Shock and Blood Transfusion
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This document discusses shock and blood transfusion. It defines shock as a state of low tissue perfusion that is inadequate for normal cellular respiration. It describes the pathophysiology of shock at the cellular, microvascular, and systemic levels. It classifies shock into hypovolemic, cardiogenic, obstructive, distributive, and endocrine types. The document also discusses blood transfusion, including definitions, indications, blood products, complications, and management of coagulopathy during massive transfusion.
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This document discusses the metabolic response to injury, including the classical concepts of homeostasis and the physiological changes that occur during injury and recovery. It describes the ebb and flow phases of the metabolic response, characterized initially by catabolism to provide substrates for survival, followed by a catabolic phase and later anabolic phase for repair. Key aspects of the response include hypermetabolism, insulin resistance, protein catabolism and redistribution, and the acute phase protein response in the liver. Avoiding unnecessary factors like continued bleeding, hypothermia, underperfusion and immobilization can help minimize the metabolic stress response to injury.
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Shock and Blood Transfusion
Shock is a state of low tissue perfusion resulting in inadequate cellular respiration. With reduced oxygen and glucose delivery, cells switch from aerobic to anaerobic metabolism, producing lactic acid and risking cell death if perfusion is not restored. Shock is classified as hypovolemic, cardiogenic, obstructive, distributive, or endocrine/neurogenic and ranges from compensated to severe.
Blood transfusion involves transfusing blood products intravenously to replace lost components. Whole blood is now rarely used, with components like red blood cells, platelets, plasma, and cryoprecipitate being transfused individually. Testing and compatibility checks are done prior to transfusion to reduce risks of reactions or infections
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Electrolytes play a vital role in maintaining homeostasis within the body. They help to regulate heart and neurological function, fluid balance, oxygen delivery, acid–base balance and much more. Electrolyte imbalances can develop by the following mechanisms: excessive ingestion; diminished elimination of an electrolyte; diminished ingestion or excessive elimination of an electrolyte. The most serious electrolyte disturbances involve abnormalities in the levels of sodium, potassium or calcium.
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The document discusses disseminated intravascular coagulation (DIC), including its causes, clinical features, diagnostic testing, management, and complications. DIC results from excessive activation of coagulation pathways leading to microthrombi formation and bleeding. It is always secondary to an underlying condition like infection, malignancy, trauma, or obstetric complications. Management involves treating the underlying cause, monitoring for bleeding and organ dysfunction, and replacing clotting factors or administering anticoagulants depending on the clinical situation. Complications can be bleeding or thromboembolic in nature. The prognosis depends on the severity of DIC and underlying condition.
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This document discusses ischemia-reperfusion injury, which occurs when blood flow returns to tissues that had previously lost their blood supply. It causes further damage beyond what occurred during ischemia alone. The two phases of injury - ischemic and reperfusion - each have unique cellular and systemic consequences. Clinically, it can cause issues like compartment syndrome, gastrointestinal/renal injury, and myocardial dysfunction. The pathophysiology involves hypoxia, inflammation, apoptosis, reactive oxygen species generation, and nitric oxide imbalance. Strategies to prevent or reduce injury include ischemic preconditioning, antioxidant therapy, anti-complement therapy, and antileukocyte therapy.
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3. Blood banks collect, test, and store blood products. They screen donations for infectious agents and determine blood type to ensure compatible transfusions. A transfusion is prepared by selecting a compatible blood type, and then confirming compatibility through cross-matching before transfusion.
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Shock is a clinical state characterized by inadequate tissue perfusion resulting from insufficient oxygen and substrate delivery to meet metabolic demands. There are several types of shock defined by etiology (hypovolemic, cardiogenic, distributive) and effects on blood pressure (compensated, decompensated). Signs of shock include tachycardia, altered mental status, and decreased urine output. Treatment involves rapid fluid resuscitation and vasoactive drugs like dopamine, epinephrine, and norepinephrine to support cardiac output as needed.
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Debridement is an important component of the wound bed preparation (WBP) management Model.
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Debridement is the removal of necrotic tissue, exudate, bacteria, and metabolic waste from a wound in order to improve or facilitate the healing process
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This document discusses fluid management and discusses several key points:
1) It outlines the typical water content of the human body which can vary from 45-75% depending on factors like age, gender, and body type.
2) It describes the importance of fluid for homeostasis, transport mechanisms, metabolic reactions, tissue texture, and temperature regulation.
3) It discusses fluid disturbances like hypovolemia which is a common issue for surgical patients and can be caused by factors like bleeding, vomiting, diarrhea, or burns.
4) It provides guidance on fluid resuscitation versus maintenance volumes and outlines some special fluids that can be used in certain clinical situations.
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This document discusses hemorrhage and shock. It covers:
1. The classification of hemorrhage based on the vessel involved, timing, volume lost, and type of intervention needed.
2. The signs and symptoms of hemorrhage and its pathophysiological effects like depletion of venous reservoirs and failure to maintain blood pressure.
3. The physiological response to hemorrhage including hemostasis, the three stages of clot formation, and new models of hemostasis involving an initiation, amplification, and propagation phase.
4. Methods for measuring blood loss are also mentioned. The document provides an overview of hemorrhage, its effects, and the body's response to stop bleeding.
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Blood transfusion
1. A blood transfusion involves transferring blood or blood products from a donor to a recipient. It is often done to replace blood lost through severe bleeding.
2. There are different types of blood transfusions depending on when the blood is collected and transfused. These include pre-operative autologous donation, intra-operative autologous transfusion, and post-operative autologous transfusion.
3. Blood banks collect, test, and store blood products. They screen donations for infectious agents and determine blood type to ensure compatible transfusions. A transfusion is prepared by selecting a compatible blood type, and then confirming compatibility through cross-matching before transfusion.
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Shock is a clinical state characterized by inadequate tissue perfusion resulting from insufficient oxygen and substrate delivery to meet metabolic demands. There are several types of shock defined by etiology (hypovolemic, cardiogenic, distributive) and effects on blood pressure (compensated, decompensated). Signs of shock include tachycardia, altered mental status, and decreased urine output. Treatment involves rapid fluid resuscitation and vasoactive drugs like dopamine, epinephrine, and norepinephrine to support cardiac output as needed.
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This document summarizes the key aspects of shock. Shock occurs when there is inadequate oxygen delivery to tissues, which can lead to cellular damage and death if left untreated. The main causes of shock discussed are hypovolaemic, septic, and cardiogenic shock. Signs and symptoms of shock include low blood pressure, fast heart rate, pale skin, confusion, and low urine output. Management involves identifying the type and stage of shock to guide fluid resuscitation and drug therapy aimed at restoring adequate circulation and oxygen delivery to tissues.
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This document summarizes shock, haemorrhage, and blood transfusion. It defines shock and describes the pathophysiology of shock at the cellular, microvascular, and systemic levels. It also classifies shock by severity and management principles. Haemorrhage is defined and classified, and its management is outlined. Blood transfusion is defined and the indications, products, and complications are discussed. Massive transfusion and its associated coagulopathy are also summarized.
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Cellular adaptations can occur through hyperplasia, hypertrophy, atrophy, or metaplasia in response to stress or changes in workload or stimulation. Hyperplasia involves an increased number of cells through cell proliferation. Hypertrophy involves cellular enlargement without an increase in cell number. Atrophy is a decrease in cell size. Metaplasia is the replacement of one adult cell type with another. Examples provided include uterine hyperplasia during pregnancy, cardiac hypertrophy in hypertension, muscle fiber atrophy after injury or disuse, and squamous metaplasia in the lungs of smokers. Dysplasia refers to alterations in cell size, shape, and organization and is a pre-cancerous condition.
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This document summarizes pathology related to white blood cells. It discusses non-neoplastic disorders like leukopenia (decreased white blood cells), neutropenia (decreased neutrophils), and reactive leukocytosis (increased white blood cells in response to infection). It also discusses neoplastic disorders of white blood cells. Specifically, it provides details on infectious mononucleosis caused by Epstein-Barr virus, including pathogenesis, morphology, and clinical features like fever, sore throat, and lymphadenitis. It also discusses cyclic neutropenia, a rare condition where neutrophil counts decrease periodically.
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Debridement is an important component of the wound bed preparation (WBP) management Model.
Cause of the wound and patient-centered concerns, debridement is a necessary step in local wound care.
Debridement is the removal of necrotic tissue, exudate, bacteria, and metabolic waste from a wound in order to improve or facilitate the healing process
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This document discusses fluid management and discusses several key points:
1) It outlines the typical water content of the human body which can vary from 45-75% depending on factors like age, gender, and body type.
2) It describes the importance of fluid for homeostasis, transport mechanisms, metabolic reactions, tissue texture, and temperature regulation.
3) It discusses fluid disturbances like hypovolemia which is a common issue for surgical patients and can be caused by factors like bleeding, vomiting, diarrhea, or burns.
4) It provides guidance on fluid resuscitation versus maintenance volumes and outlines some special fluids that can be used in certain clinical situations.
Hemorrhage and shock
This document discusses hemorrhage and shock. It covers:
1. The classification of hemorrhage based on the vessel involved, timing, volume lost, and type of intervention needed.
2. The signs and symptoms of hemorrhage and its pathophysiological effects like depletion of venous reservoirs and failure to maintain blood pressure.
3. The physiological response to hemorrhage including hemostasis, the three stages of clot formation, and new models of hemostasis involving an initiation, amplification, and propagation phase.
4. Methods for measuring blood loss are also mentioned. The document provides an overview of hemorrhage, its effects, and the body's response to stop bleeding.
Wounds, healing and tissue repair
The document discusses normal wound healing processes and phases including haemostatic, inflammatory, proliferative, and remodelling phases. It also discusses abnormal healing processes and managing different types of acute and chronic wounds. Specific topics covered include normal healing in bone, nerve, tendon tissues and abnormal healing processes. Management strategies for different wound types such as bites, puncture wounds, haematomas, degloving injuries, and compartment syndromes are provided. Chronic wounds including leg ulcers and pressure sores are also summarized.
Crush syndrome - Dr Bipul Borthakur
Crush syndrome results from prolonged pressure on muscle tissue, causing rhabdomyolysis. It is characterized by the release of toxic muscle contents into the bloodstream due to cell death. This can cause kidney damage, electrolyte abnormalities, and other systemic effects. Treatment involves aggressive fluid resuscitation, dialysis if needed, and surgery to relieve pressure on muscles through fasciotomy. Early fluid replacement within 6 hours of injury is critical to prevent complications from crush syndrome.
Shock its pathopysiology and management
This document discusses shock, including definitions, types, causes, pathophysiology, diagnosis, and treatment. It defines shock as a state of low tissue perfusion from inadequate oxygen and glucose delivery. The main types of shock discussed are hypovolemic, cardiogenic, obstructive, distributive, and septic shock. Treatment involves identifying and treating the underlying cause, restoring circulating blood volume and tissue perfusion through fluid resuscitation, and providing vasopressor support if needed to maintain blood pressure. Goals of resuscitation are optimizing oxygen delivery while avoiding fluid overload.
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Last update in diagnosis and mangement of dic
This document discusses disseminated intravascular coagulation (DIC), including its definition, pathophysiology, forms, causes, clinical presentation, diagnosis, and histological findings. DIC is an acquired syndrome characterized by widespread blood clotting and microvascular thrombosis. It can be caused by sepsis, trauma, malignancy, obstetric complications, and other conditions. Diagnosis involves scoring systems, laboratory tests showing coagulation abnormalities and thrombocytopenia, and sometimes histological evidence of microthrombi.
Damage control resuscitation
This document discusses principles of damage control resuscitation for traumatic hemorrhage. It describes how hemorrhage can lead to hypovolemic shock and coagulopathy, exacerbating blood loss. Damage control resuscitation aims to rapidly restore blood volume while limiting blood pressure increases to prevent further bleeding. It emphasizes early use of blood products rather than crystalloids to avoid dilutional coagulopathy, and maintaining hemostasis through permissive hypotension, tranexamic acid, and ratio-based blood component resuscitation. While controversial, this approach may improve outcomes compared to aggressive crystalloid resuscitation in severely bleeding trauma patients.
Sirs
The document discusses systemic inflammatory response syndrome (SIRS) and defines it as a systemic response to various stresses that includes symptoms like fever, increased heart rate, respiratory rate and white blood cell count. It outlines the progression from infection to bacteremia to sepsis, which involves SIRS criteria and a suspected or proven infection. The stages of sepsis like severe sepsis, septic shock and refractory septic shock are defined based on the presence of organ dysfunction or hypotension.
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SHOCK SYNDROMESHOCK SYNDROME
• Shock is a condition in which the cardiovascular system
fails to perfuse tissues adequately
• An impaired cardiac pump, circulatory system, and/or
volume can lead to compromised blood flow to tissues
• Inadequate tissue perfusion can result in:
– generalized cellular hypoxia (starvation)
– widespread impairment of cellular metabolism
– tissue damage organ failure
– death
ATHOPHYSIOLOGYPATHOPHYSIOLOGY
Cells switch from aerobic to anaerobic metabolism
lactic acid production
Cell function ceases & swells
membrane becomes more permeable
electrolytes & fluids seep in & out of cell
Na+/K+ pump impaired
mitochondria damage
cell death
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This document defines and classifies shock. It discusses the pathophysiology of different types of shock including hypovolaemic, cardiogenic, obstructive, distributive, endocrine, and adrenal insufficiency shock. It describes the clinical features of shock and the initial management including airway control, intravenous fluids, blood transfusion, vasopressors, and inotropes as needed.
Shock
This document provides information on shock, including its definition, types, pathophysiology, clinical features, and management. It defines shock as a state of inadequate tissue perfusion and oxygenation that can lead to organ dysfunction and death. The main types of shock discussed are hypovolemic, septic, and cardiogenic shock. For each type, the document outlines their pathophysiology, signs and symptoms, and general management approach. Overall, it serves as an overview of shock for medical students, covering the essential details of definitions, types, effects on organ systems, and clinical distinctions between compensated and decompensated states of shock.
Treatment of shock
Shock is defined as a state where the circulatory system fails to maintain adequate cellular perfusion, resulting in reduced delivery of oxygen and nutrients to tissues. There are four main types of shock: hypovolemic (caused by fluid loss), cardiogenic (caused by heart failure), obstructive (caused by obstruction of blood flow), and distributive (caused by vasodilation). Treatment for shock involves identifying the cause, managing hemodynamic and metabolic consequences, and treating complications. Interventions include fluid resuscitation, vasopressors, inotropes, and treating the underlying cause of shock. Goals of treatment are to restore adequate blood pressure, tissue perfusion and oxygen delivery, and
Shock
Shock is defined as inadequate tissue perfusion resulting in decreased oxygen delivery and buildup of waste, and can progress from early compensated stages to intermediate stages involving organ damage and late irreversible stages involving multiple organ failure. The document outlines the pathophysiology and stages of shock including effects on body systems, clinical markers, causes, and treatment focusing on restoring tissue perfusion through fluid resuscitation and management of the underlying cause.
Diagnosis, Investigations and Management of Shock
The document discusses various types of shock including hypovolaemic, cardiogenic, septic, neurogenic, endocrine, and anaphylactic shock. It describes the etiology, clinical features, investigations, and management principles for each type. It also covers the severity of shock from mild to severe, the effects of shock on different organs, and introduces the concept of multiple organ dysfunction syndrome that can occur in shock.
Shock and blood transfusion
This document discusses shock and blood transfusion. It defines shock as a state of low tissue perfusion that is inadequate for normal cellular respiration. It then describes the pathophysiology of shock at the cellular, microvascular, and systemic levels. The document also classifies different types of shock and discusses their causes and clinical features. It provides guidance on resuscitation methods for shock, including fluid therapy, vasopressor support, and monitoring. The document then discusses blood transfusion, including its history, components of blood that can be transfused, indications for transfusion, and precautions for safe transfusion.
shock surgery -bailey and love
Shock is the state of not enough blood flow to the tissues of the body as a result of problems with the circulatory system.Initial symptoms may include weakness, fast heart rate, fast breathing, sweating, anxiety, and increased thirst. This may be followed by confusion, unconsciousness, or cardiac arrest as complications worsen.
Shock is divided into four main types based on the underlying cause: low volume, cardiogenic, obstructive, and distributive shock. Low volume shock may be from bleeding, diarrhea, vomiting, or pancreatitis. Cardiogenic shock may be due to a heart attack or cardiac contusion. Obstructive shock may be due to cardiac tamponade or a tension pneumothorax. Distributed shock may be due to sepsis, spinal cord injury, or certain overdoses.
The diagnosis is generally based on a combination of symptoms, physical examination, and laboratory tests. A decreased pulse pressure (systolic blood pressure minus diastolic blood pressure) or a fast heart rate raises concerns. The heart rate divided by systolic blood pressure, known as the shock index (SI), of greater than 0.8 supports the diagnosis more than low blood pressure or a fast heart rate in isolation.
Treatment of shock is based on the likely underlying cause.[2] An open airway and sufficient breathing should be established.[2] Any ongoing bleeding should be stopped, which may require surgery or embolization.[2] Intravenous fluid, such as Ringer's lactate or packed red blood cells, is often given.[2] Efforts to maintain a normal body temperature are also important.[2] Vasopressors may be useful in certain cases.[2] Shock is both common and has a high risk of death.[3] In the United States about 1.2 million people present to the emergency room each year with shock and their risk of death is between 20 and 50%
Shock by Dr Ibrahim kimani wainaina
Shock is defined as a physiological state with reduced tissue perfusion and oxygen delivery. It can be caused by various conditions that prevent the circulatory system from meeting metabolic demands. The main types of shock are hypovolemic, cardiogenic, obstructive, distributive, and septic shock. Treatment involves identifying the underlying cause, restoring circulating blood volume, and supporting vital organ function.
Basic_Shock_Presentation[1].ppt
Shock is defined as inadequate organ perfusion and tissue oxygenation. It can be caused by hypovolaemia from blood loss, cardiac issues, or neurogenic factors. The body activates compensatory mechanisms through the cardiovascular, renal, respiratory, and cerebral systems but these fail over time without treatment. Signs of shock include decreased consciousness, fast heart rate, pale skin, and low urine output. Treatment involves fluid resuscitation, controlling bleeding, and monitoring the patient's color, breathing, pulse, and consciousness. Without adequate treatment, shock leads to multiple organ failure and death.
Shock in neonates
This document discusses shock in neonates. It defines shock and describes its consequences as inadequate tissue and organ perfusion. It outlines factors that influence adequate tissue perfusion like cardiac output, vascular tone, and blood's ability to deliver oxygen. It then describes types of shock including hypovolemic, cardiogenic, distributive, and obstructive shock. For hypovolemic shock, common causes in neonates are discussed. The document provides details on evaluating and managing neonatal shock, including fluid resuscitation, vasopressor and inotropic drug use, and investigational tests. It concludes that while neonatal shock significantly impacts mortality, management strategies have improved survival rates.
Shock
Shock is a condition where the cardiovascular system fails to adequately perfuse tissues. It can be caused by an impaired pump (cardiogenic shock), reduced circulating volume (hypovolemic shock), or maldistribution of blood flow (distributive shock). The main effects are cellular hypoxia, impaired metabolism, and organ damage or failure if not treated. Compensatory mechanisms aim to increase perfusion but eventually fail, leading to irreversible cellular damage and death if shock persists.
Shock
1. The document discusses pediatric shock, including its definition, types, pathophysiology, signs, investigations, and management.
2. The main types of shock discussed are hypovolemic, cardiogenic, distributive, obstructive, and septic shock.
3. Management of shock involves rapid recognition and resuscitation through fluid administration, vasopressors, and addressing metabolic abnormalities to restore adequate tissue perfusion.
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Shock and Blood Transfusion
- 1. SHOCK AND BLOOD TRANSFUSION Dr. Joel Danie Mathew Assistant Professor Department of General Surgery BCMCH
- 3. SHOCK A systemic state of low tissue perfusion, which is inadequate for normal cellular respiration
- 4. 6 Demand Supply Shock
- 5. Pathophysiology Cellular Microvascular Systemic - Cardiovascular, Respiratory, Renal & Endocrine
- 6. 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 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
- 7. Microvascular Hypox ia & 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 Tissue ischemia progresses Activation of immune & coagulation system
- 8. Systemic Cardiovascular Preload & afterload Compensatory baroreceptor response Increased Sympathetic activity Catecholamines release into the circulation Tachycardia Systemic vasoconstricti on
- 9. Respiratory Metabolic acidosis Inc. sympathetic stimulation Tachypnea Excretion of CO2 increased Compensatory respiratory alkalosis
- 10. Renal Decreased renal perfussion Decreased glomerular filtration -> decreased urine output Stimulate RAAS Vasoconstriction & inc. Na & water reabsorption
- 11. Endocrine Hypothalamus Adrenal cortex Vasopressin Cortisol Vasoconstriction Na & water reabsorption Sensitizing cells to catecholamines
- 13. •Hypovolemic Shock •Cardiogenic shock •Obstructive Shock •Distributive shock •Endocrine
- 14. Classification of shock Hypovolemic shock Reduced circulatory volume 1. Haemorrhagic ( Internal / external bleeding) 2. Non Haemorrhagic ( dehydration, vomiting, diarrhea, burns)
- 15. Cardiogenic Shock Primary failure of heart to pump blood to tissues Causes : MI, Cardiac dysrhythmias,valvular heart diseases, blunt myocardial injury & cardiomyopathy
- 16. Obstructive shock Reduction in preload because of mechanical obstruction of cardiac filling Causes: Cardiac tamponade Tension pneumothorax Massive pulmonary embolus Air embolus
- 17. Distributive Shock Inadequacy of intravascular volume vascular vasodilatation with hypotension low systemic vascular resistance, inadequate afterload Abnormally high cardiac output Causes : Septic shock Anaphylaxis Spinal cord injury
- 18. Endocrine shock Combination of hypovolemic, cardiogenic & distributive shock Hypothyroidism -> disordered cardiac & vascular responsiveness to circulating catecholamines -> neurogenic shock . CO falls due to low inotropy & bradycardia Adrenal insufficiency- Hypovolemia & poor response to circulating & exogenous catecholamines -> shock
- 19. Severity of Shock Compensated Decompensated
- 20. Compensated mild moderate severe Lactic acidosis + ++ ++ +++ Urine Output Normal Normal Reduced Anuric Consciousness Normal MildAnxiety Drowsy Comatose Respiratory rate Normal Increased Increased Laboured Pulse rate Mild increase Increased Increased Increased Blood Pressure Normal Normal Mild hypo Mild hypo
- 21. Resuscitation A. Conduct of resuscitation:
- 23. SHOCK STATUS:
- 24. Resuscitation C.Vasopressor & Inotrope Support:
- 25. MONITORING
- 26. HAEMORRHAGE Further haemorrhage - > ↓ Perfusion to the tissue - > unable to generate heat Coagulopathy Hypothermia Acidosis Decrease function of coagulation proteases - > coagulopathy TraumaTriad of Death
- 27. Definitions:
- 30. Blood Transfusion Definition: Process of transferring whole blood or blood components from one person (donor) to another (recipient). Indications: Acute blood loss Perioperative anemia Symptomatic chronic anemia without haemorrhage or impending surgery
- 31. Perioperative red blood cell transfusion criteria Source: Bailey & Love’s Short Practice of Surgery25th ed
- 32. Blood & Blood Products Blood component Explanation Whole blood [can be broken down to: RBC, platelets, fresh frozen plasma (FFP)] • Very rarely used • Carries greater risks of adverse reactions owing to the presence of leucocytes. Packed Red Cell • Each unit isapproximately 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 the coagulation; also contain plasma (coagulation factors), some red cells and some white cells (leukocytes)] • For patients with bleeding due to either thrombocytopenia, platelet dysfunction • Temporary thrombocytopenia occuring after radio- and chemotherapy, • Bleeding in patients with thrombocytopenia or functional platelet abnormality
- 33. 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 [supernatant precipitate of FFP and is rich in factor VIII and fibrinogen] • For Hemophilia A, von Willebrand disease, DIC, Hypofibrinogenemia (<100 mg/dl) Factor VIII concentrates • Hemophilia A, & low titer factor VIII inhibitors Factor IX Concentrates • Hemophilia B
- 35. Single transfusion incompatibility haemolytic transfusion reaction febrile transfusion reaction allergic reaction infection air embolism thrombophlebitis transfusion-related acute lung injury (TRALI)
- 36. Massive transfusion Coagulopathy Hypocalcemia Hyperkalaemia Hypokalaemia Hypothermia Iron overload
- 37. Management of coagulopathy Correction of coagulopathy isnot necessary if no active bleeding/ haemorrhage However, coagulopathy following during massive transfusion should be anticipated and managed aggressively Standard guidelines: FFP: if PTor PTT> 1.5 Xnormal; Cryoprecipitate : if fibrinogen < 0.8g/l Platelet : if platelet count < 50 x109ml
- 38. THANKYOU!