MANAGEMENT OF INTRAORAL BLEEDING

Presented by:Shashwati PaulII Year PGDept. of Periodontology

CONTENTS

Introduction

Classification of Haemorrhage

Hemostasis

Hemostatic Mechanisms

Coagulation Cascade

Laboratory Tests for Screening

Patient Evaluation before Surgery

Control of Bleeding

Local Measures

Drugs & Other Hemostatics

Dressings & Other Measures

Ligation of Vessels

Conclusion

References

INTRODUCTION

Blood is a circulating tissue composed of fluid plasma and cells (red blood cells, white blood cells, platelets).

Medical terms related to blood often begin in hemo- or hemato- from the Greek word "haima" for "blood".

Blood is a connective tissue present in fluid form.

It is circulating in the blood vessels with a constant velocity of 0.5mts/sec.

The constant motion of blood is brought about by the pumping action of heart.

Haemorrhage ( Haemo + rrhage) means the escape of blood from a blood vessel. Hemorrhage generally indicates extravasation of blood due to vessel rupture.

Hemorrhage may be external or may be enclosed within a tissue; accumulation of blood within tissue is referred to as a hematoma. Hematomas may be relatively insignificant (a bruise) or may be sufficiently large as to be fatal

Minute 1 to 2-mm hemorrhages into skin, mucous membranes, are denoted as petechiae and are typically associated with locally increased intravascular pressure, low platelet counts (thrombocytopenia), defective platelet function, or clotting factor deficiency.

Slightly larger (>3 mm) hemorrhages are called purpura. These may be associated with many of the same disorders that cause petechiae.

• Larger (>1 to 2 cm) subcutaneous hematomas (i.e., bruises) are called ecchymoses and are characteristically seen after trauma but may be exacerbated by any of the afore mentioned conditions.

• Large accumulations of blood in one or another of the body cavities are called hemothorax, hemopericardium, Hemoperitoneum or hemarthrosis (in joints).

• The clinical significance of hemorrhage depends on the volume and rate of bleeding. Rapid loss of up to 20% of the blood volume or slow losses of even larger amounts may have little impact in healthy adults; greater losses, however, may result in hemorrhagic (hypovolemic) shock.

CLASSIFICATION OF HAEMORRHAGE

Arterial Haemorrhage: Arterial bleeding is pulsatile, brisk and bright red in colour.

Venous Haemorrhage: Bleeding from veins is dark in colour and blood flows in a even stream. Due to lack of valves in veins of the facial region and extensive communication, there is relatively more flow from veins as compared to other parts of body.

Capillary Haemorrhage: In capillary haemorrhage blood oozes from the area and no bleeding point can be made out. The blood is intermediate in colour as compared to arterial and venous blood. Bleeding is not severe and is easily controlled by simple pressure with gauze pads. In coagulation disorders, there can be extensive blood loss from capillaries.

• Primary bleeding: occurs at the time of injury. Hemostatic mechanisms in the body attempt to stop the bleeding by formation of clot.

• Secondary bleeding: If the primary bleeding has stopped once, and wound starts to bleed again after 24 hours to several days, it is known as secondary bleeding. It may be due to:

(a) dislodgement of clot or (b) secondary trauma to the wound, (c) infection.

Elevation of patient's blood pressure enough to overcome pressure external to blood vessel is another common reason for secondary bleeding.

• Intermediate bleeding/ Reactionary bleeding: According to some authors bleeding occurring within eight hours after stoppage of primary bleeding is labelled as intermediate bleeding. Loose foreign body in the wound like calculus, broken bone piece, and preexisting extensive granulation tissues in the surgical site are the most common causes for the intermediate bleeding.

Internal or External Bleeding:Bleeding that is confined within the body cavity and is not apparent on the surface is known as (i) internal or concealed bleeding. Whereas, blood escaping through a wound in the skin is known as (ii) external bleeding.

Spontaneous Bleeding:Sometimes bleeding can occur without any provocation, e.g. in acquired (patients on oral hypoglycaemic agents, decreased platelets count) and hereditary coagulopathies, such type of bleeding is labelled as spontaneous bleeding.

HEMOSTASIS

There are four important steps in hemostasis

First of all the injured blood vessel, in an attempt to reduce blood flow undergoes constriction due to spasm in the vessel wall.

In the second step there is activation of platelets and formation of platelet plug. This leads to primary hemostasis.

In the third step there is activation of clotting mechanism and formation of clot leading to completion of secondary hemostasis.

In the final step there is fibrous organization of the clot or retraction of clot.

Primary Hemostasis:

• Primary hemostasis is the process of platelet plug formation at the site of injury. It occurs within

seconds of injury and is important in stopping 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.

Secondary Hemostasis:

• It is completed in several minutes and is important in bleeding from larger vessels.

Coagulation mechanism is a continuous process and there are approximately 40 substances

Procoagulants

Anticoagulants

• Normal hemostasis is the result of a set of well regulated processes that accomplish two important functions:

(1) They maintain blood in a fluid, clot free state in normal vessels; and

(2) They are poised to induce a rapid and localized hemostatic plug at a site of vascular injury.

• Both hemostasis and thrombosis are regulated by three general components the vascular wall, platelets, and the coagulation cascade.

HEMOSTATIC MECHANISMS

NORMAL HEMOSTASIS• After initial injury, there is a brief period of arteriolar vasoconstriction, largely attributable to reflex

neurogenic mechanisms and augmented by the local secretion of factors such as endothelin (a potent endothelium derived vasoconstrictor).

Endothelial injury exposes highly thrombogenic subendothelial extracellular matrix (ECM), which

allows platelets to adhere and become activated, that is, undergo a shape change and release

secretory granules. Within minutes, the secreted products have recruited additional platelets

(aggregation) to form a hemostatic plug; this is the process of primary hemostasis

Tissue factor, a membrane bound procoagulant factor synthesized by endothelium, is also exposed at the site of injury. This activates the secondary hemostasis, which takes longer than the initial platelet

plug.

Polymerized fibrin and platelet aggregates form a solid, permanent plug to prevent any further hemorrhage. At this stage, counter regulatory mechanisms (e.g., tissue plasminogen activator {t-PA}) are set into motion to limit the hemostatic plug to the site of injury .

Role of Endothelium, Platelets & Coagulation Cascade

Endothelium:Endothelial cells modulate several and frequently opposing aspects of normal hemostasis. On the one hand, the normal flow of liquid blood is maintained by endothelial antiplatelet, anticoagulant,

and fibrinolytic properties. On the other hand, after injury or activation, endothelium exhibits several procoagulant activities.

Endothelium maybe activated by infectious agents, hemodynamic factors .

Antithrombotic Properties: Antiplatelet effects: An intact endothelium prevents platelets and plasma coagulation factors from

meeting the highly thrombogenic subendothelial ECM. Nonactivated platelets do not adhere to the endothelium.

Anticoagulant effects: These effects are mediated by membrane associated heparin like molecules and by thrombomodulin, a specific thrombin receptor. They are cofactors that interact with antithrombin III to inactivate thrombin, factor Xa, and several other coagulation factors . Thrombomodulin also acts indirectly; it binds to thrombin, converting it from a procoagulant to an anti-coagulant capable of activating protein C.

Fibrinolytic effects: Endothelial cells synthesize tissue type plasminogen activator (t-PA), promoting fibrinolytic activity to clear fibrin deposits from endothelial surfaces.

Platelets:

Platelets contain two specific types of granules. Alpha granules express the adhesion molecule P-selectin on their membranes and contain fibrinogen, fibronectin, factors V and VIII, platelet factor 4 , PDGF & TGF-β.

The other granules are dense bodies, or δ granules, which contain adenine nucleotides (ADP and ATP), ionized calcium, histamine, serotonin, and epinephrine.

After vascular injury, platelets encounter ECM constituents that are normally sequestered beneath an intact endothelium these include collagen (most important), proteoglycan fibronectin, and other adhesive glycoproteins. On contact with ECM, platelets undergo three general reactions: (1) adhesion and shape change; (2) secretion (release reaction); and (3) aggregation

PLATELET MEMBRANE

Outer layer

Glycocalyx layer(Glycoprotein)

Adhesion

Inner layer

Lipoprotein layer

Various lipid molecules

Phospholipids

Activates intrinsicpathway

Normal hemostasis

+Protein enzyme-Adenyl cyclase

Enhances platelet function

Platelet adhesion to extracellular matrix is mediated largely via interactions with vWF, which acts as a bridge between platelet surface receptors and exposed collagen.

Secretion (release reaction) of the contents of both granule types occurs soon after adhesion. The process is initiated by the binding of agonists to platelet surface receptors followed by an intracellular protein phosphorylation cascade. The release of the dense body contents is especially important because calcium is required in the coagulation cascade.

• Platelet aggregation follows adhesion and secretion. Besides ADP, the vasoconstrictor thromboxane A2 (TxA2), secreted by platelets, is also an important stimulus for platelet aggregation.

The series of platelet events can be summarized as follows

Platelets adhere to ECM at sites of endothelial injury and become activated.

On activation, they secrete granule products (e.g., ADP) and synthesize TxA2.

Platelets also expose phospholipid complexes that are important in the intrinsic coagulation pathway.

Injured or activated endothelial cells expose tissue factor, which triggers the extrinsic coagulation cascade.

Released ADP stimulates the formation of a primary hemostatic plug, which is eventually converted (via ADP, thrombin, and TxA2) into a larger, definitive, secondary plug.

Fibrin deposition stabilizes and anchors the aggregated platelets.

COAGULATION CASCADE

The coagulation cascade constitutes the third component of the hemostatic process and is a major contributor to thrombosis.

The coagulation cascade is essentially a series of enzymatic conversions, turning inactive proenzymes into activated enzymes

In general, clotting of blood occurs in three stages. Formation of prothrombin activator-Initiation Conversion of prothrombin into thrombin-Amplification and Conversion of fibrinogen into fibrin- Propagation

Each reaction in the pathway results from the assembly of a complex, composed of an enzyme (activated coagulation factor), a substrate (proenzyme form of coagulation factor).

In addition to catalyzing the final steps in the coagulation cascade, thrombin also exerts a wide variety of effects on the local vasculature and inflammation; it even actively participates in limiting the extent of the hemostatic process. Most of these effects are induced via binding to a family of protease-activated receptors (PARs) that belong to the seven transmembrane G-protein-coupled receptor family.

Besides restricting factor activation to sites of exposed phospholipids, clotting is also regulated by three types of natural anticoagulants

Antithrombins (e.g., antithrombin III) inhibit the activity of thrombin.

Proteins C and S: two vitamin K dependent proteins, that are characterized by their ability to inactivate factors Va and Vllla.

Tissue factor pathway inhibitor (TFPI), a protein secreted by endothelium (and other cell types), complexes to factor Xa and to tissue factor-Va and inactivates them to rapidly limit coagulation.

FORMATION OF BLOOD CLOT

LABORATORY TESTS

Diagnostic Tests

Screening Tests

1) Clotting Time - time taken to coagulate - 5-10min (Lee-White) at 37*c - 1-3min(Wright’s method) - increases in hemophilia, Liver Diseases - decreases in Typhoid, splenectomy

2)Capillary Resistance Test - Sphygmomanometer cuff around arm - ---5min - 4cm area jst below elbow - purpuric spots

3)Partial Thromboplastin Time - Checks Intrinsic system & common pathways - aPTT –contact activator (Kaolin) is added - aPTT—68-82sec

4)Prothrombin Time

-Time required for coagulation of citrated plasma after addition of thromboplastin calcium mixture. -Normal range:10-15 sec(Quick’s method) -checks extrinsic pathway & common pathway

5)Platelet Count - 150,000-400,000/mm3

6)Bleeding Time - time required for complete stoppage of bleeding after deep needle puncture. - 1-3min

-increases in Pernicious Anemia, Aplastic anemia, Acute leukaemia, Multiple myeloma

7)Thrombin Time - 9-13sec

-Thrombin is added to pt’s blood sample as activating agent.

Fibrinogen Fibrin Blood clot

Diagnostic/ Special test

One or more screening test- +ive

For Platelet Disorders- Platelet aggregation test- Ristocetin – induced agglutination- Platelet release Reaction

Additional test for diagnosis & type of vWD:-- Ristocetin cofactor activity- Ristocetin - induced platelet aggregation- Immunoassay of vWF- Multimeric analysis of vWF- Specific assay for factor VIII

PATIENT EVALUATION BEFORE SURGERY

A careful physical examination should be noted. Assessment of the skin and mucosal surface is mandatory.

Bleeding into superficial skin and soft tissues usually seen as small capillary haemorrhages ranging from size of pinhead (petechia) to large areas of ecchymoses is usually characteristic of abnormalities of the vessels or the platelets. Haemorrhage into synovial joints is virtually diagnostic of a severe hereditary coagulation disorder.

The sex of the patient, the age when abnormal bleeding was first noted, and the family history are of particular importance in evaluating the disorders of hemostasis, since most disorders of vessels and platelets are acquired, whereas most serious coagulation disorders are hereditary, and among these, over 90 per cent occur only in males. The absence of a family history of bleeding, however, does not exclude the presence of a hereditary coagulation disorder.

The history remains the best single "screening" test for the presence of a hemorrhagic disorder, A history of surgery, major injury, or even multiple tooth extractions without abnormal bleeding is good evidence against the presence of a hereditary coagulation disorder.

Certain bleeding manifestations are more or less characteristic of the disorders of hemostasis. For example, bleeding into the synovial joints (hemarthrosis) in the absence of obvious trauma and spontaneous bleeding into the skin are rarely encountered in patients with normal hemostatic function.

Recurrent crops of petechiae, on the other hand, are strongly suggestive of an abnormality of the vessels or platelets, e.g., thrombocytopenia, and are rare in the coagulation disorders.

Profuse and often life threatening hemorrhage following trivial trauma or surgical procedures is a hallmark of the coagulation disorders

Clinical distinction between disorders of vessels and platelets and disorders of blood coagulation

Findings Disorders of Coagulation

Disorders of Platelets and Vessels(purpuric disorders

Hemarthrosis Characteristic Rare

Petechiae Rare Characteristic

Positive family history

Common Rare

Sex 95% in males Common in females

Traumatic Bleeding

Onset often delayed: rapid and voluminous

Onset immediate.Slow and persistent oozing

CONTROL OF BLEEDING

In medical and dental practice it is essential to take maximum precautions to avoid serious hemorrhage.

This admonition is particularly true for hemophilic patients, patients with hematopoietic disease, and patients receiving therapies known to affect hemostasis.

Conservative precautions, which may include the administration of clotting factors and/or hospitalization, are prudent in these cases.

In contrast, normal patients usually require no more than temporary hemostatic assistance (e.g., pressure packs, hemostatic forceps, ligation, or other locally active measures) to facilitate normal hemostasis and allow clotting to take place.

When bleeding is consequence of a specific defect in hemostasis such as hemophilia, the ideal treatment is to correct the defect. Such specific treatment, however, may not be possible because the bleeding may be due to multiple defects or no specific cause can be identified. In such case nonspecific hemostatic therapy has to be employed.

Local Measures: A perplexing hemostatic problem may arise from continued, slow oozing of blood from small

arterioles, veins, and capillaries cannot be ligated.

Measures such as pressure packs and dressings, vasoconstrictor agents, and procoagulants must be used.

Styptics or astringents, once extensively used, are no longer viewed as rational procedures for routine hemostasis in most applications.

Haemostats i.e.the mosquito or artery forceps are designed to catch bleeding points in surgical areas.

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DRUGS & OTHER HEMOSTATICS:

Drugs used for hemostatic therapy can be classified as:

i. Agents acting locallyii. Transfusional agents such as specific coagulation factorsiii. Nontransfusional agents

i. Agents acting locally: These agents control oozing of blood from minute vessels but are not effective in controlling bleeding from large vessels. They are THROMBIN: Thrombin is obtained from bovine plasma. It is stable as a dry powder stored between 2 to 8"C. It is, however, inactive below pH 5. Thrombin therapy is restricted to local application in oozing of blood. Assuming an otherwise normal clotting system, topical thrombin is often used clinically.

Topically applied thrombin (particularly in conjunction with a compatible matrix such as gelatin sponge) operates as a hemostatic, particularly if the patient is receiving oral anticoagulants.

In the event that blood flows too freely, temporary physical hemostasis must be attained before topical thrombin can be of practical value. The use of thrombin is not without problems. Currently available thrombin, especially the bovine products, may be relatively crude preparations that still contain plasmin, a fibrinolytic agent . Antibodies may also be generated to the bovine thrombin.

THROMBOPLASTIN: Thromboplastin is a powder prepared from the extracted brain and/or Lung tissue of freshly killed rabbits. It is used for determination of prothrombin time and as a local haemostatic in surgery. FlBRIN: Fibrin obtained from human plasma is used in the dehydrated form as sheets from which segments of any desired size may be cut for use on bleeding surfaces. When used in combination with a thrombin solution, it also acts as a mechanical barrier and holds thrombin in position over the bleeding area.

One of the more promising hemostatic aids to appear in recent years is fibrin sealant, also sometimes referred to as fibrin glue. With this agent, the concept of the application of topical thrombin is taken one step further.

GEL FOAM: Gel foam is a porous, pressed form of gelatin sponge used in conjunction with thrombin to control oozing of blood from surface wounds. Gel foam is usually moistened with sterile isotonic saline before use. It is completely absorbed within4to 6 weeks and hence, may be left in place after suturing of an operative wound. Gel foam is available as cones, packs, sponges and powder.

OXIDIZED CELLUI.OSE (Oxycel): Oxycel is surgical gauze treated with nitrogen dioxide, and it promotes clotting by a reaction between hemoglobin and cellulosic acid. Oxycel, when wet with tissue fluid, becomes sticky and gummy and exerts its haemostatic effect by mechanical blockage, which stimulates an artificial clot over the surface of the wound. Oxycel is usually absorbed completely within 2 to 10 days. It interferes with bone regeneration.

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MICRO FIBRILLAR COLLAGEN HEMOSTAT (Avitene): This hemostatic material is prepared from purified, bovine collagen, applied to a bleeding surface, it attracts platelets and initiate formation of a platelet plug followed by a natural clot. Used along with manual pressure it is effective in controlling capillary bleeding, even in patients on heparin or oral anticoagulants and hemophiliacs. It is non-allergenic but can promote local infection, abscess formation, and ruptured cutaneous incisions.

It is inactivated following autoclaving and hence should not be sterilised Care should be taken to avoid spillage on nonbleeding surfaces.

Astringents and Styptics The terms astringents and styptics are interchangeable, referring to different concentrations of the

same drugs. Many chemicals have vasoconstrictive or protein denaturing ability, but relatively few are appropriate for dentistry. The suitable preparations are primarily salts of several metals, particularly zinc, silver, iron, and aluminum.

Aluminum and iron salts: are quite acidic (pH 1.3 to 3.1} and therefore irritating. Furthermore, iron causes, though temporary, surface staining of the enamel, whereas silver stains may be quite permanent.

Currently, astringents are generally only used in dentistry to aid hemostasis while retracting gingival tissue.

20% ferric sub-sulfate (Monsel's solution) 8% zinc chloride

Aluminum and iron salts function by denaturing blood and tissue proteins,

It is therefore imperative that if these compounds are to be used in the practice of dentistry, they be used briefly and with copious irrigation and debridement to remove the breakdown products. They should not be applied to areas of exposed osseous material in order to avoid inflammation or complications of retarded healing such as the dry socket.

Tannic acid (0.5% to 1.0%): is an effective astringent; it also precipitates proteins, including thrombin, but is often incompatible with other drugs and metal salts used therapeutically.

ETHANOLAMINE OLEATE(ETHANOLATE)It is an irritant that causes local inflammation stimulating coagulation and fibrosis when injected locally into varicose veins. This is not used very commonly now due to alternative therapies, better surgical benefits and poor efficacy.

FERACRYLIUM (HEMOLOK, SEPGARD)

It is used locally over oozing raw surfaces for its local antiseptic and hemostatic action. It reduces capillary bleeding by forming local plasma protein complexes. It is not given orally nor i/v or i/m. It can causes local burning and irritation

SODIUM TETRADECYL SULPHATE(SYLATE-M)It is a local irritant that is used to cause local coagulation and fibrosis of veins in varicose veins. 0.5ml or 1ml of 3% solution is injected in local affected vein. Efficacy is not proven. It can cause local or systemic allergic reactions.

Vasoconstrictors

Temporary hemostasis may be obtained with adrenergic vasoconstrictor agents, generally epinephrine. Obviously, such vasoconstrictors should be applied topically or just under the mucosa only for restricted local effects and for very short periods to avoid prolonged ischemia and tissue necrosis.

Because some of the drug is absorbed systemically, particularly in inflamed and abraded tissue, cardiovascular responses may occur. Epinephrine solutions and dry cotton pellets impregnated with epinephrine are available for topical application, but other methods to control bleeding are generally preferred.

Other vasoconstrictive agents, such as 0.5% tetrahydrozoline or 0.5% oxymetazoline, have been suggested for use as better hemostatic agents for gingival cord retraction because of their much more neutral pH than epinephrine or the astringent salts

II Transfusional agents:

FIBRINOGEN: Fibrinogen. a sterile fraction from human plasma, is used for restoring normal fibrinogen levels in haemorrhagic complication caused by acute afibrinogenemia. Fibrinogen & thrombin may be employed together for local haemostasis.

ANTIHAEMOPHILIC GLOBULIN (AHG) : Haemophilia A and Christmas disease (haemophilia B) are the two most common hereditary haemorrhagic states, due to deficiency of specific clotting factors VIII and IX respectively Antihaemophilic globulin or concentrate of factor VIII (AHG) is highly effective in the treatment of classical

haemophilia-A. High potency human AHG is prepared from pooled, normal, human plasma; it is now

prepared by recombinant DNA technique. It is given in the dose of 15-60 units/kg daily.

COAGULATION FACTORS: Pure recombinant factor VIII, factor IX and factor VII are available. They are very expensive and may be associated with a greater risk of inducing inhibitor formation (IgG antibodies for VIII). thus reducing the efficacy of specific therapv.

FFP:. Fresh frozen plasma is suitable for the treatment of most coagulation disorders, since it contains all the clotting factors. Concentrate of factor VIII (purified) and partially purified preparation containing factors II. VII. IX and X are also available for ,specific deficiencies

III. Non-transfusional agents:

VITAMIN K: Adverse reactions are rare after oral administration. However, serious reactions, including fatalities, have occurred following intravenous use These reactions resemble anaphylaxis. Large doses of synthetic menadione have produced haemolytic anaemia. hvperbilirubinemia and kernicterus in newborn.

APROTININ (APROTIN, HAEMOPROT): It Is a polypeptide enzyme which inhibits serine protease and thus inhibits plasmin, kallikrein and trypsin activity. It inhibits fibrinolysis and reduces bleeding by 50% especially in surgeries

EPSILON AMINO CAPROIC ACID (HAEMOSTAT):Mechanism of action : It is a water soluble lysine analog which binds to the lysine binding sites

reversibly on plasminogen and plasmin and inhibits binding of plasmin to fibrin. It is absorbed rapidly after oral administration, 50% is excreted unchanged in urine. 4-5gm oral or I.V. infusion over 1hour followed by 1gm/hour (maximum 30gm in 24 hours)

TRANEXAMICACIDMechanism of action : It is an analog of amino caproic acid with similar action and is seven times more

potent. ETHAMSYLATE (DICYNENE, E-SYLATE, CAPSTAT)Mechanism of action : It inhibits PGI2 production and reduces capillary bleeding by stabilizing platelet

function. It is not an antifibrinolytic. Adults : Oral: 250-500mg 3 times a day or Inj. : 250-500mg I.V. 8 hourly.

Children : 10mg/kg every 8 hourly.

PROTAMINE SULPHATE:Mechanism of action : It is a low molecular weight protein which is a strong base and it combines with

heparin as an ion pair to form a stable complex devoid of anticoagulant activity. In abscence of heparin it itself can act as weak anticoagulant by interfering with platelet and fibrinogen activity. Indications: Antidote to bleeding due to heparin

VIT C & RUTIN: Vit C can control bleeding only in scurvy patients. The oral dose is 20-30 mg of rutin with 50-100mg of Vit C, repeated 3-4 times a day

Gelatin based•Gelfoam•Surgiflo•Floseal hemostatic matrixOxidised regenerative methylcellulose•Surgicel(ethicon)Glutaraldedyde based adhesive•Bioglue(cryolife)Human fibrinogen and thrombin•Tachosil(nycomed)•Tachocomb(nycomed)Fibrin glue•Tiseel(baxter)•Tissucol(baxter)•Crosseal(ethicon)•Haemaseal(haemacure)

Hemostatic collagen•Collaplug•Collatape•Helistat

Thermal Agents

• Cautery : heat is tramitted from the instrument by conduction directly to the tissues.hemostasis is achived by denaturation of proteins which results in coagulation of tissue.

• Electrosurgery: Heating occurs by induction from a alternate current source.it can be directly applied to a bleeding point after catching it with a haemostat. It seals the vessels by action of heat.

• Cryosurgery: temp ranging from -20 to-180 are used. There is dehydration and denaturation of lipid molecules.

• Argon –beam coagulator : new form of electrocautery,more effective. In this, coagulator monopolar current is transmitted to the tissues through the flow of argon gas. This allows bleeding from vessels that are smaller than 3mm in diameter to be controlled without the use of haemostats.

• Lasers : coagulates small blood vessels

• Dressings & Other Measures:

• Bleeding caused by dentoalveolar surgery can most often be controlled by applying pressure with sterile cotton gauze. If this treatment is inadequate, the clinician must localize the source of bleeding as originating either within the soft tissues or within the bony structures.

• Soft tissue bleeding may be controlled by hemostats, ligation, electrocautery, or application of microfibrillar collagen or collagen sheets (on broad bleeding surfaces). Microfibrillar collagen, made from purified bovine skin collagen, is used topically to arrest certain hemorrhagic conditions that do not respond to conventional methods of hemostasis. Collagen accelerates the aggregation of platelets and therefore may have limited effectiveness in patients with platelet disorders or hemophilia.

• Bleeding from bony structures, especially from extraction sockets, can be controlled by a variety of means. If initial attempts to achieve hemostasis with sterile cotton gauze and pressure do not succeed, a collagen plug or gelatin sponge may be inserted within the bony crypt.

The gelatin sponge facilitates platelet aggregation and can absorb 40 to 50 times its own weight in blood, both of which aid in blood coagulation. It is resorbed in 4 to 6 weeks.

Denatured cellulose sponge or gauze serves as both a physical plug and a chemical hemostatic. The apparent coagulation-promoting action stems from the release of cellulosic acid,

Two forms of cellulose sponge, oxidized cellulose and oxidized regenerated cellulose, are available.

If, during operations involving the bony processes, a "spurter" (artery) is severed, the bleeding can be controlled by taking a blunt instrument and crushing the surrounding bone into the point of_bleeding, or bone wax can be rubbed on over the bleeding bony orifice. Capillary oozing from the bone either stops spontaneously or is usually controlled when the mucoperiosteal flaps are reapproximated and sutured back over the alveolar ridges.

if bleeding is profuse, Tightly pack the sockets with iodoform gauze for 5 to 10 minutes under pressure, remove the gauze and then place pieces of absorbable hemostatic gauze in each socket before suturing the soft tissues into place.

Capillary bleeding from soft tissues at the time of operation is best controlled by suturing If, for example, after an flap surgery there is still bleeding following the insertion of the usual number of sutures, additional sutures should be inserted in that area in which bleeding occurs.

If bleeding persists, gauze pressure pads are placed over the area and firmly held in place for 5 to 10 minutes. Then, when the bleeding is controlled, additional pressure pads should be placed over this area, and the jaws held firmly together by applying an elastic bandage over the head and under the mandible for several hours.

Capillary bleeding from "raw" surfaces, such as those left after the excision of inflammatory papillary hyperplasia, hyperplastic tissue on the crest of the alveolar ridge, or epulis fissuratum, can be stopped by the careful use of the electrocoagulation instrument.

Ligation of Blood Vessels: In the event of arterial bleeding from the soft tissues, the vessel should be grasped with a hemostat and ligated by tying it directly or indirectly by the use of a circumferential suture around the soft tissue.

Palatal vessels are the most commonly severed arteries in the mouth. Less frequently traumatized or severed are the inferior alveolar artery, the sublingual artery or the external maxillary artery.

If the greater palatine artery is cut, it is practically impossible, to grasp and clamp it with a hemostat. palatal pressure, great enough to stop the bleeding, should first be applied along the course of the vessel posterior to the point of bleeding and held firmly for at least 5 to 10 minutes. This gives the body's defense mechanism an opportunity to attempt to seal off the cut vessel.

As a result of trauma (either external or from the operator's instrument), the sublingual artery in the floor of the mouth may be severed. This vessel is extremely difficult, if not impossible, to ligate when severed by a puncture wound, and the consequences can be fatal if the wound remains untreated. Bi-manual pressure (one hand inside and one hand outside the mouth) will usually control this bleeding until an appropriate ligation can be performed in the neck

Greater palatine artery: Many times pressure is sufficient to stop hemorrhage from a major vessel by pressure. If bleeding resumes on release of pressure, the palatal mucoperiosteal tissue is reflected, including the point of bleeding. The anterior palatine vessels are then ligated posterior to the bleeding point by a "stick tie" (circumferential) suture through the entire thickness of the mucoperiosteum around the anterior (greater) palatine artery. The flap is then replaced and sutured to position

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Control of hemorrhage from a severed anterior palatine artery with a "stick tie" suture passed through the mucoperiosteum medial to the cut.

Local Treatment of Intermediate or Recurrent Hemorrhage and Secondary Hemorrhage:• One or a combination of the following methods may be used:• 1. If the sutures have become loose, the area should be anesthetized and a suture inserted firmly over

the bleeding area.

• 2. Direct pressure may be applied over the bleeding area. This is asccomplished by having the patient bite firmly on gauze pressure pads over the bleeding area, or by molding soft compound blocks over the bleeding area and having the patient bite into the soft compound.

• 3. A vasoconstrictor, such as epinephrine poured on a sponge, can be applied directly to the bleeding area; this results in a constriction of the lumen of the vessel until a new clot can form.

• 4. The surgeon can also apply a local agent to speed up blood coagulation. Local agents are thrombin, fibrinogen, and thromboplastin. All these agents are placed on gauze sponges and held over the bleeding areas, or placed into the sockets with pressure.

CONCLUSION

• Control of bleeding is the most important integral part of any surgical treatment procedure. Proper prior evaluation of the patient & complete medical and family history along with precautionary lab tests are very much essential to overcome intra operative & post operative bleeding arising from undetected bleeding disorders.

• To conclude with, methods of Controlling Bleeding can be tabulated as:

Desired result

Physiologic Methods

Physical Methods Chemical Agents

Hemostasis •Vasoconstriction •Platelet plugs•Clot Retraction

•Pressure•Electrocautery•Sutures.

•Epinephrine •Astringents, •Styptics

Clotting •Procoagulants, •Thrombin, •Platelets & other •clotting factors

•Physical matrices, •Gelatin,

•Topical thrombin, •Fibrin sealant,•Antofibrinolytics

REFERENCES

Pathology – Robbins

A Textbook of Oral Surgery – Kruger

A Textbook of Oral and Maxillofacial Surgery – Neelima malik.

Textbook of Pathology – Harshmohan

Essentials of Pharmacology – Tripathi.

Contemporary Oral and Maxillofacial Surgery – Peterson.