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SHOCK & BLOOD
TRANSFUSION
BY: R. NANDINII
   GROUP K1
Overview:
                                     •   BLOOD
•   SHOCK          •   HAEMORRHAGE       TRANSFUSION
-Definition        -Definition       -Definition
-Pathophysiology   -Classification   -Indication
-Classification    -Management       -Blood products
-Severity                            -Complication
-Management
-Monitoring
SHOCK
Pathophysiology:
Cellular
                                  When perfusion to
                                  the tissue reduces

                                             Glucose within cells are exhausted
       ↓ O2 delivery to tissue
                                                Anaerobic respiration ceases

            Cell Metabolism
                                              Failure of Na/K pump in the cell
              (aerobic
                                             membrane & intracellular organelle
              anaerobic)

             Accumulation of                    Intracellular lysosome release
           lactic acid in blood                     autodigestive enzymes

                                                           Cell lysis

        Systemic metabolic
             acidosis                          Intracellular content including K
                                                released into the bloodstream
Pathophysiology:
Microvascular

        Tissue ischemia      Hypoxia &             Activate
           progresses         acidosis        complement & prime
                                                  neutrophils

        Activation Of
           Immune                                Generation of
        & Coagulation                         oxygen free radicals
            System                             & cytokine release


        Tissue oedema
                                              Injury of the capillary
            ensues →
                                                endothelial cells
        exacerbating cell
             hypoxia

                            Fluid leaks out
Pathophysiology:
Systemic
                                                          Systemic
   Cardiovascular:                                    vasoconstriction


        ↓ Preload     Compensatory                     Catecholamines
            &         baroreceptor       ↑             release into the
        Afterload       response     sympathetic          circulation
                                       activity

                                                        Tachycardia

   Respiratory:
                                        Tachypnea

                            ↑                           Compensatory
        Metabolic                                        Respiratory
                      sympathetic
         acidosis                                         alkalosis
                        response
                                        Excretion of
                                       CO2 increased
   Renal:

                           ↓ Glomerular              ↓ urine
                             filtration              output
             ↓ Kidney
             Perfusion
                            Stimulate            ↑ Na & water
                         Renin-angiotensin-      reabsorption
                            aldosterone

   Endocrine:

                                              vasoconstriction
        Hypothalamus     Vassopressin
                                                Na & water
                                               reabsorption
              Adrenal      Cortisol
              Cortex                          Sensitizing cell to
                                               catecholamine
Classification of shock:
Classification of shock:
Classification of shock:
Severity of Shock
                                                  Decompensated
                   Compensated
                                      Mild          Moderate        Severe
Consciousness        Normal        Mild Anxiety      Drowsy        Comatose
Blood Pressure       Normal          Normal           Mild ↓        Severe ↓
     Pulse Rate    Mild Increase        ↑               ↑              ↑
     Resp Rate       Normal             ↑               ↑          Laboured
    Urine Output     Normal          Normal         Reduced         Anuric
Lactic Acidosis         +              ++              ++             +++
   Compensated : Compensatory responses reduce flow to non-essential organs to
    preserve preload & flow to the lungs & brain.
   Decompensated : Further loss body’s compensatory mechanisms, Progressive
    renal, respiratory & CVS decompensation; Occurs when there’s 30-40% loss of
    Blood Volume.
Resuscitation
A. Conduct of resuscitation:
Resuscitation
B. Fluid therapy:
SHOCK STATUS:
Resuscitation
C. Vasopressor & Inotrope Support:
MONITORING
HAEMORRHAGE

Further haemorrhage               Hypothermia
 ↓ Perfusion to the
 tissue  unable to
    generate heat




               Coagulopathy                                  Acidosis

                          Decrease function of coagulation
                            proteases  coagulopathy


                              Trauma Triad of Death
Definitions:
Degree & Classification
Management:




              After control
              aggressively
              resuscitated,
              warmed and
              coagulopathy
              corrected
Transfusion
 Definition:
 Process of transferring whole blood or blood components from
 one person (donor) to another (recipient).


 Indications:
 Acute   blood loss
       to replace circulating volume & O2 delivery
 Perioperative   anemia
       To ensure adequate O2 delivery during perioperative phase.
 Symptomatic     chronic anemia without haemorrhage or impending surgery
       Hb < 6 g/dl
Perioperative red blood cell transfusion criteria




Source: Bailey & Love’s Short Practice of Surgery 25th ed
Blood & Blood Products
           Blood component                                 Explanation
Whole blood                             • Very rarely used
[can be broken down to: RBC,            • Carries greater risks of adverse reactions owing
platelets, fresh frozen plasma (FFP)]     to the presence of leucocytes.
Packed Red Cell                         • Each unit is approximately 330 ml and has a
[do not provide viable platelets or       haematocrit of 50–70%.
neutrophils]                            • For use in substantial hemorrhage & anemia,
                                          symptomatic anemia
Platelet                                • For patients with bleeding due to either
[for the coagulation; also contain        thrombocytopenia, platelet dysfunction
plasma (coagulation factors), some      • Temporary thrombocytopenia occuring after
red cells and some white cells            radio- and chemotherapy,
(leukocytes)]                           • Bleeding in patients with thrombocytopenia or
                                          functional platelet abnormality,
                                        • After massive transfusion (RBC) and
                                          thrombocytopenia
Blood & Blood Products
          Blood component                                    Explanation
Fresh frozen Plasma (FFP)                • Corrections of known congenital or acquired
[contains all coagulation factors in       coagulation factor deficiencies.
normal amounts and is free of red cells, • Treatment of microvascular hemorrhage in the
leukocytes and platelets]                  presence of prolonged PT, aPTT



Cryoprecipitate                          • For Hemophilia A, von Willebrand disease, DIC,
[supernatant precipitate of FFP and is     Hypofibrinogenemia (<100 mg/dl)
rich in
factor VIII and fibrinogen]
Factor VIII concentrates                 • Hemophilia A, & low titer factor VIII inhibitors

Factor IX Concentrates                   • Hemophilia B
Complication
 Single transfusion                        Massive transfusion
    incompatibility haemolytic               • coagulopathy;
     transfusion reaction;
    • febrile transfusion reaction;
                                              • hypocalcaemia;
    • allergic reaction;                     • hyperkalaemia;
    • infection:                             • hypokalaemia;
    – bacterial infection (usually as a
     result of faulty storage);
                                              • hypothermia.
    – hepatitis;                             Patients who receive repeated
    – HIV;                                    transfusions over long periods of
                                               time (e.g. patients with
    – malaria;
                                               thalassaemia) develop iron
    • air embolism;                           overload. (Each transfused unit of
    • thrombophlebitis;                       red blood cells contains
    • transfusion-related acute lung          approximately 250 mg of
     injury (usually from FFP).                elemental iron.)
Management of coagulopathy

    Correction of coagulopathy is not necessary if no active
     bleeding/ haemorrhage
    However, coagulopathy following during massive
     transfusion should be anticipated and managed
     aggressively
    Standard guidelines:
        FFP : if PT or PTT > 1.5 X normal;
        Cryoprecipitate : if fibrinogen < 0.8 g/l
        Platelet : if platelet count < 50 x 109 ml
THANK YOU

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Shock & blood transfusion

  • 1. SHOCK & BLOOD TRANSFUSION BY: R. NANDINII GROUP K1
  • 2. Overview: • BLOOD • SHOCK • HAEMORRHAGE TRANSFUSION -Definition -Definition -Definition -Pathophysiology -Classification -Indication -Classification -Management -Blood products -Severity -Complication -Management -Monitoring
  • 4. Pathophysiology: Cellular When perfusion to the tissue reduces Glucose within cells are exhausted ↓ O2 delivery to tissue Anaerobic respiration ceases Cell Metabolism Failure of Na/K pump in the cell (aerobic membrane & intracellular organelle anaerobic) Accumulation of Intracellular lysosome release lactic acid in blood autodigestive enzymes Cell lysis Systemic metabolic acidosis Intracellular content including K released into the bloodstream
  • 5. Pathophysiology: Microvascular Tissue ischemia Hypoxia & Activate progresses acidosis complement & prime neutrophils Activation Of Immune Generation of & Coagulation oxygen free radicals System & cytokine release Tissue oedema Injury of the capillary ensues → endothelial cells exacerbating cell hypoxia Fluid leaks out
  • 6. Pathophysiology: Systemic Systemic  Cardiovascular: vasoconstriction ↓ Preload Compensatory Catecholamines & baroreceptor ↑ release into the Afterload response sympathetic circulation activity Tachycardia  Respiratory: Tachypnea ↑ Compensatory Metabolic Respiratory sympathetic acidosis alkalosis response Excretion of CO2 increased
  • 7. Renal: ↓ Glomerular ↓ urine filtration output ↓ Kidney Perfusion Stimulate ↑ Na & water Renin-angiotensin- reabsorption aldosterone  Endocrine: vasoconstriction Hypothalamus Vassopressin Na & water reabsorption Adrenal Cortisol Cortex Sensitizing cell to catecholamine
  • 11. Severity of Shock Decompensated Compensated Mild Moderate Severe Consciousness Normal Mild Anxiety Drowsy Comatose Blood Pressure Normal Normal Mild ↓ Severe ↓ Pulse Rate Mild Increase ↑ ↑ ↑ Resp Rate Normal ↑ ↑ Laboured Urine Output Normal Normal Reduced Anuric Lactic Acidosis + ++ ++ +++  Compensated : Compensatory responses reduce flow to non-essential organs to preserve preload & flow to the lungs & brain.  Decompensated : Further loss body’s compensatory mechanisms, Progressive renal, respiratory & CVS decompensation; Occurs when there’s 30-40% loss of Blood Volume.
  • 12. Resuscitation A. Conduct of resuscitation:
  • 15. Resuscitation C. Vasopressor & Inotrope Support:
  • 17. HAEMORRHAGE Further haemorrhage Hypothermia  ↓ Perfusion to the tissue  unable to generate heat Coagulopathy Acidosis Decrease function of coagulation proteases  coagulopathy Trauma Triad of Death
  • 20. Management: After control aggressively resuscitated, warmed and coagulopathy corrected
  • 21. Transfusion Definition: Process of transferring whole blood or blood components from one person (donor) to another (recipient). Indications: Acute blood loss  to replace circulating volume & O2 delivery Perioperative anemia  To ensure adequate O2 delivery during perioperative phase. Symptomatic chronic anemia without haemorrhage or impending surgery  Hb < 6 g/dl
  • 22. Perioperative red blood cell transfusion criteria Source: Bailey & Love’s Short Practice of Surgery 25th ed
  • 23. Blood & Blood Products Blood component Explanation Whole blood • Very rarely used [can be broken down to: RBC, • Carries greater risks of adverse reactions owing platelets, fresh frozen plasma (FFP)] to the presence of leucocytes. Packed Red Cell • Each unit is approximately 330 ml and has a [do not provide viable platelets or haematocrit of 50–70%. neutrophils] • For use in substantial hemorrhage & anemia, symptomatic anemia Platelet • For patients with bleeding due to either [for the coagulation; also contain thrombocytopenia, platelet dysfunction plasma (coagulation factors), some • Temporary thrombocytopenia occuring after red cells and some white cells radio- and chemotherapy, (leukocytes)] • Bleeding in patients with thrombocytopenia or functional platelet abnormality, • After massive transfusion (RBC) and thrombocytopenia
  • 24. Blood & Blood Products Blood component Explanation Fresh frozen Plasma (FFP) • Corrections of known congenital or acquired [contains all coagulation factors in coagulation factor deficiencies. normal amounts and is free of red cells, • Treatment of microvascular hemorrhage in the leukocytes and platelets] presence of prolonged PT, aPTT Cryoprecipitate • For Hemophilia A, von Willebrand disease, DIC, [supernatant precipitate of FFP and is Hypofibrinogenemia (<100 mg/dl) rich in factor VIII and fibrinogen] Factor VIII concentrates • Hemophilia A, & low titer factor VIII inhibitors Factor IX Concentrates • Hemophilia B
  • 25. Complication Single transfusion Massive transfusion  incompatibility haemolytic  • coagulopathy; transfusion reaction;  • febrile transfusion reaction;  • hypocalcaemia;  • allergic reaction;  • hyperkalaemia;  • infection:  • hypokalaemia;  – bacterial infection (usually as a result of faulty storage);  • hypothermia.  – hepatitis;  Patients who receive repeated  – HIV; transfusions over long periods of time (e.g. patients with  – malaria; thalassaemia) develop iron  • air embolism; overload. (Each transfused unit of  • thrombophlebitis; red blood cells contains  • transfusion-related acute lung approximately 250 mg of injury (usually from FFP). elemental iron.)
  • 26. Management of coagulopathy  Correction of coagulopathy is not necessary if no active bleeding/ haemorrhage  However, coagulopathy following during massive transfusion should be anticipated and managed aggressively  Standard guidelines:  FFP : if PT or PTT > 1.5 X normal;  Cryoprecipitate : if fibrinogen < 0.8 g/l  Platelet : if platelet count < 50 x 109 ml

Editor's Notes

  1. hypothyroid : result of disordered vascular and cardiac responsiveness to circulating catecholamines. Cardiac output falls because of low inotropy and bradycardia. There may also be an associated cardiomyopathy. Thyrotoxicosis may cause a high-output cardiac failure. Adrenal insufficiency leads to shock as a result of hypovolaemia and a poor response to circulating and exogenous catecholamines. Adrenal insufficiency may result from pre-existing Addison’s disease or it may be a relative insufficiency caused by a pathological disease state such as systemic sepsis.
  2. Anaphylaxis (vasodilatation is caused by histamine release) High spinal cord injury (failure of sympathetic outflow &amp; adequate vascular tone: neurogenic shock) Sepsis (release of endotoxins by bacteria causes vasodilatation