Cerebrovascular accidents developing in the operating theater: a JSA survey for the year 2004

BACKGROUND: The incidence of cerebrovascular accidents (CVA) developing in the operating theater has not been investigated on a large scale. In 2004, the Japanese Society of Anesthesiologists (JSA) started to survey neurological as well as life-threatening events in the operating theater. The incidence of CVA developing in the operating theater was examined using data obtained by the 2004 survey. METHODS: JSA has conducted annual surveys of life-threatening and neurological events in the operating theater by sending and collecting confidential questionnaires to all JSA certified training hospitals. The recovery rate was 91% (874/960 hospitals) in 2004. Seven hundred fourteen hospitals sent valid responses, and 1,218,371 anesthesias were registered. Among these cases, 123 patients were reported to have developed CVA in the operating theater. Incidences according to age class, ASA PS and surgical sites, causes, and their outcome were investigated. The patients with ASA PS 1 or 2 were classified as having good physical status, and those with ASA PS 3-5 were classified as having poor physical status. The causes of events were classified as follows: totally attributable to anesthetic management (AM), mainly to intraoperative pathological events (IP), to preoperative co-morbidity (PC), and to surgical management (SM). RESULTS: Overall incidence of CVA was 1.01/10,000 anesthesias. The incidence in patients aged 66 years or above was 2.00/10,000 anesthesias, which was 3.83-(95% confidential interval 2.57-5.71) fold higher than that in patients aged between 19 and 65 years. The incidences in elective and emergency patients with poor physical status were 3.27 and 7.91/10,000 anesthesias, respectively, which was 7.04- (4.56-10.87) and 17.06-(10.90-26.69) fold higher than that in elective patients with good physical status, respectively. The incidences in patients undergoing thoracotomy combined with laparotomy, craniotomy, or cardiovascular surgery were 2.76, 5.96 and 11.65/10,000 anesthesias, respectively, which were 7.22- (1.64-31.76), 15.59- (8.14-29.86), and 30.52- (16.80-55.44) fold higher than that in patients undergoing laparotomy alone. Among cardiovascular surgery, thoracic aortic surgery showed the highest number of incidents (57.98/10,000 anesthesias), followed by on-pump coronary artery bypass (11.07/10,000 anesthesias). Only one patient undergoing off-pump coronary artery bypass developed CVA, resulting in an 8.14- (1.00-66.18) fold lower incidence of CVA compared to that of on-pump coronary artery bypass. AM, IP, PC and SM were responsible for 4.1%, 24.4%, 27.6% and 35.0% of CVA. The incidence of CVA caused by AM or IP was calculated to be 0.29/ 10,000 anesthesias. If patients undergoing cardiovascular surgery or craniotomy were excluded, the incidence of CVA caused by AM or IP was calculated to be 0.13/ 10,000 anesthesias (15/ 1,134,398 anesthesias). The overall outcome of CVA was as follows: uneventful recovery 9.8%, death within 30 post-operative days 26.0%, vegetative state 6.5%, and sequelae involving deficits in the central nervous system 52.0%. The outcome of CVA caused by AM or IP was as follows: uneventful recovery 20.0%, death within 30 post-operative days 22.9%, vegetative state 8.6%, or sequelae involving deficits in central nervous system 45.7%. Twenty-seven point six percent of reported CVA were considered to have been preventable. CONCLUSIONS: The overall incidence of CVA developing in the operating theater in Japan was reported to be 123 among 1.2 million anesthesias. The incidence was high in elderly patients, in patients with poor physical status, and in patients undergoing cardiovascular surgery. Because the prognosis of CVA developing in the operating theater was poor, clinical strategies for prevention, early detection, prompt diagnosis, and appropriate treatment of CVA should be established.     

Recent changes in the incidence of life-threatening events in the operating room: JSA surveys between 2001 and 2005

BACKGROUND: In Japan, the number of medical staff charged with criminal liability has been increasing since 2000, and this medico-legal trend seems to be promoting topics of medical risk management in government, academic meetings and individual hospital. A survey conducted by the Japanese Society of Anesthesiologists (JSA) has been widely accepted among JSA-certified training hospitals, and its denominator has exceeded one million since 2001. The purpose of this investigation is to examine changes in the incidence of life-threatening events in the operating theater between 2001 and 2005 based on the data of the surveys. METHODS: JSA has conducted annual surveys of life-threatening and neurological events in the operating theater by sending and collecting confidential questionnaires to all JSA certified training hospitals. Cases of life-threatening events between 2001 and 2005 were analyzed. The recovery rates ranged from 76.2% (in 2005) to 91.6% (in 2002), and the annual patient numbers available for analysis ranged from 1,051,245 (in 2005) to 1,367,790 (in 2003) during the study period. The patients with ASA PS 1 or 2 were classified as having good physical status, and those with ASA PS 3 or 4 were classified as having poor physical status. Because mortalities (within 7 postoperative days) are more common in patients with poor physical status, in emergency patients, in neonate, in the elderly, and in patients undergoing cardiovascular surgery, the mortality rate in these patients were investigated. The recovery rate from cardiac arrest without any sequelae was also investigated. The causes of events were classified as follows: totally attributable to anesthetic management (AM), mainly to intraoperative pathological events (IP), to preoperative co-morbidity (PC), and to surgical management (SM). IP consists of pulmonary thromboembolism, acute coronary syndrome, anaphylaxis and so on. The incidence of cardiac arrest and mortality are indicated per 10,000 patients. Odds ratio and 95% confidential interval are shown in comparison with the incidence in 2001 to that in 2005. RESULTS: The incidences of cardiac arrest were 6.12 in 2001, 5.79 in 2002, 5.89 in 2003, 5.09 in 2004, and 4.24/10,000 patients in 2005, respectively (odds ratio 0.69; CI 0.62-0.78). The incidences of death within 7 postoperative days due to intraoperative life-threatening events were 6.41 in 2001, 6.31 in 2002, 6.61 in 2003, 5.88 in 2004, and 4.91/10,000 patients in 2005, respectively (OR 0.77; CI 0.69-0.85). The incidences of death in patients with poor physical status (from 35.48 to 26.87/10,000 patients; OR 0.76; CI 0.66-0.86), in emergency patients (from 37.25 to 30.55/10,000 patients; OR 0.82; CI 0.72-0.93), in neonates (from 70.09 to 31.70/10,000 patients; OR 0.45; CI 0.22-0.91) and in the elderly (from 11.03 to 8.75/10,000 patients; OR 0.79; CI 0.68 to 0.92) decreased. The incidence of death in patients undergoing cardiovascular surgery ranged between 61.22 and 76.88/10,000 patients, and has not shown any significant decline. The incidences of death due to IP (from 0.65 to 0.42/10,000 patients; OR 0.64; CI 0.44-0.92), PC (from 4.14 to 3.30/10,000 patients; OR 0.80; CI 0.70-0.91) and SM (from 1.49 to 1.02/10,000 patients; OR 0.68; CI 0.54-0.87) decreased. However, the incidence of death due to AM ranged between 0.07 and 0.11/10,000 patients, and has not shown any significant decline partly because of the small number of deaths from this cause. Although recent trends in life-threatening events seemed to be favorable, the recovery rate from cardiac arrest decreased from 40.3% in 2001 to 30.7% in 2005 (OR 0.66; CI 0.51-0.84). CONCLUSIONS: The incidence of life-threatening events in the operating room and mortality due to these events seemed to have decreased during the recent five years, probably because of progress in risk management in JSA-certified training hospitals. The decrease was obvious in the recent two years. However, the results should be interpreted cautiously, because the response rate to the questionnaire in 2005 was the lowest. To confirm this trend, we should perform a follow-up survey for 2006 and continue the survey. The reasons for the deterioration in the recovery rate from cardiac arrest should also be examined.     

Acute lung injury and alveolar epithelial function

Since its original definition forty years ago, acute lung injury/acute respiratory distress syndrome has been a challenging target for both clinicians and researchers. In this review, several progresses in the past decades in the area of research concerning the pathophysiology of alveolar epithelium in this syndrome are discussed. Understanding the mechanism of tissue injury and tissue repair are key points to develop new strategy for clinical evaluation of severity of this syndrome and possible therapeutic approaches in future.     

Laparoscopic internal intestinal drainage of bile lakes in a patient with recurrence of jaundice after laparoscopic revision of Kasai portoenterostomy for biliary atresia: A case report

Bile lake, of the postoperative complications after Kasai portoenterostomy (PE) for biliary atresia, causes cholangitis that may induce progressive fibrosis of the liver. Standard treatment for bile lakes has not yet been established, but there are reports that surgical internal intestinal drainage for bile lakes effectively prevents cholangitis and maintains jaundice-free status. In this case, insertion of the percutaneous transhepatic biliary drainage into the bile lake allowed continuous drainage of large volumes of bile juice. However, reoperation following laparotomy increases the surgical risk of subsequent liver transplantation due to postoperative adhesion. Laparoscopic surgery was selected for the patient who was likely to require liver transplantation in the future. In this case, laparoscopic internal intestinal drainage of bile lakes was performed safely by a Cavitron ultrasonic surgical aspirator for the recurrence of jaundice after laparoscopic revision of PE. Cholangitis and jaundice were rapidly resolved after this surgical procedure.     

Negative inotropic action of propofol is enhanced in the acute ischemic myocardium of dogs

Purpose We investigated the effects of propofol on contractility and oxygen balance in acute ischemic myocardium and compared them with those of normal myocardium using a coronary microembolization model in dogs.Methods In open-chest dogs, the left anterior descending coronary artery (LAD) was perfused through an extracorporeal bypass from the carotid artery. Regional myocardial contractility and myocardial oxygen balance were evaluated along with segment shortening (%SS), regional myocardial oxygen consumption (MVO₂), and lactate extraction ratio (LER) of the area perfused by the LAD. Acute ischemia was produced by repeated injection of microspheres into the LAD-perfused area until %SS decreased by 50% of baseline.Results In normal myocardium, intracoronary infusion of propofol at doses of 1.2 and 2.4mg·kg^–1·h^–1 caused slight decreases in %SS to 83% ± 8% and 80% ± 10%, respectively. In ischemic myocardium, propofol caused greater decreases in %SS (59% ± 18% and 35% ± 20%, respectively). The changes in MVO₂ after propofol infusion generally paralleled the changes in %SS, but LER was not changed in either ischemic or normal myocardium.Conclusion Propofol causes a greater decrease in the contractility of acute ischemic myocardium as compared with normal myocardium in which myocardial oxygen imbalance is not involved as a mechanism.     

Endoscopic and Histologic Findings of Intraductal Lesions Presenting with Nipple Discharge

Abstract:   To improve the utility of mammary ductoscopy, we investigated the correlation between endoscopic findings and histologic findings using intraductal biopsy specimens. Seventy-one intraductal biopsy specimens obtained from 63 patients between October 2001 and March 2004 were analyzed retrospectively. All specimens were obtained from monotonous intraductal lesions immediately after observation by mammary ductoscopy and were composed of a pure histologic subtype. With regard to endoscopic findings, color was classified as yellow, red, white, or colorless, and morphology was classified as spherical, lobular, mulberry, or amorphous. The histologic subtype was classified as papillotubular, papillary, degenerated, papillary cancer, solid-type ductal carcinoma in situ (DCIS), or cribriform cancer. The relationship between histologic diagnosis, color, and morphology was investigated. Intraductal biopsy specimens included 25 specimens of carcinoma and 46 specimens of papilloma. There was no significant correlation between color and diagnosis. Fourteen of 25 carcinoma specimens were amorphous, and amorphous morphology was significantly suggestive of malignancy (p < 0.001). Further, cribriform cancer was associated with amorphous morphology and yellow color. Morphology may be a useful endoscopically delineated parameter for differentiating intraductal lesions.      

Novel SCN5A mutation (Q55X) associated with age-dependent expression of Brugada syndrome presenting as neurally mediated syncope.

BACKGROUND: An association between Brugada syndrome and neurally mediated syncope has been described. Although mutations in SCN5A have been identified in Brugada syndrome, the genetic link between Brugada syndrome and neurally mediated syncope has not been determined. OBJECTIVES: The purpose of the study was to clinically and genetically characterize a man with recurrent syncope that originally was diagnosed as neurally mediated syncope at age 8 years but subsequently manifested as Brugada syndrome at age 17 years. METHODS: The proband underwent clinical examination, which included head-up tilt test, sodium channel provocation test, and electrophysiologic study. Genetic screening of SCN5A was performed for the proband and his family members. The biophysical properties of a mutant SCN5A channel in a heterologous expression system were studied using whole-cell, patch clamp technique. RESULTS: The proband showed positive head-up tilt test, coved-type ST elevation recorded from the third intercostal space, and positive pilsicainide provocation test. Ventricular fibrillation was inducible at programmed electrical stimulation, consistent with characteristics of both Brugada syndrome and neurally mediated syncope. A novel nonsense SCN5A mutation (Q55X) was identified in the proband, his mother, and his asymptomatic brother. The heterologously expressed mutant channel was nonfunctional. CONCLUSION: We genetically determined an SCN5A mutation in a patient showing the combined phenotype of neurally mediated syncope and Brugada syndrome. Neurally mediated syncope and Brugada syndrome may share, at least in part, a common pathophysiologic mechanism.     

Cardiac Na(+) channel dysfunction in Brugada syndrome is aggravated by beta(1)-subunit

BACKGROUND: Mutations in the gene encoding the human cardiac Na(+) channel alpha-subunit (hH1) are responsible for chromosome 3-linked congenital long-QT syndrome (LQT3) and idiopathic ventricular fibrillation (IVF). An auxiliary beta(1)-subunit, widely expressed in excitable tissues, shifts the voltage dependence of steady-state inactivation toward more negative potentials and restores normal gating kinetics of brain and skeletal muscle Na(+) channels expressed in Xenopus oocytes but has little if any functional effect on the cardiac isoform. Here, we characterize the altered effects of a human beta(1)-subunit (hbeta(1)) on the heterologously expressed hH1 mutation (T1620M) previously associated with IVF. METHODS AND RESULTS: When expressed alone in Xenopus oocytes, T1620M exhibited no persistent currents, in contrast to the LQT3 mutant channels, but the midpoint of steady-state inactivation (V(1/2)) was significantly shifted toward more positive potentials than for wild-type hH1. Coexpression of hbeta(1) did not significantly alter current decay or recovery from inactivation of wild-type hH1; however, it further shifted the V(1/2) and accelerated the recovery from inactivation of T1620M. Oocyte macropatch analysis revealed that the activation kinetics of T1620M were normal. CONCLUSIONS: It is suggested that coexpression of hbeta(1) exposes a more severe functional defect that results in a greater overlap in the relationship between channel inactivation and activation (window current) in T1620M, which is proposed to be a potential pathophysiological mechanism of IVF in vivo. One possible explanation for our finding is an altered alpha-/beta(1)-subunit association in the mutant.