By

Diaa Ahmed Elsaied

Lecturer OMFS Minia University

ILO’S

1. Memorize phases of hemostasis

2. Classify hemostasis abnormalities

3. Management of bleeding disorders

4. Describe homeostasis screening tests

5. Learn management of postoperative bleeding

It is the abnormalities of hemostasis and / or coagulation,

characterized by local or extensive skin or mucocutaneous

hemorrhage derived from capillary.

The bleeding is usually spontaneous or from slight

trauma

Blood vessel injury triggers the

following sequence:

1. Vessel constricts.

2. Circulating platelets adhere to the vessel.

3. Complex series of enzymatic reactions involving

coagulation proteins, produces fibrin to form a stable

hemostatic plug .

Primary hemostasis

-- Platelet plug formation at sites of injury

Secondary hemostasis

--Plasma coagulation system

reaction resulting in fibrin

formation

Primary and secondary

hemostasis are closely linked

HEMOSTASIS

1. VASCULAR PHASE

2. PLATELET PHASE

3. COAGULATION PHASE

4. FIBRINOLYTIC PHASE

Hemostasis or normal blood

clotting is essential for

survival

WHEN A BLOOD VESSEL

IS DAMAGED,

VASOCONSTRICTION

RESULTS. 15:60sec

Contracting Vessel diameter Blood flow

This also promotes the accumulation of platelets & other

clotting factors.

Platelets Adhere To The

Damaged Surface And Form

A Temporary Plug (White

Thrombus).

< 60sec

Through Two

Separate Pathways

The Conversion Of

Fibrinogen To

Fibrin Is Complete. 3:6 Min

INTRINSIC EXTRINSIC

PROTHROMBIN

(II)

FIBRINOGEN

FIBRIN

(I) V

X

Tissue Thromboplastin Collagen

VII

XII

XI

IX

VIII

Coagulation Phase

THROMBIN

(III)

Factor I - fibrinogen

Factor II - prothrombin

Factor III - tissue thromboplastin (tissue factor)

Factor IV - ionized calcium ( Ca++ )

Factor V - labile factor or proaccelerin

Factor VI - unassigned

Factor VII - stable factor or proconvertin

Factor VIII - antihemophilic factor

Factor IX - plasma thromboplastin component, Christmas

Factor X - Stuart-Prower factor

Factor XI - plasma thromboplastin antecedent

Factor XII - Hageman factor

Factor XIII - fibrin-stabilizing factor

It is a process that prevents blood clots from growing and

becoming problematic. The primary type is a normal body

process.

Vessel wall disorders

Abnormalities of blood platelets

1) Quantitative platelets defects:

Thrombocytopenia

2) Qualitative platelets defects:

Thrombasthenia

Disturbance of coagulation in circulation

Deficiency of coagulation factors

Increase of anti-coagulation substances

Hyper function of fibrinolysis

I. VESSEL DEFECTS

II. PLATELET DISORDERS

III. FACTOR DEFICIENCIES

IV. OTHER DISORDERS

1) VITAMIN C DEFICIENCY

Scurvy cause haemorhagic features as defect in collagen

synthesis)

2) Cushing Syndrome:

resulting from excessive Corticosteroid intake or production,

leads to general protein wasting & atrophy of supporting CT.

Diagnosis is facilitated by a detailed case history and a

thorough clinical examination.

The underlying cause should be managed, if reversible.

Blood replacement and iron therapy may be necessary

following dental procedures (surgical) in involved areas

I. VESSEL DEFECTS

II. PLATELET DISORDERS

III. FACTOR DEFICIENCIES

IV. OTHER DISORDERS

Thrombocytopenia:

The number of platelets is reduced. Could be due to:

i) Decreased production in bone marrow

ii) Increased sequestration in the spleen

iii) Accelerated destruction

Thrombasthenia :

Qualitative platelet disorders. May result from defects in

any of the platelet reactions.

NORMAL 100,000 - 400,000 CELLS/MM3

,

< 100,000 Thrombocytopenia

50,000 - 100,000 Mild Thrombocytopenia

< 50,000 Sever Thrombocytopenia

•DRUG INDUCED

•thiazide diuretics

•BONE MARROW FAILURE

Viral Infections

Nutritional Deficiencies

Chemotherapy & Radiation Therapy

Infiltration of Abnormal Cells

Aplastic Anemia Leukemia Metastatic Cancer

•HYPERSPLENISM

Increase in Size Leads to Destruction of Platelets Associated with Portal Hypertension Seen in Patients with Cirrhosis

• THROMBOCYTOPATHY (adequate No but abnormal

function)

Uremia

Inherited Disorders

Myeloproliferative Disorders

Drug Induced

DRUG INDUCED

ASPIRIN IRREVERSIBLY BINDS TO THE

PLATELET FOR ITS ENTIRE LIFESPAN

(7-10 DAYS)

NSAIDS REVERSIBLY BINDS TO THE PLATELET

FOR A LIMITED TIME PERIOD

(APPROX 6 HOURS)

It is aimed at identification and correction of the

reversible defects at the earliest.

Prevention of hemorrhagic episodes.

Prompt control of bleeding when it occurs.

The management of sequelae of the disease.

Thrombocytopenias are managed with transfusions of

platelets.

I. VESSEL DEFECTS

II. PLATELET DISORDERS

III. FACTOR DEFICIENCIES

IV. OTHER DISORDERS

Hemophilia A

Hemophilia B

VON WILLEBRAND’S DISEASE

I) Secondary to drugs: -

Heparin

Coumarin

II) Disease related: -

Liver Disease

Vitamin K deficiency

Fibrinolytic Disorders

A deficiency of factor VIII, (Antihemophilic factor), is

inherited as an X-Iinked recessive trait that affects males

(hemizygous), females being the carriers (heterozygous).

SIGNS AND SYMPTOMS: -

Hemtomas – Gastrointestinal bleeding - Bleeding from

Lacerations

Hemarthroses

Hematuria

Lab Results - Prolonged PTT

It is the second most common inherited bleeding disorder,

after von Willebrand disease (vWD), with a worldwide

incidence of approximately 1 case per 5000 males.

In its severe form, this condition can cause significant

morbidity from recurrent spontaneous bleeding into

joints, muscles, and the brain.

In its more mild form, hemophilia A can lead to prolonged

oozing of blood after injuries, tooth extractions, or surgery.

It is a blood clotting disorder caused by a mutation of the

factor IX gene, leading to a deficiency of factor IX. It is

rarer than haemophilia A.

Clinical symptoms are similar to hemophilia A.

Factor IX deficiency leads to an increased propensity for

hemorrhage. This is in response to mild trauma or even

spontaneously, such as in joints or muscles.

Lab Test - Prolonged PTT

It is dependent upon the severity of disease, type and site

of hemorrhage.

Factor Replacement Therapy is considered the primary

mode of management.

Cryoprecipitate & Fresh Frozen Plasma are rarely used

because of their disadvantages of potential viral

transmission.

It is the most common hereditary coagulation abnormality

described in humans.

It arises from a qualitative or quantitative deficiency of

von Willebrand factor (vWF) & Factor VIII, a protein that

is required for platelet adhesion.

Lab Results - Prolonged BT, PTT

Signs and symptoms:

The various types of vWD present with varying degrees

of bleeding tendency, usually in the form of easy

bruising, nosebleeds and bleeding gums.

Women may experience heavy menstrual flow and blood

loss during childbirth.

Severe internal or joint bleeding is uncommon.

Desmopressin is recommended for use in cases of minor

trauma, or in preparation for dental procedures. It

stimulates the release of von Willebrand factor (vWF).

Platelet concentrate infusions may be used to control

bleeding.

Local Hemostatic agents are to be used.

ORAL ANTICOAGULANTS

COUMADIN (WARFARIN) (dose dependant, 3-5dys, onset

12-24 hrs, PT 24 hrs prior to surgery, reversed by vit K,

resist further anticoag, harmeful if stopprd suddenly)

HEPARIN (affects intrinsic & common pathway, duration

2-4 hrs, inhibit action of thrombin on fibrinogen, PTT)

ORAL ANTICOAGULANTS

Coumarin Prevents Thromboembolic Events &

is a Vit K Antagonist. Monitored by PT times.

Heparin Therapy is Monitored by PTT times.

MALABSORPTION

Various Intestinal Diseases Will Interfere w/ Bile Acid

Metabolism.

Bile Acids are Required for Vit K Absorption so You

Will See a Deficiency in Vit K Dependent Coagulation

Factors (II,VII,IX,X).

LIVER DISEASE

Jaundice Results in Malabsorption of Vit K.

Liver Disease can Result in Reduced Production of

Coagulation Factors (I,II,V,VII,IX,X).

I. VESSEL DEFECTS

II. PLATELET DISORDERS

III. FACTOR DEFICIENCIES

IV. OTHER DISORDERS

BROAD-SPECTRUM ANTIBIOTICS

Change in Intestinal Flora which Might Decrease

Vitamin K Production.

Vitamin K is Necessary for the Liver to Produce

Coagulation Factors II,VII,IX,X.

Leukopenia :

Deficient WBC , Decrease of neutrophils is most common etiology .

Physical finding are increased risk microbial infection.

Increased risk of fungal infection.

Management include :

-- Prophylactic Antibiotic.

Elevated percentage of immature WBC in peripheral circulation.

It is cancer of the WBCs that affects the bone marrow and circulating blood. It involves exponential proliferation of a clonal myeloid or lymphoid cell.

Symptoms includes:

Nausea – Fever – Weight Loss

Fatigue – Malaise - Epistaxix

Liver or spleen enlargment Bone pain & tenderness

Oral manifestation includes:

Gingival Enlargement & ulceration

Pain Erythema & oral infection

The cause of leukemia is unknown

Increased risk is associated with large doses of ionizing

radiation, certain chemicals(benzene), and infection with

specific viruses [EPV] and human lymphotropic virus

[HTLV]-1

Smoking & exposure to electromagnetic

Genetic factors may cause cytogenetic abnormalities that

affect transcriptional cascades of myeloid precursor cells.

Acute leukemia

Result from accumulation of immature , functionless WBCs in the marrow & blood

1. Acute myeloid leukemia (AML)

2. Acute lymphocytic leukemia (ALL)

Chronic leukemia

Have slower onset which allows production of larger numbers of more mature, functional cells

1. Chronic myeloid leukemia (CML)

2. Chronic lymphocytic leukemia (CLL)

Bone marrow test

1. Bone marrow aspiration :

Remove a liquid marrow sample

2. Bone marrow biopsy

Lumbar puncture:

Removes a small amount of

cerebrospinal fluid (CSF) from the space around the spine

Chemotherapy

The main treatment for many kinds of leukemia

It has 3 phases:

1- Induction

2- Consolidation

3- Maintenance

Radiation therapy

To prevent leukemia from spreading to, or treat leukemia that has spread to, the central nervous system (CNS)

Bone marrow transplant

LEUKEMIA

Anemia is a decrease in the total amount of red blood cells (RBCs) or hemoglobin in the blood, or a lowered ability of the blood to carry oxygen.

Laboratory definition:

Reduction in haemoglobin concentration

below normal

WHO criteria:

Males Hgb <13 gm/dl,

Females Hgb <12gm/dl

Symptoms:

Fatigue Weakness Dyspnea Palpitation

Headache Dizziness Angina Tinnitus

Signs:

Pallor Tachycardia Cardiac Failure

Medical & family history & perform a physical exam.

Complete blood count (CBC):- A CBC is used to count the number of blood cells in a sample of your blood. For anemia the levels of the red blood cells contained in the blood (hematocrit) and the hemoglobin in the blood is interested.

Tests for internal bleeding:- To ensure that internal bleeding is causing anemia, may also perform an endoscopy. These test can help identify sources of gastrointestinal bleeding.

Treatments for anemia depend on cause and severity. Vitamin supplements given orally (folic acid or vitamin B12) or intramuscularly (vitamin B12) will replace specific deficiencies.

Anemia treatment depends on the cause.

a) Iron deficiency anemia

b) Vitamin deficiency anemia

c) Anemia of chronic disease

d) Aplastic anemia

e) Anemia associated with bone marrow disease

f) Hemolytic anemia

g) Sickle cell anemia

Iron deficiency anemia:- Treatment for this form of anemia usually involves taking iron supplements & making changes to your diet.

• Diet as red meat, dark green leafy vegetables, dried fruits, nuts, iron-fortified cereals.

Vitamin deficiency anemia:- Treatment for folic acid & B-12 deficiency involves dietary supplements & increasing these nutrients in diet.

•If your digestive system has trouble absorbing vitamin B-12 from the food you eat, you may need vitamin B-12 shots.

Platelets Phase:

Platelet Count

Bleeding Time (BT)

Platelets Funtion Analyzer (PFA)

Coagulation Phase:

Prothrombin Time (PT)

Partial Thromboplastin Time (PTT)

Thrombin Time (TT)

NORMAL 100,000 - 400,000 CELLS/MM3

,

< 100,000 Thrombocytopenia

50,000 - 100,000 Mild Thrombocytopenia

< 50,000 Sever Thrombocytopenia

Provides Assessment Of Platelet Count & function (Quantitative & Qualitative)

NORMAL VALUE

2-8 Min

Quntative lab test for platelets function & avoid variability of BT

Normal < 193 s

Measures Effectiveness of the Extrinsic Pathway

Mnemonic - PET

NORMAL VALUE

11- 14 SECS

Measures Effectiveness of the Intrinsic

Pathway

Mnemonic - PITT

NORMAL VALUE

27 – 38 SECS

Time for Thrombin To Convert

Fibrinogen Fibrin

A Measure of Fibrinolytic Pathway

NORMAL VALUE

9-13 SECS

Dental management of the medically compromised patient

PT, aPTT, TT, BT History bleeding problem

BT, aPTT Aspirin therapy

PT Coumarin therapy

aPTT Renal dialysis (heparin)

BT – PT Possible liver disease

BT Chronic leukemia

PT Long term antibiotic therapy

BT Vascular wall alteration

TT Cancer (fibrinogenolysis)

TT PT PTT BT Platelet count Condition

- + + + + Aspirin therapy

- ++ ++ - - Coumarin therapy

- - ++ + + Heparin therapy

++ ++ ++ + + Liver disease

- - - + + Leukemia

++ ++ ++ - - Long term antibiotic

- - - + - Vascular wall defect

- - - ++ ++ Thrombocytopenia

- - ++ - - Hemophilia

++ + + - - Fibrinogenolysis

- normal, + may be abnormal, ++ abnormal

GOOD THOROUGH MEDICAL HISTORY

A PHYSICAL EXAMINATION

SCREENING CLINICAL LAB TESTS

EXCESSIVE BLEEDING FOLLOWING SURGICAL

PROCEDURE

Family HX

Personal HX

Medications

Past & Present Illness

Spontaneous Bleeding

FIVE DRUGS THAT INTERFERE WITH HEMOSTASIS

ASPIRIN

ANTICOAGULANTS

ANTIBIOTICS

ALCOHOL

ANTICANCER

Petechiae & Ecchymosis

Gingival Hyperplasia

Spontaneous Gingival Bleeding

Ulceration of Oral Mucosa

Lymphadenopathy

LOW RISK

Patients with No Hx of Bleeding Disorders

Normal Laboratory Results

MODERATE RISK

Patients on Chronic Oral Anticoagulant

Therapy. PT is 1.5 - 2 Times Control Range

Patients on Chronic Aspirin Therapy

DENTAL PATIENTS

HIGH RISK

Patients with Known Bleeding Disorders

Patients without Known Bleeding Disorders

Who Have Abnormal Laboratory Results

LOW RISK PATIENTS

Normal Protocol

MODERATE RISK PATIENTS

Anticoagulants - Consult Physician

Aspirin Therapy - BT, Consult Physician

DENTAL MANAGEMENT

HIGH RISK PATIENTS

Close Coordination with Physician

Hospitalization (Platelet Transfusion)

(Factor Replacement)

(Vit K Therapy)

(Dialysis)