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Stomatological management of anticoagulated

patients undergoing oral surgery: a narrative

review. [English translation-Original in Spanish]

::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::

Cancino, J., Fonseca, D., Parada, F., (2023) Stomatological management of anticoagulated patients undergoing oral surgery: a narrative review. Odontología Vital No. 39, Vol 2, 76-92, https://doi.

org/10.59334/ROV.v2i39.590

Javiera Cancino Diego Fonseca , Fernando Parada

1 Dental surgeon. Dentistry Faculty. Finis Terrae University, Santiago, Chile. Residency: Santiago, Chile.

ORCID: https://orcid.org/0000-0002-1956-7600 / jpcancinog@miuandes.cl

2 Resident of Maxillofacial Surgery. Dentistry Faculty. Andes University, Santiago, Chile.

ORCID: https://orcid.org/0000-0002-1672-9205 / d.fonsecaescobar@gmail.com

3 Resident of Maxillofacial Surgery. Dentistry Faculty. Andrés Bello University, Santiago, Chile.

ORCID: https://orcid.org/0000-0003-1889-245X / fdo.parada.f@gmail.com

Submitted 2023-02-09

Revised 2023-03-04

Accepted 2023-03-25

Abstract

Patients undertaking oral anticoagulant treatment may experience alterations in different stages of hemostasis, which lead to

medical/surgical implications and considerations during their care. Currently, there is no consensus regarding the dental

management of these patients, as they go through surgical procedures.

This leads to clinical protocols that follow numerous approaches, such as reducing the pharmacological intake of the

anticoagulant, replacing it with heparin, and maintaining the controlled treatment.

Objective:

To establish the stomatological management of the patient undergoing oral anticoagulant treatment through an in-depth

review of the literature.

Materials and Method:

A manual bibliographic review search of articles indexed to the PUBMED and EBSCO databases corresponding to the words

“oral surgery”, “oral bleeding”, “anticoagulants” and “dental management” was performed.

Regarding the inclusion criteria: bibliographic reviews, observational studies, clinical trials, guidelines, systematic reviews, and

meta-analyses published between November 2005 and 2022, in English or Spanish, were considered.

Conclusion:

There are multiple protocols for the care of the anticoagulated patient who will undergo a minor oral surgery procedure. It is

important to reflect on the anticoagulant used, the reason for it, its supervision, the surgical procedure that will be undertaken

by the patient, and both intraoperative and postoperative hemostatic measures to be implemented.

After analyzing the above, it is noted that reducing the intake of the drug to perform the surgical procedure may be harmful to

the patient and to the clinician, therefore it is suggested to maintain the antithrombotic treatment and carry out a correct

medical/surgical management.

Keywords

Oral surgery, anticoagulants, dental care, oral hemorrhage.

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Introduction

In the face of certain cardiovascular pathologies,

the risk of suffering a thromboembolic event

increases.

The use of oral anticoagulant therapy in primary

and secondary prevention has been shown to

reduce the risk of cardiovascular accidents and

morbidity in this type of patient (Gazit et al., 2016).

Atrial fibrillation is the most frequent indication for

receiving this treatment, with at least 3 to 6 million

people affected by this pathology in the United

States, with a projection of these values up to 6 to

16 million individuals in 2050.

In Europe, the prevalence of atrial fibrillation in

2010 was 9 million individuals older than 55 years,

and a projection of 14 million people affected in

2060 was estimated (Di Carlo et al., 2012; Kornej et

al., 2020).

Regarding the patients affected with this disease,

78% are under treatment with oral anticoagulants,

and the number is growing due to the

incorporation of new, safer drugs with a broader

therapeutic range (Grymonprez et al., 2022).

Although most dental treatments are low risk,

patients with impaired coagulation require special

care to assess the risk of bleeding they present

and thus prevent and/or manage any type of

unfortunate event (Costa-Tort et al., 2021). Given

this exponential growth in the use of chronic oral

anticoagulants, this work aims to establish the

stomatological management of patients

undergoing oral anticoagulant treatment through

an in-depth review of the literature.

Hemostasis

Hemostasis is a complex process that involves the

action of platelets, coagulation factors (Table 1),

and endothelium at the site of vascular injury.

It culminates in the blood clot formation, which

fulfills the function of preventing or limiting

bleeding. Its stages correspond to: i) primary

hemostasis, ii) secondary hemostasis, and iii)

fibrinolysis (Guerrero & López, 2015).

Primary hemostasis begins almost immediately

when the vascular lesion occurs. In this process,

platelets and the vascular wall mainly interact to

limit and stop vascular extravasation in the

capillaries, arterioles, and venules. In this stage, as a

first instance, a vascular vasoconstriction occurs

followed by the recruitment and activation of

platelets, which adhere to the injured vessel,

forming the platelet plug. This process is primarily

mediated by the prostaglandins thromboxane A2

and prostacyclin and von Willebran factor (Gale,

2011).

Secondary hemostasis, mainly coagulation factors

interact with each other, where exposure of tissue

factor at the damaged site binds and activates

factor Vll, starting a cascade of reactions that

culminates in the generation of thrombin.

This anchors circulating fibrinogen in soluble

fibrin, creating a fibrin mesh, which will reinforce

the platelet plug (Hatton et al., 2013).

Finally, in fibrinolysis, the fibrin networks present in

the fibrin clot are degraded by inhibiting the

formation of plasmin, inhibiting tissue plasminogen

activator through the release of plasminogen

activator inhibitor by endothelial

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P. 78

Identification of records through databases

IdentificationEligibility and criteriaIncluding

Documents obtained from:

PubMed (n =180) EBSCO (n

= 138)

Selected papers for title

and abstract reading (n

= 231)

Selected documents

for complete reading

(n = 100)

Documents included in

the review (n = 40)

Documents removed before review:

Duplicates (n = 87)

Documents removed by

Title and abstract (n =

131)

Excluded documents Full

text not available (n = 7)

Unrelated (n = 43)

Language (n = 10)

Figure 1 Flowchart for the selection of articles included in this review.

Coagulation cascade

The classic model of coagulation was described

by Davie and Ratnoff in 1964 and separates the

cellular and humoral phases, giving prominence

to the series of enzymatic reactions that occur

within secondary hemostasis (Kumar et al..., 2015),

which begin through the intrinsic pathway

that begins after vascular damage, with the

exposure of negatively charged surfaces that

interact with Hageman factors (FXII), antecedent

plasma thromboplastin (FXI), prekallikrein (PK) and

high molecular weight kinogens (QAPM) and the

extrinsic pathway which begins with the formation

of the Extrinsic Tenase complex made

cells. Plasmin degrades the fibrin polymer into

small fragments, which are eliminated by

macrophages (LaPelusa & Dave, 2022).

Materials and method

A manual bibliographic review search of articles

indexed to the PUBMED and EBSCO databases

corresponding to the words “buccal surgery”, “oral

hemorrhage”, “anticoagulants” and “dental care”

was performed.

Regarding the inclusion criteria, bibliographic

reviews, observational studies, clinical trials,

guidelines, systematic reviews, and meta-analyses

published between November 2005 and 2022, in

English or Spanish, were considered.

From this search strategy, a total of 322 articles

were obtained, of which 274 were excluded

(duplicates, text not available, etc.). It resulted in a

total of 44 articles for this literature review (Figure

1). The information collected was thoroughly

reviewed in its entirety.

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up of tissue factor (TF), circulating factor VIIa,

Ca++ ions and phospholipids (Smith et al., 2015).

These two pathways converge in fibrin activation,

culminating in the deposition of an insoluble clot

(Figure 2).

The formation of this clot involves enzymes

(activated coagulation factor), a substrate (an

inactive form of pro-enzymatic coagulation

factor), and a cofactor (Onishi et al., 2016).

FACTOR PLASMA

CONCENTRATION

(MG/DL)

HALF

LIFETIME

(HOURS)

FUNCTION

XII

PREKALLIKREIN

HIGH MOLECULAR

WEIGHT

VII

PROTEIN C

PROTEIN S

PROTEIN Z

VIII

THROMBOMODULIN

TISSUE FACTOR

FIBRINOGEN

0,4-0,6 45-80 In its activated form it is the intrinsic FIX

activator.

1,5-4.5 50-70 Intrinsic pathway initiator

1,5-4,5 36 Precursor of kallikrein

QUININOGENS

8-9 144-156

Cofactors in the activation of FXI and FXII

prekallikrein.

10-12 60-72 Inactive precursor of thrombin

0,05-0,06 4-6 Together with Tissue Factor initiates the

extrinsic pathway.

0,4-0,5 18-25 Inactive precursor of thrombin

0,7-1,2 24-40

Together with tissue factor initiates the

extrinsic pathway.

0,39-0,59 8-14 In its active form, it is the enzyme of the

intrinsic tenase complex.

2,5 40-60 PCa cofactor

0,22 60 Increases the inhibition of FXa by Protein Z

Inhibitor.

0,4-1,4 12-36 Prothrombinase complex cofactor

0,5-1 8-12 Intrinsic tenase complex cofactor

0 Thrombin cofactor

0 Initiates extrinsic pathway by binding to

FVIIa

200-400 90 Precursor of fibrin

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XIII 1-2 168-288

Transaminase that crosslinks fibrin

ANTITHROMBIN III 15-20 68

Serpin inhibits thrombin and factors VIIa,

IXa, Xa, Xia, XIIa and kallikrein.

HEPARIN COFACTOR

II 6,1-8,2 60 Thrombin-inhibiting serpin

PROTEIN C

INHIBITOR 0,5 23,4

Serpin inhibits PCa, thrombin, kallikrein, FXIa,

FXIIa and the C1 component.

Z PROTEIN INHIBITOR

TISSUE FACTOR

PATHWAY INHIBITOR

0,1-0,16 FXa and FXIa-inhibiting serpin

0,006 1-2

Kunitz-type inhibitor of TF/FVIIa/FXa and

PS/FXa complexes.

XII Trauma

Tissue factor

X X

XIa

XIIa

IX IXa

IXa

Prothrombin (III)

Fibrinogen (II)

Thrombin (IIa)

Fibrin (Ia)

VIIa

VII

VIIa

Intrínsec pathway Extrínsec pathway

Common pathway

Figure 2.

Coagulation cascade (adapted from Kumar et al, 2015).

Table 1.

Biochemical characteristics and function of coagulation factors (Adapted from Guerrero et ál., 2015)

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This process is calcium-dependent, which binds to

a y-carboxylated glutamic acid residue present in

factors II, VI, IX, and X. This reaction is dependent on

Vitamin K, where its reduced form is essential to

activate the aforementioned factors. Thus, Vitamin

K is an important pharmacological target for

anticoagulant drugs, since deficiency of this

cofactor prevents blood coagulation (Ufer, 2005).

Cellular model of coagulation

Described by Hoffman and Monroe in 2001, it

explains the in vivo behavior of coagulation and

replaces the cascade hypothesis, giving

prominence to the cells that participate in this

process, which are capable of directing

hemostasis, and to the importance that factor VII

activity acquires. It consists of three phases, called

the initiation, amplification, and propagation phase

(Hatton et al., 2013; Kumar et al., 2015). This model

will not be delved into, since it is not the objective of

this work.

Coagulation tests

The control of the anticoagulated patient is

carried out through various hematological tests,

which can be classified into quantitative and

qualitative, within the quantitative, we find:

-Platelet count: Usually correlates with

bleeding tendency. The normal count is

150-400,000 platelets/mm3 (Gomez et al.,

2021).

-Prothrombin time (PT), Evaluates the

function of proteins of the extrinsic pathway

(Factor VII, X, V II, and fibrinogen). The time it

takes for the fibrin plug to form is measured.

Normal values: 10-13 seconds (depending

on the type of prothrombin used and the

clot detection method) (Winter et al., 2017).

-Activated Partial Thromboplastin Time

(aPTT) Measures the function of intrinsic

pathway proteins (Factor XII, XI, IX, VIII, X, V, II,

and Fibrinogen). The time it takes for the

fibrin plug to form is recorded. Its normal

value is 25-35 seconds (Little et al., 2017).

-Thrombin time (TT): The time it takes to

coagulate a plasma when thrombin is

added. It can be found altered in the

presence of heparin and inhibitors of

thrombin formation. Its normal value is 12 to

19 seconds (Winter et al., 2017).

-“International normalized ratio (INR). It

represents the standardization of the PT. A

value of 1 indicates a coagulation level

equivalent to a patient without VKA

treatment. Values higher than this translate

as a longer time in the formation of the

blood clot and consequently more

bleeding. The objective value of the INR will

depend on the indication for which the drug

was prescribed and can range between

2.5-3.5. VKA therapy must be adjusted by

the attending physician to achieve the

desired INR (Woolcombe et al., 2022).

-Anti-factor Xa assay. It can be done by

fluorescence or chromogenic. It measures

the activity of activated coagulation factor

X. Normal values correspond to 0.5-1.2UI/ml

(Babin et al., 2017).

Within the qualitative studies, we found

-Bleeding time: Used to assess platelet

functionality, the most widely used is the

Ivy technique, whose normal value is 8 to

10 minutes (González Guerrero & Montoro

Ronsano, 2015).

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- Thromboelastogram: Evaluates the dynamics

of clot elasticity, used to assess coagulation

during surgery (González Guerrero & Montoro

Ronsano, 2015).

Types of Oral Anticoagulants

Three types of oral anticoagulants are currently

described: vitamin K-dependent (VKA), direct-acting

anticoagulants (DOAC), and heparins.

1. Vitamin K (VKA) or coumarin antagonists

Among these types of drugs are Warfarin,

Acenocoumarol, and Fenprocoumaron, all

derivatives of hydroxycoumarin, with their

pharmacokinetic and pharmacodynamic

differences (Table 2).

ANTICOAGULANT

VOLUME OF

DISTRIBUTION (L/

KG)

PROTEIN

BINDING

PLASMA

CONCENTRATION

(UMOL/L)

ELIMINATION

KINETICS

WARFARIN

ACENOCOUMAROL

FENPROCUMARON

0,08-0,13 >99% 15-8 First order

0,22-0,52 >98% 0.03-0.3 Two-phase

0,11-0,14 >99% 1,5-15 First order

They inhibit the carboxylation of vitamin

K-dependent coagulation factors: Factor II

(prothrombin), VII, IX, and X, in addition to inhibiting

protein C and S.

They are indicated for the prevention and

treatment of thrombosis and other types of

cardiovascular conditions (atrial fibrillation, venous

thromboembolism, and prosthetic heart valve)

(Conway et al., 2017).

Monitoring

VKA levels are monitored by the INR. Which must

be kept within the therapeutic range determined

by the treating physician (Exposito, 2010). A

subtherapeutic effect offers little protection

against thromboembolic events, and an INR (>4)

increases the risk of bleeding. The variability in the

response between different individuals

Warfarin is highly bound to plasma proteins, so

other substances or drugs that compete for the

binding site displace Warfarin, enhancing the

therapeutic effect of VKAs (Crader et al., 2022).

and its wide range of interactions with other drugs

and foods require frequent laboratory monitoring

(Conway et al., 2017).

Interactions

The inhibition of the expression/activity of the

CYP450 enzymes (CYP2C9 for the S-enantiomer and

CYP1A2, CYP2C19, CYP3A4 for the R-enantiomer of

Warfarin), compromised in its metabolism also

affect the effect of VKAs, therefore, plasma

concentrations of VKAs can be altered when

consumed together with drugs that modify the

expression or availability of CYP450. VKAs can be

altered when consumed

Pharmacokinetic and pharmacodynamic differences between warfarin, acenocoumarol, and

fenprocoumaron (adapted from (Ufer, 2005).

Table 2.

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together with drugs that modify the expression or

availability of CYP450, such as some antimicrobial,

antihypertensive, and anti-inflammatory drugs,

among others (Crader et al., 2022; Little et al., 2017)

(Table 2) (Table 2).

Among the adverse effects that patients under

treatment with VKA may present, we find

hemorrhagic complications, teratogenic effects

causing chondrodysplasia and nasal hypoplasia,

skin necrosis, allergic reactions, liver damage,

nephropathy, and alopecia (Patel et al., 2022)...

Drug group Increased AVK effect Decreased AVK effect

Antimicrobials

Amoxicillin with Clavulanic acid,

Azithromycin, Clarithromycin,

Levofloxacin, Ritonavir,

Tetracycline, Ciprofloxacin,

Erythromycin, Fluconazole,

Isoniazid, Miconazole

Amiodarone, Diltiazem,

Riseofulvin, Nafcillin, Ribavirin,

Rifampin, Dicloxacillin, Ritonavir

Cardiovascular

Anti-inflammatories and

immunomodulators

Fenofibrate, Clofibrate,

Propafenone, Propranolol,

Sulfinpyrazone, Aspirin

Cholestyramine, Bosentan,

Spironolactone

Mesalazine, Azathioprine

Central nervous system

Phenylbutazone, Interferon,

Aspirin, Paracetamol, Tramadol

Alcohol (in case of coexisting

liver disease), Citalopram,

Entacapone, Sertraline,

Disulfiram, Chloral hydrate,

Fluvoxamine, Phenytoin,

Tricyclic antidepressants

(Amitriptyline, Clomipramine),

Benzodiazepines

Barbiturates, Carbamazepine,

Chlordiazepoxide.

Other drugs

Anabolic steroids, Zileuton,

Zafirlukast, Fluorouracil,

gemcitabine, Levamisole

with Fluorouracil, Paclitaxel,

Tamoxifen, Tolterodine,

Thiamazole, L-Tyroxine,

L-Tyroxine, Tamoxifen,

Tamoxifen, Tamoxifen with

Fluorouracil.

Mercaptopurine, Raloxifene,

Multivitamin supplements,

flu vaccination, chelating

substances.

Table 3.

Drug interactions with vitamin K antagonists. *VKA: vitamin K antagonist.

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2. Direct-acting anticoagulants (DOAC)

These types of blood thinners have gained

popularity in recent years. DOACs are classified as

direct inhibitors of thrombin (activated factor II)

(Dabigatran) or direct inhibitors of activated

factor X (Rivaroxaban, Apixaban and Edoxaban).

They are rapidly active drugs whose main

indications are the prevention of acute myocardial

infarction in non-valvular atrial fibrillation,

thrombrophylaxis in knee or hip replacement

surgery, and the treatment/ prevention of venous

thromboembolism (Adcock & Gosselin, 2015;

Conway et al., 2017).

Monitoring.

Unlike VKAs, they do not require periodic

monitoring due to their pharmacokinetic and

pharmacodynamic predictability.

This is advantageous for patient convenience and

satisfaction. Despite this, there are various

situations in which the clinician would want to

address the precise effect of the anticoagulant to

define treatment options, such as an emergency

(e.g., trauma, hemorrhage, kidney or liver failure,

among others) (Conway et al., 2017). Tests such as

aPTT, PT, and TT have low sensitivity and specificity

for this type of drug and lack an optimal dose

response for monitoring DOACs.

For patients taking this type of anticoagulant, the

results of the mentioned tests must be interpreted

qualitatively to confirm the anticoagulant effect

(Blann & Lip, 2014). Regarding the INR, its use cannot

be recommended to monitor the use of DOACs,

since the international sensitivity index was created

as a thromboplastin correction factor specifically

for VKAs (Winter et al., 2017).

Interactions.

The pharmacokinetics of Factor Xa inhibitors may

be affected by inducers/inhibitors of CYP3A4

and/or p-glycoprotein 1. Regarding Dabigatran,

inhibitors/inducers of p-glycoprotein 1 should not

be indicated, as it is a specific substrate of this

molecule (Di Minno et al., 2017).

They report fewer adverse reactions than VKAs

(including intracerebral hemorrhage).

Gastrointestinal disturbances have been reported

with the use of Dabigatran, so if possible it should be

replaced by another type of DOAC.

3. Heparins

Heparins are highly sulfated polysaccharides used

as major anticoagulants. Indicated primarily as a

component in extracorporeal therapy to maintain

kidney blood flow during dialysis and

cardiopulmonary oxygenation (“Heparin,” 2006).

Second, it has been used to prevent/treat deep

vein thrombosis, pulmonary embolism, and

ischemic complications of unstable angina,

among others. It is administered intravenously or

subcutaneously. Its activity is due to the ability to

inhibit multiple factors in the coagulation cascade.

It binds to antithrombin as a serum protease

inhibitor and targets coagulation factors such as

Xa and IIa.

To optimize its anticoagulant activity and minimize

the risk of bleeding, Heparin variants have been

synthesized by fractionation (Beurskens et al., 2020).

The use of low molecular weight Heparin offers

different advantages over unfractionated

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Heparin, such as greater bioavailability allowing

more predictable dosing and lower prevalence of

adverse effects. Thus, low molecular weight heparin

has become the treatment of choice in clinical

situations such as venous thromboembolism,

major surgery, and acute coronary syndrome.

Unfractionated Heparin remains indicated in the

prevention of coagulation with extracorporeal

devices and patients with renal failure (Harenberg,

2011a, 2011b; Walenga et al., 2011).

Monitoring

The chromogenic anti-factor Xa assay is

considered the gold standard to investigate the

activity of low molecular weight heparins.

Regarding aPTT, it has been reported that the

prolongation of time in this assay depends on the

reagent used.

Even so, this test is not useful in its monitoring,

since this type of Heparin owes its effect mainly to

factor Xa inhibition, while aPTT prolongation is

dependent on thrombin activity (Babin et al., 2017;

Despas et al., 2016).

Adverse effects. It is reported that due to its

anticoagulant nature, bleeding or hemorrhages

are to be expected. Bleeding sites include the

adrenal gland, ovaries, and retroperitoneal area.

This complication can occur virtually anywhere

(Despas et al., 2016).

Heparin-induced thrombocytopenia is a serious

antibody-associated reaction that results in

abnormal and irreversible platelet aggregation,

leading to life-threatening thromboembolic events

(Harenberg, 2011b).

It is said that the long use of heparin can cause

Osteoporosis and, consequently, increase the risk of

fracture due to the inhibition of

osteoblastic differentiation and its function (

“Heparin”, 2006).

Bridging/Overlap Therapy

Bridging consists of substituting a long-acting

anticoagulant (usually warfarin) with a

short-acting one (usually low molecular weight

heparin) to limit the time of sub-therapeutic

anticoagulation levels and minimize

thromboembolic risk. Although there is evidence

that its use is limited, it continues to be used on a

case-by-case basis (Nazar J. et al., 2018; Polania

Gutièrrez & Rocuts, 2022).

Complications

The complications presented by patients under

TACO treatment can be classified as hemorrhagic,

which can be minor hemorrhage, major

hemorrhage, and hemorrhage that compromises

life; and non-hemorrhagic, such as skin necrosis,

peripheral emboli, alopecia, and osteoporosis

(Blann & Lip, 2014).

Dental management

Anamnesis. The patient’s clinical record must be

completed carefully, informing the reason why the

anticoagulant was prescribed, and past events of

prolonged bleeding both in the dental office and

in another context. It is important to verify all the

necessary information before performing any

invasive procedure so that the clinician has

support (Iwabuchi et al., 2014).

Assessment of bleeding risk. Dental interventions

can be divided into those in which bleeding is

unlikely and others in which it is probable (Table

3). Based on this assessment, it is possible to

determine which procedures can or cannot be

performed in the dental office without major

complications.

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Unlikely bleeding Probable bleeding

Low risk of bleeding High risk of bleeding

Infiltration of local anesthesia,

intra-ligamentary or lower

mental block.

Local truncal anesthesia

Basic periodontal examination

Removal of supragingival

plaque, calculus, and stains.

Direct restorations with

supragingival margins

Endodontics

Prints

Adjustment of orthodontic

appliances

Simple extractions (1-3 teeth

restricting the size of the

wound)

Incision and drainage

Deep periodontal probing

Root surface debridement

Direct or indirect restorations

with subgingival margins.

Complex extractions or

adjunctive extractions cause a

larger caliber wound

More than 3 extractions at the

same time

Flaps: o Elective extractions o

Periodontal surgery o

Pre-prosthetic surgery o

Periradicular surgery o

Coronary lengthening o Dental

implant surgery

Biopsies

Gingival recontouring

Assessment of the risk of bleeding in dental

procedures according to the “Scottish Dental

Clinical Effectiveness Programme”.

In patients with VKA, INR should be requested to

determine whether or not it is safe to perform the

corresponding intervention. This must be

requested at least 24 hours before the procedure,

but in patients with a stable INR, it is possible to

accept an INR of no more than 72 hours

(Woolcombe et al., 2022).

Continuing or stopping anticoagulant therapy in

this type of patient is a decision of the treating

physician and not of the dentist. In general, the

literature reports that with INR values up to 4,

invasive treatments can be performed (always

having at hand all possible bleeding control

measures).

If the INR value does not allow the procedure to be

performed, trephination may be an option while

the patient’s examinations are regularized, since it

is considered a procedure where bleeding is

unlikely to occur (Calcia et al., 2021; Winter et al.,

2017). The flow of care in these patients is

described in Figure 2.

Table 4.

Assessment of bleeding risk in dental procedures

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Is there systemic

involvement?

Need for antibiotic

prophylaxis?

Is it an emergency situation?

FollowAHA

recommendations

Follow AHA

recommendations

lnitiate definitive

treatment

lnitiate definitive treatment

Trepanation

Exodontia

Use of local hemostatic

measures

Atraumatic technique

Medical pain management

Need for antibiotic

prophylaxis?

Defer definitive

treatment

Defer definitive treatment

Assess the need for a

consultation with the attending

medie *

Trepanation ** Medical

pain management

- Rapidly progressive cellulitis

- Dyspnoea

- Dysphagia

- Facial anatomical spaces

involvement

- Fever (>38ºC)

- Severe systemic involvement

- lnmunosupression

YES

INR reading of the day

2-3.5 >3.5

Hospitalize

1NR reading of the day

• In case of persistently high INR and unable to perform overlap.

Perform exodontiain a hospital setting

•• lf trepanation is the definitive treatment, no need to request

a consultations

Assess the need for a

consultation

with the attending

medic* Trepanation **

Medical pain

management

Trepanation

Exodontia

Use of local hemostatic

measures

Atraumatic technique

Medical pain

management

Figure 3.

Flowchart of dental care in patients undergoing treatment with VKA.

For those patients taking DOAC, it is not necessary

to suspend the medication, and the procedure

can be carried out with the relevant hemostatic

measures (Caliskan et al., 2017).

In the case of patients with injectable

anticoagulants such as low molecular weight

heparin, it should be treated without interrupting

the medication. It is assumed that the risk of

bleeding in these patients is dose-dependent. In

patients using this drug with a prophylactic dose,

the risk is lower than if they were taking a VKA

(Andras et al., 2017).

Antibiotic prophylaxis. The use of preoperative

antibiotics has been described as a predictor

of postoperative bleeding, even though the

mechanism of action is not well described.

Similarly, the use of postoperative antibiotics has

been reported as a risk factor for intraoral

bleeding.

A single antibiotic dose does not significantly

affect the PT-INR of the anticoagulated patient, but

its administration should be monitored in patients

with an INR 3 for an increase in the therapeutic

range (Huang et al., 2022; Yamada et al., 2020).

Antibiotic prophylaxis, if necessary, should follow

the recommendations of the American Heart

Association (Wilson et al., 2021).

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Anesthesia Adrenaline causes local constriction of

blood vessels at the surgical site from 20 minutes

to 2 hours. The occurrence of postoperative

bleeding is affected by adrenaline at the time of

bleeding control in the dental chair and 2-3 hours

after the procedure (Inokoshi et al., 2021). Inferior

nerve block has been reported to be a risk factor

for postoperative bleeding (Huang et al., 2022). In

general, it is safe to use local anesthetics in

anticoagulated patients, as this procedure is

classified as having a low risk of bleeding (Table

3).

Surgical procedure. An atraumatic surgical

technique should be prioritized, avoiding as much

as possible extending the wound (performing only

one extraction or limiting root debridement to three

teeth), and dividing the visits in which treatment is

performed (Woolcombe et al., 2022). In general, the

evidence reports that immediate and postoperative

bleeding in simple extractions with an INR less than

3.0 is low (2%-3%) (Bajkin et al., 2014).

hemostasis. The use and selection of local

hemostasis measures will depend largely on the

degree of complexity of the intervention to be

performed.

Measures reported in the literature include the

use of sutures, alveolar fillers, and antifibrinolytic

agents to control bleeding (Iwabuchi et al., 2014).

Sutures and alveolar fillings such as oxidized

cellulose or gelite have been widely recognized as

post-extraction hemostatic measures. Even so,

not all guidelines necessarily recommend the use

of sutures over these alveolar fillers because they

can cause more damage to the perialveolar

tissue (Iwabuchi et al., 2014).

Among the antifibrinolytics described in

randomized clinical trials are tranexamic acid

(ATX) in tablets, rinse and intravenous, and

aminocaproic acid epsilon AACE) in tablets or

intravenous. These agents bind irreversibly to

plasminogen and block its interaction with fibrin.

The most studied to date is local TXA, whose

efficacy is limited to preventing oral bleeding in

anticoagulated patients (Engelen et al., 2018). Its

availability as a rinse is not available in all

countries, so injectable solutions are diluted for

intraoral use (de Vasconcellos et al., 2017).

Regarding AACE, it is described as having

antifibrinolytic potential in oral surgery, but to date,

there are no randomized clinical trials that

compare its effect with ATX (da Silva et al., 2018).

The literature reports that DOACs have a lower

incidence of postoperative bleeding than VKAs

(Manfredini et al., 2021).

Pain management. Anticoagulants can interact with

non-steroidal anti-inflammatory drugs (NSAIDs). The

patient should be recommended to take

Acetaminophen (if it is not contraindicated) over

drugs such as Aspirin, Ibuprofen, Diclofenac, or

Naproxen, since the latter increases the risk of

bleeding. If the use of an NSAID is considered, it

should be recommended for a minimum time and

with gastric protection (Kent et al., 2018).

Control. The patient should be told that in the

event of noticing a bleeding event between 24

hours and 7 days after the intervention, they

should contact the center where the intervention

was performed by telephone or go to the center in

question or another facility that can control the

bleeding (Inokoshi et al., 2021; Rocha et al., 2019).

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Postoperative bleeding event. Defined as marked

bleeding after mechanical compression with

gauze for 30 minutes. These types of events should

be monitored from the day of the procedure until

one week after the intervention.

Conclusion

There are multiple protocols for the care of the

anticoagulated patient who will undergo a minor

oral surgery procedure. It is important to consider

the anticoagulant used, the reason,

its control, the procedure to be performed on the

patient, and both intraoperative and postoperative

hemostatic measures to be performed. After

analyzing the above, it is noted that reducing the

intake of the drug to perform the procedure can be

more harmful to the patient and to the clinician,

therefore it is suggested to maintain

antithrombotic treatment and perform correct

medical/surgical management.

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