[A Case Report of Bypass Surgery for a Perforated and Unresectable Gastric Cancer].

A 74-year-old man was admitted to a clinic because of epigastralgia in June 2018. He was referred to our hospital for further examination of right hydronephrosis. He was diagnosed as having type 2 gastric cancer in the middle gastric body and lesser curvature, with an upper gastric fiber, swollen para-aortic lymph node, and right hydronephrosis by using abdominal computed tomography. PET-CT revealed no hot spot in the para-aortic lymph node but revealed a hot spot in the lower small bowel. He was admitted to our hospital because of severe abdominal pain and appetite loss and underwent a reduction and palliative surgery for the unresectable gastric cancer. The omental cavity was perforated and penetrated into the retroperitoneum. He underwent esophageal jejunal bypass and intestinal fistula tube insertion in the stomach. He had a central vein port and was discharged from our hospital. He was able to eat during his short overnight stay at our hospital after the operation but died on postoperative day 30.

Intrathecal betamethasone for cancer pain: A study of its analgesic efficacy and safety.

BACKGROUND: A preliminary study has shown effective cancer pain relief by intrathecal betamethasone (ITB). However, further evidence is needed to support this new approach. METHODS: Cancer patients with opioid-resistant pain received lumbar intrathecal administration of betamethasone 2 or 3 mg once a week for 28 days. Immediate and short-term analgesia (using a percentage pain reduction scale and a numerical rating scale, NRS) and long-term analgesia (using NRS) were assessed. Patients were classified into two groups according to the most painful site of metastasis: vertebral column and/or surrounding nerve plexus metastases (group A) and other metastases distal from the vertebral column (group B). RESULTS: A total of 104 patients received ITB. Pain relief was observed not only in the lower half but also in the upper half of the body. The proportion of group A patients who experienced immediate analgesia was 81% (47/58), which was significantly greater than that of group B (P < 0.001). A decrease in NRS scores 1 day after ITB administration was observed in significantly more patients in group A than in group B (P < 0.001). Long-term analgesia was also recorded in a greater proportion of patients in group A than in group B in the 7-day (59%, 38/64 vs 6%, 2/33) and 28-day periods (71%, 40/56 vs 31%, 8/26) (P < 0.001). No adverse effects related to neurotoxicity were recorded. CONCLUSION: Intrathecal injection of betamethasone produced analgesia for opioid-resistant cancer pain, and may be a potent therapeutic option for intolerable pain from vertebral column and/or surrounding nerve plexus metastases.

[A case of the transversus abdominis plane block in a super obese patient using a convex probe].

We report that the transversus abdominis plane block (TAP block) can be performed under ultrasound guidance using not a linear probe but a convex probe in a markedly obese patient undergoing laparoscopy-assisted distal gastrectomy. The TAP block is effective for providing perioperative analgesia. The common probe for the TAP block is a high-frequency linear probe, which can not depict the deeper tissues. We used a low-frequency convex probe for TAP block, which clearly showed the spread of local anesthetics in TAP block in a markedly obese patient. A convex probe is preferable for TAP block in markedly obese patients.

[Case of successful management with mirtazapine for prolonged pain after esophagectomy].

This case report describes a successful outcome of mirtazapine treatment in a patient with difficult post-thoracotomy pain. A 63-year-old man received thoracotomy for the resection of esophageal tumor. The pain continued 2 years after the operation. Allodynia was present in the region of the intercostal nerves from the surgical wound. Remedies such as clonazepam, amitriptyline, gabapentin, and acetaminophen were not effective, and epidural block effect was only temporal. The patient experienced a reduction in shooting pain after taking pregabalin; however, he still suffered from persistent pain and, mirtazapine was additionally administrated. One month after this, shooting and persistent pain was reduced, and the patient's appetite was improved, which had been present since the thoracotomy. Since then, his weight slightly increased and the administration of mirtazapine was stopped in accordance with the patient's request. The pain became worse again. Therefore, mirtazapine, commonly used as an antidepressant agent, was considered to be beneficial for neuropathic pain as an analgesic adjuvant.

Sevoflurane causes greater QTc interval prolongation in elderly patients than in younger patients.

BACKGROUND: Sevoflurane and droperidol prolong the QT interval, and advancing age is not only associated with a prolongation of the QT interval but is also a risk factor for drug-induced QT interval prolongation. In this study, we compared the effect of sevoflurane and droperidol on the corrected QT (QTc) interval and the dispersion of ventricular repolarization (time interval from the peak to the end of the T wave [Tp-e]) in elderly patients with those in younger patients. METHODS: Under sevoflurane anesthesia (1.5%-2.5%) with an antiemetic dose of droperidol (1.25 mg), the QT interval and the Tp-e interval, which indicates transmural dispersion of repolarization across the myocardial wall, were measured in 30 elderly patients (70 years and older) and in 30 younger patients (20-69 years) for 2 hours. The QT interval was normalized for heart rate (QTc) using 3 different formulas: Bazett, Matsunaga, and Van de Water. Data are presented as mean +/- sd. RESULTS: The elderly group was 24.4 years older (P < 0.05) than the younger group. The QTc intervals in the 2 groups before anesthesia were not significantly different. Using all 3 formulas, the QTc interval in the elderly patient group was significantly prolonged by sevoflurane (the QTc intervals at preanesthesia and 60, 75, 90, and 120 minutes after sevoflurane exposure were 0.434 +/- 0.028 seconds, 0.450 +/- 0.037 seconds, 0.463 +/- 0.037 seconds, 0.461 +/- 0.037 seconds, and 0.461 +/- 0.038 seconds, respectively, with the Bazett formula). The sevoflurane-induced QTc interval prolongation in the elderly patient group was significantly greater than that in the younger patient group (0.450 +/- 0.037 seconds vs 0.432 +/- 0.034 seconds, 60 minutes after sevoflurane exposure; 0.463 +/- 0.037 seconds vs 0.441 +/- 0.037 seconds, 75 minutes after sevoflurane exposure; and 0.461 +/- 0.038 seconds vs 0.436 +/- 0.030 seconds, 120 minutes after sevoflurane exposure with the Bazett formula), but the sevoflurane-induced QTc interval prolongation was neither further enhanced with time nor by droperidol. The Tp-e interval was not affected in either group. CONCLUSION: Sevoflurane causes greater QTc interval prolongation in elderly patients than in younger patients. Although sevoflurane does not affect the transmural dispersion of repolarization and sevoflurane-induced QTc prolongation does not advance with time and by droperidol administration, QT interval prolongation and its associated arrhythmias should be carefully monitored during sevoflurane anesthesia in elderly patients.

[Propofol triggers a marked body temperature increase in a patient with fulminant malignant hyperthermia (MH) without inducing other symptoms of MH].

A 53-year-old woman who had experienced symptoms of fulminant malignant hyperthermia (MH) by sevoflurane a week before and her MH muscle biopsy revealing positive later, underwent the right hemicolectomy under total intravenous anesthesia with propofol and fentanyl. The patient's body temperature increased at a rate of 0.6 degree C per 15 min from 37.5 to 39.4 degrees C, but other symptoms of MH, such as tachycardia, arrhythmia, acidemia, and hypoxemia, were obviously slight in comparison with those induced by sevoflurane. The body temperature decreased after discontinuation of propofol and administration of dantrorene injection. When the patient received continuous propofol infusion for the purpose of sedation in the intensive care unit again, the body temperature gradually increased to 40 degrees C. However, it decreased to 37.8 degrees C after discontinuation of propofol and dantrorene injection again. It is well recognized that propofol is not a MH trigger, but it shoud be noted that some MH patients could experience a hypermetabolic state, such as hyperthermia, even by propofol.

The differential effects of nitrous oxide and xenon on extracellular dopamine levels in the rat nucleus accumbens: a microdialysis study.

Dopamine release in the nucleus accumbens (NAC) plays a crucial role in the action of various psychotropic and addictive drugs, such as antagonists of the N-methyl-D-aspartate subtype of the glutamate. Although both nitrous oxide and xenon are N-methyl-D-aspartate receptor antagonists, they differ in their potential for producing neuropsychological toxicity; therefore, we decided to examine their effects on both spontaneous and ketamine-induced extracellular dopamine levels in the NAC. A microdialysis probe was implanted into the NAC in each of 35 rats, which were randomly assigned to one of six groups: exposure to 40% O2, exposure to 60% nitrous oxide (0.27 MAC), exposure to 43% xenon (0.27 MAC) for 60 min, and three groups exposed to either 40% O2, 60% nitrous oxide, or 43% xenon for 70 min and 80 mg/kg ketamine was given i.p. 10 min after the initiation of gas exposure. Perfusate samples were collected every 20 min, and the dopamine levels were measured using a high-performance liquid chromatography system. Nitrous oxide, but not xenon, significantly increased the dopamine level. Ketamine significantly increased the dopamine level, and this was significantly inhibited by xenon, but not by nitrous oxide. These data suggest that the difference in neuropsychological activity between nitrous oxide and xenon is partly due to their differential effects on the mesolimbic dopamine system.

[Neuromuscular blocking effects of Org 9426 (rocuronium bromide); a comparative study with vecuronium bromide in Japanese patients].

BACKGROUND: Efficacy and safety of Org 9426 were compared with those of vecuronium bromide in Japanese patients. METHODS: We studied 88 Japanese patients undergoing surgery requiring general anesthesia. Patients were allocated randomly to receive intubation dose of 0.6 mg x kg(-1), 0.9 mg x kg(-1) of Org 9426 or 0.1mg x kg(-1) of vecuronium. Following an intubation dose, patients received maintenance doses of 0.1, 0.15 or 0.2 mg x kg(-1) of Org 9426 or 0.025 mg x kg(-1) of vecuronium. The neuromuscular block was monitored with acceleromyography using TOF stimuli. Sevoflurane was administered to all treatment groups after intubation. RESULTS: The onset times of the 0.6 and 0.9 mg x kg(-1) of Org 9426 groups were 84.6 and 77.1 sec respectively, which showed statistical difference between the onset time of 0.1 mg x kg(-1) of vecuronium, 125.7 sec. The intubation condition was similar among three treatment groups. The clinical durations of 0.6 and 0.9 mg x kg(-1) of Org 9426 and 0.1 mg x kg(-1) of vecuronium were 53.4, 73.4 and 59.9 min, respectively. Clinical duration and spontaneous recovery time of maintenance dose of 0.15 mg x kg(-1) of Org 9426 were similar to those of 0.025 mg x kg(-1) of vecuronium. CONCLUSIONS: Org 9426 showed more rapid onset time than that of vecuronium and similar clinical duration and recovery times to those of vecuronium in Japanese patients.

[Airway obstruction during one-lung ventilation using a bronchial blocker and a tracheostomy tube].

We describe our experience with a 60-year-old man who had severe airway obstruction during one-lung ventilation with the tracheostomy tube using a bronchial blocker. The blocker, deriving from Univent tube, was passed through the tracheostomy tube and placed in the right main bronchus. We checked that the blocker was in appropriate place with a bronchofiberscope and obtained good one-lung ventilation with the patient in the left lateral position. However, just after the start of operation, when the skin was incised, sever hypoxia and resultant bradycardia and hypotension occurred, probably because of not only malposition of blocker but also atelectasis in the upper lobe of the dependent lung by secretion.

Ketamine attenuates hypocapnia-induced neuronal damage in the caudoputamen in a rat model of chronic cerebral hypoperfusion.

We previously demonstrated that the caudoputamen was exclusively further damaged by hypocapnia in a rat with chronic cerebral hypoperfusion which is characterized by white matter lesions (WML) and a well-established model for patients with cerebrovascular diseases and/or dementia, and suggest that this process may be the cause of long lasting postoperative delirium or brain dysfunction in such patients. In the present study, we investigated whether ketamine, a non-competitive N-methyl-D-aspartate receptor antagonist, could attenuate the neuronal damage in the caudoputamen. Ketamine, at doses of 10 and 20 mg/kg, which was given intraperitoneally before hypocapnia induction, attenuated the aggravation of WML score, neuronal damage, and astroglial proliferation in the rat caudoputamen. These results suggest that ketamine may be beneficial for preventing postoperative brain dysfunction, especially in patients with cerebrovascular diseases and/or dementia induced by hypocapnia, which is likely to occur in the mechanical ventilation used during surgery.

[NMDA receptor antagonist neurotoxicity and psychotomimetic activity].

Non-competitive NMDA receptor antagonists, in spite of their neuroprotective effects against neuronal ischemia, brain trauma, etc., cause neuronal damage in the rodent posterior cingulate and retrosplenial cortices (PC/RS), which are thought to be responsible brain regions for their psychotomimetic activity in humans. A number of anesthetics have not only GABAA receptor activating properties but also NMDA receptor antagonist properties. On the other hand, ketamine and nitrous oxide, both of which are potent non-competitive NMDA receptor antagonists and have little GABAA activating properties, are demonstrated to induce neuronal damage in the rat PC/RS. Furthermore, ketamine potentiates the neuronal damage by nitrous oxide. Although many anesthetics, such as halothane, isoflurane, barbiturates and benzodiazepines, inhibit the neuronal damage in the PC/RS by NMDA receptor antagonists, probably through GABAA receptor activation, we anesthesiologists should be aware of the risk of ketamine or nitrous oxide anesthesia, not to speak of the combined use of them, without using GABAA receptor activating agents.

Pentobarbital inhibits ketamine-induced dopamine release in the rat nucleus accumbens: a microdialysis study.

UNLABELLED: Dopamine release in the nucleus accumbens (NAC) plays a crucial role in the actions of various psychotropic and addictive drugs. Ketamine and barbiturates have psychotropic effects and addictive properties, but barbiturates prevent ketamine's psychotomimetic effects. We investigated the effects of ketamine and pentobarbital on dopamine release in the NAC. A microdialysis probe was implanted in the NAC in 35 rats, which were randomly assigned to seven groups: a normal saline intraperitoneal injection (ip) group, 50 and 100 mg/kg of ketamine ip groups, 25 and 50 mg/kg of pentobarbital ip groups, and a normal saline or 25 mg/kg of pentobarbital ip followed by 50 mg/kg of ketamine ip groups. Perfusate samples were collected every 20 min, and dopamine concentration was measured by high-performance liquid chromatography. Ketamine at doses of 50 mg/kg and 100 mg/kg significantly increased dopamine release in the NAC. Conversely, pentobarbital significantly decreased dopamine release in the NAC and inhibited the ketamine-induced dopamine release. These data suggest that the dopamine release in the NAC may be involved in ketamine-induced, but not barbiturate-induced, psychotropic effects and addiction. Inhibition of ketamine-induced dopamine release by barbiturates may be a mechanism by which they prevent ketamine emergence reactions. IMPLICATIONS: Ketamine increased dopamine release in the nucleus accumbens, which was inhibited by pentobarbital. The mesolimbic dopamine system may be involved in the psychotomimetic effects of ketamine, and the suppression of ketamine emergence reactions by barbiturates may be because of the inhibition of ketamine-induced dopamine release in the nucleus accumbens.

Ketamine-induced c-Fos expression in the mouse posterior cingulate and retrosplenial cortices is mediated not only via NMDA receptors but also via sigma receptors.

Ketamine induces marked c-fos expression in the posterior cingulate and retrosplenial cortices (PC/RS). We investigated whether NMDA and/or sigma receptors were involved in the c-Fos expression. The number of Fos-LI positive boutons in NMDA receptor knockout mice was significantly lower than that in wild-type mice. Rimcazole but not haloperidol significantly suppressed the c-Fos expression. The results indicate that the ketamine-induced c-Fos expression is mediated not only via NMDA receptors but also via sigma receptors.

Anticonvulsant effects of sevoflurane on amygdaloid kindling and bicuculline-induced seizures in cats: comparison with isoflurane and halothane.

PURPOSE: We compared the anticonvulsant effects of sevoflurane with those of isoflurane and halothane in amygdaloid kindling and bicuculline-induced seizures in cats. METHODS: In a crossover design, the effects of 70% nitrous oxide, and 0.3, 0.6, and 1.5 minimum alveolar concentration (MAC) of volatile anesthetics were studied in five cats in which the amygdala was electrically stimulated at the current used for establishing the kindled state. The effects of 0.6 and 1.5 MAC of volatile anesthetics were studied in another five cats, in which 0.2 mg.kg(-1) of bicuculline was administered i.v.. RESULTS: In the amygdaloid kindling model, all four anesthetics decreased the duration of after-discharge (AD), the rise of multiunit activity in midbrain reticular formation (R-MUA), and the behavior scores compared with findings without anesthetics. Halothane, at 1.5 MAC, significantly decreased the number of cats showing AD ( P < 0.05). In the bicuculline-induced seizure model, all five cats showed repetitive spikes during 1.5 MAC of sevoflurane, whereas only two and three cats, respectively, showed the repetitive spikes during 1.5 MAC of isoflurane and halothane. All three volatile anesthetics decreased the rise of R-MUA, the duration of the repetitive spikes, and the behavior scores. The suppression of the rise in R-MUA and the behavior scores with 1.5 MAC of sevoflurane was significantly less than that with 1.5 MAC of isoflurane. CONCLUSION: The anticonvulsant effects of sevoflurane were less potent than those of halothane in the amygdaloid kindling model and less potent than those of isoflurane in the bicuculline-induced seizure model.