A 68-year-old man with gastric adenocarcinoma was scheduled for gastrectomy. Medical history included tobacco abuse and chronic obstructive pulmonary disease (GOLD 3). Preoperative echocardiography revealed no wall motion abnormalities and ECG and blood studies were normal. With informed consent and after implementation of standard monitoring, thoracic epidural catheterisation was established (Th 8/9). Subsequent general anaesthesia and surgery were uneventful. During emergence from anaesthesia, pulseless ventricular tachycardia was detected and immediate cardiopulmonary resuscitation was commenced. Return of spontaneous circulation occurred after 1 min of chest compressions, three defibrillations with 360 J and intravenous injection of 150 mg of amiodarone. Adrenaline was not required. Appearance of a new ST-elevation on a 12-channel ECG suggestive of myocardial infarction prompted immediate transport of the patient from the operating theatre to the fluoroscopic suite. Coronary angiography revealed stenosis of the right coronary artery (RCA). During percutaneous coronary intervention (PCI), two episodes of ventricular fibrillation were successfully terminated by defibrillation (360 J) and two bare-metal stents were placed into the RCA. Intravenous anticoagulation was initiated with 5000 units of heparin and 500 mg of aspirin. After the intervention, the patient was transferred to the ICU on mechanical ventilation, receiving infusions of propofol (1.5 mg kg−1 h−1) and noradrenaline (0.1 μg kg−1 min−1). Considering the importance of cardiac stabilisation and early dual platelet inhibition on the one hand, and possible development of epidural haematoma and subsequent neurologic impairment on the other hand, the attending anaesthetists were facing a dilemma. Coagulation studies after PCI showed an activated partial thromboplastin time (aPTT) of more than 180 s, a prothrombin time (PT) of 69% and a platelet count (PLT) of 159 G l–1. Platelet function tests (PFA-100) had been ordered, but the results were still pending [later revealing normal Col/Epi (51 s) and ADP (107 s) times]. Serum creatinine (65 μmol l–1), urea (3.2 mmol l–1) and estimated glomerular filtration rate (CKD-EPI, 107 ml h–1) were normal, and creatinine clearance was not determined. After brief consultation with the attending cardiologists and haemostaseologists, the epidural catheter was removed 180 min after PCI and administration of heparin and aspirin without another measurement of aPTT (Fig. 1). For rapid assessment of neurologic function, the patient was weaned from mechanical ventilation and the tracheal tube was removed 1 h later. As sensory and motor functions were normal, no further imaging studies were performed. Ticagrelor 180 mg loading dose was administered per os 2.5 h after epidural catheter removal. Neurologic reassessment 2 weeks after catheter removal revealed no deficits. The patient was discharged to rehabilitation. Written informed consent for publication of this case was obtained from the patient.
The risks and benefits of thoracic epidural catheterisation in major abdominal surgery are well established.1 However, evidence regarding morbidity and mortality of this procedure remains controversial. Perioperative myocardial infarction in major noncardiac surgery is a rare event and even more rare in patients with epidural catheters.2 However, appropriate anticoagulant therapy is crucial for positive outcomes after acute coronary syndrome and particularly after placing stents into coronary arteries.3,4 Any withholding of dual platelet aggregation inhibition increases the risk of coronary stent thrombosis.5 Furthermore, any procoagulant stimulus and anticoagulant reversal (e.g. transfusion of packed platelet concentrates, administration of protamine or coagulation factors) should be avoided to provide functionality of stents and to prevent thrombosis. This case report illustrates the dilemma between the risk of stent thrombosis and the possible development of an epidural haematoma due to removal of an epidural catheter. Under non-urgent circumstances, guidelines recommend long periods of discontinuation of anticoagulant medication before and after epidural anaesthesia and/or epidural catheter removal, depending on anticoagulant substances and dosages used.6–8 The recommended interval for withholding ticagrelor after epidural catheter removal is 6 h.6 Combinations of anticoagulant substances, particularly the combination of heparin and aspirin, cause strong inhibition of haemostasis. Dual platelet aggregation inhibition further potentiates this effect.4
The management of emergency anticoagulant therapy after PCI in patients with epidural catheters is highly individual. Several case reports have been published, but controlled trials or cohort studies of this rare clinical problem are currently not available and seem difficult to obtain.9–11
Possible approaches may include:
- Immediate catheter removal after recognition of myocardial infarction before PCI and before initiation of any anticoagulant therapy.
- Early catheter removal after PCI and after administering heparin and aspirin under decreasing heparin effects or after confirmed normalisation of aPTT, but before loading with a second platelet aggregation inhibitor.
- Late catheter removal after PCI, after administration of heparin and aspirin and after completed loading with second platelet aggregation inhibitor. This approach should include frequent assessment of coagulation parameters and platelet function prior to catheter removal. Tirofiban, a reversible inhibitor of ADP-mediated platelet aggregation, may be used as bridging between discontinuation of a long-acting platelet aggregation inhibitor and catheter removal.9
In our patient, removal of the epidural catheter 3 h after administering heparin and aspirin was not associated with development of bleeding or neurologic impairment. Furthermore, ticagrelor administration 2.5 h after catheter removal (5 h after PCI) did not result in signs suggestive of coronary stent thrombosis. However, loading with ticagrelor was initiated earlier than suggested because perceived risk of possible stent thrombosis was considered high and the guideline of the European Society of Cardiology recommends ADP receptor blockade as early as possible.12
Retrospectively, an alternative strategy might have been immediate epidural catheter removal prior to PCI to avoid the dilemma of prioritisation of treatment as mentioned earlier. The need for cardiopulmonary resuscitation itself could be a trigger for immediate epidural catheter removal, as detection of either pulmonary embolism or cardiac infarction suggests the need for enhanced anticoagulant therapy or thrombolysis. Earliest possible weaning from mechanical ventilation and sedation should be achieved to assess neurologic function and, in case of clinical impairment, to rapidly initiate further diagnostic investigations and treatment. The question of the right time to remove an epidural catheter in a patient needing emergency anticoagulant therapy remains difficult and should be addressed in controlled trials.
Acknowledgements relating to this article
Assistance with the case report: none.
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Conflicts of interest: none.
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