4 hemorrhage rt(78) Dr. RAHUL TIWARI

09/19/16 09:09 AM 4.HEAMORRHAGE AND ITS MANAGEMENT/RT/80 1
HEAMORRHAGE AND ITS
MANAGEMENT
Dr. Rahul Tiwari – 2nd
Yr. MDS – PG Student.
Department of Oral & Maxillofacial Surgery.

DEFINITION
HISTOLOGY
CLASSIFICATION
PHYSIOLOGY
DIAGNOSIS
MANAGEMENT
COMPLICATION
CONTENTS

THE TERM HAEMORRHAGE MEANS ESCAPE OF
BLOOD FROM THE BLOOD VESSEL
HAEMORRHAGE

09/19/16 09:09 AM
4.HEAMORRHAGE AND
ITS MANAGEMENT/RT/804
Histology of vessel wall
• Tunica intima
• Tunica media
• Tunica adventitia
Vascular system

09/19/16 09:09 AM
4.HEAMORRHAGE AND
Large elastic arteries
Muscular arteries
Structure of blood vessel
Vascular system

09/19/16 09:09 AM
4.HEAMORRHAGE AND ITS
MANAGEMENT/RT/806
Arterioles
Capillaries
Vascular system

09/19/16 09:09 AM
4.HEAMORRHAGE AND
Venules
Veins
Vascular system

09/19/16 09:09 AM
4.HEAMORRHAGE AND
Arteriovenous anastomosis
Vascular system
Modified smooth
muscles

09/19/16 09:09 AM
4.HEAMORRHAGE AND
Vascular system

DEPENDING UPON THE TYPE OF
HAEMORRHAGE
CLASSIFICATION

1. ARTERIAL
2. VENOUS
3. CAPILLARY
ARTERIAL:
 Bleeding is from ruptured artery
 Pulsatile, brisk and bright red in colour
HAEMORRHAGE

VENOUS HAEMORRHAGE:
 Blood loss from vein
 Bleeding is dark in colour and flows in even stream
 There is more flow from veins of face when compared to
other parts of body due to:
- Lack of valves in veins of facial region
- Extensive communication

 Oozing from capillaries
 No bleeding point can be made out
 Intermediate in colour as compared to arterial and venous
blood
 Can be controlled by simple pressure with guaze pads as it is
not severe
 In coagulation disorders there is extensive loss from
capillaries
CAPILLARY HAEMORRHAGE

09/19/16 09:09 AM4.HEAMORRHAGE AND ITS MANAGEMENT/RT/80 14
Divided into:
• Primary
• Intermediate
•
Secondary
MECHANICAL HAEMORRHAGE

PRIMARY HAEMORRHAGE:
 Occurs at the time of injury
 Haemostatic agents in the body attempts to stop
bleeding by the formation of clot
INTERMEDIATE HAEMORRHAGE:
 Occurs within 24 hours after the operation
Causes are:
1. Loose foreign body in the wound like calculus
2.Broken bone piece
3.Pre existing extensive granulation tissue in the
extraction socket

 May occur 24 hours after surgery to
several days
CAUSES ARE
1. Dislodgement of clot
2. Secondary trauma to the wound
3. Elevation of blood pressure
4. Infection
SECONDARY HAEMORRHAGE:

INTERNAL:
-It is also called concealed bleeding
-confined within the body cavity and not
apparent on the surface
EXTERNAL:
-Blood escaping through wound in the skin
Haemorrhage can be:

This type of haemorrhage is due to the absence of
one or more factors necessary for normal
coagulation mechanism
May be genetically conditioned disorder or
acquired or through the drugs that depress the
formation of the necessary elements for coagulation
BIOMECHANICAL HAEMORRHAGE

CLASS 1CLASS 1 CLASS 2CLASS 2 CLASS 3CLASS 3 CLASS 4CLASS 4
BLOOD LOSSBLOOD LOSS UPTO 750UPTO 750 750 -1500750 -1500 1500 - 20001500 - 2000 >2000>2000
BLOOD LOSS %BLOOD LOSS % UPTO 15%UPTO 15% 15 – 30%15 – 30% 30 – 40%30 – 40% >40%>40%
PULSE RATEPULSE RATE <100<100 >100>100 >120>120 >140>140
B PB P NORMALNORMAL NORMALNORMAL DECREASEDDECREASED DECREASEDDECREASED
PULSEPULSE NORMALNORMAL DECREASEDDECREASED DECREASEDDECREASED DECREASEDDECREASED
R RATER RATE 14 -2014 -20 20-3020-30 30-4030-40 >35>35
URINEURINE >30>30 20-3020-30 5-155-15 NEGLIGBLENEGLIGBLE
4.HEAMORRHAGE AND ITS MANAGEMENT/RT/80 1909/19/16 09:09 AM

There are four important steps-
1. Injured blood vessel in an attempt to reduce blood flow
undergoes constriction due to spasm in the vessel wall
2. In the second step there is activation of platelets and
formation of platelet plug which leads to primary
haemostasis
3. In the third step there is activation of clotting mechanism
and formation of clot leading to completion of secondary
haemostasis
4. In final step there is fibrous organisation of the clot.
NORMAL HAEMOSTASIS

FACTORSFACTORS ALTERNATIVE NAMESALTERNATIVE NAMES
11 FIBRINOGENFIBRINOGEN
22 PROTHROMBINPROTHROMBIN
33 TISSUE THROMBOPLASTINTISSUE THROMBOPLASTIN
44 CALCIUMCALCIUM
55 PRO ACCELERINPRO ACCELERIN
66 NOT PRESENTNOT PRESENT
77 PROCONVERTINPROCONVERTIN
88 ANTI HAEMOPHILIC FACTORANTI HAEMOPHILIC FACTOR
99 CHRISTMAN FACTORCHRISTMAN FACTOR
1010 STUART PROWER FACTORSTUART PROWER FACTOR
1111 PLASMA THROMBOPLASTIN ANTICIDPLASMA THROMBOPLASTIN ANTICID
1212 HAGEMAN FACTORHAGEMAN FACTOR
1313 FIBRIN STABLIZING FACTORFIBRIN STABLIZING FACTOR
Procoagulant factors

COAGULATION PATHWAY

It is 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
In formation of primary haemostatic plug there is
platelet adhesion ,release of granules and platelet
aggregation
PRIMARY HAEMOSTASIS

It is the activation of clotting process in plasma that
ultimately results in the formation of fibrin which
strengthens in primary haemostatic plug
Completed in several minutes
It is important in bleeding from larger vessels
It is continuous process and there are approximately 40
substances which affect clotting
Substances which promote clotting are called pro coagulants
and those that prevent clotting are called anti coagulants
At the time of injury to the vessels these procoagulant
factors are activated and balance tilts in favour of
coagulation and formation of clot occurs
SECONDARY HAEMOSTASIS

Careful evaluation with coordinated history and physical examination provides
valuable clues as abnormality lies in
-The vessel walls
-Platelets
-In the process of coagulation
HISTORY SHOULD INCLUDE:
1.Is there any personal or family history of a bleeding tendency?
2.Has the patient undergone surgery or dental extraction previously?
3.Is there any history of haematuria , gastrointestinal haemorrhage, easy bruising ,
haemarthrosis or epistaxis?
4.Is there any history of cancer or collagen vascular disease?
5.What medications is the patient taking or has taken recently?
6.Is the patient on any special diet ?
CAREFUL EVALUATION OF THE
BLEEDING PATIENT

Assesment of skin and mucosal surface is
mandatory
Bleeding into superficial skin and soft tissue usually
seen as small capillary haemorrhages ranging from
size of pin head to large area of ecchymoses
Haemorrhage into synovial joints is virtually
diagnostic of severe hereditary coagulation
disorder
PHYSICAL EXAMINATION

MAJORITY OF THE HAEMOSTATIC DEFECTS
CAN BE SCREENED BY FOUR TESTS:
 BLEEDING TIME:
1. It is sensitive measure of platelet function
2. There is linear relationship between platelet count
and bleeding time
3. This assess the interaction between platelets and a
damaged blood vessel and the formation of a platelet
plug
4. Patients with bleeding time more than 10 min are at
increased risk of bleeding
5. BT may be abnormal in Thrombocytopenia , platelet
defects, von willebrand’s disease and in some patients
with qualitative platelet defects
6. Dukes bleeding time should not exceed 3.5 min and
Ivy method has an upper limit of 5 min
LABORATORY TESTS FOR SCREENING

PROTHROMBIN TIME:
Screens the extrinsic limb of coagulation pathway
and factors 1 , 2 and 5 of common pathway
PT is prolonged in patients who are on warfarin
therapy , vitamin k deficiency or deficiency of
factor 5 , 7 ,10 , prothrombin and fibrinogen
Normal prothrombin time is 12-14 seconds

PARTIAL THROMBOPLASTIN TIME
PTT screens the intrinsic limb of coagulation
This test tests for the adequacy of factors 8 , 9 , 10 , 11 ,
12 of intrinsic system and factors 1 ,2 and 5 0f common
pathway
PTT is prolonged in haemophilia
Normal PTT is less than 45 seconds
It is important to note that PTT is relatively insensitive to
changes in the intrinsic coagulation
A 70 percent decrease in the factor levels may still provide
normal results
Small changes in in the PTT therefore may be of great
significance

THROMBIN TIME :
Detects the qualitative abnormalities in fibrinogen and
circulating anti coagulants.
Failure of the clot to form is consistent with severe
diminution of fibrinogen
PLATELET COUNT:
Normal platelet count is 1,50,000 to 4,50,000per micro litre
of blood
When count becomes 50,000 to 1,00,000 there is mild
prolongation of bleeding time so that bleeding occurs after
severe trauma or surgery
Patients with count less than 50,000 have easy bruising
manifestated as petechia and ecchymosis during trauma
or surgery
Patients with platelet count below 20,000 have an
appreciable incidence of spontaneous bleeding ,which may be
intracranial or any other internal bleeding

Minor oral surgical procedures can be safely done ,
if the platelet count is above 80,000 to 1,00,000
other wise patient needs tansfusion of platelet
rich plasma
When abnormalities are noted in any of the
screening tests , further specific tests like Bio-
assays of coagulation factors are carried in
consultation with haematologist to get exact
diagnosis

1 LOCAL
2 SYSTEMIC
HAEMOSTATIC AGENTS

Local haemostasis is the direct control of
bleeding at the site of injury
The techniques for local haemostasis can be
classified as
1 MECHANICAL
2 THERMAL
3 CHEMICAL
LOCAL HAEMOSTATICS

1. PRESSURE AND PACKING
2. HAEMOSTATS
3. SUTURE AND LIGATION
4 EMBOLIZATION OF VESSELS
MECHANICAL METHODS

Pressure is usually able to control most of the
haemorrhages
Application of pressure basically counteracts the
hydrostatic pressure within the bleeding vessel until
such time , that a clot can form and occlude bleeding
orifice
Pressure should be applied directly over the
bleeding site firmly with gauze pack for at least 10
min
One should not be in hurry and should not lift pack
every minute to see whether bleeding has stopped
PRESSURE

Haemostats are specially designed to catch
bleeding points in the surgical area
Normally used haemostats are mosquito ,
straight and curved
Curved haemostats are used more frequently ,
because of their versatality and ease in tying
the ligature around tip of forceps
Usually thermo coagulation is done after
catching the bleeding point with artery forceps
, if vessel is small
Larger vessels are ligated with sutures
USE OF HAEMOSTATS

HAEMOSTATS

Transected blood vessel may need to be tied with
the help of ligature
Large pulsatile artery is tied with non absorbable
material like 3-0 black silk
Smaller vessels are ligated with 3-0 catgut or
polygalactin
The presence of non absorbable material in the
infected wound can lead to extrusion or sinus tract
formation
Large arteries such as External carotid artery ,
should have double transfixion suture passed
through the wall of vessel to prevent chances of
slipping of ligature
SUTURES AND LIGATION

Exact bleeding point can be localised
Agents used for Embolization include steel coils ,
polyvinyl alcohol foam , gel foam , silicon spheres ,
methyl methacrylate
Particles are placed via catheter super selectively into
the bleeding vessel usually via femoral artery
After percutaneously puncturing femoral artery a guide
wire is then inserted into the vessel followed by a
100cm long catheter
EMBOLIZATION OF VESSELS

This catheter is guided into various branches
of External carotid artery under constant
flouroscopic control
Vessels investigated for oral and peri oral
lesions include facial , lingual , transverse facial
, maxillary artery
After individual vessels are identified ,
contrast media is injected via catheter and
films are obtained
After lesions are completely mapped
angiographically the angiograms are studied
and Embolization of vessel can be carried out
by various agents

If active bleeding is occuring during
embolization , there will be preferential
flow of emboli to the traumatized area
because of faster decline of blood
pressure at bleeding site
Particles of smaller size are used to allow
them to exert their effect as distally as
possible so that haemorrhage from
collateral channels that open after
embolization is less likely
The procedure is completed when
blockage of flow into the distal branches
of artery is noted on fluoroscopy

 Principle precaution with the
embolization technique is to prevent
reflux of emboli down to E C A ,
because of entrance of emboli into I C
A could lead to cerebral embolization
and stroke
SIDE EFFECTS:
1. Transient local numbness
2. Development of aseptic necrosis
3. Fever
4. Oedema
PRECAUTIONS

1. CAUTERY
2. ELECRO CAUTERY
3. CRYOSURGERY
4. ARGON BEAM COAGULATOR
5. LASERS
THERMAL AGENTS

CAUTERY:
Heat achieves denaturation of proteins which
results in coagulation of larger areas of tissues
Heat is transmitted by instrument and conducted
directly to the tissues
Previously dental burnisher like instrument is
directly heated over flame and applied directly to
bleeding point in oral cavity

ELECTRO CAUTERY:
In electrocautery, source of heat is alternate
current
Can be directly applied or catching bleeder
with haemostat
Causes sealing of vessel through action of heat
Cannot be used for controlling bleeding from
larger vessels

ELECTROCAUTERY

CRYOSURGERY:
Extreme cooling has been used for
haemostasis
Temp ranging from -20 to -180 degrees
are used
At this temp tissues , capillaries , small
arterioles, and venules undergo cryogenic
necrosis
This is caused by dehydration and
denaturation of lipid molecules
Used to treat haemangiomas

ARGON BEAM COAGULATOR:
Represents new form of electro cautery
In this coagulator mono polar current is
transmitted to tissues through the flow of argon
gas
Tip of the coagulator is held approximately 1cm
from the tissue
Argon gas clears the surgical site of fluids to
allow the current to be focussed directly on
tissue
There is possibility of gas embolism as the
stream of gas in contact with the tissue and can
be eliminated by not placing the hand piece in
direct contact with the tissue

Lasers are commonly used for wound haemostasis
 To control bleeding encountered during
management of extraoral and intraoral vascular
lesions
Also used to control bleeding in patients who have
coagulation disorders
COMMONLY USED LASERS:
Argon , pottasium titanyl phosphate ,co2 , Nd :YAG
lasers
ACTION:
The use of laser results in contraction of collagen
that is contained within the vascular wall , causing
constriction of vascular lumen resulting in sealing of
vessels
LASERS

WHOLE BLOOD
PLATELET RICH PLASMA
FRESH FROZEN PLASMA
CRYOPRECIPITATE
CRYSTALLOIDS
COLLOIDS
SYSTEMIC AGENTS

It is indicated when there is excess blood loss with the
symptoms of hypovolaemic shock
Fresh blood contains all the factors for coagulation
Used when specific components are not available to treat
haemostatic defect
Banked blood is poor source of platelets but stable in
factor 2 , 7 , 9 , 11
Should be typed and cross matched before transfusion
Must be checked for Hepatitis B , C , HIV , Malaria
WHOLE BLOOD

Can be collected from whole blood OR directly from
patient via plasmapheresis
Plasma concentrates are viable for three days when
stored at room temperature
It is advisable to elevate the platelet levels to range
of 50,000 to 1,00,000 per microlitre to provide
adequate protection
One unit raises the platelet count to 7000 to 10000
Indicated in thrombocytopenic patients
PLATELET RICH PLASMA

FRESH FROZEN PLASMA:
One unit (150 ml) of fresh frozen plasma is usually
contains all the coagulation factors including 200 of
factor factor8 and
factor9 and 400mg of fibrinogen
CRYOPRECIPITATE:
A 15 ML of this contains 100mg of factor8 , 250mg
of fibrinogen , V W F
It is not treated to inactivate virus and is at
increased risk of viral transmission
ETHAMSYLATE:
It acts by correcting platelet adhesion
It is given as prior to surgery

FRESH FROZENFRESH FROZEN
PLASMAPLASMA
1 UNIT /ML1 UNIT /ML
CRYOPRECIPETATECRYOPRECIPETATE 5-10 UNIT/ML5-10 UNIT/ML
PLASMA DERIVEDPLASMA DERIVED
LYOPHILISEDLYOPHILISED
FACTOR 8FACTOR 8
CONSENTRATESCONSENTRATES
250-500 UNIT/VIAL250-500 UNIT/VIAL
GENETICALLYGENETICALLY
ENGINEEREDENGINEERED
FACTOR 8FACTOR 8
250-500 UNIT/VIAL250-500 UNIT/VIAL
Sources of factor 8

Quite effective in arresting the capillary bleeding and
post extraction bleeding in medullary bone
Tannic acid
Monsels solution
Mann haemostatic agent
Tea bag
CHEMICAL AGENTS

ABSORBABLE COLLAGEN HEMOSTATIC SPONGE:
(Helistat)
- Fabricated from collagen obtained from bovine deep flexor.
- On contact with blood cause aggregation of platelets which
degranulate and release coagulation factors.
- Completely absorbed within 14 – 56 days.
MICROFIBRILLAR COLLAGEN : (Avitene)
- Bovine collagen shredded into fibrils.
- Larger surface are is yielded.
- Disadvantage: When used in extraction sockets causes dry
socket.

ABSOBABLE GELATIN: (Gel
foam)
- Sponge prepared from purified gelatin solution.
- Provides a matrix on which clot may be organized.
- Completely absorbed within 4 – 6 weeks.
- Should not be used in the presence of frank
infection as it will absorb infected fluid and serve as
nidus for abscess formation.
BONE WAX:
- Mixture of beeswax and isopropyl palmitate (wax
softening agent).

HEMOSTASIS IN BLEEDING BONE:
Bleeding from small vessels emerging from the cortical
plate of maxilla or mandible can be controlled by
burnishing the entrance of the bony canal with the sharp
end of periosteal elevator or with a small hemostat.

Bone wax is possibly the most effective way to plug blood
vessels in bleeding bone.
A small piece of wax is warmed to desired consistency and
is forced into the bleeding channels to mechanically plug
them.

- Minimally resorbable. Should not be used where rapid osseous
regeneration is required and in an area that is infected or in
which periapical pathology is present.
OXIDIZED REGENERATED ABSORBABLE
CELLULOSE: (Surgicel Absorbable Hemostat)
- Prepared from the oxidation of regenerated cellulose.
- Accelerates clotting by serving as a matrix for the formation
of clot and it swells after saturation with blood.
- Material not to be left in bony cavities because of
interference with osteogenesis and risk of cyst formation.

OXIDIZED CELLULOSE: (Surgicel)
- Prepared by controlled oxidation of cellulose.
- Not resorbable, should be removed once hemostasis is
achieved.
THROMBIN: (Thrombostat)
- Bovine origin, catalyzes conversion of fibrinogen to fibrin.
TRANEXIMIC ACID: (Cyklokapron)
- Derivative of aminoacid Lysine.
- 6 -10 times potent than EACA.

- Forms reversible complex that displaces plasminogen from
fibrin, resulting in inhibition of fibrinolysis and inhibition of
conversion of plasminogen to plasmin.
FIBRIN SEALENTS: ( Tisseal )
- Synthetic fibrin type glue.
- Has 2 components: Component 1 has Fibrinogen , Factor XIII
Calcium Chloride. Component 2 has bovine thrombin and
antifibrinolytic agent.
- Increased fibrinogen concentration – increased binding
strength.
- Thrombin catalyzes conversion fibrinogen to fibrin.
- Factor XIII – initiate cross linking of fibrin clot.

Includes simple measures and is usually under taken
by placement of immobilizing external bandages
Temporary immobilization is afforded well by classical
FUNDA MAXILLA OR BARREL BANDAGE
These prevent further displacement and enhance
haemostasis and analgesia through immobilization of
fragments
Fixation of maxilla against base of skull may be
achieved by spatula dressing
TEMPORARY HAEMOSTASIS IN
MAXILLOFACIAL INJURIES

A wooden spatula or tongue depressor is
placed over the occlusal plane of the maxillary
teeth at the level of premolars
This is pulled against the base of the skull
through elastic bandage or with knotted
rubber band running over top of the head
Haemorrhage in the region of oral cavity
frequently cease after placement of gauze
pads and immobilization with FUNDA
MAXILLA OR CHIN SLING DRESSING

CHIN SLING AND SPATULA
DRESSINGS

This artery runs anteriorly from the greater palatine foramen
in sub mucosa of hard palate in groove between the horizontal
palatine process of maxilla and inner plate of alveolar process
Incision should be made parallel , rather than perpendicular to
this vessel
If accidental injury occurs bleeding is copious and application of
clamp is difficult
Most of the times , can be controlled by pressure packs
A round bolus of guaze is made of adequate size , so that it
does not cause gagging
It is kept in place by tie over sutures for 24- 48 hrs and can be
safely removed after 48 hrs
GREATER PALATINE ARTERY

It is a second branch of external carotid artery arising
just below Facial artery
Its exposure is done in sub mandibular triangle
Undertaken via sub mandibular incision of skin lying over
hyoid bone , approximately two finger breadths below the
lower margin of mandible in natural skin fold
After lower pole of sub mandibular gland and digastric
tendon exposed, the gland is turned upwards to expose
the posterior margin of mylohyoid muscle
LIGATION OF LINGUAL ARTERY

The hypoglossal nerve and lingual vein
are found over the deeply located
hyoglossus muscle which are then freed
and turned dorsally upwards
Then the hyoglossus muscle is divided to
expose the lingual artery at a point after the
branching for the base of the tongue and
ligated

Injury to this artery occurs accidentally by rotary discs or
slippage of sharp instruments working on mandibular
teeth
Can also occur while placing mandibular implant leading
to large sublingual haematoma which if not controlled can
compromise airway and may be life threatning
Local clamping of the artery and application of
electrocautery usually controlls bleeding
Because of the anatomic variation in most of the cases it
is a branch of submental artery but in significant cases it
is a branch of lingual artery
So sometimes ligation of lingual artery may not stop the
bleeding from sublingual artery, in these cases facial
artery need to be ligated
LIGATION OF SUBLINGUAL ARTERY

It is a third anterior branch of External carotid artery
Can be easily ligated at the point where it crosses lower border of
the mandible just anterior to the masseter muscle
Pulsation of the artery can be felt when the patient is asked to
clench the teeth
Facial vein lies posterior to it in majority of the cases
Marginal mandibular nerve crosses superficially over the facial
artery and vein
Sub mandibular incision is given 1-2 cm below the lower border of
the mandible
Skin , subcutaneous tissue , platysma and deep fascia are cut
The tissues are retracted upwards and artery lies just anterior to the
masseter muscle which is isolated and tied
LIGATION OF FACIAL ARTERY

Massive bleeding from the maxillary artery is not
usually controlled by nasal tamponade so, ligation
of supplying artery is required
Situated deep and direct ligation is difficult
This artery is at risk during surgery of TMJ , as it
lies medial to condylar neck
Ligation of maxillary artery can be done via
antrum through caldwell-luc approach OR ligation
of the artery can be done at the angle of the
mandible
LIGATION OF MAXILLARY ARTERY

Terminal branch of External carotid
artery
Can be managed by direct identification
of bleeding point and Electro coagulation
Pulsations of artery felt just anterior to
pre auricular region
This artery is usually encountered during
surgery of TMJ through pre auricular
incision and artery can be exposed
through same incision for ligation
LIGATION OF SUPERFICIAL
TEMPORAL ARTERY

Divides into External and Internal carotid arteries at the level of
superior thyroid cartilage
Some times division can take place at the level of hyoid bone or
slightly superior
Superior thyroid , lingual and facial are anterior branches
Occipital , posterior auricular are posterior branches
Maxillary and superficial temporal are terminal branches
LIGATION OF EXTERNAL CAROTID
ARTERY

LIGATION OF THIS ARTERY CAN BE
DONE AT TWO PLACES DEPENDING
ON SITE OF BLEEDING
1. Just above the origin of superior thyroid artery in
carotid triangle which will eliminate bleeding from
all the branches except from superior thyroid
artery
1. Can be ligated higher up in the retro mandibular
fossa , when the bleeding is exclusively from
maxillary artery or its branches

Kruger and Schilli , Oral and Maxillofacial
traumatology
 Archer , oral surgery
Cawson and scully , Dental management of
medically compromised patients
Killeys fracture of midface
Das , clinical surgery
Dental clinics of North America , LASERS
Rowe and williams maxillofacial injuries
REFERENCES

4.HEAMORRHAGE AND ITS MANAGEMENT/RT/80 8009/19/16 09:09 AM
Thank you


4 hemorrhage rt(78) Dr. RAHUL TIWARI

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