hemostasis in dentistry, intrinsic pathway, extrinsic pathway, clotting factors,

1. Haemostasis
Presented by -
Dr Parikshit S Kadam (JR 1)

2. Content
• Introduction
• Prime function of haemostasis
• Type of haemostasis
• Process of Haemostasis
• Coagulation of blood
• Clotting factors
• Laboratory Tests for Screening
• Haemostatic agents
• Bleeding Disorders
• Review of literature
• Conclusion
• References

3. Introduction
• Hemostasis is a complex physiological process involving cells
(platelets, especially but also fibroblasts), and soluble
(coagulation factors and inhibitors) and insoluble proteins
(extracellular matrix proteins)
• “Self-sealing” system to prevent excessive bleeding and
potentially life threatening states

4. Prime function of haemostasis
• To maintain blood in fluid state
• To arrest bleeding followed by trauma
• To maintain integrity of vessel wall
• To remove platelet plug when healing is complete

5. Type of hemostasis
• Primary hemostasis
 Formation of platelet plug after vessel injury
 Important in stoppage of blood from small arterioles, venules
and capillaries
• Secondary hemostasis
 Due to coagulation protein
 Completed in several minutes and important in bleeding from
large vessels

6. 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 40,000 is associated with
hemorrhagic disorders

7. 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

8. Process
Vasoconstriction
Formation of
platelet plug
Activation of
clotting mechanism
Dissolution of plug

9. VASOCONSTRICTION
• Immediate –
 Direct effect of injury
 Proportionate to the degree of trauma
• Later by humoral
 Release of 5- HT by bound platelets to the collagen

10. TEMPORARY HAEMOSTATIC PLUG
FORMATION
Platelet
adhesion
Platelet
activation
Platelet
aggregation
Formation of
temporary plug
Inhibition of
further plug
formation

12. DEFINITIVE HAEMOSTATIC PLUG
FORMATION
• Temporary plug converted to definitive plug by Process of
blood coagulation
• Results in formation tight unyielding seal

13. COAGULATION OF BLOOD
• Clotting factors
• Mechanism of coagulation
• Role of calcium in blood coagulation
• Role of vitamin –k, liver and vascular wall in haemostasis and
coagulation
• Blood clot retraction
• Blood in fluid

14. CLOTTING FACTORS
• I – FIBRINOGEN
 Soluble
 Mol wt- 3,40,000 Dalton
 6 polypeptide chain
 Con.- 0.3/100 ml blood
 It is converted into fibrin in presence of enzyme thrombin

15. • II- PROTHROMBIN
 Inactive precursor of thrombin
 Mol wt 69000 Dalton
 Synthesized in liver in the presence of vitamin K
 Conc. is 40 mg / 100 ml blood

16. • III – THROMBOPLASTIN
 Also called tissue factor or tissue thromboplastin
 Released in extrinsic pathway
• IV – CALCIUM
 Essential in all stages of coagulation
• V – LABILE FACTOR / PROACCLERIN
 Required for formation of protrombin activator
 Consumed during clotting so absent in serum

17. • VII – STABLE FACTOR / PROCONVERTIN
 For activation of factor X in extrinsic pathway
• VIII – ANTI-HAEMOPHYLLIC FACTOR A /
ANTIHAEMOPHLIC GLOBULIN
 Protein of b globulin type, synthesized in liver
 Activation of factor x
 Deficiency causes classical Haemophilia
 Inherited disease in which CT prolonged
• IX – ANTI-HAEMOPHILIC FACTOR B/ PLASMA
THROMBOPLASTIC COMPONENT
 First discovered in patient named Christmas

18. • X –STUART-PROWER FACTOR
 Along with active factor V, Ca and phopholipid forms a
complex – Prothrombin activator
 Formed in both extrinsic & intrinsic pathway
• XI – PLASMA THROMBOPLASTIN ANTICEDENT /
ANTI-HAEMOPHILIC FACTOR C
 Its deficiency causes hemorrhagic state
• XII – HAGEMAN FACTOR/ GLASS FACTOR /
CONTACT FACTOR
 Activated when comes in contact with electronegative surface
or glass or rough surface
 Its activation initiate intrinsic pathway

19. • XIII – FIBRIN STABILIZING FACTOR / FIBRINASE /
LAKI LORAND FACTOR
 Required for activation of fibrin polymer along with Ca

20. Mechanism of coagulation

24. Role of calcium in blood coagulation
• Except for first 2 steps Ca required for all steps
• Ca removal causes Anticoagulation
e.g. use of oxalates & citrates
Role of vitamin –k
 Synthesis of coagulants like Prothrombin
 Synthesis factor II, VII, IX and X

25. ROLE OF LIVER
• Synthesis of procoagulants – site of synthesis of factor
V,VII,IX,X, Prothrombin & fibrinogen
• Removal of activated procoagulants
• Synthesis of anticoagulants like – heparin, anti thrombin III &
protein C

26. ROLE OF BLOOD VESSELS
• Endothelium
 Anticoagulant role
 Barrier
 Produces heparin & α-2 macroglobulin
 Smoothness prevent aggregation
 Produces PGI2
• Coagulant role
 Von Willebrand factor (VWF)
 Tissue factor
 Plasminogen activator
• Sub endothelial tissue – collagen fibres
 Causes platelet aggregation
 Intrinsic pathway activation

27. BLOOD CLOT RETRACTION
• Clot is meshwork of fibrin with entrapped blood cells, platelets
& plasma
• Contractile proteins – Actin, myosin & thrombosthenin
• Compress fibrin meshwork squeeze out serum
• Clot reduced to 40% of its original value

28. Laboratory Tests for Screening
• Majority of defects of haemostasis can be screened by four
basic tests
1. Bleeding Time (BT)
2. Platelet Count
3. Prothrombin Time (PT)
4. Partial Thromboplastin Time (PTT)

29. Bleeding Time (BT)
• Time interval between skin prick and the arrest of bleeding
 Duke’s method – take a prick at finger skin , blood is wiped at
15 sec interval till it stops
• Normal time :- 1-6 min
 Ivy’s method – apply 40 mm Hg at upper arm with BP cuff &
take deep prick on anterior surface of skin of forearm
• Normal time – 3-6min
• BT is prolonged in thrombocytopenia, Von Willebrand’s
disease and platelet dysfunction

30. Platelet Count
• When count becomes 50,000 to 1,00,000 per cumm, there is
mild prolongation of bleeding time
• Patients with count less than 50,000 per cumm have easy
bruising manifested as petechia and ecchymoses during trauma
or surgery
• Patients with platelet count below 20,000 per cumm have an
incidence of spontaneous bleeding, which may be intracranial
or any other internal bleeding

31. • Minor oral surgical procedure can be safely done, if platelet
count is above 80,000 to 1,00,000 per cumm, otherwise patient
needs transfusion of platelet rich plasma
• Direct method – using Reese-E-Kar fluid counted in
Haemocytometer
• Indirect method – from RBC

32. Prothrombin Time (PT)
• Prothrombin time screens the extrinsic limb of coagulation
pathway (Factors V, VII and X) and factors I, II and V of the
common pathway
• It is prolonged in patients, who are on warfarin anticoagulant
therapy, vitamin K deficiency or deficiency of factor V, VII,
X, prothrombin or fibrinogen
• Normal PT is usually 12-14 second. As a general guideline for
dental procedures, the PT should be less than 1½ of the control
value

33. • Procedure – Quick’s one stage method
• Oxalated or citrated plasma of patient are added to tissue
thromboplastin & Ca chloride solution & mixture incubated at
37oc – result is conversion of fluid plasma to gel
• NT – 11-16 sec
• Importance – used to monitor pt receiving anticoagulant
therapy
• Increase in patients on oral anticoagulants, liver failure, vit K
deficiency, deficiency of factor II,V,VII,X
• Normal in Haemophilia & Christmas disease

34. Partial Thromboplastin Time (PTT)
• Partial thromboplastin time screens the intrinsic limb of
coagulation pathway and tests for the adequacy of factors VIII,
IX, X, XI, XII of intrinsic system and factors I, II, V of the
common pathway
• Normal PTT is less than 45 seconds
• It is important to note that PTT is relatively insensitive to
changes in the intrinsic coagulation system. A 70% decrease in
factor levels may still provide normal results; small changes in
PTT therefore, may be of great significance

35. • Procedure – To oxalated & citrated plasma of patients kaolin
& ca chloride are added & mixture is incubated at 37 C,
• Result is formation of plasma gel
• Importance – used to monitor Heparin therapy
• Prolonged in – haemophilia, Von-willebrand disease, liver
failure, deficiency of XII, anticoagulant therapy &
intravascular clotting

36. Deficiency PT PTT TT
VIII, IX, XI, XII - Increase -
X Increase Increase -
XIII - - -
VII Increase - -
Heparin toxicity Increase Increase Increase
Vit. K Increase - -

37. Haemostatic agents
• Local
• Systemic

38. Local Haemostatic Measures
• In a patient with normal coagulation mechanism, the control of
haemorrhage is dependent on vessel contraction, retraction and
clot formation
• During any surgical procedure, complete haemostasis must be
achieved before closure of the wound. Direct control of
bleeding at the site of injury is the best method to achieve
haemostasis
• The techniques for local haemostasis may be classified as (i)
mechanical (ii) thermal (iii) chemical

39. Mechanical Methods
• Pressure:-
 Application of pressure basically
counteracts the hydrostatic pressure
within the bleeding vessel until such
time, that a clot can form and occlude
the bleeding orifice
 Pressure is usually able to control most
of the haemorrhages.
 Pressure should be applied directly over
the bleeding site firmly over a gauze
pack for at least five minutes

40. Haemostats
• Haemostat (Mosquito, artery) forceps
are specially designed to catch bleeding
points in the surgical area. These can be
straight or curved. Curved haemostats
are used more frequently, because of
their versatility and ease in tying the
ligature around the tip of forceps
• Usually electrosurgical
thermocoagulation is done after
catching the bleeding point with artery
forceps, if the vessel is small. The large
vessels are ligated with suture

41. Sutures and ligation
• When large pulsatile artery needs to be tied, nonabsorbable
material like 3-0 black silk is preferred. Smaller vessels can be
ligated with 3-0 catgut or polygalactin
• The presence of nonabsorbable material in an infected wound
can lead to extrusion or sinus tract formation
• Large arteries with pulsation, such as external carotid artery,
should have double transfixion suture passed through the wall
of vessel to prevent chances of slipping of ligature

42. Embolization of the vessels
• With the help of angiography, the exact bleeding point can be
localized. Agents which can be used for embolization include
steel coils, polyvinyl alcohol foam, gel foam, silicon spheres
and methyl methacrylate. These particles are placed via a
catheter super selectively into the bleeding vessel usually via
femoral artery
• Vessels that are usually investigated and catheterized for
treatment of oral and perioral lesions include the facial,
lingual, transverse facial and internal maxillary arteries

43. Thermal Agents
• Cautery
 Heat achieves haemostasis by denaturation of proteins which
results in coagulation of large areas of tissue
 In cauterization, heat is transmitted from the instrument by
conduction directly to the tissues. Electrocautery has replaced
direct heat application
 When an electrosurgery unit is not available, dental burnisher
like instrument can be directly heated over a flame and applied
directly to the bleeding point in the oral cavity

44. Electrosurgery
• In electrocautery, heating occurs by induction from an
alternating current source. It is an effective and convenient
way of controlling haemorrhage
• Electrocautery can be applied directly to bleeding point or
after catching the bleeding point with haemostat. Then cautery
point is touched to the haemostat causing sealing of the vessel
through the action of heat
• It causes tissue destruction producing a burning smell and
smoke during application. This cannot control haemorrhage
from large vessels, which need to be ligated

45. Cryosurgery
• Extreme cooling has been used for haemostasis. Temperature
ranging from –20°C to –180oC are used
• At these temperatures, the tissues, capillaries, small arterioles,
and venules undergo cryogenic necrosis
• This is caused by dehydration and denaturation of lipid
molecules. Cryosurgery is specially used to treat superficial
haemangiomas

46. Argon-beam coagulator
• In this, coagulator monopolar current is transmitted to tissues
through the flow of argon gas
• This allows bleeding from vessels that are smaller than 3 mm
in diameter to be controlled without the use of haemostats or
ligatures
• The tip of the coagulator is held approximately one cm from
the tissue. A flow of argon gas clears the surgical site of fluids
to allow current to be focused directly on tissue

47. Lasers
• Lasers usually result in bloodless surgery, as these effectively
coagulate the small blood vessels during cutting of tissues

48. Chemical Methods
 Local agents
• Bone wax
 When bleeding is occurring from a bony canal, it can be
troublesome, because of inability to occlude the vessel that is
confined within bony canal
 In such a case, small quantity of bone wax can be applied to
the bleeding bone
 It acts by mechanical occlusion of the bony canal. Large
quantity of bone wax can lead to foreign body granuloma and
infection

49. Astringent agents and styptics
• Monsel’s solution contains ferric subsulphate and it acts by
precipitating proteins
• Tannic acid also helps in precipitating proteins and causes clot
formation.
• Mann haemostatic is a mixture of tannic acid, alum and
chlorobutamol. Silver nitrate and ferric chloride are other
agents, which can be used in case of minimal capillary
bleeding

50. Thrombin
• Topical use of thrombin acts by converting fibrinogen into
fibrin clot. It is very kind to tissues and quite effective. It is
applied to the bleeding surface via a pack, gelatin sponge or
surgicel

51. Gelfoam
• It is made from gelatin and is sponge like. Gelfoam has no
intrinsic haemostatic action. Its main haemostatic activity is
related to large surface area, which comes in contact with
blood and further swells on absorbing blood
• It exerts pressure along with acting as scaffold for fibrin
network. It is absorbed by phagocytosis
• Gelfoam should be moistened in saline or thrombin solution
prior to application and all the air should be removed from
interstices

52. Oxycel
• It is oxidized cellulose and on application releases cellulosic
acid, which has marked affinity for haemoglobin, leading to
formation of artificial clot
• It should be applied dry, because acid formed during wetting
process inactivates the thrombin or other haemostatic agent
• Acid produced also inhibit epithelialization, therefore, it is not
recommended for use over epithelial surfaces

53. Surgicel
• It is glucose polymer based sterile knitted fabric prepared by
the controlled oxidation of regenerated cellulose
• Its local haemostatic mechanism depends on binding of
haemoglobin to oxycellulose, allowing the dressing to expand
into a gelatinous mass, which in turn acts as scaffold for clot
formation and clot stabilization
• Surgicel can be applied dry or it can be soaked in thrombin
solution. It is removed by liquefaction and phagocytosis over a
period of one week to one month. This product does not inhibit
epithelialization and can be used over epithelial surfaces

54. Fibrin glue
• It is a biological adhesive containing thrombin, fibrinogen,
factor XIII and aprotinin.
• Thrombin converts fibrinogen to unstable fibrin clot, factor
XIII stabilizes the clot and aprotinin prevents its degradation.
• The product poses virtually no risk of transmission of viral
infections because of pasteurisation of the plasma components
and has little or no antigenic potential. This product has been
recently allowed for clinical use in UK and USA

55. Adrenaline
• Adrenaline or epinephrine, applied topically induces
vasoconstriction and thus helps in achieving haemostasis
• Extensive application or undiluted preparation can cause
systemic effects, therefore, one should be careful while using
adrenaline
• The drug is applied with the help of gauze pack in a
concentration 1:1000 over oozing sites. It can also be injected
along with local anaesthetic in concentration of 1:80,000 to
1:2,00,000

56. Systemic agents
• Fresh frozen plasma
 A unit (150 ml) of fresh frozen plasma is usually collected
from one donor and contains all coagulation factors including
200 u factor VIII, 200 u factor IX and 400 mg fibrinogen
 Fresh frozen plasma is stored at –30oC and should be infused
within two hours once defrosted

57. Whole blood
• When there is excessive blood loss due to haemorrhage, and
there are symptoms of hypovolaemic shock, whole blood
transfusion may be indicated
• Fresh whole blood contains all the factors for coagulation.
When specific blood components are not available to treat the
patient‘s haemostatic defect, whole blood may be used. It is
necessary to type and cross-match the blood before transfusion

58. • Blood must be checked for hepatitis B, C and HIV viruses
before transfusion. Banked blood is a poor source of platelets.
• Factors II, VII, IX and XI are stable in banked blood. Fresh
whole blood refers to blood that is administered within 24
hours of its donation.
• Fresh whole blood is rarely indicated because of specific
component therapy available these days. One unit of platelet
concentrates has more viable platelets than one unit of fresh
whole blood, but it is an inadequate source of factor VIII.

59. Platelet rich plasma
• It is advisable to elevate the platelet levels to the range of
50,000 to 1,00,000 cells per cu mm to provide continued
protection
• Platelets can be collected from donated whole blood or
directly from the patient via plasmapheresis
• Platelet concentrates are viable for three days when stored at
room temperature. If they are refrigerated viability decreases.
• They must be infused quickly via a short IV transfusion set
with no filter. One unit of platelet rich plasma raises the
platelet count approximately by 7,000-10,000 cells per cu mm.

60. Cryoprecipitate
• Cryoprecipitate A 15 ml vial of cryoprecipitate contains
approximately 100u factor VIII, 250 mg fibrinogen, factor
XIII and von Willebrand factor and is stored at –30oC
• Each bag of cryoprecipitate is derived from a single donor and
is not treated to inactivate viruses. Therefore, the use of
cryoprecipitate is associated with a substantial risk of viral
transmission

61. Control of Haemorrhage from Major
Arteries
• In order to control bleeding, the clinician must be able to
visualize clearly the exact point of bleeding.
• This can be achieved with the help of good light source,
adequate suction, adequate anaesthesia and sound workable
knowledge of the anatomy of the area concerned.
• One should approach bleeding problem with utmost
confidence. Majority of times, the problem arises from
inadequate preparation on the part of clinician before surgery,
poor visibility in the operative field, poor co-operation from
the patient, and incomplete armamentarium to implement the
procedure.

62. Greater Palatine Artery
• Greater palatine artery runs anteriorly from the greater palatine
foramen in the submucosa of the hard palate in a groove
between the horizontal palatine process of the maxilla and the
inner plate of the alveolar process
• The incisions over the palate should be made parallel, rather
than perpendicular to this vessel. If accidental injury occurs
bleeding is copious and application of clamp is difficult
• Most of the times, the haemorrhage can be controlled by a
pressure pack. A round bolus of gauze is made of adequate
size, so that it does not cause gagging. It is kept in place by tie
over sutures for 24 to 48 hours. Pressure pack can be safely
removed after 48 hours

63. Sublingual Artery
• Injury to sublingual artery can occur accidentally by rotating
disks or slipping of sharp instrument while working on
mandibular teeth.
• Injury to this artery during mandibular implant placement has
been reported and it may lead to large sublingual haematoma
which, if not controlled, can compromise airway and may be
life-threatening.
• It is a small artery and local clamping of the artery and
application of electrocautery usually controls the bleeding

64. • There is anatomic variation in the origin of this artery. In most
of the cases it is a branch of lingual artery, but in significant
number of cases it is a branch of submental artery, which is a
further branch of facial artery.
• So sometimes ligation of lingual artery may not stop bleeding
from sublingual artery. In that case facial artery needs to be
ligated

65. Ligation of Facial Artery
• It can be easily ligated at the point where it crosses lower
border of mandible just anterior to masseter muscle. If patient
is asked to clench the teeth, the pulsations of facial artery can
be easily felt externally
• To prevent damage to marginal mandibular branch of facial
nerve submandibular incision is given one to two cm below
the lower border of mandible. The skin, subcutaneous tissue,
platysma and deep fascia are cut. These tissues are retracted
upwards and here artery lies just anterior to masseter muscle. It
is isolated, tied and cut

66. Bleeding Disorders
• HAEMOPHILIA
 The word "Hemophilia" first appeared in a description of a
bleeding disorder condition at the University of Zurich in 1828
 Group of disorders due to hereditary deficiency of coagulation
 Characterized by Bleeding tendencies with Increased clotting
time
 Types
1. Haemophilia-A
2. Haemophilia-B
3. Haemophilia-C

67. HAEMOPHILIA-A
• Classical haemophilia due to Deficiency of factor VIII
• Sex linked recessive disease affects males and females carrier
• Tendency to bleed into soft tissues, muscle, joints , GI tracts,
urinary tracts & from nose, Severely damaged joints
• Hemorrhage into soft tissue of mouth cause respiratory
obstruction & death by suffocation
• Normal bleeding time, platelet count & PT but prolonged CT
& PTT

69. 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.

70. Treatment
• Local haemostatic measures such as application of topical
thrombin, surgicel or gelfoam is indicated
• Stabilization of clot with antifibrinolytic drugs such as
epsilon-aminocaproic acid (EACA) and tranexamic acid (5%)
mouthwash 4 to 6 times daily is indicated
• Analgesics such as aspirin and NSAIDs are contraindicated as
they alter platelet function

71. • Routine comprehensive dental care can be provided to the
patients with haemophilia on an outpatient basis, if the
practitioner is familiar with the type and severity of factor
deficiency and plans accordingly.
• Surgical procedures should be done after admitting the patient
and a minimum of 50 per cent of normal levels should be
maintained by daily monitoring of the patient
• Supragingival scaling can be managed by a single infusion of
cryoprecipitate or factor VIII concentrate coupled with
administration of 4 to 6 gm of EACA four to six times daily
for 72-96 hours after the dental procedure

72. • Inferior alveolar nerve block and posterior superior alveolar
nerve block injections should be administered only after
replacement therapy of factor VIII, because of possibility of a
dissecting haematoma
• EACA is a potent antifibrinolytic agent that inhibits
plasminogen activators present in oral secretions and stabilizes
clot formation in the oral tissues
• Tranexamic acid is a more potent and longer acting
antifibrinolytic drug. It is available as both oral and parenteral
forms. Intravenous dose is 10 mg/kg body weight, the dose
being repeated 4 to 6 hourly. It can be used as 5 per cent
mouthwash (500 mg tablet dissolved in 10 ml of water) and
this solution can be swallowed

73. Haemophilia B
• Known as Christmas Disease due to Deficiency of factor IX.
• Reccessive X-Linked disease occurs in males, transmitted by
female

74. 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.

75. HAEMOPHILIA-C
• Deficiency of PTA(Factor X)
• Inherited as Mendelian dominant affects both males &
females
• Without bleeding tendencies.
• CT may be prolonged or normal

76. Factor V Deficiency (Para hemophilia)
• 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

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

78. 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

79. 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

80. • 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)

81. • 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

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.
- PTT clotting study is normal
- PT clotting 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.
Complications
- Hemorrhage
- Gastro intestinal blleding
- Bleeding in the brain (intracranial hemorrhage)

94. Sr
no
Author
and year
Aim Results Conclusion
1 S. Al-
Mubarak
, N. Al-Ali
, M. Abou
Rass
, A. Al-
Sohail in
2007
To examine the
consequences of
temporary
withdrawal of
warfarin and/or
suturing on
bleeding and
healing pattern
following dental
extractions.
Discontinuing warfarin
reduced INR level
significantly at day 1,
which subsequently
reached <1.5 in 96 out of
104 patients (group 1 and
3). Statistical comparisons
among the different
treatment groups did not
reveal any significant
difference regarding
bleeding status or healing
pattern. Interestingly,
patients who received
sutures showed higher but
insignificant incidence of
bleeding postoperatively
compared to their
respective controls.
Dental extractions may be
safely performed for
patients on anticoagulation
therapy provided the INR
level is kept <3.0 and
effective measures of local
haemostasis are
administered. The decision
to suture should be made
on case-by-case basis, as
the trauma associated with
soft tissue handling might
outweigh its advantages in
certain situations like
simple extractions.

95. Sr no Author and
year
Aim Method Results
2 Recardo M
Rider et al
(2017)
To provide
medical/dental
management to
patient suffering from
uncontrolled bleeding
after surgical
procedures to
expose both
permanent upper
central incisors, in
which hemophilia A
was incidental finding
10 year boy with no
bleeding disoder
came with c/o lack of
eruption of upper
central incisor. 3 days
after patient came
with profuse bleeding.
Wound was sutured
and covered with
Gelfoam with surgical
splint and after 2
days, to control
bleeding, Tranexamic
acid(250 mg), vit k(5
mg) and normal saline
for 8 hours
Hemorrhage
was stopped
completely after
2 days and
after 10 days ,
child did not
show any
unusual
bleeding
experience

96. Sr no Author
and year
Aim Material and
method
Results Conclusion
3 Atanaska S.
Dinkov,
Dimitar T.
Atanasov,
Ludmila G.
Vladimirov
a-Kitova
(2017)
provides
clinical
advice on
the
manageme
nt of
patients
who
receives
Dabigatran
(vit K
antagonist)
and
requires
dental
extractions
.
course of five
patients on
dabigatran who
underwent teeth
extraction was
assessed. The
medical charts of
these patients
were investigated.
Morning dose of
dabigatran
(Pradaxa) was
omitted and teeth
extraction was
performed ≥12
hours after the
last intake of the
drug
Fourteen teeth
were extracted in
five patients
receiving
Dabigatran with
normal creatinine
clearance.
Extractions were
performed ≥12
hours after the last
administration of
dabigatran. Only
one patient has
slightly prolonged
bleeding,
successfully
controlled with
local hemostatic
measures
Simple teeth
extractions can
be safely
performed ≥12
hours after the
last
administration of
the medication in
patients with
normal creatinine
clearance
without
significantly
greater bleeding
risk than
conventional oral
anticoagulants.

97. CONCLUSIONS
• The history (medical /family history) is extremely important in
evaluating patients with disorders of haemostasis.
• 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

98. References
• Textbook of Medical Physiology by Guyton and Hall, 11th
edition.
• Textbook of pediatric dentistry scientific foundation and
clinical practice by Stewart and Barber, 1st edition.
• Pediatric oral and maxillofacial surgery by Kaban and Troulis,
1st edition.
• Textbook of oral and maxillofacial surgery by Nilima Malik,
2nd edition.
• Shafer’s textbook of oral pathology, 6th edition.

99. • Al-Mubarak S, Al-Ali N, Rass MA, Al-Sohail A, Robert A,
Al-Zoman K, Al-Suwyed A, Ciancio S. Evaluation of dental
extractions, suturing and INR on postoperative bleeding of
patients maintained on oral anticoagulant therapy. British
dental journal. 2007 Oct;203(7):E15.
• Ricardo Martínez-Rider,1 Arturo Garrocho-Rangel,1 Raúl
Márquez-Preciado,1 María Victoria Bolaños-Carmona,2
Socorro Islas-Ruiz,1 and Amaury Pozos-Guillén1. Case
Reports in Dentistry Volume 2017, Article ID 7429738, 5
pages
• Images are taken from internet sources