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.
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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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
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
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.
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)
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.
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).
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
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
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
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