Management of Bleeding in

Oral Surgery

Presented by : P. Santosh, IV BDS.

Guided By: Dr. Ramesh, MDS.,
Department of Oral and Maxillofacial
Surgery

What is Bleeding ?
Bleeding (haemorrhage)
is just escape of blood
from vessel
Hemorrhage can occur
during all surgical
procedures and its
management depends
upon whether the patient
is hematologically normal
or suffers from some
disturbance in the normal
clotting mechanism.

What causes Bleeding in oral

surgery ?
Hemorrhage following Oral Surgical
procedures can occur due to local (soft
tissue or bone) or systemic causes.
(heriditary conditions such as hemophilia, Von
Willebrands disease)
In healthy patients the postoperative
bleeding is mainly due to local causes.

Local causes
Soft tissue i.e
arterial, venous, or
capillary in nature.
Venous blood is dark
red in color and flows
steadily and heavily
Arterial bleeding is
bright red and spurting
in nature.

Bone
Bone appears to
bleed in case of injury
to inferior alveolar
artery, or from central
vascular lesions
(Hemangioma or
Vascular malformation)

Systamic causes

1. hereditary conditions ( Hemophilia)

2. thrombocytopenia
3. Leukemias
4. uncontrolled hypertension
5. oral anticoagulants like Aspirin or Warfarin
6. Chronic Liver disease
7. Vitamin k deficiency

Classification of hemorrhage
American College of Surgeons' Advanced Trauma Life
Support (ATLS)
Class I Hemorrhage involves up to 15% of blood
volume.
Class II Hemorrhage involves 15-30% of total
blood volume. Volume resuscitation with
crystalloids is all that is typically required.
Class III Hemorrhage involves loss of 30-40% of
circulating blood volume.. Fluid resuscitation with
crystalloid and blood transfusion are usually
necessary
Class IV Hemorrhage involves loss of >40% of
circulating blood volume. Aggressive
resuscitation is required to prevent death.

Types of hemorrhage
Primary Heamorrhage :
This occurs during the
surgery, as a result of
injury like cutting or
laceration of the
artery or bleeding from
bone.
This also occurs when
surgery is done in an
infected area with a lot
of granulation tissue.

Reactionary Hemorrhage
This type of bleeding occurs
within a few hours after
surgery.

Patients who have

unknowingly disturbed /
dislodged the clot are also
prone for this type of
bleeding.

Types of hemorrhage

Secondary
hemorrhage
This occurs after 7 to
10 days after surgery.
This is mainly due
to
1. Increased BP
2. opening of ligature
3. Trauma
4. infection

Types of hemorrhage
External bleeding

Internal bleeding

Spontaneous bleeding

Haemostasis??
It is stasis or arrest in flow of
blood, a natural tendency to
prevent hemorrhage (simply
blood clot formation)
This occurs in 3 steps
Vascular phase When a blood
vessel is damaged,
vasoconstriction results.
Platelet phase : Platelets

adhere to the damaged surface

to form a temporary plug.

Coagulation phase Conversion of

fibrinogen to fibrin is complete.
Fibrin tightly binds the platelets to
form a tight clot

Clinical Evaluation of patient

History:
Family history of bleeding?
Complication during
previous surgery?
History of hematuria, easy
brusing,epistaxis,
menorrahgia?
History of cancer or
collagen vascular diseases
diagnosed?
Any drug or medication
patient is on?

Examination
Anemia
Petechial spots?
Echymosis or
telengestesia?
Spleen, Liver
enlargement?
Singns of liver failure?
Bleeding in synovial
joints? ( hereditary
coagulopathies)

Lab Reports

PLATELET COUNT
BLEEDING TIME (BT)
PROTHROMBIN TIME (PT)
PARTIAL THROMBOPLASTIN TIME (PTT)
THROMBIN TIME (TT)
Others
HB- TC- DLC -CT ESR PCR
Screening test for Blood Guucose and HIV infection

Lab reports
BT : 2-8 min.PROVIDES ASSESSMENT OF

PLATELET COUNT AND FUNCTION

CT : 2-5 mins to rule out related disorders
PT: 20- 40 secs. Measures Effectiveness of
the Extrinsic Pathway
PTT : 25- 40 secs.Measures Effectiveness of the
Intrinsic
Pathway

Altered lab reports..

Platelets

100,000 - 400,000 cell/ cu mm

< 100,000
Thrombocytopenia
50,000 - 100,000
Mild Thrombocytopenia
< 50,000 Severe Thrombocytopenia

WBC 7000-11000 cells/cu mm

RBC 4-6 lakh cells / cu mm

Management of Primary Hemorrhage in

Normal patients
The management of bleeding during surgery
(Primary bleeding) can be achieved by the
following means:
1.Mechanical methods
2.Thermal agents
3.Chemical methods
4.Systemic agents
5.Ligation of related blood vessels

1.Mechanical methods

2. Thermal methods

3. Chemical methods

Ligation of vessels

Greater palatine
Lingual artery
Sublingual artery
Facial artery
Maxillary artery

Superficial temporal artery

External carotid artery

Systemic agents

Hemophilia management
Deficiency of factor VIII ( hemophilia A) or
IX (hemophilia A) or hemophilia.

Management in special patients

Haemphilia A, von Willebrands disease

Patient on Anti- Coagulant therapy
Uncontrolled Hypertensive patient
End stage liver disease
Early diagnosis:
Identification of systemic problem and referral for
physician's advice.
Use of local hemostatic aids after controlling
systemic effects of the disease is helpful

Classification of coagulation disorders

Congenital X-linked
Haemophilia A and B
Autosomal
Von Willebrand disease
Factor II, V, VII, X, XI and
XIII deficiencies
Combined II, VII, IX and
X deficiency
Hypofibrinogenaemia and
Dysfibrinogenaemia
Acquired
Liver failure

Increased consumption
Coagulation activation
Disseminated
intravascular
coagulation (DIC)
Immune-mediated
Acquired haemophilia
and von Willebrand
syndrome
Drug-induced
Inhibition of function
Heparins
Lepirudin
Inhibition of synthesis
Warfarin

Hemophilia management
Factor VIII concentrate.
Desmopressin (0.3 micro gm/ kg diluted in 100ml saline
given in 30 mins)
Tranaxemic acid (3-4 gm Tb or 0.5- 1 mg IV)
Episilon aminicaproic acid (5mg 1mg 8th hourly)
AVOID
Complicated surgeries
IV injections in severe cases
Check
INR value 2-3 , PT 20-22 secs is check and treatment is
done on patient on warffarn.
Stop aspirin prior to extractions for 5 days.
Always check BP values for a hypertensive patient.

Von Willebrands disease

It is most commonly inherited disorder, occurs
due to deficiency of von willebrands factor.
(synthesised by endothelial cells and megakaryocytes
always bound to F VII as a complex. )
Most patients with von Willebrand disease have
type 1 vWD which is characterised by a
quantitative decrease in a normal functional
protein.
Patients with type 2 disorders inherit vWF
molecules which are functionally abnormal

Von Willebrands disease

Investigations reveal:
Reduced activity of vWF and factor VIII,
and a prolongation of the bleeding time
Management:
The vasopressin receptor agonist DDAVP
raises the vWF and factor VIII levels by 34-fold, which is useful in arresting bleeding
in patients with Von Willibrands disease
and mild or moderate haemophilia A

Liver diseases..
There is reduced hepatic synthesis, e.g. of
factors V, VII, VIII, IX, X, XI, prothrombin
and fibrinogen. Thrombocytopenia may
occur secondary to hypersplenism in
portal hypertension. In cholestatic jaundice
there is reduced vitamin K absorption,
leading to deficiency of factors II, VII, IX
and X

Small note on Complications

Shock (hypovolumic)
Infection transfer during transfusion
Exsanguination ( complete loss of blood)
Death of patient

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