4 hemorrhage rt(78) dr. rahul tiwari

05/03/23 12:05 PM4.HEAMORRHAGE AND ITS MANAGEMENT/RT/80 1

HEAMORRHAGE AND ITS MANAGEMENT

Dr. Rahul Tiwari – 2nd Yr. MDS – PG Student.

Department of Oral & Maxillofacial Surgery.


DEFINITIONHISTOLOGYCLASSIFICATIONPHYSIOLOGYDIAGNOSISMANAGEMENTCOMPLICATION

CONTENTS


THE TERM HAEMORRHAGE MEANS ESCAPE OF BLOOD FROM THE BLOOD VESSEL

HAEMORRHAGE

05/03/23 12:05 PM4.HEAMORRHAGE AND ITS

MANAGEMENT/RT/804

Histology of vessel wall

• Tunica intima

• Tunica media

• Tunica adventitia

Vascular system


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Large elastic arteries

Muscular arteries

Structure of blood vesselVascular system


MANAGEMENT/RT/806

Arterioles

Capillaries



MANAGEMENT/RT/807

Venules

Veins



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Structure of blood vessel

Arteriovenous anastomosis

Vascular system

Modified smooth muscles


MANAGEMENT/RT/809

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


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 calculus2.Broken bone piece3.Pre existing extensive granulation tissue in the

extraction socket


May occur 24 hours after surgery to several days

CAUSES ARE

1. Dislodgement of clot2. Secondary trauma to the wound3. Elevation of blood pressure4. 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 1 CLASS 1 CLASS 2CLASS 2 CLASS 3CLASS 3 CLASS 4CLASS 4

BLOOD LOSS BLOOD LOSS UPTO 750UPTO 750 750 -1500750 -1500 1500 - 2000 1500 - 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

URINE URINE >30>30 20-3020-30 5-155-15 NEGLIGBLENEGLIGBLE

FLUID FLUID REPLACEMENTREPLACEMENT

CRYSTALLOIDCRYSTALLOID CRYSTALLOIDCRYSTALLOID CRYSTALLOID CRYSTALLOID AND BLOODAND BLOOD

CRYSTALLOID CRYSTALLOID AND BLOODAND BLOOD

4.HEAMORRHAGE AND ITS MANAGEMENT/RT/80 1905/03/23 12:05 PM


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 function2. There is linear relationship between platelet

count and bleeding time3. 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 TIMEPTT 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 numbness2. Development of aseptic necrosis3. 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 cauteryIn 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 lesionsAlso used to control bleeding in patients who have coagulation disordersCOMMONLY USED LASERS: Argon , pottasium titanyl phosphate ,co2 , Nd :YAG lasersACTION: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 FIt is not treated to inactivate virus and is at

increased risk of viral transmission

ETHAMSYLATE:It acts by correcting platelet adhesionIt is given as prior to surgery


FRESH FROZEN FRESH FROZEN PLASMA PLASMA

1 UNIT /ML1 UNIT /ML

CRYOPRECIPETATCRYOPRECIPETATEE

5-10 UNIT/ML5-10 UNIT/ML

PLASMA DERIVED PLASMA DERIVED LYOPHILISED LYOPHILISED FACTOR 8 FACTOR 8 CONSENTRATESCONSENTRATES

250-500 UNIT/VIAL250-500 UNIT/VIAL

GENETICALLY GENETICALLY ENGINEERED ENGINEERED 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 acidMonsels solutionMann haemostatic agentTea 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 cutThe 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 BEDONE 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 surgeryCawson and scully , Dental management of

medically compromised patientsKilleys fracture of midfaceDas , clinical surgeryDental clinics of North America , LASERSRowe and williams maxillofacial injuries

REFERENCES

4.HEAMORRHAGE AND ITS MANAGEMENT/RT/80 8005/03/23 12:06 PM

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4 hemorrhage rt(78) dr. rahul tiwari

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