1) Bleeding disorders can involve vascular, platelet, or coagulation disorders and cause symptoms like bruising, bleeding, and prolonged bleeding from minor cuts. 2) Important bleeding disorders discussed include hemophilia A (factor VIII deficiency), hemophilia B (factor IX deficiency), von Willebrand disease (a disorder of the von Willebrand clotting factor), and fibrinogen deficiency. 3) These disorders are diagnosed through tests of bleeding time and clotting factor levels and activity. Treatment involves replacing the missing clotting factor through products like cryoprecipitate, desmopressin, or clotting factor concentrates.

1. BLEEDING DISORDERS
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2. CONTENTS…
Introduction
History
- A Royal Disease
Finding the cause
Identifying clotting factors
Hemostasis
Bleeding disorders
-Vascular disorders
-Coagulation disorders
-Platelet disorders
Dental Evaluation
Dental management
Conclusions
References

3. Introduction

4. History
• In the Talmud, 2nd
century AD
•A 12th century Arab physician named Albucasis
•In the U.S., the transmission of hemophilia from mothers
to sons was first described in the early 1800s.
•In 1803, a Philadelphia physician named Dr. John Conrad
Otto wrote an account of "a hemorrhagic disposition
existing in certain families."
• The word "Hemophilia" first appeared in a description of a
bleeding disorder condition at the University of Zurich in
1828.

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6. A Royal Disease

7. Finding the Cause
 In the 20th century doctors looked for the cause of
excessive bleeding. Until then, they had believed
that the blood vessels of hemophiliacs were simply
more fragile.
 1925
Although it is probably the most common hereditary
bleeding disorder (affecting approximately 1% to 2%
of the population), von Willebrand disease was not
recognized until 1925.

8.  1937,
Patek and Taylor, two doctors at Harvard,
They called it "anti-hemophilic globulin."
 1944
Pavlosky, a doctor from Buenos Aires,
Argentina, did a lab test which showed that
blood from one hemophilic patient could
correct the clotting problem in a second and
vice-versa.

9. Identifying Clotting Factors
 In the 1960s the clotting factors were identified
and named.
 An article in Nature in 1964
 In the 1950s and early 1960s, hemophilia and
other bleeding problems were treated with whole
blood or fresh plasma. Unfortunately, there
wasn't enough of the factor VIII or IX proteins in
these blood products to stop serious internal
bleeding.
 Then, in the 1960s, cryoprecipitate was
discovered by Dr. Judith Pool

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11.  Then, later in the 1960s and early 1970s,
concentrates containing factor VIII and IX
began to be available. (freeze-dried
powdered concentrates)
 blood products carried blood-borne viruses
like hepatitis C and HIV.
 In the 1990s, modern treatment, using safer
factor concentrates, has again improved the
outlook

12. Recent progress includes:
• New clotting factor products and drugs such as desmopressin
acetate also known as DDAVP,
• New, synthetic (not derived from plasma) clotting products
that take advantage of recombinant technologies
• Better screening methods to detect and remove viruses and
other agents from factor concentrates and blood products
• Improved surgical options
• Advanced genetic testing methods
• Medically supervised home-infusion therapy
• Prophylactic treatment

13. HEMOSTASIS
 Platelets
 Coagulation factors

14. Platelets-origin
Life span : 7-14 days
Site of destruction: Spleen
Normal count : 1.5 - 4.5 lacks / cc
Increase in count : Thrombocytosis
Decrease in count : Thrombocytopenia
Decrease in platelet count below 40,000is associated with hemorrhagic disorders.

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16. a. Physiological Variations :
 Seasonal - Count is more during winter season.
 Pregnancy - Count decrease
 Exercise, excitement, injection of adrenaline, high altitude
- Increased count.
b. Pathological Variations :
 Increased platelet count seen after splenectomy idiopathic.
 Decreased platelet count is seen in
 Viral infection
 Aplastic anaemia
 Idiopathic

17. HEMOSTASIS
 Primary Hemostasis
 Blood vessel contraction
 Platelet Plug Formation
 Secondary Hemostasis
 Activation of Clotting Cascade
 Deposition & Stabilization of Fibrin
 Tertiary Hemostasis
 Dissolution of Fibrin Clot
 Dependent on Plasminogen Activation

18. Detailed Events of Coagulation
Figure 17.13b

19. Coagulation
Figure 17.13a

22. Tests of Hemostasis:
 Screening tests:
 Bleeding.T - 10m. Platelet & BV function
 Prothrombin.T – Extrinsic, aPTT – Instrinsic
 Thrombin.T – common path. (DIC)
 Specific tests:
 Factor assays – hemophilia.
 Tests of thrombosis – TT,
 Platelet function studies:
Adhesion, Aggregation, Release tests.
 Bone Marrow study

23. Disorders of Hemostasis
Classification :
• Disorders of Blood vessels
• Scurvy, senile purpura, Henoch-Schonlein syndrome.
• Disorders of Platelets
• Thrombocytopenia ITP, TTP, HUS, DIC.
• Aspirin therapy, Thrombasthenia,
• Disorders of Coagulation
• Extrinsic, intrinsic, combined.
• Other disorders
• Post transfusion purpura.

24. Vascular disorders:
Petechiae, purpura, ecchymoses
senile purpura
vitamin C deficiency (scurvy)
Connective tissue disorders
Infections – Meningococcus
Henoch-Schonlein Purpura-Immu

25. Platelet Coagulation
Petechiae, Purpura Hematoma, Joint bl.

26. Senile PurpuraSenile Purpura

27. Petechiae inPetechiae in
VasculitisVasculitis
(Rocky Mountain Spotted Fever)(Rocky Mountain Spotted Fever)

28. Henoch-Schonlein purpura
 Immune disorder
 Children
 Follows infection
 Petechiae with
edema and
itching.

29. Henoch-Schonlein purpura
20y Male, fever, painful symmetric polyarthritis for a day. During the next two days,
edema and palpable purpura developed.

30. Disorders of coagulation
 Hemophilia A(Factor VIII Deficiency)
 What Is It?
The incidence of hemophilia A is one in 10,000
live male births. About 17,000 Americans have
hemophilia.

31. Inheritance Pattern
 Hemophilia A is caused
by an inherited sex-
linked recessive trait with
the defective gene
located on the X
chromosome.

33. Genetic counseling may be
advised for carriers.
 Female carriers can be identified by testing.
 A woman is definitely a hemophilia carrier if she is:
• the biological daughter of a man with hemophilia;
• the biological mother of more than one son with hemophilia;
• the biological mother of one hemophilic son who has at least
one other blood relative with hemophilia.
A woman may or may not be a hemophilia carrier if she is:
• the biological mother of one son with hemophilia;
• the sister of a male with hemophilia;
• an aunt, cousin or niece of an affected male related through
maternal ties;
• the biological grandmother of one grandson with hemophilia.

34. Symptoms & 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
 People whose clotting activity is 5 percent of normal
may have only mild hemophilia.

36. Treatments
 In the past, mild hemophilia A was typically
treated with infusion of cryoprecipitate or
desmopressin acetate (DDAVP),
 . Today, experts recommend desmopressin
injection or Stimate nasal spray.
 cryoprecipitate

37.  Depending on the severity of the disease, DDAVP
or factor VIII concentrate -prior to dental extractions
and surgery to prevent bleeding.
 Immunization with hepatitis B vaccine.
 Gene therapy and fetal tissue implant techniques
 People who have hemophilia should also avoid
certain drugs that can aggravate bleeding problems:
 Aspirin
 Heparin
 Warfarin
 Certain analgesics such as nonsteroidal anti-
inflammatory drugs

38.  MASAC made recommendations for treatment of
hemophilia in November of 1999.
They include:
1. Factor VIII products for patients who are HIV
seronegative, including Recombinant factor VIII,
2. Immunoaffinity purified factor VIII concentrates
3. Cryoprecipitate is not recommended because of the
risk of HIV and hepatitis infection.
4. Mild hemophilia A should be treated with
desmopressin, in a DDAVP injection or Stimate
nasal spray.

39. complications
 Chronic joint deformities
 Intracerebral hemorrhage

40. Hemophilia B
(Factor IX Deficiency)
 . Hemophilia B ("Christmas disease" )
 Is a deficiency in clotting factor IX.
 Hemophilia A is seven times more common
than hemophilia B.
 The incidence of hemophilia B is one in
34,500 men.

41.  Inheritance Pattern
 Hemophilia B is caused
by an inherited sex-
linked recessive trait
with the defective gene
located on the X
chromosome. Females
are carriers of this trait.

42. Genetic counseling may be advised for carriers. Female carriers can be
identified by testing.
A woman is definitely a hemophilia carrier if she is:
 the biological daughter of a man with hemophilia;
 the biological mother of more than one son with hemophilia; • the
 biological mother of one son with hemophilia and has at least one
other
 blood relative with hemophilia.
A woman may or may not be a hemophilia carrier if she is:
 the biological mother of one son with hemophilia;
 the sister of a male with hemophilia;
 an aunt, cousin or niece of an affected male related through maternal
ties;
 the biological grandmother of one grandson with hemophilia.

43. Symptoms include:
 nosebleeds
 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
 prolonged bleeding following circumcision
 People whose clotting activity is 5% of normal may
have only mild hemophilia.

44. DIAGNOSIS:
 A doctor may suspect hemophilia in a child
whose bleeding is unusual.
 A laboratory analysis of blood samples
 Determine the severity by testing the activity
of factor IX.

45. Treatments
• Infusing the missing clotting factor.
• To prevent a bleeding crisis- taught to administer
factor IX concentrates at home at the first signs of
bleeding.
• Factor IX concentrate may be given prior to dental
extractions and surgery to prevent bleeding.
• Milder forms of hemophilia need to have dental or
other surgery, the drug desmopressin acetate
(DDAVP) may be given to improve clotting temporarily
so that transfusions can be avoided.

46. MASAC made recommendations for treatment of
hemophilia B in
November of 1999. They include
• Recombinant factor IX products for patients who are HIV
seronegative,
• Patients who are HIV-seropositive should also be treated
with high purity products such as immunoaffinity purified
and recombinant factor VIII products.
• For patients with inhibitors to factors VIII and IX, there is
Recombinant Factor VIIa (NovoSeven). Produced by baby
hamster kidney cells, no human albumin or other proteins
are used in its production, reducing virus risk.
There is also Porcine factor VIII (Hyate C) and activated
prothrombin complex concentrates

47. Complications
• Chronic joint deformities,
• Intracerebral hemorrhage
may also occur.
• Thrombosis may occur
following use of factor IX
concentrate.

48.  Von Willebrand Disease
 What Is It?
 von Willebrand disease is a hereditary
deficiency or abnormality of the von
Willebrand factor in the blood, a protein that
affects platelet function

50.  Researchers have identified many variations of the
disease, but most fall into the following classifications
• Type I: This is the most common and mildest form of von
Willebrand disease. Levels of von Willebrand factor are
lower than normal, and levels of factor VIII may also be
reduced.
• Type II: In these people, the von Willebrand factor itself
has an abnormality. Depending on the abnormality, they
may be classified as having Type IIa or Type IIb.
In Type IIa, the level of von Willebrand factor is
reduced, as is the ability of platelets to clump together.
In Type IIb, although the factor itself is defective, the
ability of platelets to clump together is actually increased.

51.  Type III: This is severe von Willebrand
disease. These people may have a total
absence of von Willebrand factor, and factor
VIII levels are often less than 10%.
 Pseudo (or platelet-type) von Willebrand
disease: This disorder resembles Type IIb von
Willebrand disease, but the defects appears to
be in the platelets, rather than the von
Willebrand factor.

52.  Inheritance Pattern
Like hemophilia, the disease is passed down through the
genes. occurs in men and women equally.
Types I and II are usually inherited in what is known as a
"dominant" pattern.
Type III von Willebrand disease, however, is usually
inherited in a "recessive" pattern.

53.  Symptoms and Diagnosis
 A parent with a history of bleeding problems.
 Typically, a child bruises easily or has bleeds
excessively after a skin cut, tooth extraction,
tonsillectomy or other surgery.
 A woman may have increased menstrual
bleeding. Bleeding may worsen at times.
 On the other hand, hormonal changes, stress,
pregnancy, inflammation and infections may
stimulate the body to increase production of the
von Willebrand factor and temporarily improve
clot formation.

54. Diagnostic signs can include:
 normal platelet count
 prolonged bleeding time
 reduced von Willebrand factor level
 reduced platelet adhesion may occur
 reduced or increased platelet aggregation
(platelet aggregation test)
 ristocetin cofactor is reduced

55. MASAC made recommendations for treatment
of von Willebrand disease in November of
1999. They include:
• Stimate, desmopressin acetate.
(DDAVP),nasal spray or injection
• Viral-inactivated factor VIII preparations rich in
von Willebrand factor, such as Alphanate,
Humate-P and Koate DVI, are
recommended.
• Cryoprecipitate is not recommended except in
life-threatening emergencies because of the
risk of HIV and hepatitis infection.

56.  Complications
After any kind of surgery, hemorrhaging may occur.
The condition is worsened by the use of aspirin and
other nonsteroidal anti-inflammatory drugs.
Women may have heavy menstrual periods as well
as risks during pregnancy and childbirth. .

57.  Factor I Deficiency (Afibrinogenemia)
 What Is It?
 Fibrinogen, also known as factor I, is needed
for most types of platelet aggregation. It's the
last step in the clotting process—the "glue"
that holds the clot together.

58.  Included under factor I deficiency are several
rare coagulation disorders known as
congenital fibrinogen defects. They include:
• afibrinogenemia
• hypofibrinogenemia
• dysfibrinogenemia

59.  Inheritance Pattern
 The disorder is not sex-linked
 It affects both males and females with equal
frequency.
 It is autosomal recessive.

60.  Symptoms and Diagnosis
Few people who have any of these
disorders suffer symptoms, although some are
predisposed to form blood clots (thrombosis).

61.  Treatments
-Many people with hypofibrinogenemia or
dysfibrinogenemia need no treatment.
-Those who require treatment may be given
cryoprecipitate or fresh frozen plasma.
The goal of treatment is to raise the patient's
fibrinogen level to 100 mg/dL for minor bleeding
and up to 200 mg/dL for surgery or severe
bleeding. (One unit of fresh frozen plasma has
about 450 mg of fibrinogen.)

62.  Complications
-Risk of thrombosis.
-In women, menstrual bleeding can be a
severe problem and must be controlled

63. Factor II Deficiency(Prothrombin)
 What Is It?
 Prothrombin is a vitamin K-dependent
proenzyme that functions in coagulation.
1)a congenital version called
hypoprothrombinemia,
2)acquired version called
dysprothrombinemia.

64.  congenital, factor II deficiency is extremely
rare.
 Acquired factor II deficiency is more common.
It results from vitamin K deficiency, severe
liver disease and therapeutic use of
anticoagulant drugs.

65.  Inheritance Pattern
 A congenital factor II deficiency is a very rare
inherited disorder that results in deficient
blood clotting. The disorder is not sex-linked
as is hemophilia.
 It affects both males and females with equal
frequency.
 It is autosomal recessive,

66. Symptoms include:
• umbilical cord bleeding at birth
• nose bleeds
• abnormal menstrual bleeding
• abnormal bleeding after delivery
• bleeding after trauma
• bleeding after surgery
• easy bruising
Signs and Tests:
• prolonged prothrombin time
• prolonged partial thromboplastin time
• factor II assay showing decreased activity
• levels of prothrombin ranging from 2% to 50% of normal

67. Treatments
MASAC made recommendations for treatment of
factor II deficiency in November of 1999.
They include:
• Prothrombin complex concentrates (PCCs) can be
used, but these products vary considerably in the
amount of factors they contain.
• Fresh frozen plasma can be used as along as it is
processed to reduce the risk of viral infection.

68.  Complications
Bleeding has to be
controlled in instances
of trauma or surgery, or
else bleeding into the
brain or skull can occur.

69.  Factor V Deficiency (Para hemophilia)
What Is It?
 Factor V deficiency is also known as Owren's
disease or parahemophilia.
 This deficit was identified in Norway in 1943. Since
then about 150 cases have been reported, occurring
in both men and women. The exact frequency of this
rare disorder is unknown, but is estimated to be one
per 1 million

70.  Inheritance Pattern
 The disorder is not sex-linked as is hemophilia.
 It affects both males and females with equal
frequency.
 It is autosomal recessive,
 Several families with combined deficiencies of factors
V and VIII have been reported.

71. Symptoms and Diagnosis
Symptoms include:
 bleeding into the skin
 excessive bruising with minor injuries
 nose bleeds
 bleeding of the gums
 excessive menstrual bleeding
 prolonged or excessive loss of blood with surgery or
trauma
Diagnosing the deficiency involves tests and signs such
as:
 factor V assay showing decreased activity
 slightly prolonged bleeding time (in some people)
 prolonged partial thromboplastin time
 prolonged prothrombin time

72. Treatments
-There are no commercially available
concentrates of factor V, so fresh plasma or
fresh frozen plasma infusions are used .
-The half-life of factor V is 24 hours.
-This is an inherited disorder; there is no known
prevention.
 Complications
-Dangerous hemorrhaging can occur if bleeding
isn't controlled quickly.
- If platelets are used as a source of factor V,
antiplatelet antibodies can be induced.

73.  Factor VII Deficiency (Proconvertin or
Stable Factor)
 What Is It?
 This extremely rare disorder can be inherited
or acquired by people who do not have
hemophilia who take Coumadin, a drug used
to inhibit blood clotting.

74.  This disorder occurs in one in 500,000 males
and females.
 Congenital factor VII deficiency should be
distinguished from acquired factor VII
deficiency, which may result from liver
disease, vitamin K deficiency or other
malabsorption conditions.

75.  Inheritance Pattern
 The disorder is not sex-linked as is hemophilia.
 It affects both males and females with equal
frequency.
 It is also autosomal recessive,
 Those who have inherited a defective factor VII
gene from only one parent will usually have only
moderate levels of the factor but no symptoms.

76. Symptoms and Diagnosis
Symptoms include:
• bleeding of mucous membranes
• spontaneous nosebleeds
• excessive bruising
• prolonged menstrual bleeding
• bleeding into muscles
• bleeding into joints
Diagnosis is made by testing for factor VII in
the blood.

77. • Signs and tests include:
-prolonged prothrombin time
-- normal partial thromboplastin time
-- decreased factor VII assay

78. MASAC made recommendations for treatment of Factor VII
deficiency in November of 1999. They include:
• Recombinant factor VIIa (NovoSeven).
• Prothrombin complex concentrates (PCCs) can be
used, but these products vary considerably in the
amount of factors they contain.
• Fresh frozen plasma can be used as along as it is
processed to reduce the risk of viral infection.
TREATMENTS

79. Complications
These can include hemorrhages, strokes or
other neurological problems related to central
nervous system bleeding.
• Fatal intracranial bleeding caused by birth
trauma has occurred.
• Menstrual bleeding may also be severe.

80. THROMBOCYTOPENIA
 Definition
 Thrombocytopenia is any disorder in which
there are not enough platelets. Platelets are
cells in the blood that help blood to clot. This
condition is sometimes associated with
abnormal bleeding.

81.  Causes, incidence, and risk factors
Thrombocytopenia is often divided into three
major causes of low platelets:
1) Low production of platelets in the bone
marrow
2) Increased breakdown of platelets in the
bloodstream (called intravascular)
3) Increased breakdown of platelets in the
spleen or liver (called extravascular

82. 1)Disorders that involve low production in the
bone marrow include:
-Aplastic anemia
-Cancer in the bone marrow
-Infections in the bone marrow (rare)
-Drugs (very rare)

83. 2)Disorders that involve the breakdown of platelets
include:
 Immune thrombocytopenic purpura (ITP)
 Drug-induced immune thrombocytopenia
 Drug-induced nonimmune thrombocytopenia
 Thrombotic thrombocytopenic purpura
 Primary thrombocythemia
 Disseminated intravascular coagulation (DIC)
 Hypersplenism (an enlarged spleen)

84.  Symptoms
-Bruising
-Nose bleeds or bleeding in the mouth
` -Rash (pinpoint red spots)
-Other symptoms may be present as well,
depending on the cause of the condition. Mild
thrombocytopenia can occur without symptoms.

85.  Signs and tests
-CBC shows low platelets
-Bone marrow aspiration or Biopsy may be
normal or may show low megakaryocytes
(platelet precursors) or an infiltrating disease.
-PTTclotting study is normal
-PTclotting study is normal
-Platelet associated antibodies may be present

86.  Treatment
Treatment depends on the cause of the condition.
In some cases, a transfusion of platelets may be
required to stop or prevent bleeding.
Expectations (prognosis)
The outcome depends on the disorder causing the
low platelet counts.
Complications
- Hemorrhage
-Gastro intestinal blleding
-Bleeding in the brain (intracranial hemorrhage)

87. DISSEMINATED INTRAVASCULAR
COAGULATION
 DIC is a syndrome arising as a complication of many
different serious and life-threatening illnesses.
1) Acute (overt) form it is a hemorrhagic disorder,
2) Chronic (nonovert) DIC, on the other hand, is more
subtle and involves thromboembolism accompanied by
evidence of activation of the coagulation system.

88. Pathogenesis of DIC

89. Table 1. Conditions underlying DIC
syndrome
 Infections
Acute DIC: Bacteria and their toxins, fungi, viruses, rickettsiae
Chronic DIC: Any chronic infection (eg, tuberculosis, abscesses,
osteomyelitis)
 Noninfectious inflammatory diseases
Inflammatory bowel disease: Crohn's disease and similar
disorders
 Obstetrical complications
Acute DIC: Abruptio placentae, abortions (especially therapeutic
abortions), amniotic fluid embolism, hemorrhagic shock
Chronic DIC: Dead fetus syndrome
 Malignancy
Acute DIC: Acute promyelocytic leukemia, acute myelomonocytic
or monocytic leukemia, disseminated prostatic carcinoma
Chronic DIC: Lung, breast, gastrointestinal malignancy

90.  Vascular disease
Acute DIC: Brain infarction or hemorrhage
Chronic DIC: Aortic aneurysm, giant hemangioma
 Venoms
Acute DIC: Snake, spider (rare)

Trauma ;
 Acute DIC: Massive tissue destruction, brain damage
 Others
Acute DIC: Heparin-induced thrombocytopenia with thrombosis
(HITT), purpura fulminans in newborns (homozygous protein C
deficiency)zDIC, disseminated intravascular coagulation.

91. Clinical and laboratory findings in DIC
 Acute DIC
Clinical findings
 Multiple bleeding sites
 Ecchymoses of skin, mucous membranes
 Visceral hemorrhage
 Ischemic tissue

92. Laboratory abnormalities
 Coagulation abnormalities:
 prolonged prothrombin time,
 activated partial thromboplastin time,
 thrombin time; decreased fibrinogen levels;
increased levels of FDP (eg, on testing for
FDP, D dimer)
 Platelet count decreased as a rule but may be
falling from a higher level yet still be normal
 Schistocytes on peripheral smear

93. Clinical and laboratory findings in DIC
 Chronic DIC
Clinical findings
 Signs of deep venous or arterial thrombosis or embolism
 Superficial venous thrombosis, especially without varicose
veins
 Multiple thrombotic sites at the same time
 Serial thrombotic episodes

94. Laboratory abnormalities
 Modestly increased prothrombin time in some patients
 Shortened or lengthened partial thromboplastin time
 Normal thrombin time in most patients
 High, normal, or low fibrinogen level
 High, normal, or low platelet count
 Increased levels of FDP (eg, on testing for FDP, D dimer)
 Evidence of molecular markers* (eg, thrombin-antithrombin
complexes, activation markers on platelet membranes,
prothrombin fragment F1+2)

95. Treatment options for DIC syndrome
 . Treat the underlying disease
Avoid delay
Treat vigorously (eg, shock, sepsis, obstetrical problems)
 Manage the DIC
Acute DIC
Without bleeding or evidence of ischemia
No treatment
With bleeding
Blood components as needed
Fresh frozen plasma
Cryoprecipitate
Platelet transfusions
With ischemia
Anticoagulants (see "with thromboembolism" below) after
bleeding risk is corrected with blood products

96. Chronic DIC
 Without thromboembolism
No specific therapy needed but prophylactic drugs
(eg, low-dose heparin, low-molecular-weight heparin)
 With thromboembolism
Heparin or low-molecular-weight heparin, trial of warfarin
sodium (Coumadin).
 *Some patients respond to warfarin, others do not. Use of
low-molecular-weight heparin for prolonged periods has
potential hazards and is expensive but can be useful when
warfarin therapy fails despite good control (international
normalized ratio [INR], 2-3).

97.  IDIOPATHIC THROMBOCYTOPENIC
PURPURA
 What is ITP?

98.  What causes ITP?
 Who gets ITP?
 How does ITP affect children?
 How is ITP diagnosed?
 How is ITP treated in children?
 How does ITP affect adults?
 How is ITP treated in adults?

99.  What about ITP in pregnant women?
 Diagnosing ITP during pregnancy can be difficult,
because platelet counts may be low for other reasons.
About 5% of women have mildly low platelet counts at
the end of a normal pregnancy. The cause of this is
unknown. The platelet count goes back to normal right
after delivery.
 A baby born to a mother with ITP may have a low blood
platelet count a few days to a few weeks after birth.
These babies are usually kept in the hospital for several
days for observation (watching to make sure they are ok)
before they go can home.

100.  Thrombotic thrombocytopenic purpura
What is thrombotic thrombocytopenic purpura?
 Thrombotic thrombocytopenic purpura (TTP) is a rare
blood condition characterised by the formation of
small clots (thrombi) within the circulation, which
results in the consumption of platelets and thus a low
platelet count (thrombocytopenia).
 What causes TTP?

101.  DRUG-INDUCED IMMUNE
THROMBOCYTOPENIA
 DRUG-INDUCED IMMUNE
THROMBOCYTOPENIA is a condition where
the use of certain drugs leads to the formation
of antibodies against platelets. These
antibodies can cause a low platelet count,
which make bleeding more likely. If these
antibodies are formed during pregnancy, they
may pass from the mother to the fetus.

102.  Thrombocytopenia (nonimmune) drug-
induced; Nonimmune
 thrombocytopenia - drug-induced
 Drug-induced nonimmune thrombocytopenia
is a reduction in normally functioning platelets
that can be caused by certain drugs.
 Platelets are important in forming blood clots.
Certain drugs may decrease the number of
platelets by damaging the bone marrow where
platelets are made. Decreased platelets may
cause easy bruising or abnormal bleeding.

103.  PRIMARY THROMBOCYTHEMIA
 Essential thrombocythemia; Essential
thrombocytosis
 Primary thrombocythemia is a condition of
overproduction of platelets without a
recognizable cause.

104. Causes, incidence, and risk factors
 Primary thrombocythemia is a slowly progressing
disorder caused by overgrowth of a type of cell that is
a precursor of blood cells. Although the platelets are
primarily affected, the red blood cells and white blood
cells are also involved
 The formation of blood clots, called thrombosis, may
coincide with bleeding episodes.
 It may even cause strokes in some people.
 Risk factors are unknown.
 The incidence is about 3 out of 100,000 people

105. Symptoms
 Nosebleeds (epistaxis )
 Bleeding from the gums
 Bleeding from the gastrointestinal tract
 Easy bruising
 Prolonged bleeding from surgical procedures or tooth
extraction
 Enlarged lymph nodes (rare)
 Bloody stools
 Headache
 Numbness of hands or feet
 Dizziness
 Ulcers on fingers or toes

106.  Signs and tests
 Bone marrow aspiration.
 CBC that shows elevated platelet count.
 Uric acid level may be elevated.
 Physical examination may show enlarged
spleen or liver

107. Treatment
 If a patient is having life-threatening complications-
platelet pheresis.
 Long-term decrease of the platelet count using
medications can reduce both bleeding and clotting
complications.
 Most common medications include hydroxyurea,
interferon-alpha, or anagrelide. For patients with a known
clotting tendency, aspirin may help decrease clotting
episodes.
 Some patients do not need any treatment.

108. Expectations (prognosis)
 The outcome varies with reports ranging from
prolonged periods without complications in some
people, to fatalities from complications related to
hemorrhage and thrombosis in others.
Complications
 Severe hemorrhage
 Thrombotic episodes (stroke, heart attack, or blood
clots in extremities)
 Acute leukemia or myelofibrosis can develop in some
patients

109. HYPERSPLENISM
 Hypersplenism is increased activity of the
spleen caused by tumors, anemia, malaria,
tuberculosis, and various connective tissue
and inflammatory diseases.
 An enlarged spleen is often accompanied by
a low level of one or more types of blood
cells. The enlarged spleen can cause
stomach pain on the left side, as well as
feeling full prematurely after eating

110. DENTAL EVALUATION
good thorough medical historygood thorough medical history
 a physical examination
 screening clinical lab tests
 excessive bleeding following surgical procedure
 Family HX
 Personal HX
 Medications
 Past & Present Illness
 Spontaneous Bleeding

111. REVIEW PATIENT’S MEDS
 FIVE DRUGS THAT INTERFERE WITH
HEMOSTASIS
 ASPIRIN
 ANTICOAGULANTS
 ANTIBIOTICS
 ALCOHOL
 ANTICANCER

112. ORAL MANIFESTATIONS
 Petechiae & Ecchymosis
 Gingival Hyperplasia
 Spontaneous Gingival Bleeding
 Ulceration of Oral Mucosa
 Lymphadenopathy

113. DENTAL PATIENTS
 LOW RISK
 Patients with No Hx of Bleeding Disorders
 Normal Laboratory Results
 MODERATE RISK
 Patients on Chronic Oral Anticoagulant
 Therapy. PT is 1.5 - 2 Times Control Range
 Patients on Chronic Aspirin Therapy
 HIGH RISK
 Patients with Known Bleeding Disorders
 Patients without Known Bleeding Disorders Who Have
Abnormal Laboratory Results

114. DENTAL MANAGEMENT
 LOW RISK PATIENTS
 Normal Protocol

115.  MODERATE RISK
PATIENTS
 Anticoagulants -
Consult Physician
 Aspirin Therapy - BT,
Consult Physician
 HIGH RISK PATIENTS
 Close Coordination
with Physician
 Hospitalization (Platelet
Transfusion) (Factor
Replacement)(Vit K
Therapy)(Dialysis

116.  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 mechanism, 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.

117. References
 Davidson’s “principles and practice of medicine-19th
edition;-Hanslet, Chilvers, Boon, Colledge, Hunters.
 Medical emergencies in the dental practice –malammed;
5th edition
 Bailey and Love’s Short practice of surgery-23rd edition;
Russel, Williams, Bulstrode;
 Complications in Oral and Maxillofacial surgery-1st edition;
Kaban, Pogrel, Perrot.
 Concise Medical Physiology;-5th edition; Chaudhari
 Systemic disease in dental treatment-1st edition;-
Michael.J.Tullman, Spencer.W.Redding.
 Clinical hematology-7th edition;-Maxwell.M.Wintrobe.
 www.hemophilia.org
 www.google.com

118. Thank you