CONTENTS
INTRODUCTION
FUNCTIONS
CONSTITUENTS OF BLOOD
GENESIS OF RBC
ANAEMIA
POLYCYTHEMIA
LEUKEMIA
CLOTTING FACTORS
CLOTTING CASCADE
BLEEDING DISORDERS
INTRODUCTION;
Blood is a specialized bodily fluid that delivers necessary substances to the body's
cells – such as nutrients and oxygen – and transports waste products away from those
same cells.
Blood is bright red when its hemoglobin is oxygenated. Blood is circulated around
the body through blood vessels by the pumping action of the heart. In lungs, arterial
blood carries oxygen from inhaled air to the tissues of the body, and venous blood
carries carbon dioxide, a waste product of metabolism produced by cells, from the
tissues to the lungs to be exhaled.
FUNCTIONS;
Constituents of blood
Blood accounts for 8% of the human body weight, with an average density of
approximately 1060 kg/m3, very close to pure water's density of 1000 kg/m3.The
average adult has a blood volume of roughly 5 liters (1.3 gal), composed of plasma
and several kinds of cells (occasionally called corpuscles); these formed elements of
the blood are erythrocytes (red blood cells), leukocytes (white blood cells), and
thrombocytes (platelets). By volume, the red blood cells constitute about 45% of
whole blood, the plasma about 54.3%, and white cells about 0.7%.
Whole blood (plasma and cells) exhibits non-Newtonian, viscoelastic fluid dynamics;
its flow properties are adapted to flow effectively through tiny capillary blood vessels
with less resistance than plasma by itself. In addition, if all human hemoglobin were
free in the plasma rather than being contained in RBCs, the circulatory fluid would be
too viscous for the cardiovascular system to function effectively.
CELLS;
In most mammals, mature red blood cells lack a nucleus and organelles.
They contain the blood's hemoglobin and distribute oxygen. The red blood
cells (together with endothelial vessel cells and other cells) are also marked by
glycoproteins that define the different blood types. The proportion of blood
occupied by red blood cells is referred to as the hematocrit, and is normally
about 45%. The combined surface area of all red blood cells of the human
body would be roughly 2,000 times as great as the body's exterior surface.
4,000–11,000 leukocytes:
White blood cells are part of the immune system; they destroy and
remove old or aberrant cells and cellular debris, as well as attack infectious
agents (pathogens) and foreign substances. The cancer of leukocytes is called
leukemia.
200,000–500,000 thrombocytes:
Plasma
About 55% of whole blood is blood plasma, a fluid that is the blood's liquid medium,
which by itself is straw-yellow in color. The blood plasma volume totals of 2.7–3.0
liters (2.8–3.2 quarts) in an average human. It is essentially an aqueous solution
containing 92% water, 8% blood plasma proteins, and trace amounts of other
materials. Plasma circulates dissolved nutrients, such as glucose, amino acids, and
fatty acids (dissolved in the blood or bound to plasma proteins), and removes waste
products, such as carbon dioxide, urea, and lactic acid.
Serum albumin
Blood-clotting factors (to facilitate coagulation)
Immunoglobulins (antibodies)
lipoprotein particles
Various other proteins
Various electrolytes (mainly sodium and chloride)
The term serum refers to plasma from which the clotting proteins have been removed.
Most of the proteins remaining are albumin and immunoglobulins.
Destruction of Hemoglobin.
When red blood cells burst and release their hemoglobin, the hemoglobin is
phagocytized almost immediately by macrophages in many parts of the body, but
especially by the Kupffer cells of the liver and macrophages of the spleen and bone
marrow. During the next few hours to days, the macrophages release iron from the
hemoglobin and pass it back into the blood, to be carried by transferrin either to the
bone marrow for the production of new red blood cells or to the liver and other tissues
for storage in the form of ferritin. The porphyrin portion of the hemoglobin molecule
is converted by the macrophages, through a series of stages, into the bile pigment
bilirubin, which is released into the blood and later removed from the body by
secretion through the liver into the bile;
Anemias
Anemia means deficiency of hemoglobin in the blood, which can be caused by either
too few red blood cells or too little hemoglobin in the cells. Some types of anemia and
their physiologic causes are the following.
Blood Loss Anemia. After rapid hemorrhage, the body replaces the fluid portion of
the plasma in 1 to 3 days, but this leaves a low concentration of red blood cells. If a
second hemorrhage does not occur, the red blood cell concentration usually returns to
normal within 3 to 6 weeks.
In chronic blood loss, a person frequently cannot absorb enough iron from the
intestines to form hemo- globin as rapidly as it is lost. Red cells are then pro- duced
that are much smaller than normal and have too little hemoglobin inside them, giving
rise to microcytic, hypochromic anemia, which is shown in
Aplastic Anemia. Bone marrow aplasia means lack of functioning bone marrow. For
instance, a person exposed to gamma ray radiation from a nuclear bomb blast can
sustain complete destruction of bone marrow, followed in a few weeks by lethal
anemia. Likewise, excessive x-ray treatment, certain industrial chemicals, and even
drugs to which the person might be sensitive can cause the same effect
Megaloblastic Anemia
The red cells grow too large, with odd shapes, and are called
megaloblasts. Thus, atrophy of the stomach mucosa, as occurs in pernicious anemia,
or loss of the entire stomach after surgical total gastrectomy can lead to megaloblastic
anemia. Also, patients who have intes- tinal sprue, in which folic acid, vitamin B12,
and other vitamin B compounds are poorly absorbed, often develop megaloblastic
anemia. Because in these states the erythroblasts cannot proliferate rapidly enough to
form normal numbers of red blood cells, those red cells that are formed are mostly
oversized, have bizarre shapes, and have fragile membranes. These cells rupture
easily, leaving the person in dire need of an adequate number of red cells.
Hemolytic Anemia.
Different abnormalities of the red blood cells, many of which are hereditarily
acquired, make the cells fragile, so that they rupture easily as they go through the
capillaries, especially through the spleen. Even though the number of red blood cells
formed may be normal, or even much greater than normal in some hemolytic diseases,
the life span of the fragile red cell is so short that the cells are destroyed faster than
they can be formed, and serious anemia results. Some of these types of anemia are the
following.
In hereditary spherocytosis, the red cells are very small and spherical rather than
being biconcave discs. These cells cannot withstand compression forces because they
do not have the normal loose, baglike cell membrane structure of the biconcave discs.
On passing through the splenic pulp and some other tight vas- cular beds, they are
easily ruptured by even slight compression.
In sickle cell anemia, which is present in 0.3 to 1.0 per cent of West African and
American blacks, the cells have an abnormal type of hemoglobin called hemo- globin
S, containing faulty beta chains in the hemo- globin molecule, as explained earlier in
the chapter. When this hemoglobin is exposed to low concentra- tions of oxygen, it
precipitates into long crystals inside the red blood cell. These crystals elongate the
cell and give it the appearance of a sickle rather than a bicon- cave disc. The
precipitated hemoglobin also damages the cell membrane, so that the cells become
highly fragile, leading to serious anemia. Such patients fre- quently experience a
vicious circle of events called a sickle cell disease “crisis,” in which low oxygen
tension in the tissues causes sickling, which leads to ruptured red cells, which causes
a further decrease in oxygen tension and still more sickling and red cell destruction.
Once the process starts, it progresses rapidly, eventu- ating in a serious decrease in
red blood cells within a few hours and, often, death.
In erythroblastosis fetalis, Rh-positive red blood cells in the fetus are attacked by
antibodies from an Rh-negative mother. These antibodies make the Rh-positive cells
fragile, leading to rapid rupture and causing the child to be born with serious anemia.
This is discussed in Chapter 35 in relation to the Rh factor of blood. The extremely
rapid formation of new red cells to make up for the destroyed cells in erythro-
blastosis fetalis causes a large number of early blast forms of red cells to be released
from the bone marrow into the blood.
Polycythemia
Secondary Polycythemia. Whenever the tissues become hypoxic because of too little
oxygen in the breathed air, such as at high altitudes, or because of failure of oxygen
delivery to the tissues, such as in cardiac failure, the blood-forming organs
automatically produce large quantities of extra red blood cells. This condition is
called secondary polycythemia, and the red cell count commonly rises to 6 to 7
million/mm3, about 30 per cent above normal.
A common type of secondary polycythemia, called physiologic polycythemia, occurs
in natives who live at altitudes of 14,000 to 17,000 feet, where the atmos- pheric
oxygen is very low. The blood count is generally 6 to 7 million/mm3; this allows
these people to perform reasonably high levels of continuous work even in a rarefied
atmosphere.
Polycythemia Vera (Erythremia). In addition to those people who have physiologic
polycythemia, others have a pathological condition known as polycythemia vera, in
which the red blood cell count may be 7 to 8 million/mm3 and the hematocrit may be
60 to 70 per cent instead of the normal 40 to 45 per cent. Poly- cythemia vera is
caused by a genetic aberration in the hemocytoblastic cells that produce the blood
cells. The blast cells no longer stop producing red cells when too many cells are
already present. This causes excess pro- duction of red blood cells in the same manner
that a breast tumor causes excess production of a specific type of breast cell. It usually
causes excess production of white blood cells and platelets as well.
In polycythemia vera, not only does the hematocrit increase, but the total blood
volume also increases, on some occasions to almost twice normal. As a result, the
entire vascular system becomes intensely engorged. In addition, many blood
capillaries become plugged by the viscous blood; the viscosity of the blood in poly-
cythemia vera sometimes increases from the normal of 3 times the viscosity of water
to 10 times that of water.
Six types of white blood cells are normally present in the blood. They are
polymorphonuclear neutrophils, polymorphonuclear eosinophils, polymorphonuclear
basophils, monocytes, lymphocytes, and, occa- sionally, plasma cells. In addition,
there are large numbers of platelets, which are fragments of another type of cell
similar to the white blood cells found in the bone marrow, the megakaryocyte. The
first three types of cells, the polymor- phonuclear cells, all have a granular
appearance.
Along with the invasion of neutrophils, monocytes from the blood enter the
inflamed tissue and enlarge to become macrophages. However, the number of
monocytes in the circulating blood is low: also, the storage pool of monocytes in the
bone marrow is much less than that of neutrophils. There- fore, the buildup of
macrophages in the inflamed tissue area is much slower than that of neutrophils,
requiring several days to become effective.
The Leukemias
Uncontrolled production of white blood cells can be caused by cancerous mutation of
a myelogenous or lymphogenous cell. This causes leukemia, which is usually
characterized by greatly increased numbers of abnormal white blood cells in the
circulating blood.
Types of Leukemia. Leukemias are divided into two general types: lymphocytic
leukemias and myeloge- nous leukemias. The lymphocytic leukemias are caused by
cancerous production of lymphoid cells, usually beginning in a lymph node or other
lymphocytic tissue and spreading to other areas of the body. The second type of
leukemia, myelogenous leukemia, begins by cancerous production of young
myelogenous cells in the bone marrow and then spreads throughout the body so that
white blood cells are produced in many extramedullary tissues—especially in the
lymph nodes, spleen, and liver.
In myelogenous leukemia, the cancerous process occasionally produces partially
differentiated cells, resulting in what might be called neutrophilic leukemia,
eosinophilic leukemia, basophilic leukemia, or monocytic leukemia. More frequently,
however, the leukemia cells are bizarre and undifferentiated and not identical to any
of the normal white blood cells. Usually, the more undifferentiated the cell, the more
acute is the leukemia, often leading to death within a few months if untreated. With
some of the more dif- ferentiated cells, the process can be chronic, some- times
developing slowly over 10 to 20 years. Leukemic cells, especially the very
undifferentiated cells, are usually nonfunctional for providing the normal pro- tection
against infection.
Effects of Leukemia on the Body
The first effect of leukemia is metastatic growth of leukemic cells in abnormal areas
of the body. Leukemic cells from the bone marrow may reproduce so greatly that they
invade the surrounding bone, causing pain and, eventually, a tendency for bones to
fracture easily.
Almost all leukemias eventually spread to the spleen, lymph nodes, liver, and other
vascular regions, regardless of whether the origin of the leukemia is in the bone
marrow or the lymph nodes. Common effects in leukemia are the development of
infection, severe anemia, and a bleeding tendency caused by thrombo- cytopenia (lack
of platelets). These effects result mainly from displacement of the normal bone
marrow and lymphoid cells by the nonfunctional leukemic cells.
Finally, perhaps the most important effect of leukemia on the body is excessive use of
metabolic substrates by the growing cancerous cells. The leukemic tissues reproduce
new cells so rapidly that tremendous demands are made on the body reserves for
foodstuffs, specific amino acids, and vitamins. Con- sequently, the energy of the
patient is greatly depleted, and excessive utilization of amino acids by the leukemic
cells causes especially rapid deterioration of the normal protein tissues of the body.
Thus, while the leukemic tissues grow, other tissues become debili- tated. After
metabolic starvation has continued long enough, this alone is sufficient to cause
death.
CLOTTING FACTORS
Factor I- FIBRINOGEN
FactorII- PROTHROMBIN
Factor XI-PTA
Combination of factor
Local systemic
Defects in coagulation
It is essential to differentiate all these causes & act quickly & decisively in
event of complication.
Those related to bleeding & those related to delayed wound healing & infection.
There is multitude of lab tests of platelet function & of the coagulation cascade.
The surgeon must often decide which of these tests to obtain to maximize the
probability of detecting occult haemostatic defect.
BT is the single best screening test for platelet function, but it has been criticized
because in some studies it does not correlate with surgical bleeding. But some authors
recommend this as a routine preoperative test because it screens for von willibrand’s
disease & platelet dysfunction. BT is useful in detecting vascular disorder i.e.
ontogenesis imperfecta, hereditary hemorrhagic telengiectasia). The test is performed
by inflating a BP cuff of 40 mm of Hg & then making a standard cut on inner surface
of forearm. Blood is removed from edge of the drop using filter paper until bleeding
has stopped
2) Prothrombin test
But screening test for abnormalities of the extrinsic, common limbs of the
coagulation the clotting time of plasma with ideal concentration of tissue
thromboplastin. Decreased level of factor 1 (afbrinogenemia), II, V
Congenital low levels of factor I. II. VII, V & X are rare But acquired defects are
common & caused by liver disease, coumadin therapy, Vit K deficiency, disseminated
intravascular coagulation, high titer lupus anticoagulant & high dose of heparin therapy.
INR is the value calculated from the ratio of Patient’s prothrombin time (PT) to
mean of normal range. This value is then corrected by multiplication by the
international sensitivity index (ISI). The ISI is based on a quantitative assessment of
responsiveness of a thromboplastin. The INR system was established to standard
discrepancies in specific thromboplastin used in the PT test. ISI is performed against
different WHO reference materials.
Although aPTT is the single most sensitive laboratory test for coagulation defects,
it must be interpreted with knowledge of its limitation. It lacks sensitivity to mild
deficiency of single clotting factors and to haemostatic defects due to coumadin. Slight
prolongation of a PTT is of no significance.
Thrombin Time: (TT)
It measures interaction between exogenously added thrombin and fibrinogen. It is
most commonly used in disseminated intravascular coagulation or in afbrinogenemia.
Platelet Counts - These are obtained on anticoagulated blood by using electronic
particles counter. The reference range being 150-450x10 3/mm3. Counts outside this
must be confirmed by using blood smear visual examination.
Activated clotting time:(aCT) It is used for assessing heparinisation of patients
intraoperatively. Whole blood is mixed with diatomaceous earth. aCT should be
prolonged by 3-4 times before cardiac bypass surgery begins.
Blood Smear - It assesses morphological abnormalities and quantitative platelet
disorder.
Mixes: - Mixing of patient plasma with an equal volume of normal plasma in a standard
test for identification of coagulation inhibitors such as lupus anticoagulants and for
confirming specific factor deficiency. If prolongation of a PTT or PT is due to specific
factor deficiency, the mix will correct to normal. If on the other hand inhibitors of
coagulation is responsible for prolonged aPTT or PT mix will not correct to normal.
Investigation Normal Range causes for
abnormality
4. Activated partial
Thromboplastin time 30-40 sec Def. of factor II,
V, VII, IX, X, XI, XII
(Hemophilia A, B,
Von Willebrands disease
DIC)
Aggregation of platelets
Platelet plug
Bleeding stopped
Coagulation cascade has been given below which shows interrelationship between
coagulation factors and platelets.
Acquired-
Vit K deficiency
Liver disease
Combined defects
- Disseminated intravascular coagulation
-Primary fibrinolysis associated with prostatic
adenocarcinoma.
2. Once exposed to sub endothelial tissue platelets release the stored contents of
granules from their cytoplasm to surrounding tissue. Granules contain many chemo
tactic factors as well as adenosine diphosphate, calcium, fibrinogen and epinephrine.
Calcium stimulates phospholipase to cleave phosopholipids providing building blocks
for prostaglandins Primary prostaglandin synthesized by platelets is thromboxane A2
that causes vasoconstriction.
3. Platelets form catalytic sources for coagulation cascade, which leads to deposition of
fibrin.
Disorders that affect total count of platelets and quality of platelets will be bound to
cause severe haemostatic defect. Following defects are discussed with management
1. Autoimmune Thrombocytopenia (AITP)
It was referred as idiopathic theombocytopenic purpura. This term is somewhat
outdated and less descriptive. Three categories of AITP are now recognized.
Although it is only known that antibodies are produced against platelets, the
mechanism of formation of antibodies is not known. Various hypothesis include
Clinical course
- Clinical features include
- Petechiae, cutaneous pupura
- Bleeding gums
- Epistaxis
- Haematuria
- Melena
- Menorrhagia
Treatment
Patient with chronic AITP are treated with steroids and spleenectomy - 80% of patient
will obtain permanent remission.
However if the child has excessive haemorhage or child is above 10 years treatment
protocol of adult AITP can be used.
If surgery has to be carried out then intravenous lgG should be given.
Cause - Blood plasma have abnormal VIII VWF causing blood to form platelet clot
- Decreased synthesis of PGI2 (prostacyclin), which is most potent inhibitor of
platelet aggregation secreted by blood endothelium.
Treatment - 90% mortality rate.
Prognosis- poor
Treatment includes - Plasma transfusion.
- Plasma pheresis
Platelet infusion should not be done as it will worsen the condition
treatment- Dialysis
- DDAVP (1-diamino-8-D arginine vasopressin) has been effective -1-12hs of
improvement.
- Infusion of cryoprecipitate -24-36hs of improvement.
4. Drug induced Thrombocytopenia
Pathogenesis is not clear. But due to interaction of drugs with platelet surface
membrane causes alteration of antigen and hence antibody production is triggered..
Atleast 6 day lag period is seen in cases without previous exposure.
- Clinical features - fever, chills, arthralgias abrupt onset of petechie, hematoma not
related to trauma.
- Rx includes immediate cessation of causative drug. Since antibodies are found in the
blood for many years, the causative drug should not be administered again.
- If severe and life threatening -Rx parallel to AITP should be carried out.
5) Ethanol induced
80% of chronic alcoholic have mild to moderate thrombocytopenia
Ethanol is directly toxic to platelets & megakaryocytes. It also causes decrease
qualitative function mainly due to decreased store production of theombaxane A2
Dental Rx in Theombocytopenia
Platelet count of 40,000/mm3 is called critical value. Usually a count of atleast
50,000 /mm3 is necessary for oral surgical procedures with conjunction of local
haemostatic measure.
Surgery can be carried out with use of DDAVP & IgG infusions as described
earlier.
Defects in coagulation
Hemophilia A-
- bleeding disorder caused by deficiency of clotting factors VIII.
- accounts for 80% of al hemophilia .
Incidence 1:10,000 of male population
Severe hemophilia with activity less than 1%
Moderate with activity less than 3-5%
Mild with activity less than 5-12%
Severity of symptoms can vary. prolonged bleeding is the hallmark of hemophilia
A and typically occurs when an infant is circumcised. Additional bleeding
manifestations when infant becomes mobile.
Mild cases may go unnoticed .Men are affected as it is due recessive gene.
However women can be carrier.
Symptoms include
- Haemarthrosis.
- Haermatomas
- Haematuria
- Bleeding from mucosal surfaces of nose and mouth.
Lab Diagnosis
Clinically patient will have increased apt but normal PT.
The factor VIII is preset in the form of complex
VIII: c – procoagulant activity of factor VIII
Complex - deficient in hemophilia
VIII : VWF – Von willebrand activity of factor VIII
complex that is deficient in Von Willebr
and’s disease
Hemophilia B
It is called as Christmas disease, but clinically indistinguishable from
hemophilia A.
- Incidence is 1:100000 .
- Found in males but females can be carriers
- Only testing for specific factor activity distinguishes hemophilia B from
hemophilia A.
- As with factor VIII, 30 % of IX activity is required for normal hemostasis
following surgery or trauma..
Management :-
Patient treatment should be based on following principles.
- Control of bleeding
- Minimum hospitalization
- Minimum chances of viral infection
- Low expenditure
As a dentist our role will be to educate patient and parents for bringing the
child to the dental clinic for preventive measures, rather than wait for extensive
procedure which require elevated factor levels & as well as hospitalization. Patient
should be taken into confidence & good rapport established.
Dental Management
- Pain Control – Intra pulpal anaesthesia is safe & can be effectively used for pulp
extirpation. Intra ligamentary injection even though not contraindicated might be
painful. Buccal, labial & palatal infiltration can be done but with caution & local
pressure applied for atleast 3-4min.
- Blocks given – Like inferior alveolar nerve block require atleast 30% of factor
level as these injections are usually given in highly vascular areas with no distinct
boundaries & filled with loose connective tissue Extravasation of blood into
oropharyngeal region can cause dysphagia, Pain, respiratory obstruction.
Periodontal procedures
It can be safely carried out provided scaling is supra gingival .
Deep subgingival scaling might have to be carried out quadrant wise with
adequate local pressure application .
Once gross scaling done subgingival scaling has to be postponed to later date
as gingiva will become the inflamed & be hyperemic – so less bleeding
- Subgingival calculus gets exposed as enlarged gingiva shrinks.
Periodontal parks can be used to as it prevents bleeding & protect the exposed areas.
Endodontic therapy:-
It is often treatment of choice as it involves minimal bleeding . care should be taken to
prevent over instrumentation.Pulpal bleeding is not a problem & stops on extirpation /
local presence.
Topical fluoride application & use of pit and fissure sealants should be
encouraged.
Stainless steel crown should be given ensuring that gingival margins are taken
care of .
Orthodontic Therapy
It can be safely carried out. But appliances should not cause any trauma.
Bleeding from minor cuts usually responds to local pressure. The use of extra oral force
& shorter treatment duration further decrease the potential of bleeding complications.
Kaneda & colleagues have reported that factor levels of 25% for deciduous &
20% for permanent teeth healing post extraction phase. 3 modalities are advocated
- continuous infusion
- Intermittent infusion
- Single concentrate infusion with antifibrinolytic agent .
Recently it was shown that post operative bleeding & the need or transfusion
after oral surgery were significantly reduced with tranexamic acid being used as a
mouthwash .
The tranexamic acid binds to lysine binding sites on plasminogen & plasmin .
This mechanism blocks the binding of plasmin to fibrin, thus acting as a potent inhibitor
of fibrinolysis .The efficiency of local antifibrinolytic Rx has been proved by
observation, that the concentration of tranexamic acid mouthwash in saliva remains
sufficiently high to suppress fibrinolysis for several house after use, while only
insignificant levels was demonstrated in plasma at the same time.
The concentration used is 5% solution poured into 5 ml + 5ml of water is used
for local irrigation & mouth wash.
Suturing with non resorbable suture can be effectively done. Resorbable
suture might cause inflammatory responses & hence increase bleeding.
Fibrin glue is hotly debated as currently used fibrin glue which mimics final
stage of blood clotting .
Because of possibility of spreading viral infection, it is not used.
- Factor VIII C replacement therapy can be calculated as 1 unit of VIII C per Kg of
body weight results in increase of 0.02 units /mm. For major surgeries value should be
0.8 – 1.0 Units /mm (80 –100%) & then maintaining at 0.3 – 0.5 units /mm
- Alternate therapy for mild & moderate hemophiliacs include the use of desmopressin
(DDAVP) – 1 deamino – 8 – d – arginine vasopressin . In hemophilic patent it is found
to increase factor VIII : C & factor VIII VWF .
The mechanism of action is unclear. The release of stored factors in vascular
endothelial cells and endogenous stores are believed to be the cause for the increase.
Current recommendation is 0.3 micro g /kg of desmopressin diluted in 50ml of normal
saline ,slow infusion over 15-30mm. The maximum raise occurs at about 90-120
minutes & persistent activity for 6 or more hours.
Side effects are mild headache, flushing & are due to increase volume & can be
usually controlled by fluid restriction.
Currently gene therapy being investigated for treatment of hemophiliacs & it is
an excellent candidate for several reasons .
- Involved proteins are delivered into circulation by a variety of cell types &
low levels of expression lead to significant improvement in management of bleeding
episodes.
- Excellent animal models exist & therapy can be easily tested
- Present gene therapy shows partial correction of hemophilia in dog & mouse
models
- Epsilon – amino capric acid (EACA or Tranexamic acid – oral dose) can also
be used.
The standard dose is 4 gm of EACA by mouth every 4-6 hrs for 7-10 days or
0.25mg/kg body weight post operatively 3-4times a day. Contraindicated in patient
with hematuria due to association with upper urinary tract obstruction.
Causes are
*Thromboplastin release
-Sepsis
- Malignancies (adenocarcinoma)
- Haemolysis
- Fat emboli
- Placental absorption
- Amniotic fluid bolus
Management
– Prognosis poor
-Aggressive Rx required. Patient may survive early complications but may end up with
late complication
It has been suggested that in recent years in many patients oral surgical
procedures can be done without alteration of then regular oral anticoagulation therapy
(OAT).
A survey conducted in USA has shown that 96% of oral surgeons prefer
alteration of anticoagulant in patients with low risk of thromboembolism .
It has been argued that oral anticoagulation regimen should be altered to low
molecular weight heparin (LMWH) used with postoperative management. The
advantage being in case of excessive bleeding there is antogonist – protamine sulphate
that could be used.
CONCLUSION:-
Treatment of patients with bleeding disorders presents a unique challenge .
Knowledge of specific coagulation defect is essential for proper management and
requires close consultation and co-ordination with patients physician & hematologist.
The conservative approach in treatment & management is recommended. When
local anesthetic is used , bleeding risk only relates to surgical site & can be controlled
with local homeostasis – Thus replacement Therapy is not absolutely necessary .
Proper oral hygiene instructions , preventive therapy & conservative management are
key for treating patient with blood coagulopathies.
REFERENCES