A 41-year-old man (height 171.5 cm, body weight 67 kg) was transferred to the regional medical center due to right hemiplegia and aphagia. Cerebral magnetic resonance imaging revealed cerebral infarction caused by occlusion of the left middle cerebral artery, while cerebral magnetic resonance angiography showed the development of a network of abnormal collateral vessels. Hence, the patient was diagnosed with MMD.
Before cerebral revascularization surgery, severe MR (III/IV) due to the prolapse of the P2 leaflet in the mitral valve was indicated by transthoracic echocardiography. Cardiac catheterization indicated elevated pulmonary arterial pressure (PAP) (systolic/diastolic/mean: 86/33/60 mmHg) and pulmonary capillary wedge pressure (32 mmHg) at the systemic arterial pressure of 120/83/102 mmHg. Hence, the patient was admitted to our university center for the surgical treatment of MR.
Preoperative single-photon emission computed tomography revealed reduced cerebral blood flow in the left cerebral hemisphere (especially in the external left frontal cortex; Fig. 1). Neurosurgeons at our center judged that the patient did not have an indication for cerebral revascularization surgery, which is used to prevent ischemic complications during the perioperative period of mitral valve plasty. This was because his left frontal lobe showed extensive cerebral infarction and no cerebral infarction symptoms were observed in the right cerebral hemisphere. Therefore, mitral valve plasty without cerebral revascularization was chosen.
In the operation room, the patient’s monitoring of electrocardiogram, oxygen saturation, systemic arterial pressure via right radial artery catheter, bispectral index, and regional cerebral oxygen saturation (rSO2) at the right and left forehead (INVOS™ 5100C, Somanetics, USA) was initiated before the administration of general anesthesia. The rSO2 values for the left and right forehead were 72 and 81 %, respectively.
General anesthesia was induced by intravenous administration of 3 mg of midazolam, 0.4 mg of fentanyl, and 50 mg of rocuronium. After tracheal intubation, a transesophageal echocardiography (TEE) probe was inserted. Then, a central venous catheter and right heart catheter were inserted via the right internal jugular vein, and central venous pressure, PAP, cardiac output, and mixed venous oxygen saturation were measured. The nasopharyngeal temperature and urinary bladder temperature were also measured.
Before CPB, general anesthesia was maintained by inhalation of sevoflurane (1–1.5 % of end-tidal concentration). The patient’s PaCO2 was maintained between 38 and 42 mmHg. Intra-aortic balloon pumping (IABP) was placed at the start of surgery and the augmented pressure was maintained. The mean arterial pressure was constantly above 70 mmHg. Before CPB, rSO2 values were almost above 80 % on both sides (Fig. 2).
During CPB, administration of sevoflurane via the oxygenator was also continued because of its cerebrovascular dilatation activity and potential preconditioning effect against focal cerebral ischemia. PaCO2 was maintained between 45 and 50 mmHg, and alpha-stat management of pH was performed. Hypothermia was induced; the temperature at the bottom of the nasopharyngeal temprature was 28 °C. We used pulsatile perfusion assist to maintain cerebral circulation during CPB with IABP. A decrease in rSO2 was observed 162 min after the initiation of CPB. Our perfusionist increased the CPB pump flow from 2.2 L/min/m2 to 2.8 L/min/m2 in order to increase cerebral blood flow. Moreover, the concentration of sevoflurane was increased to 2 %. Yet, rSO2 desaturation (15 % reduction from baseline) was not improved. We decided to increase the depth-of-anesthesia with another dose of midazolam. After administration of 3 mg of midazolam, the rSO2 values increased from 67 to 73 % on the right side and from 71 to 74 % on the left side. During CPB, the lowest values (and variation) of rSO2 in the left and right forehead were 71 % (−2 %) and 67 % (−17 %), respectively. Mitral valve plasty was performed as planned.
At the weaning from the CPB, the disappearance of MR was confirmed by TEE; the weaning was not difficult. Pulmonary hypertension also improved (PAP was 26/12 mmHg, while systemic arterial pressure was 105/56 mmHg). After CPB, inhalation of sevoflurane (1–1.5 % of end-tidal concentration) was also continued. The rSO2 values were almost above 75 % on both sides and not below the awake rSO2 values (Fig. 2). CPB and aortic cross-clamping lasted 352 min and 289 min, respectively. On the completion of the surgery, the IABP was discontinued and sevoflurane administration was stopped. The patient was transferred to the intensive care unit with ventilator support under propofol sedation.
On the 1st postoperative day (POD), the patient was weaned from the ventilator, and the patient did not complain about any new neurological deficits. We monitored the rSO2 of his forehead until the 2nd POD and no significant decrease (−20 %) of the rSO2 values was confirmed. The postoperative course was uneventful. On the 15th POD, single-photon emission computed tomography revealed that the low cerebral blood flow lesions had not changed (Fig. 3), and the patient was discharged from our hospital on the 16th POD.