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Author Topic: Blood Transfusions: Blood Products, Matching and Complications  (Read 21328 times)
Andy Battaglia
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« on: October 08, 2006, 11:05:56 PM »

This is a good resource for understanding the basics of blood , matching and complications.

From http://www.surgical-tutor.org.uk/default-home.htm?core/preop2/blood.htm~right

Blood products
ABO system

    * Consists of three allelic genes - A, B and O
    * A and B genes control synthesis of enzymes that add carbohydrate residues to cell surface glycoproteins
    * The O gene is an amorph and does not transform the glycoprotein
    * Six possible genotypes but only four phenotypes
    * Naturally occurring antibodies are found in the serum of those lacking the corresponding antigen.

ABO blood group system

    Phenotype    Genotype    Antigens    Antibodies    Frequency (%)
    O    OO    O    Anti-A, Anti-B    46
    A    AA or AO    A    Anti-B    42
    B    BB or BO    B    Anti-A    9
    AB    AB    AB    None    3

    * Blood group O = universal donor
    * Blood group AB = universal recipient

Rhesus system

    * Rhesus antibodies are immune antibodies requiring exposure during transfusion or pregnancy
    * 85% population are rhesus positive
    * 90% of Rh-negative patients transfused with Rh-positive blood develop anti-D antibodies

Cross Matching
Blood grouping

    * Patients red cells grouped for ABO and Rhesus antigens
    * Serum tested to confirm patients ABO group

Antibody screening

    * Detects atypical red cell antibodies in recipients serum

Crossmatching

    * Tests donor red cells against patients serum

Blood products

    * Whole blood
    * Packed red cells
    * Granulocyte concentrates
    * Platelet concentrates
    * Human plasma - fresh frozen plasma / freeze-dried plasma
    * Plasma protein fraction
    * Human albumin 25%
    * Cryoprecipitate
    * Clotting factors - Factor VIII / IX
    * Immunoglobulins

Complications of blood transfusion
Early

    * Haemolytic reactions (immediate or delayed)
    * Bacterial infections from contamination
    * Allergic reactions to white cells or platelets
    * Pyogenic reactions
    * Circulatory overload
    * Air embolism
    * Thrombophlebitis
    * Citrate toxicity
    * Hyperkalaemia
    * Clotting abnormalities

Late

    * Infection - cytomegalovirus / hepatitis
    * Immune sensitisation
    * Iron overload

Acute haemolytic or bacterial transfusion reactions

    * Due to acute haemolysis or bacterial contamination
    * Difficult to differentiate on clinical grounds
    * May occur after infusion of small volume of incompatible or infected blood
    * Associated with high morbidity and mortality
    * In unconscious patient bleeding due to DIC may be only sign
    * Most ABO mismatched transfusions are due to human error
    * Usually occurs soon after start of transfusion
    * Patient feels unwell and agitated
    * Symptoms include back pain and pain at infusion site
    * Associated with shortness of breath, rigors
    * Examination will show hypotension, oliguria and bleeding from venepuncture sites
    * Urinalysis will show haemoglobinuria

Management

    * Discontinue transfusion immediately and remove giving set
    * Check unit of blood against patients identity
    * Give intravenous crystalloid
    * Consider transfer to the intensive care unit
    * Take blood for FBC, plasma haemoglobin, clotting, blood cultures and repeat grouping
    * Give broad spectrum antibiotics
    * Monitor urine output and ECG

Anaphylaxis

    * Usually occurs soon after start of transfusion
    * May be seen in IgA deficient patients reacting to transfused IgA
    * Presents with circulatory collapse and bronchospasm

Management

    * Discontinue transfusion and remove giving set
    * Maintain airway and give oxygen
    * Administer adrenaline, chlorpheniramine, salbutamol
    * If the patient is IgA deficient any further transfusion must be carefully planned

Non-haemolytic transfusion febrile reaction

    * Usually occurs more than 30 minutes after start of transfusion
    * Patient feels generally well but may be shivering
    * Temperature is usually less than 38.5 °C
    * Blood pressure is usually normal

Management

    * Stop transfusion and assess possibility that this may be a more significant reaction
    * Restart transfusion at a slower rate
    * Consider the use of paracetamol
    * Hydrocortisone should not be routinely used during a transfusion

Transfusion related acute lung injury

    * Occurs following administration of plasma-containing blood components
    * Due to interaction of donor antibodies with recipient white cells
    * The clinical pictures is similar to ARDS
    * Occurs 30 minutes to several days after transfusion
    * Clinical features include fever, cough and shortness of breath
    * Chest x-ray shows perihilar shadowing
    * Treat as ARDS

Delayed haemolytic transfusion reaction

    * Occurs 5-10 days after transfusion
    * Clinical features are usually minimal
    * Possibly unexplained pyrexia or jaundice
    * Unexplained drop in haemoglobin
    * Urinalysis shows urobilinogenuria

Management

    * Check LFTs, clotting and red cell antibody screen

Autologous transfusion

    * Is the use of the patients own blood
    * Particularly useful in elective surgery
    * Accounts for 5% of transfusions in USA
    * Reduces the need for allogeneic blood transfusion
    * Reduces risk of postoperative complications (e.g. infection, tumour recurrence)
    * Three main techniques are:
          o Predeposit transfusion
          o Intraoperative acute normovolaemic haemodilution
          o Intraoperative cell salvage

Predeposit transfusion

    * Blood collection begins 3-5 weeks preoperatively
    * Between 2 and 4 units are often stored
    * Last unit collected more than 72 hours preoperatively
    * Eliminates the risk of viral transmission
    * Reduces the risk of immunological transfusion reactions
    * Reduces risk of postoperative immunosuppression seen with allogeneic transfusion
    * Collection is expensive and time-consuming
    * Only suitable for elective surgery

Intraoperative acute normovolaemic haemodilution

    * Whole blood is removed at start of operative procedure
    * Between 1.0 and 1.5 litres can be collected
    * Replaced with crystalloid or colloid solution
    * Few detrimental effects of acute anaemia have been demonstrated
    * Blood is stored in theatre at room temperature
    * Blood is re-infused during or immediately following surgery
    * Cheaper than predeposit transfusion
    * Little risk of administrative or clerical error
    * Suitable for elective or emergency surgery at which considerable blood loss anticipated

Intraoperative cell salvage

    * Shed blood is collected from operative field
    * Blood is anticoagulated with citrate or heparin and filtered to remove debris and clots
    * Cells are then washed with saline and concentrated by centrifugation
    * Concentrate is then reinfused
    * Large volumes of blood can be salvaged
    * Salvaged blood is not haemostatically intact
    * Platelets and clotting factors are consumed
    * Suitable in cardiac or trauma surgery
    * Contraindicated in contaminated operative fields and in the presence of malignancy

Bibliography

Regan F, Taylor C.  Blood transfusion medicine.  Br Med J 2002;  325:  143-147.

Sloop G D,  Friedberg R C.  Complications of blood transfusion.  How to recognise and respond to non-infectious reactions.  Postgrad Med 1995; 98:  159-162.

Vanderlinde E S,  Heal J M, Blumberg N.  Autologous transfusion.  Br Med J 2002;  324:  772-775.

Winkelstein A,  Kiss J E.  Immunohematologic diseases.  JAMA 1997;  278:  1982-1992.
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Andy Battaglia
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« Reply #1 on: January 08, 2009, 11:23:30 PM »

http://www.merck.com/mmpe/print/sec11/ch146/ch146e.html

   
   

Section
      

Hematology and Oncology
   
   

Subject
      

Transfusion Medicine
   

Complications of Transfusion
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The most common complications of transfusion are febrile nonhemolytic and chill-rigor reactions. The most serious complications are acute hemolytic reaction due to ABO incompatible transfusion and transfusion-related acute lung injury, which have very high mortality rates.

Early recognition of symptoms suggestive of a transfusion reaction and prompt reporting to the blood bank are essential. The most common symptoms are chills, rigors, fever, dyspnea, light-headedness, urticaria, itching, and flank pain. If any of these symptoms (other than localized urticaria and itching) occur, the transfusion should be stopped immediately and the IV line kept open with normal saline. The remainder of the blood product and clotted and anticoagulated samples of the patient's blood should be sent to the blood bank for investigation. Note: The unit in question should not be restarted, and transfusion of any previously issued unit should not be initiated. Further transfusion should be delayed until the cause of the reaction is known, unless the need is urgent, in which case type O Rh-negative RBCs should be used.

Hemolysis of donor or recipient RBCs (usually the former) during or after transfusion can result from ABO/Rh incompatibility, plasma antibodies, or hemolyzed or fragile RBCs (eg, by overwarming stored blood or contact with hypotonic IV solutions). Hemolysis is most common and most severe when incompatible donor RBCs are hemolyzed by antibody in the recipient's plasma. Hemolytic reactions may be acute (within 24 h) or delayed (from 1 to 14 days).

Acute hemolytic transfusion reaction (AHTR)

About 20 people die yearly in the US from AHTR. AHTR usually results from recipient plasma antibodies to donor RBC antigens. ABO incompatibility is the most common cause of AHTR. Antibodies against blood group antigens other than ABO can also cause AHTR. Mislabeling the recipient's pretransfusion sample at collection or failing to match the intended recipient with the blood product immediately before transfusion is the usual cause, not laboratory error.

Hemolysis is intravascular, causing hemoglobinuria with varying degrees of acute renal failure and possibly disseminated intravascular coagulation (DIC). The severity of AHTR depends on the degree of incompatibility, the amount of blood given, the rate of administration, and the integrity of the kidneys, liver, and heart. An acute phase usually develops within 1 h of initiation of transfusion, but it may occur later during the transfusion or immediately afterward. Onset is usually abrupt. The patient may complain of discomfort and anxiety. Dyspnea, fever, chills, facial flushing, and severe pain may occur, especially in the lumbar area. Shock may develop, causing a rapid, feeble pulse; cold, clammy skin; low BP; and nausea and vomiting. Jaundice may follow acute hemolysis.

If AHTR occurs while the patient is under general anesthesia, the only symptom may be hypotension, uncontrollable bleeding from incision sites and mucous membranes caused by an associated DIC, or dark urine that reflects hemoglobinuria.

If AHTR is suspected, one of the first steps is to recheck the sample and patient identifications. Diagnosis is confirmed by measuring urinary Hb, serum LDH, bilirubin, and haptoglobin. Intravascular hemolysis produces free Hb in the plasma and urine; haptoglobin levels are very low. Hyperbilirubinemia may follow.

After the acute phase, the degree of acute renal failure determines the prognosis. Diuresis and a decreasing BUN usually portend recovery. Permanent renal insufficiency is unusual. Prolonged oliguria and shock are poor prognostic signs.

If AHTR is suspected, the transfusion should be stopped and supportive treatment begun. The goal of initial therapy is to achieve and maintain adequate BP and renal blood flow with IV 0.9% saline and furosemide. IV saline is given to maintain urine output of 100 mL/h for 24 h. The initial furosemide dose is 40 to 80 mg (1 to 2 mg/kg in children), with later doses adjusted to maintain urinary flow > 100 mL/h during the first day.

Antihypertensive drugs must be administered with caution. Pressor drugs that decrease renal blood flow (eg, epinephrine, norepinephrine, high-dose dopamine) are contraindicated. If a pressor drug is necessary, dopamine 2 to 5 μg/kg/min is usually administered.

A nephrologist should be consulted as early as possible, particularly if no diuretic response occurs within about 2 to 3 h after initiating therapy, which may indicate acute tubular necrosis. Further fluid and diuretic therapy may be contraindicated, and early dialysis may be helpful.

Delayed hemolytic transfusion reaction

Occasionally, a patient who has been sensitized to an RBC antigen has very low antibody levels and negative pretransfusion tests. After transfusion with RBCs bearing this antigen, a primary or anamnestic response may result (usually in 1 to 4 wk) and cause a delayed hemolytic transfusion reaction. Delayed hemolytic transfusion reaction usually does not manifest as dramatically as AHTR. Patients may be asymptomatic or have a slight fever. Rarely, severe symptoms occur. Usually, only destruction of the transfused RBCs (with the antigen) occurs, resulting in a falling Hct and a slight rise in LDH and bilirubin. Because delayed hemolytic transfusion reaction is usually mild and self-limited, it is often unidentified, and the clinical clue may be an unexplained drop in Hb to the pretransfusion level occurring 1 to 2 wk posttransfusion. Severe reactions are treated similarly to acute reactions.

Febrile nonhemolytic transfusion reaction

Febrile reaction may occur without hemolysis. Antibodies directed against WBC HLA from otherwise compatible donor blood are one possible cause. This cause is most common in multitransfused or multiparous patients. Cytokines released from WBCs during storage, particularly in platelet concentrates, is another possible cause.

Clinically, febrile reactions consist of a temperature increase of ≥ 1° C, chills, and sometimes headache and back pain. Simultaneous symptoms of allergic reaction are common. Because fever and chills also herald a severe hemolytic transfusion reaction, all febrile reactions must be investigated as above, as with any transfusion reaction.

Most febrile reactions are treated successfully with acetaminophen and, if necessary, diphenhydramine (see below). Patients should also be treated (eg, with acetaminophen) before future transfusions. If a recipient has experienced more than one febrile reaction, special leukoreduction filters are used during future transfusions; many hospitals use prestorage, leukoreduced blood components.

Allergic reactions

Allergic reactions to an unknown component in donor blood are common, usually due to allergens in donor plasma or, less often, to antibodies from an allergic donor. These reactions are usually mild, with urticaria, edema, occasional dizziness, and headache during or immediately after the transfusion. Simultaneous fever is common. Less frequently, dyspnea, wheezing, and incontinence may occur, indicating a generalized spasm of smooth muscle. Rarely, anaphylaxis occurs, particularly in IgA-deficient recipients.

In a patient with a history of allergies or an allergic transfusion reaction, an antihistamine may be given prophylactically just before or at the beginning of the transfusion (eg, diphenhydramine 50 mg po or IV). Note: Drugs must never be mixed with the blood. If an allergic reaction occurs, the transfusion is stopped. An antihistamine (eg, diphenhydramine 50 mg IV) usually controls mild urticaria and itching, and transfusion may be resumed. However, a moderate allergic reaction (generalized urticaria or mild bronchospasm) requires hydrocortisone (100 to 200 mg IV), and a severe anaphylactic reaction requires additional treatment with epinephrine 0.5 mL of 1:1000 solution sc and 0.9% saline IV (see Allergic and Other Hypersensitivity Disorders: Treatment) along with investigation by the blood bank. Further transfusion should not occur until the investigation is completed. Patients with severe IgA deficiency require transfusion of washed RBCs, washed platelets, and plasma from an IgA-deficient donor.

Volume overload

The high osmotic load of blood products draws volume into the intravascular space over the course of hours, which can cause volume overload in susceptible patients (eg, those with cardiac or renal insufficiency). RBCs should be infused slowly. The patient should be observed and, if signs of heart failure (eg, dyspnea, rales) occur, the transfusion should be stopped and treatment for heart failure begun.

Typical treatment is with a diuretic such as furosemide 20 to 40 mg IV. Occasionally, patients requiring a higher volume of plasma infusion to reverse a warfarin overdose may be given a low dose of furosemide simultaneously; however, prothrombin complex concentrate (PCC) should be the first choice for such patients. Patients at high risk of volume overload (eg, those with heart failure or severe renal insufficiency) are treated prophylactically with a diuretic (eg, furosemide 20 to 40 mg IV).

Acute lung injury

Transfusion-related acute lung injury is an infrequent complication caused by anti-HLA and/or anti-granulocyte antibodies in donor plasma that agglutinate and degranulate recipient granulocytes within the lung. Acute respiratory symptoms develop, and chest x-ray has a characteristic pattern of noncardiogenic pulmonary edema. After ABO incompatibility, this is the 2nd most common cause of transfusion-related death. Incidence is 1:5,000–10,000, but many cases are mild. Mild to moderate transfusion-related acute lung injury probably is commonly missed. General supportive therapy typically leads to recovery without long-lasting sequelae. Diuretics should be avoided. Cases should be reported.

Altered oxygen affinity

Blood stored for > 7 days has decreased RBC 2,3-diphosphoglycerate (DPG), and the 2,3-DPG is absent after > 10 days. This absence results in an increased affinity for O2 and slower O2 release to the tissues. There is little evidence that 2,3-DPG deficiency is clinically significant except in exchange transfusions in infants, in sickle cell patients with acute chest syndrome and stroke, and in some patients with severe heart failure. After transfusion of RBCs, 2,3-DPG regenerates within 12 to 24 h.

Graft-vs-host disease (GVHD)

Transfusion-associated GVHD (see Transplantation: Other complications) is usually caused by transfusion of products containing immunocompetent lymphocytes to an immunocompromised host. The donor lymphocytes attack host tissues. GVHD can occur occasionally in immunocompetent patients if they receive blood from a donor who is homozygous for an HLA haplotype (usually a close relative) for which the patient is heterozygous. Symptoms and signs include fever, skin rash (centrifugally spreading rash becoming erythroderma with bullae), vomiting, watery and bloody diarrhea, lymphadenopathy, and pancytopenia due to bone marrow aplasia. Jaundice and elevated liver enzymes are also common. GVHD occurs 4 to 30 days after transfusion and is diagnosed based on clinical suspicion and skin and bone marrow biopsies. GVHD has > 90% mortality because no specific treatment is available.

Prevention of GVHD is with irradiation (to damage DNA of the donor lymphocytes) of all transfused blood products. This is done if the recipient is immunocompromised (eg, those with congenital immune deficiency syndromes, hematologic malignancies, hematopoietic stem cell transplantation; newborns), if donor blood is obtained from a first-degree relative, or when HLA-matched components, excluding stem cells, are transfused. Treatment with corticosteroids and other immunosuppressants, including those used for solid organ transplantation, is not an indication for blood irradiation.

Complications of massive transfusion

Massive transfusion is transfusion of a volume of blood greater than or equal to one blood volume in 24 h (eg, 10 units in a 70-kg adult). When a patient receives stored blood in such large volume, the patient's own blood may be, in effect, “washed out.” In circumstances uncomplicated by prolonged hypotension or DIC, dilutional thrombocytopenia is the most likely complication. Platelets in stored whole blood are not functional. Clotting factors (except factor VIII) usually remain sufficient. Microvascular bleeding (abnormal oozing and continued bleeding from raw and cut surfaces) may result. Five to 8 (1 unit/10 kg) platelet concentrates are usually enough to correct such bleeding in an adult. Fresh frozen plasma and cryoprecipitate may be needed.

Hypothermia due to rapid transfusion of large amounts of cold blood can cause arrhythmias or cardiac arrest. Hypothermia is avoided by using an IV set with a heat-exchange device that gently warms blood. Other means of warming blood (eg, microwave ovens) are contraindicated because of potential RBC damage and hemolysis.

Citrate and K toxicities generally are not of concern even in massive transfusion; however, toxicities of both may be amplified in the presence of hypothermia. Patients with liver failure may have difficulty metabolizing citrate. Hypocalcemia can result but rarely necessitates treatment (which is 10 mL of a 10% solution of Ca gluconate IV diluted in 100 mL D5W, given over 10 min). Patients with renal failure may have elevated K if transfused with blood stored for > 1 wk (K accumulation is usually insignificant in blood stored for < 1 wk). Mechanical hemolysis during transfusion may increase K. Hypokalemia may occur about 24 h after transfusion of older RBCs (> 3 wk), which take up K.

Infectious complications

Bacterial contamination of packed RBCs occurs rarely, possibly due to inadequate aseptic technique during collection or to transient asymptomatic donor bacteremia. Refrigeration of RBCs usually limits bacterial growth except for cryophilic organisms such as Yersinia sp, which may produce dangerous levels of endotoxin. All RBC units are inspected before issue for bacterial growth, which is indicated by a color change. Because platelet concentrates are stored at room temperature, they have greater potential for bacterial growth and endotoxin production if contaminated. To minimize growth, storage is limited to 5 days. The risk of bacterial contamination of platelets is 1:2500. Therefore, platelets are routinely tested for bacteria.

Rarely, syphilis is transmitted in fresh blood or platelets. Storing blood for ≥ 96 h at 4 to 10° C kills the spirochete. Although federal regulations require a serologic test for syphilis on donor blood, infective donors are seronegative early in the disease. Recipients of infected units may develop the characteristic secondary rash.

Hepatitis may occur after transfusion of any blood product. The risk has been reduced by viral inactivation through heat treatment of serum albumin and plasma proteins and by the use of recombinant factor concentrates. Tests for hepatitis are required for all donor blood (see Table 2: Transfusion Medicine: Infectious Disease Transmission TestingTables). The estimated risk of hepatitis B is 1:200,000; of hepatitis C, 1:2.6 million. Because its transient viremic phase and concomitant clinical illness likely preclude blood donation, hepatitis A (infectious hepatitis) is not a significant cause of transfusion-associated hepatitis.

HIV infection in the US is almost entirely HIV-1, although HIV-2 is also of concern. Testing for antibodies to both strains is required. Nucleic acid testing for HIV-1 antigen as well as HIV-1 p24 antigen testing is also required. Additionally, blood donors are asked about behaviors that may put them at high risk of HIV infection. HIV-0 has not been identified among blood donors. The estimated risk of HIV transmission due to transfusion is 1:2.6 million.

Cytomegalovirus (CMV) can be transmitted by WBCs in transfused blood. It is not transmitted through fresh frozen plasma. Because CMV does not cause disease in immunocompetent recipients, routine antibody testing of donor blood is not required. However, CMV may cause serious or fatal disease in immunocompromised patients, who should probably receive CMV-negative blood products that have been provided by CMV antibody-negative donors or by blood depleted of WBCs by filtration.

Human T-cell lymphotropic virus 1 (HTLV-1), which can cause adult T-cell lymphoma/leukemia, HTLV-1–associated myelopathy, and tropical spastic paraparesis, causes posttransfusion seroconversion in some recipients. All donor blood is tested for HTLV-1 and HTLV-2 antibodies. The estimated risk of false-negative results on testing of donor blood is 1:641,000.

Creutzfeldt-Jakob disease has never been reported to be transfusion-transmitted, but current practice precludes donation from a person who has received human-derived growth hormone or a dura mater transplant or who has a family member with Creutzfeldt-Jakob disease. New variant Creutzfeldt-Jakob disease (mad cow disease) has not been transmitted by blood transfusion. However, donors who have spent significant time in the United Kingdom and some other parts of Europe may be permanently deferred from donation (see Table 1: Transfusion Medicine: Some Reasons for Blood Donation Deferral or DenialTables).

Malaria is transmitted easily through infected RBCs. Many donors are unaware that they have malaria, which may be latent and transmissible for 10 to 15 yr. Storage does not render blood safe. Prospective donors must be asked about malaria or whether they have been in a region where it is prevalent. Donors who have had a diagnosis of malaria or who are immigrants, refugees, or citizens from countries in which malaria is considered endemic are deferred for 3 yr; travelers to endemic countries are deferred for 1 yr. Babesiosis has rarely been transmitted by transfusion.

Last full review/revision November 2006 by Ravindra Sarode, MD
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Little A


« Reply #2 on: January 09, 2009, 12:27:31 AM »


The reactions sound very frightening!  Other than human error, I hope that genotype testing can prevent many of the others causes of reaction. 

Sharmin
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