or excessive
alcohol consumption).56 In patients with a
therapeutic INR and epistaxis suitable for
C P J / R P C  *  M ay / J u n e  2 0 1 9  *  V O L  1 5 2 ,  N O  3 

self-management, continuation of warfarin
therapy is recommended,11,57-59 as data have
indicated that there is no increase in bleeding complications when warfarin therapy is
uninterrupted in such patients.11,59,60
* For patients taking DOACs: The patient's
current renal function, age and weight
should be assessed to ensure appropriateness
of the agent and dose. Patients should also be
assessed for any new interacting medications
that may increase DOAC levels. Several case
reports of epistaxis in patients taking dabigatran or rivaroxaban have been published,61-66
but the management strategies employed
were variable (including temporarily or
permanently stopping the DOAC, changing the DOAC to a vitamin K antagonist or
using topical tranexamic acid), offering little
insight into general recommendations.
* For patients taking antiplatelets: Again,
patients should be assessed for drug interactions that could increase antiplatelet levels. Patients taking DAPT are indeed at a
higher risk of bleeding due to the additive
platelet inhibition; however, this risk is
generally acceptable in light of the significant thrombotic risk for which it is indicated (e.g., recent placement of coronary
artery stents). There are no routinely available laboratory parameters that quantify
platelet inhibition.
* For patients taking combination anticoagulant/antiplatelet therapy, the above
factors should be assessed, as applicable.
While this combination is appropriate for
specific indications, one should be vigilant
in estimating the overall degree of thrombotic inhibition in such patients given the
cumulative effect of anticoagulants and
antiplatelets on hemostatic processes.
Third, the patient's indication for antithrombotic therapy must be evaluated, given that
this defines the specific thrombotic event the
drug is intended to prevent. An understanding
of thrombotic risk will affect the threshold at
which therapy modification is considered. Certain disease states have more refined risk stratification schemes to estimate risk, such as with
atrial fibrillation, the CHADS2 score (1 point for
each of Congestive heart failure, Hypertension,
Age 75 years or older, Diabetes mellitus and 2
points for history of Stroke or transient ischemic
173
Canadian Pharmacists Journal - May/June 2019

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