A retrospective review of 10-year trends in general anesthesia for cesarean delivery at a university hospital: the impact of a newly launched team on obstetric anesthesia practice.

BACKGROUND: The indications for general anesthesia (GA) in obstetric settings, which are determined in consideration of maternal and fetal outcome, could be affected by local patterns of clinical practice grounded in unique situations and circumstances that vary among medical institutions. Although the use of GA for cesarean delivery has become less common with more frequent adoption of neuraxial anesthesia, GA was previously chosen for pregnancy with placenta previa at our institution in case of unexpected massive hemorrhage. However, the situation has been gradually changing since formation of a team dedicated to obstetric anesthesia practice. Here, we report the results of a review of all cesarean deliveries performed under GA, and assess the impact of our newly launched team on trends in clinical obstetric anesthesia practice at our institution. METHODS: Our original database for obstetric GA during the period of 2010 to 2019 was analyzed. The medical records of all parturients who received GA for cesarean delivery were reviewed to collect detailed information. Interrupted time series analysis was used to evaluate the impact of the launch of our obstetric anesthesia team. RESULTS: As recently as 2014, more than 10% of cesarean deliveries were performed under GA, with placenta previa accounting for the main indication in elective and emergent cases. Our obstetric anesthesia team was formed in 2015 to serve as a communication bridge between the department of anesthesiology and the department of obstetrics. Since then, there has been a steady decline in the percentage of cesarean deliveries performed under GA, decreasing to a low of less than 5% in the latest 2 years. Interrupted time series analysis revealed a significant reduction in obstetric GA after 2015 (P = 0.04), which was associated with decreased use of GA for pregnancy with placenta previa. On the other hand, every year has seen a number of urgent cesarean deliveries requiring GA. CONCLUSIONS: There has been a trend towards fewer obstetric GA since 2015. The optimized use of GA for cesarean delivery was made possible mainly through strengthened partnerships between anesthesiologists and obstetricians with the support of our obstetric anesthesia team.

IFN-ß Improves Sepsis-related Alveolar Macrophage Dysfunction and Postseptic Acute Respiratory Distress Syndrome-related Mortality.

IFN-ß is reported to improve survival in patients with acute respiratory distress syndrome (ARDS), possibly by preventing sepsis-induced immunosuppression, but its therapeutic nature in ARDS pathogenesis is poorly understood. We investigated the therapeutic effects of IFN-ß for postseptic ARDS to better understand its pathogenesis in mice. Postseptic ARDS was reproduced in mice by cecal ligation and puncture to induce sepsis, followed 4 days later by intratracheal instillation of Pseudomonas aeruginosa to cause pneumonia with or without subcutaneous administration of IFN-ß 1 day earlier. Sepsis induced prolonged increases in alveolar TNF-α and IL-10 concentrations and innate immune reprogramming; specifically, it reduced alveolar macrophage (AM) phagocytosis and KC (CXCL1) secretion. Ex vivo AM exposure to TNF-α or IL-10 duplicated cytokine release impairment. Compared with sepsis or pneumonia alone, pneumonia after sepsis was associated with blunted alveolar KC responses and reduced neutrophil recruitment into alveoli despite increased neutrophil burden in lungs (i.e., "incomplete alveolar neutrophil recruitment"), reduced bacterial clearance, increased lung injury, and markedly increased mortality. Importantly, IFN-ß reversed the TNF-α/IL-10-mediated impairment of AM cytokine secretion in vitro, restored alveolar innate immune responsiveness in vivo, improved alveolar neutrophil recruitment and bacterial clearance, and consequently reduced the odds ratio for 7-day mortality by 85% (odds ratio, 0.15; 95% confidence interval, 0.03-0.82; P = 0.045). This mouse model of sequential sepsis → pneumonia infection revealed incomplete alveolar neutrophil recruitment as a novel pathogenic mechanism for postseptic ARDS, and systemic IFN-ß improved survival by restoring the impaired function of AMs, mainly by recruiting neutrophils to alveoli.

Early-phase Innate Immune Suppression in Murine Severe Sepsis Is Restored with Systemic Interferon-ß.

BACKGROUND: Sepsis is a leading cause of death in the intensive care unit. Immune modulatory therapy targeting sepsis-associated proinflammatory responses has not shown survival benefit. Here, the authors evaluated innate immunity at the early stage of murine mild or severe peritoneal sepsis induced by cecal ligation and puncture, and the effect of systemic interferon-ß, a potent inflammatory mediator, on severe sepsis as well as its mechanism of action. METHODS: Mild and severe sepsis was induced in C57BL/6 mice by cecal ligation and puncture with 22- and 18-gauge needles for puncture, respectively. Interferon-ß (700 U/g) was subcutaneously administered either before or 12 h after cecal ligation and puncture for the severe sepsis group. RESULTS: Severe sepsis resulted in significantly lower 6-day survival rates than mild sepsis (n = 48, 25% vs. n = 11, 81.8%, P = 0.002), significantly less phagocytic capacity of peritoneal exudate cells, and lower CXC chemokine receptor-2 expression on circulating neutrophils at 24 h after cecal ligation and puncture. Interferon-ß administration 12 h after cecal ligation and puncture associated with significantly improved survival (n = 34, 52.9%, P = 0.017) increased the number and function of peritoneal exudate cells, peritoneal/systemic inflammatory cytokine/chemokine concentrations, and CXC chemokine receptor-2 on neutrophils, compared with the severe sepsis controls. However, those responses were not observed in the prophylactic interferon-ß group (n = 24). Interferon-ß increased lipopolysaccharide-induced interleukin-6 messenger RNA/protein expression of lipopolysaccharide-tolerant murine peritoneal macrophages, which was not observed in nontolerant cells. CONCLUSIONS: In severe sepsis, immune suppression occurs within 24 h and is associated with worse mortality. Interferon-ß given after the onset of peritonitis restores impaired innate immunity in vivo and in vitro.

A Case of a Cardiac Resynchronization Therapy-Defibrillator Exhibiting a Lower and Alternately Variable Basic Rate.

A cardiac resynchronization therapy defibrillator (CRT-D) (Medtronic Inc. Protecta XT) was implanted in a 67-year-old man who had cardiac sarcoidosis with extremely low cardiac function. He had ventricular tachycardia which was controlled by catheter ablation, medication and pacing. The programmed mode was DDI, lower rate was 90 beats/minute, paced AV delay was 150 ms, and the noncompetitive atrial pacing (NCAP) function was programmed as 300 ms.After his admission for pneumonia and heart failure, we changed his DDI mode to a DDD mode because he had atrial tachycardia, which led to inadequate bi-ventricular pacing. After a while, there were cycle lengths which were longer than his device setting and alternately varied. We were able to avoid this phenomenon with AV delay of 120 ms and NCAP of 200 ms.NCAP is an algorithm which creates a gap above a certain period after the detection of an atrial signal during the postventricular atrial refractory period of the pacemaker. This is to prevent atrial tachycardia and repetitive non-reentrant ventriculoatrial (VA) synchrony in the presence of retrograde VA conduction. But in this case, NCAP algorithm induced much lower rate than the programmed basic lower rate. This situation produced some arrhythmias and exacerbated symptoms of heart failure. This had to be paid attention to, especially when the device was programmed at high basic heart rate.

Farnesyltransferase inhibitor FTI-277 reduces mortality of septic mice along with improved bacterial clearance.

Treatment with statins, inhibitors of HMG-CoA reductase, extends the survival of septic mice. However, the molecular mechanisms underlying the cholesterol-lowering, independent beneficial effects of statins in sepsis are poorly understood. The inhibition of protein isoprenylation, namely farnesylation and geranylgeranylation, has been proposed as a mediator of the pleiotropic protective effects of statins, although direct evidence is lacking. Major features of sepsis-induced immune suppression include T-cell dysfunction, which is characterized by apoptosis of splenic T cells, increased CD4(+)Foxp3(+) regulatory T cells (Tregs), and suppression of type 1 helper T-cell response [e.g., interferon-γ (IFN-γ) secretion] in mice. Here, we show that the induction of sepsis by cecal ligation and puncture (CLP) resulted in increases in farnesyltransferase activity and farnesylated proteins in the spleen relative to sham operation. Treatment with farnesyltransferase inhibitor N-[4-[2(R)-amino-3-mercaptopropyl]amino-2-phenylbenzoyl]methionine methyl ester trifluoroacetate salt (FTI-277) (25 mg/kg b.wt. i.p.) at 2 h after CLP blocked the increase in farnesylated proteins and improved survival and bacterial clearance of septic mice. FTI-277 reverted to or mitigated sepsis-induced apoptosis in spleen and thymus, increased splenic CD4(+)Foxp3(+) Tregs, and suppressed IFN-γ secretion and proliferation of splenocytes in response to anti-CD3+CD28 antibodies in mice. Moreover, FTI-277 promoted macrophage phagocytotic activity in septic mice. These results indicate that elevation in protein farnesylation plays a role in derangements in immune function and mortality of septic mice. These findings suggest that prevention of immune dysfunction might contribute to FTI-277-induced improvement in survival of septic mice. These data highlight protein farnesyltransferase as a novel potential molecular target to reduce the mortality of patients with sepsis.

Successful treatment of bepridil-induced intraoperative torsades de pointes by isoproterenol infusion.

BACKGROUND: Several types of antiarrhythmic drugs are known to induce QT prolongation and torsades de pointes. CASE PRESENTATION: An 84-year-old man was scheduled for open gastrectomy for residual cancer. He had been prescribed bepridil for atrial fibrillation that converted to sinus rhythm with prolonged QT interval in the operating room. After the surgery was initiated under general and epidural anesthesia, the patient's heart rate decreased to 50/min and multifocal premature ventricular contractions appeared, followed by several episodes of torsades de pointes, each lasting for 5 to 15 s. Infusion of isoproterenol was started (0.01 µg/kg/min), and the heart rate was maintained at around 80/min. Premature ventricular contractions disappeared, and torsades de pointes did not recur during the surgery. The operation was completed uneventfully. The serum bepridil concentration was found to be extremely high postoperatively. CONCLUSIONS: Bepridil-induced intraoperative episodes of torsades de pointes were successfully treated by increasing the heart rate with isoproterenol.

[Intraoperative coronary spasm during caesarean section under spinal anesthesia].

A 37-year-old woman without history of ischemic heart disease or any coronary risk factors was scheduled for caesarean section. Under spinal anesthesia, the patient's blood pressure (BP) decreased to 93/72 mmHg. Although 6 mg of ephedrine was administered intravenously, BP continued to decrease to 75/40 mmHg and she complained of nausea. In addition to additional ephedrine (12 mg), phenylephrine (0.1 mg) and atropine (0.5 mg) were administered. BP increased to 170/100 mmHg, but electrocardiogram (ECG) showed ST elevation in I and aV(L), ST depression in II, III, aV(F), and frequent premature ventricular beats, and the patient complained of chest discomfort. Coronary dilators and lidocaine promptly reversed the ST elevation, premature ventricular beats and discomfort. The operation was started promptly and was uneventful. Although BP decreased again to 75/45 mmHg at the beginning of the operation, we did not use vasopressors to avoid the relapse of myocardial ischemia. The anesthetic course was uneventful thereafter. This cardiac event seemed to be derived from coronary spasm caused by acute sympathetic stimulation. The observations in this case suggest that the possibility of intraoperative coronary spasm should be considered even in a healthy patient.

Synergistic cytoprotection by co-treatment with dexamethasone and rapamycin against proinflammatory cytokine-induced alveolar epithelial cell injury.

BACKGROUND: One of the main pathophysiological manifestations during the acute phase of sepsis is massive production of proinflammatory mediators. Clinical trials involving direct suppression of inflammatory mediators to relieve organ dysfunction in sepsis have been extensively performed; however, the clinical outcomes of such trials remain far from satisfactory. Given the need for better sepsis treatments, we have screened various agents with anti-inflammatory properties for cytoprotective effects. In this study, we identified dexamethasone and rapamycin as clinically applicable candidates with favorable synergistic effects against inflammatory cytokine-induced cytotoxicity in vitro and further explored the molecular mechanisms underlying the augmented cytoprotective effects exerted by co-treatment with both drugs. METHODS: Human alveolar epithelial cell-derived A549 cells were stimulated with a mixture of inflammatory cytokines, TNF-alpha, IL-1beta, and IFN-gamma, which induce cellular injury, including apoptosis. This in vitro model was designed to simulate acute lung injury (ALI) associated with sepsis. The cells were co-treated with dexamethasone and rapamycin under cytokine stimulation. Conditioned medium and cell lysates were subjected to further analysis. RESULTS: Either dexamethasone or rapamycin significantly attenuated cytokine-induced cytotoxicity in A549 cells in a dose-dependent manner. In addition, the simultaneous administration of dexamethasone and rapamycin had a synergistic cytoprotective effect. The applied doses of dexamethasone (10 nM) and rapamycin (1 nM) were considerably below the reported plasma concentrations of each drug in clinical setting. Interestingly, distinct augmentation of both of c-Jun inhibition and Akt activation were observed when the cells were co-treated with both drugs under cytokine stimulation. CONCLUSIONS: A synergistic protective effect of dexamethasone and rapamycin was observed against cytokine-induced cytotoxicity in A549 cells. Augmentation of both of c-Jun inhibition and Akt activation were likely responsible for the cytoprotective effect. The combined administration of anti-inflammatory drugs such as dexamethasone and rapamycin offers a promising treatment option for alveolar epithelial injury associated with sepsis.

Nitrosative stress and pathogenesis of insulin resistance.

Insulin resistance is a major causative factor for type 2 diabetes and is associated with increased risk of cardiovascular disease. Despite intense investigation for a number of years, molecular mechanisms underlying insulin resistance remain to be determined. Recently, chronic inflammation has been highlighted as a culprit for obesity-induced insulin resistance. Nonetheless, upstream regulators and downstream effectors of chronic inflammation in insulin resistance remain unclarified. Inducible nitric oxide synthase (iNOS), a mediator of inflammation, has emerged as an important player in insulin resistance. Obesity is associated with increased iNOS expression in insulin-sensitive tissues in rodents and humans. Inhibition of iNOS ameliorates obesity-induced insulin resistance. However, molecular mechanisms by which iNOS mediates insulin resistance remain largely unknown. Protein S-nitrosylation, a covalent attachment of NO moiety to thiol sulfhydryls, has emerged as a major mediator of a broad array of NO actions. S-nitrosylation is elevated in patients with type 2 diabetes, and increased S-nitrosylation of insulin signaling molecules, including insulin receptor, insulin receptor substrate-1, and Akt/PKB, has been shown in skeletal muscle of obese, diabetic mice. Akt/PKB is reversibly inactivated by S-nitrosylation. Based on these findings, S-nitrosylation has recently been proposed to play an important role in the pathogenesis of insulin resistance.

Development of a local anesthetic lidocaine-loaded redox-active injectable gel for postoperative pain management.

Although local anesthesia is commonly applied for pain relief, there are several issues such as its short duration of action and low effectiveness at the areas of inflammation due to the acidic pH. The presence of excessive amount of reactive oxygen species (ROS) is known to induce inflammation and aggravate pain. To resolve these issues, we developed a redox-active injectable gel (RIG) with ROS-scavenging activity. RIG was prepared by mixing polyamine-b-poly(ethylene glycol)-b-polyamine with nitroxide radical moieties as side chains on the polyamine segments (PMNT-b-PEG-b-PMNT) with a polyanion, which formed a flower-type micelle via electrostatic complexation. Lidocaine could be stably incorporated in its core. When the temperature of the solution was increased to 37°C, the PIC-type flower micelle transformed to gel. The continuous release of lidocaine from the gel was observed for more than three days, without remarkable initial burst, which is probably owing to the stable entrapment of lidocaine in the PIC core of the gel. We evaluated the analgesic effect of RIG in carrageenan-induced arthritis mouse model. Results showed that lidocaine-loaded RIG has stronger and longer analgesic effect when administered in inflamed areas. In contrast, while the use of non-complexed lidocaine did not show analgesic effect one day after its administration. Note that no effect was observed when PIC-type flower micelle without ROS-scavenging ability was used. These findings suggest that local anesthetic-loaded RIG can effectively reduce the number of injection times and limit the side effects associated with the use of anti-inflammatory drugs for postoperative pain management. STATEMENT OF SIGNIFICANCE: 1. We have been working on nanomaterials, which effectively eliminate ROS, avoiding dysfunction of mitochondria in healthy cells. 2. We designed redox injectable gel using polyion complexed flower type micelle, which can eliminates ROS locally. 3. We could prepare local anesthesia-loaded redox injectable gel (lido@RIG). 4. Drug release could be extended by local administration of lido@RIG. 5. Deprotonation of lidocaine improved anesthetic effect because ROS were eliminated locally by RIG. 6. Local inflammation could be also suppressed by lido@RIG.

iNOS as a Driver of Inflammation and Apoptosis in Mouse Skeletal Muscle after Burn Injury: Possible Involvement of Sirt1 S-Nitrosylation-Mediated Acetylation of p65 NF-κB and p53.

Inflammation and apoptosis develop in skeletal muscle after major trauma, including burn injury, and play a pivotal role in insulin resistance and muscle wasting. We and others have shown that inducible nitric oxide synthase (iNOS), a major mediator of inflammation, plays an important role in stress (e.g., burn)-induced insulin resistance. However, it remains to be determined how iNOS induces insulin resistance. Moreover, the interrelation between inflammatory response and apoptosis is poorly understood, although they often develop simultaneously. Nuclear factor (NF)-κB and p53 are key regulators of inflammation and apoptosis, respectively. Sirt1 inhibits p65 NF-κB and p53 by deacetylating these transcription factors. Recently, we have shown that iNOS induces S-nitrosylation of Sirt1, which inactivates Sirt1 and thereby increases acetylation and activity of p65 NF-κB and p53 in various cell types, including skeletal muscle cells. Here, we show that iNOS enhances burn-induced inflammatory response and apoptotic change in mouse skeletal muscle along with S-nitrosylation of Sirt1. Burn injury induced robust expression of iNOS in skeletal muscle and gene disruption of iNOS significantly inhibited burn-induced increases in inflammatory gene expression and apoptotic change. In parallel, burn increased Sirt1 S-nitrosylation and acetylation and DNA-binding capacity of p65 NF-κB and p53, all of which were reversed or ameliorated by iNOS deficiency. These results indicate that iNOS functions not only as a downstream effector but also as an upstream enhancer of burn-induced inflammatory response, at least in part, by Sirt1 S-nitrosylation-dependent activation (acetylation) of p65 NF-κB. Our data suggest that Sirt1 S-nitrosylation may play a role in iNOS-mediated enhanced inflammatory response and apoptotic change, which, in turn, contribute to muscle wasting and supposedly to insulin resistance after burn injury.

[Retrospective analysis of critical perioperative myocardial infarction].

BACKGROUND: Myocardial infarction, a major complication of non-cardiac surgery, impacts on perioperative morbidity and mortality. METHODS: We retrospectively reviewed the intensive care unit records and anesthesia charts of non-cardiac surgical patients needing cardiac intensive care for myocardial infarction from April 1998 to December 2000 at the University of Tokyo Hospital and analyzed data obtained from these records. RESULTS: Four cases were detected. Three were vascular patients. The myocardial infarction occurred in two patients preoperatively, in one intraoperatively, and in another postoperatively. Hypovolemia was considered as an important contributing factor. All the patients developed shock abruptly and cardiac arrest followed in three. Three needed intra-aortic balloon counterpulsation, and one of these needed percutaneous cardiopulmonary support. Emergent percutaneous coronary intervention was performed in all cases and resuscitation was successful temporarily in all patients. However, the clinical outcome was poor; three died in our hospital and one transferred to another hospital became severely disabled. CONCLUSIONS: Surgical patients can be asymptomatic although they have significant coronary artery disease. Most of the events occurred abruptly without preexisting myocardial ischemia, suggesting the pathophysiology causing acute coronary syndrome. Thorough cardiac examination, including coronary angiography is recommended preoperatively in patients with strong coronary risks, especially in vascular patients.

[Intraoperative coronary spasm in non-cardiac surgery].

BACKGROUND: Cardiovascular events are one of the most critical perioperative complications. The purpose of this study is to investigate the clinical characteristics, effective treatments, and clinical outcome of intraoperative coronary spasm through a review of the published literature. METHODS: Reports of intraoperative coronary spasm were identified using the Medline database (1977-2000) or by manually searching the Journal of Anesthesia (1987-2000). The clinical characteristics of intraoperative coronary spasm were analyzed in the 56 patients who had developed coronary spasm during non-cardiac surgery. RESULTS: The mean patient's age was 58 +/- 13 years. The majority of patients were men (75%), Japanese (78%), and had no history of chest pain (75%). Regional anesthesia, vasopressors, alkalosis, hypotension, inadequate depth of anesthesia, and vagal stimulation were noted as major contributing factors. More than half of the patients showed severe hypotension and 30% developed cardiovascular collapse. However, coronary dilators, and nitrates in particular, were very effective for the treatment, and the clinical outcome was relatively good (one death and three cases of myocardial infarction). CONCLUSIONS: Intraoperative coronary spasm may develop in patients with no history of chest pain. Some of the intraoperative conditions themselves are potent vasoconstricting factors. Once coronary spasm occurs, immediate administration of a full dose of coronary dilators is recommended.

[Anesthetic management of patients with dilated cardiomyopathy undergoing non-cardiac surgery].

BACKGROUND: A considerable amount of data are available regarding cardiac risk in patients with coronary artery disease, but not with patients with cardiomyopathy, undergoing non-cardiac surgery. METHODS: Reports of the anesthetic management of patients with dilated cardiomyopathy (DCM) undergoing non-cardiac surgery were identified using Medline and the Igaku-chuou-zassi (Japana Centra Revuo Medicina) database (1981-2001). The data were analyzed in terms of patient characteristics, methods of intraoperative care, and clinical outcome. RESULTS: Seventy-three patients were included. The mean value of the preoperative left ventricular ejection fraction (EF) was 31%. About 70% of patients revealed poor ventricular function (EF < 35%). EF did not correlate with the severity of congestive heart failure (CHF). Major complications occurred in 6 cases and minor ones in 23 cases. A history of CHF, advanced NYHA classification and lack of preoperative diagnosis of DCM were suggested as perioperative risk factors. CONCLUSIONS: Careful planning is inevitable in anesthesia for patients with DCM, although the rate of major perioperative complications is relatively low. Evaluation of cardiac reserve is more important than the resting value of ejection fraction. In order to clearly elucidate risk factors for adverse perioperative outcomes, further analysis will be necessary as more cases are documented.

[Lessons learned from anesthetic management of pheochromocytoma resection: a report of three cases].

The anesthetic management of patients with pheochromocytoma, in which drastic hemodynamic changes may occur, is still a challenge to even the most experienced anesthesiologist, although the perioperative mortality has been reduced remarkably. We report three patients who developed unexpected major complications during elective resection of a pheochromocytoma. The Case 1 patient was a 46 year-old woman who developed ventricular tachycardia immediately after administration of ephedrine for transient hypotension induced by excessive phentolamine. Even a mild beta adrenergic agent may cause extraordinary stimulation to myocardium under alpha blockade. The Case 2 patient was a 44 year-old man who needed intensive vasodilating therapy due to an exaggerated cardiovascular response to intraoperative surgical stress. He developed severe metabolic acidosis resembling hyperdynamic shock before resection of the tumor, although blood pressure was controlled within the expected range. The Case 3 patient was a 60 year-old woman who did not receive preoperative alpha blocker therapy because she lacked cardiovascular symptoms. However, she revealed a high level of systemic vascular resistance after induction of general anesthesia and needed moderate inotropic support to compensate for an abrupt reduction of vascular resistance after resection of the tumor. The pathophysiology of the disease is complex and anesthetic care must be tailored in accordance with each patient's situation.

[Successful anesthetic management of patients with poor ventricular function using the phosphodiesterase III inhibitor, olprinone, during major cardiovascular procedures].

We administered olprinone, a newly developed phosphodiesterase III inhibitor, commencing before induction of general anesthesia to patients with poor ventricular function during major cardiovascular procedures. Case 1 patient underwent off-pump CABG for acute myocardial infarction. Although he was in a shock state, olprinone improved the contractility of viable myocardium, increased the cardiac index, and decreased the pulmonary artery pressure. Case 2 patient underwent off-pump CABG for unstable angina. Olprinone significantly increased the cardiac index and the mixed venous oxygen saturation. Case 3 patient underwent graft replacement for rupture of a dissected descending aorta. Although he showed ischemic cardiomyopathy with diffuse hypokinetic left ventricle, olprinone drastically improved the contractility of the heart. Olprinone was very effective for improving ventricular dysfunction; its institution prior to induction of anesthesia made successful anesthetic management possible without resorting to a mechanical assist device like the intra-aortic balloon pump.

[Intraoperative coronary spasm in patients without a history of anginal chest pain].

We report three cases of intraoperative coronary spasm that developed during non-cardiac surgical procedures. None of the patients had a history of anginal chest pain. The presumed contributing factors were: 1) suction of the trachea during general anesthesia, 2) hyperventilation and hypotension during induction of general anesthesia, and 3) hyperventilation during neuroanesthesia. Coronary vasodilators were administered and all cases recovered promptly without any clinical sequelae. A review of the literature reveals that the majority of patients who developed intraoperative coronary spasm had no history of anginal chest pain. Some of common intraoperative conditions such as hyperventilation, hypotension, and inadequate depth of anesthesia, were reported to be potent precipitating factors for coronary spasm. In recent years, a larger proportion of surgical patients have coronary risk factors. Careful anesthetic management is required to prevent intraoperative coronary spasm even in patients without a history of coronary artery disease.

[Anesthetic management of patients with hypertrophic obstructive cardiomyopathy undergoing non-cardiac surgery].

BACKGROUND: A considerable amount of data are available regarding cardiac risk in patients with coronary artery disease undergoing non-cardiac surgery, but few data are available regarding risk for patients with cardiomyopathy. METHODS: Reports on the anesthetic management of patients with hypertrophic obstructive cardiomyopathy (HOCM) undergoing non-cardiac surgery were identified using Medline and the Igaku-Chuou-Zassi (Japana Centra Revuo Medicina) database (1981-2002). The data were analyzed in terms of patient characteristics, methods of intraoperative care, and clinical outcome. RESULTS: Sixty nine patients were included. The mean value of the left ventricular outflow tract pressure gradient (LVOTPG) was 63 mmHg. Twenty two cases were diagnosed as severe HOCM in terms of pressure gradient (LVOTPG > or = 50 mmHg) and clinical manifestations. Major complications, such as cardiac arrest and refractory shock, occurred in 10 cases. However, these perioperative risks were not correlated with severity of HOCM. CONCLUSIONS: Careful planning is inevitable in anesthesia for patients with HOCM. Although the rate of major perioperative complications is relatively low, they can occur unexpectedly and resemble the natural course of HOCM. In order to clearly elucidate risk factors for adverse perioperative outcomes, further analysis will be necessary as more cases are documented.

[Usefulness of multi-lead electrocardiogram and transesophageal echocardiography for the detection and evaluation of intraoperative coronary spasm].

We describe a case of coronary spasm in a 59-year-old man undergoing an emergent abdominal aortic replacement for ruptured aortic aneurysm. The patient was brought to the operating room in a state of hypovolemic shock, and was successfully resuscitated through intensive volume expansion by rapid infusion devices. Twenty minutes after cross-clamping of the abdominal aorta, ST-segment elevation on the lead III of electrocardiogram (ECG) and dyskinesis in the inferior wall shown by transesophageal echocardiography (TEE) were noted. Coronary spasm was suspected, and isosorbide dinitrate was administered intravenously without delay, leading to prompt reversal of ischemic changes. A number of reports have suggested that care should be taken against coronary spasm in non-cardiac surgery as well as cardiac surgery, especially in patients with coronary risk factors. Monitoring by multi-lead ECG and TEE is a powerful method by which to detect and evaluate intraoperative myocardial ischemia.