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Purpose We evaluated the safety and efficacy of long-term administration of dexmedetomidine in patients in the intensive care unit (ICU). Primary endpoint was the incidence of hypotension, hypertension, and bradycardia. Secondary endpoints were withdrawal symptoms, rebound effects, the duration of sedation with Richmond Agitation-Sedation Scale (RASS) ≤ 0 relative to the total infusion time of dexmedetomidine, and the dose of additional sedatives or analgesics. Methods Dexmedetomidine 0.2–0.7 μg/kg/h was continuously infused for maintaining RASS ≤ 0 in patients requiring sedation in the ICU. Safety and efficacy of short-term (≤24 h) and long-term (>24 h) dexmedetomidine administration were compared. Results Seventy-five surgical and medical ICU patients were administered dexmedetomidine. The incidence of hypotension, hypertension, and bradycardia that occurred after 24 h (long-term) was not significantly different from that occurring within 24 h (short-term) (P = 0.546, 0.513, and 0.486, respectively). Regarding withdrawal symptoms, one event each of hypertension and headache occurred after the end of infusion, but both were mild in severity. Increases of mean arterial blood pressure and heart rate after terminating the infusion of dexmedetomidine were not associated with the increasing duration of its infusion. The ratio of duration with RASS ≤ 0 was ≥ 85 % until day 20, except day 9 (70 %) and day 10 (75 %). There was no increase in the dose of additional sedatives or analgesics after the first 24-h treatment period. Conclusions Long-term safety of dexmedetomidine compared to its use for 24 h was confirmed. Dexmedetomidine was useful to maintain an adequate sedation level (RASS ≤ 0) during long-term infusion.

A 69-year-old male patient with esophageal cancer underwent video assisted subtotal esophagectomy after neoadjuvant chemotherapy and radiation (50 Gy). Adhesion between esophagus and the aorta was so severe that the aortic arch was damaged and massive bleeding occurred during manipulation of the esophagus. However, as we had expected and prepared for the incident, we successfully managed it and emergency thoracic endovascular aortic repair could be performed by cardiac surgeons immediately. Preanesthetic careful consideration and preparation for surgical incidents are necessary for anesthesiologists.

病変が言語中枢や運動中枢に近接している場合, 術後の神経脱落症状を防ぐため, 術中に患者をawakeとし脳機能のマッピングとモニターしながら開頭手術を行うawake craniotomyが選択される. 上気道の確保, 全身痙攣の確実なコントロール, 心理的な配慮が重要なポイントとなる. 通常の全身麻酔に比べ, より慎重な患者評価を行い, さらに患者との信頼関係を築かなければならない. 術中のマッピングを確実にするには, 前投薬などそれ以前に投与する麻酔薬を最小限にする努力が必要である. 体位は半側臥位または側臥位となるが, 圧迫点すべてにパッドを入れ, 体幹と頭部のねじれがないよう, また頸部は軽度伸展位とし, 気道が自然に開通しやすいようにする. 鎮静はプロポフォールの持続投与, 鎮痛はエピネフリン添加の局所麻酔薬により頭皮神経のブロックと皮切部の浸潤麻酔により行う. レミフェンタニル, デクスメデトミジンなど新しい麻酔薬と, ラリンジアルマスクの利用などにより快適かつ安全な管理が可能となりつつある.

The aim of the present study was to examine whether hypoxic pulmonary vasoconstriction (HPV) is preserved during one-lung ventilation combined with thoracic epidural anesthesia (TEA) in dogs. Using a separately ventilated left lower lobe (LLL) in situ, the pressure-flow (P-Q) curve was obtained. The HPV response was assessed by the shift of the P-Q curve, changes in blood flow diversion rate (FDR) and decrease in PaO2 during hypoxic gas ventilation of LLL. In the control group (n = 7), the shift of P-Q curve, changes in FDR, and decrease in PaO2 remained constant during four consecutive hypoxic stimulations. In the TEA group (n = 6), the P-Q curve shifted to the left during hyperoxia, but the magnitude of the shift during hypoxia was unchanged. FDR and decrease in PaO2 were significantly reduced compared with baseline values (P0.05 with analysis of variance). TEA reduced heart rate, cardiac output, mean arterial pressure, mean pulmonary arterial pressure, and mixed venous oxygen tension. Our results suggest that TEA did not affect the primary pulmonary vascular tone at baseline or during lobar hypoxia, but enhanced the diversion of blood flow and arterial blood oxygenation during lobar hypoxia. This enhanced HPV response probably reflects hemodynamic changes, such as decreased cardiac tension, due to sympathetic nerve activity blockade by TEA.

小児に対する前投薬として,ミダゾラム注腸投与の効果を,1～6歳の小児109例を対象とし,投与時間(導入30分前と60分前),投与量(0.2mg/kgと0.4mg/kg)および年齢(1～3歳と4～6歳)に分けて検討した.鎮静スコア1(導入時にマスクを嫌がるもの)を無効,スコア2～4を有効,スコア5を過剰鎮静として評価すると,30分前投与群で,投与量に関係なく,年長児の有効率(92～100%)は年少児(54～58%)に比較して有意に高く,この傾向は投与時間を導入60分前にしても同様であった.以上の結果からミダゾラム0.2～0.4mg/kgの30～60分前注腸投与法は,年少児での有効性は十分でないが,4～6歳の就学前児童の前投薬としては有用な方法と思われた.

Volatile anesthetics are generally considered to possess a vasodilator action. Some of their actions on pulmonary vessels, however, are not clearly understood. We examined the effects of various volatile anesthetics on pulmonary vessels using an in situ rabbit isolated-lung perfusion model. We prepared a rabbit constant-flow lung-perfusion model by sending blood to the pulmonary artery and removing blood from the left atrium, and observed the changes in pulmonary arterial perfusion pressure caused by inhalation of 0.5, 1, 2, and 3 minimum alveolar concentration (MAC) volatile anesthetics: halothane, enflurane, isoflurane, and sevoflurane, in random order. These volatile anesthetics increased pulmonary arterial perfusion pressure in a dose-dependent manner and caused the pulmonary arteries to constrict. In particular, halothane at all concentrations induced significantly greater pulmonary vasoconstriction than the other volatile anesthetics. Therefore, it is suggested that volatile inhalation anesthetics induce the pulmonary arteries to constrict, and halothane exhibits the most potent pulmonary vasoconstrictor effect among the volatile anesthetics tested.

Objective: To investigate whether prostaglandin E 1 (PGE 1 ) directly inhibits hypoxic pulmonary vasoconstriction in dogs. Design: Prospective, longitudinal study. Setting: University research laboratory. Subjects: Six mongrel dogs in vivo. Interventions: The left thorax of anesthetized and ventilated dogs was opened and the left lower lobe was separately ventilated. The tip of the thermodilution pulmonary artery catheter was introduced into the left lower lobe pulmonary artery. The left lower lobe was ventilated with hyperoxic (95% oxygen and 5% CO 2 ) or hypoxic (95% nitrogen and 5% CO 2 ) gas. By manipulating the occluders placed on both pulmonary arteries, blood flow in the left lower lobe was regulated. Continuous pressure-flow plots for the left lower lobe were then obtained. Measurements and Main Results: Measurements included continuous pressure-flow plot generation, thermodilution cardiac output and blood flow in the left lower lobe, and blood gas analysis. Alveolar hypoxia of the left lower lobe caused blood flow in the left lower lobe to decrease from 371.8 ± 63.4 to 95.0 ± 23.4 mUmin and shifted the pressure-flow plot to the right, with a decreased slope and with an increase in the pressure-axis intercept. Subsequently, systemic venous infusion of PGE 1 at a rate of 0.3 μg/kg/min had no effect on the pressure-flow plot configuration, blood flow in the left lower lobe, pulmonary vascular resistance, systemic vascular resistance, and Pao 2 . However, there was a decrease in the pressure-axis intercept of the pressure-flow plot. Infusion of PGE 1 at a rate of 3.0 μg/kg/min (high-dose) during hypoxia reduced pulmonary vascular resistance and systemic vascular resistance by 19% and 25%, respectively, and returned the pressure-flow plot toward normal while blood flow in the left lower lobe increased to 122.6 ± 21.0 mUmin. Consequently, Pao 2 decreased from 270 ± 31 to 144 ± 32 torr (36.0 ± 4.1 to 19.2 ± 4.3 kPa). Conclusion: High-dose PGE 1 essentially inhibits hypoxic pulmonary vasoconstriction, at the expense of a deterioration in pulmonary gas exchange and systemic blood pressure in dogs.

Congenital afibrinogenemia is a rare autosomal recessive hemorrhagic disorder, and thrombotic complications occurring spontaneously or after infusion of fibrinogencontaining preparations have been reported in afibrinogenemic patients [1]. We report a case of mesenteric venous thrombosis due to fibrinogen replacement in a patient with congenital afibrinogenemia. A 19-year-old male with congenital afibrinogenemia had previously undergone uneventful surgical procedures for splenic rupture, intracranial bleeding, and mandibular abscess (2002) with preoperative supplement of fibrinogen concentrate. He was urgently admitted to the Critical Care Medical Center and diagnosed with diffuse peritonitis in 2003. After prophylactic administration of ten units of fresh-frozen plasma (FFP), resection of the small intestine was performed. Numerous thromboses were detected in the mesenteric veins of the resected specimen. The color of the remaining small intestine darkened during wound closure and mesenteric circulation worsened. Continuous infusion of unfractionated heparin (Novo Heparin 1000, Mochida Pharmaceutical Co., Japan) at 500 units/h was initiated following a 2000-unit bolus. The following day, massive resection of the small intestine, leaving only 60 cm of small intestine, was performed due to necrosis identified during a second-look operation. In 2004, emergency surgery was performed for adhesive intestinal obstruction without hemostatic complications by prophylactic administration of fibrinogen concentrate and unfractionated heparin. Perioperative laboratory data from 2002, 2003, and 2004 are shown in Table 1. In 2002, data revealed undetectable plasma fibrinogen levels by the functional assay, undetectable prothrombin time (PT) and activated partial thromboplastin time (APTT), and thrombocytosis. Supplementation with 9000 mg of fibrinogen raised fibrinogen levels to 1.91 g/l and normalized PT and APTT. In 2003, fibrinogen levels, PT, APTT, and platelet count after preoperative administration of ten units of FFP were approximately the same as in 2002. However, excessively high levels of hemostatic and inflammatory markers preoperatively indicated a hypercoagulable and inflammatory state. While perioperative heparin infusion in the first operation suppressed levels of hemostatic markers, the levels of those in the second-look operation were still above normal range. In 2004, preoperative tests again showed undetectable plasma fibrinogen level and PT, but APTT was normal. Values for all hemostatic markers, WBC, and C-reactive protein (CRP) were markedly elevated compared to reference ranges, but platelet count was normal. Supplementation with fibrinogen concentrate and intraoperative heparin administration resulted in a plasma fibrinogen concentration of 1.03 g/l and an APTT of 44.7 s. Fibrinogen level measured using both functional and immunological assays was 0.1 g/l at 5 days after administration of 1000 mg of fibrinogen concentrate. Prothrombin activation increases and increased thrombin generation has been observed in afibrinogenemia [2]. Thrombin represents a potent activator of platelets and platelet aggregation [3]. Tefferi et al. [4] reported marked thrombocytosis occurring in 22.0% of postsplenectomy patients. Furthermore, Remijn et al. [1] showed that the absence of fibrinogen results in large but loosely packed platelet aggregates and suggested that afibrinogenemic patients could be at risk for thrombosis. Thus, hypercoagulable states due to increased prothrombin activation and platelet aggregation may exist in our patient. Compensative reaction for severe intestinal inflammation and/or heparin-induced thrombocytopenia [5] may have been considerable for the reduced platelet count in 2004, Y. Takasugi (*) . Y. Shiokawa . R. Kajikawa . J. Oh . Y. Koga Department of Anesthesiology, Kinki University School of Medicine, 377-2 Ono-Higashi, Osaka-Sayama, Osaka, 589-8511, Japan e-mail: yoshihiro.takasugi@nifty.com Tel.: +81-72-3660221 Fax: +81-72-3660206

Background In vitro studies have shown that isoflurane, enflurane, and halothane inhibit the hypoxic pulmonary vasoconstriction (HPV) with essentially the same potency. The aim of this study is to compare the effects of sevoflurane and isoflurane on HPV in constant-flow perfused rabbit lungs. Methods Constant-flow perfused lungs from Japanese white rabbits were tested. The lungs were divided into three groups: isoflurane alone (n = 6), sevoflurane alone (n = 6), and sevoflurane with ibuprofen pretreatment (n = 6). Baseline HPV responses were measured as the pulmonary arterial pressure increased after changing inspired oxygen concentration from 95% for 15 min to 3% (with 5% CO2) for 5 min without anesthetic administration. Next, three different concentrations of anesthetics were added to the inspired gas for 15 min in random order. The HPV response in the presence of anesthetic was expressed as a percentage of the pressor response in the absence of anesthetics, and dose-response relationships were calculated using the nonlinear least-squares method. Results Isoflurane and sevoflurane both depressed the HPV response in a dose-related manner. The half-inhibition values (ED50) of HPV with isoflurane and sevoflurane were 0.85 +/- 0.22 MAC and 1.00 +/- 0.12 MAC (mean +/- SD), respectively, and were not statistically different. Ibuprofen pretreatment did not alter ED50 and slope of dose-response curve, although the absolute value of pressor response in the sevoflurane group with ibuprofen pretreatment was greater than that in the sevoflurane alone group at every concentration of sevoflurane. Conclusions Sevoflurane inhibits the HPV response in a dose-related manner, and its potency is similar to that of isoflurane in vitro. Cyclooxygenase products do not mediate the inhibition of HPV by sevoflurane.

The effect of preanesthetic 20 mg of famotidine on gastric fluid volume and pH were studied in patients scheduled for elective surgery. One hundred and twenty-eight patients were divided into four groups-control, intravenous, intramuscular and oral with 32 patients in each group. Patients in placebo group received no famotidine and served as control. Patients in the intravenous and intramuscular groups were administered famotidine one hour before surgery. Patients in the oral group were administered famotidine the night before and on the morning of surgery. Gastric volume in the control group was 19.1 +/- 10.8 ml; in the intravenous group, 7.4 +/- 6.4 ml; in the intramuscular group, 7.3 +/- 6.9 ml; and in the oral group, 7.1 +/- 6.9 ml. Gastric pH was 3.4 +/- 2.3, 6.8 +/- 1.1, 6.9 +/- 1.6, and 6.7 +/- 1.2 in groups one through four, respectively. When compared to the control group, famotidine significantly decreased gastric volume and increased gastric pH. There were no statistical differences among the different modes of administration. No adverse effects were observed in this study. It is concluded that preanesthetic management of 20 mg of famotidine reduced the risk of acid aspiration pneumonitis.

•There are many reports on complication of tracheal intubation, but the development of acute respiratory distress associated with subcutaneous emphysema, pneumomediastinum and bilateral pneumothorax is a rare complication during general anesthesia. It has also been reported that tracheal perforation may be predisposed to such complication1-5. This is a report of an unexpected and dramatic experience we had of a case under anesthesia.

To the Editor: Anti-N-methyl-D-aspartate-receptor (NMDAR) encephalitis is caused by serum antibodies against NMDAR, and is often associated with tumors [1]. Its symptoms include psychosis, seizures and disturbance of consciousness, all of which resemble the symptoms induced by NMDA antagonists, such as ketamine. We report a patient with anti-NMDAR encephalitis, and we had difficulty treating the patient because no primary tumor was found. A 57-year-old woman, who had a cough and fever, developed to status epilepticus, and consciousness disturbance. Examinations revealed elevated anti-NMDAR antibodies, but no obvious primary tumor could be found with a CT scan. However, fluorodeoxyglucose positron emission tomography showed an accumulation of fluorescence in a right enlarged obturator lymph node (Fig. 1, Supplementary material), indicating augmented metabolism, and lymph node removal was scheduled. After epidural catheter placement, anesthesia was induced with propofol, and the trachea was intubated. Anesthesia was maintained with 60 % nitrous oxide and 1.5 % sevoflurane with epidural anesthesia. The surgery was completed without complications. After tracheal extubation, the patient was transferred to the intensive care unit. The patient’s postoperative course was uneventful. Her lymph node was histopathologically normal, but we postulated that the lymph node would produce ectopic NMDAR. The patient’s level of consciousness improved gradually. There are some anesthetic drugs that serve as NMDAR antagonists, such as ketamine and nitrous oxide. Pryzbylkowski et al. [2] have recommended avoiding such drugs for anesthesia in a patient with anti-NMDAR encephalitis, and we should not have used nitrous oxide for anesthesia. In conclusion, we encountered a patient with anti-NMDAR encephalitis without a responsible tumor, but removal of a metabolically active enlarged lymph node markedly improved the symptoms.