In this prospective study involving 125 patients, we analyzed epidural analgesia failure after major abdominal surgery using computed tomography (CT) epidurographies to compare the incidence of dislodgement of epidural catheters and leakage of solution from the epidural space between two groups of patients: patients with successful or failed epidural analgesia. Our hypothesis was that the incidence of dislodgement and leakage should be low when epidural analgesia is successful. A thoracic epidural catheter was inserted before general anesthesia and secured by subcutaneous tunneling. Bupivacaine (0.25%) was administered during surgery followed by continuous epidural analgesia with 0.125% bupivacaine (10 mL/h) and morphine (0.25 mg/h) for 48 h. Failure was defined as a visual analog scale pain score at rest more than 30 mm and/or interruption of epidural analgesia before 48 h for any reason. When failure was not due to unintentionally withdrawn, kinked catheters or adverse events (n = 11), a CT scan with contrast injection was performed. Control CT scans were also performed in patients with adequate analgesia (i.e., the success group). The incidence of failure was 24.8% (n = 31). CT scans in the failure group (n = 20) showed seven patients with catheters outside the epidural space, nine with normal distribution, one with unilateral spread, and three with leakage of solution outside the epidural space. In the success group, CT scans (n = 19) showed 11 patients with normal distribution, five with unilateral spread, and three with leakage. We conclude that the major cause of epidural analgesia failure was dislodgment of the catheter. CT scans were mostly useful for detecting leakage of injectate, which may be the early phase of dislodgment.

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We carried out a randomized prospective study in 60 patients who had undergone major abdominal surgery for cancer. For postoperative pain control, 30 patients received continuous extradural infusion of 0.125% bupivacaine 12.5 mg h-1 and morphine 0.25 mg h-1 (EXI group) and 30 received patient-controlled analgesia (PCA) with intravenous morphine (1 mg bolus, 5-min lock-out and maximum dose 20 mg 4h-1). Both groups had general anaesthesia. The two groups were compared for postoperative pain scores, satisfaction, sedation and oxygen saturation. Oxygen saturation was recorded continuously the night before surgery and for two consecutive postoperative nights. Episodes of moderate desaturation (90% > SpO2 85%) were more frequent in the EXI group than in the PCA group (P < 0.05). Pain scores were lower in the EXI group compared with the PCA group at rest and while coughing (P < 0.05). No significant difference was found for patient sedation and satisfaction.

BackgroundPatients with congenital afibrinogenemia suffer from spontaneous recurrent severe bleeding. While fibrinogen concentrates are known to effectively treat bleeding episodes, thrombotic complications often occur upon replacement therapy, rendering clinical management highly challenging.Case PresentationWe hereby report a case of combined afibrinogenemia and congenital antithrombin deficiency manifested by recurrent life-threatening bleeding, as well as spontaneous severe arterial occlusion, such as acute coronary syndrome and stroke, and venous thromboses like pulmonary embolism.Secondary fibrinogen prophylaxis is recommended following any initial life-threatening bleeding episode in patients with afibrinogenemia, yet the high associated risk of thrombosis illustrates the complexity of choosing the most effective prophylaxis strategy combining fibrinogen concentrate with antithrombotic agent for optimal protection against the risk of both severe bleeding and thrombosis. For our patient, the thrombin generation assay objectively confirmed her prothrombotic tendency.ConclusionThis case may help us better understand the pathophysiology of arterial thrombosis in afibrinogenemia, while highlighting the difficulty of managing such complications.