A 78-year-old woman (height: 1.6 m; weight: 71 kg) with sudden onset of left abdominal pain was diagnosed with an impending AAA rupture and was transferred to this hospital for surgical management. The patient had no remarkable medical history. Before surgery, her vital signs were blood pressure, 89/67 mmHg; heart rate, 104 beats per minute; respiratory rate, 34 breaths per minute; and oxygen saturation, 98% in room air. Blood tests indicated a hemoglobin level of 7.4 g/dL, normal renal function, and absence of any coagulation disor- ders. Electrocardiography indicated a normal sinus rhythm with no evidence of ischemia. Transthoracic echocardiography (TTE) showed normal left ventricular function (ejection frac- tion 450%) and no obvious valvular disease. A contrast- enhanced computed tomographic (CT) scan confirmed the presence of a 60-mm ruptured infrarenal AAA. A contrast- enhanced CT scan of the entire aorta found no evidence of dissection, intramural hematoma, or penetrative ulcers along the entire length of the ascending aorta. After the placement of peripheral intravenous and arterial catheters, the patient was transferred to the operating room for surgical repair of the AAA. Anesthesia was induced, unevent- fully, with 250 μg of fentanyl, 2 mg of midazolam, and 100 mg of rocuronium. She was intubated with a 7.0-mm endotracheal tube and received inhaled sevoflurane as maintenance anes- thesia. Thereafter, a central venous catheter was inserted through the right internal jugular vein. After her abdomen was opened, the hemorrhage from the aneurysm became uncontrollable. She suffered cardiopulmo- nary arrest (CPA) due to hemorrhagic shock. Therefore, a left anterolateral incision was made, and the cardiothoracic surgeon initiated cardiac massage. Moreover, the descending aorta was clamped through the incision. Thus, cardiopulmonary resusci- tation was attempted, and spontaneous circulation returned after approximately 24 min; hence, the surgery was resumed. Her activated coagulation time (ACT) was 340 seconds without heparin administration; therefore, heparin was not administered during the surgery. The infrarenal abdominal aorta and left and right common iliac arteries were identified and clamped. Thereafter, the patient underwent infrarenal abdominal aorta replacement with an I-graft (20 11 mm; Hemashield Gold, MAQUET, San Jose, CA). After the proximal aortic site was unclamped, the patient's blood pressure suddenly fell. Although appropriate medical and fluid therapies were administered, her vital signs remained unstable. Consequently, a TEE probe was inserted, which indicated the presence of an AAD extending along the aorta proximally from the aortic arch to the descending aorta. At that time, the dissection was limited to the aortic arch on the proximal side. After the distal site was unclamped, the patient suffered another CPA due to hypovolemic shock and required blood volume infusion and cardiac massage. She recovered quickly and underwent another TEE examination thereafter. TEE indicated that the dissection extended to the ascending aorta—which was suggestive of a retrograde type-A AD (Fig 1) —and showed the presence of moderate-to-severe AR, the absence of any apparent pericardial effusion, and the absence of any abnormal cardiac wall motion or coronary involvement. Within the visual field of the TEE, no entry site of the dissection was observed. After discussing the management of this patient with the cardiothoracic surgeons, conservative treatment was adopted for treating the dissection. After I-graft replacement for the AAA was completed, the patient was transferred to the intensive care unit (ICU) with an open abdomen and was intubated. She received an infusion of 0.1 μg/kg/min of norepinephrine and 0.7 μg/kg/min of epi- nephrine. The total amount of bleeding due to surgery was 1,074 mL, whereas 7,070 mL of blood were collected in the cell saver canister (Sorin Group, Milan, Italy). The patient required 34 U of packed red cells, 32 U of fresh frozen plasma, and 30 U of platelet concentrates to resolve the loss caused by hemorrhage during the surgery. Finally, her ACT was found to be 191 seconds without heparin administration.
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