Coagulation of blood right from haematopoiesis, platelets, endothelial injuries, development of clotting factors, coagulation cascade, applied aspect of coagulation related disorders and much more.

1. Dr. Balraj Shukla
Department of Pedodontics & Preventive Dentistry
College of Dental Sciences & Research Centre

2. Contents
 Introduction to Hematopoiesis
 Blood and its functions
 Platelets
 Pathophysiology of the endothelium
 Hemostasis
 Clotting Factors
 Coagulation Cascade
 Clot retraction & dissolution
 Neonatal vs Adult Haemostasis
 Vitamin K in pediatrics
 Anti-clotting mechanism in the body
 Tests for Clotting
 Disorders of blood coagulation
 Anti-coagulant therapy
 Dental management of patients on anti-coagulants
 Conclusion
 References

3. HAEMATOPOESIS

6. Functions of Blood
Transportatio
n
Dissolved
gases,
nutrients,
hormones,
metabolic
wastes
Regulation
pH, Body
temperatur
e
Protection
Pathogens,
Toxins,
Infections,
Coagulatio
n

7. PLATE
LETS• Disc-shaped
• No nucleus
• Remain in bloodstream for 5-9 days
• Removed by macrophages in liver & spleen

8. Pathophysiology of the Endothelium

10. The Endothelial cell

11. Endothelial injuries
• Formation of endothelial gaps
- Most common mechanism of vascular leakage
- Elicited by histamine, leukotrienes, bradykinin, etc.
- Occurs in venules more often
- Reversible injury and lasts for 15-30 minutes
- A.k.a. Immediate Transient Response
• Direct endothelial injury
- Due to injurious stimulus like burns, bacterial
infection, etc.
- Leakage starts immediately and lasts for several hours
till the vessels are repaired.
- Affects venules, arterioles and capillaries
- A.k.a. Immediate Sustained response

12. • Delayed prolonged leakage
- Injury that begins after 2-12 hours and lasts for several days
- Affects venules and capillaries
- Caused by thermal injuries, radiations, bacterial toxins.
• Leukocyte-mediated endothelial injury
- More commonly seen in acute inflammation
- Leukocytes that adhere to endothelium may get activated
such that they release toxic oxygen species and
proteolytic enzymes that cause endothelial injury.
- Restricted to venules and capillaries.
• Leakage from new blood vessels
- Occurs during angiogenesis when immature endothelial
cells do not form proper intercellular junctions

14. VASOCONSTRICTION
MAJOR FACTORS CAUSING VASOCONSTRICTION:
• Thromboxane A2 from platelet membranes
• Serotonin from dense granules of platelets
• Endothelin made from injured endothelium
• Neurogenic reflex by pain receptors
OTHER FACTORS:
• Bradykinin
• Fibrinopeptides

15. PLATELET PLUG FORMATION
• PLATELET
ADHESION
- vWF – Bridge
between
exposed
collagen and
platelet surface
• PLATELET SECRETION
- Initially adhered platelets
release clotting factors
from the alpha & dense
granules.
- Calcium binds to
phospholipids and
provides a surface for the
clotting factors to bind to.
• PLATELET AGGREGATION
- Thromboxane A2 released
by activated platelets
attract more platelets to
bind.
- ADP enlarges the platelet
aggregate to a platelet plug.
- ADP binding also forms the
basis for Thrombin
generation and binding of
Fibrinogen to the platelet
plug.

16. Clotting Factors
 Coagulation occurs through a series of reactions
due to the activation of a group of substances.
The substances necessary for clotting are called
Clotting factors.

17. CLOTTING FACTORS
FACTORS NAME
I Fibrinogen
II Prothrombin
III Thromboplastin (Tissue Factor)
IV Calcium
V Labile Factor (Proaccelerin/ Accelerator globulin)
VI Factor Va/Accelerin
VII Stable Factor
VIII Antihemophilic Factor (Antihemophilic globulin)
IX Christmas Factor
X Stuart-Prower factor
XI Plasma thromboplastin antecedent
XII Hageman factor (contact factor)
XIII Fibrin-stabilizing factor (fibrinase)

18. FACTOR
I
Fibrinogen
 Source : Liver
 Pathway : Both extrinsic and intrinsic
 Activator : Thrombin
 Function : When fibrinogen is converted into fibrin
by thrombin, it forms long strands that compose
the mesh network for clot formation.

19. FACTOR
II
Prothrombin
 Source : Liver
 Pathway : Both Extrinsic and Intrinsic
 Activator : Prothrombin activator
 Function : Prothrombin is converted into
thrombin which then activates fibrinogen
into fibrin

20. FACTOR III
Thromboplastin/Tissue
Factor
 Source : Platelets(Intrinsic) and Damaged
endothelium lining the blood vessel (Extrinsic)
 Pathway : Both extrinsic and intrinsic
 Activator : injury to blood vessel
 Function : Activates factor VII (a)

21. FACTOR IV
Calcium
 Source : Bone and absorption from food in GIT
(intrinsic) and the blood vessel ( Extrinsic)
 Pathway : Both extrinsic and intrinsic
 Function : Works with many clotting factors for
activation of the other clotting factors. [These are
called Calcium dependent steps.]

22. FACTOR V
Proaccelerin/ Labile factor/ Ac-
Globulin
 Source : Liver and platelets
 Pathway : Both extrinsic and intrinsic
 Activator : Thrombin
 Function : Works with factor X to activate
Prothrombin

23. FACTOR VII
Proconvertin/Serum Prothrombin
conversion accelerator/ Stable factor
 Source : Liver
 Pathway : Extrinsic
 Activator : factor III (Tissue factor)
 Function : Activates factor X which works with
other factors to convert prothrombin into
thrombin.

24. FACTOR VIII
Anti-Hemoplytic factor/ Antihemophilic
factor or globulin/ Antihemophilic factor
 Source : Endothelium lining blood vessel and
platelets (plug)
 Pathway : Extrinsic
 Activator : Thrombin
 Function : Functions with factor IX and calcium to
activate factor X. Converts prothrombin to
thrombin.
 Deficiency leads to : Hemophilia A

25. FACTOR IX
Christmas Factor/ Plasma
Thromboplastin Component/ Anti-
hemophilic factor-B
 Source : Liver
 Activator : Factor XI and Calcium
 Function : Works with Factor VIII and calcium
to activate Factor X
 Deficiency leads to : Hemophilia B

26. FACTOR X
Stuart-Prower
factor/Antihemophilic Factor B
 Source : Liver
 Pathway : Intrinsic, Extrinsic
 Activator : Factor VII (Extrinsic) / Factor IX +
Factor VIII + Calcium (intrinsic)
 Function : Works with platelet phospholipids to
convert prothrombin into thrombin. This reaction
is made faster by activated Factor V.

27. FACTOR XI
Plasma Thromboplastin Antecedent/
Antihemophilic Factor C
 Source : Liver
 Pathway : Intrinsic
 Activator : Factor XII + Prekallikrein and
Kininogen
 Function : Works with calcium to activate Factor
IX
 Deficiency leads to : Hemophilia C

28. FACTOR
XII
Hageman Factor
 Source : Liver
 Pathway : Intrinsic
 Activator : Contact with collagen in the torn wall of
blood vessels
 Function : Works with prekallikrein and kininogen
to activate Factor XI. Also activates plasmin
which degrades clots.

29. FACTOR
XIII
Fibrin Stabilizing
Factor
 Source : Liver
 Activator : Thrombin and calcium
 Function : Stabilizes the fibrin mesh network of
a blood clot by helping fibrin strands to link to
each other. Thus, it also helps to prevent fibrin
breakdown (fibrinolysis) activates plasmin
which degrades clots.

30. PREKALLIKREIN / FLETCHER
FACTOR
 Source : Liver
 Pathway : Intrinsic
 Function : Works with kininogen and Factor XII to
activate Factor XI.

31. KININOGEN/FITZGERALD
FACTOR
 Source : Liver
 Pathway : Intrinsic
 Function : Works with prekallikrein and Factor XII
to activate Factor XI.

32. We are
here

33. STAGES OF BLOOD CLOTTING
Formation of prothrombin activator
Conversion of prothrombin into thrombin
Conversion of fibrinogen into fibrin

34. Formation of Prothrombin Activator
 Formation of prothrombin activator occurs through 2
pathways :
i. Intrinsic pathway – initiated by platelets within the
blood
ii. Extrinsic pathway – initiated by tissue thromboplastin
formed from injured tissues

37. Conversion of Prothrombin into
Thrombin
Blood clotting is all about thrombin formation. Once
thrombin is formed, it definitely leads to clot formation.
Steps :
 Prothrombin activator converts prothrombin into thrombin
in the presence of calcium ions (factor IV).
 Once formed thrombin initiates the formation of more
thrombin molecules. The initially formed thrombin
activates factor V which in turn accelerates formation of
both extrinsic & intrinsic prothrombin activator which

38. Conversion of Fibrinogen into
Fibrin
• Thrombin converts fibrinogen into activated fibrinogen
which is called fibrin monomer.
• Fibrin monomer polymerizes with other monomer
molecules and form loosely arranged strands of fibrin.
• Later these loose strands are modified into dense and
tight fibrin threads by fibrin-stabilizing factor (factor
XIII) in the presence of calcium ions.
• All the tight fibrin threads are aggregated to form a
meshwork of stable clot.

39. Clot Retraction & Dissolution
Clot contains
fibrin, platelets
and plasma.
Contractile
proteins like
actin, myosin &
thrombosthenin
compress the
fibrin network to
squeeze out the
serum.
Clot now
reduced by 40%
to its original size
after 30-45
minutes.
Blood vessel
lining thus pulled
closer to each
other.
Fibroblasts and
new endothelial
cells repair the
lining.
So what happens to
the clot?

40. Neonatal vs Adult
Haemostasis
Compone
nt
Neonatal Adult
Coagulatio
n Factors
Decreased Factors II, VII, IX,
X, XI, XII
Prolonged action of
Fibrinogen, Factor V, XIII
Increased Factor VIII
Decreased thrombin
generation
Primary
Hemostasi
s
Increased VWF
Normal Platelet count,
Decreased Platelet Function
Enhanced Primary
Hemostasis
Fibrinolysis Decreased Plasminogen Hypofibrinolytic state
Natural
Coagulatio
n Inhibitors
Decreased AT, PC, PS Reduced capacity to inhibit
activated proteins
(Lippi et al, Sem Thromb Hemost 2007, 33,816-820 Guzzetta et al, Ped
Anesthesia 2010, 21, 3-9)

41. Vitamin K
 Hydrophobic, Lipophilic vitamin that contains a
Naphthoquinone ring
 3 types: Phylloquinone (K1), Menaquinone (K2),
Menadione (K3)
 Recommended daily intake:Men 120 micrograms/day
Women 90 micrograms/day
Infants (first 6 months of
life)
2 micrograms/day
Infants (7-12 months) 2.5 micrograms/day
Children (1-3 years) 30 micrograms/day
Adolescents 75 micrograms/day

42. Vitamin K deficiency in neonates
Endogenous Exogenous
Insufficient intestinal colonization
by bacteria
Low concentration of Vitamin K
in breast milk (1-4
micrograms/litre)
“ Vitamin K is poorly transmitted across the
placental barrier. At birth, its levels are often
below the detection limit of 0.02 ng/mL, yet
haemostasis is still ‘‘appropriate’’ and the vast
majority of infants do not bleed. In breast-fed
infants given no vitamin K supplement,
measurable levels are normally found 12 hours
after birth and adult levels of 0.4 ng/mL by Day
4.”
- Lippi et al, 2007, Coagulation testing in

43. Vitamin-K Deficiency Bleeding (VKDB)
 Disorder wherein blood coagulates immediately upon Vit K
supplementation
 INR = 4, Normal count of platelets and fibrinogen
EARLY VKDB (6-12%)
- Within 24 hours of birth
- Seen in infants whose
mothers have been
taking drugs that inhibit
Vitamin K
- Anticonvulsants
(Phenytoin,
Barbiturates),
Antituberculosis
(Isoniazid, Rifampicin),
Antibiotics
(Cephalosporins),
Coumarin derivatives
(Warfarin)
CLASSICAL VKDB
(0.44-1.5%)
- Within 24 hours &
7 days of birth
- Due to
delayed/insufficie
nt feeding
- Bruises, GIT
Bleeding
LATE VKDB
- Between the age of 2-
12 weeks
- Exclusively associated
with breast feeding
- 1:20,000 prevalence
- 20% mortality rate
- 50% chances of
intracranial
haemorrhage
- Persistent neurological
damage

44. Natal and neonatal teeth extraction
 Tooth should be at least 1 mm mobile
 Child should be at least 10 days old
 Vitamin K i.m. dose of 0.5-1 mg must be administered prior
to extraction

45. ANTICLOTTING MECHANISM IN THE
BODY PHYSICAL FACTORS
- Continuous circulation of
blood
- Smooth endothelial lining of
blood vessels
 CHEMICAL FACTORS
- All clotting factors are in
inactive state
- Presence of heparin and
antithrombin which are produced
by liver

46. TESTS FOR CLOTTING
Bleeding Time
It is the time interval from oozing of blood after a cut
or injury till arrest of bleeding. Its normal duration is 3
to 6 minutes. It is prolonged in thrombocytopenia &
thrombopathy.
Clotting time
It is the time interval from oozing of blood after a
cut or injury till the formation of clot. Its normal
duration is 3 to 8 minutes. It is prolonged in
hemophillia.

47. Prothrombin time
 It is the time taken by blood to clot after adding tissue
thromboplastin to it. Blood is collected and oxalated so
that, the calcium is precipitated and prothrombin is not
converted into thrombin. Thus, the blood clotting is
prevented when calcium is added to this blood.
 Normal duration of Prothrombin time is about 12-14
seconds.
 It is prolonged in deficiency of prothrombin and other
factors like factors I, V, VII, X. However, it is normal in
hemophilia.Activated Partial Thromboplastin time
 It is used to check the efficacy of anticoagulant therapy.
 Normal duration of aPTT is 30-40 seconds.
 It measures the Factors I, II, V, VIII, X, XI & XII.

48. Tourniquet test
 Clinical test to determine patient’s capillary fragility.
 It is a diagnostic test for thrombocytopenia and dengue
fever.
 Inflate blood pressure to a point midway the systolic and
diastolic pressure for 5 minutes.
 Presence of more than 20 petechiae in an area of 6.25 cm
square indicates positive result.

49. INTERNATIONAL NORMALIZED RATIO
(INR)
 The INR was devised to standardize
the measurements of PT.
 For each batch of tissue factor, the
manufacturer assigns an
International Sensitivity Index (ISI)
which indicates the activity of tissue
factor with a standardized sample.
Normal ISI is between 1.0 to 2.0.

51. Classification of Bleeding disorders
 INTERNAL
- Haematoma
(Petechiae, Purpura,
Ecchymosis)
- Hemopericardium
- Hemoperitoneum
- Hemarthrosis
- Haemothorax
- Hematomyelia
- Intracranial
haemorrhage
 EXTERNAL
- Epistaxis
- Haemoptysis
- Haematemesis
- Haematochezia
- Melena
- Menorrhagia
- Haematuria

52. Disorders of Primary
Haemostasis
 Vessel Wall abnormalities
- Hereditary Haemorrhagic
Telangiectasia
- Ehlers-Danlos syndrome
 Qualitative disorder of
platelets
- Bernard-Soulier Syndrome
- Thrombasthenia
 Quantitative disorder of
platelets
- Thrombocytopenic purpura
Disorders of Secondary
Haemostasis
 Congenital bleeding
disorders
- Haemophilia
- Parahaemophilia
- Von Willebrand’s disease
 Acquired bleeding disorders
- DIC
- Liver or Renal disease
 Thrombosis
- Antithrombin III deficiency
- Protein-C & Protein-S
Classification of Coagulation disorders

53. Hereditary Haemorrhagic
Telangiectasia Autosomal dominant disorder characterized by cherry-like
red lesion appearing as multiple localized angiomatas on
lower face, tongue, lips fingers, toes and oral mucous
membrane.
 Telangiectasia or crushed spider-like appearance
represents permanently enlarged capillaries which are
present just under the skin.
• Treatment includes:
- Septal dermoplasty in
patients with frequent
epistaxis
- Pressure pack
- Sclerosing agents like
Sodium morrhuate or
Sodium Tetradecyl
Sulphate

54. Ehlers-Danlos Syndrome
 Originally a connective tissue disorder
 Manifests include collagen synthesis disorder wherein
capillaries are poorly supported by subcutaneous
collagen. Hyperextensibility of these capillaries leads to
ecchymosis.

55. Bernard-Soulier Syndrome
 Autosomal recessive bleeding disorder characterized by
Giant platelets, prolonged bleeding time and low platelet
count.
 Bleeding gums, Epistaxis and unusual menstrual cycles
can be observed.
 Occurs due to deficiency of Glycoprotein lb, which is a
receptor for von Willebrand factor.
• Treatment includes:
- Platelet transfusion
- Administration of
tranexamic acid in
episodes of bleeding

56. Glanzmann’s thrombasthenia
 Hereditary chronic haemorrhagic disease characterized
by defect in platelet aggregation due to defective
membrane protein
 Spontaneous gingival bleeding from the oral cavity, onset
of menarche, hemarthrosis, prolonged bleeding time.
• Treatment includes:
- No specific treatment
- Platelet infusion:
Microfibrillar collagen
preparation with
fibrinolytic inhibitors
can be given for
patients indicated for
oral surgery.

57. Thrombocytopenic Purpura
 Also known as
Werlhof’s disease/
Haemorrhagic purpura
 Increase in
megakaryocytes inside
the bone marrow and
decrease in circulating
blood platelets.
 Clinical features
manifest when platelet
count drops below
1,00,000/mm3

58. Clinical features:
- Petechiae, ecchymosis, epistaxis, haemorrhagic bullae
- Most commonly seen at the junction of hard and soft palate.
- Increased bleeding time and normal clotting time.
- Seen in the age ranges of 2-6 years and 20-50 years.
Treatment:
- Supportive treatment of 2mg/kg
prednisolone daily in children &
1mg/kg in adults daily. Should be
continued till platelet count reaches
normal level.
- Splenectomy indicated if platelet
count does not reach normal level in 3
to 4 days.
- I.V. Ig is given 1g/kg if bleeding is life
threatening.
- Gingival bleeding can be controlled by
Gelfoam/absorbable cellulose/1.5%

59. Thrombocytosis
 Platelet count exceeds
400,000
platelets/microlitre.
Seen in elderly patients.
 2 types: Primary &
Secondary
Primary: Chronic
myeloproliferative or
myelodysplasia
Secondary: Reactive
thrombocytosis, caused
due to other disease or
condition
 Epistaxis, Skin
haemorrhage,
spontaneous gingival

60. Haemophilia
 Haemophilia is an X-linked recessive disorder of
blood coagulation. Can be of three types:
- Haemophilia A
- Haemophilia B
- Haemophilia C (Autosomal dominant)

61. Haemophilia A
 Deficiency of factor VIII
 Affects 1/10,000 individuals
 Occurs in babies only after 6 months of age
 Normal factor VIII level: 50-150%
 Affects males predominantly
 Hemarthrosis or joint haemorrhage (more common in
children)
 Subcutaneous haemorrhage
 Intracranial bleeding (rare)
 Persistent bleeding from lip, tongue and gingiva
 Haematoma from the floor of mouth
 Tooth eruption and exfoliation may lead to prolonged
haemorrhage

62.  Classification based on AHG (Anti-Haemophilic Globulin):
- Mild: less than 4% of AHG
- Moderate: 1% to 3% of AHG
- Moderate to Severe: 0 to 0.9% of AHG
- Severe: 0% of AHG
 Treatment:
- Fresh frozen plasma
- Factor VIII concentrate
- Genetic counselling
- Synthetic analogue of Desmopressin (anti-diuretic) in
combination with Tranexamic acid (anti-fibrinolytic) and
Epsilon Amino-Caproic acid (anti-fibrinolytic).

63. Haemophilia B
 Deficiency of factor IX
 Affects 1/30,000 individuals
 Affects males predominantly
 Phenotypically indistinguishable from Haemophilia A
 Distinguishable from Haemophilia A by modification of
prothrombin consumption time and partial
thromboplastin time
 Treatment includes administration of Factor IX
concentrate

66. HAEMOPHILIA C
 Autosomal recessive
disorder, deficiency of
factor XI
 Only type of haemophilia
that can occur in girls as
well
 Fourth most common
coagulation disorder
 Heavy nosebleeds,
Haematuria, Heavy
menstrual bleeding
 Treatment: Factor XI
concentrate
PARAHAEMOPHILIA
 Deficiency of factor V,
reduction in plasma
proaccelerin
 Autosomal dominant
disorder
 Affects both sexes
 Spontaneous epistaxis,
bleeding into the GIT,
Menorrhagia
 Cutaneous ecchymosis,
hamartoma
 Spontaneous gingival
bleeding
 Intraocular haemorrhage into

67. Von Willebrand’s disease
 Pseudohaemophilia/ Vascular
haemophilia/Vascular purpura
 Autosomal dominant, more
common in childhood and
females
 vWF is a carrier protein for
factor VIII
 Most common hereditary clotting
disorder
 vWF is responsible for platelet
adhesion to subendothelium,
regulation of plasma level of
factor VIII coagulation activity
and thereby haemostasis.
 Most common sites of bleeding
Treatment:
• Transfusion of plasma
and cryoprecipitate
• Desmopressin as
nasal spray to control
nasal bleeding
• vWF containing Factor
VIII concentrates for
prophylaxis in major
surgeries.

68. Disseminated Intravascular
Coagulation Acquired bleeding disorder which can be acute or chronic
 Acute DIC is clinically severe with depletion of multiple clotting
factors like fibrinogen, prothrombin, factor V, factor VIII and also
reduced platelets.
 Gingival bleeding is the most common oral manifestation
Treatment:
- Platelets transfusion
and Cryoprecipitate
- Treatment of other
exacerbating factors
like acidosis,
dehydration, renal
failure, hypoxia and
septicaemia.

69. Thrombosis
Arterial thrombosis
Venous thrombosis
Mechanism
Typically from rupture of
atherosclerotic plaques.
Typically from a combination of
factors from Virchow’s triad.
Location Left heart chambers, arteries
Venous sinusoids of muscles and
valves in veins
Diseases
Acute coronary syndrome
Ischemic stroke
Limb claudication/ischemia
Deep venous thrombosis
Pulmonary embolism
Composition Mainly platelets Mainly fibrin
Treatment
Mainly antiplatelet agents (ASA,
clopidogrel)
Mainly anticoagulants (heparins,
warfarin)

70. ANTICOAGULA
NTSSUBSTANCE MoA USES
Heparin Suppresses action of
thrombin
Activates Antithrombin III
Inactivates the active forms
of clotting factors IX, X, XI &
XII
- To prevent intravascular
blood clotting during
surgeries
- During dialysis
- During cardiac surgeries
- To preserve blood before
transfusion
EDTA Remove calcium from the
blood
- Administered i.v. in cases
of lead poisoning
- In laboratories as an
anticoagulant
Ammonium &
Potassium oxalates
Reduce the blood calcium
level
- Only in vitro use as it is
poisonous in vivo
Warfarin Inhibition of carboxylation
of Vitamin K dependent
factors like factors II, VII, IX
& X
- Deep venous thrombosis,
Arterial embolism, Ischaemic
attacks, Serious
haemorrhage

71. ANTICOAGULANTS
 In vitro: Heparin, Sodium Citrate, Sodium Oxalate, Sodium
edetate
 In vivo:
- Parentral: Unfractioned heparin, LMWHs,
Fondaparinux, Lepirudin
- Oral: Coumarin derivatives (Warfarin), Phenindione,
Dabigatran etexilate

72. Inhibits
epoxide
reductase

74. HEPARIN WARFARIN
Naturally occurring Synthetic
Used both in vivo and in vitro Used only in vivo
Parenterally (i.v., s.c.) Orally
Rapid onset, short duration of action Delayed onset, long duration of action
Therapy monitored by aPTT Therapy monitored by INR
Protamine Sulphate is the antagonist Vitamin K1 & fresh frozen plasma is the
antagonist
Safe during pregnancy Teratogenic potential
PEDIATRIC DOSAGE
NEONATES & INFANTS
Initial dosage: 75-100 units/kg I.V. bolus
Maintenance dosage: 25-30 units/kg/hr
i.v. infusion
CHILDREN
Same initial dosage, Maintenance
dosage reduced to 18-20 units/kg/hr/i.v.
infusion
NEONATES & CHILDREN
Initial dose: 0.2mg/kg orally
Maintenance dose (to maintain INR
between 2-3)
Infants: 0.33mg/kg
Teenagers: 0.09mg/kg
Dosage later adjusted based on INR
levels

75. Dental management of patients on
Anticoagulant therapy

76. What Happens for Patients Who Are Having a Minor
Procedure, Such as a Tooth Extraction or Skin Cancer
Removal?
For patients having minor dental work, such as a tooth extraction
or root canal, it may not be necessary to stop warfarin. Some
dentists allow patients to continue warfarin (especially if there are
concerns about stopping it), so long as they take a special
mouthwash called tranexamic acid (Amicar) just before and 3
times daily for 1 to 2 days after the dental procedure, to help
prevent bleeding. For patients having minor skin procedures or
cataract surgery, interruption of warfarin is often not required
because there is minimal bleeding.
- American Heart Association (Circulation)

77. Low risk procedures
No change in
anticoagulation
medication. NOACs like
Warfarin, Dabigatran
and Rivaroxaban can be
continued. (Root canal
treatment,
uncomplicated
extraction of 1 to 3
teeth, minor
reconstructive
procedures)
Moderate risk
procedures
Withdrawal of coumarin 2
days before and
verification of INR on day
of procedure
High risk
procedures
Heparin protocol
recommended (INR
>4, extraction of
more than 3 teeth).
Surgery and anticoagulants
Heparin bridging
therapy
with LMWH & UFH
• Discontinue warfarin 2-3 days before
hospitalization
• Check aPTT, INR, CBC and Platelet count
• Heparin bolus dosage: 80 units/kg
• Drip infusion dosage: 18 units/kg
• Check APTT 6 hours after initial dosage
• Adjust dosage of heparin accordingly
• If APTT levels are therapeutic on 2 successive
occasions, the next tests should be conducted

78. During dental surgery
 No NSAIDs should be used
 Use regional block LA only if essential
 Prefer resorbable sutures in invasive procedures

79. Post-op management of patients on
anticoagulation therapy
 Warfarin is restarted 10 mg dose on night of surgery (2-5 mg in
children)
 Check INR
 Mouth rinsing is avoided
 Oral penicillin 250-500 mg QID for 7 days
 Tranexamic acid mouth wash – 10mL, 5% solution used four
times a day, for 2 minutes for 7 days.
 Paracetamol for post-operative pain. Codeine can be given in
conjunction to enhance its effect.
 Cold diet and minced food

80. CONCLUSI
ON

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83. THANKYOU