Survey of patients whose lungs could not be ventilated and whose trachea could not be intubated in university hospitals in Japan.

PURPOSE: We conducted a survey to clarify the actual circumstances in which the lungs could not be ventilated and the trachea could not be intubated (CVCI). METHODS: A questionnaire was mailed to all the university hospitals in Japan, asking about CVCI they had experienced during induction of anesthesia in 1998, and before 1997. RESULTS: Answers were obtained from 60 of 83 institutes. CVCI occurred in 26 of 151 900 cases of general anesthesia (0.017%) in 1998. Eighteen cases occurred after induction of anesthesia by several induction methods. Five cases occurred after repeated attempts at tracheal intubation by laryngoscopy and fiberscopy in patients under awake or anesthetized conditions. In the remaining 3 cases, the situation of occurrence was not documented. Patients with CVCI had anatomical abnormalities around the upper airways, mostly from acquired diseases. CVCIs after induction of anesthesia were successfully treated by restoration of spontaneous respiration, blind intubation, laryngeal mask airway, and transtracheal approaches, and CVCIs after repeated attempts at intubation were treated mostly by transtracheal approaches. No serious consequences occurred in any patients in 1998. Twenty cases were reported before 1997, and 2 were specific, in which CVCI followed malplacement of a tracheal tube, and serious consequences, death and brain damage, respectively, followed. In other patients, no serious consequences occurred, although cardiac arrest occurred in 1 patient. CONCLUSION: This survey demonstrates that CVCI can occur in any situation in which the airway is not established. Furthermore, effective treatments may be different depending on the situation, and delayed recognition of tracheal tube misplacement may lead to a serious outcome.

Facilitation of ischemia-induced release of dopamine and neuronal damage by dexamethasone in the rat striatum.

Glucocorticoids have been reported to aggravate ischemia-induced neuronal damage in both humans and experimental animals. Because an excess release of neurotransmitters is closely related to the outcome of ischemic neuronal damage, we evaluated the effects of dexamethasone on monoaminergic release and histological outcome. Changes in the extracellular concentrations of monoamines and their metabolites in the striatum produced by occlusion of the middle cerebral artery for 20 min were measured using a microdialysis high-performance liquid chromatography procedure, and the effects of intracerebroventricular administration of dexamethasone (10 microg) were evaluated in halothane-anesthesized rats. The histological outcome was evaluated by light microscopy 7 days after ischemia. Additionally, the effects of lesioning of the substantia nigra were estimated. The extracellular concentrations of neither dopamine nor serotonin were affected by the administration of dexamethasone in the nonischemic state. The occlusion of the middle cerebral artery produced a marked increase in the extracellular concentration of dopamine in the striatum, the peak value being 240 times that before ischemia. The preischemic administration of dexamethasone enhanced the increase in dopamine level during ischemia, and the peak value in the dexamethasone group was 640% of that in the vehicle group. After 7 days, ischemic neuronal damage in the dexamethasone group was severe compared with that in the vehicle group. In rats receiving the substantia nigra lesion, the ischemic release of dopamine was abolished, and the aggravation of ischemic neuronal damage by dexamethasone was completely alleviated. Changes in the release of monoamines may be a contributing factor in the development of the ischemic neuronal damage induced by glucocorticoids.

[Is local anesthesia necessary for venipuncture?].

We evaluated the necessity of local anesthesia for the venipuncture pain in 27 healthy adult volunteers by using a visual analogue scale (VAS) from 0 to 10. The pain scales were measured three times: at the time of percutaneous intravenous cannulation (20 G polyurethane catheter) without local anesthesia as well as the skin infiltration with local anesthetics (0.5% lidocaine 0.5 ml; 25 G needle), and after intravenous cannulation. The measurements were done twice, once by an expert staff and once by a novice staff with an interval of three days. VAS values were significantly higher (2.4 +/- 1.1) for the percutaneous intravenous cannulation without local anesthesia than both for the skin infiltration with local anesthetics (1.4 +/- 0.6) and for the evaluation after intravenous cannulation (0.7 +/- 0.8), independent of who inserted the catheter. VAS values were significantly lower (2.1 +/- 1.0) when the percutaneous intravenous cannulation without local anesthesia was performed by expert staff than when it was performed by novice staff (2.7 +/- 1.1; P < 0.05). We conclude that local anesthesia is necessary when novice staff performs the percutaneous intravenous catheterization.

Percutaneous cervical cordotomy and subarachnoid phenol block using fluoroscopy in pain control of costopleural syndrome.

We examined the efficacy of percutaneous cervical cordotomy (PCC) and subarachnoid phenol block using fluoroscopy (SAPB-F) for control of chest and/or back pain from costopleural syndrome. The efficacy of each block was evaluated by changes in pain score (PS), analgesic dose and performance status 1 week after the block, as well as by the complications. Between 1980 and 1986, PCC was performed in 10 patients. SAPB-F was performed in 13 patients between 1987 and 1991. Pain was not well controlled by analgesics in any of these patients. For PCC the follow-up period was 94.7 +/- 71.1 days. PS (VAS, 0-10) reduced from 8.5 +/- 0.9 to 3.0 +/- 2.7. No analgesics were needed in 4 patients. Pain recurred in 1 patient. Hemiparesis occurred in 2 patients. General fatigue occurred in 6 patients. In 4 patients with these complications performance status deteriorated and did not recover during the follow-up period. For SAPB-F the follow-up period was 71.8 +/- 44.0 days. SAPB-F was designed to achieve selective phenol deposit at the targeted nerve root. PS decreased from 7.5 +/- 1.9 to 2.7 +/- 2.6. No analgesics were needed in 5 patients. Pain recurred in 3 patients. There were no complications and no changes in performance status. From this study we concluded that PCC is an effective method of pain control for costopleural syndrome, but a risk of serious complications is involved. SAPB-F is an effective and safe method and should be the first choice of nociceptive pathway block.