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25 Trillion – RBC’s – most abundant cells in the body Total body cell counts to 100 trillion. All the blood in the circulation traverses the entire circuit of the circulation an average of once each minute when the body is at rest, and as many as six times each minute when a person becomes extremely active. The average blood volume of adults is about 7% of body weight, or about 5 liters. About 60% of blood is plasma and 40% is RBC’s. Hemorrhage : The escape of blood from the vessels or bleeding. Classification : a) According to size i.

Petechias – pin point


Purphra – up to 1 cm


Ecehymosis – larger


Hamatoma – massive accumulation of blood within a tissue

b) According to types 1.

Arterial hemorrhage : Recognized as bright red blood, spurting as a jet which rises and falls in time with pulse.


Venous hemorrhage : Dark red blood, study copious flow.


Capillary hemorrhage : Bright red, often rapid ooze.


Primary hemorrhage


Secondary hemorrhage


Reactionary hemorrhage

Hemostasis and blood coagulation:


The term hemostasis means prevention of blood loss. Whenever a vessel is severed or ruptured, hemostasis is achieved by several mechanisms. 1) Vascular spasm 2) Formation of platelet plug 3) formation of a blood clot as a result of blood coagulation 4) eventual growth of fibrous tissue into the blood clot to close the hole in the vessel permanently. 1) Vascular constriction: The trauma to the vessel wall causes the vessel to contract; this instantaneously reduce the flow of blood from the vessel rupture. The contraction results from nervous reflexes, local humoral factors from the traumatized tissues and blood platelets. 2) Formation of platelet plug : Many very small vascular holes do develop (thousands) thought the body each day – it is often sealed by platelet plug rather than by a blood clot. Platelet repair of vascular openings is based on several important functions of the platelet it self. When platelets come in contact with a damaged vascular surface, such as collagen fibers in the vascular wall, the platelets themselves immediately change their characteristics drastically. They begin to swell, they assume irregular forms with numerous irradiating pseudopods protruding from their surfaces; their contractile proteins contract forcefully and cause the release of granules that contain multiple active factors. They become sticky so that they adhere to collagen in the tissue and to a protein called von willebrand factor that spreads through the plasma; they secrete large quantities of ADP; and their enzymes form thromboxane A2. The ADP and thromboxane act on the nearby platelets to activate them as well and the stickness of these additional


platelets cause them to adhere to the originally activated platelets. Therefore, at the site of any rent in a blood vessel wall, the damaged vascular wall or extravascular tissues. Elicit activation of successively increasing numbers of platelets that themselves attract more and more additional platelets, thus forming platelet plug. In the subsequent process of blood coagulation, fibrin threads form, these attach tightly to the platelets, thus constructing a unyielding plug. If there is a large hole a blood clot in addition to the platelet plug is required to stop bleeding. 3) Blood coagulation in the ruptured vessel: The third mechanism for hemostasis is formation of the blood clot. The colt begins to develop in 15 to 20 seconds if the trauma to the vascular wall has been severe and in 1 to 2 minutes if the trauma has been minor. Activator substances from, traumatized vascular wall, from platelets and from blood proteins adhering to the traumatized vascular wall initiate the clotting process. Mechanism of blood coagulation: More than 50 important substances that affect blood coagulation have been found n the blood and in the tissues. Clotting factors in blood and their synonyms: Factor I : Fibrinogen. Factor II : Prothrombin. Factor III : Tissue thromboplastin or tissue factor. Factor IV : Calcium. Factor V : Proacceleria or labile factor Factor VI : Serum prothrombin conversion accelerator or pro convertin or stable factor Factor VII : Antihemophilic factor (AHF) or antihemophilic factor A.


Factor VIII : Plasma thromboplstin component (PTC) or christmas factor or antihemophilic factor B. Factor IX : Stuart factor Factor X : Plasma thromboplastin anticedent (PTA) or antihemophilic factor C. Factor XI : Hageman factor. Factor XII : Fibrin stabilizing factor. Factor XIII : Fletcher factor. Factor XIV : High molecular weight kininogen. Factor XV : Platelets. a) Some that promote coagulation called procoagulants. b) Others that inhibit coagulation called anticoagulants. Whether blood will coagulate depends on the balance between these two group of substances. In the blood stream the anticoagulants normally predominate, so that blood does not coagulate while it is circulating in the blood vessels. But when a vessel is ruptured, procoagulants in the area of the tissue damage become “activated� and override the anticoagulants and then a clot does develop. In the field of blood coagulation it is accepted fact that clotting takes place in three essential steps, they are 1. In response to rupture of the vessel or damage to the blood itself, a complex cascade of chemical reactions occur in the blood involving more than a dozen blood coagulation factors. The net result is formation of a complex of activated substances collectively called prothrombin activator. 2. The prothrombin activator catalyzes the conversion of prothrombin in to thrombin.


3. The thrombin acts as an enzyme to convert fibrinogen in to fibrin fibers that enmesh platelets, blood cells and plasma to form the clot.

1) Initiation of coagulation : formation of prothrombin activator : Mechanism that initiate the clotting in first place, are, set into play by a) Trauma to the vascular wall and adjacent tissues. b) Trauma to the blood or c) Contact of blood with damaged endothelial cells or with collagen and other tissue elements outside the blood vessel. In each instance this leads to the formation of prothrombin activator, which then causes prothrombin conversion to thrombin and all subsequent clotting steps. Prothrombin is a plasma protein an alpha2 – globulin. It is present in normal plasma in a concentration of about 15 mg/dl. It is a unstable protein that can split easily into smaller compounds, one of which is thrombin. Prothrombin is formed continually by the liver, vit. K is required by liver for normal formation of prothrombin. Either lack of vit. K or R the presence of liver disease that prevents normal prothrmobin formation can cause the prothrmbin level so low that a bleeding tendency results. Prothombin activator is generally considered to be formed in two ways, although, in reality, the two ways interact constantly with each other, 1) By the extrinsic pathway that begins with trauma to the vascular wall and surrounding tissues and 2) By intrinsic pathway that begins is blood itself.


1) Extrinsic pathway for initiating blood clotting : TISSUE TRAUMA



Activated X Ca++

Platelets phospholipids III


Prothrmobin activator



Thrmobin Ca++

a) Release of tissue factor : Traumatized tissue releases a complex of several factors called tissue factor, that functions mainly as a proteolytic enzyme. b) Activation of factor X : The tissue factor further complexes with blood coagulation factor VII and in the presence of calcium ions, acts enzymatically on factor X to form activated factor X (Xa). c) Effect of activated factor X (Xa) to form prothrombin activator :



activated factor

X combines


with tissue

phospholipids that are part of tissue factor or WHG additional phospholipids released from platelets, as well as with factor V to form complex called prothrombin activator. Within a few seconds, in the presence of calcium ions this splits prothrombin to form thrombin. Once the clotting process is begun activated factor V becomes a additional strong accelerator of prothrombin activation. This is known as positive feed back effect of thrombin in accelerating the entire process. Intrinsic pathway for initiating clotting : The second mechanism for initiating the formation of prorthmbin activator and therefore for initiating begins with trauma to the blood itself or exposure of blood to collagen in a traumatized vascular wall and continues through the following reactions, Blood trauma or contact with collagen XII

Activated XII (HMW kinogen, prekallikerin) XI

Activated XI Ca++ IX

Activated IX VIII

Thrombin X

Ca++ Activated X

Platelet phosphalipid and factor III


Prothrombin activator Prothrombin

Thrombin Ca++


a) Activation of factor XII and release of platelet phospholipids : Trauma to the blood or exposure of the blood or exposure of the blood to vascular wall collagen alters two important clotting factors in the blood-factor XII and the platelets. When factor XII is disturbed it gets converted









Simultaneously the blood trauma also damages the platelets, either because of adherence to collagen or to a wettable surface and this releases platelet phosphalipid containing lipoprotein called platelet factor 3 which also plays a role in subsequent clotting reactions. b) Activation of factor XI : The activated factor XII acts enzymatically on factor XI to activate this as well, which is the second step in the intrinsic pathway. This reaction also requires HMW kininogen and it is accelerated by prekallikrein. c) Activation of factor IX by activated factor XI : The activated factor XI then acts enzymatically on factor IX to activate this factor also. d) Activation of factor X – role of factor VIII : The activated factor IX, acting in concert with factor VIII and with the platelet phospholipids and factor 3 from the traumatized platelets activates factor X. it is clear that when either factor VIII or platelets are in short supply this step is deficient. Factor VIII is the factor that is missing in the person who has classic hemophilia. Platelets are the clotting factor that is lacking in the bleeding disease called thrombocytopenia. e) Action of activated factor X to from prothrombin activator – role of factor V :


This step in the intrinsic pathway is the same as the last step of the extrinsic pathway i.e. activated factor X combines with factor V and platelet or tissue phospholipids to from the complex called prothrombin activator. The prothrombin activator initiates within seconds the cleavage of prothrombin to from thrombin, there by setting in to motion the final clotting process. Role of calcium ions in to intrinsic and extrinsic pathway : Except for first two steps in the intrinsic pathway calcium is required for all the reactions, therefore in the absence of calcium blood clotting will not occur. In living person calcium ion concentration rarely falls low enough to affect significantly kinetics of clotting. When blood is removed from body, it can be prevented from clotting by reducing calcium ion concentration below threshold level for clotting either by deionizing or by a. Reacting with substances like citrate ions. b. Precipitating calcium with substances like oxalate ions. Interaction between intrinsic and extrinsic pathway : Clotting is initiated simultaneously by both pathways. The tissue factor initiates extrinsic pathway, factor XII and platelets contact with collagen initiates intrinsic pathway. Another important interaction between the two systems is caused by proteolytic effects of thrombin to activate enzymes in the intrinsic pathway. Intravascular clotting sometimes results from factors that activate intrinsic pathway. Eg : Antigen – antibody reaction. Drugs or debris that enter circulation. In important difference between the 2 pathways is that the extrinsic pathway can be explosive in nature, once initiated its speed of occurrence is limited only by amount of tissue thromboplastin released and quantities of factor X,


VII and V in blood with severe tissue trauma clotting can occur in as little as 15 seconds. On the other hand, intrinsic pathway is much slower to proceed, usually requires 1 to 6 minutes to cause clotting. STAGE – 2 : Conversion of prothrombin into thrombin : Prothrombin activator converts prothrombin into thrombin is the presence of calcium. Thrombin itself can accelerate this reaction by positive feed back mechanism. (i.e. activation of factor V which inturn accelerates formation of both extrinsic and intrinsic prothrombin activator). STAGE 3 : Conversion of fibrinogen into fibrin : Thrombin is a protealytic enzyme and converts soluble fibrinogen into insoluble fibrin by removing 4 low molecular weight peptides from each molecule of fibrinogen forming a molecule of fibrin monomer that has automatic capability of polymerizing with other monomer molecules to from long fibrin threads. Initially the fibrin monomer molecules are held together by weak noncovalent hydrogen bonding and no cross linkage, therefore clot is weak and easily broken. This is modified later into a dense tight aggregate by fibrin stabilizing factor in the presence of calcium ions and activation by thrombin, covalent bonds and multiple cross linkage takes place. Fibrinogen : 

It is a high molecular weight protein (3,40,000)

Cone in blood 100 to 700 mg/dl.

Formed in liver


Thrombin Fibrinogen

Activated fibrinogen


Loss of 4 polypeptides Loose strands of fibrin Ca++ Fibrin (Tight clot)

Fibrin stabilizing factor

Prothrombin activating factor


Factor X Ca++ Factor V Thrombin

Blood clot : The fibrin threads run in all directions to form a meshwork which entrape RBC’s, WBC’s and platelets. The entire mass of fibrin meshwork and the blood cells entrapped within this is called blood clot. This clot adheres to the opening of damaged blood vessels and prevents blood loss. Clot retraction : A few minutes after clot is farmed, it begins to contract and express a straw colored fluid called serum within 20 to 60 min.


Serum differs from plasma as it lacks fibrinogen and other clotting factors and hence can’t clot. Platelets are necessary for clot retraction and failure of clot retraction indicates that number of platelets in circulating blood is low. Electron micrographs of platelets in the blood clot show that they become attached to the fibrin threads together. Further more, platelets entrapped in the clot continue to release procoagulant substances, one of which is fibrin stabilizing factor, which causes more and more cross linking bonds between the adjacent fibrin threads. In addition the platelets themselves contribute directly to clot contraction by activating the platelet thrombosthenin, actin and myosin molecules, which are contractile proteins and cause strong contraction of the platelet spicules attached to fibrin. As the clot retracts, the edges of the broken blood vessel are pulled together, thus possibly or probably contributing to the ultimate state of hemostasis. Lyses of blood clot: The lyses of blood clot inside the blood vessel are called fibrinolysis. This occurs by a substance known as plasma or fibrinolysin. The








profibrinolysin. When a clot is formed, a large amount of plasminogen is trapped along with other plasma proteins. The injured tissues and vascular endothelium release a powerful activator called tissue plasminogen activator that a day or later after bleeding stops, convert plasminogen to plasmin. It digests the fibrin threads and other substances in the surrounding blood, such as fibrinogen, factors V, VIII and XII and prothrombin. Therefore plasmin causes lysis of clot and also destruction of many clotting factors, these by causing hypocoagulability of blood. Plasmins inhibitor :


Small amount of plasmin is formed in the blood all the time, which could seriously impede the activation of clotting system, blood also contains another factor α2 – antiplasmin, that bonds with plasmin and inhibits it. Therefore the rate of plasmin formation must raise above a certain clinical level before it becomes effective. The lysis of blood clot allows slow clearing (over several days) of extraneous clotted blood in the tissue and allows reopening of clotted vessels. Hemorrhage. Hemorrhage in dental practice is commonly encountered after extractions, and during endodontic therapy is noticed in the following situations: – Acts as a sign of vital pulp – Sign of perforation – Over instrumentation – During treatment of C shaped canals – Perforating internal resorption – From perforations, during access opening preparations – Endodontic surgeries There are four methods by which the dentist can detect the patient who may have a bleeding problem 1)



Bleeding problems in relatives


Bleeding problems following operations and tooth extractions


Bleeding problems following trauma (cuts, etc)


Medications that may cause bleeding problems - Aspirin - Anticoagulants - Long- term antibiotic therapy.



Presence of illnesses that may have associated bleeding problems -Leukemia - Liver disease - Hemophilia - Congenital heart disease

f) 2)

Spontaneous bleeding from nose, mouth, ears etc. Physical examination


Jaundice, pallor


Spider angiomas






Oral ulcers


Hyperplastic gingival tissues




Screening laboratory tests a)

PT- prothrombin time - normal 11 to 15 sec.


APTT- activated partial throboplastin time – normal is 25 to 35 sec



TT – thrombin time – normal is 9 to 13 sec


BT – bleeding time – normal 1 to 6 minutes


Platelet count – normal 140,000 to 400,000/m3 Surgical procedure – excessive bleeding following surgery may be

first clue to underlying bleeding problem.

COAGULANTS These are agents which promote coagulation, and are indicated in hemorrhagic states.


Fresh Whole Blood or Plasma provide all the factors needed for coagulation and are the best therapy for the deficiency of any clotting factor; also they act immediately. Other drugs used to restore hemostasis are :1. Vitamin K

K1 (from plants) K2 ( produced by bacteria) K3 ( synthetic)

2. Miscellaneous

Fibrinogen Anti hemophilic factor Rutin Adrenochrome Monosemicarbazone

Daily requirement of Vit K of adult – 50 to 100 mg / day.

LOCAL HEMOSTATICS (STYPTICS) Def- These are substances used to stop bleeding from a local approachable site. They are particularly effective on oozing surfaces Eg: Tooth socket Open wounds They should never be injected Eg. 1. Thrombin : hemophilia, neurosurgery, skin grafting - sprayed on the bleeding surface. 2. Fibrin : Prepared from Human plasma and dried and used as sheets / foam for covering or packing bleeding substances and gets absorbed in the body. 3. Gelatin Foam : it is spongy gelatin, available in various shapes. It is moistened with saline and used for packing wounds, gets absorbed in 1 to 2 months. 4. Russels viper venom : applied locally, acts as thermoplastin. 5. Vasocomtrictors lile – 1% sol of Adrenaline may be soaked is sterile cotton guage and packed, stops epitaxis and other similar bleedings.


6. Astringents : like tannic acid is used for bleeding guns. Other substances which hasten clotting are: -

Extracts of Lungs and Thymus - they have thromboplastin which causes rapid coagulation.


Sodium or Calcium Alginate – enhance clotting by activating hageman factor


Oxidized cellulose – causes clotting by activating hageman factor It is normal for blood to seep from the site of a surgical procedure for

several has after operation cloane the mouth with a mild rise (1/2 salt, ½ glass water H2O) talking x strong mouth rinses may stimulate bleeding should be controlled for few days. It bleeding continues a becomes profuse, try to locate the exact spot the blood is coming from by gently flushing the mouth clean looking is a mirror. Once you determine where it is coming from, hold a price of gauge, some toweling or a tea bag against the tissue and bone, apply firm but gentle premise for 10 min with out moving the finger away from the site. Do this is a sitting position. If heavy bleeding continues, call the surgeons office.

ANTICOAGULANTS Def : These are substances which prevent or postpone coagulation. They may act inside body (is vivo) ; outside body ( in vitro) or used both in vivo and in vitro. 1. -

Heparin It is a naturally produced anticoagulant, a conjugated polysaccharide, it is produced in mast cells and basophiles. Mast cells are situated immediately outside the capillaries in large no of tissues or


organs which contain more connective tissue. These wandering cells are abundant in liver and lungs. -

Commercial heparin is prepared is almost pure form. It is extracted from liver and other organs of animals.

Mechanism of Action It prevents clotting by its antithrombin activity. It also combines with antithrombin III (a protease inhibitor present in circulation) and a)

Removes thrombin from circulation


Inactivates the active form of other clotting factors like IX, X, XI, XII.


It also activates antithrombin III.

Uses : as a anticoagulant both in vivo and in vitro. Clinical use Intravenous injection of heparin (0.5 to 1 mg ./ kg body wt) causes bleeding time to increase from normal 6 min to 30 or more minutes. The action of heparin lasts app 3 to 4 hrs till it is destroyed by an enzyme in the blood known as heparinase. In clinics hyparin is used is :1)

To prevent intravascular blood clotting during surgery.


During dialysis when blood is passed through artificial kidney.


During cardiac surgery, which involves passing blood through heart lung machine


After collecting blood from donor, if transfusion into the recipient is delayed, it is used as an anticoagulant.

During treatment if too much is administered and serious bleeding crises occurs, then protamine acts specifically as an antiheparin,by inactivating heparin because it carries strong positive electrical charges, whereas heparin carries strong negative charges. Use in laboratory


As an anticoagulant while collecting blood for various investigations. 2.

Coumarin Derivatives Dicoumoral and Warfarin are the derivatives of coumarin.

Mechanism of action It competes with Vit K for reactive sites is the enzymatic processes for formation of prothrombin factors VII, IX, X all of which form in the liver and require Vit K. It blocks the action of Vit K. After effective dose is administered, the coagulant activity decreases to approximately 50 % of normal at end of 12 hrs and to 20% at end of 24 hrs. The process is not blocked immediately must await consumption of pro thrombin and other factors already present in plasma. Normal coagulation returns 1 to 3 days after discontinuing therapy. Uses – they are used as oral anticoagulants in clinical practice. 3.



Ethylene Diamine Tetra Acetic acid or sodium salt of EDTA is a strong anticoagulant.

Mechanism of Action -

by removing calcium from blood

Uses -

Administered intravenously in case of lead poisoning


Also used as anticoagulant in lab (in vitro).

4. -

Oxalate Compounds It prevents coagulation by forming calciumoxalate, which is precipitated later, thus they reduce blood calcium level. It is used as in vitro anticoagulant.

5. -

Citrates Sodium, Ammonium or Potassium citrate can be used as anticoagulants in lab (invitro). Citrate combines with calcium is blood


to form calcium citrate and the reduction is calcium level prevents coagulation. -

Citrate is also used in blood blank as Acid Citrate Dextrose (ACD) or Citrate Phosphate Dextrose (CPD) to store blood.


Heparan Heparan sulphate has a weak heparin like activity and is produced

mainly by vascular endothelium. The �2 macroglobulin is also a thrombin inhibitor. 7.

Protein C Thrombin can bind with a compound called thrombomodulin

(produced by vascular endothelium) and causes changes is thrombin, which now acts on protein C to convert it into activated protein C which is an anticoagulant. It acts on VIIIa, so that factor VIII is inactivated. Protein C is produced by the liver. For formation of activated protein C, a co-factor protein S is required. Role of vit K. liver and vascular wall is hemostasis and coagulation. Physical methods to prevent clotting 1)

Cold : reducing temperature to about 50C postpones clotting.


Collecting blood in a container with smooth surface : like a silicon coated container prevents clotting.This is by inhibition of platelet activation and formation of pro thrombin activator.

Vit K - Helps in synthesis of a) Procoagulants, factor VII, IX, IX, X and prothrombin b) Circulatory anticoagulant, protein C. - vit K deficiency causes hemorrhagic disorders.


Liver :

It is the site for synthesis of

a) Procoagulants like factors V, VII, IX, X, prothrombin and fibrinogen b) Anticoagulants, heparin, antithrombin III and protein C. - Liver failure thus can cause signs and symptoms of hypocoagulabiity as well as hypercoagulability. Vascular Walls a)

Sub endothelial layer is highly thrombogenic. Contact with blood triggers off coagulation.


Endothelial layer is primarily opposing clotting as it is a barrier between blood and subendothelial layer. But also releases some procoagulants.


Vasospasm is an aid to hemostasis

BLOOD COAGULATION TESTS - BT, CT, platelet count, prothrombrin time,thrombin time, activated partial thromboplastin time. 1) Bleeding Time : This is the time interval from oozing of blood after a cut or injury till arrest of bleeding.Normal duration is 1- 6 mins. It is prolonged in purpura and by the lack of platelets. 2) Clotting Time This is the time taken by the blood to clot after collecting from body. Normal duration is 6 to 10 min.It is prolonged in hemophilia. 3) Prothrombin Time It gives an indication of the total quantity of prothrombin in blood. The blood is collected and oxalated so that, the prothrombin is not converted into thrombin, thus blood clotting is prevented. Then a large


quantity of tissue thromboplastin with calcium is added to this blood. Calcium nullifies the effect of oxalate, and the tissue thromboplastin activates prothrombin and blood clotting occurs. During this procedure, the time taken by blood to clot after adding tissue thromboplastin is called prothrombin time. Normal duration is about 12 sec. It is prolonged in deficiency of prothrombin and other factors I, V, VII and X. However, it is normal in Hemophilia. The test to measure the prothrombin time is -

Quickies one stage method

BLEEDING DISORDERS 1) Bleeding caused by Vit K deficiency : -

Except for few most of the clotting factors are produced in liver. Therefore liver diseases – hepatitis, cirrohosis and acute yellow atrophy – depress clotting system


Vit K is needed for formation of – prothrombin,factor VII, factor IX, factor X and proteinC in liver. Therefore Vit K deficiency causes insufficiency of these factors – bleeding.


Vit K is synthesized in GIT by bacteria. In GIT disease, deficiency occurs as a result of poor absorption of fats from GIT because Vit K is fat soluble and ordinarily absorbed into blood along with fats.


Other cause – failure of liver to secrete bile into GIT (due to obstruction of bile duct or liver disease) become lack of bile prevents adequate fat digestion and absorption, therefore poor Vit K absorption.


Ordinarily, if Vit K is given to deficient patient 4 to 8 hrs before operation and liver parenchymal cells are at least one – half


normal in function, sufficient clotting factors will be produced to prevent excessive bleeding. 2) Hemophilia It is a sex linked inherited disease, transmitted as a recessive trait. Causes : It is caused by deficiency of Factor VIII and IX. Factor VIII – classical hemophilia or hemophilia A. Factor IX – Christmas disease or hemophilia B. 85% of people with hemophilia are affected by Hemophilia A and remaining 15% by Hemophilia B. It occurs due to lack of formation of prothrombin activator, hence coagulation time is prolonged. Bleeding time and prothrombin time are normal. Both the factors are transmitted genetically by way of female chromosome, therefore they will never have hemophilia because at least one of her two ‘X’ chromosomes will have appropriate genes. However if one of her X chromosome is deficient, she will be a hemophilia carrier, transmitting the disease to half of her male offsprings and transmitting the carrier states to half her female offsprings. Bleeding will not occur except after trauma, but the degree of trauma required to cause severe and prolonged bleeding may be so mild that it is hardly noticeable. Bleeding lasts for literally weeks after extraction of a tooth. Factor VIII is composed of 2 separate components, a very large component with mol.wt in millions and another smaller component with molecular weight of about 2,30,000 .This small component is most important in intrinsic pathway of clotting, and its deficiency of this part of factor VIII that causes classical hemophilia. Hemophilia C – caused by deficiency of Plasma thromboplastin antecedent (PTA factor XI)


- Not sex linked, transmitted to both male and female decedents by male and probably females. Oral signs and symptoms – bleeding from slight cause (tooth brush) – large clots develop around teeth. - Shedding and eruption of teeth may be associated with oozing of blood for days or weeks. Tooth extraction – Ist indication of disease Treatment : Injection of purified factor VIII. (unfortunately cost of factor VIII is very high and availability is limited because it is gathered only from human blood and in extremely small quantities.

DENTAL MANAGEMENT Heamophilia A Conservative dentistry If conservative treatment is not tolerated without anaesthesia,papillary or intraligamentary infiltration may achieve sufficient analgesia. Care must be taken not to let the matrix band injure the periodontal tissues (to be safe –rubberdam is used) Endodontics Topical application of 10% cocaine to exposed pulp is choice for vital pulp extirpation. Treatment- replacement of missing factors either by plasma /plama fractions is primary form of therapy.Factor VIII is found in only fresh plasma,but factor IX remains stable and active for long periods in stored plasma.Factor VII can also be replaced by cryprecipitate(cryofactor VIII).Epsilon-amino caproic acid (Amicar) a drug that blocks action of fibrinolysin has also been found to be helpful ad given prior to and following dental extractions.Factor IX deficiency can be treated by fresh or stored plasma as well as by the use


of prothrombin complex concentrates that contain factors VII,IX,X.Factor IX is replaced with fresh plasma. 3) Von Willebrand Disease Characterized clinically by spontaneous bleeding from mucous membrane; from wounds; and prolonged bleeding time in presence of normal platelet count – Transmitted as an autosomal dominant disorder. Type I : reduced quantity of circulating VWF. Von Willebrand factor is a protein secreted by endothelial cells and platelets. This proteins is responsible for adherence of platelets to endothelium of blood vessels during hemostasis after an injury. Type II - Deficiency of the larger component of factor VIII Von Willibrand disease. 4) Purpura Here bleeding time is prolonged, however clotting time is normal. Persons have a tendency to bleeding from many small venules or capillaries resulting is small punctuate hemorrhagic spots through all the body tissues, the skin displays many small purplish (Purpuric) blotches / spots, hence the name purpura. They depending on cause : Thrombocytopenic purpura – platelets are very important for repair of minute breaks is capillaries and other small vessels. In bone marrow disease, the platelet production is affected causing deficiency state, the number falling below a value of app 50,000 / lt (normal 150,000 to 300,000). The deficiency of platelets (thrombocytopenia) leads to purpura, which is called Thrombocytopenic purpura. Levels as low as 10,000 / ml are frequently lethal. b) Thromboesthenic purpura purpra occurring due to abnormal platelets is circulation, although the number be normal.


c) Idiopathic thrombocytopenic purpura It is the purpura occurring due to unknown causes. The platelet count is reduced due to development of specific antibodies which may occur after transfusion of blood from another person, but usually they result from development of autoimmunity to the persons own platelets the cause is unknown. Treatment : Relief from bleeding for 1 to 4 days can often be effected is the patient by giving fresh whole blood transfusions. Also, Spleenectomy is very helpful, sometimes effecting almost a complete cure,because spleen removes large number of platelets, particularly damaged ones from blood. Thrombosis : Def: coagulation of blood inside the blood vessel is called throbisis or Intravascular blood clotting. Complications : Thrombus – during thrombosis, there is occlusion of lumen of blood vessels by solid mass of platelets, red cells /or clot, which is called Thrombus. The thrombsis due to agglutination of RBC is called Agglutinative thrombsis. Embolism and Embolus Embolism is the process in which the thrombus or part of it is detached and carried in blood stream to arrest the blood flow in any part or region of the body. Embolus – it is the thrombus or part of it, which causes embolism. eg. obstruction of blood flow in lungs – pulmonary embolism Brain – cerebral embolism Heart – coronary embolism Infarction and Infarct


Infarction is the stoppage of blood supply to any organ or part of the organ due to embolism. Infarct – it is the affected area. eg. Myocardial infarction. Causes : a. Injury to blood vessels – during infection or mechanical obstruction the endothelial lining of between is damaged and this initiates thrombosis. b. Roughened endothelial lining – infection, damage or arteriosclerosis, the endothelium becomes rough and initiates clotting. c. Sluggishness of blood flow – decreased rate of blood flow causes aggregation of

platelets and formation of thrombosis slowness of

blood flow. occurs in reduced cardiac action, hypotension and low metabolic rate, prolonged conferment to led and immobility of links. d. Agglutination of RBC – it can occur by foreign antigens or toxic substances. The clotting occurs inside the blood vessel during agglutination of RBC. e. Toxic Thrombosis - it is common due to action of chemical poisons like arsenic compounds, mercury, poisonous mushrooms and snake venom. f. Congenital absence of Protein C Protein C is a circulating anticoagulant, which inactivates factors V and VIII, Thrombosis occurs is the absence of this protein. Congenital absence causes thrombosis and death in infancy. Disseminated intravascular coagulation This occurs due to initiation / activation of clotting mechanism is widespread areas of circulation, resulting from the presence of large amounts of traumatized or dying tissue in the body that releases tissue thromboplastins into the blood.


The clots are small but numerous and plug a large share of small peripheral blood vessels. This occurs especially is septisemic shock in which either circulating bacteria or bacterial toxins – especially endotoxins – activate the clotting mechanisms. The plugging of small peripheral vessels greatly diminishes delivery of oxygen and other nutrients to the tissues – a situation that exacerbates shock picture. A particular effect of DIC that the patient frequently begins to bleed. The reason for this is that so many of the clotting factors are removed by the widespread clotting that too few procoagulants remains to allow normal emostaris of the remaining blood. Clinical considerations During day to day clinical practice it is very important for the dentist to take up all the precautionary measures as well as to follow judiciously the principles and steps of various treatment modalities to prevent any under hemorrhage to occur. 1)

Immediate Root fillings : Some operators, provided the pulp is vital and with out evidence of

gross infection, insert a root filling immediately after preparation of canal. This has 2 drawbacks – organisms may remain after preparation and may survive, later causing periapical disease. Following trauma of pulpectomy, haemorrhage may occur when the vasoconstrictor action of anesthetic solution ceases ,the root filling prevents blood entering the root canal, hemorrhage into periapical region takes place – leading to apical periodontitis – discomfort – significantly more post – operative pain. 2)

Prevention of Discoloration Discoloration of tooth subsequent to RCT can in most instances be

prevented by giving proper attention to various aspects of treatment.


It is important that the opening into the pulp chamber is large enough to permit the removal of all pupal debris in crown.After removal of vital pulp all traces of blood should be eliminated from the pulp chamber. Haemorrhage should have ceased by the time the pulp cavity is dressed and sealed. Large strands of tissue coronal to level at which pulp was severed should not be allowed to remain, since they are likely to bleed later and the above said may enter the dentinal tubules and discolour the tooth.


During Surgical Treatment Good anesthesia is essential during surgical endodontics.Profound

long lasting anesthesia can be achieved using 2% lignocaine (lidocaine) with 1.80.000 adrenaline (epinephrine). The vasoconstrictor in such a anesthetic prolongs the duration of anesthesia

and helps to induces

heamostasis to provide a blood free operative site. If bleeding from edge of incision and from cancellous bone is present, then packing the bone cavity with a length of ribbon gauze, 1 cm wide soaked is 1/1000 adrenaline should be tightly packed into the cavity, the flap replaced, and left for a minute or so. Following its removal, localized bleeding is ceased. After surgery flap is returned to original position and stabilized with sutures, firm pressure is then applied to tissue flap with gauze soaked is saline for several minutes. This minimizes size of blood clot between tissue and cortical bone, so that there will be less post operative swelling and discomfort and proper fast healing. Some post operative instructions to patient to prevent bleeding 1. Avoid strenuous activity until next day, since this tends to make wound bleed. 2. Don’t smoke / drink alcohol


3. Don’t retract lip or cheek to inspect region as it will pull on tissue flap. 4. Brush normally on other quadrants, avoid surgical site till sutures are removed. Measurement of acute blood loss :Assessment and management of blood loss must be related to the pre – existing circulating blood volume, which can be derived from patients weight :

infant 80 to 85 ml / kg adult 55 to 75 ml / kg

Measuring blood loss - Blood clot if the size of clenched fist is roughly equal to 500 ml. -

Swelling in closed # (tibia) 500 to 1500 ml


Swab weighing – in the operating theater, blood loss can be measured by weighing swabs after use and subtracting the dry wt. The resulting total obtained (1g = 1 ml) is added to the role of blood collected in suction / drainage bottles.

Treatment -

Restore blood volume immediately.


Pressure and packing – first aid treatment is a pressure dressing which should be bound on tightly. Eg digital pressure (fore finger and thumb), cloth rag (epistaxis)


Packing – rolls of wide gauze.


Position and rest – elevation of limbs eg recaptured varicose veins, employs gravity to reduce bleeding and causes vasoconstriction.

BLOOD TRANSFUSION Indications 1. Major road traffic accident


2. chronic blood loss 3. post operative in patient with malignancies bleeding disorders 4. intra operative – major surgery Advantages : - Volume replacement - Increase O2 carrying capacity - Replacement of clotting factors

Complication – Pyrexia - Platelet sanitization -

-Plasma allergy


-Renal failures

CONCLUSION For normal existence of man the coagulation of blood is of at most importance as without this function man would be to death. Hence it is very important to record a proper history and take all the caution while treating before its too late, as it is said its better to prevent than to cure.

Blood clotting/Dental implant courses by Indian dental academy  

The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide r...

Blood clotting/Dental implant courses by Indian dental academy  

The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide r...