Anesthesia and analgesia
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Anesthesia and analgesia · Nov 1997
Is epidural anesthesia in labor associated with chronic low back pain? A prospective cohort study.
The association between epidural anesthesia during labor and subsequent postpartum low back pain remains unclear. The objective of this follow-up cohort study was to determine whether epidural anesthesia was associated with chronic back pain 1 yr after delivery. We contacted 329 women by telephone and asked them to complete a standardized questionnaire 1 yr (+/-1 mo) after delivery. One hundred sixty-four women had received epidural analgesia for labor and delivery, and 165 had not. Subjects were asked to quantify their back pain (yes/no, numeric rating score, and interference with daily activities). Differences between the two groups were tested by using the chi2 test and the Mann-Whitney U-test, and logistic regression was used to control for confounding variables. The response rate was 244 of 329 (74%). Responders and nonresponders were similar in their demographic and clinical characteristics. There was no difference in the prevalence of back pain between women who had received epidural anesthesia (12 of 121, 10%) and those who had not (17 of 123, 14%). The adjusted relative risk of low back pain at 1 yr (epidural versus nonepidural) was 0.63 (95% confidence interval 0.25, 1.56). There were also no differences between the two groups on numeric rating scores or level of interference with activities. This prospective follow-up study demonstrated no association between epidural anesthesia for labor and delivery and chronic back pain 1 yr after delivery. ⋯ We evaluated the presence of low back pain 1 yr after delivery in two groups of women-those who chose epidural analgesia for labor and those who did not. There was no increased risk of back pain in women who had used epidural analgesia. This finding is consistent with those of other North American studies.
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Anesthesia and analgesia · Nov 1997
Comparative StudyDose-related biochemical markers of renal injury after sevoflurane versus desflurane anesthesia in volunteers.
Sevoflurane (CH2F-O-CH[CF3]2) reacts with carbon dioxide absorbents to produce Compound A (CH2F-O-C[=CF2][CF3]). Because of concern about the potential nephrotoxicity of Compound A, the United States package label (but not that of several other countries) for sevoflurane recommends the use of fresh gas flow rates of 2 L/min or more. We previously demonstrated in humans that a 2-L/min flow rate delivery of 1.25 minimum alveolar anesthetic concentration (MAC) sevoflurane for 8 h can injure glomeruli (i.e., produce albuminuria) and proximal tubules (i.e., produce glucosuria and urinary excretion of alpha-glutathione-S-transferase [alpha-GST]). The present report extends this investigation to fasting volunteers given 4 h (n = 9) or 2 h (n = 7) of 1.25 MAC sevoflurane versus desflurane at 2 L/min via a standard circle absorber anesthetic system (all subjects given both anesthetics). Markers of renal injury (urinary creatinine, albumin, glucose, alpha-GST, and blood urea nitrogen) did not reveal significant injury after anesthesia with desflurane. Sevoflurane degradation with a 2-L/min fresh gas inflow rate produced average inspired concentrations of Compound A of 40 +/- 4 ppm (mean +/- SD, 8-h exposure [data from previous study]), 42 +/- 2 ppm (4 h), and 40 +/- 5 ppm (2 h). Relative to desflurane, sevoflurane given for 4 h caused statistically significant transient injury to glomeruli (slightly increased urinary albumin and serum creatinine) and to proximal tubules (increased urinary alpha-GST). Other measures of injury did not differ significantly between anesthetics. Neither anesthetic given for 2 h at 1.25 MAC produced injury. We conclude that 1.25 MAC sevoflurane plus Compound A produces dose-related glomerular and tubular injury with a threshold between 80 and 168 ppm/h of exposure to Compound A. This threshold for renal injury in normal humans approximates that found previously in normal rats. ⋯ Human (and rat) kidneys are injured by a reactive compound (Compound A) produced by degradation of the clinical inhaled anesthetic, sevoflurane. Injury increases with increasing duration of exposure to a given concentration of Compound A. The response to Compound A has several implications, as discussed in the article.
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Anesthesia and analgesia · Nov 1997
Clinical TrialAcute normovolemic hemodilution can replace preoperative autologous blood donation as a standard of care for autologous blood procurement in radical prostatectomy.
Predonation of autologous blood (PAD) is a standard of care for patients undergoing radical prostatectomy, but recent studies have shown that PAD is not cost-effective. Acute normovolemic hemodilution (ANH) is an alternative autologous blood procurement technique that is much less costly than PAD. We compared the efficacy and costs of ANH alone to ANH combined with PAD. Two hundred-fifty patients who predonated fewer than 3 units of autologous blood before radical prostatectomy underwent ANH to a target hematocrit of 28%. Perioperative hematocrit levels, transfusion outcomes and costs, and postoperative outcomes were compared for patients who predonated 0, 1, or 2 units of blood before surgery. A computer model was used to estimate the savings in red blood cells (RBC) associated with each autologous intervention. ANH alone resulted in a 21% allogeneic transfusion rate and contributed a mean net savings of 112 mL RBC in blood conservation (equivalent to 0.6 unit of blood). The addition of 1 or 2 units of PAD reduced allogeneic exposure rates to 6% or 0%, respectively. Overall, patients who predonated blood had a mean net loss of 198 mL of RBC (equivalent to 1 blood unit), due to both an absence in compensatory erythropoiesis and to the wastage of 60% of the blood units donated. Patients who underwent ANH alone had a 60% reduction in mean total transfusion costs ($103 +/- $102) compared with patients who predeposited 2 units of autologous blood in addition to ANH ($269 +/- $11, P < 0.05). We conclude that ANH can replace PAD as an autologous blood option because it is less costly and equally effective. A combination of ANH and PAD can further decrease allogeneic blood exposure, but it increases transfusion costs and wastage. ⋯ A patient's own blood can be obtained for use in surgery by predonation or acute normovolemic hemodilution on the day of surgery. Both blood collection techniques decrease the need for blood bank transfusions, but acute normovolemic hemodilution is less expensive and more convenient for patients.
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Anesthesia and analgesia · Nov 1997
Risk factors for neurologic deterioration after revascularization surgery in patients with moyamoya disease.
To investigate the risk factors for postoperative neurological deterioration in patients with moyamoya disease, we retrospectively reviewed the perioperative course of 368 cases of revascularization surgery in 216 patients with this disease. Risk factors anecdotally associated with postoperative ischemic events were analyzed by comparing groups with or without a history of such events on the operative day. Ischemic events were noted in 14 cases (3.8%), 4 of which were defined as strokes and the others as transient ischemic attack (TIA). Postoperative neurological deterioration more often developed in patients who suffered from frequent TIAs, had precipitating factors for TIA, and underwent indirect nonanastomotic revascularization. The authors conclude that the incidence of postoperative ischemic events were related more to the severity of moyamoya disease and the type of surgical procedure than to other factors, including anesthetic management. ⋯ Although preventing stroke is the major concern for patients with moyamoya disease, risk factors for perioperative cerebral ischemia have not been clarified. We retrospectively analyzed the perioperative course in 368 cases with this disease and found that the severity of the disease and type of surgical procedure were major determinants of postoperative cerebral ischemia.
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Anesthesia and analgesia · Nov 1997
Clinical TrialPostoperative pharmacokinetics and sympatholytic effects of dexmedetomidine.
Dexmedetomidine is a selective alpha2-adrenoceptor agonist with centrally mediated sympatholytic, sedative, and analgesic effects. This study evaluated: 1) pharmacokinetics of dexmedetomidine in plasma and cerebrospinal fluid (CSF) in surgical patients; 2) precision of a computer-controlled infusion protocol (CCIP) for dexmedetomidine during the immediate postoperative period; and 3) dexmedetomidine's sympatholytic effects during that period. Dexmedetomidine was infused postoperatively by CCIP for 60 min to eight women, targeting a plasma concentration (Cp) of 600 pg/mL. Before, during, and after infusion, blood was sampled to determine plasma concentrations of norepinephrine, epinephrine, and dexmedetomidine, and CSF was sampled to determine dexmedetomidine concentrations (C[CSF]). Heart rate and arterial blood pressure were measured continuously from 5 min before until 3 h after the end of infusion. During the infusion, Cp values generally exceeded the target value: median percent error averaged 21% and ranged from -2% to 74%; median absolute percent error averaged 23% and ranged from 4% to 74%. After infusion, C(CSF) was 4% +/- 1% of Cp. Because C(CSF) barely exceeded the assay's limit of quantitation, CSF pharmacokinetics were not determined. During the infusion, norepinephrine decreased from 2.1 +/- 0.8 to 0.7 +/- 0.3 nmol/L; epinephrine decreased from 0.7 +/- 0.5 to 0.2 +/- 0.2 nmol/L; heart rate decreased from 76 +/- 15 to 64 +/- 11 bpm; and systolic blood pressure decreased from 158 +/- 23 to 140 +/- 23 mm Hg. We conclude that infusion of dexmedetomidine by CCIP using published pharmacokinetic parameters overshoots target dexmedetomidine concentrations during the early postoperative period. Hemodynamic and catecholamine results suggest that dexmedetomidine attenuates sympathetic activity during the immediate postoperative period. ⋯ We studied the pharmacokinetic and sympatholytic effects of dexmedetomidine during the immediate postoperative period and found that during this period, the published pharmacokinetic data slightly overshoot target plasma dexmedetomidine concentrations. We also found that heart rate, blood pressure, and plasma catecholamine concentrations decrease during dexmedetomidine infusion.