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An 85-year-old man suffering from severe aortic ste- nosis underwent transurethral resection of the prostate (TUR-P) under spinal anesthesia producing analgesia below T7. TUR-P was performed uneventfully with repeated injections of phenylephrine 0.05 to 0.1 mg which kept systolic blood pressure around 100 mmHg. Refractory hypotension occurred in the intensive care unit two hours after spinal anesthesia when the patient continued to speak ; systolic blood pressure fell to 60 mmHg from 100 mmHg, and discontinuance of speak- ing restored the blood pressure, although injections of phenylephrine had no effect Four episodes of hypoten- sion occurred before the movement of lower extremi- ties was restored, 5.5 hours after spinal anesthesia. Refractory hypotension might have been the result of a decrease in venous return caused by increased intra- thoracic pressure during speaking, and sympatholysis and decreased abdominal compression by spinal anes- thesia combined with complicating cardiac dysfunction.

The cardioprotective effects of glucocorticoids in the acute setting of ischemia/reperfusion have been experimentally demonstrated in animals1–7 and humans.8 Although the mechanisms underlying glucocorticoid cardioprotection are not known with certainty, glucocorticoids are reported to preserve cellular function in ischemia thereby prolonging the period of myocardial viability. In previous studies, glucocorticoids were reported to improve lactate imbalance and prevent the leakage of intracellular enzymes caused by myocardial ischemia.6,7 At the same time, deleterious effects of glucocorticoids on ischemia-induced neuronal damage have been shown in various animal models, despite the ability of glucocorticoids to alleviate cerebral edema caused by traumatic brain injury and hemorrhage.9–13 Further, steroids are not indicated for traumatic brain injury in humans, as they do not improve clinical outcomes.14 Because adenosine 5′-triphosphate (ATP) provides energy to maintain membrane functional integrity in both the heart and brain, and ATP depletion precedes loss of cellular viability, the different effects of the agents in ATP utilization in the heart and brain during ischemia could well explain differences in ischemia-induced organ injury. In the present study, therefore, we investigated the effect of dexamethasone, a glucocorticoid without mineralocorticoid activity, on ischemia-induced reduction of ATP in the mouse heart and brain. In addition, we examined the effect of metyrapone, a potent inhibitor of the synthesis of glucocorticoids, to assess the role of endogenous glucocorticoids. We hypothesized that ATP levels would be diminished in neuronal tissue subjected to dexamethasone and improved in cardiac tissue subjected to dexamethasone. In contrast, ATP levels would be improved in neuronal tissue subjected to metyrapone and diminished in cardiac tissue subjected to metyrapone.

Sepsis is a severe pathologic event, frequently causing death in critically ill patients. However, there are no approved drugs to treat sepsis, despite clinical trials of many agents that have distinct targets. Therefore, a novel effective treatment should be developed based on the pathogenesis of sepsis. We recently observed that an old hypnotic drug, bromvalerylurea (BU) suppressed expression of many kinds of pro- and anti-inflammatory mediators in LPS- or interferon-γ activated alveolar and peritoneal macrophages (AMs and PMs). Taken the anti-inflammatory effects of BU on macrophages, we challenged it to septic rats that had been subjected to cecum-ligation and puncture (CLP). BU was subcutaneously administered to septic rats twice per day. Seven days after CLP treatment, 85% of septic rats administrated vehicle had died, whereas administration of BU reduce the rate to 50%. Septic rats showed symptoms of multi-organ failure; respiratory, circulatory and renal system failures as revealed by histopathological analyses, blood gas test and others. BU ameliorated these symptoms. BU also prevented elevated serum-IL-6 level as well as IL-6 mRNA expression in septic rats. Collectively, BU might be a novel agent to ameliorate sepsis by preventing the onset of MOF.

We present a case of continuous subarachnoid block for the treatment of refractory cancer pain in the shoulder and upper extremity on the right side of the patient. The catheter tip was placed in the subarachnoid space close to the nerve roots on the right side at the height of C5 corresponding to the painful region. Until the patient died, his pain was controlled with infusions of bupivacaine (30-58.7 mg/d) and morphine (2-19.6 mg/d) for 120 days during which upper extremity function was not disturbed and respiratory function and performance status were improved. This case suggests continuous subarachnoid block at the low cervical level is useful for refractory cancer pain in the shoulder and upper extremity.

Inflammatory reactions play an important role in ischaemia/reperfusion injury in various organs. Since histamine H4 action has been shown to prevent the development of ischaemia/reperfusion liver injury, we examined the effects of dimaprit, a histamine H2/H4 receptor agonist, on ischaemia-induced cytokine release and liver damage. Male Wistar rats (300 g) were subjected to warm ischaemia for 30 min. by occlusion of the left portal vein and hepatic artery under halothane anaesthesia. Saline or dimaprit (20 mg/kg, subcutaneously) was injected immediately after reperfusion of blood flow. Transient ischaemia provoked severe liver damage 24 hr after reperfusion, and the plasma concentrations of alanine transaminase and aspartate transaminase were 4600 IU/l and 13,200 IU/l, respectively. The values in the dimaprit group were 55% and 46% of those in control animals, respectively. Dimaprit also reduced the infarct size to 50%. Liver ischaemia markedly increased interleukin-12 levels 2–24 hr after reperfusion. The dimaprit treatment depressed the values to 40–64% of those in the corresponding control group 4–24 hr after reperfusion. Since interleukin-12 facilitates cell-mediated cytotoxicity, the protective effect of dimaprit may be attributed to regulation of cytokine release during reperfusion.

A decrease in the serum ratio of branched-chain amino acids (BCAAs) to aromatic amino acids (Fischer ratio) reflects the severity of hepatic encephalopathy, and clinical improvement by dietary augmentation with BCAAs has been demonstrated. As behavioral alteration results from changes in central neurotransmission, we investigated the role of BCAA administration on changes in the levels of central neurotransmitters in acute liver injury. Male Wistar rats were subjected to liver ischemia by occluding the left portal vein and hepatic artery for 90 minutes. A 4% BCAA solution containing valine, leucine, and isoleucine was intraperitoneally administered 3 times (8 mL/kg, each) at 1 hour, 6 hours, and 24 hours after vascular reperfusion, and changes in the extracellular concentrations of neurotransmitter amino acids, monoamines, and their metabolites were evaluated in the striatum by a microdialysis procedure. Although the extracellular concentration of dopamine was affected by neither liver ischemia nor BCAA injections, the level of 3,4-dihydroxyphenylacetic acid, a metabolite of dopamine, decreased to 34% in the ischemic group 24 hours after reperfusion. The 3,4-dihydroxyphenylacetic acid level was normalized by treatments with BCAAs. The improvement of deranged cerebral dopaminergic activity may be a contributing factor in the improvement of hepatic encephalopathy by BCAAs.

Background and Objectives Because the histaminergic system in the brain is involved in regulation of pain, the relationship between central histaminergic activity and neuropathic pain is of interest. Methods Neuropathic pain was induced in rats by partial ligation of the left sciatic nerve, and changes in the extracellular concentration of histamine in the right striatum were examined by a microdialysis procedure 2 weeks later. The nociceptive threshold was determined with von Frey tests, and effects of histaminergic ligands were examined. Results Although the extracellular concentration of histamine did not differ between the sham-operated and ligated groups, histaminergic activity assessed by metoprine-induced accumulation of histamine was facilitated in ligated animals. The metoprine treatment ameliorated neuropathic pain in ligated animals, although the agent did not affect the threshold in sham-operated rats. Either intracerebroventricular (ICV) administration of histamine (30 μg) or intraperitoneal (IP) administration of l -histidine (370 mg/kg) decreased the nociceptive threshold in ligated rats. However, a high dose of histamine (180 μg ICV) increased the nociceptive threshold. Ranitidine (100 μg ICV), an H2 antagonist, increased the threshold, whereas pyrilamine (15 μg ICV), an H1 antagonist, showed no remarkable change. Administration of thioperamide (30 μg ICV), an H3 antagonist, increased the threshold, although systemic administration of the agent (3.6 mg/kg IP) decreased it. Conclusions Blockade of supraspinal histamine H2 receptors or stimulation of spinal H3 receptors may contribute to alleviation of neuropathic pain.

Inflammation is a crucial factor in the development of ischemia-induced brain injury. Since facilitation of central histaminergic activity ameliorates reperfusion injury, effects of postischemic administration of l -histidine, a precursor of histamine, and thioperamide, a histamine H3 receptor antagonist, on inflammatory cell infiltration were evaluated in a rat model of transient occlusion of the middle cerebral artery. After reperfusion for 12, 24, or 72 h following 2 h of occlusion, brain slices were immunohistochemically stained with antibodies against myeloperoxidase and CD68, which were markers of polymorphonuclear leukocytes and macrophages/microglia, respectively. After reperfusion for 12–24 h, the number of neutrophils on the ischemic side increased markedly, whereas the increase was not observed on the contralateral side. Administration of l -histidine (1000 mg/kg × 2, i.p.), immediately and 6 h after reperfusion, reduced the number of neutrophils to 52%. Simultaneous administration of thioperamide (5 mg/kg, s.c.) further decreased the number of neutrophils to 32%. Likewise, the ischemia induced increase in the number of CD68-positive cells after 24 h was suppressed by l -histidine injections. The l -histidine administration decreased the number of CD4+T lymphocytes on both ischemic and contralateral sides after 12 h, and concurrent administration of thioperamide prolonged the effect. Although administration of mepyramine (3 nmol, i.c.v.) did not affect suppression of leukocyte infiltration, ranitidine tended to reverse the effect of l -histidine. These data suggest that enhancement of central histaminergic activity suppresses inflammatory cell recruitment after ischemic events through histamine H2 receptors, which may be a mechanism underlying the protective effect of l -histidine.

Background and Objectives: Epidural block in the midthoracic region is difficult, even with fluoroscopically guided methods, because of the inability to view the interlaminar space on radiographs. We have, therefore, proposed fluoroscopically guided epidural block for the midthoracic region, as well as other thoracic and lumbar regions, by use of the pedicle as a landmark to show the height of the interlaminar space. Methods: Twenty patients scheduled to receive an indwelling epidural catheter at Th6-7, Th9-10, Th12-L1, or L3-4 were studied. The skin insertion site was at the junction of a line parallel to the vertebral column that passed through the middle of the pedicle and the lower border of vertebral body, immediately inferior to the target interlaminar space on an anteroposterior radiograph. The needle was walked up the lamina, and the interlaminar space was sought near the midline of the vertebra at the height of the pedicle. Results: Epidural block was easily performed in all cases. No difference was observed in the angulation of the epidural needle among the groups; the mean inward and upward angulation were 38° and 63°, respectively, although the skin insertion site relative to the spinous process was different among the groups. Conclusions: This study showed the usefulness of our fluoroscopically guided method for the midthoracic region, and other thoracic and lumbar regions. We propose an alternative method for a blind epidural approach at Th6-7, Th9-10, Th12-L1, or L3-4.

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.

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.

Background Trigeminal neuralgia is a neuropathic disorder characterized by episodes of intense pain in the face. Drug therapy is the first choice of treatment. However, in cases where drug therapy are contraindicated due to side effects, patients can get pain relief from lengthy neurosurgical procedures. Alternatively, a peripheral trigeminal nerve block can be easily performed in an outpatient setting. Therefore it is a useful treatment option for the acute paroxysmal period of TN in patients who cannot use drug therapy. We performed real-time ultrasound guidance for infraorbital nerve blocks in TN patients using a high concentration of tetracaine dissolved in bupivacaine. In this report, we examine the efficacy of our methods. Patients As approved by the Institutional Review Board, the medical records in our hospital were queried retrospectively. Six patients with TN at the V2 area matched the study criteria. All patients could not continue drug therapy with carbamazepine due to side effects and they received an ultrasound-guided infraorbital nerve block with a high concentration of tetracaine dissolved in bupivacaine. Methods The patient was placed in the supine position and the patient’s face was sterilized and draped. An ultrasound system with a 6-13 MHz linear probe was used with a sterile cover. The probe was inserted into the horizontal plane of the cheek just beside the nose and was slid in the cranial direction to find the dimple of the infraorbital foramen. The 25G 25 mm needle was inserted from the caudal side just across from the probe using an out-of-plane approach. To lead the needle tip to the foramen, needle direction was corrected with real-time ultrasound guidance. After the test block with lidocaine (2%, 0.5 ml), a solution of tetracaine (20 mg) dissolved in bupivacaine (0.5%, 0.5 ml) was injected. During each injection, the spread of the agent around the nerve was confirmed using ultrasound images. Results Ten blocks were performed for six patients. Immediately after the procedure, all 10 blocks produced analgesia and relieved the pain. In the three blocks, pain was experienced in a new trigger point outside of the infraorbital nerve region (around the back teeth) within a week after the block and pain were relieved using other treatment. Two patients developed small hematomas in the cheek but they disappeared in a week. All patients did not complain about other side effects including paraesthesia, hyperpathia, dysaesthesia, or double vision. Hypoaesthesia to touch and pain in the infraorbital region were observed in all blocks after 2 weeks. Conclusions We performed real-time ultrasound-guided infraorbital nerve block for TN with a high concentration of tetracaine dissolved in bupivacaine. Our method achieved a high success rate and there were only minor and transient side effects. Implications Real-time ultrasound-guided infraorbital nerve block is one of the useful options to treat the acute paroxysmal period of TN at the infraorbital nerve area. Ultrasound-guided injections may become the standard practice for injecting peripheral trigeminal nerves. Using this high concentration of tetracaine as a neurolytic agent is effective and appears to have only minor side effects.

Objective: Uraemia often provokes various neurological disorders, such as mental changes, malperception, confusion, seizures and coma. Since changes in neurotransmissions induce neurological symptoms, we investigated changes in the monoamine metabolism and motor activity in uraemic rats. Design: Prospective, randomised, controlled animal study. Subjects: Male Wistar rats. Interventions: Acute renal failure was induced by occlusion of bilateral renal arteries for 60 min, and the motor activity and brain monoamine turnover were examined 48 h later. The brain monoamine turnover was evaluated by the depletion of norepinephrine (NE) and dopamine (DA) induced by α-methyl-p-tyrosine (α-MT), or the accumulation of 5-hydroxyindoleacetic acid (5-HIAA) induced by probenecid. Measurements and results: Marked damage in renal function was found in animals subjected to renal ischaemia 48 h after the operation. The motor activity of the uraemic rats was impaired. The turnover of DA in the striatum, mesencephalon and hypothalamus was decreased in these rats. The turnover of NE and 5-hydroxytryptamine (5-HT) was unchanged in all regions examined. Conclusions: Suppression of the central DA turnover appears to be involved in the impairment of motor activity in uraemic rats.

Preoperative massive subcutaneous emphysema before intubation is extremely rare. However, this complication may be potentially lethal, depend on the condition of air spreading. Subcutaneous emphysema which occurs intra- or postoperative period is sometimes iatrogenic because the air is introduced into the tissue space through the hole injured by the operation. But the emphysema in this case occurred preoperatively by the pressure of the bag valve mask, because the patient had an intra-oral wound, which reaches the submental space. In this report, we describe an extremely rare case of preoperative massive emphysema of the patient with the mandibular fracture.

Background Glucocorticoids have been reported to aggravate ischemic brain damage. Because changes in the activities of various neuronal systems are closely related to the outcome of ischemic damage, the authors evaluated the effects of dexamethasone on the monoaminergic systems and ischemic neuronal damage. Methods The right middle cerebral artery was occluded for 2 h, and the tissue concentrations of monoamines and their metabolites were determined in the cerebral cortex and the striatum of rats. The turnover of 5-hydroxytryptamine was compared in animals injected with saline and those injected with dexamethasone twice (2 mg/kg in each injection) by evaluating the probenecid-induced accumulation of 5-hydroxyindoleacetic acid. The turnovers of norepinephrine and dopamine were estimated from the alpha-methyl-p-tyrosine-induced depletion of norepinephrine and dopamine, respectively. The effect of dexamethasone on the infarct volume was evaluated by triphenyltetrazolium chloride stain in rats subjected to 2 h of occlusion. Results Dexamethasone did not affect the cortical 5-hydroxytryptamine or 5-hydroxyindoleacetic acid contents. However, it suppressed the turnover of the cortical 5-hydroxytryptamine on both sides. Dexamethasone reduced the turnover of the striatal 5-hydroxytryptamine and facilitated the dopamine turnover. In rats subjected to 2 h of occlusion and 2 h of reperfusion, the infarct volume was 10.5 times greater in the group that received dexamethasone than in the animals that received saline. Conclusions Dexamethasone suppresses the inhibitory serotonergic system and facilitates the excitatory dopaminergic system in the rat telencephalon. This may be a mechanism by which dexamethasone aggravates ischemic neuronal injury.

Glucocorticoids exacerbate neuronal damage due to hypoxia, ischemia, seizure and hypoglycemia. Because the release of glutamate is closely involved in neuronal damage, the effects of dexamethasone on the ischemia-induced accumulation of extracellular amino acids (aspartate, glutamate, and glycine) were investigated in the gerbil hippocampal CA1 region by a microdialysis-high-performance liquid chromatography procedure in vivo. There were no differences in the extracellular concentrations of amino acids before ischemia between the control group and the dexamethasone (3m microg, i.c.v.)-injected group. The concentration of glutamate reached 246% of that before ischemia within 2.5 min of transient forebrain ischemia. Dexamethasone augmented the increase in glutamate to 508% of that before ischemia. This finding suggests that glucocorticoids aggravate ischemic neuronal damage by causing glutamate to accumulate in the extracellular space.

We have developed some indices to evaluate the phase III slope in CO2 elimination curves. The indices were applied to 12 mechanically ventilated patients in ICU to determine their stability under various ventilator settings. Fco2-sl[30-90] and[Formula: see text] expressed the mean incline of phase III slope in Fco2-volume curves and[Formula: see text]-volume curves, respectively. Fco2-SR and[Formula: see text]-SR expressed the ratio of the slopes in the first and second halves of the phase III portion in both curves. The indices were also applied to 108 elective surgery patients to determine their usefulness in predicting ventilatory efficiency during general anesthesia. In the first study, Fco2-sl[30-90] and[Formula: see text][30-90] correlated with ETco2, Vd/Vt and the volume of CO2 expired, but Fco2-SR and[Formula: see text]-SR were independent of these parameters.[Formula: see text]-SR did not show any significant changes under various ventilator settings except for application of PEEP. In the second study, those with impaired preoperative respiratory function had significantly larger values for[Formula: see text].[Formula: see text] was as sensitive as parameters such as VD/VT, arterial to end-tidal CO2 tension difference (a-ET·Dco2), and volume pressure index (VPI) in prediting poor respiratory functions. We concluded that[Formula: see text] is a useful index for evaluating the phase III slope in CO2 elimination curves.

症例44歳男性,クモ膜下出血に対し緊急クリッピング術を行なった。前投薬はアトロピンのみとし,フェンタニルとベクロニウムにより挿管した。この時直腸温37.8℃だった。GOとイソフルラン0.2～0.4%で麻酔を維持した。導入1時間30分後より,25分間でETCO2は40より66mmHg,直腸温は39.1より40.0℃まで急激に上昇した。MHと診断し治療を開始した。ダントロレン投与が有効で,ETCO2は80mmHgを最高に15分間で34mmHgまで低下した。体温のピークはETCO2よりも15分遅れ41.7℃を最高に低下していった。MHの原因はイソフルランと推察した。またETCO2の変化は体温よりも先行し,診断および治療効果の判定に有用であった。

硬膜外カテーテルは種々の原因により閉塞,自然抜去等のトラブルが起こる.73歳の女性のS状結腸癌に対し,前方切除術が行われた.麻酔は硬膜外麻酔と全身麻酔で行った.術後,鎮痛のために硬膜外カテーテルからボーラス注入中に患者が動き,その後薬液注入ができなくなった.カテーテルを調べたところ,皮下へ3cm進入し,進入したカテーテルが皮下で屈曲していた.硬膜外カテーテルは,抜去だけでなく皮下へ進入することもあり得ることに注意する必要がある.

We experienced an incident of the stricture caused by the degradation of an O-ring in the oxygen outlet of the central piping. The event was identified by the intermittent decrease of the central piping oxygen supply pressure into the anesthesia machine. In this case, pressure was judged normal by periodical checking. But the malfunction became clear when the parts of outlet were replaced, because similar incidents frequently had occurred. The cyclical rhythm of the declining oxygen supply pressure means that oxygen supplies decreases with the increase of oxygen consumption, and it may be a sign of serious malfunction. Therefore, it is necessary to check the pressure deviations under use of high-flow oxygen.

In order to clarify the mechanism of reference of pain following cordotomy (ROPC), the authors investigated ROPC in 66 patients undergoing percutaneous cervical cordotomy (PCC) and examined the features of ROPC and the correlation between the occurrence of ROPC and the pre-operative pain states, as well as the results of PCC. ROPC was observed in 7 patients. It occurred immediately after PCC in 6 of 7 patients and 6 h after PCC in 1 patient. The pain was referred horizontally and cranially from the region rendered totally or largely analgesic by PCC to the normally innervated region. The region to which the pain was referred was not fixed. The referred pain disappeared by rendering the region where referred pain was felt analgesic with additional PCC. There was no correlation between the occurrence of ROPC and pre-operative pain states, or the results of PCC. From these results we postulate that: (1) ROPC occurs via a subsidiary pathway consisting of ascending chains of short neurons connecting dorsal horn neurons longitudinally and latitudinally; (2) the subsidiary pathway is inhibited under normal conditions by feedback inhibition from second-order neurons and/or higher central neurons of the nociceptive pathway; and (3) ROPC results from the release of the feedback inhibition by cordotomy.

Preoperative massive subcutaneous emphysema before intubation is extremely rare. However, this complication may be potentially lethal, depend on the condition of air spreading. Subcutaneous emphysema which occurs intra- or postoperative period is sometimes iatrogenic because the air is introduced into the tissue space through the hole injured by the operation. But the emphysema in this case occurred preoperatively by the pressure of the bag valve mask, because the patient had an intra-oral wound, which reaches the submental space. In this report, we describe an extremely rare case of preoperative massive emphysema of the patient with the mandibular fracture.

A 76-year-old man was referred to our pain clinic for the treatment of bilateral lower extremity pain due to metastasis of renal cell carcinoma to the sacrum. The pain could not be controlled with narcotics, antidepressant or the epidural block. The characteristics of pain were like those of benign disease, being spontaneous, not exacerbated by body movement, and having a dysesthetic nature with chill sensations. Therefore, spinal cord stimulation (SCS) was performed, relieving the pain until death, 6 months after its induction. This case shows the usefulness of SCS for neuropathic cancer pain that shows signs similar to those of benign disease.

A 36-year-old woman was scheduled for the right lower lobe resection under the left one-lung ventilation with a double-lumen tube (DLT). Difficult intubation due to limited (1.5 cm) mouth opening was recognized following the induction of anesthesia. Fiberoptic oral intubation by the DLT was successfully performed under the ventilation via the nostrils using a small-size, child mask covering only the nose (nasal mask). Ventilation was well maintained using the nasal mask, and the gas leakage was coped with tightening the lips with the tube and using a high flow of oxygen. This nasal mask ventilation method is useful and safe in cases of difficult intubation by DLT in which no other proper methods are available.

Nerve block is useful for the treatment of acute pain and cancer pain; however the treatment's effectiveness with regard to non-cancer chronic pain is controversial. Of the non-cancer diseases, trigeminal neuralgia and spinal facet joint pain, in which long-term pain relief can be obtained by the nerve block without serious complications in most of patients, are well suited for the nerve block. Systemic reviews for the treatment of radicular pain from spine disorders with the nerve block showed contradictory long-term results. In other chronic pains, the effectiveness of nerve blocks has not been proved, although anecdotal reports suggests that a small proportion of patients respond well to the nerve block. Further study is necessary to examine what kinds of pains and patients will be relieved with the nerve block.

The management of opioid resistant cancer pain is a significant issue for palliative medicine. Certain types of pain can be relieved effectively using nerve blocks without exacerbating and sometimes improving daily activity as long as proper patient selection and technique are employed. Continuous epidural and subarachnoid block, celiac plexus block, superior hypogastric plexus block, subarachnoid phenol block and percutaneous cervical cordotomy are common pain treatment procedures. In our pain clinic, these procedures were performed on about 20% of cancer pain patients, most of whom experienced pain relief without serious complications. Proper use of nerve blocks and neuroablative procedures can undoubtedly improve the management of cancer pain and should be a significant component of the strategy for cancer pain relief.

Object. The clinical features, possible causes, and contributing factors associated with novel spontaneous pain following unilateral cordotomy were investigated to clarify the mechanism and clinical importance of this pain. Methods. Forty-five patients who underwent cordotomy for severe unilateral cancer pain were included in this study. New pain occurred in 33 (73.3%) of 45 patients. Pathological conditions of tissue demonstrated on imaging corresponded to new pain in eight patients, referred pain in five, and neither of these in 15 patients. New pain was centered opposite the site of the original pain in a mirror-image location in 28 patients and rostral to the original pain in five patients. It was temporary in seven patients, weaker than the original pain in 25, and as severe as the original pain in one patient. The incidence of moderate or severe pain was significantly higher in patients with confirmed tissue disease (six of eight patients) than in those without (six of 20 patients). An important contributing factor to the occurrence of new pain was the achievement of analgesia by performing the cordotomy. Conclusions. The present results indicate that new pain occurs frequently after unilateral cordotomy. Nonetheless, cordotomy may still be indicated for unilateral uncontrollable pain because new pain, when present, was weaker and more easily controlled than the original pain in nearly all cases. The authors speculate that new pain may represent a type of referred pain from the original painful area or may arise from sensitization of contralateral spinal nociceptive circuits due to metastasis or tumor infiltration, and that new pain is potentiated by the interruption of descending inhibitory pathways.

Glucocorticoids have been reported to aggravate ischemic neuronal damage. Because energy failure is a crucial factor in the development of ischemic neuronal injury, the effects of dexamethasone on histologic outcome and energy metabolism were investigated in gerbil brain. Dexamethasone (3 μg, i.c.v.) was administered 1 h prior to ischemia, and its effect on delayed neuronal death caused by 2 min of bilateral common carotid artery occlusion was observed in hippocampal CA1 pyramidal neurons. The brain concentration of ATP after various durations of decapitation ischemia was determined, and the effect of dexamethasone (3 μg, i.c.v.) was examined. Na + ,K + -activated adenosine triphosphatase (Na + ,K + -ATPase) activity was evaluated after the administration of the agent. Forebrain ischemia for 2 min produced neuronal damage in animals pretreated with dexamethasone, although neuronal damage was not observed in vehicle-injected animals. Decapitation ischemia for 0.5 and 1 min reduced the brain ATP concentration to 44% and 15% of the basal level, respectively. Dexamethasone attenuated the ischemia-induced reduction in ATP, and the values were 58% and 25% of the basal level, respectively. Na + ,K + -ATPase activity at pH 6.7 was suppressed to 47% by dexamethasone treatment (3 μg, i.c.v.), whereas the activity at pH 7.4 was not influenced by the agent. The results show that a contributing factor to the aggravation of ischemic neuronal damage may be a disturbance in Na + ,K + -ATPase despite adequate levels of ATP.

Objective: To investigate the action of prostaglandin E1 on hepatic encephalopathy. Design: Prospective, randomised, controlled animal study. Setting: University animal laboratory. Subjects: Male Wistar rats. Interventions: After passive avoidance learning, acute liver failure was induced by occlusion of the left portal vein and the hepatic artery for 90 min. Then memory retention was evaluated 48 h later. The effects of prostaglandin E1 on memory retention were examined in animals treated with the agent systemically (intravenous injections with prostaglandin E1 twice before and after surgery, 20 µg/kg each time) and animals treated with the agent topically (intracerebroventricular injection with prostaglandin E1, 0.1 µg/h for 48 h beginning at liver ischaemia). Measurements and results: Marked damage was found on plasma analysis in animals subjected to liver ischaemia, and the memory retention was also impaired. Intravenous administration of prostaglandin E1 improved both the liver injury and memory retention. However, intracerebroventricular administration of prostaglandin E1 alleviated neither. Conclusion: These findings show that prostaglandin E1 contributes to the amelioration of hepatic encephalopathy by improving liver function.

Transient forebrain ischemia was induced in gerbils, and the effect of a pre-ischemic treatment with metyrapone (100 mg/kg) on delayed neuronal death in hippocampal CA1 neurons was evaluated. The effect of metyrapone on the ischemic release of amino acids in the CA1 region was also examined by microdialysis. Hippocampal slices were used for the evaluation of the hypoxia-induced intracellular Ca2+ increase by microfluorometry. The metyrapone treatment morphologically improved the damage provoked by 3 min of ischemia, although it did not alleviate the damage by 5 min. Ischemia for 3 min produced a 306% increase in the glutamate concentration in perfusates, and metyrapone suppressed the peak value to 42% of that in the control group. The extent of the increase in fluorescence intensity by intracellular Ca2+ was lower by 16% in slices from metyrapone-treated animals than in controls 600 s after induction of hypoxia. The removal of Ca2+ from the perfusion medium suppressed the hypoxic Ca2+ increase, and the increase was further reduced in slices pretreated with metyrapone. The increase in the level of endogenous glucocorticoids, which occurs in cerebral ischemia, may aggravate ischemic neuronal damage.

The changes in the extracellular concentrations of rat striatal H2O2, dopamine (DA) and its metabolites during middle cerebral artery (MCA) occlusion and reperfusion were simultaneously examined by microdialysis, and the relationship between the ischemia-induced release of DA and the generation of H2O2 was estimated by assessing the effect of the lesion of the substantia nigra (SN). In the rats without SN lesions, a significant increase in the striatal H2O2 level was observed during the ischemia and reperfusion phases. In the rats with SN lesions, the ischemia-induced H2O2 production was not attenuated. These results suggest that DA is not an important source of H2O2 in cerebral ischemia and reperfusion.

The central histaminergic action on ischemia-induced neuronal damage was examined by evaluating the histological outcome and the direct current (DC) potential shift in the hippocampal CA1 region in gerbils. An intracerebroventricular administration of histamine (10-100 nmol) improved the delayed ischemic damage in hippocampal CA1 pyramidal cells produced by 3 min of transient forebrain ischemia. A high dose (75 nmol) of mepyramine, an H1 antagonist, aggravated ischemia-induced neuronal damage, but not a low dose (0.75 nmol). Administration of cimetidine (4 nmol) and ranitidine (3 nmol), H2 antagonists, aggravated the neuronal damage. An injection of histamine (100 nmol) prolonged the onset time of the ischemia-induced sudden shift in the extracellular DC potential (anoxic depolarization; AD) to 133% of that in control animals. Administration of mepyramine (75 nmol) did not markedly change the AD, whereas injections of cimetidine (40 nmol) and ranitidine (3 nmol) reduced the onset latency to 47 and 45%, respectively. These findings suggest that the central H2 action serves to protect neurons by delaying the onset of AD in gerbils.

To the editor: Recently, Tsuji et al. [1] reported an interesting case in which an epidural block did not produce any anesthesia, and epidurography showed misplacement of the catheter into the lumbar quadratus muscle. We agree with them that the catheter was threaded into the lumbar quadratus through an intervertebral foramen. We now would like to give a few comments on the importance of epidurography and on the incidence of misplacement of an epidural catheter via intervertebral foramen. Epidurography is very useful to investigate the cause of failure in continuous epidural block. We perform epidurography by two steps. First, a small amount of iotrolan (0.2-0.5 ml [2]) is injected to take radiographs which show both the course of the inserted catheter and the position of the catheter tip. Then, a few milliliters of the contrast medium is added to determine the spread of the medium in the epidural space. Misplacement of an epidural catheter via intervertebral foramen is not rare. The incidence of transforaminal escape of an epidural catheter was 6.1% in our 99 chronic pain patients who were t reated with continuous epidural block [3]. According to the other investigations performed by Hehre et al. [4], Sfinchez et al. [5], and Itoh et al. [6], the incidence was 1.4% in 1780 cases, 6.7% in 90 cases, and 16.4% in 385 cases, respectively. As Tsuji et al. [1] ment ioned in their report, it is important not to push the catheter too far into the epidural space to prevent misplacement of a catheter. According to Bonica [2], a catheter length of 4cm in the epidural space is quite sufficient. Other means of preventing this failure include avoiding stiff catheters [7], not directing the catheter downward [2], and not inserting a catheter when paresthesia from stimulation of a nerve root is noted [7].

The patency of the airway via each orifice was examined during general anesthesia in 112 patients by occluding other orifices in order to develop a method in which fiberoptic endotracheal intubation (FEI) and ventilation could be performed via different orifices. Ventilation was well maintained via the mouth in 61 (54.5%), via bilateral nostrils in 87 (77.7%), and via the unilateral right and left nostril in 67 (59.8%) and 73 (65.2%) patients, respectively. With the aid of an artificial airway, ventilation was well maintained via the mouth in 112 (100.0%), via bilateral nostrils in 111 (99.1%), and via the unilateral right and left nostril in 106 (94.6%) and 105 (93.8%) patients, respectively. Based on these findings, we developed a method in which FEI is performed via the nostril, while ventilation is performed with a mask applied over only the mouth.

We have developed some indices to evaluate the phase III slope in CO