The presentation deals with the basics of hemorrhage i.e. classification, etiology. It also covers the mechanism of hemostasis and the various methods to achieve hemostasis. Hope you like it! Suggestions and feedback will always be well appreciated. :)

1. HEMORRHAGE AND ITS MANAGEMENT
Presented By:
Akshat Sachdeva
BDS Final Year
Manav Rachna Dental College
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2. WHAT IS HEMORRHAGE?
• Denotes the escape of blood from a blood vessel.
• Any damage to the vasculature leads to the outflow of blood.
• Blood carries oxygen and nutrients to the tissues and is vital for body
functions.
• Loss of blood due to any reason beyond a certain point is potentially
life threatening and may lead to exsanguination (blood loss to a degree
sufficient to cause death).
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3. CLASSIFICATION OF HEMORRHAGE
1. Depending on the SOURCE OF BLEEDING:
i) External Hemorrhage: When bleeding is revealed and seen outside,
e.g. epistaxis.
ii) Internal Hemorrhage: Bleeding is concealed and not seen outside,
e.g. intracranial hematoma.
2. Depending on the NATURE OF BLEEDING VESSEL:
i) Arterial Hemorrhage: Bright red in color. Blood emitted as a jet with
each heartbeat.
ii) Venous Hemorrhage: Dark red in color. Blood flow is steady.
iii) Capillary Hemorrhage: Bright red in color. Generalized ooze of
blood instead of blood flow.
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4. 3. Depending upon TIME OF HEMORRHAGE:
i) Primary Hemorrhage: Occurs at the time of trauma or surgery.
ii) Reactionary Hemorrhage: Occurs within 24 hours of trauma or
operation.
iii) Secondary Hemorrhage: Occurs after 7 – 14 days of trauma or
operation.
4. Depending upon VOLUME OF BLOOD LOSS:
i) Mild Hemorrhage: Blood loss ≤ 500 mL.
ii) Moderate Hemorrhage: Blood loss 500 – 1000 mL.
iii) Severe Hemorrhage: Blood loss ≥ 1 L.
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5. Depending upon SPEED OF BLOOD LOSS:
i) Acute Hemorrhage: Massive bleeding in short span of time.
ii) Chronic Hemorrhage: Slow bleeding small in quantity for long time.
6. Depending upon PERCENTAGE OF BLOOD LOSS:
i) Class I: Up to 15%.
ii) Class II: Between 15 – 30%.
iii) Class III: Between 30 – 40%.
iv) Class IV: More than 40%.

6. ETIOLOGY
• Trauma.
• Infections.
• Congenital malformations.
• Surgical (intraoperative/postoperative).
• Due to systemic diseases (viral infection, scurvy, allergy).
• Abnormalities in clotting factor (hemophilia A, multiple myeloma).
• Abnormalities in platelets (leukemia, ITP, thrombocytosis,
thrombocytopenia).
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7. HEMOSTASIS
• Mechanism of cessation of extravasation of blood.
• Four important steps:
 Injured blood vessel undergoes constriction due to spasm.
 Activation of platelets and formation of platelet plug. This leads to
primary hemostasis.
 Activation of clotting mechanism and formation of clot leading to
completion of secondary hemostasis.
 Fibrous organization of clot or retraction of clot.
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8. Mechanism of Hemostasis 8

9. PRIMARY HEMOSTASIS
• Process of platelet plug formation at the site of injury.
• Occurs within seconds of injury and is important for stoppage of
blood from small arterioles, venules and capillaries.
• There is platelet adhesion, release of granules and platelet aggregation
resulting in formation of primary hemostatic plug.
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11. SECONDARY HEMOSTASIS
• Activation of clotting process in plasma that results in formation of
fibrin which strengthens the primary hemostatic plug.
• Completed in several minutes and is important in bleeding from larger
vessels.
• Some substances promote clotting (called procoagulants) and some
prevent clotting (called anticoagulants).
• There is a complex interaction of various factors of coagulation in the
formation of a clot.
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12. 12Coagulation Mechanism

13. Coagulation mechanism can be broken down into series of 4 reactions:
Reaction 1:
• Intrinsic or contact phase of coagulation.
• Factors VIII, IX, XI, XII along with calcium and plasma proteins take
part.
• Partial thromboplastin time screens this.
Reaction 2:
• Extrinsic pathway for initiation of coagulation.
• Release of tissue thromboplastin from injured tissues.
• Protease complex formed between factor VII, calcium and tissue
thromboplastin, which activates factor X.
• Prothrombin time screens this.
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14. Reaction 3:
• Factor X is activated by proteases generated in the previous two
reactions.
Reaction 4:
• Prothrombin is converted into thrombin in presence of factor V,
calcium and phospholipids.
• Main role of thrombin is conversion of fibrinogen into fibrin.
• It also activates factor V, VIII and XIII and helps in platelet
aggregation and secretion.
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15. CLINICAL EVALUATION
• Evaluation of patient with co – ordinated history and physical
examination provides valuable clues.
• History should include following questions:
1. Is there any personal or family history of bleeding tendency?
2. Has the patient undergone surgery or extractions previously?
3. Any history of hematuria, GIT hemorrhage, epistaxis?
4. What medication is the patient taking or has taken recently?
• Note for any splenomegaly, hepatomegaly.
• Hepatic insufficiency should be assessed.
• Assessment of skin and mucosal surfaces.
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16. LABORATORY TESTS
1. Bleeding Time (BT):
• Patients with BT more than 10 minutes have increased risk of
bleeding.
• Various methods for measuring BT, e.g. Ivy, Duke and template.
• BT is prolonged in thrombocytopenia, Von – Willebrand’s disease and
platelet dysfunction.
2. Platelet count:
• Normal count: 1.5 – 4.5 lakhs per cumm of blood.
• When count becomes 50,000 – 1 lakh per cumm, there is mild
prolongation of BT.
• Patients with count less than 50,000 per cumm have easy bruising.
• Minor oral surgical procedures can be done if count is above 80,000 –
1 lakh per cumm.
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17. 3. Prothrombin Time (PT):
• Normal PT is usually 12 – 14 seconds.
• Prolonged in patients on warfarin anticoagulant therapy, vitamin K
deficiency or deficiency of factor V, VII, X, prothrombin or
fibrinogen.
4. Partial Thromboplastin Time (PTT):
• Prolonged in hemophiliacs.
• Normal PTT is less than 45 seconds.
• PTT is relatively insensitive to changes in intrinsic coagulation
system.
• Small changes in PTT may be of great significance.
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18. METHODS OF ACHIEVING HEMOSTASIS
MECHANICAL METHODS
• Pressure.
• Hemostat.
• Sutures and Ligation.
CHEMICAL METHODS
Local Agents:
• Adrenaline.
• Thrombin.
• Surgicel.
• Oxycel.
• Surgicel Fibrillar.
• Gelatine Sponge.
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19. • Microfibrillar Collagen.
• Fibrous Glue.
• Styptics and Astringents.
• Alginic Acid.
• Natural Collagen Sponge.
• Bone Wax.
• Ostene.
Systemic Agents:
• Whole Blood.
• Platelet Rich Plasma.
• Fresh Frozen Plasma.
• Cryoprecipitate.
THERMAL AGENTS
• Cautery.
• Electrocautery.
• Cryosurgery.
• Lasers. 19

20. MECHANICAL METHODS
1. PRESSURE
• Immediate measure for capillary or venous bleeding.
• Firm pressure should be applied over the bleeding site using either
fingers or gauze for at least 5 minutes.
• This would control most hemorrhages by counteracting the hydrostatic
pressure of the bleeding vessel.
2. HAEMOSTAT
• Application of haemostat at the bleeding point helps in direct occlusion
of the bleeding vessel
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21. 3. SUTURES AND LIGATION
• Severed blood vessels may be tied with ligatures. A ligature replaces
the hemostat as a permanent method of effective hemostasis.
• For large pulsatile artery, a trans – fixation suture to prevent slipping is
indicated.
• Non – resorbable sutures such as silk and polyethylene are used as they
evoke less tissue reaction.
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22. CHEMICAL METHODS
Local Agents:
1. ADRENALINE
• Topical application of adrenaline brings about vasoconstriction of
bleeding capillaries.
• Available in ampoule, which is applied with the help of gauze.
• Concentration of 1 in 1000 is used for hemostasis over the oozing site.
2. THROMBIN
• Helps in converting fibrinogen into fibrous clot.
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23. 3. SURGICEL
• Oxidized cellulose polymer obtained by dissolving pure alpha-
cellulose in an alkaline solution.
• Acts by forming acid products from partial dissolution that coagulates
the plasma proteins to form a black or brown sticky gelatinous clot.
• Applied surgicel resorbs from the site in 4 to 8 weeks.
• Disadvantage is that the surgicel clot is not formed by normal
physiological mechanism.
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24. 4. SURGICEL FIBRILLAR:
• Modified surgicel or oxidised regenerated cellulose in layers that can be
adapted to irregular surfaces and inaccessible areas.
• Complete resorption occurs in 2 weeks.
5. GELATINE SPONGE OR GELFOAM OR SURGIFOAM:
• Formed from purified pork skin gelatin.
• Completely absorbable material.
• Has the capacity to absorb 45 times its weight in blood.
• Resorbs completely in 4 to 6 weeks.
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25. 4. OXYCEL
• Oxidized cellulose polymer product.
• This absorbable hemostatic material is manufactured by controlled
oxidation of cellulose using nitrous dioxide.
• Cellulosic acid present in it has affinity for hemoglobin which leads to
the formation of artificial clot.
• Should be applied on the dry surface as the acid formed during the
wetting process inactivates the thrombin.
• The platelets plug into its meshwork like surface & helps in clot
formation.
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26. 6. MICROFIBRILLAR COLLAGEN (AVITENE)
• Collagen derived from bovine skin cause contact activation in addition
to direct platelet aggregation.
• Absorption time is 3 months.
7. FIBRIN GLUE
• Biological adhesive which contains thrombin, fibrinogen, factor XIII,
aprotinin.
• Thrombin converts fibrinogen to unstable fibrin clot, factor XIII
stabilizes the clot and aprotinin prevents its degradation.
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27. 8. STYPTICS & ASTRINGENTS
• Precipitates protein & arrests bleeding.
• Commonly used styptics & astringents are Monsel’s solution
containing ferric subsulfate & tannic acid.
• Thrombin & gelatin sponge are now widely used.
9. ALGINIC ACID
• Placed over the bleeding sites, a protective film is formed over the
bleeding site, this film compresses the capillaries & stabilizes the blood
clot.
10. NATURAL COLLAGEN SPONGE
• White sponge material, fully absorbable. It stimulates the platelet
aggregation thereby enhancing hemostasis.
• Activates coagulation factors XI & XIII.
• Preferred in patients who are susceptible for hemorrhage after dental
surgical procedures.
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28. 11. FIBRIN SPONGE
• Obtained from bovine material.
• Chemically treated to avoid allergic reactions.
• Applied on the bleeding site especially in post extraction socket.
• Fully absorbed by the tissues within 4-6 weeks.
12. OSTENE (a new water soluble bone hemostatic agent)
• New bone hemostatic agent, made of water-soluble alkylene oxide
copolymers.
• Showed no incidence of adverse response in the cortical defect site,
medullary cavity or the surrounding tissue.
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29. 13. BONE WAX
• Sterilized, non – absorbable mix of waxes.
• Consists of seven parts by weight of wax (white bees wax, paraffin wax
& an isopropyl ester of palmitic acid), two parts of olive oil and one part
of phenol.
• Indicated in cases of bleeding from the bone or from chipped edges of
bone.
• Bone wax is softened with the fingers to desired consistency & then
applied over the bleeding site.
• Its hemostatic mechanism is through mechanical obstruction of the
osseous cavity containing the bleeding vessels.
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Systemic Agents:
1. Whole Blood:
• Fresh whole blood refers to blood that is administered within 24 hours
of its donation.
• Whole blood transfusion indicated when there is excessive blood loss.
• Contains all factors for coagulation.
• Must be checked for HIV, hepatitis B, C viruses.
2. Platelet Rich Plasma:
• Platelets can be collected from donated whole blood.
• Platelet concentrates are viable for 3 days when stored at room
temperature.
• Must be infused quickly via short i.v. tranfusion set.
• One unit raises platelet count by approx 7,000 to 10,000 cells per
cu mm.

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3. Fresh Frozen Plasma:
• Unit of fresh frozen plasma is collected from one donor and contains
all coagulation factors.
• Stored at -30°C, should be infused within 2 hours once defrosted.
4. Cryoprecipitate:
• Stored at -30°C.
• Each bag is derived from single donor and is not treated to inactivate
viruses.
• Associated with a substantial risk of viral transmission.

32. THERMAL AGENTS
Heat achieves hemostasis by denaturation of proteins.
1. Cautery:
• Heat is transmitted from instrument by conduction directly to the
tissues.
• Electro – cautery has replaced direct heat application.
• Dental burnisher like instrument can be directly heated over flame and
applied directly to the bleeding point.
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33. 2. Electrocautery:
• Most widely used.
• Electrocautery can be applied directly to bleeding point.
• Cautery point is touched to the hemostat, causing sealing of vessel
through action of heat.
• Causes tissue destruction producing burning smell and smoke during
application.
• Effective and convenient way of controlling hemorrhage.
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 Advantages of electrocautery:
• Permits any degree of hemorrhage control.
• Provides clear and improved view.
• Increases efficiency.
• Reduces chair side time.
• Gives pressure – less cutting.

35. 3. Cryosurgery:
• Extreme cooling has been used for hemostasis.
• Temperature ranging from -20°C to -180°C are used.
• Tissues, capillaries, small arterioles and venules undergo cryogenic
necrosis.
• Caused by dehydration and denaturation of lipid molecules.
• Specially used to treat superficial hemangiomas.
4. Lasers:
• Lasers usually result in bloodless surgery.
• Effectively coagulate the small blood vessels during cutting of tissues.
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36. REFERENCES
1. Textbook of Oral and Maxillofacial Surgery by Neelima Anil Malik
(3rd edition).
2. Textbook of Oral and Maxillofacial Surgery by S.M. Balaji (2nd
edition).
3. Textbook of Surgery for Dental Students by Sanjay Marwah (1st
edition).
4. Essentials of Pathology for Dental Students by Harsh Mohan (4th
edition).
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