This is a presentation on hemorrhage and shock in oral and maxillofacial surgery

1. HEMORRHAGE AND SHOCK:
ITS MANAGEMENT IN ORAL SURGERY
Dr. Genene Getachew
Dental intern at jimma
university, Ethiopia
-2024 -
1

2. OUTLINE
• Introduction
• Definition of Hemorrhage
• Classification of hemorrhage
• Hemostasis
• Clinical Evaluation of the Bleeding Patient
• Shock
• Classification of shock
• Managements of shock
2

3. Introduction
• Hemorrhage is related to bleeding or
abnormal flow of blood
• It can occur in greater or lesser degree during
all surgical procedures and its management
depends on situation of the patient.
• Usually hemorrhage is followed by shock
3

4. HEMORRHAGE
Definition
• Hemorrhage (Hemo + rrhage) denotes the
escape of blood from a blood vessel
• Any damage to the vasculature leads to out
flow of blood
• Loss of blood due to any reason beyond a
certain point is potentially life threatening and
may lead death.
4

5. Classification of hemorrhage
based on source
of blood loss
Arterial hemorrhage
-bright red in color
Venous
hemorrhage
-dark in color
Capillary
hemorrhage
-bluish bright red in
color
Based on time of
occurrence
Primary hemorrhage
-Occurs at time of
surgery or extraction
Intermediate hemorrhage
-occurs within eight hours
Secondary hemorhage
-bleed again after 24 hours to several days
-causes: trauma, clot dislogement, infection
Visualisation of
hemorhage
Internal hemorrhage
External
hemorrhage
5

6. Based on source of blood loss
arterial hemorrhage
• is bleeding from a ruptured artery.
• is pulsatile, brisk and bright red in color.
venous hemorrhage
• Loss of blood from a vein
• is dark in color and blood flows in an even stream.
capillary hemorrhage
• blood oozes from the area and no bleeding point can be
made out.
• The blood is bluish bright red in color
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7. Based on time of occurrence
Primary hemorrhage
• occurs at the time of injury.
intermediate hemorrhage
• bleeding occurring within 8 hours after
stoppage of primary bleeding .
Causes: calculus, broken bone piece, and
preexisting extensive granulation tissue
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8. Cont..
secondary hemorrhage
wound starts to bleed again after 24 hours to
several days
It may be due to:
– dislodgment of clot;
– secondary trauma to the wound;
– infection
– elevation of patient’s blood pressure
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9. Internal or External Bleeding
internal or concealed bleeding
 confined within the body cavity and is not
apparent on the surface
external bleeding
 blood escaping through a
wound in the skin
9

10. Cont..
Spontaneous Bleeding
• occur without any provocation, e.g. in
acquired (patients on oral hypoglycemic
agents—decreased platelets count) and
hereditary coagulopathies
10

11. HEMOSTASIS
mechanism of stoppage of bleeding
• Stages of hemostasis
»Vascular stage
»Platelet stage
»Coagulation cascade
» fibrous organization
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12. Primary Hemostasis
• process of platelet plug formation at the site of
injury
• occurs within seconds of injury
• is important in stoppage of blood from small
arterioles, venules and capillaries.
• Platelet adhesion, release of granules and
platelet aggregation resulting in formation of a
primary hemostatic plug
12

13. Secondary Haemostasis
• the activation of clotting process in plasma
• it ultimately results in the formation of fibrin
which strengthens the primary haemostatic
plug.
• completed in several minutes
• important in stopping bleeding from larger
vessels
13

14. Cont...
• Coagulation mechanism is a continuous process
• there are approximately 40 substances, which affect
clotting
• Pro-coagulants
• those promote clotting
• Anticoagulants
• prevent clotting
 Normally, there is fine balance between these factors and
blood usually does not coagulate inside the body.
14

15. Cont..
• Whenever there is an injury to the vessels
these procoagulant factors are activated
and balance tilts in favor of coagulation and
there is formation of a clot.
15

16. Coagulation reactions
Reaction 1
• is intrinsic or contact phase of coagulation.
• In this phase, mainly factors VIII, IX, XI, XII
along with calcium and plasma proteins take
part.
• Partial thromboplastin time (PTT) screens this
intrinsic limb of the coagulation
16

17. Cont..
Reaction 2
• is extrinsic pathway for initiation of coagulation.
• there is release of tissue thromboplastin from
injured tissues.
• A protease complex is formed between factor VII,
calcium and tissue thromboplastin, which
activates factor X and takes part in reaction III—
the common pathway.
• Prothrombin time (PT) {laboratory test} screens
the extrinsic limb of coagulation.
17

18. Cont..
Reaction 3
• factor X is activated by proteases
generated in previous two reactions
18

19. Cont..
Reaction 4
• prothrombin is converted into thrombin in the
presence of factor V, calcium and phospholipids.
• Thrombin has got multiple functions in
hemostasis.
• Its main role is conversion of fibrinogen
into fibrin, but it also further activates factor V,
VIII and XIII and helps in platelet aggregation and
secretion
19

20. 20

21. Cont..
21

22. 22

23. Clinical evaluation of the Bleeding
Patient
• history and physical examination
• bleeding abnormality resides in:
– the vessels walls,
– platelets
– in the process of coagulation.
23

24. history should include
• family history of a bleeding tendency?
• Has the patient undergone surgery or dental extractions
previously?
• Is there any history of hematuria, gastrointestinal
hemorrhage, easy bruising, hemarthrosis, menorrhagia, or
epistaxis?
• Is there any history of cancer or collagen vascular
disease?
• What medications is the patient taking or has taken recently?
• Is the patient on any special diet?
24

25. physical examination should note
• adenopathy, splenomegaly, or hepatomegaly
• signs of jaundice, telangiectasias, or any other
stigma of liver disease
• skin and mucosal surface is mandatory
25

26. Laboratory Tests for Screening
Bleeding Time;
• sensitive measure of platelet function
• prolonged in thrombocytopenia, Von
Willebrand’s disease and platelet dysfunction
Platelet Count;
• Minor oral surgical procedure can be safely done,
if platelet count is above 80,000 to 1,00,000 per cumm
• otherwise patient needs transfusion of platelet rich
plasma
26

27. Prothrombin Time;
• screens the extrinsic limb of coagulation pathway
(Factors V, VII and X) and factors
I, II and V of the common pathway
• prolonged in patients, who are on warfarin
anticoagulant therapy, vitamin K deficiency or
deficiency of factor V, VII, X, prothrombin or fibrinogen
• Normal PT is usually 12 to 14 seconds.
27

28. Partial Thromboplastin Time
• screens the intrinsic limb of coagulation pathway
and tests for the adequacy
of factors VIII, IX, X, XI, XII of intrinsic system and
factors I, II, V of the common pathway.
• prolonged in hemophiliacs.
• Normal PTT is less than 45 seconds
If both the tests are prolonged, then factor II, V,
X or vitamin K deficiency and liver disease are
suspected
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29. Hemostatic measures
• In normal coagulation mechanism, hemorrhage
control based on vessel contraction, retraction,
and clot formation
• During any surgical procedure, complete
hemostasis must be achieved before closure of
the wound.
• Direct control of bleeding at the site of injury is
the best method to achieve hemostasis.
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30. Local methods/measures
 mechanical
 thermal
chemical
30

31. Mechanical Methods
Pressure:
• Counteracts the hydrostatic pressure within the
bleeding vessel
• applied directly over the bleeding site firmly over a
gauze pack for at least five minutes
• not lift pack every minute to see whether bleeding has
stopped or not
31

32. Cont..
• hemostat(Mosquito, artery) forceps
• are specially designed to catch bleeding points in the
surgical area.
• These can be straight or curved.
• Usually, electrosurgical thermo-coagulation is done
after catching the bleeding point with hemostat
forceps, if the vessel is small.
32

33. cont..
Sutures and ligation:
When large pulsatile artery needs to be tied, non-
absorbable material like 3-0 black silk is preferred.
Smaller vessels can be ligated with 3-0 catgut
Large arteries with pulsation, such as external
carotid artery, should have double transfixion
suture passed through the wall of vessel to prevent
chances of slipping of ligature.
33

34. cont..
Embolization of the vessels
• With the help of angiography, the exact
bleeding point can be localized.
• Agents used for embolization :
steel coils, polyvinyl alcohol foam, gel foam,
silicon spheres and methyl methacrylate
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35. Thermal Agents
Cautery
• by denaturation of proteins which results in
coagulation of large areas of tissue.
• heat is transmitted from the instrument by
conduction directly to the tissues
• control hemorrhage from large vessels, which
need to be ligated
35

36. Cont..
Electro-surgery
• heating occurs by induction from an
alternating current source.
• Electro-cautery can be applied directly to
bleeding point or after catching the bleeding
point with hemostat.
• This cannot control hemorrhage from large
vessels, which need to be ligated.
36

37. cont..
Cryosurgery
• Extreme cooling has been used for hemostasis
• Temperature ranging from –20ºC to–180ºC are used
• tissues,capillaries, small arterioles, and venules
undergo cryogenic necrosis.
• caused by dehydration and denaturation of lipid
molecules
• used to treat superficial hemangiomas
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38. Chemical Methods
• Astringent agents and styptics:
• Monsel’s solution: contains ferric sub-sulfate
and acts by precipitating proteins
• effective in capillary bleeding control
and post extraction bleeding in medullary
bone.
• Mann hemostatic is a mixture of tannic acid,
alum and chlorobutamol.
• Silver nitrate and ferric chloride are can be
used in case of minimal capillary bleeding.
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39. Cont..
• Tannic acid also helps in precipitating proteins
and causes clot formation
• home remedy
39

40. Bone wax
• small quantity applied to the bleeding bone canal
• acts by mechanical occlusion of the bony canal.
• Large quantity of bone wax can lead to foreign body granuloma and
infection
Thrombin
• When applied topically it converts fibrinogen into fibrin clot
• applied to the bleeding surface via a pack, gelatin sponge or surgicel
40

41. Gelfoam
• It exerts pressure along with acting as scaffold for
fibrin network.
• It is absorbed by phagocytosis.
• should be moistened in saline or thrombin
solution prior to application and all the air should
be removed from interstices.
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42. Oxycel
• oxidized cellulose
• affinity for hemoglobin, formation of artificial
clot
• Acid produced also inhibit epithelialization
• not recommended for use over epithelial surfaces
42

43. Surgicel:
• It is glucose polymer
• Its local hemostatic mechanism depends on
binding of hemoglobin to oxycellulose, allowing
the dressing to expand into a gelatinous mass,
which in turn acts as scaffold for clot formation
and clot stabilization.
• Surgicel can be applied dry or it can be soaked in
thrombin solution
43

44. Fibrin glue:
• biological adhesive containing thrombin,
fibrinogen, factor XIII and aprotinin
• Thrombin converts fibrinogen to unstable
fibrin clot, factor XIII stabilizes the clot and
aprotinin prevents its degradation
44

45. Adrenaline:
• Applied topically induces vasoconstriction and thus helps
in achieving hemostasis.
• Extensive application or undiluted preparation can cause
systemic effects,
• should not be used in patients who have hypertension or
previously existing cardiac disease.
• vasoconstrictor effect is reversible and one should be
careful to watch for recurrence of bleeding when its
effect wears off
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46. Systemic agents
• Whole blood
• Platelet rich plasma
• Fresh frozen plasma
• Cryoprecipitate
46

47. Control of Hemorrhage from major
arteries
Greater
Palatine
Artery
Ligation
of Facial
Artery
Ligation
of
Lingual
Artery
Ligation
of
Maxillary
Artery
Superfici
al
Temporal
Artery
Ligation
of
External
Carotid
Artery in
Carotid
Triangle
External
Carotid
Artery
47

48. Shock
• is a pathophysiologic condition, clinically
recognized as a state of inadequate perfusion.
• Due to inadequate blood flow, there is
inadequate delivery of nutrients to the tissues
and inadequate removal of cellular waste
products from the tissue cells, which results in
disruption of vital organ functions
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49. Classification of shock
– Hypovolemic shock
– Cardiogenic shock
– Septic shock
– Neurogenic shock.
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50. Hypovolemic Shock
• results from a decrease in the circulating or
effective intravascular volume.
• most common type of shock in the victim of
maxillofacial trauma.
• Classified as:
• hemorrhagic and non hemorrhagic
A) Hemorrhagic shock is due to loss of blood
from the body as a result of injury.
50

51. Cont..
B) In non hemorrhagic shock,
 there is massive fluid shift from intravascular
compartment to extravascular compartment.
Caused by burns, crush injuries, pancreatitis,
peritonitis, pleural effusion and ascites.
Water loss
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52. Clinical features of shock
Blood loss Clinical features
Mild Postural hypotension; patient feeling
cold; tachycardia; cool, pale, moist skin;
collapsed neck veins; concentrated urine
Moderate Thirst; supine hypotension and
tachycardia; oliguria or anuria
Severe Agitation, confusion; supine hypotension
and tachycardia are invariably present;
rapid deep respiration
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53. Monitoring
• Vital signs should be monitored periodically.
• Continuous electrocardiography, pulse oximetry
should be performed
• Arterial blood gases, pH and electrolyte levels are
monitored.
• Central venous pressure should be monitored.
• In patients with moderate and severe shock, fluid
therapy is monitored by right heart
catheterization with a balloon tipped
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54. Treatment
• Fluid replacement: When hemorrhage is
massive, type specified matched transfused
blood is the preferred method to correct
hypovolemia.
• Initial resuscitation is done with crystalloids,
such as normal saline or Ringer’s lactate.
• After initial resuscitation, albumin or starch
solution can be used, as these restore
intravascular volume more effectively
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55. Cardiogenic Shock
• occurs as a result of inadequate cardiac output,
impaired oxygen delivery, and reduced tissue
perfusion.
Treatment
• identify the cause, maintaining adequate systemic
blood pressure, cardiac output and tissue perfusion
with volume expansion and inotropic drugs.
• Dopamine
• It is diluted in normal saline or 5% dextrose drip and
given at 5–10 µg/kg/min.
• norepinephrine and dobutamine can be used.
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56. Septic Shock
• describes the clinical syndrome corresponding to
acute circulatory failure resulting from serious
infection.
• Gram-negative bacteria, fungi, viruses and
parasites
• arterial hypotension associated with altered
mental status, changes in organ perfusion and
signs of organ failure, such as reduction in urine
output, increased blood lactate levels (>2 mEq/L)
reflect alteration in cellular metabolism.
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57. Management of septic shock
• should be based on:
– early and effective volume replacement;
– restoration of tissue perfusion;
– adequate oxygen supply to cells and;
– control of infection with antibiotic therapy and
control of source of infection.
– Dopamine
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58. Neurogenic Shock
• results without any loss of blood volume
• Vasovagal syncope
management
• Placing the patient in supine position
• This increases the blood flow from the
periphery to the cerebral tissues thus aiding in
recovery.
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59. Reference
• Neelima (textbook of oral and maxillofacial
surgery) 4th edition
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60. Thank you!
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