shock and blood trasfution problems and complications

Blood

1. Shock and blood transfusion Dr:Avtandil bolqvadze 2022

2. LECTURE OVERVIEW Shock-pathophysiology Classification of shock Severity of shock Resuscitation-the principles and priorities of resuscitation Monitoring for patient in shock Haemorrhage Classification of haemorrhage Management of haemorrhage Blood and blood products Blood groups-ABO, RH system Blood transfusion-indications, cross-matching Complications of blood transfusion

3. shock Shock is a systemic state of low tissue perfusion that is inadequate for normal cellular respiration If perfusion is not restored in a timely fashion this lead to cell die Shock is a life threatening

4. pathophysiology At cellular level Deprivation of 02 Anaerobic metabolism Accumulation of lactic acid-met. Acidosis Failure of Na /K pumps-intracellular lysosomes activate release autodigestive enzymes-cell lysis

5. Pathophysiology Microvascular changes Ischemia progresses Hypoxia an acidosis –activate complement and neutrophilis Generation of oxygen free radicals and cytokine release Injury of the capillary endothelial cells Damaged endothelium becomes leaky, fluid leaks out Oedema, cellular hypoxia

6. Compensatory mechanisms Cardiovascular preload and afterload reduction Baroreceptor response Increased sympathetic activity Release of catecholamines into the circulation Tachycardia and systemic vasoconstiction Respiratory Metaboloc acidosis and increased sypmthetic responcse Increased respiratory rate and minute ventilation Increases the excertion of carbon dioxide(produces a compensatory respiratory alkalosis) Renal Low perfusion to kidneys Activation:renin-angiotension-aldosterone system Vasoconstriction and increased resorbtion of sodium and water Endocrine Decereased preload(activation of baroceceptors ) releases vasopressin from hypothalamus(antiduretic hormone) systemic vasoconstictor Decereased preload(activation of baroceceptors ) releases cotrizol from the adrenal cortex resorbtion of sodium and water

7. Calssification of shock Hypovolaemic shock- associated with reduced circulating volume Cardiogenic shock- associated with insufficient pumping function of the heart Obstructive shock-associated with mechanical obstruction of cardiac filling Distributive shock-associated with inadequate organ perfusion,vascular dilatation with hypotension Endocrine shock

8. Hypovolaemic shock Haemorrhagic causes Gi bleeding Abdominal aortic Aneurysm rupture Trauma Postpartum hemorrhage ectopic pregnancy Non haemorrhagic causes Dehydration Vomiting,diarrhoea Bowel obstruction Acute pancreatitis Urinary loss(diabetes)

9. Cardiogenic shock Causes Myocardial infarction Cardiac dysrhythmias Valvular heart disease(aortic, mitral valve stenosis,…) Dilated Cardiomyopathy Congential heart diseases Blunt myocardial injury

10. Obstructive shock Causes Tension pneumothorax Cardiac tamponade Massive pulomonary embolus/air embolus

11. Distributive shock Septic shock Causes-release of bacterial toxins Anaphylactic shock-severe systemic allergic reaction Causes:bee stings, drug, food allergies, I.V contrast allergies Neurogenic shock-failure of symphathetic outflow and adequate vascular tone Causes:acute spinal cord injury Endocrine shock Causes Hypo and hyperthyroidism Adrenal insufficiency

12. Stages/Severity of shock Compensated shock : In compensated shock there is adequate compensation to maintain central blood volume and preserve flow to the kidneys ,lungs and brain Tachycardia and cool peripheries (clinical signs) There may be no other clinical signs There is a systemic metaboloc acidosis within the underperfused organs Although clinically occult, this state will lead to multiple organ failure and death if prolonged

13. Stage/Severity of shock Decompensated shock: Further loss of circulating volume overloads the body,s compensatory mechanisms and there is progressive renal, respiratory and cardiovascular decompensation

14. Cardiac output is the term that describes the amount of blood the heart pumps each minute Systemic vascular resistance(SVR) is  the resistance in the circulatory system that is used to create blood pressure, the flow of blood and is also a component of cardiac function . Central venous pressure (CVP) is  the pressure in the thoracic vena cava near the right atrium .  mixed venous oxygen saturation (SvO2) refers to  the oxygen content of blood that returns to the heart after meeting tissue needs . Norm:50-70% A base deficit  indicates an excess of acid

15. Shock –General treatment principles Although treatment should be aimed at the underlying etiology of shock, the most critical aspect of treatment is the prompt restoration of normal hemodynamics Priorities: Pulse, ventilation, and oxygenation Fluids(unless pt has cardiogenic shock) “Pressors”(vasopressors and inotropes) Everything else

16. Shock -General treatment priciples From a hemodynamic perspective there are three main categories of treatment for shock Iv fluids-increases cvp,left ventricular and diastolic volume Vasopressors-increases svp (systemic vascular rsistance) Inotropes-increases contractility,cardiac output

17. Shock-General treatment principles shock Iv fluids CVP Vasopressors SVR Inotropes contractility hypovolemic + Temporary use only - distributive + + +/- cardiogenic - - + obstructive +/- +/- +/-

18. Monitoring for patients in shock Minimum ECG Pulse oximetry Blood pressure Urine output Additional modalities Central venous pressure Invasive blood pressure Cardiac output Serium lactate Mixed venous oxygen saturation

19. haemorrhage Definition: the loss of blood from the circulatory system or the escape of blood from the blood vessels into surrounding tissue

20. Classification of haemorrhage Clinical classification: Revealed or external -blood leakes from blood vessels either through a natural opening such as the mouth, nose, ear, vagina, anus or through a brake in the skin Concealed or internal -blood leakes from blood vessels inside the body such es within chest, abdomen, pelvis,retroperitoneum or in the limbs Causes :deep chest or abdominal wound,any cut into muscle or fracturing of bone, bleeding ulcers,ruptured aortic aneurysm Signs : Anxiety and restlessness Excessive thirst(polydipsia) Nausea and vomiting Cool,moist and pale skin(cold and clammy) Rapid breathing(tachypnea) Rapid ,weak pulse(tachycardia)

21. Classification of haemorrhage Varietis of bleeding Arterial bleeding:blood loss is rapid and profuse,the color of blood is bright red, blood spurts as the heart beats, can cause death quickly Venous bleeding: blood loss is a steady flow,the color of blood is dark Capillary bleeding:blood flow is slow,the color of blood is red but less bright

22. Classification of haemorrhage According to the time of wound Primary haemorrhage :occurs immediately(a cut finger or an operation incision) Reactionary haemorrhage :occurs in first 24-hr after operation(dislodgement of a clot by resuscitation, normalisation of blood pressure, technical failure-slippage of a ligature secondary haemorrhage :occurs 7-14 days after injury. If infection are present, walls of blood vessels may be eroded and may burst ,causing secondary haemorrhage

23. management External bleeding management: Direct pressure In direct pressure Elevation tourniquet

24. Classification of haemorrhagic shock

25. management Internal bleeding- management Airway Breathing Circulation Blood transfusion Fluids surgery

26. GI bleeding-Endoscopic and laparoscopic image

27. Blood groups according to ABOsystem Blood is divided into four groups according to presence or absence of certain antigen on the surface of RBCs We have two tipes of antigen on RBC A antigen B antigen We have four possibilities of presence or absence of these two types of antigens Absence of both A and B antigens ………..group O Presence of A antigen………………group A Presence of B antigen………………group B Presence of both A and B antigens …………….group AB

28. Genetic determination of ABO antigens Humans have three different gens for expression ABO genes(A,B and O genes).gene O is functionless. These genes are on two chromosomes(pair9) 6 possible combinations (genotypes)and 4 group AA…….group A --- 42% AO…….group A ---42% AB…….group AB –3% BB…….group B --- 9% BO…….group B --- 9% OO…….group O ---46%

29. Agglutinins(antibodies) Found in plasma Are mostly of IgM type(gamma globulin) Landsteiner,S Law(for ABO system) states that if an atigen is absent, the corresponding abtibody is present Conversely, if an antigen is present on the surface of the RBC, the corresponding antibody is absent in the plasma

30. Rhesus system Rh factor is an atigen present in RBC. This antigen was discovered by Landsteiner and Wiener It was first discovered in Rhesus monkey and hence the name Rh factor. There are many Rh antigens but only the D antigen is more antigenic in human The persons having D antigen are called Rh positive and those without D antigen are called Rh negative 85 % of people are Rh positive and 15% are Rh negative Percentage of Rh positive people is more among black people Rh group system is different from ABO group system because the antigen D does not have corresponding natural antibody (anti-D). However if Rh postitive blood is transfused to a Rh negative person anti-D is developed in that person On the other hand, there is no risk of complications if the Rh positive person receives Rh negative blood

31. Blood and blood products Whole blood Packed red cells -are spun-down and concentrated packs of red blood cells, 330ml max,HCT-50-70% Fresh-frosen plasma(FFP) -is removed from fresh blood and stored at -40-50 C, contains coagulation factors Cryoprecipitate -contains factorVII and fibrinogen. Stored at -30 C Platelets - are prepared by using a centrifuge to separate the platelet-rich plasma from the donated unit of whole blood. platelet concentrates contain about 60mL of plasma and small numbers of red blood cells and leukocytes Prothrombin complex concentrates(PCC) -contain factor II, IX, X Autologous blood

32. Blood transfusion Blood transfusion is the process of transferring blood or blood components from one person (the donor) into the bloodstream of another person(the recipient) Richard lower pioneered the first blood transfusion from animal to human in 1665 at the Royal Society In 1840 Dr. James Blundell, performed the first successful whole blood transfusion to treat haemophilia

33. Indications for blood transfusion Acute blood loss-to reduce hypovolemia and improve oxygen carrying capacity of blood Perioperative anaemia-to ensure adeuate oxygen delivery during perioperative phase Symptomatic chronic anaemia-aplastic anaemia, leukemias, hemophilia,clotting and bleeding disorders

34. Precautions to be taken before the transfusion of blood Donor must be healthy, without any diseases like: Diseases caused by virus like hepatitis, AIDS Sexually transmitted diseases such as syphilis Only compatible blood must be transfused Both matching and cross –matching must be done Rh compatibility must be confirmed

35. Complications of blood transfusion Incompatibility haemolytic transfusion reaction-the reactions may be mild causing only fever and hives(skin disorder characterized by itching) or may be severe leading to renal failure, shock and death Febrile transfusion reaction Allergic reaction Infection-hepatitis,bacterial infection,HIV Air embolism Thrombophlebitis Coagulopathy Hypocalcaemia Hyperkalaemia hypokalaemia Hypothermia Iron overload