Equipment list for difficult airway management.
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Biomedical subjects
Publications and source records attributed to S Kiyama.
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To examine the education of trainees with regard to difficult airway management, we sent a questionnaire to all 89 Japanese University Departments of Anaesthesia (to be answered by a person who was responsible for teaching trainees) and all 280 Royal College of Anaesthetists' Tutors in the UK. The presence or absence of a formal training module for difficult airway management, timing and methods of training, types of airway devices that should be taught, and tutors' expertise with various techniques and devices were surveyed. Sixty-seven of the 89 Japanese tutors (75%) and 167 of 280 UK tutors (60%) replied to the questionnaire. Only 19 of 67 (28%) Japanese anaesthetists and 33 of 167 (20%) UK anaesthetists who replied, indicated that they had a difficult airway training module. In six Japanese departments (9%) and 115 (69%) UK departments, equipment for percutaneous transtracheal ventilation was readily available. Airway devices and techniques that tutors considered necessary to be mastered in the first 2 years of training, differed considerably between Japan and the UK, with notable differences in the use of gum elastic bougies and awake intubation. A training module for difficult airway management is often not provided and equipment for emergency transtracheal ventilation is often unavailable in both countries.
OBJECTIVE: To evaluate the effect of clusterin overexpression on radiation-induced tumour growth rates and apoptosis in human prostate LNCaP cells, as prostate cancer cells are relatively resistant to radiation-induced apoptosis and local recurrences are common, but overexpression of the anti-apoptotic protein clusterin can accelerate progression to androgen-independence and to confer a chemoresistant phenotype in various prostate cancer models. MATERIALS AND METHODS: Western blot analysis and immunohistochemistry were used to compare clusterin expression levels in parental (P) and clusterin-transfected (T) LNCaP cells in vitro and in vivo. The effects of radiation on clusterin-expression in both parental LNCaP/P and clusterin-transfected LNCaP/T tumours were analysed by Northern blot analysis. The cellular response to radiation was determined up to 3 weeks after irradiation using tetrazolium and re-growth assays, and cell-cycle analysis by flow cytometry. RESULTS: Clusterin mRNA expression increased from undetectable to low levels in LNCaP/P tumours after radiation and more than three-fold in LNCaP/T tumours. Clusterin overexpression decreased the radiosensitivity in a time-dependent manner, reducing the extent of growth arrest and apoptosis by up to 54%. Re-growth assays showed that the improved survival rates of LNCaP/T cells after radiation did not change after 3 days, remaining constant over 3 weeks. CONCLUSIONS: These results identify clusterin as a promoter of cell survival that may help mediate resistance to radiation-induced apoptosis. Furthermore, clusterin overexpression seems to provide an extended protection against radiation-induced cell cycle arrest and apoptosis.
AIMS: Withdrawal of angiotensin-converting enzyme (ACE) inhibitors may affect the progression of chronic renal failure and an insertion/deletion (I/D) polymorphism of the ACE gene may influence it. METHODS: We retrospectively collected patients with chronic glomerulonephritis and benign nephrosclerosis who discontinued ACE inhibitor use. The relationship between the decline of renal function after the withdrawal and the influencing factors such as ACE gene polymorphism, blood pressure and proteinuria were evaluated using multiple regression analysis. RESULTS: Forty-two patients (initial serum creatinine 0.5 - 6.5 mg/dl) had been treated and discontinued ACE inhibitor use. Only patients with the II or DI genotypes of the ACE gene developed the deterioration of renal function, starting at 2 months after the withdrawal. Stepwise regression analysis revealed that the level of proteinuria after the withdrawal, presence of the insertion of ACE gene and serum creatinine level at the time of withdrawal mainly influenced the decline of renal function after the withdrawal (adjusted R2 = 0.48). CONCLUSION: Withdrawal of ACE inhibitor causes the deterioration of renal function in patients with the II or DI genotypes, high proteinuria after the withdrawal, and high serum creatinine level at the withdrawal, which probably causes the rebound increase in serum ACE activity.
Tracheal intubation was facilitated with an intubating laryngeal mask (ILM) in two patients with difficult airways. Target-controlled infusion (TCI) of propofol and fentanyl was used for sedation during placement of an ILM. An ILM was inserted smoothly. Spontaneous ventilation and oxygenation were well maintained throughout the induction. Both patients were satisfied with intravenous sedation using TCI for awake instrumentation of their airways.
We here report the case of a 38-year-old male with back pain and vomiting occurring after exercise. Serum creatinine level was elevated, and he was admitted to our hospital with diagnosis of acute renal failure (ARF). He had experienced similar attacks at least 4 times, including the present episode, from the age of 22 years. After admission, the patient was managed only by resting, and remission was nearly attained in about 1 month. The renal biopsy specimen performed on day 15 showed findings of acute tubular necrosis, thickening of the tubular basement membrane, and interstitial fibrosis. After remission, the serum uric acid level was 0.7-0.8 mg/dl, fractional excretion of uric acid was 0.63, and the possibility of other diseases facilitating the excretion of uric acid was denied. Therefore, ARF associated with idiopathic renal hypouricemia was diagnosed. Since only mild responses were observed in a pyradinamide loading test and a benzbromarone loading test, the case was considered to be a presecretary reabsorption disorder type. Renal function tests showed the almost complete recovery of the glomerular filtration rate (GFR: 114 ml/min/1.73 m2), but the urine concentrating ability was markedly decreased (specific gravity 1.019 and osmolarity 516 mOsm/kgxH2O in Fishberg test). Past data from this patient indicated that this renal dysfunction had been persisting for ten years. We examined 9 patients with renal hypouricemia and focused on the differences between the two groups (with or without complications). Four patients had a history of exercise-induced ARF or calculus. The urine concentrating ability was significantly lower in these patients (group A) than in the other patients without complications (group B). The glomerular filtration rate in group A was within the normal range, but was lower than in group B. These results suggested the possibility that patients with renal hypouricemia with complications may have chronic renal dysfunction in the future.
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Endothelin-1 (ET-1) is thought to play a significant role in acute renal failure induced by cyclosporin A (CsA). The cDNA sequence encoding endothelin-converting enzyme-1 (ECE-1), which produces the active form of ET-1 from big ET-1, was recently reported. To elicit the role of ECE-1 in the glomerular and tubular dysfunction induced by CsA, the effects of CsA on mRNA and protein expression of ECE-1 in rat kidney and on mRNA expression of prepro-ET-1 and ET A- and B-type receptors in glomeruli were studied. ECE-1 mRNA was detected in glomeruli and in whole nephron segments. ECE-1 mRNA expression was downregulated in all nephron segments at 24 h after CsA injection. Protein levels were also downregulated in glomeruli and in the outer and inner medulla. CsA rapidly increased prepro-ET-1 mRNA expression in glomeruli at 30 to 60 min after injection; this rapid increase was followed by an increase in plasma ET-1 levels. These increases were followed by decreased expression of ECE-1, ET A-type receptor, and ET B-type receptor mRNA at 6 h after injection, and serum creatinine levels were increased at 24 h after CsA injection. It is suggested that downregulation of glomerular and tubular ECE-1 expression may be caused by increased ET-1 synthesis in CsA-induced acute renal failure.
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The processed electroencephalogram (pEEG) was monitored in eight patients undergoing gynaecological laparotomy under combined extradural and nitrous oxide-isoflurane anaesthesia. Pre-incisional mean spectral edge frequency 95 percentile (SEF95) and median frequency (MF) were 11.67 (SD 1.63) Hz and 3.74 (0.24) Hz, respectively. After skin incision, both SEF95 and MF decreased to 6.61 (2.04) Hz and 2.72 (0.32) Hz, respectively (P < 0.001). An increase in mean arterial pressure after incision suggested inadequate depth of anaesthesia. After introduction of extradural analgesia, these variables returned to pre-incisional values (SEF95 11.65 (1.73); MF 4.02 (0.41)). Reduction of end-tidal isoflurane from 1.0% to 0.5% after extradural analgesia did not cause significant pEEG changes. pEEG may assist anaesthetists to recognize adequacy of combined general-extradural anaesthesia.
Despite widespread recognition of the potential role of the processed electroencephalogram (pEEG) as a monitor of depth of anaesthesia, few studies have examined the effects of surgical stimuli on the intraoperative pEEG. Two groups of gynaecological patients (n = 10 in each group), with or without pre-incisional extradural analgesia, undergoing gynaecological laparotomy under nitrous oxide and isoflurane anaesthesia were monitored with routine haemodynamic observations and pEEG. Patients who received pre-incisional extradural analgesia showed no significant changes in pEEG variables during surgery (mean spectral edge frequency 95 percentile (SEF95) 13.3 (SD 1.4) Hz), whereas in all patients without pre-incisional extradural analgesia, a significant decrease in SEF95 was noted (6.5 (1.1) Hz after incision compared with a pre-incisional value of 12.5 (1.4) Hz) together with an increase in arterial pressure (paradoxical response). In the latter group, SEF95 and arterial pressure returned to pre-incisional values after extradural analgesia was established during operation. During emergence from anaesthesia, both groups showed a significant increase in SEF95 (25.7 (1.4) Hz). This study suggests that intraoperative pEEG arousal response was different from changes detected when anaesthesia was terminated at the end of surgery. Surgical stimuli in the absence of adequate analgesia induced a paradoxical arousal response.
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Left ventricular hypertrophy is reported to be common in chronic hemodialysis patients, and also to increase the risk for mortality in chronic hemodialysis patients. An echocardiographical and clinical study was carried out to investigate the risk factors for left ventricular hypertrophy in 151 non-diabetic chronic hemodialysis patients without valvular diseases or myocardial infarction in two hemodialysis units in Fukuoka, Japan. The left ventricular mass index (LVMI) correlated positively to age, systolic blood pressure and interdialysis weight gain while it correlated negatively to the duration of hemodialysis therapy and hematocrit. Resorting to a multivariate analysis, the LVMI was found to positively correlate to age and the systolic blood pressure while it correlated negatively with the duration of hemodialysis therapy and the hematocrit level. These findings suggest that hypertension and anemia may thus be independent risk factors for left ventricular hypertrophy.
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