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Types of Hemorrhage?
- Primary Hemorrhage
- Reactionary hemorrhage
- Secondary hemorrhage
Pathophysiology and management of complications of blood transfusion. [TU 2062]
Enumerate the complication of massive blood transfusion. Discuss the diagnosis and management of DIC. [TU 2060]
Short notes on hazards of blood transfusion. [TU 2057,62]
Complications of massive BT. Discuss management of DIC. [TU 2073/7]
Enumerate the complications of massive blood transfusion. Discuss in short methods of diagnosis and mgmt. Of DIC.[TU 2060/6]
What is massive blood transfusion?
Massive BT is defined as a volume equivalent or exceeding the patients own volume transfused within a 12 hour period.
Massive transfusion implies a single transfusion greater than 2500 mL or 5000 mL transfused over a period of 24 hours.
Complications of blood transfusion?
A. Transfusion reactions
- 1. Acute Non hemolytic reactions
- a. Hypersensitivity reactions
- b. Febrile non-hemolytic reactions
- 2. Hemolytic reactions
- a. Acute immune hemolysis - Recipient’s antibodies to ABO antigens result in a rapid intravascular hemolysis of donor RBCs mediated by activation of complement.
- b. Delayed hemolytic reaction - results from an anamnestic Ab response to donor Rh or non-ABO antigens causing an extravascular hemolytic reaction.
3. Transfusion related acute lung injury (TRALI)
4. Graft Vs Host Disease (GVHD)
C. Complications of massive blood transfusion
- B. Infective complications
- 1. Viral - CMV, EBV, HBV, HCV, HIV, HTLV
- 2. Parasitic - Malaria
- 3. Bacterial - Yersinia, Pseudomonas, Enterobacter
What is TRALI?
- Its is a clinical syndrome with acute hypoxemia and non-cardiogenic pulmonary edema.
- Usually occurs within 1 to 2 hours of transfusion (anytime up to 6 hours later). Theories:
- - Donor blood containing anti-leukocyte Ab.
- - Mediators of inflammation form in stored blood
- Patient develops fever, SOB, cough and hypoxemia.
- CXR shows the picture of ARDS with perihilar infiltrates.
- Support can vary from supplemental oxygen to intubation and ventilation.
- Most cases resolve on their own but some can be fatal.
Describe briefly about GVHD. [TU 2066]
Activated Donor T cells damage host epithelial cells after an inflammatory cascade that begins after the preparative regimen.
These donor (eg, graft) cells may recognize patient (eg, host) cells as foreign, thereby initiating a graft-versus-host reaction which may lead to GVHD.
What are the complications of massive blood transfusion?
- A) Alteration in coagulation system
- B) Complications Of Citrate Transfusion
- C) Hypothermia
- D) Hyperkalemia -
- E) Volume overload - Transfusion associated cardiac Overload (TACO)
Reason for alteration of coagulation system?
- Acidosis and hypothermia
- Dilution of plasma clotting factors
- Reduction of platelet count - each 10-12 unit can produce 50% fall in platelet count.
Complications of citrate?
- Metabolic alkalosis - each 1mmol of citrate releases 3 mEq of bicarbonate.
- Hypocalcemia - due to citrate binding to ionized calcium.
What is cryoprecipitate. Describe its uses and hazards related to its use. [TU 2062/12]
- Cryoprecipitate is the insoluble material that comes out of solution after plasma is frozen and thawed at 4°C (between 1 and 6°C).
- It is rich in certain plasma proteins, especially fibrinogen.
- Cryoprecipitate contains most of the fibrinogen (factor I), factor VIII, factor XIII, von Willebrand factor (VWF), and fibronectin derived from one unit of Fresh Frozen Plasma (FFP).
- Uses -
- - Fibrinogen disorders
- - Liver disease
- - Disseminated intravascular coagulation (DIC), or uremia after desmopressin are found to be ineffective
- - Hemophilia A
- - Von Willebrand disease (VWD)
- - Factor XIII deficiency when a purified/recombinant factor is unavailable.
Cryoprecipitate is ineffective for reversing anticoagulation and for replacing coagulation factors other than factors VIII, XIII, fibrinogen, or von Willebrand factor.
Discuss the recent concept of autologous blood transfusion. [TU 2063/2]
Explain the mechanism of reperfussion injury. Write briefly the measures taken to prevent this injury. [TU 2067/2]
What is a reperfusion injury? What are its causes? How do you manage a case of reperfusion injury? [TU 2057,56]
Reperfusion (reoxygenation) injury is the tissue damage caused when blood supply returns to the tissue after a period of ischemia or lack of oxygen (anoxia, hypoxia). The absence of oxygen and nutrients from blood during the ischemic period creates a condition in which the restoration of circulation results in inflammation and oxidative damage through the induction of oxidative stress rather than restoration of normal function.
Metabolic acidosis from liberation of lactate may produce myocardial depression and hypotension, which is usually transient but more persistent acidosis can occur. Release of potassium from necrotic and injured muscle may lead to significant hyperkalemia which requires urgent treatment.
- - The initial management of the systemic complications of reperfusion injury is focused on restoration of intravascular volume, followed by prevention and treatment of associated metabolic abnormalities including hyperkalemia, metabolic acidosis and myoglobinuria which may lead to acute kidney injury.
- - Therapeutic hypothermia
- - Hydrogen sulfide treatment
Discuss various ways to control the bleeding in surgical practice. [TU 2066/5]
Discuss in short the methods of diagnosis and management of disseminated intravascular coagulopathy (DIC) [TU 2057]
Describe in short the pathophysiology of DIC. Outline the principle of management of DIC. [TU 2065/5]
Short note on DIC. [TU 2054,56]
Disseminated intravascular coagulation is a pathological process characterized by the widespread activation of the clotting cascade that results in the formation of blood clots in the small blood vessels throughout the body. This leads to compromised tissue blood flow and can ultimately lead to multiple organ damage. In addition, as the coagulation process consumes clotting factors and platelets, normal clotting is disrupted and severe bleeding can occur from various sites.
- Causes -
- • Solid tumors and blood cancers (particularly acute promyelocytic leukemia)
- • Obstetric complications: abruptio placentae, pre-eclampsia or eclampsia, amniotic fluid embolism, retained intrauterine fetal demise, septic abortion, post partum haemorrhage
- • Massive tissue injury: severe trauma, burns, hyperthermia, rhabdomyolysis, extensive surgery
- • Sepsis or severe infection of any kind
- • Transfusion reactions
- Pathophysiology - In DIC, the processes of coagulation and fibrinolysis are dysregulated, and the result is widespread clotting with resultant bleeding.
- • Characteristic history (this is important because severe liver disease can essentially have the same laboratory findings as DIC)
- • Prolongation of PT and aPTT
- • A rapidly declining platelet count
- • High levels of fibrin degradation products, including D-dimer
- • The peripheral blood smear may show fragmented red blood cells (known as schistocytes) due to shear stress from thrombi
- Treatment of DIC is centered around treating the underlying condition. Transfusions of platelets or fresh frozen plasma can be considered in cases of significant bleeding, or those with a planned invasive procedure. The target goal of such transfusion depends on the clinical situation. Cryoprecipitate can be considered in those with a low fibrinogen level.
Management of excessive intra operative bleeding. [TU 2073]
Mention the causes of hemorrhage and its management. How to control the bleeding in an operative field and how to prevent post operative bleeding? [TU 2070]
Explain homeostasis. [Tu 2065/5]
Describe the technique of Central venous line insertion. Enlist its complications. [TU 2055,62,64/5]
Mention various preparation of blood products for transfusion and indications for their use. [TU 2059]
Describe various coagulopathies in surgical practice. [TU 2068/2]
Mention various preparations of blood product for transfusion and indications for their use. [TU 2059]
What is tumor angiogenesis? What is the role of angiogenesis inhibitor in cancer therapy. [TU 2062]
Pathophysiology of body’s response to infection. [TU 2056]
Short note on triage, necrotizing fasciitis, surgical audit. [TU 2055]