Dr. Ch VT- The topic describe about the general as well the the dental aspect too. The classification, clinical features and management. The dental conditions associated with haemorrhage and shock has been highlighted with their management

1. Good Morning
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2. 2

3. Contents
 Introduction
 Haemorrhage-
 Classification
 Pathophysiology
 Management
 Shock
 Classification
 Pathophysiology
 Management
 Dental Significance
3

4. Introduction
 Haemorrhage is said to be pertaining to bleed or the
abnormal flow of blood.
 Shock is a life threatening condition characterized
by poor tissue perfusion with impaired cellular
metabolism, manifested in turn by serious
physiological abnormalities.
4

5.  Haemorrhage can occur to a greater or lesser degree
during all surgical procedures and it’s management
depends upon whether the patient is hematologically
normal or suffers from some disturbance in the normal
clotting mechanism.
 Usually haemorrhage is followed by shock as there is
blood loss which in turn leads to reduced tissue
perfusion
5

6. Haemorrhage
Term “Haemorrhage” comes fromGreek.
“haima”(Blood) + “rhegumai” (To Break forth)
The bleeding may occur externally or interally
into serous cavities e.g. haemothorax,
haemoperitoneum etc into a hollow viscus.
6

7. Important terms
 Cardiac Cycle
 The repetitive pumping action that produces
pressure changes that circulate blood
throughout the body
 Cardiac Output
 Is a product of stroke volume and heart rate.
Stroke volume- volume of blood ejected in each
cycle
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8. Cardiac Output
 Normal CO = 5 to 6 liters per minute (LPM)
 Increase up to 30 LPM during stress or exercise
 Heart Rate X Stroke Volume
 Influenced by:
 Strength of contraction
 Rate of contraction
 Amount of venous return available to the ventricle (preload)
8

9.  Haematoma- Extravasation of blood into the
tissues with resultant swelling.
 Ecchymosis-Large extravasation of blood into
skin and mucous membrane.
 Petechiae - minute pin-head sized haemorrhages.
 Haemangioma- collection/cluster of blood vessels
9

10. Etiology
The blood loss may be large or sudden (acute), or small
repeated bleeds may occur over a period of time
(chronic).
Trauma
Vessel wall trauma
e.g. penetrating wound in the heart or great vessels, during
labour etc.
Spontaneous
e.g. Rupture of an aneurysm, septicaemia, acute
leukaemia’s,scurvy.
10

11.  Inflammation
e.g. bleeding from chronic peptic ulcer,
typhoid ulcers, syphilitic involvement
of the aorta.
 Vascular diseases
e.g. atherosclerosis.
 Elevated pressure within the vessels
e.g. cerebral and retinal haemorrhages in
systemic hypertension etc.
11

12. CLASSIFICATION
According to the source of haemorrhage, it is classified in two
ways:-
A. 1. EXTERNAL HAEMORRHAGE
2. INTERNAL HAEMORRHAGE
B.1. ARTERIAL
2. VENOUS HAEMORRHAGE
3. CAPILLARY HAEMORRHAGE
12

13. 1.External haemorrhage- revealed outside or can be seen
externally.
Eg-
Epistaxis
Haematemesis
2.Internal haemorrhage- is not seen outside, it is a concealed
haemorrhage.
E.g-
 Bleeding peptic ulcer,
 Ruptured ectopic gestation
 Fracture of major bones-Sometimes this haemorrhage may be
revealed or can be external. 13

14. Nature of the Haemorrhage
1. Arterial haemorrhage
Bright red in colour
Jets out which rises and falls in time with the pulse.
Pulsation of artery seen
Easily controlled as it is visible
2. Venous haemorrhage
Darker red
Never jets out but oozes out.
Non-pulsatile
Difficult to control-veins get retracted. 14

15. 3. Capillary haemorrhage
Red in colour
Oozes out slowly
If continues for many hours, blood loss
becomes serious, as in haemophilia.
15

16. 16
Venous haemorrhage whether primary or
reactionary, is exceedingly difficult to bring
under control.

17. The Time of Appearance of Haemorrhage,
• At the time of injury or operation.
PRIMARY
HAEMORRHAGE
• After 6-12hrs of surgery
• Cause- Hypertention, Sneezing,
Coughing, Retching
REACTIONARY
HAEMORRHAGE
• After 7-14 days
• Cause- infection and sloughing of a
vessel wall
SECONDARY
HAEMORRHAGE
17

18. Duration of Haemorrhage
 Acute- Occurs suddenly
Eg- oesophageal Variceal bleeding due to portal
hypertention
 Chronic- Haemorrhoids, duodenal ulcer, TB Ulcer of
ileum
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19. Pathophysiology
19

20. 20

21. MEASUREMENT OF ACUTE BLOOD LOSS
It is important to measure how much patient has lost blood. This amount
should always be replaced.
The blood loss detected by the methods is usually less than the actual
loss. This is because a considerable amount of water is lost via lungs,
from the wound and by evaporation of sweat from skin.
This loss of plasma and water constitutes 20% more than blood loss
detected by various methods.
21

22. The best method of detecting is by weighing swabs. The other
methods are as follows:-
1. Blood clot size- a clenched fist is roughly equal to 500ml.
2. Swelling in closed fractures-
Moderate swelling in closed fracture of tibia = 500-1500 ml
blood loss.
Moderate swelling in fractured shaft of femur is 500-2000ml.
(Ruscoe Clarke)
22

23. 3. Swab weighing – Blood loss can be measured by
weighing the swabs before and after use and adding the
total so obtained (1g = 1ml) to the volume of blood
collected in the suction or drainage bottles. (In extensive
wounds , the blood loss estimation is of no use)
4. Measurement of central venous pressure
23

24. 5. Haemoglobin level (12-16 g/dl)- There is no immediate change in
haemorrhage, but within few hours the level is lowered by
haemodilution i.e movement of fluid into the vascular compartment
in order to restore the blood volume.
The degree of dilution gauged by haematocrit reading (PCV).
PCV is measured on capillary blood and read in mm.
Men- 40-56 %
Women – 35-48 %
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25. Treatment
 Includes 3 steps
 Physiologic response
 Treatment of shock
 Surgical methods
25

26. Starling’s Law of the Heart
 When the rate at which blood flows into the heart from
the veins (venous return) changes, the heart
automatically adjusts its output to match inflow.
 The more blood the heart receives the more it pumps…
 Increased end diastolic volume increases
contractility.
 Increases stroke volume.
 Increases cardiac output.
26

27. Managing shock
Hospitalisation
Intravenous
line
Blood
transfusion
Oxygen
Dopamine
As soon as possible
Iv Adm. Of RL/Plasma
eg: Hetastarch, Gelatin
Done to optimize ventricular
preload
If PO2 < 70mmHg O2
should be given by face mask
or nasal catheter.With careful monitoring of
pulse rate, BP, Urine, Cardiac
output, Hb% PCV
2microgm/kg/min: Renal Vasodilation.
5-15microgm/kg/min: Increase BP,
Improves Cardiac output
27

28. Surgical Methods
 Application of artery forceps- (Spencer well’s forceps)
for bleeding from vein, arteries and capillaries
 Application of ligatures- for bleeding vessels
 Cauterisation
 Application of bone wax- to control bleeding from bone.
Eg: Horsley’s wax)
 Silver clips- for bleeding from cerebral vessels.
28

29. Haemorrhage in Dentistry
 Significant or major hemorrhages are not that common.
However, uncontrolled and persistent bleeding can occur in
some patients after dental extraction.
 Therefore, it is still important to achieve proper hemostasis
in all patients during oral surgical procedures.
29

30.  Haemorrhage following Oral Surgical procedures
can occur due to local or systemic causes.
 In healthy patients the postoperative bleeding is
mainly due to local causes
30

31. Causes
 Local causes- originate in either soft tissue or
bone.
 Bone bleeding- from nutrient canals in the
alveolar region, central vessels, such as the
inferior alveolar artery, or from central
vascular lesions (Hemangioma or Vascular
malformation).
31

32.  Systemic causes-
 Hemophilia
 Von Willebrand’s disease
 Patients with thrombocytopenia
 Leukemia
 Patients with uncontrolled hypertension.
32

33. Investigations
Laboratory
 Platelet count- 100,000 - 400,000 cells /mm3
 Bleeding time (BT)-2-8 Min
 Prothrombin time (PT)-10-15 Sec
 Partial Thromboplastin Time (PTT)-25-40 Sec
 Thrombin time (TT)-9-13 Sec
 INR<3
 Blood pressure- 120/80 mmHg (Healthy Adult)
33

34. Management
 Lower doses (30% of normal) of clotting factor concentrates.
 Oral rinse of an antifibrinolytic agent (tranexamic acid)
following extraction 10 ml of a 5% solution.
 Single dose of factor, in cases of severe hemophilia A
(elevating the factor VIII level to 101 IU/dL).
 Desmopressin, (derivative of hormone vasopressin) increase factor
VIII level in some patients with mild or moderate forms of
hemophilia A or type 1 von Willebrand disease
K.D Tripathi 4th Edition 34

35.  Fibrin glue as a local hemostatic.
 In Endodontics-
The use of 4% sodium hypochlorite for irrigation and calcium
hydroxide paste appears to minimise this problem
Prophylactically- if patient is Haemophilic, adm.of coagulant
factor prior to treatment.
Andrew Brewer , Maria Elvira Correa GUIDELINES FOR DENTAL TREATMENT OF
PATIENTS WITH INHERITED BLEEDING DISORDERS World Federation of
Hemophilia, 2006
35

36. Local Measures ( Synthetic Materials)
 Surgicel (Oxidised RegeneratedCellulose)
 Gelfoam with activated thrombin.
 Avitene (Microfibrillar Collagen).
 Etik Collagen (Packed collagen).
 Tranexamic acid 5%.
 Irrigation of wound with Tranexamic acid.
 Pressure with oral packs
36

37. SHOCK
37

38.  Definition- Shock is a physiologic state characterized by
systemic reduction in tissue perfusion, resulting in
decreased tissue oxygen delivery.
 Shock is a condition when despite normal oxygen
content of arterial blood, the oxygen delivery fails to
meet the metabolic requirements of the tissues.
( Davidson)
38
Shock

39. 39

40. 40

41. Types of Shock
41
Hypovolemic
Cardiogenic
Distributive
Obstructive
Neurogenic
Anaphylactic
Septic

42. 42

43. Etiopathogenesis
43

44. Hypovolaemic (etiology)
 Definition- medical condition in which rapid loss of
intravascular blood or plasma volume results in multiple organ
failure due to inadequate perfusion
 Blood loss.
 Haemorrhage
 Plasma / body water loss.
 Electrolytes imbalance.
 Vomiting.
 Diarrhea.
 Dehydration.
44

45. Pathophysiology
45

46. 46
Haemorrhage from systemic venules & small veins
Decreased filling of the right heart
Decrease of filling of the pulmonary vasculature
Decrease filling of the left atrium & ventricle
Decrease in left ventricular stroke volume
Drop in arterial blood pressure
shock

47. SIGN & SYMPTOMS
MILD HYPOVOLEMIA (<20% of blood loss)
Mild tachycardia but relatively few external signs especially in a
supine resting young patient
 Cool extremities
 Diaphoresis
 Anxiety
MODERATE HYPOVOLEMIA (20-40% of blood loss)
 Pt becomes increasingly anxious & tachycardic
 Although normal blood pressure can be maintained in the supine
position, there may be significant postural hypotension &
tachycardia
 Mild oliguria
CLINICAL MANIFESTATION OF HYPOVOLEMIC
SHOCK
47

48. 48
SEVERE HYPOVOLEMIA (>40%)
 Blood pressure declines & unstable even in supine position
 Marked tachycardia
 Marked oliguria
 Mental status deterioration (coma)

49.  The impaired ability of the heart to pump
blood
 Dysfunction of the right or left ventricle
or both (rare)
 Most common cause is MI
 Occurs when > 40% of ventricular mass
damage
 Mortality rate of 80 % or MORE
49
Cardiogenic shock

50. Cardiogenic
etiology
 Valvular heart disease
 Myocardial infarction.
 Cardiac arrhythmias.
 Cardiomyopathy
50

51. Pathophysiology Of Cardiogenic
Shock
Left vetricular output decreases
Filling of left heart decreases
Right heart unable to pump blood
to lungs
Dysfunction of right ventricle
Failure of the left heart
Engorgement of pulmonary vasculature
Left ventricular and systemic arterial blood
pressure decreases
Left ventircle unable to maintain stroke
volume
Dysfunction of left ventricle
51

52. Treatment Of Cardiogenic Shock
52
 Clear airway with adequate oxygenation
 In case of right sided failure caused by massive
pulmonary embolus- large doses of heparin is given iv
 For pain- proper sedative like morphin is given
 Fulminant pulmonary edema is treated using diuretics

53. Neurogenic Shock
53
 A type of distributive shock that results from
the loss or suppression of sympathetic tone
 Causes massive vasodilatation in the venous
vasculature,  venous return to heart,  C.O.
 Can occur within 30 minutes of a spinal cord
injury at the fifth thoracic (T5) vertebra or
above
 Can be in response to spinal anesthesia

54. Vasovagal Shock
54
 It is a type of neurogenic shock
 Pooling of blood in the limbs due to dilatation of
peripheral vasculature
 Reduced venous return to the heart-low cardiac output-
bradycardia
 Blood flow to brain is reduced- cerebral hypoxia &
unconsiousness

55. Etiological Factors Of Vasovagal
Shock
55
 Anxiety
 Overwhelming fear or grief
 Site of bleeding
 Severe pain

56. Pathophysiology of Neurogenic Shock
Disruption of sympathetic nervous system
Loss of sympathetic tone
Venous &arterial vasodilation
Decreased venous return
Decreased stroke volume
Decreased cardiac output
Decreased cellular oxygen supply
Impaired tissue perfusion
Impaired cellular metabolism 56

57. Clinical Features
57
 Peculiar feature: skin remains warm, pink and well
perfused
 Urine output is normal
 Rapid heart rate
 Low blood pressure

58. Treatment
58
 Trendelenburg position: displaces blood from systemic
venules and small veins into the right heart & thus
increases cardiac output.
 Fluid administration
 Vasoconstrictor

59. Anaphylactic Shock
 Serious allergic reaction that is rapid in onset and may
cause death.
 Acute, life-threatening hypersensitivity reaction to an
antigen a person is allergic to.
59

60. Etiological factors of anaphylactic
shock
60
 Insect bites and stings
 Foods
 Medications
 Penicillins/sulphonamides
 Cephalosporins, tetracyclins
 Vaccines & toxoids
 Aspirin
 NSAIDS

61. 61

62. Pathophysiology
62
 Release of inflammatory mediators and cytokines from mast
cells and basophils, typically due
 Immunologic
 Non -immunologic

63. 63
(IgE)
binds
Antigen
Antigen-bound IgE
activates
receptors on mast cells and basophils.
release of inflammatory mediators (histamine)
increase the contraction of bronchial smooth muscles
vasodilation, increase the leakage of fluid from blood
vessels, and cause heart muscle depression
Immunologic

64. Non immunologic
64
 Non-immunologic mechanisms involve substances
that directly cause the degranulation of mast cells and
basophils.
 These include agents such as contrast
medium, opioids, temperature (hot or cold), and
vibration.

65. Management of Anaphylactic
shock
65
 Airway management
 Supplemental oxygen
 Large volumes of intravenous fluids, and close
monitoring.
 Administration of epinephrine is the treatment of
choice with antihistamines and steroids(for
example, dexamethasone )

66. Septic Shock(Etiology)
 Gram +ve Bacteria
 Gram –ve Bacteria
 Fungi / Virus
 Protozoa
66

67. Treatment of septic shock
67
 Prompt diagnosis and treatment is an effective way to
reduce the mortality
 Treatment is divided into two groups
1. Early surgical debridement or drainage and using
appropriate antibiotics
2. Fluid replacement, steroid administration & use of
vasoactive drugs

68. Treatment of septic shock
68
 Debridement or drainage under local or general
anasthesia as soon as possible after initial stability.
 Antibiotics given based on specific culture and
sensivity test.
Broad spectrum antibiotics started initially
Cephalothin(6-8 gm/day i.v in 4-6 divided doses),
gentamicin (5 mg/Kg/day), Clindamycin or
chloromycetin

69. Treatment of septic shock
69
 Fluid replacement-provide the sufficent blood volume to the
vital oragns.
 Mechanical ventilation with endotracheal intubation in late
septic shock.
 Short term , high dose steroid therapy in cases not responding
to the other methods of the treatment.
An initial dose of 15-30 mg/kg body wt of methyl
prednisolone or equivalent dose of dexamethasone i.v is given
in 5-10 mins

70. Obstructive (Etiology)
 Cardiac Tamponade
 Pulmonary Embolism
 Tension Pneumothorax
 Air embolism
70

71. Stages of shock
 Initial : The cells become leaky and switch to anaerobic
metabolism.
 Non-progressive:(compensated stage) Attempt to
correct the metabolic upset of shock.
 Progressive: (decompensated stage ) Eventually the
compensation will begin to fail.
 Refractory : Organs fail and the shock can no longer be
reversed.
71

72. 72

73. Management
73

74. Management
 Monitoring
 Blood pressure
 Heart rate
 Respiratory rate
 Urine output
 Blood CBC
 Pulse- oximetry
 ECG
 U/S , CT , X-ray
74

75. Guidelines
 Treat the cause
 Improve Cardiac function
 Improve Tissue perfusion
75

76. Prehospital Care
Prevention of further injury & transportation of patient to hospital as
rapidly as possible
Prehospital intervention includes
 Immobilization of the patient
 Securing adequate airway
 Ensuring ventilation
 Maximizing circulation
76

77. Maximise O2 Delivery
 Airway assessment should be immediate.
 Depth &rate of respiration assessed.
 Any interfering pathology should be addressed immediately
 High flow supplemental oxygen administered & ventilatory
support given
77

78. Commonly Used IV Fluids
 Normal saline(0.9% NaCL): isotonic salt water.
 Lactated ringer’s (RL): isotonic, 273 mOsm/L.
 D5W: hypertonic, 406 mOsm/L.
 Hypertonic saline(3% NaCl): 1026 mOSm & 513 mEq/L
Na.
79

79. Other Therapy
Treatment By The Head-down Position. in hemorrhagic and neurogenic
shock when BP is too low,placing the patient in trendenlenburg position
promotes venous return, thereby also increasing C.O.
First essential step in the treatment of many types of shock.
OXYGEN THERAPY.
Frequently is far less beneficial, because the problem in most types of
shock is not inadequate oxygenation of the blood by the lungs but
inadequate transport of the blood after it is oxygenated
80

80. Treatment with Glucocorticoids (Adrenal Cortex Hormones That
Control Glucose Metabolism).
(1) Frequently increase the strength of the heart in the late stages of
shock;
(2) It stabilize lysosomes in tissue cells and thereby prevent release of
lysosomal enzymes into the cytoplasm of the cells, thus preventing
deterioration from this source; and
(3) Aid in the metabolism of glucose by the severely damaged cells.
81

81. Conclusion
 Haemorrhage and shcok are the conditions
best treated by prevention and proper
investigation and knowing the patient.
“NEVER Treat A Stranger”
– Sir William Osler
82

82. 83
 D. J. Perry,1 T. J. C. Noakes2 and P. S. Helliwell3 Guidelines for
the management of patients on oral anticoagulants requiring
dental surgery DOI: 10.1038/bdj.2007.892 ©British Dental
Journal 2007; 203: 389-393
 Harrison internal medicine- 18th edition
 Davidson – Principles & Practice of Medicine
 A concise textbok of surgery- S. Das- 4th edition
 Human physiology for BDS- AK Jain-3rd Edition
 Textbook of clinical medicine-SN Chug
 Manipal Manual of surgery-K. Rajagopal Shenoy
References