Mlt502 groupa


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  • Advocate temporary disqualification of donor. - If these donors have antibodies to high-frequency leukocyte antigens, such as HNA-3a, HLA-A2, and HLA-B12, they should be disqualified from plasma or platelet donation; otherwise, if these findings are negative, they should be returned to the donor pool.Multiparous = women who is having born more than 1 childAdministration of diuretics is not recommended because the condition is not caused by volume overload and because this measure may exacerbate hypotension.
  • Mlt502 groupa

    1. 1. According to Medscape, Online Medical Dictionary, transfusion reaction can be define as reaction of the body to a transfusion of blood that is not compatible with its own blood during or within 24 hours of a blood transfusion. Transfusions are given: a) To restore lost or depleted blood components b) To improve clotting time c) To improve the ability of the blood to deliver oxygen to the body’s tissues.
    2. 2. What is Acute Hemolytic Transfusion? Types of transfusion reaction associated with hemolysis. It occur as soon as possible after blood is being transfused. AHTR also known as ‘Immediate Hemolytic Transfusion Reaction’. Types of AHTR 1)Immune Mediated 2)Non-immune Mediated
    3. 3. • IMMUNE MEDIATED cause by : - Anti A, Anti B or both - Rh - Kell -Duffy • This result in severe intravascular hemolysis and later cause extravascular. • NON IMMUNE MEDIATED occurs when there are damage of RBC before transfusion which result in hemoglobinemia and hemoglobinuria. Patient shows asymptomatic or milder symptoms.
    4. 4. Sign and Symptoms Fever Hemoglobinemia hemoglobinuria Red or dark urine Chills Hypotension Renal failure DIC (Disseminated intravascular coagulation) Back pain
    5. 5. Management 1)When reaction become more severe : - stop transfusion and inform doctor for immediate patient review. -check vital sign and respiratory status. - check patient ID and recheck again detail on blood unit and compatibility label or tag. 2) Inform transfusion service immediately. 3)Administered low dose of dopamine for hypotension patient (1-5ug/kg/min) 4) Monitor urine output commonly using catheterisation.
    6. 6. Complication  Acute kidney failure.  Anemia  Lung problems  Shock Treatment  Mild symptom can be treated with : - paint reliever and acetaminophen can reduce fever and discomfort. -intravenous
    7. 7. Prevention  Prevent mislabeled  Collect the correct sample.  Must form bedside check before administer blood product.  Make sure correct bar coding of blood component and patient ID.  Transfusion practice should be done by experience physician and nurse.
    8. 8. Definition : hypersensitivity reaction to a particular allergen 2 types of allergic reaction: • urticaria transfusion reaction • anaphylactic transfusion reaction
    9. 9. • Simple allergic reaction • Usually begin minutes after infusion • The reaction is simple to diagnose and do not cause significant problems to the patient. • Patient are treated with an antihistamine such as diphenhydramine (Benadryl).
    10. 10. Mechanism of urticaria transfusion reaction • Urticaria transfusion reaction caused by soluble allergenic substances in donor product • The recipient IgE antibody will reacts against this allergenic subtances, most commonly a donor plasma protein resulting in a "type I hypersensitivity" reaction • Histamine and other substances are released from mast cells and basophils through interaction with IgE. • The secretions result in the formation of pruritic (itchy) raised, red-rimmed "wheals" on the skin of the recipient.
    11. 11. Sign & symptom of urticaria transfusion reaction: • No fever •Erythema • Cutaneous flushing • Angioedema • Nausea • Vomiting • Diarrhea minor2010.JPG
    12. 12. Treatment of urticaria transfusion reaction: Temporarily stop the transfusion Maintain intravenous access Give diphenhydramine 20–50 mg IV If the symptoms resolve, restart the transfusion slowly If the symptoms do NOT resolve, stop the transfusion
    13. 13. •Rapidly developing and serious allergic reaction • This reaction affects a number of different body systems at one time. • Severe anaphylactic reactions can be fatal • Associated with IgA deficiency deficiency •Patient treated with epinephrine
    14. 14. Mechanism of anaphylactic transfusion reaction • Usually caused by exposure of an antigen to a sensitized patient. •Reaction commonly occur when recipient has no IgA antibody and transfusion was elicits anti-IgA response of recipient • The "classic" type of anaphylaxis involves IgE antibodies on the surface of a mast cell targeted against an offending antigen. When the patient is exposed to the antigen a second time, the IgE stimulates the mast cells, leading to an outpouring of histamine.
    15. 15. Sign and symptoms of anaphylactic transfusion reaction: • Hypotension • Tachycardia • Chest pain • Loss of consciousness • Arrhythmia • Wheezing • No fever • Patient can have upper and lower airway obstruction such as hoarseness and dypsnea iles/anaphylaxis%20baby%20gif.gif
    16. 16. Treatment of anaphylactic transfusion reaction: Stop the transfusion Maintain IV access with normal saline Administer oxygen Intubation may be needed Epinephrine is most effective medication for treatment of anaphylaxis Steroid and H1-receptor antagonists have been used Observe the patient closely Report the reaction to the transfusion medicine service
    17. 17. • TRALI=Transfusion Related Acute Lung Injury • TRALI is a complication of allogenic blood transfusion that typically manifested by shortness of breath due to noncardiogenic pulmonary edema,fever and hypotension. • It can cause transfusion-associated mortality.
    18. 18. • There are two types of mechanisms that involve with the TRALI which are: ▫ A) Immunologic Mechanism ▫ B) Nonimmunologic Mechanism • Mechanism of TRALI pathogenesis is differ among patients.
    19. 19. A)Immunologic mechanism Principle Types of Alloatibodies involve • Involve antibody-mediated event. • Alloantibodies are responsible for TRALI. • Anti-human leukocyte antigen(anti-HLA) class I or class II antibody • Also associated with antilymphocyte,antimonocyte • Specific neutrophil alloantigen:HNA-1a,HNA-1b,HNA3a and HNA-2a
    20. 20. Donor alloantibody interact with recipient leukocyte antigen Increased vascular permeability lead to capillary leak and pulmonary tissue damage Activation of complement cascade,cytokines Initiate antigenantibody interacion Activation of complement components and neutrophils Produce inflammatory mediators.
    21. 21. B) Nonimmunologic Mechanism • It involve soluble mediator-mediated not antibody mediated event. • In this mechanism, antigranulocyte or anti-HLA antibodies are not detected in either recipient or donor • It is suggested that the granulocyte activation is mediated by a soluble lipid substance that will accumulate during the storage of the products • It also postulated that, biologically active lipids or interleukins is generated and present in increased concentration in stored blood products. • All this event cause pathogenesis of TRALI due to nonantibody mediated.
    22. 22. Biologically active lipids that accumulate during the storage Alveolar damage Pulmonary edema Increase in permeability of pulmonary circulation
    23. 23. Sign and Symptoms • Acute hypoxemia and noncardiogenic pulmonary edema (NPE). • Acute onset of respiratory compromise. • Severe hypoxemia within 6 hours of beginning transfusion caused by a decrease in pH and pO2 and an increase in pCO2 levels in arterial blood gas analysis. • Progressive dyspnea • Cyanosis • Fever (increase of 1-2˚C) • Tachycardia • Hypotension (may not respond to IV fluid resuscitation) • Frothy sputum (yellow or pink in color)
    25. 25. TREATMENT AND PREVENTION • Mild TRALI needs supplemental oxygen therapy. • Severe TRALI may require mechanical ventilation and ICU support. • Upgrade blood transfusion guidelines which will be minimize the unnecessary transfusions are occurred. • Advocate temporary disqualification of donors implicated in TRALI reactions until leukocyte antibody testing can be completed. • Rejected all multiparous females from plasma donation. • No administration of diuretics
    26. 26. What is GVHD?? • Graft-versus-host disease or GVHD is a term used to describe a battle between the transplanted stem cells and the patient’s body. This is a complication that occurs when the new stem cells (the graft) reject or assume body (the host) as foreign. • GVHD is rare in autologous transplants (stem cells come from own blood or bone marrow), it occurs in approximately 50% of patients who have an allogeneic (donor) transplant. • GVHD is less likely to occur if the donor and recipient are matched – have identical tissue or “HLA (human leukocyte antigen)” types.
    27. 27. How GVHD develops? • GVDH occur when the transplant affects recipient immune system. T cells from donor’s bone marrow or stem cells will contain some T cells. T cells are a type of white blood cells that function to attack and destroy cells that recognize as foreign and can be harmful to the host. • T cells don’t attack body own cells, because they recognize proteins on the cells called HLA (human leukocyte antigens). HLA is inherited protein. Apart from identical twins HLA is unique to each person. • Tissue typing is a blood test to check how closely recipient and donor HLA matches. . If recipient and donor have very similar HLA, the chances of GVDH are lower. The more differences there are between recipient HLA and donor, the more likely recipient are to get GVHD. • After a transplant recipient bone marrow starts making new blood cells from the donor stem cells. These new blood cells have the donor's HLA pattern. They recognize the HLA pattern on recipient body cells as different (foreign) and may begin to attack some of them. The GVHD may affect different areas of body. Most commonly it affects the skin, digestive system (including the bowel and stomach) and liver.
    28. 28. Types of GVHD Two types of GVHD:  Acute GvHD: occur early when the bone marrow starts to engraft around two to four weeks after the transplant ▫ It often causes an itchy red skin rash. If the bowel, stomach or liver are affected, nausea and vomiting, diarrhea and a jaundice may be develop. ▫ Acute GvHD is more likely to affect recipient if:  Recipient have a transplant at an older age  the donor is unrelated or not such a close match to recipient  Chronic GvHD: occurs after day 100 after transplant. It may develop as a continuation of acute GVHD or occur without any prior history of acute GVHD. Chronic GVHD is usually less serious.
    29. 29. Signs and Symptoms of GVHD Acute GVHD Involve three main body systems: 1. Skin • a rash on the skin surface but it is mostly seen on the hands, feet, abdomen and face. • itching, redness on areas of the skin that initially looks sun-burnt. 2. Liver • Jaundice (yellow coloring of the skin or eyes) 3. Gastrointestinal Tract • Abdominal pain or cramps, nausea, vomiting, and diarrhea
    30. 30. Chronic GVHD • • • • • • • • • soreness or dryness of the mouth or eyes lung and liver complications changes in skin pigmentation hair loss weight loss vaginal dryness Cough shortness of breath joint problems
    31. 31. Possible benefits of GVHD • Although GVDH may have a serious even life threatening problem, it may give a benefit too. In case of transplant for leukaemia, having mild GVHD may be a good thing. • As well as attacking recipient body cells, the donor T cells will also attack any remaining leukaemia or cancer cells. Doctors call this the graft versus disease effect, or graft versus leukaemia effect (GVL). • The graft means "the donor T cells". There may also be graft versus disease effect after a transplant for lymphoma or myeloma.
    32. 32. Risk factors for GVHD • Unrelated donor transplants Risk of developing GVDH is greater if donor and recipient is not related • Mismatched donors If you have a mismatched transplant your donor will be as close an HLA match as possible. But sometimes the best available bone marrow donor is still a slight mismatch. This increases the risk of GVHD. • High numbers of T cells in the donated stem cells or bone marrow Donated stem cells or bone marrow that contain high numbers of T cells are more likely to cause GVHD. This is called a T cell replete stem cell transplant. Whilst this type of transplant may cause more GVHD, it may also lower the chance of relapse. • Age The older recipient and donor are, the greater recipient risk of developing GVHD. • Having a donor of a different sex to you If donor is a different sex to recipient, the risk of GVHD is slightly increased. This is particularly true if a male has a female donor who has had children or been pregnant in the past.
    33. 33. LABORATORY DIAGNOSIS • Several lab and imaging tests that can be done to diagnose and monitor problems caused by GVHD : ▫ Liver function tests  Elevation of the alkaline phosphatase concentration an early sign of liver involvement by GVHD  Hypoalbuminemia is usually due to GVHD-associated intestinal protein leak and a negative nitrogen balance ▫ Serum electrolytes and chemistries  Potassium, magnesium, bicarbonate levels can be altered  Massive diarrhoea and diminished oral intake can lead to serious electrolyte abnormalities • A biopsy of the skin, mucus membranes in the mouth, or other parts of the body can help to confirm the diagnosis.
    34. 34. Prevention and treatment • Way to prevent GVDH ▫ Tissue typing.  Tissue typing is a process to match the transplanted donor cells as closely as possible to the host or patient cells.  Of all the proteins in the body, it is crucial to try to match up the proteins called HLA antigens that are found on the surface of all the cells. The mixture of HLA proteins belonging to each of us is inherited equally from our parents. The closer the HLA match between the donor and host tissues, the less likely the outcome of GVHD for the host (patient). ▫ Intake of drug before transplant (esp. Stem cell transfusion)  Drug given such as cyclosporine and methotrexate, tacrolimus (Prograf®) and methotrexate, tacrolimus and mycophenolate mofetil (CellCept®) and Prograf and sirolimus (Rapamune®). • Treatment ▫ Intravenously administered glucocorticoids, such as prednisone.  But this medicines have side effects, including kidney and liver damage so close monitoring is needed.
    35. 35. DEFINITION Bacterial contamination of blood component is the second most common caused of death in transfusion reaction Platelet contamination is the most common blood component that easily contaminated due to the storage temperature (room temperature) may facilitate bacterial growth Infusion of contaminated component may be asymptomatic or cause fever with evidence of sepsis or septic shock and death Bacterial psychrophilic gram negative bacteria (pseudomonas, coliforms and achromobacters) are common contaminants
    36. 36. TYPES OF BACTERIA BLOOD COMPONENTS ORGANISMS PACKED RBC Yersinia enterolotica Pseudomonas fluorescnes Serratia liquefaciens PLATELETS Stahplycoccus epedermidis Staphylococcus aureus Bacilus cereus Propionibacterium spp. Micrococcus spp. Group C Streptococcus
    37. 37. Sources of bacterial contamination External ▫ Venipuncture site ▫ Contaminated needle ▫ Collecting set Internal ▫ Blood collected from donor suffers mild bacterimia or infection
    38. 38. ETIOLOGY ETIOLOGY FOR PLATELET CONTAMINATION  Platelets is contaminated with bacteria because the storage for platelets is at room temperature with gently agitation which facilitate the bacterial growth  The most common organism contaminating platelets are rapidly growing aerobic organisms  Organism may contaminate the platelet from the skin of donor venipuncture site or from equipments that is used during collection and processing ETIOLOGY FOR PACKED RBC CONTAMINATION  Being stored at 4 oC, most common organism that associated with packed RBC contamination are psychrophilic bacteria which can withstand cold temperature such as Yersinia enterolotica  Donor infected with Yersinia enterolotica may have bacteremia during donation of blood because infection may be asymptomatic  Transfusion of packed RBC with Yersinia spp. Contaminated unit may caused rapid development of life-threatening gram negative sepsis in recipient
    39. 39. Develop within minutes to up to 2 hours from start of transfusion  Hypertension  Nausea  Vomiting  Diarrhea fever  Oliguria  Shock  Dyspnoea, wheezing and/or cough  Respiratory distress  Bleeding: endotoxin induce DIC SIGN AND SYMTOMPS
    40. 40. PATHOGENESIS AND CLINICAL MANIFESTATION PATHOGENESIS OF BACTERIAL CONTAMINATION:  The psychrophilic organisms multiples at 4oC  These organism pseudomonas, coliform and achromobacter are all gram negative bacilli produces endotoxin that present in the cell wall of these organisms  These organisms metabolises citrate and produces endotoxins consisting of lipid polysaccharide and amino acids  Endotoxins are pyrogenic and causes granulocytosis and thrombocytopenia, gram negative septicimia, endotoximic shock  Fall in cardiac output leads to endotoximic shock that triggers disseminated intravascular coagulation (DIC) which is responsible for the fatal outcome rather than bacterimia CLINICAL MANIFESTATION OF BACTERIAL CONTAMINATION:  Clinical manifestation may be observed after introduction of contaminated blood in the form of circulatory collapse  At the beginning, there may be fall in body temperature subsequently it rises  It then effects the brain, the respiratory system and gastrointestinal tract resulting in conciousness or semiconciousness, dyspnea, vomitting and loose motion  Treatment consists of immediate discontinuation of blood transfusion, vigrous management of endotoximic shock to avoid occurrence of DIC through suitable antibiotics
    41. 41. PREVENTION GENERAL  Written procedure for all aspects of procuring, issuing, and administering transfusion must be prepared.  Improve the technique for proper use of equipment, intravenous solutions, and drugs used during the administration of blood and blood component.  Equipment must be properly maintained and records kept of how and when items are used.  Medications that can be given intravenously must never be injected into blood bags which only use intravenous access devices. BACTERIAL CONTAMINATION FOR PLATELETS     The storage time of platelets must be shorten as logically possible Order platelet concentrated for transfusion only when the patient is ready to receive them After platelet concentrates are pooled, it must be use within 4 hours Once platelets have been delivered to the appropriate location, hang the bag and start transfusion immediately  No platelet concentrates can be leaved unattended in an uncontrolled, unmonitored environment  If platelet concentrates are ordered for a patient but then not transfused, it must be return as soon as possible to the transfusion service for the appropriate storage.
    42. 42. MANAGEMENT  Blood culture from the recipient must be done  Save and collect all blood component units transfused within 90 minutes of the reaction diagnosis  Obtain recipient`s post transfusion blood sample for transfusion reaction investigation Management for Post-transfusion sample and blood component  Send all the blood sample to the microbiology laboratory for gram stain as soon as possible  Reactions are potentially fatal and they must be detected and treated immediately if suspected with bacterial contamination  Start with aggressive broadspectrum antibiotic therapy and give supportive care such as corcticosteroids.  The patient`s intravascular volume should be maintained with crystalloid solution and possible vasopressor drugs such as dopamine
    44. 44. • Each unit of blood contains 250mg of iron as iron can be found in Hb molecule. • Iron is released when RBCs is destroyed. • Human lack major mechanisms for iron excretion, thus iron is accumulated in liver, spleen, heart and endocrine organ as hemosiderin. • Frequent blood transfusion has high risk of iron overload.
    45. 45. • The diseases that require frequent transfusion include: • Thalassemia • Sickle cell disease • Aplastic anemia • Signs and symptoms of hemosiderosis: • • • • • • Muscle weakness Fatigue Weight loss Mild jaundice Anemia Cardiac arrhythmias
    46. 46. • Complications that may occur: • Tissue damage • Heart failure • Liver failure • Diabetes • Hypothyroidism • Treatment: chelating agent  desferrioxamine, deferiprone, desferasirox  binds to iron and helps remove it through the urine or feces.
    47. 47. Picture of kidney under the microscope. The brown area contains hemosiderin. Retrieved from:
    48. 48. References • Borton, D. C. (2011, April 20). Patient.Co.UK. Retrieved from Blood Transfusion Reactions: transfusion-reaction • rgic.html • • •