[Two cases of pulmonary embolism in spinal surgeries].

We experienced two cases of pulmonary embolism (PE) in the perioperative period. Although the incidence of perioperative PE is low, it may lead to a critical outcome. The first case is a 59-year-old man without risk factors of PE, scheduled for laminectomy. The end tidal CO2 of 25 mmHg and Pa(CO2) of 48 mmHg developed at the same time during the operation, suggesting PE. He was diagnosed as PE by pulmonary perfusion scan later. The second case was a 71-year-old woman with hypertension and diabetes mellitus, scheduled for laminectomy. Although there were no events during the surgery, she complained of chest pain and dyspnea after the operation. Blood gas analysis showed Pa(O2) of 55 mmHg (FI(O2) 0.4). She was also diagnosed as PE by pulmonary perfusion scan. Both patients made satisfactory progress by appropriate diagnosis and treatment. PE may occur in spite of prevention, and it is important to find out the signs of PE and to prepare for the occurrence of PE.

[Control of postoperative bladder spasm by caudal anesthesia in children undergoing ureteral reimplantation].

BACKGROUND: For management of postoperative bladder spasm by the ureteral reimplantation, general anesthesia and epidural anesthesia are selected in many hospitals, but epidural anesthesia is not a common technique for various complications and risks. We examined whether postoperative bladder spasms can be prevented by general anesthesia combined with single shot caudal anesthesia. METHODS: We studied 18 patients undergoing ureteral reimplantation. Premedicated by diazepam syrup (0.5 mg x kg(-1), maximum dose 10 mg). In combination with caudal anesthesia with 0.3% ropivacaine (3 mg x kg(-1), maximum dose 60 mg), general anesthesia was maintained with oxygen, nitrous oxide and sevoflurane. For the evaluation of pain relief we used face pain scale when the patients returned to the ward, postoperative 5 hours, 24 hours and at discharge. RESULTS: At postoperative 5 and 24 hours, some patients had a pain scale of above 3. But, those under pain scale 1 was 83%. At discharge, all patients were evaluated as pain scale 0 or 1. CONCLUSIONS: General anesthesia combined with single shot caudal anesthesia suppressed postoperative bladder spasm. All patients were discharged within 3 postoperative days.

Ascorbate inhibits apoptosis of Kupffer cells during warm ischemia/reperfusion injury.

BACKGROUND/AIMS: This study sought to determine whether ascorbate (Asc), a scavenger of reactive oxygen species, inhibits apoptosis of hepatic cells consisting of hepatocytes, Kupffer cells, and sinusoidal endothelial cells (SECs) in the rat liver after warm ischemia/reperfusion (I/R) injury. METHODOLOGY: Hepatic warm ischemia (69% of the total liver) was induced for 30 min, followed by reperfusion for 60 min. In some animals, ascorbate (at 1 or 10 mg/kg) was infused intravenously immediately before the onset of reperfusion. Hepatic cell apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL). Mitochondrial release of cytochrome c into the cytoplasm was assessed by Western blot analysis, and the activation of caspase-3 in liver tissue was determined by colorimetric assays. RESULTS: Assays of cytochrome c release and caspase-3 showed increased levels of these apoptotic related proteins and enzyme activity. While few apoptotic hepatocytes or SECs were detected in the ischemic group by TUNEL staining, the number of TUNEL-positive Kupffer cells was approximately 4.5-fold greater than that seen in the sham-treatment group. Ascorbate treatment reduced this increase in apoptotic Kupffer cells. CONCLUSION: The hepatic cells most vulnerable to oxidative stress in the first hour of reperfusion were Kupffer cells. These may play a key role in hepatic warm I/R injury.

[Assessment of sublingual PCO2 during selective cerebral perfusion].

We monitored sublingual tissue PCO2 (PSLCO2) continuously with an ISFET (ion-sensitive field effect transistor) based PCO2 sensor during and after surgical treatment for descending aortic aneurysm. Using femoro-femoral bypass and a beating heart technique, distal end of aneurysm was clamped and then selective cerebral perfusion was performed into the left subclavian and left common carotid arteries. Aneurysmectomy and reconstructive surgery were carried out with proximal end of the left common carotid artery being clamped. Upon starting selective cerebral perfusion, PSLCO2 increased abnormally. PSLCO2 increased from 38 mmHg just after induction of anesthesia to the maximum value of 87 mmHg during selective cerebral perfusion. Three hours after arriving in the intensive care unit, the patient developed convulsion and anisocoria and the computed tomography showed cerebral infraction. Since the blood flow to the tongue is fed through the internal and external carotid arteries, the increase in PSLCO2 is supposed to be caused by the decrease of blood flow to the tongue during selective cerebral perfusion. The monitoring of PSLCO2 may be a useful method to estimate the brain blood flow during selective cerebral perfusion.

[Successful anesthetic management of three patients with cardiac dysfunction for non-cardiac surgery using olprinone hydrochloride].

Non-cardiac surgery presents significant risks to patients with cardiac dysfunction. The relative safety of different anesthetic techniques has been studied without mentioning any clear indication. The depression of myocardial contractility by anesthetic agents limits their use in patients with cardiac dysfunction, especially for induction of anesthesia. We used olprinone hydrochloride perioperatively in the anesthetic management of three patients. In all cases, anesthetic induction, intraoperative course and the postoperative period proceeded uneventfully. We consider that perioperative use of continuous olprinone hydrochloride infusion may be suitable for patients with cardiac dysfunction for non-cardiac surgery.