ACTA Odontológica Venezolana

print version ISSN 0001-6365

ACTA odontol. Venez v.42 n.2 Caracas 2004

DENTAL MANAGEMENT OF PATIENTS WITH

HEMORRHAGIC DISEASES AND ANTICOAGULANT
THERAPY.
REVIEW OF THE LITERATURE.

Marisol Benito Mariluz Benito, Alexis Moron, Cecilia Bernardoni, Saul Pereira, Miriam
Bracho, Nancy Rivera.

La Universidad del Zulia. School of dentistry. Service Autonomous University

Hospital. Dentistry service. "Care for patients with systemic diseases area".

OVERVIEW

Medical history is essential in the management of any type of patient, the symptoms and
signs that may suggest hemorrhagic disease can be of two types: those who are more
frequent in the alterations of coagulation factors and those that are more common in
disorders of platelet and vascular primary hemostasis and are generally known as purple or
syndrome purpuric. The petechiae are small capillary bleeding, usually pinpoint, are typical
in syndrome purpuric, and tend to be more intense or confluent at pressure
sites. Ecchymosis, is the infiltration of the skin or mucous membranes of extravasated
blood (the typical moreton or Cardinal), are usually associated with petechiae in syndrome
purpuric, but might be of good size, disorders of coagulation and hiperfibrinoliticos
syndromes. Hematomas, collection of blood extravasada in muscle or deep tissues, are most
frequent in the system of coagulation defects, as does also the hemarthrosis, hemorrhage
almost pathognomonic intra-articular of severe inherited disorder of coagulation
(hemophilia A and B). Purpuric bleeding is characterized by bleeding Mucocutaneous
(petechia, ecchymosis, menses, hematuria, or digestive bleeding). They are usually multiple
and sometimes appear superficial injuries after bleeding begins immediately after vascular
rupture, all these clinical manifestations are important that the dentist will recognize them
in order to provide better dental treatment to patients with bleeding disorders and prevent
unwanted complications.
Keywords: Hemostasis, coagulation, hemorrhage, hemophilia, purple, Petechia,
ecchymosis, Hematoma, dental management.

ABSTRACT

The clinical history has a great significance in the management of any patient, symptoms
and signs suggesting bleeding disease can be mainly of two types: the most frequently
observed in the alterations of the factors of clotting and those, the commonest in
disturbance of primary hemostasis, vascular or platelet, known as purple or purpuric
syndrome. Petechiae - small pointform capillary bleeding; they are common in cases of
syndrome purpuric, and they can be more intense or confluent in sites of
pressure. Ecchymosis is the infiltration on the skin or mucoses of extravasated blood
(purpure injury), they are usually associated with petechiae in the purpuric
syndrome; However, they can be seen in large size in clotting disturbances and
hiperfibrinolytic syndromes. Hematoma - collection of extravasated blood in deep tissues or
muscles are frequent in clotting system defects, as well as hemarthrosis. It is an intra joint
hemorrhage almost pathognomonic of inherit clotting severe disturbance (Hemophilia A
and B).

The bleeding is characterized by mococutaneous hemorrhages purpuric, (petechiae,

ecchymosis, menorrhages, hematuria or bleeding of the digestive system). Usually, they are
multiple, and sometimes they appear after superficial injuries, the bleeding start, shortly
after the vascular rupture. All those clinical manifestations are important for the dentist
Knowledge to avoid non desirable complications

Key Words: Hemostasis, Clotting, Bleeding, Hemophilia, Purpura, Petechiae, Ecchymosis,

Hematoma, Management in Dentistry.

Been to arbitration: 16/10/2002 accepted for publication: 13/06/2003

INTRODUCTION

Hemostasis is the set of physiological mechanisms that help stop bleeding and to minimize
blood loss and involves at least three closely related mechanisms: vasoconstriction, the
agglomeration (Adhesion and aggregation) or primary hemostasis, activation of coagulation
or hemostasis secondary factors. (1) the platelets have a half-life of 7 to 9 days. In its interior
are substances thromboxane A2, ADP or acquire plasma serotonin. Platelets are essential
for clotting have a substance called platelet-derived Factor 3 (2). The normal number of
platelets is between 150,000 and 450,000 platelets per mm3 of blood. The platelet numbers
lower than 100,000 x mm3 are considered expressive of thrombocytopenia and over
450,000 x mm3 is called thrombocytosis (1). Hemostasis starts sticking Von Willebrand
Factor collagen in the wound of the vascular wall. Von Willebrand Factor molecules have
the property of joining on the one hand the collagen that forms the subendotelio and on the
other hand to recipients that exist in the membrane of platelets, called glycoprotein
IB (2,3). Platelets attached to collagen subendotelio change form and release its contents
primarily ADP, thromboxane A2, creating an atmosphere of substances proagregantes
possessing the ability to add on the first adherent platelets platelets. (2.3)
These substances and others released by adherent platelets have the ability to alter the form
of platelets and expose other types of receptors (glycoprotein IIb-IIIa), causing the adhesion
of platelets each other. This adhesion of platelets each other are called platelet aggregation
and is carried out through bridges of Fibrinogen. (2,3) The platelet count measures the
number of platelets and the normal value varies from 150,000 to 450,000 X3mm, the time
of bleeding allows to know the quality of platelets in their Hemostatic function and its
normal time is 1 to 5 minutes. Platelet aggregation measures the degree of platelet pieces,
especially when they have qualitative alterations. Its normal value is: 70-100%. (4) the final
step to achieve definitive hemostasis, is the participation of so-called Clotting proteins. The
intervention of the clotting factors is possible via several routes: intrinsic and extrinsic
pathway linking at the end to reach the common route, in order to form a fibrin mesh to
protect the blood clot. (4)

After that fibrin clot is formed to repair or stop the bleeding from the injured vessel, it must
be destroyed to restore normal blood flow. This process in which fibrin is degraded
ezimaticamente, is called fibrinolysis and is performed by a physiological system whereby
a precursor called plasminogen into plasmin which destroys the clot(1,2).

In the oral cavity, the dental pulp and the alveolus, they have a high content of activators of
plasminogen, which can contribute to bleeding after extraction. The prophylactic use of
antifibrinolytic drugs reduces or prevents bleeding post-extraction in patients with defects
in platelets or coagulation (1).

The intrinsic coagulation Via can be evaluated through the TPT (partial thromboplastin
time) which is 25 to 40 " (2.4), the variation in more or less than 2.5" is considered abnormal,
an increase in the value of the TPT with respect to the control or witness could be indicative
of an alteration at the level of factor VIII or IX (factors Antihemofilicos)(2.4). "The PT
(prothrombin time) whose value is 12 to 14 " (2.4), the variation in more or less 2.5" is
considered abnormal;This time elongation may suggest liver disease since the hepatocyte is
the producing cell except for Von Willebrand factor clotting factors therefore patients with
liver cirrhosis can show elongation in prothrombin time as well as patients with gallstones
or bile duct obstruction since bile enables the absorption of vitamin K , and not be absorbed
there is a decrease of the factors that depend on it are: Factor II, VII, IX, x. the TP increased
in this case could be standardised with parenteral administration of Vit K. Another cause
that can cause an elongated TP is broad-spectrum antibiotic therapy for an extended time
since it destroys Vit K-producing gut bacteria and deficiency of the previously mentioned
factors (2). The common route is evaluated through TT (Thrombin time), your time is
of 10 16 "and the variation in more or less 2.5" is considered abnormal. This test measures
the time that transforms Fibrinogen into fibrin. The time is extended in cases of quantitative
deficiencies of Fibrinogen, presence of anticoagulants heparinicos or presence of
Fibrinogen degradation products, as for example in disseminated intravascular
coagulation. (2)

There are a number of diseases where the blood vessels instead of primary and secondary
hemostasis mechanisms are affected, these diseases are the vascular purple, which
correspond to a heterogeneous group of clinical disorders not thrombocytopenic
characterized by hemorrhagic manifestations located primarily in skin, lesions at the level
of the nasal, oral mucosa, gastrointestinal and urogenital tract are also described and the
main defect is an abnormality in the microvasculature, that may be endothelial with with or
without commitment to subendotelio. The anatomical integrity of the vascular bed is
essential for maintaining a hemostatic balance, factors such as the capillary endothelium,
fibrillar extracellular membrane, the subendothelial connective tissue and the presence of
glycosaminoglycans as intercellular adhesive and they are necessary elements in the
structure of the microcirculation alterations bring as a consequence disorders in vascular
permeability or defect in the ability of the capillary bed to maintain its integrity (increased
vascular fragility). To be found in this group of diseases, generally, changes in the number
or the function of platelet or clotting factors (2).

Disorder in the number of platelets

Autoimmune thrombocytopenic purpura: It presents clinically in two ways: acute and

chronic. The acute form occurs predominantly in children, which may spontaneously
transfer and its prognosis is favorable when it comes to immunosuppressive especially type
steroid. Large amount of megakaryocytes frequently accompanied by morphological
alterations, may be seen in bone marrow vacuolated. Generally presents little or no platelet
production (less than 20,000 x3mm). The chronic form occurs more frequently in adults and
is characterized by thrombocytopenia moderate between 30,000 to 80,000 x3mm, increased
megakaryocytes in bone marrow and shortening of the platelet life (1).

There is tendency to hemorrhage from the mucosa, presence of petechiae, ecchymosis,

purple and hemorrhagic vesicles particularly on the palate and buccal mucosa, pallor of the
mucosa may occur since blood loss causes anemia in the patient(1.5). The diagnosis is made
based on the clinical history and confirmed with laboratory tests where we find:
thrombocytopenia, bleeding time lengthened, poor retraction clot and sometimes anaemia
by bleeding(1).

The quality of platelet disorders

Glanzmann's Thrombasthenia: is an autosomal recessive disorder. It is characterized by a

normal platelet count but the bleeding time is elongated and almost zero clot retraction. The
disorder characterized by deficiency of recipients IIb-IIIa platelet membrane therefore there
will be no platelet aggregation. It is classified as type I and type II. Type I being the most
frequent more or less 70% of cases the GPIIb-IIIa practically are absent. What happens is
that platelets may be not linked to Fibrinogen, factor Von Willebrand and fibronectin that
lack them the physiological receptor and therefore there is no platelet aggregation. Type II
is characterized by the amount of GPIIb-IIIa is reduced between 5 and 25%, but not absent,
allowing some degree of clot retraction but not enough to support a normal platelet
aggregation(1,2,6).

In patients with Glanzmann epistaxis, gingival hemorrhage and menorrhagia are frequent
demonstrations. Surgery and other invasive procedures are complicated by excessive
bleeding. (6)
Bernard Soulier syndrome: Is a recessive autosomal characterized by moderate
thrombocytopenia, large platelets, very prolonged bleeding time, with normal platelet
aggregation with ADP, arachidonic acid and bovine Von Willebrand factor. The hemostatic
defect is due to the absence or deficiency of platelet membrane glycoproteins IB complex
molecular which makes that platelets may no adhere to subendotelio, this glycoprotein is
the physiological receptor for Von Willebrand factor. (2)

Disorders acquired platelet inhibitors

Chronic renal failure: Uremic poisoning has special effect on platelets, which leads to a
hemorrhagic disposition. Hemorrhagic disorders may be increased in patients under
hemodialysis therefore applied, e.g. mechanical damage heparin suffering platelets to hit
against the walls of the ducts of the hemodialysis unit (7).

Drugs: As we know aspirin and NSAIDs characterized by inhibiting prostaglandin

synthesis, since they inhibit the enzyme cyclooxygenase of fatty acids (or prostaglandin
endoperoxide synthase), which converts arachidonic acid to prostaglandins, thromboxane
A2 and prostacyclin. To inhibit the troboxano inhibit the aggregation of platelets.

Von Willebrand disease : It is a bleeding disorder that is inherited inherited as autosomal

dominant which, in the majority of cases, is characterized by normal platelet count but a
prolonged bleeding time, elongated TPT and increased capillary fragility. The Von
Willebrand factor (VWF) is a glycoprotein that is circulating in plasma forming a complex
with factor VIII(1). It is classified as type I, type IIA, type IIB and type III.

Type I: It is the most common, has a mild or moderate decline in vW factor. In milder
cases, though hemostasis is clearly affected the level vW factor is immediately below the
normal limit (50% activity or 5 mg/L.) Endothelial cells derived from the umbilical cord of
patients with disease of vW in crops synthesize and secrete limited quantities of the meter
of VWF and have reduced from double to quadruple of the mRNA of the VWF (2,8,9).

Type II: Much less frequent are characterized by normal or near-normal levels of the
altered protein. Those who suffer from the disease of vW type IIA variety have deficits of
detectable forms of the meter of high and medium molecular weight VWF by
electrophoresis in SDS-agarasa. This is because well a capacity to secrete the multimers of
the high molecular weight VWF or proteolysis of these multimers shortly after exiting the
endothelial cell and enter the circulation. The variety in type IIb also lost the high
molecular weight multimers. However in type IIb disease, this is due to improper bonding
of the VWF, platelets. Total antigens of the VWF and Factor VIII levels are normal (2,8,9).

Type III: About one in every million people suffer from a severe form of vW, which is
phenotypically recessive disease. They present Antigen factor vW undetectable or activity
and a factor VIII low enough so to any other hemarthrosis as well as hemophilia. (2,8,9).

The proper treatment of the disease of VW depends on the symptoms and the type of
underlying disease. There are two alternatives. One is to use crioprecipitados, a fraction of
plasma VWF-enriched, and the other in hiring concentrates of factor VIII that preserves the
high molecular weight VWF multimers. Concentrates of factor VIII are very purified and
have been treated with heat to destroy HIV; they are indicated to treat all hereditary forms
of the disease of VW. Other therapeutic action that avoids the use of plasma is to administer
(1-desamino-8 d-arginine vasopressin) DDAVP or desmopressin, an analogue of
vasopressin, which increases plasma levels of factor of vW in normal patients and patients
with mild vW. Disease type I patients are the best candidates for treatment with DDAVP. In
patients with disease of vW varieties DDAVP should not be used without previously testing
efficiency, since the patient type IIa sometimes not pattern the multimers or hemostasis and
in patients improves type IIb can even worsen the effect when the meter, and induce an
intravascular aggregation of platelets and descend the same count. The DDAVP is
ineffective in patients with the severe form of the disease of vW (2,8,9,10,11).

In severe cases of the disease the most common manifestations are epistaxis, bleeding,
gastrointestinal and Genitourinary tracts and for women by menorrhagia and postpartum
bleeding. In Von Willebrand Disease Type I complex FVIII/VWF increases during
pregnancy to improve this form the clinical manifestations (1.2). Oral manifestations that
may occur in this disease are: gingivorragias, petechiae or ecchymosis in oral mucosa. In
some cases the disease has been detected by bleeding after dental surgery. (1)

Von Willebrand disease is currently considered as the most frequent hereditary bleeding
disease. Epidemiological studies by Nilsson et to the in 1984 referred to a frequency in
Sweden of 70 cases for every million inhabitants and Diez-Ewald et to the Venezuela in
1991, based on the number of cases identified in 5 years, they estimated a rate of 73 cases
per million in the city of Maracaibo(12), the diagnosis can be made based on the clinical
history and is confirmed by laboratory tests where time bleeding and the TPT are
elongated (1).

Hemophilia: is a group of hereditary diseases linked to the X chromosome. The disorder is

due to the deficiency of factor VIII (hemophilia A) or deficiency of factor IX (hemophilia
B) and only affects men as the female wearer. From a genetic point of view, it is important
to know: If a carrier of hemophilia conceives a son, has the same chance of having a
hemophilic a normal child child, and in the event that you have a girl also there is the same
chance to be bearer or to be normal, all a haemophiliac daughters are carriers, a
haemophiliac does not spread disease to his sons (1).

The clinical manifestations are the same in both diseases and will depend on the degree of
the factor deficit. Patients with less than 1% factor (severe hemophilia) (1,2,13), will present
bleeding to minimal injury (1) , bleeding into joints and muscles with functional alterations
of the members. When the deficit is between 1 and 5% (1, 2,13) , is known as moderate
haemophilia where spontaneous haemorrhages and the hemarthrosis are occasional(1), when
the factor is between 6% and 25% deficit (1,2,13), hemophilia is mild and characterized by
cause severe bleeding after minor, such as amigdelectomia and extractions surgeries(1).

At the level of the oral tissues, hemorrhage can affect lips as a result of injuries at the site
when the child begins to walk. Gums can be seat of hemorrhage. The eruption and collapse
of temporary teeth are not usually accompanied by large blood loss, but on the other hand,
the eruption of the permanent teeth is followed by bleeding at the level of the dental
alveolus which can result in death of the tooth (1.14).

The hemarthrosis is a common complication in the joints of hemophiliacs who support

weight. Although they are rare in the joint temporomandibular (TMJ), two cases have been
reported. (15)

Dental behavior in patients with hemorrhagic diseases

Bleeding disorders are one of the most interesting problems to be considered by the dentist
in their daily practice. The propensity to profuse bleeding makes them a special group that
deserves careful attention to avoid the post-operative complications. Research of a bleeding
disorder requires very careful laboratory and a clinical study. The clinical history is the
most important support for the diagnosis of diseases. Develop clinical history are recorded
in family history and personal of bleeding, use of drugs, nutritional deficiencies, etc., as
well as the start of bleeding, its nature, location and whether spontaneous or provoked. The
type of hemorrhage can be oriented to the etiologic diagnosis, so for example, if the
hemorrhage is type Petechial or dotted equimotico do suspect a platelet disorder, while
Frank bleeding disorders in coagulation plasmatic factors suggest. The start of haemorrhage
during childhood and their persistence throughout the patient's life suggest a congenital
bleeding disorder. When bleeding occurs in a male may indicate that it's a hemophilia. If
early symptoms of bleeding are recent should consider the possibility of liver problems or
ingestion of drugs.

Medical history is important in these cases that never should be considered normal
hemostasis of a patient with normal laboratory tests if you have a history of abnormal or
pathological bleeding. We must, however, apply in all patients where a bleeding disorder is
suspected lab tests that allow to verify or orient their coagulation profile. These laboratory
studies are as follows:

Platelet count: that measures the amount of platelets and whose normal value varies
between 150,000 to 500,000 x mm3.

Bleeding time: allows to know the quality of platelets in their Hemostatic function and its
normal time is 1 to 5 min.

Retraction of the clot: It measures the platelet function and it starts at 30 minutes and must
be completed within 24 hours.

Coagulation time: measures the total process of hemostasis and their normal time goes
from 4 to 10 min.

TPT: It measures the intrinsic pathway of coagulation and it should not be above 5 "with
respect to the witness; otherwise it would be pathological.
TP: It measures the extrinsic pathway and it should not be above 2.5 "with respect to the
witness; otherwise it will be pathological.

TT: It measures the last phase of coagulation, i.e. the transformation of Fibrinogen to
fibrin. and it should not be above 2.5 "with respect to the witness; otherwise it would be
pathological.

Fibrinogen: Essential for clotting factor and whose normal value is between 200-400mgs.

Factor XIII: must be present (1)

Dental management of patients with platelet problems

The purple are the most common cause of all hemorrhagic diseases more or less specific,
still unchanged by the use of more frequently used hemostatics in dental practice. It is
therefore important to follow certain standards for dental treatment of these patients:

Work as a team with the medical specialist in haematology for the care of these
patients. While it does not have safety by the hematologist that may be the surgical
procedure will be postponed.

Prior to dental intervention the number of platelets should be above 100,000 platelets per
mm3.

It is necessary to take all measures such as Thrombin topical in combination with oxidized
cellulose as well as the use of antifibrinolytic drugs for the protection of the clot and
prevention of hemorrhage.

Avoid tissue suture and prefer local hemostasis with gauze.

The diet or food should be soft to avoid injuries in gum.

Emergencies must attend under any circumstances using clinical criteria suitable for the
solution of the problem, such as: local hemorrhages use hemostatics mentioned above, as
well as the compression with gauze to try to achieve haemostasis, otherwise is sent to the
specialist. In cases of toothache by pathology pulp is necessary to remove pulp tissue to
place a paste with analgesic anti-inflammatory properties thus allowing the pain relief and
subsequently the Endodontic treatment will continue. The use of anesthetic technique
troncular will be avoided in certain cases.

Contraindicated the use of aspirin for pain relief, instead use acetaminophen.

You should be a good oral hygiene that includes the correct use of the toothbrush, since this
is the best prevention to help control bacterial plaque and prevent the formation of
calculation able to cause bleeding emergency.
Therapy of substitution in these disorders is the concentrated platelet (1).

Dental management of patients with disorders of coagulation plasmatic factors

In the past, tooth extraction in patients with hemophilia and Von Willebrand disease
required transfusion and prolonged hospitalization. Replacement therapy with concentrates
of clotting factors improved the situation, but there was the risk of viral infection and the
formation of inhibitors of factors. Currently, recombinant (not plasma-derived) products
reduce the risk. Treatment with desmopressin (DDAVP), which produces the release of
factor VIII and Von Willebrand (VWF) in patients with mild hemophilia and Von
Willebrand disease, is an alternative to the transfusion of concentrates of clotting
factors. Other forms of therapy, such as antifibrinolytic and local Haemostatic methods,
agents are necessary but not sufficient in many patients. The common objectives of the
dental extraction for patients with bleeding disorders is to prevent bleeding and avoid the
use of products derived from plasma, wherever possible (16).

The oral care of hemophiliacs, represents a challenge for professionals dealing with
health. He is known for Hematologists and dental care than most of the hemophiliac
patients are carriers of caries multiple and advanced by the fear of bleeding by the brushing
dental (15). It is suitable to teach prevention and motivation necessary to achieve a proper
oral health and prevent serious complications with the immediate help of the haematologist.

Recommended standards for dental treatment of hemophiliac patient

Anaesthetics by blocking should only be administered in severe and moderate hemophiliacs

previously prepared and authorized by the hematologist (1).

Avoid anesthesia truncal (1.14) due to the dangers of avoiding deep bleeding. Prefer the
infiltrating anesthesia, intrapulpar intraligamentary (1.15).

Using premedication with sedatives, and hypnotics in major surgical procedures and very
especially in nervous and apprehensive patients. Which must be given by mouth and avoid
the parenteral route to avoid bruising.

Only perform essential surgery (1.15), avoid the elective surgery (14).

Primary teeth must not be removed before its natural fall, should be with the least possible
trauma. Not must be removed more than 2 teeth per session, removing shrapnel, bone, scale
etc., which makes it difficult for hemostasis. Local hemostasis with gauze is performed
every 30 minutes. In the post operative, antifibrinolytic drugs in the form of mouthwash are
indicated by three to four minutes repeating every 6 hours for 5 to 7 days. Gauze dampened
with the antifibrinolytic for 20 minutes (1) should be placed in the extraction site.

When the patient suffers from post-operative bleeding must be again evaluated by the team
treating to decide if it is again trasfundido with factor replacement and continue therapy via
oral (1).
You must avoid the use of suture; If necessary, (1) performed with Nonabsorbable silk suture
to prevent the inflammatory response, which has antifibrinolitica action. (11)

The treatment and curettage should be performed authorization of the hematologist and the
use of antifibrinolytic drugs in the post-operative (1).

Endodontic treatment or therapy pulp is one of the most suitable techniques for
hemophiliacs patients (1.14), since it allows us to retain and maintain necessary
teeth. Remember that the teeth with necrotic pulp endodontic cases is not necessary the use
of anesthesia. The instrumentation must be made without exceeding the apical constriction
in order to prevent bleeding (1).

Surgical-dental treatments is suitable the isolation of the surgical field with rubber
dam (1,14,15) for several reasons: the cutting tools of high speed can cause injury to the mouth,
especially in children, besides the rubber dam retracts the lips, cheeks, tongue and protects
them from any laceration. Clips or Staples pair the dam should be placed by causing
minimal trauma to the gums.

In the case required prosthesis or treatment orthodontic avoid apparatus that gingival tissues
are injured (1.15).

Abscesses with painful symptoms, the patient will receive antibiotic and analgesic
medication remembered avoid NSAIDs and recommended the use of acetaminophen. The
time to drain the abscess, the patient should receive replacement therapy raising factor
between 30-50%, depending on the factor of deficit. (1)

In cases of Pathology pulp should be remove the pulp and place medication intraconducto
analgesic and anti-inflammatory for pain control and then continue
treatment (1). Treatments, endodontic must beware not to pass the constriction apical
otherwise could introduce hemorrhage (14).

The deficit factor substitution implies the hematologist and will depend on the type of
severity of the disorder. In haemophilia A and Von Willebrand used replacement therapy is
Cryoprecipitate or factor concentrate VIII and other plasma disorders and hemophilia B is
used fresh and concentrated factor IX plasma (1,14,15).

In the treatment of the hemophiliac is required the collaboration of the parents of the
patient, should explain the need for their children early periodic dental examination to
eliminate on the one hand the fear and apprehension to dental treatment; in order to prevent
possible installation and development of carious or periodontal processes that involve
bleeding emergency. (1) since starting with prevention is can instill in patients with bleeding
disorders the benefits of maintaining oral health(1.15).

Dental management of patients with anticoagulant therapy

Regime of anticoagulant therapy in patients suffering from acute myocardial infarction,
stroke or prosthetic valve replacement is conducted. As it is a long-term treatment, the
number of patients requiring extraction under these conditions is increasing. In these cases
the treatment is complicated not only by the medical condition of the patients, but also for
its anticoagulant treatment. (17)

Today the warfarin sodium is the most widely used oral anticoagulant, but requires careful
control of laboratory, since its activity may be affected by several factors, including the
individual response of the patient, the diet or the simultaneous administration of other
drugs. For the monitoring of the treatment used the prothrombin time (PT), although since
1983 the World Health Organization recommends the use of the INR (International
normalized ratio), as a way to standardize the TP among the different
laboratories. (4.18) normal value is 0.87 to 1.3 which measures the degree of
anticoagulabilidad obtained with the use of anticoagulants coumarins (INR = PT
(patient) /TP normal). (4)

Some authors have pointed out that it is not necessary to vary the dose of coumadin when
the INR is approximately 4(19), patients with prosthetic valves with the recommended value
of the INR 3.5 (20.4), and equal risk of thromboembolism; they can be treated without
removing the anticoagulant therapy oral (20).

Many protocols have been suggested in the past. These included administering heparin
before treatment, adjust, or reduce the dose of warfarin days before treatment. Patients
under treatment with warfarin sodium and that require tooth extraction need to be handled
in such a way as to carry out treatment without great risk of bleeding post op or
thromboembolic events if you discontinue the medication. (21)

Sindet-Petersen et al. in 1989, recommended immediately after extraction application of

gauze soaked in local compressed tranexamic acid for a few minutes and then mouth rinses
every 6 hours for 7 days, guideline which was used by others. (22)

There are authors who use the prior control of INR, and after the extractions supplied
tranexamic acid, synthetic antifibrinolytic agent to apply in principle with a compressive
bandage and subsequently using mouthwashes for two minutes every six hours for two
days. (21.4)

Conclusions

Knowledge of the various hemorrhagic diseases is essential, since dentistry at all times
professional activates the hemostatic process in their patients and can discover the same
alterations during surgical dental procedures. In addition you must familiarize oneself with
the handling of these disorders that require multidisciplinary teamwork in order to give the
patient the best care and minimize the complications of his condition.

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Universidad Central de Venezuela

Faculty of dentistry,
ACTA Odontológica Venezolana,
Los Chaguaramos
Postal code 47136-1041-
Caracas, Venezuela
www.actaodontologica.com

fundacta@actaodontologica.com