A 31-year-old male requires an emergency blood transfusion.
Which ONE of the following statements is TRUE?
Answer: B: Fully cross-matched blood refers to blood that is: ABO and Rh typed; screened for antibodies; and compatibility tested with the donor’s blood to identify the potential for a transfusion reaction. This involves mixing the donor’s RBCs and serum with the recipient’s red blood cells (RBCs) and serum. Testing is performed immediately after mixing, after incubation at 37°C for varying times, and with and without an antiglobulin reagent to identify surface immunoglobulin or complement. When properly cross-matched, each unit of blood product can be administered with the expectation of safety. Full cross-match takes approximately 60 minutes, which is too long in an emergency situation.
In an emergency situation, three alternatives to fully cross-matched blood, in order of preference, exist:
1. Type-specific blood with an abbreviated crossmatch (takes approximately 30 minutes) This includes testing for ABO and Rh compatibility. In addition, the recipient’s serum is screened for unexpected antibodies, and an immediate ‘spin’ cross-match is performed at room temperature as opposed to 37°C.
2. Type-specific blood (takes approximately 2 minutes) Testing is only done for ABO and Rh compatibility, without screen or immediate spin cross-match. Type-specific blood that is not cross-matched has been given in numerous military and civilian series without serious consequences. While the type-specific blood is being transfused, the antibody screen and the cross-match are carried out in the laboratory. It is rare that a few minutes cannot safely be expended to allow the blood bank to release type-specific blood.
3. Group O blood (immediately available) Either Rh+ or Rh- blood can be given in an emergency situation because immediate transfusion reactions do not occur due to rhesus incompatibility. However, Rh- patients may become sensitised if Rh+ blood is given and they theoretically carry the risk of experiencing a transfusion reaction if exposed again to Rh-incompatible blood. However, significant, subsequent transfusion reactions with CHAPTER 8 HAEMATOLOGICAL AND ONCOLOGICAL EMERGENCIES Rh-incompatible blood sensitised to the Rh factor are very rare. Many nowadays advise the routine use of the more widely available O Rh+ packed cells in all patients for whom the Rh factor has not been determined, except in females of childbearing age, for whom future Rh sensitisation may be an important consideration.
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Regarding a multi-trauma patient with critical bleeding requiring a massive blood transfusion, which ONE of the following statements is TRUE?
Answer: D: In adults, ‘massive transfusion’ may be defined as a transfusion of half of one blood volume in 4 hours, or more than one blood volume in 24 hours (approximately 10 units PRBC).
In trauma patients with critical bleeding, early transfusion of FFP and platelets is associated with reduced mortality and subsequent RBC requirements. The exact ratio of PRBC to platelets to FFP that should be used during massive transfusion is controversial. Traditionally, a ratio of PRBC to FFP of 1:4 has been used but data from both civilian and military experience reveal that patients receiving more than 10 U PRBC show decreased mortality when they simultaneously receive FFP in a ratio of PRBC to FFP of 1:1, rather than 1:4. Evidence now suggests that in trauma patients with critical bleeding requiring massive transfusion, a ratio of ≤2:1:1 of RBCs :FFP:platelets is associated with reduced mortality. Another consensus article examining the use of blood products worldwide supported the administration of platelets in a massive transfusion protocol in a 1:1:1 ratio with PRBC and FFP; however, further research is needed to recommend target ratio of RBC:FFP:platelets. The National Blood Authority Australia recommends that institutions develop a massive transfusion protocol (MTP) that includes the dose, timing and ratio of blood component therapy for use in trauma patients with, or at risk of, critical bleeding requiring massive transfusion as the use of a protocol is associated with reduced mortality.
There is limited data to support or refute the use of rFVIIa in trauma patients and the indications for administration of rFVIIa in cases of traumatic haemorrhage remain unclear. Much of the current use of rFVIIa is for patients with critical bleeding unresponsive to conventional measures of surgical haemostasis and adequate component therapy. This use remains controversial, particularly because of concerns about the risk of potential thrombotic complications. Currently, the routine use of rFVIIa in trauma patients with critical bleeding requiring massive transfusion is not recommended because of its lack of effect on mortality and variable effect on morbidity. Furthermore, rFVIIa is approved in Australia and New Zealand only for the control of bleeding and prophylaxis for surgery in patients with inhibitors to coagulation factors FVIII or FIX, congenital factor VII deficiency and Glanzmann’s thrombasthenia. Any use outside of these indications is considered ‘off-licence’.
In trauma patients with, or at risk of, significant haemorrhage, TXA should be considered. A recently published randomised controlled trial has demonstrated improved survival in trauma patients who received TXA. In this international, multicentre randomised controlled trial of more than 20,000 patients, TXA (loading dose 1 g over 10 minutes, followed by infusion of 1 g over 8 hours) demonstrated a significant reduction in all-cause mortality at 4 weeks after injury and risk of death from bleeding. The investigators strongly endorse the importance of early administration of TXA in bleeding trauma patients and suggest that trauma systems should be configured to facilitate this recommendation. In patients presenting late (several hours after injury) the clinician should be more cautious and make an assessment of the individual benefits and risks of this treatment, since the drug is likely to be much less effective and possibly even harmful. A recent Cochrane review demonstrated that TXA safely reduces mortality in bleeding trauma patients without increasing the risk of adverse events. Given the above evidence, TXA should be considered as an adjunct in these patients and should be administered as part of a locally adapted MTP in the setting of overall patient management, including strict attention to the control of bleeding, physiological and metabolic parameters, coagulation status and temperature maintenance.
A 35-year-old female receives a blood transfusion in the emergency department (ED) for symptomatic chronic anaemia. A full cross-match was performed prior to administration. One hour into the transfusion the nurse informs you that the patient has developed a fever of 38.3°C. She is otherwise well with normal vital signs.
Which ONE of the following is TRUE?
Answer: A: It is not uncommon for patients to develop a fever during transfusion of blood products. Although fever is usually due to a febrile non-haemolytic reaction, more serious haemolytic reactions and bacterial contamination can be fatal and should always be considered.
Immediate haemolytic transfusion reactions occur when the recipient’s antibodies recognise and haemolyse the donor’s red blood cells. It is most commonly due to ABO incompatibility and usually is the result of human error; incorrect cross-matching or inadvertent administration of wrong blood to the wrong patient. The clinical manifestation of acute haemolysis includes fever, chills, low back pain, flushing, dyspnoea, tachycardia, shock, haemoglobinuria and an anxious feeling of impending doom. The risk of morbidity and mortality is usually proportional to the amount of blood received before recognition of the transfusion reaction. Therefore, in non-emergent blood transfusions, the initial rate of blood transfusion is low for the first 30 minutes to allow for identification of a transfusion reaction while minimising the volume of blood transfused.
A febrile, non-haemolytic reaction is defined as an increase in temperature of 1°C or higher during or up to 6 hours after the transfusion of blood products. It is one of the more common transfusionrelated complications, occurring in 1 per 300 units of PRBC infused and is not commonly due to an interaction between recipient antibodies and donor leucocytes with release of cytokines. The clinical manifestation includes fever, rigors, headaches, myalgias, tachycardia, dyspnoea and chest pain. Febrile reaction is usually self-limited and will respond to antipyretics.
Sepsis due to bacterial contamination is an uncommon cause of fever because both the citrate preservative and refrigeration kill most bacteria. Initially, it may be difficult to differentiate a febrile reaction from a more serious haemolytic transfusion reaction or sepsis. Accordingly, if any patient develops a fever attributable to a transfusion, the transfusion should be stopped immediately, the blood bank should be informed and blood samples should be collected from the opposite arm to transfusion for retype and repeat cross-match, direct and indirect Coombs’, full blood count (FBC), coags, urea and electrolytes test (U&E), haptoglobin, indirect bilirubin, lactate dehydrogenase (LDH), plasma free Hb, urine for Hb and the blood returned to the bank for testing. While lab confirmation is being performed, the sequel of haemolysis is treated supportively. Transfusion reactions are due to a specific interaction between a particular unit and a particular patient, therefore if a blood transfusion is still indicated, blood can be collected for retype and cross-match and a new unit should be transfused.
Regarding anticoagulation therapy with warfarin, which ONE of the following statements is TRUE?
Answer: C: Two brands of warfarin are currently available, Coumadin and Marevan. These two brands have not been shown to be bioequivalent and are therefore not interchangeable; subsequently, it is important that a patient remains with one or other of the currently available brands.
Warfarin acts by inhibiting the synthesis of functional vitamin K-dependent coagulation factors II, VII, IX and X (extrinsic coagulation pathway). Additionally, it blocks the synthesis of antithrombin protein C and protein S, which is responsible for the transient state of increased thrombogenesis at the start of warfarin therapy. For this reason, patients with acute thromboembolic events, such as deep vein thrombosis (DVT), pulmonary embolism (PE) or embolic stroke, should be given heparin or low molecular weight heparin concurrently when starting warfarin. The heparin or low molecular weight heparin can be ceased after a minimum period of 5 days of combined therapy with warfarin and after the INR has been in the therapeutic range for 48 hours. A minimum of 5 days of heparin should be given, even if the INR reaches the desired level beforehand. Patients at less immediate risk, such as patients in stable atrial fibrillation without embolic events, may be safely started on warfarin without concurrent heparin.
The major adverse effect of warfarin is an increased bleeding tendency and many factors can increase the risk. A patient’s risk of bleeding is greatest in the first 3 months of starting warfarin therapy. Age, especially age >70 years, is one of the strongest risk factors for bleeding. Generally, elderly people have increased sensitivity to the anticoagulant effect of warfarin and require a lower mean daily dose than younger patients. In one study, recent antibiotic use was the second greatest risk factor (after age) for overanticoagulation. Other risk factors include a history of past bleeding, previous stroke, history of falls, liver disease, chronic renal failure, change in interacting medications, change in, or poor, nutrition and large fluctuations of INR. Although the bleeding risk increases as the INR increases, 50% of bleeding episodes occur while the INR is <4.0.
A 60-year-old male is referred by his general practitioner (GP) with an INR of >10. He has no active bleeding. He is on warfarin for atrial fibrillation.
Which ONE of the following is the MOST appropriate action?
Answer: B: When managing a patient with supratherapeutic INR levels it is important to determine (1) the cause or precipitating event, (2) the presence or absence of bleeding, (3) if bleeding is absent, the risk of bleeding, and (4) the indication for warfarin therapy, as this will determine the subsequent managing strategy. The decision of which combination of reversal agents to use is based on the urgency (presence of significant bleeding or risk of bleeding), the completeness of reversal required (normalisation of INR or therapeutic INR), the level of INR and the risk of thrombosis when the anticoagulation is reversed.
In this scenario there is no evidence of clinically significant bleeding but there is also no additional information to determine this patient’s risk for bleeding. In the absence of bleeding, current consensus guidelines of the Australasian Society of Thrombosis and Haemostasis recommend the following therapy based on the risk of bleeding in patients with an INR >9.0:
Oral vitamin K1 is the route of choice as the intravenous route, although it produces a more rapid reversal, may be associated with anaphylactic reactions. There is no evidence that this rare, but serious, complication can be avoided by using low doses. In Australia and New Zealand, vitamin K1 is a mixed micelle-based formulation, and may not carry the same risk of allergies, including anaphylaxis, as earlier formulations. The formulation of injectable vitamin K1, while not approved for oral use by government regulatory agencies in Australia and New Zealand, is preferred for the reversal of anticoagulation because of its dosing flexibility. Additionally, intravenous administration also carries the risk of overcorrection (subtherapeutic INR). To temporarily reverse the effect of warfarin when there is a need to continue warfarin therapy, vitamin K1 should be given in a dose that will quickly lower the INR to a safe, but not subtherapeutic, range and will not cause resistance once warfarin is reinstated. For most patients, 1.0–2.0 mg of oral vitamin K1 is sufficient. If the INR is particularly high, as in this case, 5 mg orally may be required. Large doses of vitamin K1 may produce some resistance to reanticoagulation with warfarin, and this can be avoided by giving smaller doses. Larger doses are appropriate if a clinical decision has been made to discontinue further warfarin treatment.
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