This seminar includes hemostasis,mechanism of blood clotting and associated blood dyscrasias commonly seen in children and their treatments with a note on antifibrinolytics

2. CONTENTS
 HEMOSTASIS
 STEPS IN BLOOD CLOTTING
 FIBRINOLYTICS
 ANTICOAGULANTS
 TESTS FOR CLOTTING
 BLEEDING DISORDERS IN PEDIATRICS
 ANTIFIBRINOLYTICS
 CONCLUSION
 REFERENCES

3. HEMOSTASIS : Defined as the body's normal physiological response
for the prevention and stopping of bleeding/haemorrhage.
• It results in the blocking of any vascular breach.
• Generally, it helps: ensure blood fluidity and blood vessel
integrity.

4. MECHANISMS:
Hemostasis occurs when blood is present outside of
the body or blood vessels.
It is the instinctive response for the body to stop
bleeding and loss of blood.
During hemostasis three steps occur in a rapid
sequence:
1 - Primary/Vasoconstriction
2 – Secondary/Platelet plug formation
3 – Tertiary/Coagulation

5. Primary Haemostasis :
• Primary haemostasis is by vasoconstriction after injury.
• This reduces the outflow of escaping blood after injury.
• Circulating platelets are exposed to subendothelial collagen, which causes
the release of intra- cytoplasmic granules that stimulate platelet aggregation
and helps to form the soft primary plug.
Abnormalities in primary haemostasis:
• Abnormal platelet number or function
• Abnormal von willebrand factor

6. Secondary Haemostasis :
• The aggregation of platelets is the second phase of
haemostasis.
• Therefore it is aka ‘the platelet phase’.
Abnormalities in secondary haemostasis:
• Defects in the coagulation cascade cause more
serious bleeding than do defects of primary
haemostasis.
• They include bleeding into cavities (chests, joints,
cranium).

8. Tertiary Haemostasis:
• It is the third and final phase.
It is divided into 2 pathways:
 The extrinsic pathway
 The intrinsic pathway

9. STEPS OF BLOOD CLOTTING:
Coagulation/clotting is defined as the process in which blood looses
its fluidity and becomes a jelly like mass few minutes after it is shed
out or collected .
In general blood clotting occurs in three stages:
 Formation of prothrombin activator
 Conversion of prothrombin into thrombin
 Conversion of fibrinogen into fibrin

10. CLOT RETRACTION:
After the formation the blood clot starts contracting and after about
30-45 minutes a straw coloured fluid called serum oozes out of the
clot.
• The contractile protein namely,
- Actin
- myosin and
- thrombosthenin
in the cytoplasm of platelets are responsible for clot retraction.

11. Fibrionlysis:
• It is the lysis of blood clot inside the blood
vessel and helps to remove the clot from the
lumen of the blood vessel
• This process requires a substance called
plasmin or fibrinolysin.
t-pa = tissue plasminogen

12. Anticoagulants:
The substances which prevent or postpone coagulation of blood are anticoagulants.
These are of three types:
• To prevent blood clotting inside the body
• To prevents clotting blood that is collected from the body
• To prevent blood clotting both invitro and invivo
Various anticoagulants commomly used are: - Heparin
- Coumarin derivatives
- EDTA
- Oxalate compounds
- Citrates
- Procoagulants

13. OTHER SUBSTANCES WHICH PREVENT BLOOD CLOTTING
Physical methods:
• cold
• collectng blood in a container with smooth
surface
Procoagulants:
• Thrombin
• Snake venom
• Extract from lungs and thymus
• Calcium or sodium alginate
• Oxidized cellulose

14. TESTS FOR CLOTTING:
Bleeding time
– Time taken for a standardized skin puncture to stop bleeding
– Measures platelet plug formation in vivo (assessment of platelet
response to limited vascular injury)
– Normally between 3 and 10 minutes
– Prolonged bleeding times are found in patients with platelet function
defects

15. Coagulation tests:
– Performed using blood collected into citrate, which neutralizes
calcium ions and prevents clotting.
– The prothrombin time (PT)
– The partial thromboplastin time (PTT)
– The thrombin time (TT)

16. The prothrombin time (PT):
• Time needed for the plasma to clot in the presence of tissue thromboplastin and
calcium
• Evaluates the ability of blood to clot properly
• Normal time for clotting is 10-14s
• It is normal in hemophilia.
• Prolong PT results from def of: – Factor V
– Factor VII
– Factor X
– Prothrombin
– Fibrinogen .

17. The partial thromboblastin time (PTT) :
• Time needed for the plasma to clot in the presence of a surface activator
(kaolin), cephalin and calcium.
• Normal time of clotting is 30-40s
• This test is done to investigate the bleedind disorders.
• Prolong PPT results from def of:
– Factor V
– Factor VIII
– Factor IX
– Factor X
– Factor X1
– Prothrombin
– Fibrinogen

18. THROMBIN TIME (TT) :
• Measures clotting time of plasma after adding thrombin
• Normal clotting time is 14-16s
• Used to detect heparin in plasma or fibrinogen abnormalities.
• Prolong TT results from:
– Deficiency of fibrinogen
– Dysfibrinogenaemia

19. • The international normalized ratio (INR) is a standardized
number that's figured out in the lab.
• If you take blood thinners, also called anti-clotting
medicines or anticoagulants, it's especially important to
check your INR.
• The INR is figured out using the results of the prothrombin
time (PT) test

20. Anticlotting mechanism in the body :
Under physiological conditions intravascular clotting does not occur.it is because of the
presence of some physiochemical factors in the body.
Physical factors:
• Continuous circulation of blood
• Smooth endothelial lining of blood vessels
Chemical factors:
• Presence of natural anticoagulants i,.e heparin produced in the liver
• Production of thrombomodulin by endothelium of blood vessels
• All the clotting factors are in in active stage

21. BLEEDING DISORDERS IN PEDIATRICS
1)HEREDITARY COAGULATION DISORDERS
- HEMOPHILIA A
- HEMOPHILIA B
- VON WILLEBRANDS DISEASE
2)ACQUIRED COAGULATION DISORDRS
- VITAMIN K DEFICIENCY
- DIC
- LIVER DISEASE
- MASSIVE TRANSFUSION SYNDROME
- COAGULATION DISORDER DUE TO ANTIBODIES
3)PLATELET DISORDERS
THROMBOCYTOPENIC PURPURA
- IDIOPATHIC
- THROMBOCYTIC
- DRUG INDUCED

22. Coagulation defects, purpura and other haemorrhagic conditions
•(D65) Disseminated intravascular coagulation (defibrination syndrome)
• Afibrinogenaemia, acquired
• Consumption coagulopathy
• Diffuse or disseminated intravascular coagulation (DIC)
• Fibrinolytic haemorrhage, acquired
• Fibrinolytic purpura
• Purpura fulminans
•(D66) Hereditary factor VIII deficiency
• Haemophilia A
•(D67) Hereditary factor IX deficiency
• Christmas disease
• Haemophilia B
•(D68) Other coagulation defects
• (D68.0) Von Willebrand's disease
• (D68.1) Hereditary factor XI deficiency
• Haemophilia C
• (D68.2) Hereditary deficiency of other clotting factors
• (D68.3) Haemorrhagic disorder due to circulating
anticoagulants
• (D68.4) Acquired coagulation factor deficiency
• (D68.8) Other specified coagulation defects
• (D68.9) Coagulation defect, unspecified
ICD- 10 CLASSIFICATION

23. •Purpura and other haemorrhagic conditions(D69.0) Allergic purpura
• anaphylactoid purpura
• Henoch-Schönlein purpura
•(D69.1) Qualitative platelet defects
• Bernard-Soulier syndrome (giant platelet)
• Glanzmann's disease
• Grey platelet syndrome
• Thromboasthenia (haemorrhagic)(hereditary)
• Thrombocytopathy
•(D69.2) Other nonthrombocytopenic purpura
•(D69.3) Idiopathic thrombocytopenic purpura
• Evans' syndrome
•(D69.4) Other primary thrombocytopenia
•(D69.5) Secondary thrombocytopenia
•(D69.6) Thrombocytopenia, unspecified
•(D69.8) Other specified haemorrhagic conditions
•(D69.9) Haemorrhagic condition, unspecified

24. HAEMOPHILIA :
• X linked disorder resulting from a deficiency in clotting factor VIII
(Hemophilia A or classic) or factor IX (Hemophilia B or Christmas Disease) .
• Affects males, females are carriers.
3 forms of hemophilia are seen:
• Severe- < 1% of normal factor VIII
• Moderate – 1% - 5%
• Mild – 5% – 25%

25. ORAL MANIFESTATIONS:
• Petechiae
• Ecchymoses
• Spontaneous gingival bleeding can occur
• Prolonged massive bleeding even from simple tooth exfoliation or extraction.
• Associated with anaemia induced pallor and pseudoaphthae.

26. PERIODONTAL CONSIDERATIONS:
• Periodontal health is of critical importance for the hemophiliac for 2
primary reasons:
• Hyperemic gingival contribute to spontaneous and induced gingival
bleeding.
• Periodontitis is leading cause for tooth morbidity necessitating extractions.
• In all but severe hemophiliacs, scaling can be carried out without LA.
• Periodontal surgery requires LA and factor VIII replacement to a level
between 50 to 75%
Naveen Kumar J, Anil Kumar R, Varadarajan R, Sharma N. Specialty dentistry for the hemophiliac: Is there a protocol
in place?. Indian J Dent Res 2007;18:48-54

27. HEMOPHILIA- A :
• Treatment = factor replacement
– Bleeding is treated by administration of factor VIII concentrate by intravenous
infusion.
– 1 IU is the amount of procoagulant present in 1 ml of normal plasma
– Minor bleeding: the factor VIII level should be raised to 20-30% and DDVAP can
be used
– Severe bleeding: the factor VIII should be raised to at least 50% as in joints,soft
tissue and oral bleeds
– Major surgery: the factor VIII should be raised to 100% preoperatively and
maintained above 50% until healing has occurred.

28. Synthetic vasopressin (Desmopressin) An analogue of vasopressin
• Intravenous, subcutaneous or intranasal
• DDAVP causes rise in factor VIII and VWF through release from
stored sites in endothelial cells
• 1.5mg/ml
• Repeated administration may result in tachyphylaxis and reduction
in response due to depletion of storage sites
• Produces a rise in factor VIII in mild hemophilia
• It avoids the complications associated with blood products
• It is ineffective in severe haemophilia

29. HEMOPHILIA B
• Also known as Christmas disease
• Caused by a deficiency of factor IX
• The inheritance and clinical features are identical to hemophilia A
• Only can be distinguished by specific coagulation factor assays
• Hemophilia B is treated with factor IX concentrates
Clotting factor concentrates are administered in different regimens depending on
the severity which can be divide into
- Replacement therapy
- Primary prophylactic/long term
- Secondary prophylactic/long or short trem

30.  Replacement therapy administered after bleeding episode has occurred
or as therapy administered on regular schedule to prevent or suppress
bleeding episodes
 primary prophylaxis is long term treatment for prevention of joint
diseases instituted before or after minimal haemarrthrosis has occurred
 Secondary prophylaxis may be long or short term but is instituted after
hemarthrosis has occurred to interrupt bleeding

31. DENTAL CONSIDERATIONS:
• Local anaesthetic injections or surgery can be followed by persistent bleeding for
days.
• The hemorrhage cannot be controlled by pressure alone.
• Bleeding tendency may be aggravated by NSAIDs.
• In all but severe haemophiliacs, non surgical dental treatment can usually be
carried out under antifibrinolytic cover.
• Extractions and dentoalveolar surgery should be carefully planned. A factor VIII
level between 50 and 75% is required.
• Mild hemophiliacs requiring such surgeries can be managed usually without
factor replacements. Desmopressin and tranexamic acid are primary alternative.
• Post operative suturing is desirable.
Guidelines for dental treatment of patients with inherited bleeding disorders
Andrew Brewer,Maria Elvira Correa

32. VON WILLBRAND’S DISEASE:
• Hereditary coagulation abnormality caused by either:
– Reduced level of vWF
– Abnormality in vWF Due to Point mutation or Major deletion
• VWF is a protein that has two roles:
– It promote adhesion of platelets to the endothelium
– It is a carrier molecule for factor VIII, protecting it from premature destruction
• So in VWD there is:
– Defective platelet function
– Factor VIII deficiency

33. • VWD has been classified into three types:
– Type 1 VWD • Characterized by a mild reduction in VWF and is usually inherited as
an autosomal dominant
– Type 2 VWD • Loss of high-molecular-weight multimers, and it too is usually
inherited as an autosomal dominant
– Type 3 VWD • Characterized by severe reduction in VWF and usually inhereted as
autosomal recessive
Clinical features:
– Typically there is mucus membrane bleeding (epistaxis, menorrhage...)
– The severity of symptoms are variable with types
• Type 1, 2 usually mild symptoms
• Type 3 severe symptoms

34. ORAL MANIFESTATIONS :
• Gingival bleeding is the most common finding- in about 30 – 40% of the diseased.
• Uncontrollable bleeding during dental procedures like gingival manipulation and
pulpectomy.

35. DENTAL CONSIDERATIONS:
• Aspirin and NSAIDs should be avoided.
• Local infiltration anaesthesia should generally be used.
• Nerve block anaesthesia is generally contra indicated because
injections delivered into loose alveolar tissue (highly vascular regions)
may produce bleeding or a dissecting hematoma that could obstruct
the patient’s airway.
• Conscious sedation can be given, but care must be taken not to
damage the vein.
• General anaesthesia must be given in hospital.
• Intubation is a possible hazard because of the risk of submucosal
bleeding in the airway.Dental management of patients with inherited bleeding disorders: a multidisciplinary approach

36. PERIODONTAL CONSIDERATIONS:
• Gingival haemorrhage is more common than in haemophilia.
• Even minor gingival manipulation can lead to uncontrollable
bleeding.
• Cryoprecipitate or other anti fibrinolytic agents should be
administered to minimize bleeding.
• Post operative diet should be soft and semi solid to minimize
trauma to the gingiva.
Dental management of patients with inherited bleeding disorders: a multidisciplinary approach

37. TREATMENT:
– Depends on the severity of the condition
– May be similar to that of mild haemophilia, including the
use of Desmopressin where possible
- DDAVP may be used in patients with type 1 VWD
– Factor VIII or Von willebrand factor concentrates should be
used to treat bleeding or to cover surgery in patients who
require replacement therapy

39. ACQUIRED COAGULATION DISORDERS
1.VITAMIN K DEFICIENCY
- Vitamin K is a fat soluble vitamin
– Obtained from green vegetables and bacterial synthesis in the gut
– Important on coagulation factors II, VII, IX and X and on proteins C.
– Without it, these factors cannot bind calcium.
Vitamin K deficiency
– haemorrhagic disease of the newborn
– Biliary obstruction
– Malabsorption of vitamin K
– Vitamin K antagonist drugs

40. DENTAL MANAGEMENT OF A CHILD WITH INCIDENTALLY DETECTED HEMOPHILIA: REPORT OF A
CLINICAL CASE
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
An 8.10-year-old boy without history of significant bleeding events presented with his parents to the Pediatric
Dentistry Postgraduate Clinic complaining of lack of eruption of both permanent upper central incisors. The
parents manifested a good general health status of their son and no reported previous significant bleeding
episodes (e.g., from gingiva during tooth brushing), medical disorders (particularly bleeding diathesis), or
exposure to surgical interventions. On the oral examination, both incisors were palpable and covered with a
fibrous gingival tissue, not associated with previous bleeding
A signed informed consent was obtained from the parents before the treatment. It was decided to perform a
vestibular squared incision over the gingiva with flap apical reposition, to expose the incisal third of both
incisor crowns. The surgical procedure was carried under local anesthesia, employing a water-irrigated laser
hand-piece system and sutures in both sides of the flap . The patient was discharged without apparent local
or systemic complications and with postoperative hygiene/diet instructions.

42. Three days later the patient returned to the clinic exhibiting gingival profuse bleeding, difficult to control with
external pressure application by means of wet gauze . After consulting with the Pediatric Hematologist and
because there was not history of spontaneous bleeding or other hemorrhagic events, routine laboratory blood
tests for blood clotting times were carried out. The results were within the normal limits, except for the aPTT,
which was considered slightly lower. Then, the wound was resutured and covered with Gelfoam with a surgical
splint. After 2 days, the bleeding persisted and the child looked pale and weak. New laboratory specific tests,
including quantification of factors VIII and IX and Von Willebrand, were performed. The clot factor VIII
manifested a deficit of 6% regarding the normal plasmatic level; according to this information, the child was
diagnosed as having mild hemophilia A. To control the bleeding, the patient was intravenously infused with
tranexamic acid (250 mg), vitamin K (5 mg), and normal saline, for 8-hours; after this time, the hemorrhage was
finally stopped, and the patient discharged. At the final examination, 10 days after the event, the child did not
show additional unusual bleeding episodes or any other oral/systemic complications.

43. LIVER DISEASE
– Biliary obstruction results in malabsorption of vitamin K and therefore
decresed synthesis of factors II, VII, IX and X
– Also there are decreased in factor V and fibrinogen
– Dysfibrinogenemia
– Thrombocytopenia.
– Functional abnormalities of platelets
– Hypersplenism associated with portal hypertension
– DIC

44. DISSEMINATED COAGULATION DISORDERS (DIC)
There is widespread deposition of fibrin within blood vessels with
consumption of coagulation factors and platelets occurs as a consequence
of many disorders which release procoagulant material into the circulation
or diffuse endothelial damage or generalized platelet aggregation.
CLINICAL FEATURES:
– Bleeding, particularly from venipuncture
– Purpura
– Generalized bleeding in GIT, oropharynx, lungs, urogenital tract, vaginal
bleeding
– Less frequently, microthrombi may cause skin lesions, renal failure, gangrene.

45. PATHOGENESIS:
1. DIC may triggered by the entry of procoagulant material into
circulation:
– Amniotic fluid embolism
– Premature separation of placenta
2. Initiated by widespread endothelial damage and collagen exposure:
– Septicemia
– Severe burns
3. Widespread intravascular platelet aggregation
– Some bacteria, viruses and immune complexes may have direct
effect on platelets.

46. TREATMENT
– Treat underlying cause
– Supportive therapy with fresh frozen plasma (FFP) and platletes
concentrates
– Cryoprecipitate may also required

47. PLATELET DISORDERS :
• Platelet disorders may be the result of alteration in platelet numbers, either
- decreased (thrombocytopenia)
- increased (thrombocythemia),
• Thrombocytopenia has platelet count < 1,50,000
• Altered platelet function (thrombocytopathia) with normal platelet count
• Platelet disorders may be:
Quantitative- Thrombocytopenic purpura
Qualitative- Disorders of platelet function

48. CAUSES:
• Failed platelet production
• Thrombocytopenia
• von Willebrand’s disease.
• Excessive platelet Destruction
• Idiopathic Thombocytopenic Purpura
• DIC
• Abnormal platelet Function
• Abnormal platelet Regulation

49. THROMBOCYTOPENIC PURPURA
• Thrombocytopenia is a bleeding disorder characterised by a platelet count below
the normal range.
• Reduced counts may be due to:
- Failure of platelet production
- Disordered platelet distribution
- Increased platelet destruction.
• It may be: - Auto- immune or Idiopathic
- Drug induced

50. IDIOPATHIC THROMBOCYTOPENIC PURPURA
• Aka auto – immune thrombocytopenic purpura.
• ITP is one of the most common causes of thrombocytopenia.
• Can lead to purpura and prolonged bleeding.
DRUG INDUCED THROMBOCYTOPENIC PURPURA
• Reactions of drugs or toxins resulting in a low platelet count and bleeding tendency.
• Common offenders are:
• Quinidine
• Sulfonamides
• Heavy alcohol consumption.

51. GENERAL FEATURES:
Hallmarks are:
• Abrupt appearance of petechial hemorrhages.
• Purpura
• Bruises after trauma
• Petechiae cover extensive surface area appearing rash like, but are tender and
do not itch.
• Located chiefly on arms, lower leg, upper chest and neck.
• In severe cases- mucosal bleeding of the GIT may occur.

52. ORAL MANIFESTATIONS
• Include petechiae
• Ecchymoses
• Post operative haemorrhage.
• Sumucous purpura may be conspicous and sometimes
seen as “blackcurrant jelly” blood blisters.

53. DENTAL CONSIDERATIONS
• Regional local anaesthetic block injections can be given.
• Major surgery requires platelets more than 75x 10 9 /l.
• Conscious sedation can be given.
• General anaesthesia can be given in an hospital.
• Avoid aspirin and other NSAIDs.
PERIODONTAL CONSIDERATIONS
• Gingiva is soft, swollen and friable.
• Bleeding occurs on the slightest provocation and is difficult to control.
• The severity of the gingival condition is dramatically alleviated by removal
of the local factors.
Dental management of patients with inherited bleeding disorders: a multidisciplinary approach

54. OUTCOME AND MANAGEMENT IN NEONATAL THROMBOCYTOPENIA DUE TO
MATERNAL IDIOPATHIC THROMBOCYTOPENIC PURPURA.
van der Lugt NM1, van Kampen A, Walther FJ, Brand A, Lopriore E.
OBJECTIVES:Pregnant women with Idiopathic thrombocytopenic purpura (ITP) can deliver neonates with severe
thrombocytopenia. Clear evidence declaring the pathophysiological cause of this neonatal thrombocytopenia is lacking, as
antiplatelet antibodies are not always detectable in maternal serum. Severe neonatal thrombocytopenia below 50 × 10(9) /l is
reported in 8-13% of the neonates from mothers with ITP and intracranial haemorrhage (ICH) in 0-2·9%. Evidence about the
optimal postnatal treatment is scarce. Our objective was to evaluate the outcome and management in neonates with passive ITP
.
MATERIALS AND METHODS:All neonates from mothers with ITP born between 1980 and 2011 were included. Platelet counts
during the first 10 days, presence of Intra cranial hemorrhage and postnatal treatment were recorded. Maternal characteristics
were analysed as possible risk factors for severe neonatal thrombocytopenia.
RESULTS: Sixty-seven neonates were included. Severe thrombocytopenia (<50 × 10(9) /l) occurred in 20/67 (29·9%) neonates.
In three neonates, platelet count rose spontaneously, 18 neonates were treated (one with persistent moderate thrombocytopenia)
with the following: platelet transfusions (3), prednisone (2), intravenous immunoglobulin (IVIG) (1), platelet transfusions and IVIG
(11), platelet transfusion and prednisone (1). Recurrence of low platelet counts after transfusions was commonly seen. Risk
factors for severe neonatal thrombocytopenia were a previous sibling with severe thrombocytopenia and low maternal platelet
nadir during pregnancy.
CONCLUSION:In this cohort, severe neonatal thrombocytopenia occurs more frequently than previously reported. To maintain a
platelet count above 50 × 10(9) /l, often multiple transfusions and IVIG are required. Multiple transfusions may be avoided by
starting IVIG, when platelet count falls below 50 × 10(9) /l after the first platelet transfusion.

55. GLANZMANN'S THROMBASTHENIA – A RARE CASE REPORT OF
SPONTANEOUS GINGIVAL BLEEDING
Vijayalakshmi Venkat, Sruti Kalluri, Satheesha Reddy Bandalore Hanumantha
Glanzmann's thrombasthenia is a rare congenital bleeding disorder which is associated with mutations in the
genes encoding glycoproteins, GPIIB or GPIIIA resulting in platelet dysfunction.
It is an autosomal recessive disorder where platelet count is normal or subnormal, bleeding time is prolonged,
and there is deficiency or absence of platelet aggregation. Because of this deficiency of platelet function, it
manifests as a bleeding disorder characterized by mucocutaneous hemorrhage of varying severity. The gene
responsible is carried on the long-arm of chromosome 17 at q.
A female patient about 10 years of age reported to the department with a chief complaint of bleeding gums
since 4 days. Her medical history showed multiple episodes of bleeding from the gums since 4 days which
was spontaneous. There was also prolonged bleeding following minor trauma and hemetemesis.
There was no significant family history of bleeding disorder. She
also give history of taking tablet. She has been taking livogen and
tranaxemic acid for the past 3 years, and three units of blood has
been transfused till now.

56. Intraoral examination revealed spontaneous gingival bleeding from upper and lower tooth causing stains
all over the surface. Dental caries with pulpal involvement was seen in 54. Numbers 54 and 83 showed
grade II mobility. Considering the history and clinical examination, a provisional diagnosis of
Glanzmann's thrombasthenia was given.
the patient was then subjected to hematological investigation which showed normal platelet count of
1,78,000/mm 3, normal prothrombin time (11.2 s), normal partial thromboplastin time (28.5s), and normal
thrombin time (14.9s), but bleeding time was prolonged >15 min. Factor VIII, fibrinogen, and von
Willebrand factor showed normal values.
Oral prophylaxis was done in the Department of Pedodontics and she was
advised to take vitamin C supplements daily and to use soft tooth brush with
fluoridated tooth paste. The treatment for grossly decayed 54 was delayed,
taking into consideration the health condition of the child until hemorrhage had
been controlled. She was referred to the general physician to obtain consent for
the same. The recall schedule for this child was every 2 weeks initially which
showed improvement in oral hygiene, followed by once in 3 months and then
once in 6 months, stressing the importance of maintaining oral hygiene at all
appointments.

57. ANTIFIBRINOLYTIC AGENTS
Antifibrinolytic agents are an adjunctive therapy for dental management of
patients with bleeding disorders.
These agents include: - ε – amino caproic acid
- Tranexamic acid
Hemophilic patients form loose,friable clots that are easily dislodged,especially
in the oral cavity where fibrinolysis is increased.
Antifibrinolytics prevent clot lysis within the oral cavity and are often used as
an
adjunctive therapy

58. DOSES:
• In children ε – amino caproic acid is given immediately before dental treatment in
initial loading dose of 100-200 mg/kg upto maximum of 10 grams.
- Subsequently 50-100mg/kg orally every 6 hours for 5-7 days with maximum
dose of 5 grams
• Maximum dose of tranexamic acid is 25mg/kg i.e 1500 mg every 8 hourly
- Doses of 10-15 mg/kg weight have been reported to be effective depending on
the severity
Side effects:
Headache,Nausea,Dry mouth,Urinary tract bleeding,DIC

59. CONCLUSION

60. REFERENCES
1.Concise medical physiology, Chaudhuri, IV edition.
2.Essentials of medical physiology – Sembulingam
3. Robbin’s Basic Pathology, Seventh Edition.
4.Carranza’s Clinical Periodontology, X edition.
5.Naveen Kumar J, Anil Kumar R, Varadarajan R, Sharma N. Specialty dentistry for
the hemophiliac: Is there a protocol in place?. Indian J Dent Res 2007;18:48-54
6.Dental management of patients with inherited bleeding disorders: a
multidisciplinary approach
7.Guidelines for dental treatment of patients with inherited bleeding disorders
Andrew Brewer,Maria Elvira Correa