Anesthesia and analgesia
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Anesthesia and analgesia · Feb 2002
Randomized Controlled Trial Clinical TrialThe effect of nitrous oxide on jugular bulb oxygen saturation during remifentanil plus target-controlled infusion propofol or sevoflurane in patients with brain tumors.
During propofol/fentanyl anesthesia, a large percentage of patients have jugular bulb oxygen saturation (SjO(2)) <50%. The incidence is less with isoflurane/N(2)O. We evaluated the effect of N(2)O on SjO(2) during remifentanil-based anesthesia with concurrent propofol or sevoflurane in 20 adults undergoing brain tumor surgery. Anesthesia was randomized: Group 1 (n = 10), target-controlled infusion propofol; and Group 2 (n = 10), thiopental 2-3 mg/kg followed by sevoflurane 0.9% end-tidal. Jugular bulb and arterial blood samples for gas analysis were withdrawn during the administration of oxygen 33% with nitrogen 67% and then with N(2)O 67%. All samples were drawn before surgery and 20 min after the addition of the study gas and with an ETCO(2) 26-28 mm Hg and mean arterial pressure >90 mm Hg. Both groups had similar demographic and physiologic data. In the Propofol group, SjO(2) was 50% +/- 10% with nitrogen and 52% +/- 9% with N(2)O (not significant); in the Sevoflurane group, however, N(2)O 67% increased SjO(2) from 56% +/- 13% to 66% +/- 12% (P < 0.01). This indicates that N(2)O does not reduce the incidence of low SjO(2) values during propofol anesthesia. ⋯ This study demonstrates that nitrous oxide can increase jugular bulb venous oxygen saturation when added to sevoflurane/remifentanil anesthesia, but not to propofol/remifentanil anesthesia, in patients with brain tumors.
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Anesthesia and analgesia · Feb 2002
Randomized Controlled Trial Clinical TrialAre lactated Ringer's solution and normal saline solution equal with regard to coagulation?
Crystalloids represent an attractive strategy to alleviate intravascular volume deficits. Crystalloid hemodilution was associated with hypercoagulability in in vitro and in vivo studies. The influence of different crystalloids on coagulation in the surgical patient is not well studied. In a prospective, randomized study in patients undergoing major abdominal surgery, we used either lactated Ringer's solution (RL) (n = 21) or 0.9% saline solution (SS) (n = 21) exclusively for intravascular volume replacement over 48 h to maintain central venous pressure between 8 and 12 mm Hg. Activated thrombelastography (TEG) using different activators (intrinsic TEG, extrinsic TEG, heparinase TEG, aprotinin TEG) was used to measure coagulation time, clot formation time, and maximum clot firmness. Measurements were performed after induction of anesthesia (T0), immediately after surgery (T1), 5 h after surgery (T2), and on the morning of the first (T3) and second (T4) postoperative days. RL 18,750 +/- 1890 mL and 17,990 +/- 1790 mL of SS were infused during the study period. Acidosis was seen only in the SS-treated group. Blood loss was not different between the groups. Fibrinogen and antithrombin III decreased similarly at T1 and T2 in both groups, most likely because of hemodilution. Differences in TEG data from normal baseline were seen only immediately after surgery and 5 h thereafter, indicating mild hypercoagulability in the intrinsic TEG (RL, from 147 +/- 130 s to 130 +/- 11 s; SS, from 146 +/- 12 s to 131 +/- 12 s). There were no differences in coagulation between RL- and SS-treated patients. We conclude that in major abdominal surgery intravascular volume replacement with crystalloids resulted in only moderate and abbreviated changes in coagulation. No differences in activated TEG and blood loss were seen between an RL- and an SS-based intravascular volume replacement regimen. ⋯ In 42 patients undergoing major abdominal surgery, either lactated Ringer's solution or 0.9% saline solution were exclusively used for volume therapy for 48 h. Activated thrombelastography revealed some mild hypercoagulability after surgery. No differences in coagulation were seen between the two intravascular volume replacement strategies.
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Anesthesia and analgesia · Feb 2002
Autoantibodies associated with volatile anesthetic hepatitis found in the sera of a large cohort of pediatric anesthesiologists.
Anesthetic-induced hepatitis is thought to have an immune-mediated basis, in part because many patients who develop hepatitis have serum autoantibodies that react with specific hepatic proteins. The present study shows that pediatric anesthesiologists also have these serum autoantibodies. Moreover, levels of these autoantibodies are higher than those of general anesthesiologists. We collected sera from 105 pediatric and 53 general anesthesiologists (including 3 nurse anesthetists), 20 halothane hepatitis patients, and 20 control individuals who were never exposed to inhaled anesthetics. Serum cytochrome P450 2E1 (P450 2E1) and 58-kd hepatic endoplasmic reticulum protein (ERp58) autoantibodies were measured by enzyme-linked immunosorbent assays. Positive values were 2 SD above median control values. Two multiple regression models were constructed. Pediatric anesthesiologists, like halothane hepatitis patients, had higher serum autoantibody levels of ERp58 and P450 2E1 than general anesthesiologists and controls, which was possibly because of their increased occupational exposures to anesthetics. Female anesthesiologists had higher levels of ERp58 autoantibodies than male anesthesiologists, whereas female pediatric anesthesiologists had higher levels of P450 2E1 autoantibodies than all other anesthesiologists. One female pediatric anesthesiologist had symptoms of hepatic injury. Because most anesthesiologists do not develop volatile anesthetic-induced hepatic injury, the findings suggest that pathogenic ERp58 and P450 2E1 autoantibodies may not directly cause volatile anesthetic hepatitis. Female anesthesiologists have high levels of these autoantibodies; however, the majority of these individuals do not develop hepatitis, suggesting that autoantibodies may not have a pathological role in volatile anesthetic-induced hepatitis. ⋯ Environmental exposure of anesthesiology personnel to certain inhaled anesthetics can induce the formation of autoantibodies that have been associated with anesthetic hepatitis. Female anesthesiologists have high levels of these autoantibodies; however, the majority of these individuals do not develop hepatitis, suggesting that autoantibodies may not have a pathological role in volatile anesthetic-induced hepatitis.
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Anesthesia and analgesia · Feb 2002
Clinical Trial Controlled Clinical TrialEpidural infusion pressure in degenerative spinal disease before and after epidural steroid therapy.
The analgesic mechanism of epidural steroids in reducing pain associated with degenerative spinal disease (DSD) is poorly understood. We report increased inline epidural infusion pressure in patients with DSD and assess whether this phenomenon is affected by administration of an epidural steroid injection. We collected data during epidural placement for routine surgery or epidural steroid therapy. Using a 17-gauge Tuohy needle, with patients in the right lateral decubitus position, loss of resistance to 2 mL of saline identified the epidural space. Two minutes later the needle was attached to saline-filled tubing connected to a pressure transducer (Baxter PX 260 pressure monitoring kit with Truwave TM disposable pressure transducer). In the first part of the study, 4 successive boluses of 3 mL of local anesthetic were administered at a rate of 6 mL/min to 15 patients (age 47 +/- 6 yrs) with radicular back pain and magnetic resonance imaging (MRI) or computed tomography (CT) evidence of DSD, and to 8 control patients with no history of back pain (age 44 +/- 5 yr) while inline epidural infusion pressure was measured. In the second part of the study 44 patients with low back pain and MRI or CT evidence of DSD presenting to the pain clinic were infused with 8 mL of 0.125% bupivacaine and 40 mg of methylprednisolone (20 mg/mL) at a rate of 6 mL/min while inline epidural infusion pressure was measure and recorded. This was repeated 3 wk later. Initially, DSD patients had significantly increased infusion pressures over normals, which most likely reflects outflow resistance or obstruction. A significant decrease in inline epidural infusion pressure was observed after epidural steroid treatment. This change in pressure may indicate efficacy from epidural steroid injection. ⋯ During injection into the epidural space we observed increased resistance in patients with degenerative spinal disease. This resistance was significantly less when measured 3 wk after an epidural steroid injection. This change in pressure may indicate efficacy from epidural steroid injection.
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Anesthesia and analgesia · Feb 2002
Venous air emboli occur during release of positive end-expiratory pressure and repositioning after sitting position surgery.
We studied the effect of positive end-expiratory pressure (PEEP) release and positioning on the occurrence of venous air embolism (VAE). Eighteen consecutive patients (8 women, 10 men; ASA grade I-III) undergoing neurosurgery in the sitting position were studied. After induction of anesthesia ventilation was controlled with a PEEP of 5 cm H(2)O in an oxygen-air gas mixture. A transesophageal echocardiographic (TEE) probe was inserted. Preoperatively, a patent foramen ovale was excluded in all patients. TEE monitoring was performed during surgery, during PEEP release at the end of surgery with the patient still in the sitting position, and during change of the patient position into the supine position. The severity of VAE was differentiated as follows: grade 1 = only microbubbles; grade 2 = microbubbles and decrease of end-tidal carbon dioxide partial pressure (PETCO(2)) by more than 1.5 mm Hg; grade 3 = microbubbles combined with a decrease of PETCO(2) by more than 1.5 mm Hg, and a decrease of mean arterial blood pressure by at least 20 mm Hg. During surgery, VAE with a grade of 1, 2 or 3 occurred in 7, 4, and 2 patients, respectively. After PEEP release, VAE of grades 1, 2, and 3 were observed in 7, 2, and 1 patients, respectively. During repositioning from sitting to supine position, VAE of grades 1, 2, and 3 was observed in 6, 1, and 1 patients, respectively. The patient with VAE grade 3 needed inotropic support until 2 h after surgery to maintain sufficient blood pressure. No patient showed any sign of paradoxical arterial embolism or cardiac dysfunction. We conclude that VAE occurs not only during surgery in the sitting position, but also with release of PEEP and during repositioning to the supine position. ⋯ This study shows that venous air embolism (VAE) occurs not only during surgery in the sitting position but also during positive end-expiratory pressure release and repositioning of the patient into the supine position. Continuous monitoring for VAE should be performed until the patient is returned to the supine position.