Long-term survival and late complications after repair of ruptured abdominal aortic aneurysms

PURPOSE: Long-term survival and late vascular complications in patients who survived repair of ruptured abdominal aortic aneurysms (RAAA) is not well known. The current study compared late outcome after repair of RAAA with those observed in patients who survived elective repair of abdominal aortic aneurysms (AAA). METHODS: The records of 116 patients, 102 men and 14 women (mean age: 72.5 (8.3 years), who survived repair of RAAA (group I) between 1980 to 1989 were reviewed. Late vascular complications and survival were compared with an equal number of survivors of elective AAA repair matched for sex, age, surgeon, and date of operation (group II). Survival was also compared with the age and sex-matched white population of west-north central United States. RESULTS: Late vascular complications occurred in 17% (20/116) of patients in group I and in 8% (9/116) in group II. Paraanastomotic aneurysms occurred more frequently in group I than in group II (17 vs. 8, p = 0.004). At follow-up, 32 patients (28%) were alive in group I (median survival: 9.4 years) and 53 patients (46%) were alive in group II (median survival: 8.7 years). Cumulative survival rates after successful RAAA repair at 1, 5, and 10 years were 86%, 64%, and 33%, respectively. These were significantly lower than survival rates at the same intervals after elective repair (97%, 74%, and 43%, respectively, p = 0.02) or survival of the general population (95%, 75%, and 52%, respectively, p < 0.001). Coronary artery disease was the most frequent cause of late death in both groups. Vascular and graft-related complications caused death in 3% (3/116) in group I and 1% (1/116) in group II. Cox proportional hazards modeling identified age (p = 0.0001), cerebrovascular disease (p = 0.009), and number of days on mechanical ventilation (p = 0.01) to be independent prognostic determinants of late survival in group I. CONCLUSIONS: Late vascular complications after repair of RAAA were higher and late survival rates lower than after elective repair. These data support elective repair of AAA. As two-thirds of the patients discharged after repair of RAAA are alive at 5 years, aggressive management of RAAA remains justified.     

Ondansetron versus droperidol or placebo to prevent nausea and vomiting after otologic surgery

This study compares the preoperative administration of ondansetron with that of droperidol or saline solution for the prevention of nausea and vomiting in otologic surgery patients. A total of 120 otherwise healthy individuals were randomly assigned to receive either saline solution, ondansetron (4 mg intravenously), or droperidol (25 microg/kg intravenously) before anesthetic induction. Intraoperative and postanesthesia care unit times were recorded along with incidence of nausea, vomiting, pain, nausea and recovery scores, and the administration of rescue antiemetics. Similar assessments were made during the next 24 hours. Demographics were similar, but more males received ondansetron. Anesthetic recovery scores were lower after administration of droperidol than after ondansetron. Incidence of nausea was similar between groups, but severity was greater with placebo and droperidol than with ondansetron. More vomiting occurred with placebo than with ondansetron or droperidol. No intergroup differences in rescue antiemetic administration were noted, however. Twenty-four hours later, more patients receiving placebo had nausea or vomited than patients receiving droperidol or ondansetron. Fewer women in the ondansetron group vomited than in the other two groups. Ondansetron 4 mg intravenously is as effective as droperidol and better than saline solution in preventing nausea and vomiting in patients undergoing otologic surgery. No cost advantage as determined by lower use of rescue antiemetics or shorter postanesthesia care unit times was noted after ondansetron therapy.     

Sleep apnea in 81 ambulatory male patients with stable heart failure. Types and their prevalences, consequences, and presentations

BACKGROUND: Heart failure is a highly prevalent disorder that continues to be associated with repeated hospitalizations, high morbidity, and high mortality. Sleep-related breathing disorders with repetitive episodes of asphyxia may adversely affect heart function. The main aims of this study were to determine the prevalence, consequences, and differences in various sleep-related breathing disorders in ambulatory male patients with stable heart failure. METHODS AND RESULTS: This article reports the results of a prospective study of 81 of 92 eligible patients with heart failure and a left ventricular ejection fraction < 45%. There were 40 patients without (hourly rate of apnea/hypopnea, 4 +/- 4; group 1) and 41 patients with (51% of all patients; hourly rate of apnea/hypopnea, 44 +/- 19; group 2) sleep apnea. Sleep disruption and arterial oxyhemoglobin desaturation were significantly more severe and the prevalence of atrial fibrillation (22% versus 5%) and ventricular arrhythmias were greater in group 2 than in group 1. Forty percent of all patients had central sleep apnea, and 11% had obstructive sleep apnea. The latter patients had significantly greater mean body weight (112 +/- 30 versus 75 +/- 16 kg) and prevalence of habitual snoring (78% versus 28%). However, the hourly rate of episodes of apnea and hypopnea (36 +/- 10 versus 47 +/- 21), episodes of arousal (20 +/- 14 versus 23 +/- 11), and desaturation (lowest saturation, 72 +/- 11% versus 78 +/- 12%) were similar in patients with these different types of apnea. CONCLUSIONS: Fifty-one percent of male patients with stable heart failure suffer from sleep-related breathing disorders: 40% from central and 11% from obstructive sleep apnea. Both obstructive and central types of sleep apnea result in sleep disruption and arterial oxyhemoglobin desaturation. Patients with sleep apnea have a high prevalence of atrial fibrillation and ventricular arrhythmias.     

Recombinant tissue plasminogen activator for the treatment of spontaneous adult intraventricular hemorrhage

BACKGROUND: Intraventricular hemorrhage (IVH) has a poor prognosis with mortality rates of between 80 and 100% when all four ventricles are involved. Fibrinolytic therapy has been reported to improve overall outcome. METHODS: Patients with severe primary IVH were treated by direct intraventricular injection of recombinant tissue plasminogen activator (rt-PA) into the lateral ventricles, followed by cerebrospinal fluid (CSF) drainage if the intracranial pressure rose above 20 mm Hg. RESULTS: Over a 15-month period from 1995 through 1996, 10 patients were treated, (4 male and 6 female, mean age 35 years; range, 21-55 years). The mean Glasgow Coma Scale score on admission was 6 (range, 4-8) and the mean Graeb score for severity of IVH on the first CT scan was 10 (range, 8-12). Angiography was negative in five cases but identified arteriovenous malformations in three, a post-traumatic pseudoaneurysm in one, and Moya-moya disease in one. The mean total dose requirement of rt-PA was 8.25 mg (range, 6-12 mg) with a significant reduction in the mean Graeb score after 7 days to 3.9 (range, 2-7, p<0.0001). Outcome at 3 months was death in one case (mortality 10%), severe disability in two (20%), moderate disability in three (30%), and good result in four (40%). Four patients (40%) required subsequent CSF shunting. No complications of rehemorrhage, infection, or catheter obstruction were encountered. CONCLUSION: Intraventricular fibrinolysis with rt-PA seems to be safe and effective for the treatment of severe IVH.     

Insulin-stimulated glycogen synthesis in cultured hepatoma cells: differential effects of inhibitors of insulin signaling molecules

In rat HTC hepatoma cells overexpressing human insulin receptors, insulin stimulated glycogen synthesis by 55-70%. To study postreceptor signaling events leading to insulin-stimulated glycogen synthesis in these cells, we have employed pathway-specific chemical inhibitors such as LY294002, rapamycin and PD98059 to inhibit phosphatidylinositol-3-kinase (PI3K), p70 ribosomal S6 kinase and mitogen-activated protein kinase (MAPK) kinase/MAPK, respectively. LY294002 (50 microM) completely abolished insulin-stimulated glycogen synthesis whereas rapamycin (2-20 nM) partially inhibited it. Neither LY294002 nor rapamycin significantly affected the basal glycogen synthesis. However, PD98059 (100 microM) significantly inhibited the basal glycogen synthesis without affecting insulin-stimulated glycogen synthesis. In these cells, insulin at 100 nM decreased glycogen synthase kinase 3 alpha (GSK3 alpha) activity by 30-35%. LY294002, but neither rapamycin nor PD98059, abolished insulin-induced inactivation of GSK3 alpha. These data suggest that insulin-stimulated glycogen synthesis in rat HTC hepatoma cells is mediated mainly by PI3K-dependent mechanism. In these cells, inactivation of GSK3 alpha, downstream of PI3K, may play a role in insulin-stimulated glycogen synthesis.     

The changing pattern of intestinal tuberculosis: 30 years' experience

SETTING: Although the incidence of tuberculosis had been decreasing for many years, it has recently risen. OBJECTIVES: To investigate the changes in the pattern and distribution of intestinal tuberculosis and to alert surgeons to the importance of maintaining a high index of suspicion for this disease entity. DESIGN: Retrospective analysis of 134 patients with intestinal tuberculosis discharged from the Veterans General Hospital in Taipei from 1965 to 1995. All records, bacteriological examinations and pathological specimens were reviewed and extracted onto a standard questionnaire. RESULTS: A decline in the case numbers of intestinal tuberculosis was noted after 1975. However, there seems to be a slight rise in case numbers since 1990. The average age of those patients after 1990 (64.8 years) is higher than those before 1990 (44.4 years). None of our patients had clinical signs of human immunodeficiency virus (HIV) infection. Most patients (81.3%, 109/134) had not received a definite diagnosis until surgery. Active pulmonary tuberculosis was found in 37 patients (29.1%). CONCLUSION: The possible reasons for the rise in cases of intestinal tuberculosis in our patients may be linked to an increased life expectancy, the reappearance of some formerly 'silent' tuberculosis cases, and relapse in patients having received incomplete antituberculosis chemotherapy. Its insidious and non-specific clinical presentation makes the diagnosis of intestinal tuberculosis difficult. An increased index of suspicion and greater familiarity with the disease may shorten the time of diagnosis and may also prevent some unnecessary operations.     

A functional role for mitochondrial protein kinase Calpha in Bcl2 phosphorylation and suppression of apoptosis

Phosphorylation of Bcl2 at serine 70 may result from activation of a classic protein kinase C (PKC) isoform and is required for functional suppression of apoptosis by Bcl2 in murine growth factor-dependent cell lines (Ito, T., Deng, X., Carr, B., and May, W. S. (1997) J. Biol. Chem. 272, 11671-11673). Human pre-B REH cells express high levels of Bcl2 yet remain sensitive to the chemotherapeutic agents etoposide, cytosine arabinoside, and Adriamycin. In contrast, myeloid leukemia-derived HL60 cells express less than half the level of Bcl-2 but are >10-fold more resistant to apoptosis induced by these drugs. The mechanism responsible for this apparent dichotomy appears to involve a deficiency of mitochondrial PKCalpha since 1) HL60 but not REH cells contain highly phosphorylated Bcl2; 2) PKCalpha is the only classical isoform co-localized with Bcl2 in HL60 but not REH mitochondrial membranes; 3) the natural product and potent PKC activator bryostatin-1 induces mitochondrial localization of PKCalpha in association with Bcl2 phosphorylation and increased REH cell resistance to drug-induced apoptosis; 4) PKCalpha can directly phosphorylate wild-type but not phosphorylation-negative and loss of function S70A Bcl2 in vitro; 5) stable, forced expression of exogenous PKCalpha induces mitochondrial localization of PKCalpha, increased Bcl2 phosphorylation and a >10-fold increase in resistance to drug-induced cell death; and () PKCalpha-transduced cells remain highly sensitive to staurosporine, a potent PKC inhibitor. Furthermore, treatment of the PKCalpha transformants with bryostatin-1 leads to even higher levels of mitochondrial PKCalpha, Bcl2 phosphorylation, and REH cell survival following chemotherapy. While these findings strongly support a role for PKCalpha as a functional Bcl2 kinase that can enhance cell resistance to antileukemic chemotherapy, they do not exclude the possibility that another Bcl2 kinase(s) may also exist. Collectively, these findings identify a functional role for PKCalpha in Bcl2 phosphorylation and in resistance to chemotherapy and suggest a novel target for antileukemic strategies.     

Esophageal resection for cancer

Currently, relatively safe, reliable resection techniques are available for most patients with esophageal carcinoma who present with nonmetastatic disease. For optimal results, the surgeon must be familiar with both transhiatal and transthoracic approaches and must individualize the approach depending on the tumor size and location and the patient's functional status. Whereas post-resection survival rates are good for patients with early-stage disease (Stage I or IIa), most patients present with locally advanced, Stage III disease. Although some progress has been made in the past decade in regard to early diagnosis among patients with Barrett's metaplasia undergoing endoscopic surveillance and additional progress has been made in adapting multimodality treatment programs successfully to patients with locally advanced disease, the overall cure rate for patients with esophageal carcinoma remains low.