Asystole Triggered by the Mouth Opening With a Dental Mouth Gag Under General Anesthesia During Pediatric Oral Surgery: Report of a Rare Case.

The trigeminovagal reflex manifests as a sudden onset of bradycardia, hypotension, and cardiac arrest in response to the stimulation of the trigeminal nerve. The incidence of trigeminovagal reflex in maxillofacial surgical procedures is approximately 1.6%. We report a case of asystole in a pediatric patient in whom a dental mouth gag triggered the trigeminovagal reflex during oral surgery. The patient was a 5-year-old boy who was scheduled to undergo extraction of maxillary supernumerary teeth. After tracheal intubation, anesthesia was maintained with sevoflurane and remifentanil. At the beginning of the surgery, his mouth was opened with a dental mouth gag, and electrocardigram showed asystole for 20 seconds. Thereafter, his heart rate spontaneously returned to basal value within 60 seconds. Since sufficient mouth opening was required to conduct the surgery, his mouth was opened again with the gag. When the interincisal distance exceeded about 40 mm, his heart rate suddenly decreased, but spontaneously returned to baseline within 60 second. The subsequent anesthetic course was uneventful.

Efficacy of prophylactic doses of intravenous nitroglycerin in preventing myocardial ischemia under general anesthesia: A systematic review and meta-analysis with trial sequential analysis.

STUDY OBJECTIVE: To evaluate the efficacy of intravenous nitroglycerin (TNG) in preventing intraoperative myocardial ischemia (MI) under general anesthesia. Moreover, we analyzed the hemodynamic changes in heart rate (HR), mean blood pressure (MBP), and pulmonary capillary wedge pressure (PCWP) associated with TNG administration both before and after the induction of anesthesia. DESIGN: Meta-analysis. SETTING: Operating room, cardiac surgery or non-cardiac surgery, all surgeries were elective measurements. We performed a computerized search of articles on PubMed, Scopus, and the Cochrane Central Register of Controlled Trials. Meta-analysis was performed using Review Manager. The data from the individual trials were combined using a random-effects model to calculate either the pooled relative risk (RR) or the weighted mean difference (WMD) with 95% confidence interval (CI). We conducted trial sequential analysis (TSA). The primary outcome was the incidence of MI and the secondary outcomes were hemodynamic changes (HR, MBP, and PCWP). MAIN RESULTS: Using electronic databases, we selected 10 trials with a total of 353 patients for our review. Prophylactic intravenous TNG did not significantly decrease the incidence of MI (RR=0.61; CI, 0.33 to 1.13; P=0.12; I2=55). TSA corrected the CI to 0.05 to 7.39 and showed that 9.5% of the required information size was achieved. In terms of hemodynamic changes, intravenous TNG significantly reduced MBP in comparison with the placebo (MBP pre-induction: WMD=-7.27; 95% CI -14.2 to -0.33; P=0.04; I2=97%; MBP post-induction: WMD=-5.13; 95% CI -9.17 to -1.09; P=0.01; I2=73%). CONCLUSIONS: Our analyses showed that prophylactic intravenous TNG does not reduce the incidence of intraoperative MI. Moreover, TSA suggests that further studies are necessary to confirm the results (GRADE: very low). Prophylactic doses of intravenous TNG significantly reduced the MBP both pre and post anesthesia induction (GRADE: very low).

[Endotracheal intubation in an adult patient fitted with a Leksell frame using a Pentax Airwayscope with a pediatric-type INTLOCK blade (ITL-P)].

Several previous reports have established the Pentax Airwayscope (Pentax AWS, S-100, HOYA-PENTAX, Tokyo, Japan) as an efficient tool for tracheal intubation in adult patients. The Pentax AWS is often successfully used with an INTLOCK blade; to date, however, INTLOCK blades have been released for neonatal and pediatric patients only. In this case, we performed tracheal intubation using a Pentax AWS attached to a pediatric-type INTLOCK blade (ITL-P) in an adult patient fitted with a Leksell Stereotactic frame (Elekta, Sweden). The patient weighed 45 kg and was 154 cm tall, and was scheduled for a tumor biopsy due to glioblastoma in the brain stem. The patient was preoperatively fitted with a Leksell frame on her head. The patient was not premedicated and was monitored with electrocardiography (ECG), noninvasive blood pressure, and pulse oximetry. Following pre-oxygenation, general anesthesia was induced using propofol 4.0 microg x ml with target-controlled infusion and remifentanil 0.25 microg x kg(-1) hr(-1). After loss of consciousness, we administered 30-mg rocuronium boluses. We initially attempted tracheal intubation first using a Macintosh laryngoscope and then a Pentax AWS, but we could not achieve tracheal intubation with either of these instruments. Upon switching to a Pentax AWS with an ITL-P, we successfully achieved tracheal intubation without any complications. Anesthesia was maintained uneventfully with 3.0 microg x ml(-1) propofol and remifentanil 0.10 to 0.25 microg x kg(-1) x hr(-1) in oxygen and air. Further study is needed to facilitate the effective use of the Pentax AWS and the ITL-P in such cases.

[Endotracheal intubation for a neonatal patient complicated with Arnold-Chiari malformation using a Pentax airway scope with a neonatal-type INTLOCK blade (ITL-N)].

Several previous reports have established the Pentax Airway Scope (Pentax AWS, S-100, HOYA-PENTAX, Tokyo, Japan) as an efficient tool for endotracheal intubation in adult patients. To date, however, there are no reports on its use with the INTLOCK blade for neonatal and pediatric patients. In this case, we performed tracheal intubation using a Pentax AWS attached to a neonatal-type INTLOCK blade (ITL-N) twice, 1 day and 10 days after birth, in a neonatal patient complicated with Arnold-Chiari malformation. The patient weighed 2.2 kg and was 47 cm tall. The first operation consisted of the repair of a meningocele ; the second was for the insertion of an indwelling Ommaya reservoir. We initially attempted tracheal intubation using a Miller's laryngoscope in the first operation and a Macintosh laryngoscope in the second, but we could not achieve tracheal intubation with either of these instruments. Upon switching to a Pentax AWS with an ITL-N, however, we successfully achieved tracheal intubation in both operations. Further research is needed to facilitate the effective use of the Pentax AWS in such cases.

Endothelin-1 stimulates cyclin D1 expression in rat cultured astrocytes via activation of Sp1.

Endothelins (ETs), a family of vasoconstrictor peptides, are up-regulated in several pathological conditions in the brain, and induce astrocytic proliferation. We previously observed that ET-1 increased the expression of cyclin D1 protein. Thus, we confirmed the intracellular up-regulation of cyclin D1 by ET-1 in rat cultured astrocytes. Real-time PCR analysis indicated that ET-1 (100 nM) and Ala(1,3,11,15)-ET-1 (100 nM), a selective agonist of the ETB receptor, induced a time-dependent and transient increase in cyclin D1 mRNA. The effect of ET-1 was diminished by an ETB antagonist (1 µM BQ788) or inhibitors of Sp1 (500 nM mithramycin), ERK (50 µM PD98059), p38 (20 µM SB203580) and JNK (1 µM SP600125), but not inhibitors of NF-κB (10 µM SN50 and 100 µM pyrrolidine dithiocarbamate). The binding assay for Sp1 indicated that ET-1 increased the binding activity of Sp1 to consensus sequences, and two oligonucleotides of the cyclin D1 promoter including the Sp1-binding sites diminished the effect of ET-1. Western blot analysis showed that ET-1 induced time-dependent and transient phosphorylation of Sp1 on Thr453 and Thr739 via the ETB receptor. ET-1-induced phosphorylation of Sp1 was attenuated by PD98059 and SP600125. Additionally, ET-1 increased the incorporation of bromodeoxyuridine (BrdU) in cultured astrocytes and the number of BrdU-positive cells decreased in the presence of PD98059, SP600125 and mithramycin. These results suggest that ET-1 increases the expression of cyclin D1 via activation of Sp1 and induces astrocytic proliferation.

[Emergency incompatible red cell transfusion to a patient whose blood type was suspended from identification].

We report a case of a 59-year-old woman who presented with hypovolemic shock and compensated acidosis (preoperative arterial blood gases: pH 7.3, P(CO2) 31.9 mmHg, Pa(O2) 112.3 mmHg, base excess -9.8, Hb 6.4 g x dl(-1)) due to perforated descending colon, necessitating emergency surgery. Tracheal intubation had been performed preoperatively. Prior to induction of anesthesia, blood pressure was 106/74 mmHg, heart rate 119 beats x min(-1), and Sp(O2) 100% breathing room air. Anesthesia was induced with remifentanil influsion at a rate of 0.05 mg x kg(-1) x min(-1), sevoflurane 1% and rocuronium bromide 30mg, and was maintained with oxygen, air, remifentanil and sevoflurane. For a critical hypovolemia, in accordance to the guidelines for intraoperative critical hemorrhage and the Japanese practical guidelines for blood components therapy, we started to transfuse incompatible red cell (O+) since the identification of blood typing was suspended. The duration of surgery was 104 min, with an intraoperative total bleeding of 125 ml. Four units of total blood transfusion and 3,050 ml of infusion of Ringer's acetate solution were administered. The patient was transferred to ICU with tracheal intubation. No adverse reactions associated with blood type incompatibility were recognized.

[Anesthetic management for a pediatric patient of Klippel-Trenaunay syndrome with giant head by hydrocephalus].

Klippel-Trenaunay syndrome (KTS) is a rare disorder associated with the triad of 1) capillary vascular malformation, 2) varicose veins and/or venous malformation, 3) and soft tissue and/or bony hypertrophy. A six-month old, 6.0-kg-weight male pediatric patient was scheduled for ventriculo-peritoneal shunt operation for hydrocephalus caused by obstructive aqueductus cerebri. At the age of three months, he was diagnosed as KTS by extensive capillary vascular malformation and soft tissue hypertrophy of the right leg. Physical examination showed prominent vascular malformation over his anterior thoracic and abdominal wall, and soft tissue hypertrophy was only on his right leg. Simultaneously, he was complicated with congenital hydrocephalus because of obstructive aqueductus cerebri. His head and skull were enlarged and his head measurement reached 55 cm (chest measurement 32 cm). Anesthetic management of KTS patients should be prepared with blood transfusion against massive hemorrhage and hypovolemic shock. Furthermore, KTS patients should be always considered to have airway difficulty due to the soft tissue hypertrophy, upper and airway hemangiomas. Therefore, we planned safer tracheal intubation following practice guidelines for management of the difficult airway.

Induction of non-apoptotic cell death by morphinone in human promyelocytic leukemia HL-60 cells.

As previously suggested, codeinone (oxidation product of codeine) induces non-apoptotic cell death, characterized by marginal caspase activation and the lack of DNA fragmentation in HL-60 human promyelocytic leukemia cells, which was inhibited by N-acetyl-L-cysteine. Whether, morphinone, an oxidative metabolite of morphine, also induced a similar type of cell death in HL-60 cells was investigated. Morphinone showed slightly higher cytotoxic activity against human tumor cell lines (oral squamous cell carcinoma HSC-2, HSC-3, HSC-4, NA, Ca9-22, promyelocytic leukemia HL-60, cervical carcinoma HeLa) than against normal oral human cells (gingival fibroblast HGF, pulp cells HPC, periodontal ligament fibroblast HPLF). Morphinone also induced an almost undetectable level of internucleosomal DNA fragmentation in the HL-60 cells. Morphinone did not activate caspase-8 or -9 in these cells. Morphinone dose-dependently activated caspase-3 in both HL-60 and HSC-2 cell lines, but to a much lesser extent than actinomycin D. Electron microscopy demonstrated that morphinone induced mitochondrial shrinkage, vacuolization and production of autophagosome and the loss of cell surface microvilli, without destruction of cell surface and nuclear membranes in the HL-60 cells. The autophagy inhibitor 3-methyladenine (0.3-10 mM) slightly inhibited the morphinone-induced cytotoxicity, when corrected for its own cytotoxicity. These data suggest that morphinone induces non-apoptotic cell death in HL-60 cells.

Effect of anticancer agents on codeinone-induced apoptosis in human cancer cell lines.

The possible apoptosis-inducing activity of codeinone, an oxidative metabolite of codeine, without or with anticancer drugs, was investigated. Codeinone induced internucleosomal DNA fragmentation in human promyelocytic leukemia cells (HL-60), but not in human squamous cell carcinoma cells (HSC-2). Codeinone dose-dependently activated caspase-3 in both of these cells, but to a much lesser extent than that attained by actinomycin D. This property of codeinone was similar to what we have found previously in alpha,beta-unsaturated ketones. Codeinone did not activate caspase-8 or caspase-9 in these cells. The cytotoxic activity of codeinone against HSC-2 cells was inhibited by N-acetyl-L-cysteine, but somewhat additively stimulated by sodium ascorbate, epigallocatechin gallate, hydrogen peroxide, sodium fluoride, 5-fluorouridine, cisplatin, doxorubicin and methotrexate. These data suggest that codeinone has possible antitumor potential, in addition to its action as a narcotic analgesic, even though it induces incomplete apoptosis-associated characteristics.