Haemostatic Alteration In Cardiopulmonary Bypass Surgery

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Open cardiac surgery produces significant activation of coagulation, fibrinolysis, and platelets, despite the use of heparin. This is due to the presence of the cardiopulmonary bypass circuit. The following are well-documented alterations.186

1. Platelet defects during CPB: A qualitative platelet abnormality exists in virtually 100% of patients during CPB and usually reverses within an hour or so after completion of CPB. The blood-material surface interaction and shear effects of flow through the circuit traumatise platelets. CPB produces thrombocytopenia, platelet fragmentation, and platelet function abnormalities, including a reduced response to aggregation stimuli. This is due to discharge ofalpha granules and loss ofplatelet membrane receptors, such as, GpIb and GpIIb/GpIIIa. As P-selectin is expressed on the inner surface of a-granules, their release produces increased platelet surface expression of P-selectin. Activated platelets are also able to bind leucocytes forming polymorphonuclear- and monocyte-platelet conjugates. The degree of impairment in platelet function correlates with the duration of CPB and with the level of hypothermia. The defect occasionally persists longer and sometimes results in bleeding. The level of hypothermia used during the procedure and contact with the synthetic surface of the oxygenator contribute to the haemostatic defect. Moderate hypothermia (2832° C) is used during CPB to reduce tissue ischaemia and preserve the myocardium. This affects platelet number and function. The generation of thrombin-antithrombin (TAT) complexes is greater during and after hypotheremic bypass compared to normothermic bypass. Postoperative blood loss and transfusion requirements also appear to be greater in patients undergoing hypothermic CPB.195 Transfusion of platelet concentrates promptly controls the bleeding. Despite abnormalities in platelet number and function, there is no evidence that routine perioperative transfusion of

Moderate to high PTP

Determine PTP of DVT

Negative

DVT confirmed

Negative

Positive

Serial US or venography

Negative

DVT excluded

Negative

DVT confirmed

Low PTP

Venous US

D-dimer test

Positive

Positive

D-dimer test

Venous US

Positive

Fig. 14 Algorithm for diagnosing DVT based on clinical assessment of pre-test probability (PTP), venous ultrasonography (US), and d-dimer testing.

platelet concentrates is necessary (Office of Medical Application of Research, National Institute of Health, UK Health Department 1989). Many patients with coronary artery disease may be taking aspirin. Patients taking aspirin before CPB surgery are at risk of excessive blood loss during the procedure. It is, therefore, recommended that aspirin be discontinued 5 to 10 days before CPB surgery.186,187

2. Thrombocytopenia: Platelet counts after bypass are generally between 50 and 150 x 109/l.

Thrombocytopenia itself is rarely a cause for postoperative bleeding.

3. Failure to neutralise the heparin completely is rarely seen with modern techniques. Use of thrombin time (TT) and reptilase time quickly clarifies the presence of excessive heparin. Following initial adequate heparin neutralisation, the re-appearance of active heparin in the circulation may occur 2 to 6 hours later. This rebound effect is caused by the delayed return of sequestered extravascular heparin, which occurs when peripheral perfusion improves.186

4. DIC: This does not occur regularly during the CPB procedure. In the postoperative period, DIC occurs uncommonly and usually reflects other problems, such as, poor cardiac output, acidosis, and sepsis.

5. Fibrinogenolysis: Activation of fibrinolysis measured by D-dimer levels has been shown to peak during CPB. There is a wide variation in fibrinolytic response to CPB. The increased fibrinolytic activation is mainly due to an increase in t-PA and to lesser extent by contact activation that is maximal at the first passage of blood through the extracorporeal circuit. Some of the t-PA is released from the coronary circulation after cardioplegic arrest has been performed. During CPB the peak of TAT levels precede high D-dimer levels, suggesting the majority of t-PA released is from the endothe-lium secondary to thrombin generation. One study showed that peak D-dimer levels correlate with postoperative bleeding. Recent studies indicate that fibrinogenolysis is much less frequent during bypass than previously believed and probably accounts for bleeding uncommonly. Nonetheless, if the euglobulin clot lysis time is shortened and there is no evidence ofDIC, judicious use oftranex-amic acid sometimes dramatically halts bleeding.186,188,189

6. Activation of coagulation during CPB: Despite systemic heparinisa-tion, CPB produces significant activation of coagulation compared to other thoracic operations not requiring CPB. The thrombo-genic effect of the extracorporeal circuit is the main stimulus with surgical cutting playing a lesser role. The time course of activation of coagulation show a significant increase on initiation of CPB and a rapid fall at the end of CPB. CPB surgery is associated with a drop in the plasma levels of most coagulation factors, which is primarily attributable to haemodilution. As with platelet concentrates, it is not necessary to routinely transfuse FFP during CPB. Inappropriate use of FFP in CPB surgery is common and has logistic and economic implications.190 Selective deficiency of high molecular weight von Willebrand factor multimers and associated prolongation of bleeding time with haemorrhagic tendency have been described in both adults and children with valvular heart disease or congenital cardiac defects. Surgical correction of the defect results in normalisation of the multimer pattern.186

7. Haemodilution: Is a consequence of extracorporeal circulation, but the fall in haematocrit, platelet count, and plasma proteins including coagulation factors is about 25 to 30%. Therefore, it is not sufficient to cause bleeding.

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