shock and blood transfusion by dr chandrakant sabale

1. SHOCK AND BLOOD TRANSFUSION
DR CHANDRAKANT SABALE

2. SHOCK
 Shock is a systemic state of low tissue perfusion that is inadequate
for normal cellular respiration.

4. PATHOPHYSIOLOGY
 Cellular
 Microvascular
 Systemic - Cardiovascular,
Respiratory, Renal & Endocrine

5. CELLULAR
 When perfusion to tissue reduces Dec O2 delivery to tissues Cell metabolism
( aerobic -> anaerobic)
 Accumalation of lactic acid in blood
 Systemic metabolic acidosis
 Glucose within cells are exhausted and Anaerobic respiration ceases
 Failure of Na/K pump in the cell membrane & intracellular organelle
Intracellular lysosome release autodigestive enzymes.
 Cell lysis & intracellular contents inc K released into bloodsream

6. MICROVASCULAR
 As Tissue ischemia progresses
 Hypoxia & acidosis
 Activate compliment & prime neutrophils
 Generation of O2 free readicals & cytokine release
 Injury to capillary to endothelial cells
 Further activation of immune system
 Endothelial damage – leaky- tissue edema

7. CARDIOVASCULAR
 Decreased Preload & afterload
 Compensatory baroreceptor response resluting in increased Sympathetic
activity and Catecholamines release into the circulation
 This results in Tachycardia and Systemic vasoconstriction

8. RESPIRATORY
 The metabolic acidosis and increased
sympathetic response result in an
increased Respiratory Rate and minute
ventilation to increase the excretion of
CO2.

9. RENAL
 Decreased renal perfussion leads to
Decreased glomerular filtration and
decreased urine output
 It Stimulate RAAS Vasoconstriction & inc.
Na & water reabsorption.

10. CLASSIFICATION OF SHOCK
 Hypovolemic Shock
 Cardiogenic shock
 Obstructive Shock
 Distributive shock
 Endocrine

11. HYPOVOLEMIC SHOCK
 Reduced circulatory volume
 1. Haemorrhagic ( Internal / external
bleeding)
 2. Non Haemorrhagic ( dehydration,
vomiting, diarrhea, burns)

12. CARDIOGENIC SHOCK
 Primary failure of heart to pump
blood to tissues
 Causes : MI, Cardiac
dysrhythmias,valvular heart diseases,
blunt myocardial injury &
cardiomyopathy

13. OBSTRUCTIVE SHOCK
 Reduction in preload because of
mechanical obstruction of cardiac
filling
 Causes: Cardiac tamponade
Tension pneumothorax
Massive pulmonary embolus
Air embolus

14. DISTRIBUTIVE SHOCK
 Inadequacy of intravascular volume leads to
vascular vasodilatation with hypotension low
systemic vascular resistance, inadequate afterload
which finally results in Abnormally high cardiac output
 Causes : Septic shock
Anaphylaxis
Spinal cord injury

15. ENDOCRINE SHOCK
 It is combination of hypovolemic,
cardiogenic & distributive shock.
 Causes of endocrine shock
hypo- and hyperthyroidism
adrenal insufficiency

16. CLINICAL FEATURES AND SEVERITY OF SHOCK
 cold, pale, or clammy skin
 excessive sweating
 fast heart rate
 shallow and rapid breathing
 Drowsiness And fainting
 Blue or gray lips or fingernails
 Irritability
 Anxiety and dizziness
 enlarged pupils
 nausea or vomiting

17. SEVERITY OF SHOCK

18. MANAGEMENT: RESUSCITATION
 Immediate resuscitation manoeuvres for patients presenting in shock are to
ensure a patent airway and adequate oxygenation and ventilation.
 The timing and nature of resuscitation will depend on the type of shock and
the timing and severity of the insult.
 Rapid clinical examination will provide adequate clues to make an appropriate
first determination.
 If there is initial doubt about the cause of shock, it is safer to assume the
cause is hypovolaemia.

19. FLUID THERAPY
 First-line therapy, is intravenous access and
administration of IV fluids. Access should be through
short, wide-bore catheters.
 Type of IV fluids: crystalloids or Colloids ?
 The shock status determined dynamically by the
cardiovascular response to the rapid administration of a
fluid bolus(250-500 mL ) and the cardiovascular responses
in terms of HR, BP and CVP are observed.
 If blood lost then replace with blood.

20. VASOPRESSOR AND INOTROPIC SUPPORT
 DISTRIBUTIVE SHOCK:
Vasopressor agents -phenylephrine, noradrenaline
 CARDIOGENIC SHOCK:
Required to increase cardiac output and therefore oxygen delivery.
The inodilator dobutamine is the agent of choice.

21. MONITORING
 Minimum
ECG
Pulse oximetry
Blood pressure
Urine output
Additional modalities
Central venous pressure
Invasive blood pressure
Cardiac output Base deficit and serum
lactate

22. HEMORRHAGE
A)Haemorrhage may be revealed or concealed.
Revealed – external haemorrhage
Concealed – is contained within the body cavity.
B) Primary, reactionary and secondary haemorrhage
Primary -immediately due to an injury (or surgery).
Reactionary -delayed haemorrhage (within 24 hours) and is usually due to dislodgement
of a clot by resuscitation, normalisation of blood pressure and vasodilatation.
Reactionary -may also be due to technical failure, such as slippage of a ligature.
Secondary - due to sloughing of the wall of a vessel. It occurs 7-14 days after injury.

23. CLASSIFICATION OF HAEMORRHAGIC SHOCK

24. MANAGEMENT
 Identify haemorrhage and Immediate resuscitative manoeuvres.
 Identify the site of haemorrhage- history (previous episodes,
known aneurysm, non-steroidal therapy GI bleeding) or
examination.
 Haemorrhage control – Damage control Surgery.

25. BLOOD TRANSFUSION
 Process of transferring whole blood or its components from one person
(donor) to another person(recipient)
 Blood transfusion can be life saving after trauma or haemorrhage
 For some it may be important for sustaining life as in conditions like Beta
Thalassemia Major

26. HISTORY OF BLOOD TRANSFUSION

27. • In the late 19th Century ,Halsted had transfused blood to his own sister
suffering from post partum haemorrhage,with the blood drawn from
his own veins.
• In 1937,Bernard Fantus created the concept of first hospital based
“blood bank” in the United States
• Charles Drew (1940-1950) a surgeon at Columbia University showed
how blood can be separated into RBCs and plasma and that plasma
can be frozen for a long time

28. BLOOD AND BLOOD COMPONENTS
• Blood is collected from donors who have been previously screened before
donating, to exclude any donor whose blood may have the potential to harm
the patient, or to prevent possible harm that donating a unit of blood may
have on the donor.
• A maximum of three times each year.
• Each unit is tested for evidence of hepatitis B, hepatitis C, HIV-1, HIV-2 and
syphilis.
• Donations are leukodepleted as a precaution against variant Creutzfeldt–
Jakob disease (this may also reduce the immunogenicity of the transfusion).
• The ABO and rhesus D blood groups are determined, as well as the presence
of irregular red cell antibodies. The blood is then processed into
subcomponents

29. WHOLE BLOOD
 Advantage over packed cells as it is coagulation factor rich and, if fresh, more
metabolically active than stored blood

30. PACKED RED CELLS
 Packed red blood cells are spun-down and concentrated packs of red blood
cells.
 Each unit is approximately 330 mL and has a haematocrit of 50–70%.
 Packed cells are stored in a SAG-M solution (saline–adenine–glucose–
mannitol)
to increase shelf life to 5 weeks at 2–6°C.
 (Older storage regimes included storage in CPD:
citrate–phosphate–dextrose solutions,
which have a shelf life of 2–3 weeks.)

31. FRESH-FROZEN PLASMA
 Rich in coagulation factors and is removed from fresh blood and stored at
−40 to −50°C with a 2-year shelf life.
 It is the first-line therapy in the treatment of coagulopathic haemorrhage
 Rhesus D-positive FFP may be given to a rhesus D-negative
woman although it is possible for
seroconversion to occur with large
volumes owing to the presence of
red cell fragments, and
Rh-D immunisation should be considered.

32. CRYOPRECIPITATE
 A supernatant precipitate of FFP and is rich in factor VIII and fibrinogen.
 It is stored at −30°C with a 2-year shelf life. It is given in low fibrinogen states
or factor VIII deficiency.

33. PLATELETS
 Platelets are supplied as a pooled platelet concentrate and contain about 250
× 109 /L.
 Platelets are stored on a special agitator at 20–24°C and have a shelf life of
only 5 days.
 Given to patients with thrombocytopenia or with platelet dysfunction who are
bleeding or undergoing surgery

34. PROTHROMBIN COMPLEX CONCENTRATES
 Highly purified concentrates prepared from pooled plasma.
 They contain factors II, IX and X. Factor VII may be included or
produced separately.
 It is indicated for the emergency reversal of anticoagulant (warfarin)
therapy in ucontrolled haemorrhage.

35. AUTOLOGOUS BLOOD
 It is possible for patients undergoing elective surgery to predonate their own
blood up to 3 weeks before surgery for retransfusion during the operation
 Similarly, during surgery blood can be collected in a cell-saver which washes
and collects red blood cells which can then be returned to the patient.

36. INDICATIONS OF BLOOD TRANSFUSION
 : ● Acute blood loss, to replace circulating volume and maintain oxygen
delivery;
 ● Perioperative anaemia, to ensure adequate oxygen delivery during
the perioperative phase;
 ● Symptomatic chronic anaemia, without haemorrhage or impending
surgery.

37. TRANSFUSION TRIGGER
 A haemoglobin level of 6 g/dL is acceptable in patients who are not actively
bleeding, not about to undergo major surgery and are not symptomatic.
 There is some controversy as to the optimal haemoglobin level in some
patient groups, such as those with cardiovascular disease, sepsis and
traumatic brain injury. Although, conceptually, a higher haemoglobin level
improves oxygen delivery.

39. BLOOD GROUP AND CROSS MATCHING
 The term blood group is applied to any well-defined system of red blood cell
antigens which are inherited characteristics.
 Over 20 blood group systems having approximately 400 blood group antigens are
currently recognised.
 The ABO and Rhesus (Rh) blood group systems are of major clinical significance.
 Other minor and clinically less important blood group systems are:
 Lewis system, P system, I system, MNSsystem, Kell and Duffy system, and Luthern
system.

40. ABO SYSTEM

42.  Red blood cells of type O and A2 have large amounts of another antigen
called H substance which is genetically different from ABO but is a precursor
of A and B antigens.
 An O group individual who inherits A or B genes but fails to inherit H gene
from either parent is called Oh phenotype or Bombay blood group.
 In such rare individual, despite the presence of all the three antibodies in
serum (anti-A, anti-B
 and anti-H), the red cells are not agglutinated by the antisera.

43.  Rhesus system:
 The Rh allelic genes are C or c, D or d and E or e, located on chromosome 1. One set of 3
genes is inherited from each parent giving rise to various complex combinations.
 The corresponding antigens are similarly named Cc, Ee and only D since no d antigen
D antigen is most strongly immunogenic and, therefore, clinically most important.
All Rh antibodies in Rh-negative individuals are acquired from immunisation such as by
transfusion and during pregnancy, resulting in fatal haemolytic transfusion reaction and
haemolytic disease of the newborn .

44.  A pre-transfusion compatibility testing is essential prior to any blood
transfusion. The procedure consists of the following:
 1. ABO and Rh(D) grouping of the patient (recipient).
 2. Antibody screening of the patient’s serum to detect the
 presence of clinically significant antibodies.
 3. Selecting the donor blood of the same ABO and Rh group.
 4. Cross-matching the patient’s serum against donor red cells
 to confirm donor-recipient compatibility.

45. CROSS MATCHING
 All transfusions are preceded by ABO and rhesus typing of both donor and
recipient blood to ensure compatibility.
 The recipient’s serum is then mixed with the donor’s cells to confirm ABO
compatibility and to test for rhesus and any other blood group antigen–
antibody reaction.
 Full cross-matching of blood may take up to 45 minutes in most laboratories.
 In more urgent situations, ‘type specific’ blood is provided which is only
ABO/rhesus matched and can be issued within 10–15 minutes.
 Where blood must be given emergently, group O (universal donor) blood is
given (O− to females, O+ to males).

46. THE PRECAUTIONS
 When blood transfusion is prescribed and blood is administered, it is essential
that the correct patient receives the correct transfusion.
 Two healthcare personnel should check patient details against the prescription
and the label of the donor blood.
 In addition, the donor blood serial number should also be checked against the
issue slip for that patient.
 Provided these principles are strictly adhered to the number of severe and fatal
ABO incompatibility reactions can be minimised.

47. BEFORE TRANSFUSION
 the following with the medical record, patient ID band, and the blood product
label:
 Informed consent
 Patient identification number
 Patient name
 Blood group and type
 Expiration date
 Inspection of blood product for clots or unusual color

48. BEFORE THE TRANSFUSION
REMEMBER TO…
 Begin IV line with normal saline
 (Never use D5/DNS and RL solution instead of saline )
 Review the signs and symptoms of a transfusion reaction with the patient
 Advise patient to report any chills, itching, hives, swelling, rash, shortness of breath, fever,
low back pain, nausea, or anything unusual
 Use blood within 30 minutes after its arrival from the blood bank
 Establish a baseline
 Obtain vital signs
 Auscultate lungs
 Assess for JVP

49.  Assess the patient ,look for any reaction in the initial stage ,of no reaction one
can proceed and blood transfusion should be completed within 4 hrs
 If two back to back transfusion are to be given then Inj Lasix 20 mg IV (Blood
pressure should be assessed to avoid hypotension) should be given in
between transfusions
 During transfusion, monitor vitals at regular intervals

50. IF YOU SUSPECT A REACTION...
 Stop blood transfusion immediately
 Inj Avil 2 cc iv stat
 Inj Hydrocortisone 100 mg iv stat
Continue saline infusion and monitor for vitals

51. SOME MORE POINTS ….

52. DAMAGE CONTROL RESUSCITATION
 Permissive hypotension until definitive surgical control
 Minimal crystalloid use
 Initial use of 5% hypertonic saline
 Early use of blood products (PRBCs,FFP,Platelets,cryoprecipitates)
 Consider drugs to treat coagulopathy (rFVIIa,prothrombin concentrate,TXA)

53. WHOLE BLOOD RESUSCITATION
 Used by military surgeons
 Activation of walking blood bank when received warning about incoming
casualties
 Blood is withdrawn and mixed with 50 to 100 ml of citrate-phosphate-
dextrose,which binds calcium and prevents clotting in the bag
 The bag of fresh blood is then transfused within minutes after donation
 (Look for hypocalcemia which can occur due to CPD,as it can lead to
coagulopathy )

54. RESUSCITATION WITH 1:1:1
• The PROMMT study demonstrated that during massive transfusion that
patients transfused with PRBCs,FFPs,Platelets in the ration of 1:1:1 or 1:1:2 was
associated with improved survival .
• It prevents MODS,ARDS,infection,venous thromboembolism or sepsis .

55. MASSIVE TRANSFUSION PROTOCOL
 It improves survival in trauma patients
 MASSIVE TRANSFUSION PROTOCOL AT THE UNIVERSITY OF ARIZONA
COOLER 1 COOLER 2 COOLER 3 COOLER 4 COOLER 5 COOLER 6
UNITS OF
PRBCS
2 4 6 6 6 6
UNITS OF FFP 6 6 6 6
UNITS OF
PLATELETS
1 1 1
UNITS OF
CRYOPRECIPITA
TE
20 10

56.  In Massive Transfusion Protocol directive for severely injured patients ,blood bank should
bring a cooler with 2 units of unmatched O-negative blood that can be used for resuscitation
 (Usually patient’s blood sample should be drawn before the unmatched blood is transfused)
 If patient requires more PRBCs before cross matched blood is available ,4 units of O negative
blood should be made available .If cross matched blood is available then it should be
preferred
 For patients requiring more than 6 PRBCs ,7 to 12 units of PRBCs should be transfused along
with 6 units of FFPs and 1 unit of apheresis platelets .
 Uncrossmatched blood is predictor of complications such as ARDS and sepsis

57. TRANSFUSION REACTIONS
 Immunological transfusion reaction
 1.Haemolytic transfusion reaction
 - Intravascualar haemolysis - ABO incompatibility
 Restlessness, anxiety, flushing, chest or lumbar pain, tachypnoea, tachycardia and nausea, followed by
shock and renal failure.
 - Extravascular haemolysis - Immune antibodies of Rh system
 Less severe, consist of malaise and fever mostly
 Delayed reactions in which the patient develops anaemia due to destruction of red cells in the RE
system

58.  2. Transfusion-related acute lung injury (TRALI).
 Results from transfusion of donor plasma containing high levels of anti-HLA antibodies which bind to
leucocytes of recipient.
 These leucocytes then aggregate in pulmonary micromutation and release mediators of increased
vascular permeability resulting in acute pulmonary oedema and signs and symptoms of respiratory
failure.
 3. Other allergic reactions are as follows
 i) Febrile reaction
 ii) Anaphylactic shock on transfusion of blood from other
 human subjects.
 iii) urticaria may occur.
 iv) Transfusion-related graft-versus-host disease mediated by donor T lymphocytes may occur.

59. NON IMMUNE TRANSFUSION REACTION
 - Circulatory overload
 - Massive transfusion - results in dilutional thrombocytopenia and
dilution of coagulation factors.
 -Transmission of infections
 - Air embolism
 - Thrombophlebitis
 -Transfusion haemosiderosis

60. COMPLICATIONS
 .
 Complications from a single transfusion include:
 ● incompatibility haemolytic transfusion reaction;
 ● febrile transfusion reaction;
 ● allergic reaction;
 ● infection:
 ● bacterial infection (usually due to faulty storage);
 ● hepatitis;
 ● HIV;
 ● malaria;
 ● air embolism;
 ● thrombophlebitis;
 ● transfusion-related acute lung injury (usually from FFP)

61. Complications from massive transfusion(transfusion of more than 10 PRBCs in
24 hrs ) include:
● coagulopathy;
● hypocalcaemia;
● hyperkalaemia;
● hypokalaemia;
● hypothermia
In addition, patients who receive repeated transfusions over long periods of
time (e.g. patients with thalassaemia) may develop iron overload. (Each
transfused unit of red blood cells contains approximately 250 mg of elemental
iron.)

62. MANAGEMENT OF COAGULOPATHY
 Prevention of dilutional coagulopathy is central to the damage control resuscitation of
patients who are actively bleeding.
 It is best to match each red cell unit with one unit of FFP and one of platelets (1:1:1). This will
reduce the incidence and severity of subsequent dilutional coagulopathy.
 Crystalloids and colloids should be avoided for the same reason.
 The balanced transfusion approach cannot, however, correct coagulopathy.
 Therefore, coagulation should be monitored routinely, either with point-of-care testing
(thromboelastometry) or with laboratory tests (fibrinogen, clotting times)
 The antifibrinolytic tranexamic acid is the most commonly administered. It is usually
administered empirically to bleeding patients because effective point-of-care tests of
fibrinolysis are not yet routinely available.

63. CONTINUED…
 FFP : If PT or PTT is x 1.5 normal
 Cryoprecipitate :If fibrinogen is < 0.8 g/l
 Platelet : 50 x 109 /L

64. BLOOD SUBSTITUTES
 Blood substitutes are an attractive alternative to the costly process of
donating, checking, storing and administering blood, especially given the
immunogenic and potential infectious complications associated with
transfusion.
 Blood substitutes are either biomimetic or abiotic..

65.  Examples :
 1)Hemoglobin oxygen carriers -
 - Derived from outdated human blood,bovine/swine blood,transgenic E.coli
 e.g. HBOC 201,PolyHeme,Hemoglobin in liposomes
 2)Perflurocarbons
 3)Pyruvate Ringer’s solution,L-Lactate,etc.
 4)Dried plasma

66. THANK YOU
THANK YOU