Showing papers in "Anesthesiology in 1992"

Postoperative nausea and vomiting. Its etiology, treatment, and prevention.

Abstract: In a recent editorial, Kapur described perioperative nausea and vomiting as "the big 'little problem' following ambulatory surgery."257 Although the actual morbidity associated with nausea is relatively low in health outpatients, it should not be considered an unavoidable part of the perioperative experience. The availability of an emesis basin for every patient in the postanesthesia recovery unit is a reflection of the limited success with the available therapeutic techniques.257 There had been little change in the incidence of postoperative emesis since the introduction of halothane into clinical practice in 1956. However, newer anesthetic drugs (e.g. propofol) appear to have contributed to a recent decline in the incidence of emesis. Factors associated with an increased risk of postoperative emesis include age, gender (menses), obesity, previous history of motion sickness or postoperative vomiting, anxiety, gastroparesis, and type and duration of the surgical procedure (e.g., laparoscopy, strabismus, middle ear procedures). Anesthesiologists have little, if any, control over these surgical factors. However, they do have control over many other factors that influence postoperative emesis (e.g., preanesthetic medication, anesthetic drugs and techniques, and postoperative pain management). Although routine antiemetic prophylaxis is clearly unjustified, patients at high risk for postoperative emesis should receive special considerations with respect to the prophylactic use of antiemetic drugs. Minimally effective doses of antiemetic drugs can be administered to reduce the incidence of sedation and other deleterious side effects. Potent nonopioid analgesics (e.g., ketorolac) can be used to control pain while avoiding some of the opioid-related side effects. Gentle handling in the immediate postoperative period is also essential. If emesis does occur, aggressive intravenous hydration and pain management are important components of the therapeutic regimen, along with antiemetic drugs. If one antiemetic does not appear to be effective, another drug with a different site of action should be considered. With the availability of new antiserotonin drugs, the incidence of recurrent (intractable) emesis could be further decreased. Research into the mechanisms of this common postoperative complication may help in improving the management of emetic sequelae in the future. As suggested in a recent editorial, improvement in antiemetic therapy could have a major impact for surgical patients, particularly after ambulatory surgery. Patients as well as those involved in their postoperative care look forward to a time when the routine offering of an emesis basin after surgery becomes a historical practice.

Effects of intravenous dexmedetomidine in humans. II. Hemodynamic changes.

Abstract: Dexmedetomidine (DMED) is a novel clonidine-like compound known to have sedative, analgesic, and cardiovascular stabilizing qualities. DMED is a more highly selective alpha 2-adrenergic agonist than clonidine. This investigation examined the hemodynamic effects of four selected iv doses in consenting healthy male volunteers. In a randomized, double-blind, placebo-controlled trial subjects received 0 (n = 9), 0.25 (n = 6) 0.5 (n = 6), 1.0 (n = 6), or 2.0 (n = 10) micrograms/kg of DMED by infusion (2 min). ECG, heart rate (HR), arterial blood pressure (MABP), bioimpedance cardiac output (CO), and plasma catecholamines concentrations (CA) were monitored from 90 min before to 360 min after infusion. Plasma DMED concentrations were measured. DMED produced a maximum decrease in MABP at 60 min of 14%, 16%, 23%, and 27% for the 0.25, 0.5, 1.0, and 2.0 micrograms/kg groups, respectively (P < .05). At 330 min MABP remained below baseline by 8% and 17% at the two largest doses (P < .05). Both HR and CO decreased maximally by both 17% at 105 min. The two largest doses produced a transient (peak at 3 min lasting < 11 min) increased in MABP (16 +/- 2.5 and 24 +/- 10 mmHg, respectively; P < .05) with a concomitantly reduced CO (41%, 2 micrograms/kg; P < .05) and HR (22%, 2 micrograms/kg; P < .05), whereas systemic vascular resistance doubled. Even the lowest dose decreased CA immediately to values close to 20 pg/ml for 5 h. A 2-min iv infusion of DMED produced a transient increase in MABP and a longer lasting decrease in MABP and CA. These DMED doses were well tolerated in the healthy volunteers.

Effects of intravenous dexmedetomidine in humans. I. Sedation, ventilation, and metabolic rate.

Abstract: Dexmedetomidine (DMED) is a highly selective centrally acting alpha 2-adrenergic agonist thought to provide significant sedation without appreciable ventilatory effects. This double-blind, placebo-controlled experiment evaluated four dose levels of DMED (0.25, 0.5, 1.0, and 2.0 micrograms/kg intravenously over 2 min) in 37 healthy male volunteers. Measurements of sedation, arterial blood gases, resting ventilation, hypercapnic ventilatory response (HVR), and metabolic rate (O2 consumption and CO2 production) were performed at baseline, 10 min after DMED infusion, and thereafter at the end of each subsequent 45-min period. DMED caused sedation resulting in loss of responsiveness in most of the subjects administered 1.0 and 2.0 micrograms/kg; sedation was evident for 195 min following 2.0 micrograms/kg (P < .05). Ten minutes following infusion of 1.0 and 2.0 micrograms/kg, PaCO2 had increased by 5.0 and 4.2 mmHg, respectively (P < .05), and 60 min following 2.0 micrograms/kg, VE had decreased by 28% (P < .05). The placebo group showed a progressive increase in the HVR slope (50% increase by 330 min following the infusion; P < .05). Overall, across all the DMED doses, the slope was decreased (P < .05) at all times after DMED. The calculated ventilation at a PaCO2 of 55 mmHg was decreased (39%; P < .05) 10 min following 1.0 and 2.0 micrograms/kg, returning to control values by 285 min following 2.0 micrograms/kg. O2 consumption increased 16% (P < .05) at 10 min following 2.0 micrograms/kg; CO2 production decreased (22% at 60 min). By 5 h postinfusion, both had returned to normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Context-sensitive half-time in multicompartment pharmacokinetic models for intravenous anesthetic drugs.

Abstract: Elimination half-life is the pharmacokinetic parameter used most commonly to describe duration of pharmacologic action, including that expected of intravenous anesthetic drugs administered by continuous infusion. Little consideration has been given, however, to the relevance of elimination half-life in describing plasma (central compartment) drug concentrations in the context of relevant infusion durations. Therefore, simulations were performed with multicompartment pharmacokinetic models for six intravenous anesthetic drugs. These models had elimination half-lives ranging from 111 to 577 min. The input in each simulation was an infusion regimen designed to maintain a constant plasma drug concentration for durations ranging from 1 min to 8 h and until steady state. The time required for the plasma drug concentration to decline by 50% after terminating each infusion in each of the models was determined and was designated the "context-sensitive half-time," where "context" refers to infusion duration. The context-sensitive half-times were markedly different from their respective elimination half-lives and ranged from 1 to 306 min. The half-times were explained by posing each pharmacokinetic model in the form of a hydraulic model. These simulations demonstrate that elimination half-life is of no value in characterizing disposition of intravenous anesthetic drugs during dosing periods relevant to anesthesia. We propose that context-sensitive half-times are a useful descriptor of postinfusion central compartment kinetics.

Incidence and risk factors for side effects of spinal anesthesia

Abstract: We prospectively studied 952 patients to identify the incidence of hypotension (systolic blood pressure < 90 mmHg), bradycardia (heart rate < 50 beats/min), nausea, vomiting, and dysrhythmia during spinal anesthesia. Historical, clinical, and physiologic data were correlated with the incidence of th

Preemptive analgesia. Clinical evidence of neuroplasticity contributing to postoperative pain.

Abstract: Recent evidence suggests that surgical incision and other noxious perioperative events may induce prolonged changes in central neural function that later contribute to postoperative pain. The present study tested the hypothesis that patients receiving epidural fentanyl before incision would have less pain and need fewer analgesics post-operatively than patients receiving the same dose of epidural fentanyl after incision. Thirty patients (ASA physical status 2) scheduled for elective thoracic surgery through a posterolateral thoracotomy incision were randomized to one of two groups of equal size and prospectively studied in a double-blind manner. Epidural catheters were placed via the L2-L3 or L3-L4 interspaces preoperatively, and the position was confirmed with lidocaine. Group 1 received epidural fentanyl (4 micrograms/kg, in 20 ml normal saline) before surgical incision, followed by epidural normal saline (20 ml) infused 15 min after incision. Group 2 received epidural normal saline (20 ml) before surgical incision, followed by epidural fentanyl (4 micrograms/kg, in 20 ml normal saline) infused 15 min after incision. No additional analgesics were used before or during the operation. Anesthesia was induced with thiopental (3-5 mg/kg) and maintained with N2O/O2 and isoflurane. Paralysis was achieved with pancuronium (0.1 mg/kg). Postoperative analgesia consisted of patient-controlled intravenous morphine. Visual analogue scale pain scores were significantly less in group 1 (2.6 +/- 0.44) than in group 2 (4.7 +/- 0.58) 6 h after surgery (P less than 0.05), by which time plasma fentanyl concentrations had decreased to subtherapeutic levels (less than 0.15 ng/ml) in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Sympathetic responses to induction of anesthesia in humans with propofol or etomidate.

Abstract: Anesthetic induction with propofol commonly results in hypotension. This study explored potential mechanisms contributing to hypotension by recording cardiovascular responses including sympathetic neural activity from patients during induction of anesthesia with propofol (2.5 mg.kg-1 plus 200 micrograms.kg-1.min-1) or, for comparison, etomidate (0.3 mg.kg-1 plus 15 micrograms.kg-1.min-1). Twenty-five consenting, nonpremedicated, ASA physical status 1 and 2, surgical patients were evaluated. Measurements of R-R intervals (ECG), blood pressure (radial artery), forearm vascular resistance (plethysmography), and efferent muscle sympathetic nerve activity ([MSNA] microneurography: peroneal nerve) were obtained at rest and during induction of anesthesia. In addition, a sequential bolus of nitroprusside (100 micrograms) followed by phenylephrine (150 micrograms) was used to obtain data to quantitate the baroreflex regulation of cardiac function (R-R interval) and sympathetic outflow (MSNA) in the awake and anesthetized states. Etomidate induction preserved MSNA, forearm vascular resistance, and blood pressure, whereas propofol reduced MSNA by 76 +/- 5% (mean +/- SEM), leading to a reduction in forearm vascular resistance and a significant hypotension. Both cardiac and sympathetic baroslopes were maintained with etomidate but were significantly reduced with propofol, especially in response to hypotension. These findings suggest that propofol-induced hypotension is mediated by an inhibition of the sympathetic nervous system and impairment of baroreflex regulatory mechanisms. Etomidate, conversely, maintains hemodynamic stability through preservation of both sympathetic outflow and autonomic reflexes.

Relative Risk Analysis of Factors Associated with Difficult Intubation in Obstetric Anesthesia

Abstract: Difficult tracheal intubation, often unexpected, has been identified as the commonest contributory factor to anesthetic-related maternal death. The ability to predict such cases preoperatively would be of great value. Preoperative airway assessment and potential risk factors for difficult tracheal intubation were recorded in 1,500 patients undergoing emergency and elective cesarean section under general anesthesia. Airway assessment using a modified Mallampati test recorded oropharyngeal structures visible upon maximal mouth opening. Potential risk factors documented were obesity; short neck; missing, protruding, or single maxillary incisors; receding mandible; facial edema; and swollen tongue. Subsequent to induction of anesthesia, the view at laryngoscopy and difficulty at intubation were graded. There was a significant (P less than 0.001) correlation between the oropharyngeal structures seen and both the veiw at laryngoscopy and difficulty at intubation. Univariate analysis demonstrated a significant association between difficult intubation and short neck (P less than 0.001), obesity (P less than 0.0001), missing maxillary incisors (P less than 0.02), protruding maxillary incisors (P less than 0.001), single maxillary incisor (P less than 0.0001), and receding mandible (P less than 0.003). Neither facial edema (P = 0.414) nor swollen tongue (P = 0.141) were found to be associated with difficult intubation. Multivariate analysis removed obesity and missing and single maxillary incisors as risk factors. Obesity was eliminated because of its strong association with short neck. The probability of experiencing a difficult intubation for various combinations of risk factors was determined.(ABSTRACT TRUNCATED AT 250 WORDS)

A Hypnotic Response to Dexmedetomidine, an α2 Agonist, Is Mediated in the Locus Coerüleus in Rats

Abstract: Dexmedetomidine, the highly selective alpha 2-adrenergic agonist, produces a dose-dependent hypnotic response in rats through a central mechanism. Because the locus coeruleus (LC) contains pathways involved in the maintenance of vigilance and a high prevalence of alpha 2 adrenoceptors, we investigated the role of this brainstem nucleus in the hypnotic response to dexmedetomidine. The experimental model consisted of chronic, stereotactically cannulated rats (n = 157) in which the hypnotic response to dexmedetomidine was assessed by the duration of the loss of their righting reflex. Correct placement of the cannula was confirmed histologically at necropsy. The hypnotic response to dexmedetomidine 0.3-333.3 micrograms administered into the LC increased in a dose-dependent fashion. Dexmedetomidine 6.6 micrograms injected 2 mm lateral to the LC did not cause the animals to lose their righting response. Atipamezole 0.07 micrograms-12 micrograms, a selective alpha 2-adrenergic antagonist, blocked the hypnotic response to dexmedetomidine 6.6 micrograms when both were administered into the LC. Also, atipamezole 0.7-30 micrograms, administered into the LC, blocked in a dose-dependent manner the hypnotic response to intraperitoneal (ip) dexmedetomidine 50 micrograms.kg-1. Atipamezole injected into the LC did not block the hypnotic response to pentobarbital 40 mg.kg-1 ip. Prazosin, an alpha 1-adrenergic antagonist, 4.2 micrograms into the LC or 1.0 mg.kg-1 ip, did not alter the hypnotic response to dexmedetomidine 6.6 micrograms into the LC. The present data suggest that alpha 2-adrenergic receptors in the LC appear to be a major site for the hypnotic action of dexmedetomidine.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of the antinociceptive effects of pre- and posttreatment with intrathecal morphine and MK801, an NMDA antagonist, on the formalin test in the rat.

Abstract: Current thinking emphasizes that protracted small afferent input can evoke mechanisms that mediate a significant potentiation of spinal nociceptive processing and that this facilitory component has a unique pharmacology. To investigate the behavioral parallels of this spinal facilitation, we evaluated the effects of pre- and post-treatment of intrathecal morphine (mu agonist) and MK801 (N-methyl-D-aspartate [NMDA] antagonist) on the formalin test. Intraplantar formalin resulted in a biphasic appearance of flinching behavior (phase 1 = 0-5 min; phase 2 = 10-60 min). Morphine and MK801 were administered intrathecally 15 min before formalin injection in the pretreatment study and 9 min after formalin injection in the posttreatment study. Pretreatment with intrathecal morphine produced comparable dose-dependent suppressions of the phase 1 and phase 2 behaviors (ED50 = 0.5 micrograms [95% CI = 0.3-0.9] and 0.3 micrograms [95% CI = 0.1-0.7], respectively). Posttreatment with morphine also resulted in comparable suppression of the phase 2 response (ED50 = 0.2 micrograms [95% CI = 0.1-0.3]). At the highest dose of intrathecal morphine (10 micrograms), an almost complete suppression of formalin-evoked behavior was observed. Pretreatment with MK801 inhibited the second-phase response more strongly than the first-phase response (ED50 = 1.6 micrograms [95% CI = 0.5-5.7] vs. 0.1 microgram [95% CI = 0.3 - 0.4], respectively). In contrast, posttreatment with the highest dose of MK801 had no effect on the phase 2 response.(ABSTRACT TRUNCATED AT 250 WORDS)

Postoperative myocardial ischemia. Therapeutic trials using intensive analgesia following surgery. The Study of Perioperative Ischemia (SPI) Research Group.

Abstract: Recent data suggest that postbypass and postoperative myocardial ischemia are related to adverse cardiac outcome following myocardial revascularization. Therapeutic trials to suppress postoperative ischemia are warranted. Because anesthetics can suppress a variety of physiologic responses to stress as well as myocardial ischemia intraoperatively, we examined whether use of intensive analgesia in the stressful postoperative period could decrease postoperative ischemia. In 106 patients undergoing elective myocardial revascularization, we standardized the anesthetic prior to bypass (sufentanil 5-10 micrograms/kg [induction] and 4.2-6.0 micrograms.kg-1.h-1 [infusion] supplemented with up to 0.5 mg/kg of diazepam). During bypass, patients were randomly assigned to receive either morphine sulfate (group M, n = 54, up to 2 mg/kg) or sufentanil (group S, n = 52, 1 microgram/kg and 1 microgram.kg-1.h-1). In the intensive care unit (ICU), group M received low-dose analgesia (morphine sulfate 1-10 mg intravenously every 30 min, average dose = 2.2 +/- 2.1 mg/h), while group S continued to receive intensive analgesia (infusion of sufentanil at 1 microgram.kg-1.h-1). Both groups received supplemental midazolam in the ICU (group M = 1.1 +/- 1.1 mg/h; group S = 0.6 +/- 0.6 mg/h; P = 0.01). All analgesic and sedative-hypnotic medications were discontinued at 18 hours following myocardial revascularization. Using continuous two-channel electrocardiographic (ECG) monitoring (CC5 and CM5), we documented and characterized ECG changes consistent with ischemia during the preoperative, intraoperative (pre- and postbypass), and postoperative (on- and off-treatment) periods. The total ECG monitoring time was 8,486 h, averaging 81 h per patient. During the prebypass (anesthetic control) period, groups M and S had a similar incidence, but group S episodes were more severe: maximum ST-segment change (median), S versus M: -1.8 mm versus -1.4 mm (P = 0.04). During the postbypass period, both groups had a similar incidence of ischemia, but episodes in group S were less severe: maximum ST-segment change, S versus M: -1.8 mm versus -2.7 mm (P = 0.0005). During the ICU-on-therapy period, the incidence of ischemic episodes was less in group S patients, and the severity was less: area-under-the-ST-time curve, S versus M: -21 mm.min versus -161 mm.min (P = 0.05). After discontinuation of the drug regimen in the ICU, the incidence and severity of ischemic episodes was similar. The incidence of hypotension, hypertension, and tachycardia was similar in both groups in both the intraoperative and ICU periods.(ABSTRACT TRUNCATED AT 400 WORDS)

Up-and-down regulation of skeletal muscle acetylcholine receptors. Effects on neuromuscular blockers.

Abstract: Multiple factors alter the interaction of muscle relaxants with the NMJ. This review has focused on the aberrant responses caused principally by alterations in AChRs (table 1). Many pathologic states increase (up-regulate) AChR number. These include upper and lower motor neuron lesions, muscle trauma, burns, and immobilization. Pre- or postjunctional inhibition of neurotransmission by drugs or toxins also up-regulate AChRs. These include alpha- and beta-BT, NDMR, anticonvulsants, and clostridial toxins. We speculate that other bacterial toxins also up-regulate AChR. With proliferation of AChRs, agonist drug dose-response curves are shifted to the left. The exaggerated release of potassium when depolarization occurs with the use of agonists such as SCh and decamethonium can be attributed to the increased number of AChR. Thus, SCh should be avoided in patients who are in the susceptible phase (see section V). In the presence of increased AChR, the requirement for NDMR is markedly increased. Thus, the response to NDMR may be used as an indirect estimator of increased sensitivity to SCh (table 1). The most extensively studied pathologic state in which there is a decrease in AChRs is myasthenia gravis; there is immunologically mediated destruction and/or functional blockade of AChRs. The pathophysiologic and pharmacologic changes in LEMS are quite distinct from those of myasthenia gravis. Decreased AChRs in myasthenia gravis result in resistance to agonists and increased sensitivity to competitive antagonists. In conditioning exercise, the perturbed muscles show sensitivity to NDMR that may be due to decreased AChRs. Chronic elevations of ACh observed with organophosphorus poisoning or chronic use of reversible cholinesterase inhibitors results in down-regulation of AChRs. In this condition, SCh should be avoided because its metabolic breakdown would be impaired; the requirement for NDMR may be decreased. All of the varied responses to SCh and NDMR, which are associated with concomitant changes in AChRs, are analogous to drug-receptor interactions observed in other biologic systems.

Multicenter Study of General Anesthesia III. Predictors of Severe Perioperative Adverse Outcomes

Abstract: Little information is available about the incidence of severe adverse outcomes, and even less information is available about the identification and quantification of independent predictors of severe perioperative adverse outcomes. The purpose of this study was to identify and quantitate independent predictors of severe perioperative adverse outcomes in a prospective randomized clinical trial of general anesthesia in 17,201 patients. Twenty-nine prognostic variables for 15 severe outcomes in 847 patients were tested by multiple stepwise logistic regressions from which 20 significant (P less than 0.05) predictors were identified. A history of cardiac failure or myocardial infarction less than or equal to 1 yr; ASA physical status 3 or 4; age greater than 50 yr; cardiovascular, thoracic, abdominal or neurologic surgery; and the study anesthetics were significant predictors of "any severe outcome, including death." There were 17 significant predictors for 10 severe cardiovascular outcomes in 608 patients, including a history of ventricular arrhythmia, hypertension, cardiac failure, myocardial ischemia, myocardial infarction less than or equal to 1 yr or myocardial infarction greater than 1 yr, and smoking; ASA physical status; age; cardiovascular, thoracic, abdominal, eyes-ears-nose-throat/endocrine, neurologic, musculoskeletal, or gynecologic surgery; and the study anesthetics. There were 9 significant predictors for 4 severe respiratory outcomes in 163 patients, including a history of cardiac failure, myocardial ischemia, or chronic obstructive pulmonary disease; obesity; smoking; male gender; ASA physical status; abdominal surgery; and the study anesthetics. Colinearity between related prognostic variables (such as disease and ASA physical status) was assessed using progressively segregated groups of variables in eight stepwise logistic regressions. We conclude that the comprehensive stepwise logistic regression of 29 prognostic variables reported here provides a valid estimate of the risks of severe perioperative outcomes associated with general anesthesia.

Intraarticular morphine, bupivacaine, and morphine/ bupivacaine for pain control after knee videoarthroscopy

Abstract: Evidence has accumulated that opioids can produce potent antinociceptive effects by interacting with opioid receptors in peripheral tissues. This study sought to compare the effects of morphine with those of bupivacaine administered intraarticularly upon pain following arthroscopic knee surgery. In a double-blind, randomized manner, 33 patients received either morphine (1 mg in 20 ml NaCl; n = 11), bupivacaine (20 ml, 0.25%; n = 11), or a combination of the two (n = 11) intraarticularly at the completion of surgery. After 1, 2, 3, and 4 h and at the end of the 1st and 2nd postoperative days, pain was assessed by a visual analogue scale, and supplemental analgesic requirements were recorded. Pain scores were significantly greater in the morphine group than in the other two groups at 1 h. There were no significant differences at 2 and 3 h. From 4 h until the end of the study period, pain scores were significantly greater in the bupivacaine group than in the other two groups. Analgesic requirements were significantly greater in the morphine group than in the other groups at 1 h but were significantly greater in the bupivacaine group than in the other groups throughout the remainder of the study period. We conclude that intraarticular morphine produces an analgesic effect of delayed onset but of remarkably long duration. The combination of these two drugs results in satisfactory analgesia throughout the entire observation period.

Responses of plasma adrenocorticotropic hormone, cortisol, and cytokines during and after upper abdominal surgery.

Abstract: There is currently accumulating evidence for bidirectional communication between the neuroendocrine and immune systems. Various cytokines have been suggested to be involved in the stimulation of stress hormone secretion during the times of infection and inflammation. To assess the possible involvement and pathophysiologic significance of cytokines in the mechanisms responsible for the perioperative stress response of the hypothalamo-pituitary-adrenal axis, we observed the changes of plasma adrenocorticotropic hormone and cortisol levels together with those of plasma endotoxin and cytokine levels. In patients undergoing pancreatoduodenectomy, perioperative stimulation of adrenocorticotropic hormone and cortisol secretion was accompanied by a significant elevation of plasma cytokine levels. Application of epidural block up to the upper thoracic levels failed to suppress this stress response effectively. In patients undergoing unilateral total hip replacement, the response of plasma hormone levels was smaller and briefer with no significant increase of plasma cytokine levels. Application of epidural block up to the lower thoracic levels suppressed this hormonal response almost completely. In patients undergoing pancreatoduodenectomy, a significant elevation of plasma endotoxin level was followed by a gradual but significant elevation of plasma tumor necrosis factor alpha and interleukin-6 levels. It seems likely that the stimulatory effects of these cytokines on the secretion of adrenocorticotropic hormone and cortisol might be involved in the development of the greater and more prolonged stress response of hypothalamo-pituitary-adrenal axis. Our present study suggests that not only neural input from the surgical wound but also stimulation of cytokine production were responsible for the development of the stress response of the hypothalamo-pituitary-adrenal axis during and after upper abdominal surgery.(ABSTRACT TRUNCATED AT 250 WORDS)

Epidural versus general anesthesia, ambient operating room temperature, and patient age as predictors of inadvertent hypothermia.

Abstract: To elucidate the multifactorial nature of perioperative changes in body temperature, the influence of several clinical variables, including anesthetic technique, ambient operating room temperature, and age, were evaluated. Perioperative oral sublingual temperatures were measured in 97 patients undergoing lower extremity vascular surgery randomized to receive either general (GA) or epidural (EA) anesthesia. Surgery and anesthesia were performed in operating rooms (OR) with a relatively warm mean ambient temperature (24.5 +/- 0.4 degrees C) (GA, n = 30; EA, n = 33) or relatively cold mean ambient temperature (21.3 +/- 0.3 degrees C) (GA, n = 21; EA, n = 13). Patients were 35-94 yr old, with a mean age of 64.5 +/- 1.1 yr. A regression analysis was performed to determine the variables that correlated with intraoperative decrease in temperature and postoperative rewarming rate. The major correlates of greater intraoperative decrease in temperature were 1) GA (P = 0.003); 2) cold ambient OR temperature (P = 0.07); and 3) advancing patient age (P = 0.03). There was significant interaction between ambient OR temperature and type of anesthesia (P = 0.03): there was a greater intraoperative decrease in temperature with GA compared to EA in a cold OR but a similar decrease with GA and EA in a warm OR. The data also suggest an interaction between type of anesthesia and patient age (P = 0.06), showing a greater decrease in temperature with GA compared to EA in the younger patients, but a similar decrease between GA and EA in older patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Three posterior percutaneous celiac plexus block techniques. A prospective, randomized study in 61 patients with pancreatic cancer pain.

Abstract: Variations and refinements of the classic retrocrural technique of neurolytic celiac plexus block (NCPB) for pancreatic cancer pain (PCP) have been proposed over the last 30 yr to improve success rates, avoid complications and enhance diagnostic accuracy. The aim of this prospective, randomized study was to assess the efficacy and morbidity of three posterior percutaneous NCPB techniques in 61 patients with PCP. The 61 patients were randomly allocated to three NCPB treatment groups: group 1 (20 patients, transaortic plexus block); group 2 (20 patients, classic retrocrural block); and group 3 (21 patients, bilateral chemical splanchnicectomy). The quality and quantity of pain were analyzed before and after NCPB. No statistically significant differences (P greater than 0.05) were found among the three techniques in terms of either immediate or up-to-death results. Operative mortality was nil with the three techniques and morbidity negligible. NCPB abolished celiac PCP in 70-80% of patients immediately after the block and in 60-75% until death. Because celiac pain was only a component of PCP in all patients, especially in those with a longer time course until death: 1) abolition of such pain did not ensure high percentages of complete pain relief (immediate pain relief in 40-52%; pain relief until death in 10-24%); 2) NCPB was effective in controlling PCP in a higher percentage of cases if performed early after pain onset, when the pain was still only or mainly of celiac type and responded well to nonsteroidal antiinflammatory drug therapy; and 3) the probability of patients remaining completely pain-free diminished with increased survival time.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of isoflurane and nitrous oxide in subanesthetic concentrations on memory and responsiveness in volunteers.

Abstract: Awareness, defined as conscious memory during anesthesia, has been a problem in anesthesia practice. To determine the effect of isoflurane and nitrous oxide (N2O) on memory, 17 healthy adult volunteers were randomly assigned to receive isoflurane or N2O and received the alternate agent 1–2 weeks lat

The Effects of Sevoflurane, Halothane, Enflurane, and Isoflurane on Hepatic Blood Flow and Oxygenation in Chronically Instrumented Greyhound Dogs

Abstract: Inhalational anesthetics produce differential effects on hepatic blood flow and oxygenation that may impact hepatocellular function and drug clearance. In this investigation, the effects of sevoflurane on hepatic blood flow and oxygenation were compared with those of enflurane, halothane, and isoflurane in ten chronically instrumented greyhound dogs. Each dog randomly received enflurane, halothane, isoflurane, and sevoflurane, each at 1.0, 1.5, and 2.0 MAC concentrations. Mean arterial blood pressure and cardiac output decreased in a dose-dependent fashion during all four anesthetics studied. Heart rate increased compared to control during enflurane, isoflurane, and sevoflurane anesthesia and did not change during halothane anesthesia. Hepatic arterial blood flow and portal venous blood flow were measured by chronically implanted electromagnetic flow probes. Hepatic O2 delivery and consumption were calculated after hepatic arterial, portal venous, and hepatic venous blood gas analysis. Hepatic arterial blood flow was maintained with sevoflurane and isoflurane. Halothane and enflurane reduced hepatic arterial blood flow during all anesthetic levels compared to control (P less than 0.05), with marked reductions occurring with 1.5 and 2.0 MAC halothane concomitant with an increase in hepatic arterial vascular resistance. Portal venous blood flow was reduced with isoflurane and sevoflurane at 1.5 and 2.0 MAC. A somewhat greater reduction in portal venous blood flow occurred during 2.0 MAC sevoflurane (P less than 0.05 compared to control and 1.0 MAC values for sevoflurane). Enflurane reduced portal venous blood flow at 1.0, 1.5, and 2.0 MAC compared to control. Halothane produced the greatest reduction in portal venous blood flow (P less than 0.05 compared to sevoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)

Reaction of sevoflurane and its degradation products with soda lime. Toxicity of the byproducts.

Abstract: Sevoflurane previously has been reported to undergo extensive degradation in the presence of soda lime. To more completely characterize the extent and significnce of this reaction, we studied degradation of sevoflurane with and without soda lime, as well as the toxicity and mutagenicity of the degradation products. Two degradation products detected were CF2 = C(CF3)OCH2F (compound A) and CH3OCF2CH(CF3)OCH2F (compound B). During circulation of 1%, 2%, and 3% sevoflurance in a closed anesthesia circuit for 8 h, peak concentrations of compound A were 13.3 +/- 0.27, 30.2 +/- 0.10, and 42.1 +/- 1.07 ppm at 2 h, respectively. The concentrations of compound B did not exceed 2 ppm. The temperature of the soda lime was 43.3 +/- 2.8 degrees C at 1 h and increased gradually to 47.9 +/- 1.5 degrees C after 8 h. In closed flasks with soda lime, the magnitude of the decrease in sevoflurance concentrations (3%) and of the increase in compound A concentrations was temperature dependent. The peak concentrations of compound A at 23 degrees C, 37 degrees C, and 54 degrees C were 32.8 +/- 6.8 at 2 h, 46.6 +/- 1.0 at 0.5 h, and 78.5 +/- 2.3 ppm at 0.5 h, respectively. The LC50 (50% lethal concentration) of compound A in Wistar rats was 1,090 ppm in males and 1,050 ppm in females exposed for 1 h. The LC50 was 420 ppm in males and 400 ppm in females exposed for 3 h. The chronic toxicity of compound A in Wistar rats was studied by exposing rats 24 times, for 3 h each, to initial concentrations of 30, 60, or 120 ppm in a ventilated chamber. At all concentrations, there were no apparent effects other than a loss of body weight in females (120 ppm) on the final day (P < 0.01). Compound A did not induce mutation on the reverse (Ames) test at less than 2,500 micrograms/dish (culture medium 2.7 ml) with activation by S-9 mixture, and below 1,250 micrograms/dish (culture medium 2.7 ml) without activation, in four strains of S. typhimurium and in 1 strain of E. coli. Exposure of fibroblasts to 7,500 ppm of compound A for 1 h, compound A did not induce structural change. In a study of acute toxicity of compound B, there was no toxicity in Wistar rats after 3 h of exposure at 2,400 ppm. The reverse (Ames) test for compound B was negative at 625-1,250 micrograms/dish.(ABSTRACT TRUNCATED AT 400 WORDS)

Inhaled nitric oxide after mitral valve replacement in patients with chronic pulmonary artery hypertension.

Abstract: Patients with mitral valve disease can develop pulmonary artery hypertension that persists after mitral valve replacement. In 1987, nitric oxide (NO) was reported to be an important factor accounting for the biologic activity of endothelium-derived relaxing factor. Inhaled NO was subsequently report

Stress hormone response during and after cardiopulmonary resuscitation

Abstract: The purpose of this study was to assess whether plasma adrenocorticotropin, cortisol, vasopressin, and renin concentrations are higher in resuscitated than in nonresuscitated patients during cardiopulmonary resuscitation, and whether there are possible correlations between these hormones and blood pressure or heart rate in the immediate postresuscitation phase. Of 34 consecutive patients (36-85 yr of age) with out-of-hospital cardiac arrest, 20 could be successfully resuscitated and admitted to hospital, whereas in the remaining 14 patients restoration of spontaneous circulation could not be achieved. During cardiopulmonary resuscitation, median adrenocorticotropin, cortisol, vasopressin, and renin concentrations in the external jugular vein were 237 pg/ml, 32.6 micrograms/dl, 122 pg/ml, and 46.5 ng/l, respectively, in resuscitated patients, and 45 pg/ml (P = 0.018), 18.4 micrograms/dl (P = 0.481), 88 pg/ml (P = 0.049), and 11 ng/l (P = 0.017), respectively, in nonresuscitated patients. Median adrenocorticotropin, cortisol, vasopressin, and renin concentrations were 101 pg/ml, 34.6 micrograms/dl, 22 pg/ml, and 25 ng/l, respectively, 60 min after successful resuscitation. No significant correlations were found between hormone levels and blood pressure or heart rate, but there was a significant negative correlation between the interval from collapse to the start of cardiopulmonary resuscitation and plasma cortisol concentrations during cardiopulmonary resuscitation (Spearman rank correlation coefficient = -0.967, P less than 0.001), indicating an impaired cortisol release from the adrenal cortex. The lower hormone concentrations of the nonresuscitated patients measured during cardiopulmonary resuscitation might indicate an impairment in neuroendocrine response.

A randomized comparison of intravenous versus lumbar and thoracic epidural fentanyl for analgesia after thoracotomy.

Abstract: Administration of large doses of fentanyl is a popular method to provide postoperative analgesia after thoracotomy. It is however unclear whether epidural lumbar (L) or epidural thoracic (T) administration of fentanyl confers any major advantage over intravenous (iv) infusion. Using a randomized prospective study design, we compared the potential benefits of L, T, and iv fentanyl administration after thoracotomy in 50 patients. Epidural catheters were not injected during surgery. Postoperatively a fentanyl infusion (5 micrograms/ml) was started at 1 microgram.kg-1.h-1 after a bolus of 1 microgram/kg and adjusted to maintain a score < or = 30/100 at rest using a visual analog scale (VAS) for pain. Data were prospectively collected before surgery, at fixed intervals during the 48 h of fentanyl infusions, and the day of discharge. There was no difference between the groups in overall quality of analgesia at rest and after coughing, quantity of fentanyl delivered (L = 1.15 +/- 0.38, T = 1.22 +/- 0.23, iv = 1.27 +/- 0.3 micrograms.kg-1.h-1), incidence of pruritus needing treatment (L = 2, T = 1, iv = 0 patients), need to decrease fentanyl infusion rate because of side effects (L = 2, T = 2, iv = 4 patients), importance of pulmonary infiltrates, or arterial blood gas values. One patient (L group) needed naloxone (0.04 mg iv). Intravenous patients were more frequently nauseated (P = .009) and needed boluses of fentanyl more often (L = 3 +/- 9, iv = 6 +/- 12, T = 4 +/- 8; P = .04).(ABSTRACT TRUNCATED AT 250 WORDS)

Prevalence of Latex Sensitization among Hospital Physicians Occupationally Exposed to Latex Gloves

Abstract: Patients undergoing surgery who have a history of occupational exposure to latex gloves may be predisposed to intraoperative anaphylaxis caused by latex allergy. Thus, medical personnel who routinely wear latex gloves may be at higher risk than the general population. The prevalence of latex sensiti

Prevention of Intraoperative Hypothermia by Preoperative Skin-Surface Warming

Abstract: Background:Intraoperative hypothermia initially results from internal redistribution of heat facilitated by anesthesia-induced vasodilatlon. Preinductlon skin-surface warming minimizes postinduction hypothermia in anesthetized volunteers. However, its efficacy might be reduced in surgical situations

Oral ketamine preanesthetic medication in children.

Abstract: The authors sought to define a dose of oral ketamine that would facilitate induction of anesthesia without causing significant side effects. Forty-five children (ASA Physical Status 1 and 2; aged 1-7 yr) were assigned randomly in a prospective, double-blind fashion to three separate groups that received either 3 mg/kg, 6 mg/kg, or no ketamine mixed in 0.2 ml/kg cola-flavored soft drink. They also were evaluated preoperatively and postoperatively for acceptance of oral ketamine as a premedicant, reaction to separation from parents, emotional state, and emergence phenomena. The authors detected no episodes of respiratory depression, tachycardia, or arterial hemoglobin desaturation before, during, or after surgery. The 6 mg/kg dose was well accepted; provided uniform, predictable sedation within 20-25 min; and allowed calm separation from parents and good induction conditions. The 3 mg/kg dose did not always cause sedation and calm separation from parents. Neither dose of ketamine increased the incidence of laryngospasm, prolonged recovery times, or caused emergence phenomena. The authors conclude that an oral dose of 6 mg/kg ketamine is easily administered and well accepted in young children and provides predictable, satisfactory premedication without significant side effects.