The classical description of coagulation pathways includes an intrinsic pathway and an extrinsic pathway in which clotting factors are designated with Roman numerals (Fig. 13.1). Each pathway consists of a cascade in which a clotting factor is activated and in turn catalyses the activation of another pathway. The intrinsic pathway involves the sequential activation of factors XII, XI and IX. The extrinsic pathway involves the activation of factor VII by tissue factor, and is sometimes called the tissue factor pathway. Of the two pathways, the extrinsic pathway is considered to be the more important because abnormal expression of the intrinsic pathway does not necessarily result in abnormal clotting. The intrinsic pathway may have an additional role in the inflammatory response.

Both the intrinsic and extrinsic pathways result in a final common pathway which involves the activation of factor X. Activated factor X in turn converts prothrombin to thrombin (factor II to IIa), which allows the conversion of fibrinogen to fibrin (factor I to Ia). Fibrin then becomes cross-linked to form a clot.

It is important to note that this description of intrinsic and extrinsic pathways is essentially a description of what happens in laboratory in vitro conditions. The in vivo process is much more of an interplay between platelets, circulating factors and the endothelium.

The following steps can be conceptualized (Fig. 13.1):

Initiation. Damaged cells express tissue factor (TF) which, following activation by binding with circulating factor VIIa, initiates the coagulation process by activating factor IX to factor IXa and factor X to factor Xa. A rapid binding of factor Xa to factor II occurs, producing small amounts of thrombin (factor IIa).

Amplification. The amount of thrombin produced by these initiation reactions is insufficient to form adequate fibrin, so a series of amplification steps occurs. Activated factors IX, X and VII promote the activation of factor VII bound to tissue factor. Without this step, there are only very small amounts of activated factor VII present. In addition, thrombin generates activated factors V and VIII.

There is a parallel system of anticoagulation, involving antithrombins and proteins C and S, which help prevent an uncontrolled cascade of thrombosis. Thrombin binds to thrombomodulin on the endothelium. This prevents the procoagulant action of thrombin. In addition, the thrombin–thrombomodulin complex activates protein C. Along with its cofactor, protein S, activated protein C (APC) proteolyzes factor Va and factor VIIIa. Factor Va increases the rate of conversion of prothrombin to thrombin and factor VIIIa is a cofactor in the generation of activated factor X. Inactivation of these two factors therefore leads to marked reduction in thrombin production. Activated protein C also has effects on endothelial cells and leukocytes, independent of its anticoagulant properties, including anti-inflammatory properties, reduction of leukocyte adhesion, and chemotaxis and inhibition of apoptosis.

Antithrombin is a serine protease inhibitor which is found in high concentrations in plasma. It inhibits the action of activated factors VII, X, XI, XII and thrombin. It is the site of action of heparin, which increases its rate of action several thousand-fold.

In addition, platelet adhesion and aggregation are normally inhibited in intact blood vessels by the negative charge present on the endothelium, which prevents platelet adhesion, and by substances which inhibit aggregation such as nitric oxide and prostacyclin.

Controlled fibrinolysis occurs naturally, involving the conversion of plasminogen to plasmin, which in turn degrades fibrin. Plasminogen can be activated by naturally occurring tissue plasminogen activator and urokinase.

Common laboratory tests used to investigate coagulation include:

The activated prothrombin time (PT), which tests for factors involved in the extrinsic coagulation pathway (prothrombin, factors V, VII, X), normal range 12–14 s, but often expressed as a ratio (the international normalized ratio, INR)

The activated partial thromboplastin time (APTT, also known as the kaolin cephalin clotting time, KCCT), which tests for factors present within the intrinsic pathway (including factors I, II, V, VIII, IX and X), normal range 26–33.5 s, often also expressed as a ratio (APTTR)

Thromoboplastin time (TT), which tests for the presence of fibrinogen and the function of platelets, normal range 14–16 s

Fibrinogen assay, normal range 1.5–4 g L^− 1

HAEMATOLOGICAL DISORDERS AND THEIR IMPACT ON ANAESTHESIA

Anaemia

Anaemia occurs as a result of decreased red cell production or increased loss due to bleeding or destruction. A number of congenital or acquired conditions can result in anaemia (Table 13.1). Anaemia is defined as a haemoglobin less than 13 g dL^− 1 (men) or 12 g dL^− 1 (women), but the level of anaemia at which physiological dysfunction occurs in everyday life, or under the stress of surgery, is unclear.

TABLE 13.1

Causes of Anaemia

^*Causes of MAHA include vasculitis, disseminated intravascular coagulation (DIC), HELLP syndrome (Haemolysis, Elevated Liver enzymes, Low Platelets) and thrombotic thrombocytopaenic purpura/haemolytic uraemic syndrome (TTP/HUS) (see Table 13.2).

Symptoms associated with anaemia include dyspnoea, angina, vertigo and syncope, palpitations and limited exercise tolerance. These symptoms may be better tolerated in younger patients or in those in whom the onset is more gradual. Anaemia detected in the preoperative period should ideally be investigated and treated prior to surgery. This is true of even relatively mild anaemias because patients with a low haemoglobin concentration at the outset are more likely to receive blood transfusions as a result of their surgery, and there are occasions on which simple treatments, for example pre-operative iron supplementation, may prevent this. Anaemia is classically subdivided into three diagnostic categories:

microcytic, hypochromic anaemia (anaemia with a low mean cell volume, MCV < 78 fL, and low mean cell haemoglobin, MCH < 27 pg); common causes include iron deficiency anaemia, chronic blood loss, anaemia of chronic disease, thalassaemia or sideroblastic anaemia.

macrocytic anaemia (MCV < 100 fL); common causes include vitamin B₁₂ or folate deficiency/malabsorption, alcoholism, liver disease, myelodysplasia or hypothyroidism. If the reticulocyte count is high (> 2.5%), acute blood loss or haemolytic anaemia may be considered.

normocytic normochromic anaemia (normal MCV and MCH); common causes include anaemia of chronic disease, aplastic anaemia, haematological malignancy, or bone marrow invasion or fibrosis. If the reticulocyte count is high, this may also represent acute blood loss or haemolysis.

Inherited and Other Coagulopathies

Various conditions and drugs are known to be associated with increased blood loss during surgery (Tables 13.2 and 13.3). If a patient presents with a known condition or with a history of abnormal bleeding (e.g. menorrhagia or excessive bleeding after previous minor injuries), blood should be sent for a coagulation profile including a platelet count, prothrombin time (PT), thrombin time (TT) and activated partial thromboplastin time (APTT). A platelet count is often done as part of the full blood count, which is considered routine before major surgery. In contrast, coagulation screens should not be considered routine. They are designed for specific investigation of patients with bleeding disorders, not as screening tests. They have a low probability of detecting an abnormality in the absence of any relevant history.

TABLE 13.2

Conditions Which are Known to Increase Blood Loss

^*Heparin-induced thrombocytopaenia (HIT)

^**HELLP syndrome (Haemolysis, Elevated Liver enzymes, Low Platelets)

^†Thrombotic thrombocytopaenic purpura/haemolytic uraemic syndrome (TTP/HUS)

TABLE 13.3

Drugs which are Known to Increase or Reduce Blood Loss

^*Citrate may be used to anticoagulate some dialysis machines, and may be used to ‘lock’ central lines (i.e. keep them from becoming blocked with blood clot)

^**Activated Protein C has been used in the treatment of severe sepsis

^***Used in various angioplasty procedures; mechanism of action depends on drug being released by the stent

^†See Table 13.8

Reproduced from Levi M, Toh CH, Thachil J, Watson HG. Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology. British Journal of Haematology 2009; 145(1): 24–33. © Blackwell Publishing.

Patients known to have inherited abnormalities of coagulation, such as haemophilias A and B, and von Willebrand disease, need specialist haematology input because they are likely to need supplementation of specific factor concentrates prior to surgery, guided by factor assays. This is particularly true of patients known to have antibodies (inhibitors) to the factor in question. Due to the incidence of spontaneous joint or muscle haemorrhage in patients with severe disease, it is rare for them to present for unrelated surgery with an occult diagnosis of haemophilia. Less severe disease (e.g. patients who are heterozygous for haemophilia and have abnormally low factor concentrations) or acquired disease (e.g. acquired von Willebrand disease) may occasionally present unexpectedly during surgery, and a suspicion of abnormal clotting during surgery should prompt the anaesthetist to send blood samples for assessment of the coagulation profile.

In the past, the use of factor concentrates from pooled donor units meant that many patients with haemophilia were infected with HIV or hepatitis viruses, and older patients may therefore be infected.

Depending on the type of haemophilia, tranexamic acid (an antifibrinolytic), desmopressin (DDAVP) or repeated factor infusions may need to be given intraoperatively. The use of desmopressin may be associated with water retention and, potentially, acute hyponatraemia.

Acquired coagulopathy can also occur as an acute event, for example: following major trauma, during major haemorrhage or in the presence of disseminated intravascular coagulopathy (DIC). In major haemorrhage, clotting factors can become depleted if not replaced promptly. The management of coagulopathy in major haemorrhage should be guided by clinical urgency and laboratory tests (Fig. 13.2).

FIGURE 13.2 Sample major haemorrhage protocol.

Intramuscular injections are not recommended in coagulopathic patients because of the risk of intramuscular haemorrhage, and the use of NSAIDs may exacerbate the bleeding tendency.

Coagulopathy of Trauma: Patients who have suffered major trauma have a high incidence of coagulopathy. This is multifactorial and complex but certainly appears before administration of intravenous fluids or blood products, so is not solely an iatrogenic haemodilution effect. The factors associated with coagulopathy are listed in Table 13.4. These factors interact in particular in the ‘lethal triad’ of hypothermia, acidosis and coagulopathy. The effect of hypothermia is not seen in routine coagulation testing because these are performed at 37°C.

TABLE 13.4

Factors Associated with Coagulopathy in Trauma

Physiological dilution of clotting factors
Hypothermia
Acidosis
Red cell loss
Trauma-induced fibrinolysis
Injury-related inflammation
Hypoperfusion
Hypocalcaemia
Genetic predispositions
Iatrogenic – dilution by fluids, anticoagulant effects of intravenous fluids

Most trauma centres now have well defined policies for managing major blood loss (see below). Following publication of the CRASH-2 study, tranexamic acid (1 g as soon as possible after injury, followed by 1 g given over 8 h) is recommended for patients presenting with major trauma.

Disseminated Intravascular Coagulation (DIC): In DIC, the microcirculation of different organs becomes damaged by fibrin clots generated by coagulation pathways which become hyperactive. The pathophysiological production of so many fibrin clots results in a consumptive coagulopathy rendering the patient susceptible to haemorrhage as a result of surgery or other invasive procedures. The causes of DIC are shown in Table 13.2. If DIC is suspected, the cause should be identified and corrected wherever possible. The diagnosis of DIC can be difficult to make and relies upon evaluating the results of several aspects of a coagulation profile. A scoring system exists to evaluate the likelihood of DIC (Table 13.5). Patients who develop DIC in the perioperative period, or who require surgery to treat the cause of DIC (e.g. patients with intra-abdominal sepsis), are at increased risk of major haemorrhage. They are likely to need replacement of consumed coagulation factors in the form of platelets, fresh frozen plasma and cryoprecipitate. Haematological advice should be sought whenever DIC is suspected.

TABLE 13.5

Diagnostic Scoring System for Disseminated Intravascular Coagulation (DIC)

Adapted from the ISTH Diagnostic scoring system for DIC

Occasionally, DIC may present as a predominantly thrombotic condition, and in these cases, the use of heparin may be indicated.

Drug-Induced Coagulopathies: A list of drugs known to increase blood loss is shown in Table 13.3. If possible, provision should be made to discontinue these preoperatively, taking into account the amount of ‘wash-out’ time which may be required. For example, vitamin K inhibitors such as warfarin can take up to 5 or 6 days, and irreversible platelet inhibitors such as aspirin and clopidogrel may take up to 7 days (the time it takes to generate new platelets). In patients in whom continued anticoagulation is considered essential, for instance those at high risk of venous thromboembolic disease, ‘bridging’ therapy during the wash-out period with shorter-acting anticoagulants such as an unfractionated heparin infusion or low molecular weight heparins (LMWHs) may be considered. These shorter acting agents can be stopped closer to the time of surgery in order to minimize the amount of time the patient is without anticoagulants. In the case of LMWHs, this should be 24 h before surgery, with the last dose being reduced to half normal. In the case of an unfractionated heparin infusion, this can be stopped 2–6 h prior to surgery and the level of anticoagulation monitored by measuring the APTT of the patient’s blood.

For patients who have discontinued warfarin therapy, it is advised that the patient’s INR is tested on the day of surgery. An INR of < 1.5 is normally considered safe for most surgical procedures, although lower ratios may be preferred by surgeons working in highly sensitive areas, for example neurosurgery.

If surgery is required urgently, it may be necessary to reverse the effects of anticoagulant therapy acutely. This should be done under the guidance of a haematologist, but in the case of heparin may involve the use of protamine. Rapid reversal of vitamin K-dependent coagulopathy can be achieved safely with prothrombin complex concentrates (PCC). Vitamin K takes hours to work and should be given at the same time in order to reduce the risk of postoperative coagulopathy. In less urgent situations, vitamin K can be given alone, or the warfarin simply stopped for a few days. In acute circumstances where drugs are thought to be affecting platelet function, platelet transfusions may be considered.

Thrombocytopaenia: Thrombocytopenia is usually defined as a platelet count less than 100 × 10⁹ L^− 1, but the point at which thrombocytopaenia becomes clinically important depends upon the clinical scenario. Conditions which can result in thrombocytopaenia are shown in Table 13.2. In patients whose platelet count is low, or platelet function is thought to be impaired, a perioperative platelet transfusion may be required.

In the majority of patients with thrombocytopaenia, spontaneous bleeding is unlikely to occur if the platelet count is greater than 10 × 10⁹ L^− 1. There is no clear consensus as to what level of platelet count is acceptable for any given procedure, but the following guidance has been suggested:

≥ 20 × 10⁹ L^− 1 – for a minor intervention (e.g. insertion of a urinary catheter or nasogastric tube)

≥ 30 × 10⁹ L^− 1 – for the insertion of a central venous catheter under ultrasound guidance

≥ 60–80 × 10⁹ L^− 1 – for epidural insertion or neuraxial blockade

≥ 80 × 10⁹ L^− 1 – for uncomplicated surgery

≥ 100 × 10⁹ L^− 1 – major haemorrhage, major trauma or CNS trauma

It should be noted that platelet transfusions are relatively contra-indicated in haemolytic uraemic syndrome/thrombotic thrombocytopaenic purpura (HUS/TTP) where their use may precipitate further thrombosis. In such cases, the risk of transfusion should be weighed against the risk of bleeding.

One cause of thrombocytopaenia of particular note in the perioperative setting is heparin-induced thrombocytopaenia (HIT). HIT is an antibody-mediated reaction which is thought to occur after exposure to heparin occurring concurrently with a physiological insult such as surgery. It is more strongly associated with unfractionated heparin than LMWHs, usually occurs 4–6 days after exposure and results in a falling platelet count, the nadir of which is 30–50% lower than the patient’s ‘normal’ value. HIT rarely results in acute haemorrhage, but is thought to be associated with a pro-thrombotic tendency requiring the patient to be treated with an alternative anticoagulant such as danaparoid (warfarin is not suitable in this situation). Several scoring systems exist to evaluate the likelihood of HIT, and a laboratory ELISA can be used for confirmation.

INTERVENTIONAL PROCEDURES AND REGIONAL ANAESTHESIA IN COAGULOPATHIC PATIENTS

Interventional procedures such as the insertion of central venous catheters, epidural block or regional nerve blocks constitute a significant risk in coagulopathic patients in terms of haemorrhage or haematoma formation. Of particular note are the risks of airway obstruction from failed jugular venous catheter insertion, and paralysis caused by epidural haematoma formation.

It is likely that the routine use of ultrasound imaging has reduced the risks associated with many procedures, but in profoundly coagulopathic patients it may still be advisable to resort to alternative, ‘safer’ techniques; for example, central venous catheterization of the femoral vein may be preferable to the subclavian or internal jugular routes.

The level of coagulopathy at which various procedures can be considered ‘safe’ is far from clear. Regarding thrombocytopaenia, suggested platelet counts have been mentioned in the previous section, whilst INR and APTT ratios of ≤ 1.4 have been considered relatively safe for most procedures undertaken by anaesthetists.

Safe levels of clotting factors in patients with inherited disorders such as haemophilia are not known, and in these cases a risk/benefit analysis will be necessary.

Drugs causing coagulopathic problems which are difficult to measure present specific problems. A variety of consensus statements, based on evidence from case series, exist on the safety of neuraxial blockade in differing circumstances. Typical responses include:

LMWH (thromboprophylaxis dose): needle insertion should be delayed until 12 h after last dose; epidural catheters should be removed at least 12 h after the last dose and at least 4 h before the next dose

Subcutaneous unfractionated heparin thromboprophylaxis: needle insertion should be delayed until 4 h after the last dose; epidural catheters should be removed at least 1 h before the next dose

NSAID therapy, including low-dose aspirin, can be continued and does not seem to represent an increased risk

Ticlopidine: should be discontinued 14 days prior to neuraxial blockade

Clopidogrel: should be discontinued 7 days prior to neuraxial blockade

GIIb/IIIa inhibitors: should be discontinued 9–48 h prior to neuraxial blockade.

It should be noted that evidence in this area is sparse, and that these guidelines are incomplete, difficult to extrapolate into different settings (e.g. regional anaesthetic techniques with lower associated risk) and may not represent best practice. When in doubt, senior anaesthetic and/or specialist haematological advice should be sought.

THROMBOSIS AND ACUTE ISCHAEMIC EVENTS

All hospital patients should undergo an assessment of their risk of developing venous thromboembolism (VTE) in order to ensure that appropriate prophylactic measures are taken. Reassessment should be undertaken after 24 h, and at any time that the patient’s clinical condition changes. Any assessment should weigh the risk of developing VTE against the risk of bleeding which might occur when pharmacological prophylaxis is prescribed (Tables 13.6 and 13.7). Methods of pharmacological prophylaxis include subcutaneous low molecular weight heparins, subcutaneous unfractionated heparin and newer anticoagulants such as fondaparinux, dabigatran and rivaroxaban. Antiplatelet agents such as aspirin are not considered to provide adequate protection against VTE when used in isolation.

TABLE 13.6

Conditions which are Known to Increase Thrombosis Risk

*Acquired*	Antiphospholipid syndrome Cardiac failure Diabetes Heparin-induced thrombocytopaenia Hyperlipidaemia Malignancy Myeloproliferative disorders Nephrotic syndrome Oral contraceptive pill (oestrogen therapies) Paroxysmal nocturnal haemoglobinuria Polycythaemia TTP/HUS*
*Congenital*	Antithrombin deficiency Dysfibrinogenaemia Factor V Leiden variant (activated protein C resistance) Hyperhomocysteinaemia Protein C deficiency Protein S deficiency Prothrombin genetic variant

^*Thrombotic thrombocytopaenic purpura/haemolytic uraemic syndrome (TTP/HUS)

TABLE 13.7

Risk Assessment for Venous Thromboembolism (VTE)

Adapted from the NICE guidelines, Venous thromboembolism: reducing the risk, 2010

Mechanical methods of VTE prophylaxis are often also used, either as an adjunct to pharmacological methods, or as an alternative to them where the bleeding risk is considered high. Mechanical methods include anti-embolism stockings, and foot-impulse or pneumatic compression devices (both stockings and compression devices may be thigh or knee length). There is very little evidence to support the use of any one mechanical device rather than the alternatives. Mechanical methods may not be appropriate in patients with damaged skin, peripheral neuropathy, oedema, peripheral arterial disease, or other conditions in which fitting the devices might be problematic or cause damage.

In patients who are at very high risk of both bleeding and thromboembolic events, the pre-emptive insertion of a vena cava filter may be required.

PATIENTS WITH HAEMATOLOGICAL MALIGNANCY

Unless the patient has an intercurrent coagulopathy or neutropaenia, the anaesthetic implications of haematological malignancies are relatively limited. If a patient has been treated previously with chemotherapeutic agents, special attention should be made to preoperative cardiorespiratory assessment because some agents increase the risk of pulmonary fibrosis, pneumonitis, cardiomyopathy and hypertension. Patients who are likely to undergo haematopoietic stem cell transplants (bone marrow transplants), or who are treated with purine analogue, and who are needing blood product transfusions, are likely to need ‘special measures’ such as irradiated blood products or blood which is confirmed to be negative for cytomegalovirus (CMV negative). These patients should be discussed with a haematologist prior to transfusion.

BLOOD PRODUCTS AND BLOOD TRANSFUSION

The transfusion of whole blood is relatively uncommon and donated blood is usually separated into its constituent components, which are then available for transfusion. A wide range of blood products are available, the most common of which are listed in Table 13.8, along with their indications. Units of packed red cells are most commonly transfused during the resuscitation of acute haemorrhage, or as a treatment of symptomatic anaemia.

TABLE 13.8

Indications and Uses of Blood Products

^*Albumin may be used safely for volume resuscitation, but there is little evidence to suggest that it is associated with improved outcomes when compared with other resuscitation fluids. It may be associated with worse outcomes when used in certain conditions such as traumatic brain injury.

^**The use of human albumin solution to correct hypoalbuminaemia is contentious. Hypoalbuminaemia is associated with increased mortality in critically ill patients, but actively correcting it is not clearly associated with improved outcome. Hyperoncotic albumin has also been used in the management of adult respiratory distress syndrome (ARDS).

Red cell concentrates are commonly leukocyte depleted and resuspended to a haematocrit of 0.6. In the UK, the red cells are usually suspended in an additive solution: SAGM (Saline maintains isotonicity; Adenine as an ATP precursor to maintain red cell viability; Glucose for red cell metabolism; Mannitol to reduce red cell lysis). These additives are designed to extend the safe storage period and the packed red cells are kept refrigerated at 4 °C. Currently, red cells can be stored for up to 5–6 weeks. There is ongoing debate as to whether the ‘storage lesion’ which occurs during this time is clinically relevant, with some studies suggesting that outcomes are worse for patients who have had ‘old’ blood transfused.

Red Cell Storage Lesion

A variety of biochemical and immunological changes occur during red cell storage which may have clinical impact.

2,3-DPG concentrations fall rapidly (undetectable within 2 weeks). The clinical consequence is less clear, probably because 2,3-DPG concentrations are restored to normal very rapidly following transfusion.

ATP depletion occurs during storage, particularly beyond 5 weeks, and is associated with morphological changes. As with 2,3-DPG, ATP normalizes promptly following transfusion and the morphological changes reverse.

Haemoglobin has been shown to be an important part of the control of regional blood flow due to its interaction with nitric oxide. This ability is lost early (days) following blood storage, but the clinical impact of this is not yet clear.

Morphological changes during storage are complex, but in general, red cells become less deformable; these changes may be only partly reversible.

It has long been recognized that red cell transfusion can have systemic immunological effects including effects on organ transplants, infection and malignancy. The causes of these effects are not clear but may involve residual leukocytes and immunological mediators released by red cells.

In patients who are asymptomatic and not actively bleeding, current evidence suggests that there is no benefit in transfusion provided that the haemoglobin concentration is 7 g dL^− 1, or greater. This ‘trigger’ of 7 g dL^− 1 is derived from the ‘Transfusion requirements in critical care’ trial (TRICC trial, Herbert P., et al, New England Journal of Medicine, 2009). Despite the publication of this study, there remains doubt as to what the ‘safe’ level of anaemia is for patients with some specific conditions, including ischaemic heart disease, head injury and acute burns. For patients who are symptomatic, or who are actively bleeding, a higher target haemoglobin concentration of 9–10 g dL^− 1 is often adopted.

Packed red cells must be checked before they are transfused to ensure that the donated blood is compatible with the recipient’s blood, the most important aspect of which is ABO and Rhesus D (RhD) compatibility.

Patients of blood group O can receive only group O donated blood

Patients of blood group A can receive group O or group A donated blood

Patients of blood group B can receive group O or group B donated blood

Patients of blood group AB can receive groups O, A, B or AB donated blood

Patients with RhD positive blood can receive RhD positive or RhD negative blood

Patients with RhD negative blood will preferentially be given RhD negative blood, but occasionally may be transfused RhD positive blood unless they are an RhD negative female patient with child-bearing potential, in which case they should only ever receive RhD negative blood.

Other, less common, red blood cell antibody/antigen reactions may also occur, and if time allows, a full cross-match should be undertaken. In more urgent situations a more limited approach may be necessary (Fig. 13.2).

The transfusion of FFP also depends upon ABO grouping, but is more complex. Group O FFP may only be given to group O patients, whilst FFP of groups A, B and AB may given to any recipient, but only if it does not contain a ‘high-titre’ of anti-A or anti-B activity. If possible, the transfused unit of FFP should be of the same group as the recipient.

The transfusion of blood products is not without risk, and, if possible, should not be done without the informed consent of the recipient. A list of the most common complications of transfusion is shown in Table 13.9. Of particular note are the risks associated with the transfusion of incompatible blood products, which are considered to be ‘Never Events’ within the UK (the equivalent to ‘No Pay’ events within the US system). A ‘zero-tolerance’ approach to pre-transfusion sampling, and blood product checking and administration is recommended, which includes:

TABLE 13.9

Errors and Complications of Blood Transfusion (as Classified and Defined by the SHOT Report 2009)

^*Special requirements include irradiated blood, or blood where cytomegalovirus is absent (CMV negative blood) – for indications see text

taking blood samples from one patient at a time

hand-writing all blood sample tubes and forms at the bedside after sampling, having positively identified the patient by full name, date of birth and hospital identification number

patient identification should involve checking any identification band which the patient is wearing as well as a verbal confirmation from the patient of full name and date of birth, if possible

all blood products should be prescribed on a record which also contains the above patient identification

all blood products should be checked prior to administration, and the patient’s identity confirmed for a second time; all the patient details present on the prescribed unit of blood must match exactly the verbal response from the patient, the patient’s identification band and the prescription record, and this should be confirmed by a second person performing an independent check

if there are any discrepancies, the transfusion should not go ahead

the details of the transfused product, including any serial numbers, should be recorded on the transfusion record

In Europe there is a legal obligation to keep a permanent record of all blood products that have been transfused.

MAJOR HAEMORRHAGE

When major haemorrhage occurs, it is often necessary to transfuse large volumes of both packed red cells and products which promote clotting, such as fresh frozen plasma (FFP), cryoprecipitate and platelets. Major haemorrhage protocols have been developed in order to aid this process, an example of which is shown in Figure 13.2. If possible, the transfusion of red cells and clotting products should be guided by laboratory results, or by near-patient testing (for example near-patient haemoglobinometers or thromboelastography – TEG). However, waiting for confirmation of coagulopathy before administering appropriate therapy is likely to lead to greater blood loss, use of more blood products and worse outcome. Major trauma is well recognized as causing early coagulopathy even before any fluids or blood products are given.

There is no universal agreement about the relative proportions of RBC:FFP:platelets:cryoprecipitate that should be given. However, there is reasonable evidence to suggest that early aggressive prevention/control of coagulopathy is beneficial in terms of overall blood product use and probably outcome.

Good communication among all members of the team and the haematology department are crucial to the management of major haemorrhage, whatever the setting. Prevention/correction of coagulopathy should always go hand in hand with control of the bleeding source.