Shock & blood transfusion

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  • 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.
  • Anaphylaxis (vasodilatation is caused by histamine release) High spinal cord injury (failure of sympathetic outflow & adequate vascular tone: neurogenic shock) Sepsis (release of endotoxins by bacteria causes vasodilatation
  • Shock & blood transfusion

    1. 1. SHOCK & BLOODTRANSFUSIONBY: R. NANDINII GROUP K1
    2. 2. Overview: • BLOOD• SHOCK • HAEMORRHAGE TRANSFUSION-Definition -Definition -Definition-Pathophysiology -Classification -Indication-Classification -Management -Blood products-Severity -Complication-Management-Monitoring
    3. 3. SHOCK
    4. 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. 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. 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. 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
    8. 8. Classification of shock:
    9. 9. Classification of shock:
    10. 10. Classification of shock:
    11. 11. Severity of Shock Decompensated Compensated Mild Moderate SevereConsciousness Normal Mild Anxiety Drowsy ComatoseBlood Pressure Normal Normal Mild ↓ Severe ↓ Pulse Rate Mild Increase ↑ ↑ ↑ Resp Rate Normal ↑ ↑ Laboured Urine Output Normal Normal Reduced AnuricLactic 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. 12. ResuscitationA. Conduct of resuscitation:
    13. 13. ResuscitationB. Fluid therapy:
    14. 14. SHOCK STATUS:
    15. 15. ResuscitationC. Vasopressor & Inotrope Support:
    16. 16. MONITORING
    17. 17. HAEMORRHAGEFurther haemorrhage Hypothermia ↓ Perfusion to the tissue  unable to generate heat Coagulopathy Acidosis Decrease function of coagulation proteases  coagulopathy Trauma Triad of Death
    18. 18. Definitions:
    19. 19. Degree & Classification
    20. 20. Management: After control aggressively resuscitated, warmed and coagulopathy corrected
    21. 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. 22. Perioperative red blood cell transfusion criteriaSource: Bailey & Love’s Short Practice of Surgery 25th ed
    23. 23. Blood & Blood Products Blood component ExplanationWhole blood • Very rarely used[can be broken down to: RBC, • Carries greater risks of adverse reactions owingplatelets, 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 anemiaPlatelet • For patients with bleeding due to either[for the coagulation; also contain thrombocytopenia, platelet dysfunctionplasma (coagulation factors), some • Temporary thrombocytopenia occuring afterred 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. 24. Blood & Blood Products Blood component ExplanationFresh 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 theleukocytes and platelets] presence of prolonged PT, aPTTCryoprecipitate • For Hemophilia A, von Willebrand disease, DIC,[supernatant precipitate of FFP and is Hypofibrinogenemia (<100 mg/dl)rich infactor VIII and fibrinogen]Factor VIII concentrates • Hemophilia A, & low titer factor VIII inhibitorsFactor IX Concentrates • Hemophilia B
    25. 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. 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
    27. 27. THANK YOU

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