Changes of local brain tissue oxygen pressure after vasopressin during spontaneous circulation

Summary. Background. Brain tissue oxygen pressure (PbtO₂) correlates to cerebral blood flow (CBF) during spontaneous circulation, with one important regulator being nitric oxide (NO). Although it is established that arginine vasopressin (AVP) improves CBF and global cerebral oxygenation during cardiopulmonary resuscitation, it is unknown whether similar beneficial effects are present during spontaneous circulation. The purpose of this study was to investigate the effects of AVP with and without pre-treatment with the NO synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) on local brain tissue oxygenation in a beating heart model.Methods. Following approval of the Animal Investigational Committee, nine healthy piglets underwent general anaesthesia, and were instrumented with a probe in the cerebral cortex to measure PbtO₂. Each animal was assigned to receive AVP (0.4U·kg^–1), and after a wash-out period, L-NAME (25mg·kg^–1 over 20min) followed by AVP (0.4U·kg^–1). After each AVP administration, nitroglycerine (25µg·kg^–1 over 1min) as a NO donor was infused to test the vascular reactivity independently from NOS inhibition.Findings. Three minutes after administration of AVP, PbtO₂ increased significantly (P<.05; mean±SEM, 31±11 versus 43±14mmHg, +39%), compared with baseline. After pre-treatment with L-NAME, the changes of PbtO₂ after AVP were not significant (32±11 versus 28±10, –13%) when compared with the baseline.Conclusion. In this beating heart porcine model, local brain tissue oxygenation was improved after AVP alone, but not after inhibition of NO synthesis with L-NAME.     

Comparison of anesthetic effects of epidural and intravenous administration of buprenorphine during operation

Thirty six patients were received epidural anesthesia with or without buprenorphine (BPN) during upper abdominal surgery. They were divided into three groups of 12 patients as follows; G-I received 20ml of 1% lidocaine epidurally, G-II received 20ml of 1% lidocaine epidurally and 0.6mg BPN intravenously, G-III received 20ml of 1% lidocaine with 0.6mg BPN epidurally. Additional 5ml of 1% lidocaine was given to any patient if systolic blood pressure or heart rate increased 10% compared to control value. Trachea was intubated following anesthetic induction with thiopental. The lungs were ventilated with a mixture of N₂O/O₂ (33%) and pancuronium was used for muscle relaxation. The total required doses of lidocaine in G-II and G-III were decreased 60% compared to control group (G-I) (P 0.05). The mean period of time until the first administration of pentazocine for postoperative pain was 13 ± 10hr (mean ± SD) in G-II and 19 ± 24hr in G-III compared to 5 ± 4hr in G-I (P 0.001). The dose of the administration of pentazocine that was required for pain relief during the first 48 postoperative hr in G-III was 54 ± 10mg (mean ± SD) compared to 150 ± 21mg in G-I (P 0.02) and 106 ± 28mg in G-II (P 0.05). Recovery from anesthesia in G-III was more rapid than that in G-I (P 0.05). The Pa_{CO 2} values in G-II and G-III increased 15% compared to control group at about 4hr and 8hr after administration of BPN, but any clinical treatment was not needed for them. Nonrespiratory side effects, e.g., nausea, vomiting, fatigue and headache, were comparably common in all groups. Mild hematuria associated with acute hypotension occurred in two patients in G-II (17%) immediately after the intravenous injection of 0.6mg of BPN. The results showed that 0.6mg of BPN given epidurally demonstrated better anesthetic and more potent postoperative analgesic effects and lesser side effects than 0.6mg of BPN given intravenously in patients undergoing upper abdominal surgery.(Yonemura E, Fukushima K.: Comparison of anesthetic effects of epidural and intravenous administration of buprenorphine during operation. J Anesth 4: 242–248, 1990)     

Bench test assessment of the new Raumedic Neurovent-P ICP sensor: a technical report by the BrainIT group

Summary. Background. In clinical practice, fiberberoptic and piezo-electric ICP probes are often used for measuring intracranial pressure (ICP). A number of similar technologies, although performing well in bench test studies, have been shown to exhibit unacceptable zero drift, fragility or both during trials conducted under clinical conditions. Recently, a new technology has become available, the Neurovent-P (Raumedic AG+CO, Raumedic, Germany). As a pre-requisite for a clinical trial, we have conducted and report on bench test studies to confirm the manufacturers long term zero-drift performance for this technology.Method. In a test rig static tests (recording of 20mmHg pressure) and dynamic tests, ranging from 5 to 50mmHg have been performed.Findings. 10 ICP probes have been tested for a total of 60 days. All the catheters, after the connection with the ICU monitor displayed a static pressure of 0±1mmHg and did not required pre-insertion alteration. At five days, mean zero drift was 0.6±0.9mmHg. Overall, zero drift ranged from 0 to 2mmHg. At a fixed static pressure of 20mmHg, the mean recorded value was 20.6±0.8mmHg, ranging from 19 to 23mmHg. A regression analysis of the relationship between the applied pressure and the recorded pressure during the dynamic tests of the 10 catheters yielded a correlation coefficient R² of 0.997. Applying the Altman and Bland method to assess the bias and confidence limits for the Raumedic catheter responses during the dynamic tests against the applied gold-standard hydrostatic column pressures, the average bias of –0.66±0.85mmHg, with 95% CLs of –2mmHg and 1mmHg.Conclusions. Mean zero drift, after five days, was very small and long-term continuous recording of a stable pressure was very precise. The response at dynamic tests, i.e. the changes of pressure in a wide range, was excellent. The average bias of the Raumedic catheter compared with the hydrostatic column is very small. After this bench test, the next and most critical step will be to conduct a trial of this promising technology under more demanding clinical environment.     

Combined effects of Inversed Ratio Ventilation (IRV) with positive end-expiratory pressure ventilation (PEEP) on cardiorespiratory function in acute respiratory failure

Combined effects of inversed ratio ventilation (IRV) with positive end-expiratory pressure (PEEP) on cardiorespiratory function were examined in 24 patients with acute respiratory failure. Patients were divided into two groups: the IRV group (n = 12) who showed no significant increase in Pa_{O 2} with a 6cmH₂O of PEEP and PEEP group (n = 12) who were ventilated mechanically with PEEP only at maximum level of 10cmH₂O. In IRV group step-wise prolongation of the I:E ratio from 1:1.9 to 2.6:1 or 4:1 was applied as a Pa_{O 2} was improved and in PEEP group also level of PEEP was increased from 0, 5 to 10cmH₂O after one hour period irrespective of Pa_{O 2}. Inversed ratio ventilation and PEEP increased significantly Pa_{O 2}/Fi _{O 2}, the increase being observed 6hrs (I:E = 2:1) and 2hrs (10cmH₂O) after starting IRV or PEEP. Further improvement of oxygenation was not observed in IRV even if I:E ratio was prolonged up to 2.6:1 or 4:1. These results suggested that combinations of IRV with PEEP were effective and an I:E ratio of 2:1 may be optimal, and IRV is advantageous compared to PEEP, but will take more long time to improve oxygenation than PEEP.(Sari A, Toriumi T, Yamashita S, et al.: Combined effects of inversed ratio ventilation (IRV) with positive end-expiratory pressure ventilation (PEEP) on cardiorespiratory function in acute respiratory failure. J Anesth 5: 105–113, 1991)     

Dose-finding study of intravenous midazolam for sedation and amnesia during spinal anesthesia in patients premedicated with intramuscular midazolam

Purpose We investigated the effective and safe dose of intravenous midazolam for sedation and amnesia during spinal anesthesia in patients premedicated with intramuscular midazolam.Methods One hundred and eighty patients aged 20–50 years scheduled for spinal anesthesia received midazolam 0.06mg·kg^–1 and atropine 0.01mg·kg^–1 intramuscularly 15min before entering the operating room. Spinal anesthesia was performed with 0.5% hyperbaric tetracaine. Five minutes after starting surgery, midazolam 0 (control group), 0.01, 0.02, 0.03, 0.04, or 0.05mg·kg^–1 was intravenously administered (30 patients each). Blood pressure, heart rate, respiratory rate, percutaneous oxygen saturation (S_{p O 2}), verbal response, eyelash reflex, and involuntary body movement were measured every 5min for 30min. Memory during surgery was also investigated.Results The number of the patients with loss of verbal response, with loss of eyelash reflex, and with no memory during surgery were significantly larger in the groups receiving midazolam 0.03mg·kg^–1, 0.04mg·kg^–1, and 0.02mg·kg^–1, respectively. The decrease in blood pressure or increase in respiratory rate with decrease in S_{p O 2} was significantly larger in the groups receiving midazolam 0.03mg·kg^–1 or 0.05mg·kg^–1, respectively.Conclusion For sedation and amnesia of the patients aged 20–50 years in spinal anesthesia with about 1h duration receiving intramuscular midazolam 0.06mg·kg^–1 as a premedication, intravenous midazolam 0.02mg·kg^–1 might be effective and safe.     

EnHurane supresses phrenic nerve-diaphragm Transmissionin vivo

We examined the effects of enflurane on the diaphragmatic function in 15 pentobarbital-anesthetized, mechanically ventilated dogs. They were divided into three groups of five animals each, according to the administered concentration of enflurane. The diaphragmatic function was assessed from transdiaphragmatic pressure (Pdi) and integrated diaphragmatic electromyography (Edi) developed at functional residual capacity against an occluded airway during bilateral supramaximal phrenic nerve stimulation at 0.5, 10, 20, 50 and 100Hz under quasiisometric condition. After a control measurement, enflurane was administered at a constant end-expired concentration (0, 0.5 and 1MAC) and the measurement was repeated after 1 hour of exposure. The Pdi amplitude generated by single twitch (0.5Hz) and during 10, 20 and 50Hz stimulation was unchanged between the groups. No change in Pdi during 100Hz stimulation was noted during 0 and 0.5MAC exposure, while it was reduced by 1MAC of enflurane. When the values of Pdi were expressed as % of maximum Pdi (%Pdi,max) that developed during control measurement and analyzed in terms of %Pdi,max—stimulus frequency relationship, a significant decrease in %Pdi,max was noted for 100Hz stimulation in 0.5 and 1MAC groups compared to the control. Similarly, Edi during 100Hz stimulation obtained in 0.5 and 1MAC groups was markedly depressed compared to the control. Edi during 50Hz stimulation was also decreased at 1MAC. Relative changes in Edi following enflurane administration were greater than the corresponding changes of Pdi. These results demonstrate that enflurane impairs diaphragmatic function through its inhibitory effects on neuromuscular transmission.(Kochi T, Ide T, Isono S, et al.: Enflurane supresses phrenic nerve-diaphragm transmission in vivo. J Anesth 5: 260–267, 1991)     

Quantitative determination of atracurium in human plasma using high-performance liquid chromatography

The authors have established a new method for extraction and determination of atracurium in human plasma that employs a reversed phase high-performance liquid chromatography (HPLC). This method made use of a fluorescent spectrophotometer at an excitation wavelength of 240nm and an emission wavelength of 310nm. The mobile phase was made of a phosphate buffer, distilled water and acetonitrile (20V:30V:50V). The analytical column used was a Little Champ C₁₈.In a Bond Elute C₁₈ extraction column, which had been prewashed with a phosphate buffer and a 50% methanol solution, atracurium was extracted from acidified plasma samples using a mixture of methanol and phosphate buffer. A standard curve was prepared by the internal standard method using metocurine. A high linear correlation between atracurium concentration and the ratio of the atracurium peak height to the metocurine peak height was observed (r = 0.9994). The lowest threshold for detection of atracurium was 15ng/ml. When the plasma concentrations of atracurium were determined in 2 clinical cases, t_1/2 was 2.10 and 1.73min and t_1/2 was 15.57 and 21.57min, respectively. These results indicate that this method of extraction and determination is appropriate for studying the pharmacokinetics of atracurium because it allows a high reproducibility, and provides an extremely accurate, simple and quick analysis.(Okutani R, Kono K, Frederic M. deBros et al.: Quantitative determination of atracurium in human plasma using high-performance liquid chromatography. J Anesth 2: –, 1988)     

Postoperative Renal Function After Elective Abdominal Aortic Aneurysm Repair Requiring Suprarenal Aortic Cross-Clamping

Purpose To examine postoperative renal function after suprarenal aortic cross-clamping performed without renal hypothermia in patients undergoing elective abdominal aortic aneurysm (AAA) surgery.Methods Between 1991 and 2000, 18 patients underwent surgery for a juxtarenal AAA, which required a suprarenal aortic cross-clamp. All AAAs were repaired with a proximal anastomosis just below the renal arteries. We divided the patients into two groups according to the duration of the renal ischemia: <45min (n = 12) and 45min (n = 6). The postoperative changes in renal function were analyzed.Results There were no hospital deaths and none of the patients needed permanent hemodialysis. The postoperative peak in the serum creatinine level after suprarenal cross-clamping for 45min was significantly higher than that after cross-clamping for <45min. The percentage changes in serum creatinine and blood urea nitrogen were correlated positively with the duration of renal ischemia, and were significantly greater in the group with renal ischemia of <45min than in the group with prolonged renal ischemia (45min).Conclusions Suprarenal aortic cross-clamp without performing renal hypothermia is safe and able to be tolerated well by the patient during elective AAA surgery, although careful attention must be paid to limiting the period of renal ischemia.     

Effects of calcium and temperature on tension in isolated canine coronary artery

The effects of calcium and temperature on the tension of isolated canine coronary arterial strips were studied.In 20mEq·l ^–1 K solution, the tension was significantly increased from 0mg with 0mEq·l ^–1 Ca to 33 ± 18mg with 0.2mEq·l ^–1 Ca at 37°C, from –40 ± 18mg with 0mEq·l ^–1 Ca to –17 ± 11mg with 0.2mEq·l ^–1 Ca at 30°C, from –77 ± 19mg with 0mEq·l ^–1 Ca to –52 ± 17mEq·l ^–1 with 1mEq·l ^–1 Ca at 25°C, from –88 ± 13mg with 0mEq·l ^–1 Ca to –41 ± 18mg with 2mEq·l ^–1 Ca at 20°C, from –125 ± 16mg with 0mEq·l ^–1 Ca to –116 ± 13mg with 2mEq·l ^–1 Ca at 15°C. Ca higher than 0.2mEq·l ^–1 produced a dose-dependent increase in tension between 37°C and 15°C. In spite of the presence of 4mEq·l ^–1 Ca, the development of tension was strongly supressed by lowering the temperature below 20°C, and completely inhibited at 10°C. The rate of a decrease in tension caused by cooling was about 5.5mg·°C^–1.This study demonstrated that Ca²⁺ produced a dose-dependent increase in tension in high-K solution, which was suppressed as the temperature was lowered.(Yoshida K, Fujii Y, Ina H, et al.: Effects of calcium and temperature on tension in isolated canine coronary artery. J Anesth 5: 172–176, 1991)     

Enzyme inhibition by analgesic and hypnotic agents on anaerobic dehalogenation of halothane

Enzyme inhibition on anaerobic dehalogenation of halothane by various analgesic or hypnotic agents was investigated in vitro using rat liver microsomal fraction. The production rate of chloro-difluoro-ethylene (CDE) and chloro-trifluoro-ethane (CTE), anaerobic metabolites of halothane, was measured when various concentrations of analgesic or hypnotic agents (fentanyl, morphine, pentazocine, buprenorphine, ketamine, diazepam, chlorpromazine and hydroxyzine) were supplemented. Inhibitor constant (Ki) of each agent was calculated and compared with each other. The activity of NADPH-cytochrome c reductase (fp₂) and NADH-ferricyanide reductase (fp₁) was measured when each agent was added. The values of inhibitor constants (Ki) for CDE and CTE formation were in the following order from large to small values; morphine (656µM and 2570µM), chlorpromazine (49.7µM and 68.1µM), ketamine (24.9µM and 64.4µM), fentanyl (23.9µM and 34.6µM), hydroxyzine (19.2µM and 50.8µM), diazepam (17.0µM and 13.9µM), buprenorphine (11.2µM and 22.4µM), and pentazocine (1.96µM and 6.67µM) respectively. Pentazocine inhibited the formation of CDE 300 fold greater than morphine. The activity of fp₂ and fp₁ did not change by the addition of these analgesic or hypnotic agents. These results indicate that various analgesic or hypnotic agents, which are commonly used with halothane in clinical anesthesia, suppress the anaerobic dehalogenation of halothane in vitro. They also imply that the suppression of production of halothane metabolites is the result of direct enzyme inhibition on cytochrome P-450, since these agents did not affect the activity of fp₂ and fp₁ which are flavoproteins existing in the microsomal electron transport system.(Yamanoue T, Kikuchi H, Fujii K, et al.: Enzyme Inhibition by Analgesic and Hypnotic Agents on Anaerobic Dehalogenation of Halothane. J Anesth 5: 331–337, 1991)     

Erythemas caused by electrodes while monitoring neuromuscular blockade: three cases

Skin erythemas formed in three patients during surgery at the sites where negative electrodes had been attached to stimulate the ulnar nerve for a neuromuscular transmission monitor (Relaxograph). The patients were all women, aged 52, 62, and 74 years, and general anesthesia lasted 8h 20min, 4h 50min, and 8h 45min, respectively. The electrodes used were disposable ECG electrodes in the first two patients and one designed for a neuromuscular monitor in the third; all were carbon-coated and then covered with gel. However, when the electrodes were detached from the lesion, they all showed loss or damage of the carbon coating under the gel. We recommend balancing the merit of monitoring with the risk of complications, even when applying an apparently safe, noninvasive monitor.     

Inhaled Nitric Oxide Therapy After Fontan-Type Operations

Purpose Inhaled nitric oxide (NO) therapy is a newly developed strategy designed to reduce pulmonary vascular resistance after the Fontan-type operation. We reviewed our experience to evaluate its efficacy and true indications.Methods We retrospectively examined 47 children who received inhaled NO therapy after the Fontan-type operation between August 1996 and December 2002. The maximal dose of NO ranged from 5 to 30ppm (median 10ppm), and the duration of inhaled NO therapy ranged from 5h to 52 days (median 2 days).Results Inhaled NO significantly decreased the central venous pressure (CVP), from 16.2 ± 2.2 to 14.6 ± 2.2mmHg (P < 0.0001), and the transpulmonary pressure gradient between the CVP and left atrial pressure, from 9.9 ± 2.9 to 8.4 ± 2.7mmHg (P < 0.0001). It also increased the systolic systemic arterial pressure from 71.9 ± 15.2 to 76.8 ± 14.5mmHg (P < 0.05). In 26 patients with additional fenestration, inhaled NO led to a significant improvement in SaO₂ from 90.1% ± 9.6% to 93.3% ± 7.9% (P < 0.01). However, patients with a CVP <15mmHg or a transpulmonary pressure gradient <8mmHg, or both, after the Fontan-type operation, showed no significant changes in hemodynamics during inhaled NO therapy.Conclusions We propose that a CVP 15mmHg or a transpulmonary pressure gradient 8mmHg, or both, after Fontan-type operations are appropriate indications for inhaled NO therapy.     

Effects of Cilostazol on Human Venous Smooth Muscle

In this study, we evaluated the effect of therapeutic doses of cilostazol on human venous smooth muscle. Saphenous vein rings (two to four per patient sample) were suspended in tissue baths for isometric tension recordings. At the beginning of the experiment, optimal tension for isometric contraction was achieved for each ring in a stepwise fashion in the presence of norepinephrine (10^–2 M). Norepinepherine was then added cumulatively in half-molar increments and isometric tension developed by the rings was measured, thereby obtaining a dose-response curve. Following washout and reequilibration, the rings were precontracted with a 30-50% submaximal dose of norepinepherine determined from the dose-response curve and allowed to contract until a stable plateau was reached. Cilostazol was then added in a cumulative manner (680-2,720 g/L), and the tension generated was recorded. A total of 76 venous rings were tested, and all relaxed in the presence of cilostazol. The amount of relaxation increased as the concentration of cilostazol increased. Relaxation of 15±1.9% (mean±SEM) at low cilostazol doses (680 g/L) to 37±3% at high cilostazol doses (2,720 g/L) was demonstrated. A second finding of this study was demonstrated when the patient samples were divided according to the presence or absence of risk factors for arteriosclerosis. The specific risk factors examined included diabetes mellitus, smoking, hypercholesterolemia, and hypertension. The presence or absence of hypertension (n=52) or hypercholesterolemia (n=18) did not affect the amount of relaxation of the venous rings. Smokers (n=46) had less relaxation 16±2.4% (680 g/L) to 41±3.6% (2,720 g/L) compared to nonsmokers (n=53) who relaxed 22±3.5% (680 g/L) to 48±5.7% (2720 g/L). This did not reach statistical significance at any concentration cilostazol (p=0.11-0.18). Diabetics (n=53) did have statistically significantly less relaxation at every concentration of cilostazol compared to nondiabetics (n=11, p < 0.05). All venous rings relaxed in the presence of cilostazol. Veins of nondiabetics relaxed statistically significantly more than those of diabetics. Smokers had less relaxation than non-smokers, but this was not statistically significant. We are the first to demonstrate that human venous smooth muscle cells undergo relaxation when exposed to therapeutic concentrations of cilostazol.     

Vitamin C may be beneficial in the prevention of paracetamol-induced renal damage

Background There is no specific treatment for paracetamol-induced renal damage. Vitamin C is an outstanding chain-breaking antioxidant and a free radical scavenger. The present study was undertaken to determine whether large doses of vitamin C are useful in the treatment of paracetamol-induced renal damage.Methods Renal injury was induced in rats by the administration of 1g/kg body weight paracetamol intraperitoneally. Some rats received intraperitoneal injections of vitamin C (250, 500, or 1000mg/kg body wt) at 1.5h, 6h, 9h, or 16h after the administration of paracetamol, and the rats were killed 24h after the administration of paracetamol.Results Renal injury was accompanied by a decrease in nonprotein thiol and protein thiol in the kidneys of paracetamol-treated rats. The administration of vitamin C to the paracetamol-treated rats prevented renal damage either completely or partially. Lower doses of vitamin C were beneficial in the prevention of paracetamol-induced renal injury when administered early and higher doses were beneficial when administered later. In the paracetamol-treated rats that responded to vitamin C, renal nonprotein thiol level and protein thiol were restored almost completely. Interestingly, a highly significant inverse correlation was obtained between renal nonprotein thiol level and plasma creatinine.Conclusions Megadoses of vitamin C may be beneficial in the treatment of paracetamol-induced renal damage. The mechanism of protection by vitamin C appears to be the regeneration of nonprotein thiol.     

Secondary growth of a cortical necrosis: effect of NOS inhibition by aminoguanidine post insult

Summary ¶Background. A cortical tissue necrosis from a focal freezing injury expands to 140% of its initial volume within 24hrs in rats. Previous studies of our laboratory have shown that administration of the NOS inhibitor aminoguanidine (AG) prior to trauma attenuates this process of secondary brain damage. Objective of the present study was to analyse whether this agent is also protective when treatment commences after the insult. Method. A highly standardized freezing lesion was induced in the brain cortex of 30 anaesthetized rats. The animals were divided into three experimental groups. Animals of group I (sham-5min, n=10) were sacrificed 5min after trauma for quantitative histomorphometric assessment of the primary cortical lesion. Animals of group II (sham-24h, n=10) received isotonic saline (16.7ml/kg b.w., i.p.) at 15min and 8hrs after trauma. In the treatment group (group III, AG-24h, n=10), AG was administered (100mg/kg b.w.) also at 15min and 8hrs after trauma. 24hrs later – the time point of maximal lesion spread – the animals of group II and III were sacrificed for quantification of the secondary lesion growth. Findings. The focal freezing injury produced a cortical necrosis volume of 6.07±1.04mm³ immediately after trauma (group I). After sham treatment, the necrosis expanded to 8.39±1.57mm³ within 24hrs (group II) corresponding to a lesion growth of 138% compared to the primary necrosis (p<0.01 vs. group I). In animals treated with AG after the trauma (group III), the volume of necrosis was significantly attenuated at 24hrs to 6.77±0.87mm³ representing an expansion of the lesion to only 112% (p<0.05 vs. group II). Thus, AG was inhibiting the secondary growth of necrosis by no less than 69%. Interpretation. The findings demonstrate that AG retains its neuroprotective potential against secondary brain damage from trauma even when administration begins after trauma.Published online October 20, 2003     

Hospital Readmissions Following Abdominal Aortic Aneurysm Repair

In-hospital outcomes associated with abdominal aortic aneurysm (AAA) repair are well described. However, little is known about post-discharge readmission rates, lengths of stay, associated mortality, and costs. We examined 206 consecutive patients who underwent AAA repair at two American hospitals between 1998 and 2000. Index hospitalization and 6-month readmission data were extracted from a resource and cost accounting system used by both hospitals. Among the 206 patients, 183 survived until discharge (mortality rate 11.2%). Among the surviving patients, 38 (21.0%) were readmitted within 6 months. Half of the readmissions occurred within two weeks of discharge, with patients presenting with a diverse array of complications. Nonelective repair and diabetes mellitus were independent predictors of hospital readmission (OR=2.83, 95% CI=1.25-6.40, p=0.01; OR=6.60, 95% CI=1.02-42.4, p=0.047, respectively). For each readmission, the mean length of stay was 10.7±2.5 days and the mean cost was $13,397±3,381. The cumulative number of hospital days during the 6 months post-discharge was 17.7±3.5 days for each readmitted patient and the mean per-patient total cost was $23,262±5,478. The mortality rate among readmitted patients was 13.2%. Overall, readmissions following AAA repair accounted for a cost >50% over and above the cost of the readmitted patients index hospitalization. Hospital readmissions are common during the 6 months following AAA repair. Patients who are readmitted experience long lengths of stay and high mortality rates, and their care incurs high costs.Dr. Eisenberg is a Physician-Scientist of the Quebec Foundation for Health Research. Dr. Pilote is a Physician-Scientist of the Canadian Institutes for Health Research.     

Elevation of the extracellular glutamate concentration in the hippocampus after total cerebral ischemia related to the deterioration of the recovery in EEG and evoked potentials in dogs

The concentrations of extracellular glutamate (Glu), aspartate (Asp) and glycine (Gly) were measured by microdialysis method in the cortex and hippocampus before, during and after 15min of total cerebral ischemia in dogs. The correlations between the concentrations of amino acids and the changes in EEG and evoked potentials (EP) after ischemia were evaluated. Total cerebral ischemia was achieved by occluding the ascending aorta and the caval veins. The concentrations of Glu in the hippocampus significantly increased from 1.73 ± 0.59 (mean ± SEM) nmol·ml^–1 at pre-ischemia to 5.46 ± 1.34 (P 0.05) during ischemia and 14.37 ± 3.70 (P 0.01) 0–15min after ischemia, and returned to the pre-ischemic level 30min after ischemia. The concentration of hippocampal Glu 0–15min after ischemia had significant negative correlations with the EEG-EP scores (0 = serious deterioration of electrical function and 6 = normal electrical function) 30min, 3hr and 5hr after ischemia (r = –0.69, P 0.05:r = –0.67, P 0.05:r = –0.70, P 0.05, respectively). The increase of the extracellular Glu concentration in the hippocampus immediately after ischemia may aggravate the neurological outcome after total cerebral ischemia.(Ono K, Iwatsuki N, Tajima T, et al.: Elevation of the extracellular glutamate concentration in the hippocampus after total cerebral ischemia related to the deterioration of the recovery in EEG and evoked potentials in dogs. J Anesth 7: 334–340, 1993)     

Wear of ultra-high-molecular-weight polyethylene cup articulating with 22.225 mm zirconia diameter head in cemented total hip arthroplasty

A number of studies have highlighted the increasing incidence of aseptic cup loosening with increasing depth of cup penetration by the metal head. We present our experience with a 22.225mm diameter zirconia head on a 9–10 taper articulating with an ultra-high-molecular-weight polyethylene (UHMWPE) cup in cemented total hip arthroplasties. We prospectively studied the wear of the UHMWPE cup articulating with a 22.225mm diameter zirconia head in cemented total hip arthroplasties. A total of 339 patients (153 men, 186 women, 373 hips) were included. The patients mean age at surgery was 52 years (17–76 years), with 41% age 50 years or younger. Their mean weight was 72.4kg (24–125kg). At a mean follow-up of 4.3 years (0–8 years) the mean penetration rate of the cup was 0.03mm/year (0–0.51mm/year). Altogether, 289 (77.5%) showed no measurable wear, 38 (10.2%) had a penetration rate of 0.11mm/year or less, 33 (8.9%) had a rate of 0.12–0.2mm/year, and in 13 (3.5%) the rate was more than 0.2mm/year. Ceramic–UHMWPE is the next stage in the evolution of total hip arthroplasty for addressing wear and any possible related issues.     

Enhancement of lidocaine-induced epidural anesthesia by deoxyaconitine in the rabbit

Purpose.Aconiti tuber has been used in traditional Oriental medicine to alleviate pain. The antinociceptive property of aconiti tuber is due to the action of its extracted alkaloids such as deoxyaconitine. The purpose of this study was to investigate the effect of epidural deoxyaconitine on epidural lidocaine anesthesia. Methods.Five adult rabbits were used. Three different combinations of drugs were injected into the epidural space, in the following order: first (combination A), 1.5ml of 2% lidocaine; second (combination B), 1.5ml of 2% lidocaine and 150µg deoxyaconitine; and third (combination C), 3mg nor-binaltorphimine followed by 1.5ml of 2% lidocaine and 150µg deoxyaconitine 30min later. The latency of onset and the duration of three end-points (sensory loss in the tail, loss of weight-bearing ability, and flaccid paresis of hind limb) were measured. Results.Onset times for the three end-points were not changed by deoxyaconitine or by nor-binaltorphimine. The duration of sensory loss was 27.0 ± 2.7min, the duration of loss of weight-bearing ability was 33.0 ± 2.7min, and the duration of flaccid paresis was 21.0 ± 4.2min in the combination A group. In the combination B group, deoxyaconitine extended the time of sensory loss by 80%, the time of loss of weight-bearing by 50%, and that of flaccid paresis by 60% compared with the combination A group. In the combination C group, this phenomenon was partially antagonized by pretreatment with nor-binaltorphimine, a -opioid antagonist. Conclusions.Based on our observations, deoxyaconitine enhanced epidural lidocaine anesthesia in the rabbit, and this effect seemed to be partly mediated by -opioid receptors.     

Percutaneous and Open Renal Revascularizations Have Equivalent Long-Term Functional Outcomes

Atherosclerotic renal artery stenosis is a significant cause of poorly controlled hypertension and progressive renal dysfunction leading to ischemic nephropathy and other end-organ damage. The optimal treatment of renovascular disease contributing to hypertension and renal dysfunction is not known. This study compares the anatomic and functional outcomes of both open and endovascular therapy for chronic, symptomatic atherosclerotic renal artery disease. We performed a retrospective analysis of records from patients who underwent renal arterial interventions, endovascular or open bypass, between January 1984 and January 2004. Principal indications for intervention were hypertension (51%), chronic renal insufficiency (13%), and hypertension and elevated creatinine (36%). A total of 247 patients (109 males; mean age 69±10, range 44–89 years) underwent 314 interventions (109 open procedures; 205 angioplasties, 71% with stent placement). There was a significant difference in 30-day mortality (4% vs. <1%; p < 0.005) between the open and endoluminal groups, but not at 1, 3, or 5 years. Patients in the open group had a higher primary patency rate at 5 years (83±5% vs. 76±6%; p=0.03), but patients in the endoluminal group had a higher assisted primary patency rate at 5 years (92±5% vs. 84±5; p=0.03). There was no significant difference between both treatment groups in cumulative freedom from presenting symptom or in freedom from dialysis and renal-related death. Patients who presented with hypertension were more likely to have shown improvement in their blood pressure with endoluminal intervention at 1, 3, and 5 (59±6% endoluminal vs. 83±5% open; p=0.01) years. From these results we conclude that open repair and endoluminal repair of atherosclerotic renal artery stenosis have similar immediate and long-term functional and anatomic outcomes. Patients who present with hypertension may have greater benefit with an endoluminal repair.Presented at the Twenty-ninth Annual Meeting of the Peripheral Vascular Surgery Society, Anaheim, CA, June 4-5, 2004.