Haemorrhage and shock

1. 1
HAEMORRHAGE
&
SHOCK

2. BLOOD COAGULATION
When a tissue is damaged
Prothrombin is converted into its active form
thrombin
(In the presence of calcium)
Fibrinogen then transformed by thrombin to
fibrin
Mesh is formed by platelets and other blood
cells to form clot

3. CLOTTING FACTORS
3
I. FIBRINOGEN
II. PROTHROMBIN
III. TISSUE FACTOR( THROMBOPLASTIN)
IV. CALCIUM( CA2+)
V. LABILE FACTOR, PROACCELERIN, AC-
GLOBULIN
VI. STABLE FACTOR

4. CONTD…
VII. ANTIHAEMOPHILIC GLOBULIN( AHG),
ANTIHAEMOPHILIC FACTOR A
VIII. CHRISTMAS FACTOR, PLASMA
THROMBOPLASTIN COMPONENT(PTA),
ANTIHAEMOPHILIC FACTOR B
IX. STUART POWER FACTOR
X. PLASMA THROMBOPLASTIN
ANTECEDENT( PTA), ANTIHAEMOPHILIC
FACTOR C
XI. HAGEMAN FACTOR
XII. FIBRIN STABILISING FACTOR 4

5. CLASSIFICATION
BY ATLS Based on blood volume
1. Class I Haemorrhage
2. Class II Haemorrhage
3. Class III Haemorrhage
4. Class IV Haemorrhage
5

6. CONTD…
World Health Organization
 Grade 0 - no bleeding
 Grade 1 - Petechial bleeding;
 Grade 2 - mild blood loss (clinically
significant);
 Grade 3 - gross blood loss, requires
transfusion (severe);
 Grade 4 - debilitating blood loss, retinal or
cerebral associated with fatality
6

7.  According to Origin:
 Mouth
Hematemesis, Haemoptysis
 Anus
Hematochezia
 Urinary tract
Hematuria
 Upper head
Intracranial haemorrhage
Cerebral haemorrhage
Intracerebral haemorrhage
Subarachnoid haemorrhage (SAH) 7

8. Lungs
Pulmonary haemorrhage
Gynaecologic
Vaginal bleeding
Postpartum haemorrhage
Breakthrough bleeding
Ovarian bleeding.
Gastrointestinal
Upper gastrointestinal bleed
Lower gastrointestinal bleed
Occult gastrointestinal bleed
8

9. 9
According to source
• Capillary
• Venous
• Arterial
According to situation
• External (Revealed haemorrhage)
• Internal (Concealed haemorrhage)
• Subcutaneous/intramuscular

10. According to the time of wound:
• Primary haemorrhage
• Reactionary or intermediate haemorrhage
• Secondary haemorrhage
10

11. CAUSES
1.Traumatic Injury
Abrasion
Excoriation
Hematoma
Laceration
Incision
Puncture Wound
Contusion
Crushing Injuries
Ballistic Trauma 11

12. 2. Medical condition
Intravascular changes
Intramural changes
Extra vascular changes
12

13. SIGNS & SYMPTOMS OF
HAEMORRHAGE
Blood coming from an open wound.
Bruising
Shock, which may cause any of the
following symptoms:
• Confusion or decreasing alertness
• Clammy skin
• Dizziness or light-headedness after an
injury
• Low blood pressure
• Paleness (pallor) 13

14. Contd…
• Rapid pulse, increased heart rate
• Shortness of breath
• Weakness
Symptoms of internal bleeding may also
include:
• Abdominal pain and swelling
• Chest pain
14

15. • External bleeding through a natural opening
– Blood in the stool(appears black, maroon,
or bright red)
– Blood in the urine (appears red, pink, or
tea-colored)
– Blood in the vomit (looks bright red, or
brown like coffee-grounds)
– Vaginal bleeding (heavier than usual or
after menopause)
• Skin colour changes that occur several days
after an injury (skin may black, blue, purple,
yellowish green) 15

16. CONTROL OF
HAEMORRHAGE
16

17. Apply direct pressure:
• with gloved hand,
• sterile dressing(s).
Bleeding stopped? YesNo
Elevate extremity:
• above victim’s heart,
continue direct pressure
Locate pressure point,
apply pressure:
• maintain direct pressure
over wound
Treat for shock:
• care for wound,
• seek definitive care
Bleeding stopped?
Bleeding stopped?
No
Bleeding from
extremity?
No
Apply tourniquet
(last resort)
Yes
No
Definitive therapy
17

18. Apply pressure directly to
wound site:
–Gloved hand, dressing
–If dressing soaks
through, add more
gauze on top and press
harder
18
Direct pressure

19. If possible, raise wound site
above level of victim’s heart
19
Elevate wound site

20. Find proximal “pressure
point” and press on it
(radial, ulnar, brachial,
axillary, femoral arteries—
not carotid)
Apply direct pressure to site
20
Pressure points
Yes
Yes

21. Tourniquet
Apply band above injury site, tighten to stop
bleeding:
–Last resort—risky
–Note time of application
–Reassess frequently
21

22. 22
FIRST AID IN EXTERNAL
BLEEDING
Bring the sides of wound together and press
firmly.
Press on the pressure point for 10-15 min.
Place the causality in comfortable position
and raise the injured Part and reassure him.
Apply a clean pad larger than the wound and
press it firmly with the palm until bleeding
becomes less.
If bleeding continues do not take off original
dressing but add more pads.
Bandage, it but not too tightly.

23. CONTROL OF INTERNAL
HAEMORRHAGE
The organ is emptied of blood clots
if possible.
The vessels are encouraged to
contract.
Packing
Surgical ligature
Internal pressure.
23

24. FIRAT AID IN INTERNAL
BLEEDING
Lay the causality down with head low; raise
his legs by Use of pillow.
Keep him calm and relaxed. Reassure him.
Do not allow him to move.
Keep up the body heat with thin blankets or
coat.
24

25. CONTD…
Do not give anything to eat or drink
aspiration may occur.
Do not apply ice bags or hot water
bottles to chest or abdomen.
Take him to the hospital as early as
possible.
Transport gently
25

26. RESTORATION OF BLOOD
VOLUME
Transfusion under increased
pressure
 Pressure cuff
 Pressure pump administration
26

27. NURSING MANAGEMENT
Risk for bleeding related to
pregnancy related complications,
postpartum complication, treatment
related side effects, circumcision,
DIC, inherent coagulopathies, GI
disorders, aneurysm, impaired liver
function, trauma or history of falls.
27

28. 28
Shock

29. DEFINITION
1. Shock can be best be defined as a condition
in which tissue perfusion is inadequate to
deliver oxygen and nutrients to support vital
organs and cellular function.
2. Shock is a syndrome characterized by
decreased tissue perfusion and impaired
cellular metabolism. This results in an
imbalance between the supply of and
demand for oxygen and nutrients.
29

30. Contd….
3. Shock is a condition where the
tissues in the body do not receive
enough oxygen and to allow cells to
function.
4. Shock is defined as failure of the
circulatory system to maintain
adequate perfusion to vital organs.
30

31. 31
Shock
Homeostasis
–cellular state of balance
–perfusion of cells with oxygen and
glucose is one of its cornerstones
–Transfer of waste materials from the
cell to blood for elimination

32. 32
Shock
Inadequate oxygenation or
perfusion causes:
Inadequate cellular oxygenation
Shift from aerobic to anaerobic
metabolism

33. 33
AEROBIC METABOLISM
6 O2
GLUCOSE
METABOLISM
6 CO2
6 H2O
36 ATP
HEAT (417 kcal)
Glycolysis: Inefficient source of energy production; 2
ATP for every glucose; produces pyruvic acid
Oxidative phosphorylation: Each pyruvic acid is
converted into 34 ATP

34. 34
ANAEROBIC METABOLISM
GLUCOSE METABOLISM
2 LACTIC ACID
2 ATP
HEAT (32 kcal)
Glycolysis: Inefficient source of energy production; 2
ATP for every glucose; produces pyruvic acid

35. 35
Anaerobic Metabolism
Occurs without oxygen
– oxydative phosphorylation can’t occur
without oxygen
– glycolysis can occur without oxygen
– cellular death leads to tissue and organ
death
– can occur even after return of perfusion
∀⇒ organ or organism death

36. VASCULAR RESPONSES
Oxygen attaches to the haemoglobin
molecule in red blood cells, and the blood
carries it to body cells.
Central regulatory mechanisms
Local regulatory mechanisms
36

37. B.P REGULATION
Three major components of the circulatory
system blood volume, the cardiac pump, and
the vasculature must respond effectively to
complex neural, chemical, and hormonal
feedback systems to maintain an adequate
blood pressure and ultimately perfuse body
tissues.
Mean arterial blood pressure = cardiac output
× peripheral resistance
37

38. CONTD…
Cardiac output is determined by stroke
volume (the amount of blood ejected at
systole) and heart rate.
Blood pressure is regulated by the
baroreceptors (pressure receptors) located in
the carotid sinus and aortic arch.
Chemoreceptor’s, also located in the aortic
arch and carotid arteries, regulate blood
pressure and respiratory rate using much the
same mechanism in response to changes in
oxygen and carbon dioxide concentrations in
the blood. 38

39. CONTD…
The kidneys also play an important role in
blood pressure regulation.
Adequate blood volume, an effective cardiac
pump, and an effective vasculature are
necessary to maintain blood pressure and
tissue perfusion.
39

40. STAGES OF SHOCK
Initial Stage
Compensatory
Stage
Progressive
Stage
Irreversible
Stage

41. INITIAL STAGE
Initially, the body compensates
with the onset of shock.
No changes are noted clinically.
Changes are beginning to occur
on the cellular level.

42. COMPENSATORY STAGE
Activation of SNS - activation of epinephrine
and nor epinephrine.
Vasoconstriction, increased heart rate, and
increased contractility of the heart contribute
to maintaining adequate cardiac output.
Kidneys release renin into blood
formation of angiotensin & release of
aldosterone, ADH

43. Decreased CO
SNS stimulation
Epinephrine &
nor epinephrine
released
Vasoconstriction
Increased SVR
Renin secreted by
kidney
Angiotension
Aldosterone
ADH
Increase blood volume
hydrostatic pressure
fluid pulled into
capillary
Blood Pressure Maintained

44. CLINICAL
MANIFESTATIONS
Normal B.P
Increased respiratory rate
Skin- cold & clammy
Hypoactive bowel sounds
Decreased urine output
Mental status changes- confusion
44

45. MANAGEMENT
MEDICAL MANGEMENT
• Fluid replacement
• Medication therapy
NURSING MANAGEMENT
• Monitoring tissue perfusion
• Reducing anxiety
• Promoting safety
45

46. PROGRESSIVE STAGE
Vicious circle of compensation
eventually leads to decompensation.
Mean arterial pressure starts to fall -
SBP below 90.

47. CLINICAL FEATURES
RESPIRATORY:
o rapid & shallow
o Crackles
o Decreased arterial oxygen
o Increased CO2
o Pulmonary edema
o Interstitial inflammation & fibrosis
o ARDS 47

48. CARDIOVASCULAR:
o Dysrhythmias
o Ischemia
o Rapid HR- > 150 bpm
o Chest pain
o Rised cardiac enzyme levels
NEUROLOGIC
o Mental status changes-Confusion
o Lethargy
o Dilated pupils, sluggish reaction to light
48

49. RENAL EFFECTS
o Acute renal failure
HEPATIC EFFECTS
o susceptible to Infection
o Elevated liver enzymes& bilirubin
levels
49

50. GI EFFECTS
o Stress ulcer
o Bloody diarrhea
o Bacterial toxin translocation
HEMATOLOGIC EFFECTS
o DIC
50

51. MEDICAL MANAGEMENT
IV FLUIDS& MEDICATIONS
Early enteral support
Antacids, histamine-2 blockers, or
anti-peptic agents.
51

52. NURSING MANAGEMENT
Preventing complications
Promoting rest and comfort
Supporting family members
52

53. IRREVERSIBLE STAGE
Severe organ damage
Low B.P
Complete renal and liver failure
Multiple organ dysfunction
progressing to complete organ
failure has occurred, and death is
imminent.
53

54. MANAGEMENT
MEDICAL
 Same as progressive stage
 Antibiotic agents & immunomodulation
therapy
NURSING
 Offering brief explanations to the patient
 Provide opportunities for the family to
see, touch, and talk to the patient.
54

55. OVERALL MANAGEMENT
IN SHOCK
Fluid replacement
Vasoactive medications
Nutritional support
55

56. TYPES OF SHOCK
Hypovolemic Shock
Cardiogenic Shock
Distributive Shock
–Neurogenic shock
–Septic shock
–Anaphylactic shock

57. Most common type of shock
–Decreased intravascular volume
• Primary cause = loss of blood or body
fluids from an internal or external
source
57
HYPOVOLEMIC SHOCK
Scalp laceration 3rd
degree/full thickness burn

58. CONTD…
• INTERNAL: Hemorrhage, severe
burns, severe dehydration
• EXTERNAL: Trauma, Surgery,
Vomiting, Diarrhoea, Diuresis,
Diabetes insipidus
58

59. CLINICAL FEATURES
A rapid, weak, thready pulse
Cool, clammy skin
Rapid and shallow breathing
Hypothermia
Thirst and dry mouth
Cold and mottled skin (Livedo
reticularis)
59

60. MANAGEMENT
MEDICAL
 Treatment of the underlying cause
- Fluid & blood replacement
- Redistribution of fluid by positioning
 Pharmacologic therapy
NURSING
o Administering blood & fluids safely
o oxygen
60

61. CARDIOGENIC SHOCK
PATHOPHYSIOLOGY
Decreased cardiac contractility
Decreased stroke volume and
cardiac output
Pulmonary congestion, Decreased
systemic tissue perfusion,
Decreased coronary artery perfusion61

62. MANAGEMENT
MEDICAL
 Correction of underlying causes
 Initiation of first-line treatment
• Supplying supplemental oxygen
• Controlling chest pain
• Providing selected fluid support
62

63. CONTD…
• Administering vasoactive
medications
• Controlling heart rate with
medication or by implementation of
a transthoracic or intravenous
pacemaker
• Implementing mechanical cardiac
support 63

64. NURSING
 Preventing cardiogenic shock.
 Monitoring hemodynamic status.
 Administering medications and
intravenous fluids.
 Maintaining intra-aortic balloon
counter pulsation.
64

65. Circulatory or distributive shock –
abnormal displacement of blood
volume in the vasculature.
65
DISTRIBUTIVE SHOCK
Urticaria/anaphylaxis Meningococcic sepsis

66. TYPES
1.Septic shock
2. Neurogenic shock
3. Anaphylactic shock
66

67. RISK FACTORS
Septic shock- immuno suppression,
extremes of age, malnourishment,
chronic illness, invasive procedures.
Neurogenic shock – spinal cord
injury, spinal anesthesia, depressant
action of medications, glucose
deficiency.
Anaphylactic shock- penicillin
sensitivity, transfusion reaction.bee
sting allergy, latex sensitivity. 67

68. SEPTIC SHOCK
Caused by widespread infection.
Vasodilation
Maldistribution of blood volume
Decreased venous return
Decreased stroke volume
Decreased cardiac output
Decreased tissue perfusion
68

69. MANAGEMENT
MEDICAL
• identifying and eliminating the
cause of infection.
• Fluid replacement.
PHARMACOLOGIC THERAPY
• Antibiotic sensitivity.
• 3rd
generation cephalosporin +
amino glycoside 69

70. NUTRITIONAL THERAPY
• Nutritional supplementation - within
the first 24 hours .
• Enteral feedings
NURSING MANAGEMENT
• Follow aseptic technique.
• Monitor for signs of infection.
• Monitor hemodynamic status, fluid
intake& output& nutritional status.
• Daily weight & close monitoring of
serum albumin.
70

71. NEUROGENIC SHOCK
vasodilation occurs as a result of a
loss of sympathetic tone.
may have a prolonged course
(spinal cord injury) or a short one
(syncope or fainting)
Dry, warm skin & bradycardia.
71

72. MANAGEMENT
MEDICAL
1. Restoring sympathetic tone through
stabilization of a spinal cord injury
or, in the instance of spinal
anaesthesia, by positioning the
patient properly.
2. Specific treatment depends on its
cause. If hypoglycemia (insulin
shock) is the cause, glucose is
rapidly administered. 72

73. NURSING
• Elevate and maintain the head of
the bed at least 30 degrees.
• . In suspected spinal cord injury,
neurogenic shock may be
prevented by carefully immobilizing
the patient.
• Applying elastic compression
stockings and elevating the foot of
the bed
73

74. • Check the patient daily for any
redness, tenderness, warmth of the
calves, and positive Homans sign
(calf pain on dorsiflexion of the
foot).
• Administering heparin or low-
molecular-weight heparin
(Lovenox) as prescribed, applying
elastic compression stockings, or
initiating pneumatic compression of
the legs may prevent thrombus
formation. 74

75. • Performing passive range of motion
of the immobile extremities.
• In the immediate post injury period,
the nurse must monitor the patient
closely for signs of internal bleeding
that could lead to hypovolemic
shock.
75

76. ANAPHYLACTIC SHOCK
Caused by severe allergic reaction
when a patient who has already
produced antibodies to a foreign
substance (antigen) develops a
systemic antigen–antibody
reaction.
76

77. Due to antibody responses
Release of histamine Vasodilatation
Increased capillary Permeability
Severe bronchoconstriction
Decreased oxygen supply and
utilization
Inadequate tissue Perfusion
77

78. MANAGEMENT
MEDICAL
 Removing the causative antigen
(e.g., discontinuing an antibiotic
agent), administering medications
that restore vascular tone, and
providing emergency support of
basic life functions.
78

79.  Epinephrine
 Diphenhydramine
 Nebulized medications ( albuterol)
 cardiopulmonary resuscitation
 ET Intubation or tracheotomy
NURSING
 Assessing all patients for allergies
or previous reactions to antigens
and communicating the existence
of these allergies or reactions to
others. 79

80.  Assess the patient’s understanding
of previous reactions and steps
taken by the patient and family to
prevent further exposure to
antigens.
 Advise the patient to wear or carry
identification that names the
Specific allergen or antigen.
 When administering any new
medication, the nurse observes the
patient for an allergic reaction. 80

81.  Identify patients at risk for
anaphylactic reactions to contrast
agents (radiopaque, dye-like
substances that may contain
iodine) used for diagnostic tests.
 Take immediate action if signs and
symptoms occur, and must be
prepared to begin cardiopulmonary
resuscitation if cardio respiratory
arrest occurs.
81

82.  In addition to monitoring the
patient’s response to treatment, the
nurse assists with intubation if
needed, monitors the
hemodynamic status, ensures
intravenous access for
administration of medications, and
administers prescribed medications
and fluids, and documents
treatments and their effects.
82

83.  Community health and home care
nurses whose role includes
administering medications,
including antibiotic agents, in the
patient’s home or other settings
must be prepared to administer
epinephrine subcutaneously or
intramuscularly in the event of an
anaphylactic reaction.
83

84. PREVENTION OF SHOCK
Preoperatively:
 His blood should be adequate in
quantity and volume.
 His tissues should be adequately
hydrated.
 He should be mobile.
 Patient should be kept warm on his
journey from ward to theatre.
84

85. Post operatively:
 Fluid and electrolyte replacement
normal saline, dextrose 5%, plasma
and rest and relief from the pain
continues.
 Gentle handling by nursing staff
will help in prevention of shock.
 Diuretics like mannitol .
 If oliguria persists furosemide can
be given.
 Dopamine

86. COMPLICATIONS
1. ARDS
2. Multiple Organ Failure
86

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Edition. New Delhi:
Elsevier Publications; 2008.
Page No: 67-81
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Elsevier Publications; 2011.
Page No: 1722-1744
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Emergency Bleeding Control
9. Http:// Nursing Care plans
BlogSpot. In/ 2012
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91. 10. En.Wikipedia.Org/ Wiki/ Bleeding
11. En. Wikipedia. Org/ Wiki/ Shock
12. Journals. Iwww.Com/ Shock
Journal
91