Anaemia

Where possible, anaemia should be corrected before elective surgery. UK national guidance advocates the identification of preoperative iron deficiency before planned surgery and has stated that iron-deficient patients should not have planned surgery without preoperative intervention.

Clinical pathways for dealing with iron-deficient patients have the potential to significantly reduce transfusions. In addition, perioperative measures such as cell salvage and low volume blood sampling reduce transfusion requirements.

Preoperative autologous blood donation is discouraged in the UK because of concerns about sterility, storage and short shelf-life (<6 weeks).

Abnormalities of Haemostasis

It is important to identify patients with a bleeding history. A tool such as the International Society of Thrombosis and Hemostasis Bleeding Assessment Tool (ISTH BAT) questionnaire is more sensitive and specific than laboratory tests (i.e. PT, APTT, platelet count).

Patients taking anticoagulants and antiplatelet agents should be given explicit instructions regarding cessation before surgery.

Mild thrombocytopenia is common in elderly patients. More marked thrombocytopenia may be secondary to immune thrombocytopenia, right heart failure, hepatic impairment, drug therapy, haematinic deficiency or myelodysplasia. Where time allows, a platelet count of <75 × 10⁹ l^–1 should prompt haematology referral to establish if the cause is reversible.

The minimum platelet count required for cardiac surgery is debated. The question is confounded by antiplatelet and anticoagulant drug therapy. In most centres, a platelet count of 100 × 10⁹ l^–1 is regarded as the minimum necessary for elective cardiac surgery. In life-threatening situations, a platelet count of ~35 × 10⁹ l^–1 may be tolerated, albeit with a greater risk of bleeding and transfusion.

A prednisolone ‘challenge’ (1 mg kg^–1) may temporarily increase the platelet count in the perioperative period. A positive response is not absolutely indicative of steroid-responsive immune thrombocytopenia as some patients with myelodysplasia may show a transient response.

In the setting of urgent or emergent surgery, platelet administration at the start of surgery should be considered in patients with a platelet count of <70 × 10⁹ l^–1 and post CPB-transfusion in patients with a platelet count 70–90 × 10⁹ l^–1. Earlier platelet transfusion is not recommended because of the risk of human leucocyte antigen sensitization.

Antiplatelet Agents

Virtually all cardiac surgery patients take aspirin. Aspirin irreversibly blocks cyclooxygenase, leading to permanent platelet inactivation (Box 36.1). Upon cessation, normal platelet production restores platelet function in 8 days, meaning that patients exhibit 10% platelet recovery per day. For this reason, many centres no longer advocate stopping aspirin before surgery (Box 36.1).

Around 30% of patients exhibit a degree of in vitro resistance to clopidogrel. By contrast, there is little resistance to prasugrel and ticagrelor. Patients undergoing cardiac surgery within 5 days of discontinuing clopidogrel, ticagrelor or prasugrel have greater perioperative blood loss. In unstable patients, the decision to discontinue adenosine diphosphate (ADP) receptor blockers must balance the risks of bleeding and coronary ischaemia.

Congenital Haemolytic Anaemia and Haemoglobinopathy

With the exception of sickle cell disease (HbAS, HbSS), no special precautions are necessary. There is general agreement that moderate and deep hypothermia should be avoiding in patients with sickle cell trait.

Case series from Ghana and India have demonstrated that patients with sickle cell disease (HbSS) can successfully undergo cardiac surgery without additional precautions. In the UK however, patients with sickle cell disease invariably undergo preoperative red cell exchange to achieve HbS 25–30% and Hb concentration 100 g l^–1. Allogenic blood should be Rhesus and Kell matched and ideally less than 10 days old.

Hereditary spherocytosis requires no special precautions. Where it is suspected, a preoperative haematology opinion should be sought to exclude rarer congenital red cell membrane disease. Some patients who have undergone splenectomy for congenital haemolytic anaemia may have abnormal blood films that can be confused with hereditary spherocytosis.

Patients with cryohydrocytosis, a subtype of hereditary stomatocytosis, may develop hyperkalaemia during cooling followed by hypokalaemia on rewarming.

Cold Agglutinins

Most patients will show a degree of autoagglutination if their blood is cooled to 4 °C. A number of elderly patients may have significant cold agglutination. This may be idiopathic or associated with low-grade lymphoma. Clinically relevant cold agglutinins are evident at room temperature or even at 37 °C.

The incidental finding of autoagglutination is typically followed by a direct antiglobulin test (DAT). If this proves positive for complement immunoglobulin M (IgM) or IgG a thermal range of agglutination (4–37 °C) is obtained.

Treatment ranges from plasma exchange, immunosuppression, avoidance of cold cardioplegia, maintenance of normothermia to avoidance of surgery altogether. Where lymphoma is thought to be the cause, targeted chemo/immune therapy may induce agglutinin remission sufficient to permit surgery.

Anticoagulants

The management of patients on warfarin is largely governed by the original indication for anticoagulation. Patients who have AF without high-risk features can usually stop their warfarin 5 days before surgery without bridging. Similarly, patients on direct-acting oral anticoagulants (DOACs) for AF can stop their DOAC at the recommended time point and have prophylactic low-molecular-weight heparin (LMWH) from the time of admission. Higher-risk patients typically require bridging with an infusion of unfractionated heparin (UFH).

High-risk patients typically restart anticoagulation 6–8 h after the surgery with UFH or LMWH, whereas in low-risk patients, prophylactic LMWH can be used.

Dabigatran and other alternatives to UFH may have an increased role because of the availability of reversal agents. Idarucizumab (Praxbind^®) is licensed for dabigatran reversal and andexanet alfa (Andexxa^®) has recently been FDA-approved for reversal of rivaroxaban and apixaban.

Where interruption of thrombotic therapy is considered within 6 weeks of a venous thromboembolic (VTE) event the insertion of a removable embolus filter should be considered in discussion with a haematologist. If one is placed, it is absolutely paramount that a removal date is agreed prior to insertion as any filter that remains in situ becomes an indication for long-term anticoagulation in its own right.

In patients with a known thrombophilia (e.g. factor V Leiden, antiphospholipid syndrome), extended thromboprophylaxis should be considered. The decision to anticoagulate should be based on actual past thrombotic events rather than perceived risk.

Thrombolytic Agents

These drugs are currently indicated in the early management of acute MI. On rare occasions, a patient presenting with stroke in association with an, as yet, undiagnosed acute type A aortic dissection may receive thrombolytic therapy. It is not uncommon therefore, for the anaesthetist to be presented with a patient who has recently received drugs such as streptokinase or recombinant tissue plasminogen activators (t-PA; alteplase, reteplase). The surgical team needs to be aware of the half-lives of individual drugs and appreciate that their effects may persist for several days.

Heparin Resistance

In patients requiring therapeutic anticoagulation, heparin resistance is widely defined as the need for greater than 35,000 IU UFH per day to achieve a therapeutic APTT. In the setting of cardiac surgery with CPB, failure to achieve an ACT of >450 s after UFH 350 IU kg^–1 is usually considered as representing heparin resistance. Causes include: antithrombin deficiency, elevated concentrations of factor VIII, fibrinogen or heparin binding protein; and increased heparin clearance. In addition, patients with a chronic aortic dissection and chronic obstructive pulmonary disease are reported to be at a greater risk of heparin resistance. It should be borne in mind that heparin itself may produce antithrombin deficiency.

Antithrombin deficiency can usually be treated with either antithrombin concentrate or FFP. In patients with elevated clotting factor concentrations an anti-Xa assay may be used as an alternative to ACT or APTT monitoring. In patients with increased heparin binding or heparin clearance, an alternative anticoagulation strategy may be required.

Alternatives to Heparin

A number of agents have been used as alternatives to UFH. These include argatroban, prostacyclin and bivalirudin. Dosing, monitoring and reversal of these infrequently used drugs are challenging. The use of these drugs should be preceded by a current literature search and a haematology consult. The short half-life of some of these drugs means that stasis of blood with the extracorporeal circuit must be avoided to prevent clotting. When used to avoid patient exposure to UFH, it is important to ensure that heparin-coated equipment is not inadvertently used.