A 17-year-old girl with a height of 150 cm and weight of 55 kg was referred to our hospital for disturbance of consciousness and right hemiparesis. She was diagnosed with acute subdural and subcortical hemorrhage due to ruptured AVM, and emergency craniotomy was performed under general anesthesia. She had a surgical history of left Blalock–Taussig shunt at the age of 2 months, bidirectional Glenn operation at the age of 3 years, and Fontan palliation (extracardiac conduit total cavopulmonary connection without fenestration of the atrium) at the age of 5 years for her congenital hypoplastic left heart syndrome (HLHS), double outlet right ventricle, atrioventricular septal defect, pulmonary atresia, and absence of inferior vena cava. She had received aspirin, warfarin, propranolol, imidapril, furosemide, and spironolactone preoperatively. Her activities of daily living were maintained. Preoperative transthoracic echocardiography (TTE) showed normal systolic and diastolic function of the univentricular chamber with trivial atrioventricular valve regurgitation.
In addition to the American Society of Anesthesiologists’ standard monitors, monitoring of arterial blood pressure (ABP), CI, and SVV was started via the left radial artery after confirming the equivalence of non-invasive blood pressure on her right arm. After induction of general anesthesia using target-controlled infusion of propofol at 3 μg/ml, remifentanil infusion at a rate of 0.2 μg/kg/min, and 40 mg of rocuronium, tracheal intubation was performed. Positive pressure ventilation was started with respiratory rate at 16 breaths/min, tidal volume 330 ml, I:E ratio 1:2, positive end-expiratory pressure 0 cmH2O, and peak airway pressure 20 cmH2O. We inserted a central venous catheter via the right internal jugular vein under X-ray fluoroscopy to a length of 11 cm and started continuous CVP monitoring. After positioning the CVP transducer at the same height as the patient’s heart, the initial value of CVP was 15 mmHg; we therefore attempted to maintain this value intraoperatively.
After the incision of the dura, rapid bleeding from the AVM was observed, and CVP suddenly decreased to less than 5 mmHg (Fig. 1). We first rapidly administered 500 ml of crystalloid, 500 ml of colloid, and 720 ml of fresh frozen plasma. We did not transfuse packed red blood cells at this time because high values of hematocrit (approximately 45%) were observed preoperatively. After that, approximately 1000 ml of blood loss was observed and hematocrit decreased to 29%. Then, we started to administer packed red blood cells to prevent an excess decrease in hematocrit. After fluid and blood transfusion, CVP gradually recovered to 10–15 mmHg. Approximately 1700 ml of rapid blood loss was observed in 30 min. Low CVP values (<5 mmHg) continued for approximately 20 min. In contrast, there was only a slight rise in SVV from 5 to 8%. CI was kept within an acceptable range (2.9–3.5 l/min/m2). Heart rate (HR) and ABP were also maintained without the use of inotropes or vasopressors. AVM resection and external decompression ended with a total operation time of 383 min, and the patient was transferred to the intensive care unit under sedation and controlled ventilation. In total, 1960 ml of blood loss and 540 ml of urine volume were observed. A total of 2500 ml of crystalloid and 800 ml of colloid were administered, and 840 ml of packed red blood cells, 1680 ml of fresh frozen plasma, and 400 ml of platelets were transfused.
Three days after surgery, the patient was still under controlled ventilation, but her hemodynamic state and circulatory monitoring values were stable (HR 75 bpm, ABP 110/50 mmHg, CVP 13 mmHg, CI 4.5 l/min/m2, and SVV 5%). At that time, ventricular systolic function and diastolic dimension measured by TTE were similar to those observed before surgery.
