DEPARTMENT OF ORAL AND MAXILLOFACIAL

SURGERY

BLEEDING DISORDERS AND MAXILLOFACIAL

VASCULAR ANOMALIES
SEMINAR NO:4 DATE:26/11/18

GUIDED BY: PRESENTED BY:

DR.NISHANT .R. CHOURASIA DR.MANIMALA PRIYA BABY
PROFESSOR & HOD OF OMFS YEAR(2018-2021)
 INTRODUCTION

•A group of disorders characterized by defective hemostasis

with abnormal bleeding

•The cause may or may not be related to platelet

abnormalities

•These causes are broadly divided into 4 groups:

1. Due to vascular abnormality
2. Due to platelet abnormality
3. Disorder of coagulation factor
4. Combination of all these as in disseminated intravascular
coagulation
 CLOTTING FACTORS

Factor 1 Fibrinogen
Factor Prothrombin
Factor 3 Tissue thromboplastin
Factor 4 Calcium ions
Factor 5 Labile factor
Factor 7 Stable factor
Factor 8 Antihemophillic Factor
Factor 9 Christmas Factor
Factor 10 Stuart-Prower Factor
Factor 11 Plasma thromboplastin antecedent
Factor 12 Hageman Factor
Factor 13 Fibrin stabilising Factor
 HEMOSTASIS

1.Vascular phase
2.Platelet phase
3.Coagulation phase
4.Fibrinolytic phase
Hemostasis

Primary Hemostasis
•Blood vessel contraction
•Platelet Plug Formation
Secondary Hemostasis
•Activation and clotting cascade
•Depostion and Stabilization of Fibrin
Tertiary Hemostasis
•Dissolution of Fibrin clot
•Dependent on Plasminogen Activation
 So What Causes Bleeding
Disorders?

VESSEL DEFECTS
PLATELET DISORDERS
FACTOR DEFICIENCIES
OTHER DISORDERS
 Classification:

•Disorders of blood vessels

•Scurvy,Senile purpura,Henoch-Schonlein
syndrome

•Disorders of coagulation
•Extrinsic.intrinsic,combined

•Disorders of Platelets
•Thrombocytopenia ITP,HUS,DIC
•Aspirin therapy,Thrombasthenia

•Other disorders
•Post transfusion purpura
 VASCULAR DISORDERS

•Vascular disorders rarely causes serious bleeding;any

bleeding into skin or mucus membrane starts
immediately after trauma but stops within 24-48 hours.
•Vascular disorders are a rare cause of bleeding
problems;they include Marfan, Ehler-Danlos and
Osler-Rendu- Weber syndrome
 OSLER-WEBER-RENDU
SYNDROME(HEREDITARY HAEMORRHAGIC
TELANGIECTASIA)

General aspects
•Hereditary haemorrhagic
telangiectasia is an autosomal
dominant condition with a high
penetrance,as 97% of people
affected exhibit symptoms
•There is vascular dysplasia
leading to telangiectasia and
arteriovenous malformation in
the skin,mucosa and viscera
Clinical features
•Interestingly,HHT usually presents in adolescence.
•Telangiectasia on the skin or any part of the
oral,nasal,conjuctival,respiratory,gastrointestinal or
urogenital mucosa,or brain and liver,leads to bleeding
•Associated features include:
•Heamorrhage of the gastrointestinal tract,which
can result in iron deficiency anemia
•Respiratory arteriovenous malformations,which
can present as dyspnoea,cyanosis or finger –
clubbing.
•Liver arteriovenous malformations that can cause
cirrhosis,which can further exacerbate the bleeding
tendency,and high output cardiac failure

.
General management
•Investigations include capillary microscopy,
computed tomography,magnetic resonance imaging
and angiography,
•Treatment is by cryosurgery or by argon laser
treatmet.

Dental aspects
•Telangiectasias may be seen in any part of the mouth
and may be conspicious on the lips and tongue.
•Regional local anesthesia should be avoided because
of the risk of deep bleeding.
•Concious sedation can be given if required.
 SURGICAL MANAGEMENT

•Septal dermoplasty:It is done in patient who has got repeated

attacks of epistaxis.in this involved muosa is removed and
replaced by skin graft
•Pressure pack:Spontaneous haemorrhage may be controlled by
pressure packs,particularly nasal bleeding
•Sclerosing agents:Sclerosing agents such as sodium
morrhuate or sodium tetradecyl sulfate injected into the lesion
is useful
•Electrocautery:Electocautery is also useful,prophylactically in
a lesion that is likely to cause bleeding
•LASER ablation
•Other therapy:Other therapy like progesterone,estrogen,iron
replacement therapy and occasionally blood transfusion is also
indicated in severe patient
 PLATELET DISORDERS

•Platelets originate from bone marrow megakaryocytes

and have a life span of about 1 week,before they are
destroyed in spleen.
•Thrombopoetin,the megakaryocyte-stimulating hormone
is produced in the liver and kidneys,so liver,kidney or
bone marrow disease can each cause thrombocytopenia.
•Platelet numbers or function, if impaired,can cause a
bleeding tendency,purpura and abnormal laboratory
investigation results.
•Drugs,bone marrow invasion,autoimmune diseases and
other disorders can reduce platelet number.
Thrombocytopenia can arise from:
 IDIOPATHIC THROMBOCYTOPENIC PURPURA
•This involves autoantibody-mediated platelet
destruction,the most common antibody being directed
against the platelet GP2b-3a receptor.
•Features include petechiae,ecchymosis and
postoperative haemorrhage.
Surgical management
•Full blood picture and platelet counts are indicated.
•Corticosteroids or immunosuppressives are the main
treatments.
•Splenectomy or spleenic irradiation,followed by
thrombopoietin therapy is needed.
•Eltrombopag and romiplastin are thrombopoietin
receptor agonists which stimulate platelet production
and used to treat ITP.
•Dental extractions may be covered by these agents
 GLANZMANN DISEASE

•Glanzmann disease is a rare autosomal recessive disorder

caused by either deficient or abnormal glycoprotein platelet
receptors.
•Defects in the GP 2b-3a complex lead to defective platelet
aggregation and subsequent bleeding,usually presenting in
infancy or early childhood with bruising or petechiae following
minimal or unrecognised trauma,or epistaxis.
•The platelet count is normal but platelet aggregation is
defective .
General management
•Management includes avoiding trauma and
avoiding analgesics such as aspirin
•Minor bleeding intraorally can be managed by
tranexamic acd
•Major bleeding may require platelet transfusion.
•Recombinant human-activated factor 7 has been
used in patients with antibodies to GP 2b-3a
receptors
Disorders of coagulation
 HAEMOPHILLIA A

General aspects
•Haemophillia a is an X-linked disorder resulting
from a deficiency in blood clotting factor 8, a key
component of the coagulation cascade.
•Haemophillia mainly affects males
•All daughters of an affected male are carriers but
sons are normal.
•The female carriers will transmit the disorder to
half of her sons and the carrier state to half of her
daughters.
Hemophillia A
 Symptoms and diagnosis

•Bruising
•Spontaneous bleeding
•Bleeding into joints and
associated pain and swelling
•Gastrointestinal tract and urinary
tract hemorrhage
•Blood in the urine or stool
•Prolonged bleeding from cuts,
tooth extraction and surgery
General management
•The diagnosis of heamophillias is based on the clinical
presentation, a positive family history ,coagulation studies
and clotting factors assays.
Laboratory findings in haemophillia
•Normal prothrombin time
•Prolonged activated partial thromboplastin time
•Reduced factor 8
•Reduced factor 9
•Haemophilliacs should be under the care of recognised
hemophilliac centres,where the primary aim is to prevent
and treat bleeding with the missing clotting factor,using a
specific factor concentrate.
•Factor 8 must be replaced to adequate levels during
episodes of bleeding.
•Patients usually recognise early symptoms of bleeding
even before the manifestations of physical signs.
•This is often described as tingling sensation or aura
•Acute bleeds should be treated as quickly as
possible,preferably within 2 hours.
•Desmopressin can raise factor 8 level adequately to
control bleeding in patients with mild and possibly
moderate,hemophillia A
 Surgical considerations

•Prophylactic Medications ,as prescribed by World

Federation Of Hemophillia.
 HEMOPHILLIA B

•Christmas disease- deficiency in clotting factor 9

Symptoms include:

•Nose bleeds,Bruising
•Spontaneous bleeding
•Bleeding into joints and associated pain and swelling
•Gastrointestinal tract and urinary tract hemorrhage
•Blood in the urine or stool.
General management
•The activated partial thromboplastin time is
prolonged with a normal prothrombin time
•Treatment is with factor 9 concentrate
• A dose of 20 units of factor 9 per kilogram body
weight is given intravenously 1 hour
preoperatively
 VON WILLEBRAND DISEASE

•von Willebrand disease is the most common inherited

bleeding disorder and is caused by von Willebrand factor
deficiency.
•Inheritance is usually autosomal dominant and disease
affects males or females
•Von Willebrand factor is a protein expressed both in
platelets and blood vessel endothelial cells;it is
synthesized in endothelium and megakaryocytes has
binding sites for collagen and for platelet glycoprotein
receptors.
von Willebrand Factor acts in two ways:
•It normally binds to GP1b and acts as a carrier for
factor8,increasing factor 8 half-life by protecting it from
proteolytic degradation thus a deficiency of von
Willebrand Factor also leads to a low factor 8
concentration in the blood
•von Willebrand Factor also mediates platelet adhseion
to damaged vascular endothelium,enhancing platelet
aggregation.Thus a deficiency of von Willebrand Factor
leads to defective platelet adhesion,which in turn causes
a secondary deficiency in factor 8
Clinical features:
•von Willebrand Factor causes bleeding that has
features similar to those caused by platelet dysfunction
•The common pattern is bleeding from and purpura of
mucus membrane and the skin.
•Gingival hemorrhage is more common
•Excessive haemorrgage occur after sugeries
•The pattern is distinct fro that of hemophillia
•Bruising ,epistaxis and prolonged bleeding during
surgeries are the most common features
The amount of bleeding depends on the type and
severity of vWD but manifests with:
•Frequent or hard to stop bleeds
•Easy bruising
•Heavy menstrual bleeding
•Longer than normal bleeding after
injury,surgery,childbirth or dental care
Other common bleeding events including:
•Blood in the stool
•Blood in the urine
•Bleeding into joints
General management
•von Willebrand Factor is characterised by the laboratory
findings:
Prolonged activated partial thromboplastin time
Low levels of von Willebrand Factor
Reduced platelet aggregation
•Factor 8 must be replaced to adequate levels during
episodes of bleeding
•Desmopressin can raise factor 8 level adequately to
control bleeding in patients
Treatment
•The most commonly used types of treatment are:
Desmopressin acetate
von Willebrand Factor replacement
Antifibrinolytic agents
 HAEMOPHILLIA C

•Common in ashkenazi jews

•Factor 11 deficiency is inherited as an autosomal
disorder with either homozygosity or compound
heterozygosity
•Patients with factor 11 deficiency cannot activate
thrombin,this results in rapid fibrinolysis which is
responsible for the bleeding tendency seen in this
disorder
•Fresh-frozen plasma or factor 11 is required
 ACQUIRED COAGULATION DEFECTS

•Acquired haemorrhagic disorders are more prevalent than

congenital diseases
•Important causes include anticoagulant therapy and liver
disease,vit k deficiency or malabsorption,disseminated
intravascular coagulation,fibrinolytic states, amyloidosis
and autoimmune disorders
 LIVER FAILURE

•Liver failure leads to impaired synthesis of vitamin k

dependent clotting factors such as factor 2,7,9,10 and
fibrinogen leading to prolonged PT and INR
•Patients with liver failure may also have oesophageal
varices associated with portal hypertension,and serious
bleding from these is possible
•During bleeding fresh frozen plasma may be needed.
•Treatment with high-dose vitamin K increases levels of
these clotting factors
 DRUGS

•Anticoagulants are given to prevent and treat

thromboembolic disease
•Commonly used anticoagulants are coumarin warfarin for
long term treatment and heparin for short term treatment
•Warfarin is the most commonly used oral anticoagulant
•It is a vitamin k antagonist ,which acts by inhibiting the
post translational glutamate carboxylation of blood
coagulation factors 2,7,9 and 10
 WARFARIN

•Surgery is the main oral health –care hazard to the

patient on warfarin
•The INR is used as a guideline to care and should be
checked on the day of operation or,within 24 hours
prior to surgery
•Anticoagulant traetment should not be altered ,since
it does not necessarily reduce bleeding significantly n
contrast it may cause hypercoagulability and rebound
thrombosis
•LA regional block injections ,or those in the floor of
mouth may be a hazard ,since bleeding into the
fascial spaces of the neck can threaten airway patency
•If surgery is to be limited ,such as the uncomplicated
forceps extraction of 1-3 teeth,and the INR is below 4.0,with
no risk factors present,local hemostatic measures alone
should suffice
•Postoperative bleeding may be minimized by the use of
oxidized cellulose,collagen sponges and sutures.
•If surgery is not to be simple or minor, the INR is over 4.0
or other risk factors are present ,the patient should be treated
in specialist centres
 ASPIRIN AND ANTIPLATELET DRUGS

•Aspirin irreversibly impairs platelet aggregation and is

used long-term in the prevention of cardiovascular events
and stroke in patients at risk
•In patients with no other cause for a bleeding tendency
who are receiving upto 100mg aspirin daily,in general for
uncomplicated extractions of 1-3 teeth there is no need to
interfere with aspirin treatment
•In patients with no other cause of bleeding tendency who
are receiving doses of aspirin higher than 100mg daily,if
there is concern the current value of the bleeding time
should be established
•If it is over 20 miniutes ,surgery should be postponed.
VITAMIN K DEFICIENCY AND MALABSORPTION

•Vitamin k is fat soluble vitamin present in the diet and also

synthesized by the gut flora
•It is absorbed in the small gut, in the presence of bile salts.
•After transport to liver,vit k is used for synthesis of factors
2,7,9 and 10
Haemorrhagic disease may ,therefore result from interference
with vitamin k use by
 Anticoagulants
 Malabsorption
 Obstructive jaundice
 Severe liver disease
Dental aspects
•Dental management in vitamin K deficiency may be
complicated by the clotting defect and the underlying
disorder,particularly obstructive jaundice.
•The underlying disorder should preferably be corrected but
vitamin K can be given if surgery is urgent
•Phytomenadione is the most potent and rapidly acting form and
should preferably be given intravenously
•Liver disease is an important cause of bleeding disorder related
to:impaired vitamin K metabolism,failure of synthesis or
overconsumption of normal clotting factors
•Antifibrinolytic treatment and fresh frozen plasma may
sometimes be effective
 THROMBOTIC DISORDERS

•Superficial vein thrombosis may complicate intravenous

injections,particularly of diazepam,but does not lead to
pulmonary embolism
•Treatment of acute episodes of thrombosis is by
subcutaneous injection or infusion of heparin
 DEEP VEIN THROMBOSIS AND
THROMBOEMBOLIC DISEASE

•Blood contains natural anticoagulants,mainly

antithrombin which inhibits several activated coagulation
factors including thrombin,factor 9a and factor 10a,by
forming a stable complex with various factors
•Deep vein thrombosis and subsequent pulmonary
embolism are important sequlae and causes of death .
•Factors that increase the risk of thrombosis include:
Injury to a vein
Slowed blood flow
Increased oestrogen
Coagulation disorders
Chronic medical disorders
Clinical features of DVT
•Venous thrombosis usually affects the deep
calf veins and there the most common
symptoms include:
Pain,especially on flexing the
ankle(Homan sign)
Swelling
Tendernes
Redness
General management of DVT
•Prophylaxis against venous thromboembolism is important but
not reliably effective
•The calves must not rest on hard objects during surgery and
stasis may be eliminated by calf contractions
•Early mobilization and leg movements postoperatively must be
encouraged
•Heparin anticoagulation is the most effective method of
preventing thromboembolism
•DVT is often diagnosed clinically but confirmed using:
Duplex ultrsound to evaluate the vein blood flow
Venography
Blood D- dimer test
Clinical features of pulmonary
embolism
•Pulmonary embolism can occur without
any symptoms of a DVT but features can
include:
Dyspnoea
Arrythmias
Chest pain
Anxiety
Haemoptysis
Low blood pressure,light
headedness or fainting
General management of Pulmonary Embolism
•Massive pulmonary embolism and cardiac arrest
requires emergency care and early treatment with
thrombolytics and anticoagulants
External cardiac massage which breaks the
embolus
Oxygen
Intravenous heparin
A thrombolytic agent,such as streptokinase
 DENTAL ASPECTS OF THROMBOSIS

•Venous thrombosis may affect the deep calf veins

as a consequence of immobility,pressure on the
calf and increased blood coagulability which
follows GA and surgery
•Thrombophilia and hypofibrinolysis may possibly
underlie so called neuralgia-inducing cavitational
ostonecrosis or Ratner bone cavities, which may
cause severe pain
•NICO appears to be due to resistance to activated
protein C or to low protein levels c levels
•Bone sites most frequently involved are
mandibular molars, maxillary molars and
maxillary incisors
 DISSEMINATED INTRAVASCULAR
INTRACOAGULATION

•Disseminated intravascular coagulation is an uncommon,complex

process with potentially fatal activation of the hemostasis related
mechanisms within the circulation.
•Uncontrolled consumption of clotting factors and intravascular
deposition of platelets may result in serious coagulapathy and
thrombocytopenia
•DIC may be caused by many conditions ,including
sepsis,adenocarcinoma,acute myeloid leukemia,obstetric
complications such as amniotic fluid,embolus,incompatible blood
transfusions,burns,cancers or severe trauma
•DIC can lead to thrombosis,bleeding,hemolysis and shock.
Treatment
•DIC is an acute emergency and any hypoxia or acidosis should
be corrected ,and heparinization,replacement of clotting factors
and platelets or antifibrinolytic therapy given as appropriate.
APPROACH TO BLEEDING DISORDERS IN DENTAL
TREATMENT

Evaluation of bleeding dsorders

Take history
Physical examination
Screening clinical laboratory tests
Observation of excessive bleeding following a
surgical procedure
History
Bleeding problems in relatives
Bleeding problems following operations and tooth
extractions,trauma
Use of drugs for prevention of coagulation or pain
Spontaneous bleeding from nose,mouth etc
Physical examination
Jaundice
Petechiae
Purpura
Ecchymosis
Spider angioma
Oral ulcer
Hyperplasia of gingiva
Haemarthrosis
Icterus Petechiae Purpura

Ecchymosis Spider angioma Oral ulcers

Heamarthrosis Hyperplasia of gingiva
 HEAMOSTASIS SCREENING TESTS

•Screening tests are done to show if there is a

bleeding disorder,but further tests needed to define
the disorder
I. Bleeding time
II. Prothrombin time
III.Thrombin time
• Once the hemostasis screening tests have
indicated that there is a bleeding disorder ,specific
tests required,such as
I. Factor assays-Hemophillia
II. Tests of thrombosis
III.Platelet function studies
IV.Bone marrow study
 PLATELET /THROMBOCYTE COUNT

The number of platelets in a specified volume of

blood
Platelets play a vital role in Haemostasis.
Normal range=1,50,000-4,00,000/cu.mm of blood
Thrombocytopenia=less than 1,40,000/cu.mm of blood
Clinical bleeding problem=less than 50,000/cu.mm of
blood
Spontaneous bleeding with life threatening=less than
20,000lcu.mm of blood
 PROTHROMBIN TIME

Activated by tissue thromboplastin

It is used to check the extrinsic pathway factor(F 7) and
the common pathway(F5,10,prothrombin and fibrinogen)
Normal range:11 to 15 seconds
International normalised ratio(INR)
Surgery can be done under INR less than
3.0
When INR=3.0-3.5,consultation is needed
Delay surgery when INR more than 3.5
Dental management of bleeding disorders
Replacement therapy:
1. Platelet concentrate:thrombocytopenia
2. Fresh frozen plasma:liver disease,haemophillia
B,vWD
3. Factor 8/9 concentrate:Hemophillia A and B
4. DDAVP:Hemophillia A,vWD
Antifibrinolytic therapy
1. E-aminocaproic acid
2. Tranexamic acid

Local heamostatic methods

 Splints,pressure packs,sutures,gelfoam with
thrombin,suricel,microfibrillar collagen
 APPROACH TO MAXILLOFACIAL
VASCULAR ANOMALIES

•The most crucial step in evaluating a patient with a

maxillofacial vascular anomaly is to determine
whether the vascular lesion is a tumor or a
malformation
•History and physical examination provide an
accurate diagnosis
•Vascular malformations unlike hemangioma ,are
almost always noticed at birth and grow
proportionately with the patient
•Spontaneous expansion of a vascular malformation
or bleeding secondary to trauma or infection can
cause an acute painful swelling
•Vascular malformations frequently cause bony
distortions,destruction or hypertrophy
•The distinction between a vascular tumor versus
vascular malformation is extremely important because
of the major implications for prognosis and treatment
•Vascular malformations do not grow by cellular
proliferation,but rather expand by dilation of abnormal
channels and formation of collateral vessels
Clinical examination
Infantile hemangioma-Infantile hemangioma have
distinct margins ,whereas others are diffuse lesions
throughout the upper dermis
•Early superficial infantile hemangiomas are bright red
,whereas deep lesions may not exhibit cutaneous or
mucosal discoloration
•Infantile hemangioma is firm to palpation,and there are
no pulsations
•Infantile hemangiomas are fast -flow lesions during the
proliferating phase and slow-flow during regression
•Frequently, dilated cutaneous veins are visible in the area
of tumor.
• By the time the patient is 1 year of age,infantile
hemangiomas begin to exhibit the first signs of involution
•The bright red color of a superficial lesion deepens ,small
central areas on the surface become gray and the lesion is
less tense on palpation
•Deep hemangiomas ,with intact overlying skin soften and
gradually involute,just as do the bright superficial lesions.
•Involution is complete by 5-8 yrs
Vascular malformations-vascular malformations vary in
color and configuration depending on the vessels
involved
•capillary malforamations are pink during infancy,darken
during childhood ,and become deep purple in older patients
•They are smooth in children,with the texture of normal
skin,whereas in adults the surface often becomes pebbly
and slightly raised.
•Venous malformations are bluish,soft and easily
compressible;phleboliths are often palapated
•Venous abnormalities expand with valsalva maneuver
•Enlargement can follow injury or partial ressection or can
occur with puberty,pregnancy or medication
Lymphatic lesion-lymphatic lesions are colorless wheras
combined lymphatic-venous malformations are deep purple-
blue in color.
•Expansion often occurs as coincident with any upper
respiratory tract infection
•This anomalous lymphatic tissue seems unable to control
the periodic seedling with oral microorganisms
•Macrocystic lesions of the head and neck usually can be
trnsilluminated
•Lymphatic malformations can expand suddenly secondary
to bacterial infection
Arteriovenous lesions- arteriovevous lesions are warm and
sometimes tender and if there is macroshunting ,pulsation and
bruit can be appreciated
Radiological studies
•Magnetic resonance imaging with gadolinium enhancement is the
standard technique for studying vascular lesions
•MRI is useful in demonstrating a deep hemangioma from a
lymphatic or venous malformation
•Plain radiography and CT demonstrates bony changes in relation
to vascular lesions
•Typical sleletal changes include increased size of the underlying
bone,hypertrophy,distortion in shape,or decreased skeletal density,
such as bony destruction
 Management of infantile hemangioma

Observation:most infantile hemangiomas are small and produce

no functional or long-term problems for the patient
•The child should be observed while the tumor proliferates and
ultimately undergoes involution
Local treatment for ulceration and bleeding:it is common for
infantile hemangioma of the lip to ulcerate
•These ulcerated areas should be treated by frequent cleaning
and application of topical antibiotics iontment
•If there is bleeding this usually can be demonstrated by local
pressure.
Pharmacologic treatment:
•For small hemangiomas less than 2 cm in
diameter,intralesional injection of upto 3 to 5mg/kg
triamcinolone is given
•Systemic coticosteroids are used for larger ,destructive or
life endagering lesions
•Prednisolone at a dosage of 2 to 3 mg/kg/day is
administered each morning for 2 weeks
Surgical management:excision of an infantile hemangioma
is indicated for a well localised tumor that is ulcerated
,bleeding producing airway obstruction of interfering with
vision.
Management of arteriovenous malformations
•Super-selective arterial or retrograde venous embolization is used
for palliation of pain,bleeding or cogestive heart failure
•Arterial embolization for occlusion of the nidus followed 24 to
72 hours later by surgical excision
•Sclerotherapy or insertion of platinum coils placed by direct
puncture of the nidus,in conjunction with aterial and venous
occlusion ,may be used if there are tortuous vessels .
CONCLUSIONS
•The history (medical/family history) is extremely important in
evaluating patients with disorders of hemostasis

•Dental extractions are a very common major stresses of the

haemostatic mechanisms,and a prior history of excessive bleeding
following an extraction is important

•So,thorough understanding and knowledge about bleeding

disorders is very much needed for dental professionals to minimize
the complications of many treatment procedures.
References
•Davidsons .Principles& practice of medicine.22nd
edition:2014:991-994
•Crispian Scully.Scully’s medical problems in dentistry.7th
edition:New delhi:2014:212-233
•Leonard kabban.Pediatric oral and maxillofacial surgery.1st
edition:Saunders:2004:275-284