Hemorrhage and Shock and Blood Transfusion.pptx

This is described in detail for surgery subject topic shock, hemorrhage, blood transfusion for points vise it's introduction, cause, effect, pathophysiology, management, treatment for medical student for notes type and easy language to study with diagram description for helpful for surgery medicine

1. Shock & Hemorrhage - By Dr. Nisit Patel

2. Shock Shock is the most common and therefore the most important cause of death of surgical patients.

3. Shock – Definition Shock is a systemic state of low tissue perfusion that is inadequate for normal cellular respiration. With insufficient delivery of oxygen and glucose , cells switch from aerobic to anaerobic metabolism. If perfusion is not restored in a timely fashion, cell death ensues.

4. 1. Cellular Perfusion to tissue decreased Cells deprived of O2 Switch from aerobic to anaerobic metabolism By product – Lactic Acid Cause Metabolic Acidosis Glucose also exhausted So no energy / ATP Failure of Na + /K + pump Intracellular lysosomes release Cell lysis/death 2. Microvascular As tissue ischaemia progresses… Activation of the immune and coagulation systems Hypoxia and acidosis activate complement Generation of oxygen free radicals and cytokine release Injury of the capillary endothelial cells Damaged endothelium loses its integrity and becomes ‘leaky’ Fluid leaks out and tissue oedema occurs, exacerbating cellular hypoxia Shock – Pathophysiology

5. 3. Systemic CVS Increased sympathetic activity R elease of catecholamines Results in tachycardia and systemic vasoconstriction Respiratory System Metabolic acidosis and increased sympathetic response Increased respiratory rate and minute ventilation To increase the excretion of carbon dioxide Shock – Pathophysiology

6. 3. Systemic Renal decreased perfusion pressure in the kidney leads to reduced filtration at the glomerulus and a decreased urine output RAAS is activated further vasoconstriction and increased sodium and water reabsorption by the kidney Endocrine vasopressin ( a nti d iuretic h ormone) is released from the hypothalamus in response to decreased preload and leads to vasoconstriction and resorption of water in the renal collecting system Cortisol is also released Shock – Pathophysiology

7. 4. Ischaemia–reperfusion syndrome During the period of systemic hypoperfusion Cellular and organ damage progresses due to the direct effects of tissue hypoxia and local activation of inflammation The cellular and humoral elements activated by the hypoxia (complement, neutrophils, microvascular thrombi) are flushed back into the circulation where they cause further endothelial injury to organs such as the lungs and the kidneys. This leads to acute lung injury, acute renal injury, multiple organ failure and death . Reperfusion injury can currently only be attenuated by reducing the extent and duration of tissue hypoperfusion. Shock – Pathophysiology

8. Shock – Classification There are numerous ways to classify shock, but the most common and most clinically applicable is one based on the initiating mechanism. All states are characterised by systemic tissue hypoperfusion, and different states may coexist within the same patient

9. 1. Hypovolaemic shock It is due to a reduced circulating volume Hypovolaemia may be due to haemorrhagic or non- haemorrhagic causes. Non- haemorrhagic causes include poor fluid intake (dehydration), excessive fluid loss due to vomiting, diarrhoea, urinary loss (e.g. diabetes), evaporation. Hypovolaemia is probably the most common form of shock, and to some degree is a component of all other forms of shock. Shock – Classification

10. 2. Cardiogenic shock It is due to primary failure of the heart to pump blood to the tissues . Causes of cardiogenic shock include myocardial infarction, cardiac dysrhythmias, valvular heart disease, blunt myocardial injury and cardiomyopathy. Cardiac insufficiency may also be due to myocardial depression caused by endogenous factors (e.g. bacterial and humoral agents released in sepsis) or exogenous factors, such as pharmaceutical agents or drug abuse. Shock – Classification

11. 3. Obstructive shock In obstructive shock there is a reduction in preload due to mechanical obstruction of cardiac filling. Common causes of obstructive shock include cardiac tamponade, tension pneumothorax, massive pulmonary embolus or air embolus. In each case, there is reduced filling of the left and/or right sides of the heart leading to reduced preload and a fall in cardiac output. Shock – Classification

12. 4. Distributive shock Distributive shock describes the pattern of cardiovascular responses characterising a variety of conditions, including septic shock, anaphylaxis and spinal cord injury . Inadequate organ perfusion is accompanied by vascular dilatation with hypotension , low systemic vascular resistance, inadequate afterload and a resulting abnormally high cardiac output. Shock – Classification

13. 5. Endocrine shock May present as combination of hypovolaemic , cardiogenic or distributive shock Causes of endocrine shock include hypo- and hyperthyroidism and adrenal insufficiency Shock – Classification

14. Shock - Severity

15. Compensated As shock progresses, the body’s cardiovascular and endocrine compensatory responses reduce flow to non-essential organs to preserve preload and flow to the lungs and brain. In compensated shock, there is adequate compensation to maintain central blood volume and preserve flow to the kidneys, lungs and brain . Apart from a tachycardia and cool peripheries (vasoconstriction, circulating catecholamines ), there may be no other clinical signs of hypovolaemia . Although clinically occult, this state will lead to multiple organ failure and death if prolonged, due to the ischaemia –reperfusion effect . Shock - Severity

16. Decompensated Further loss of circulating volume overloads the body’s compensatory mechanisms and there is progressive renal, respiratory and cardiovascular decompensation . In general, loss of around 15% of the circulating blood volume is within normal compensatory mechanisms. Blood pressure is usually well maintained and only falls after 30–40% of circulating volume has been lost. Shock - Severity

17. Initially there is tachycardia, tachypnoea , a mild reduction in urine output and the patient may exhibit mild anxiety. BP is maintained although there is a decrease in pulse pressure. The peripheries are cool and sweaty with prolonged capillary refill times. Shock - Severity Decompensated – Mild Shock

18. As shock progresses, renal compensatory mechanisms fail, renal perfusion falls and urine output dips below 0.5 mL/kg per hour. There is further tachycardia, and now the BP starts to fall. Patients become drowsy and mildly confused . Shock - Severity Decompensated – Moderate Shock

19. In severe shock, there is profound tachycardia and hypotension. Urine output falls to zero Patients are unconscious with laboured respiration. Shock - Severity Decompensated – Severe Shock

20. Shock – C/F Compensated Mild Moderate Severe Lactic Acidosis + ++ ++ +++ Urine Output Normal Normal Reduced Anuric Conscious Level Normal Mild Anxiety Drowsy Comatose Respiratory Rate Normal Increased Increased Laboured Pulse Rate Mild increase Increased Increased Increased BP Normal Normal Mild Hypotension Severe Hypotension

21. Shock – Consequences Unresuscitable Shock Patients who are in profound shock for a prolonged period of time become ‘ unresuscitable ’. Cell death follows from cellular ischaemia and the ability of the body to compensate is lost. Death is the inevitable result. Multiple Organ Failure The result of prolonged systemic ischaemia and reperfusion injury is end-organ damage and multiple organ failure . It is defined as two or more failed organ systems. There is no specific treatment for multiple organ failure. Multiple organ failure currently carries a mortality of 60% ; thus, prevention is vital by early aggressive identification and reversal of shock.

22. Shock – Effects of Organ Failure

23. Shock – Resuscitation Immediate resuscitation manoeuvres for patients presenting in shock are to ensure a patent airway and adequate oxygenation and ventilation . Once ‘airway’ and ‘breathing’ are assessed and controlled, attention is directed to cardiovascular resuscitation.

24. Conduct of Resuscitation In patients who are actively bleeding (major trauma, aortic aneurysm rupture, gastrointestinal haemorrhage ), it is counterproductive to institute high-volume fluid therapy without controlling the site of haemorrhage . Increasing blood pressure merely increases bleeding from the site while fluid therapy cools the patient and dilutes available coagulation factors. Thus operative haemorrhage control should not be delayed and resuscitation should proceed in parallel with surgery. Shock – Resuscitation

25. Fluid Therapy In all cases of shock, regardless of classification, hypovolaemia and inadequate preload must be addressed before other therapy is instituted. First-line therapy, therefore, is intravenous access and administration of intravenous fluids . Access should be through short, wide-bore catheters that allow rapid infusion of fluids as necessary. Shock – Resuscitation

26. Fluid Therapy – Type of Fluids There is no ideal resuscitation fluid , and it is more important to understand how and when to administer it. No overt difference in response or outcome between crystalloid solutions (normal saline, Hartmann’s solution, Ringer’s lactate) or colloids (albumin or commercially available products). Most importantly, the oxygen carrying capacity of crystalloids and colloids is zero . If blood is being lost, the ideal replacement fluid is blood , although crystalloid therapy may be required while awaiting blood products. Shock – Resuscitation

27. Fluid Therapy – Dynamic Fluid Response The shock status can be determined dynamically by the cardiovascular response to the rapid administration of a fluid bolus. In total, 250–500 mL of fluid is rapidly given (over 5–10 minutes) and the cardiovascular responses in terms of heart rate, blood pressure and central venous pressure are observed. Patients can be divided into ‘responders’, ‘transient responders’ and ‘non-responders ’. Shock – Resuscitation

28. Vasopressor and inotropic support It is not indicated as first-line therapy in hypovolaemia . Administration of these agents in the absence of adequate preload rapidly leads to decreased coronary perfusion and depletion of myocardial oxygen reserves. Vasopressor agents (phenylephrine, noradrenaline) are indicated in distributive shock states (sepsis, neurogenic shock) where there is peripheral vasodilatation. In cardiogenic shock, or where myocardial depression has complicated a shock state inotropic therapy may be required to increase cardiac output and therefore oxygen delivery. The inodilator dobutamine is the agent of choice Shock – Resuscitation

29. Shock – Resuscitation Trendelenburg position — head down position, used in patient in shock Correction of acid-base balance: Acidosis is corrected by using 8.4% sodium bicarbonate IV . Steroid is often life-saving. 500–1000 mg of hydrocortisone can be given. Antibiotics in patients with sepsis; proper control of blood sugar and ketosis in diabetic patients Nasal oxygen to improve oxygenation or ventilator support Ventilator and ICU/critical care management

30. Shock – Monitoring

31. Hemorrhage Hemorrhage is treated by arresting the bleeding – not by fluid resuscitation or blood transfusion

32. Hemorrhage – Classification

33. Hemorrhage – Pathophysiology

34. Hemorrhage – C/F

35. Hemorrhage – Signs of Significant Loss

36. Hemorrhagic Shock Classification Class Blood loss Features I Up to 15% (< 750 ml) Normal II Blood loss 15–30% (750–1500 ml) Palor , thirsty, tachycardia III Blood loss 30–40% (1500–2000 ml) Hypotension, tachycardia, oliguria, confusion IV Blood loss > 40% (> 2000 ml) Rapid pulse, low BP, anuria, unconsciousness, MODS

37. Hemorrhage – Measurement of Blood Loss Clot size of a clenched fist is 500 ml. Blood loss in a closed tibial fracture is 500–1500 ml; In a fracture femur is 500–2000 ml. Weighing the swab before and after use is an important method of on-table assessment of blood loss Hb % and PCV estimation. Measurement of CVP or PCWP. Investigations specific for cause: U/S abdomen, Doppler and often angiogram in vascular injury, chest X-ray in haemothorax , CT scan in major injuries, CT scan head in head injuries Mops used during major surgery should be kept in a rack so that quantity of bleeding during surgery can be assessed approximately

38. Hemorrhage – Effects

39. Hemorrhage – Treatment Stop the blood loss : Pressure Packing Position and rest Operative procedures. Restoring the lost blood : Fresh whole blood transfusion Plasma expanders Blood transfusion is required if Hb % is < 8 g% One unit of blood should raise 1 gm% of haemoglobin Damage control surgery Arrest hemorrhage Control sepsis Protect from further injury Nothing else

40. Hemorrhage – Treatment

41. Hemorrhage – Treatment Catheterisation , foot end elevation, monitoring. Oxygen support/intubation/ventilator and critical care. Pressure, packing and head down ( Trendelenburg ) position to restore BP and blood supply of brain Wound exploration and proceeding, i.e. ligation of the small vessel, suturing the wound part, vessel suturing (anastomosis), excision of the tissues Laparotomy for liver or spleen or mesentery or bowel injuries, suturing, splenectomy Topical applications for local ooze— Oxycel , gauze soaked with adrenaline, bone wax for oozing from bone and other local haemostatic agents (collagen, thrombin)

42. Blood Transfusion

43. BT – Indications Acute blood loss following trauma, >15% of total body volume in otherwise healthy individuals (liver, spleen, kidney, GIT injuries, fractures, haemothorax , perineal injuries). During major surgeries —abdominoperineal surgery, thoracic surgery, hepatobiliary surgery. Following burns. In septicaemia . As a prophylactic measure prior to surgery. Whole blood is given in acute blood loss. Packed cells are given in chronic anaemia . Blood fractions are given in ITP, haemophilias

44. BT – Donor Criteria Donor should be fit without any serious diseases like HIV1 and HIV2 and hepatitis infections and malaria . Weight of donor should be >45 kg

45. BT – Complications Congestive cardiac failure (CCF) Transfusion reactions HBV, HCV Incompatibility: Major and minor reactions with fever, rigors, pain, hypotension Pyrexial reactions due to pyrogenic ingredients in the blood Allergic reactions Sensitisation to leucocytes and platelets Immunological sensitization Infections Serum hepatitis HIV infection Bacterial infection Malaria transmission Epstein- barr virus infection Cytomegalovirus infection Syphilis, Yersinia Babesia microti infection Trypanosoma cruzi infection

46. BT – Complications Air embolism, Thrombophlebitis Allergic Reaction Febrile transfusion reaction Coagulation failure Dilution of clotting factors DIC Dilutional thrombocytopenia occurs in patients with massive blood transfusion TRALI - transfusion-related acute lung injury Circulatory overload causing heart failure Haemochromatosis in patients with CRF receiving repeated blood transfusions Citrate intoxication causes bradycardia and hypocalcaemia. For every four units of blood 10 ml of 10% calcium chloride or gluconate should be infused intravenously Iron overload