Anesthesia and analgesia
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Anesthesia and analgesia · Feb 1998
Randomized Controlled Trial Clinical TrialIntravenous lidocaine speeds the return of bowel function, decreases postoperative pain, and shortens hospital stay in patients undergoing radical retropubic prostatectomy.
Postoperative ileus is a concern among surgical patients. Epidural anesthesia and analgesia with local anesthetics can decrease the duration of ileus. Significant systemic absorption of local anesthesia occurs during epidural use. In this study, we examined whether many of the beneficial effects on bowel function seen with epidural lidocaine are also present when the drug is given parenterally. Forty patients undergoing radical retropubic prostatectomy were studied with one half of the patients receiving a lidocaine bolus (1.5 mg/kg) and infusion (3 mg/min, unless weight <70 kg, then 2 mg/min); the other half received a saline infusion. A blind observer recorded the patient's daily pain score, the time the patient first experienced flatulence and had the first bowel movement, and the total use of analgesics. Lidocaine-treated patients first experienced flatulence in a significantly shorter time (P < 0.01) than control patients. Lidocaine patients' hospital stay was also significantly shorter (P < 0.05); on average, they spent 1.1 fewer days in the hospital. I.V. lidocaine initiated before anesthesia and continued 1 h postoperatively significantly sped up the return of bowel function. Lidocaine patients were also more comfortable postoperatively. Many of the bowel function benefits attributed to epidural lidocaine are also present when the drug is administered parenterally. Additionally, the length of hospital stay was reduced in lidocaine-treated patients. ⋯ This study prospectively examined whether I.V. lidocaine could affect the return of bowel function after radical prostate surgery. Lidocaine-treated patients had shorter hospital stays, less pain, and faster return of bowel function. In this population, lidocaine infusion can be a useful adjunct in anesthetic management.
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Anesthesia and analgesia · Feb 1998
Randomized Controlled Trial Clinical TrialAdding sodium bicarbonate to lidocaine enhances the depth of epidural blockade.
It is controversial whether adding CO2 or sodium bicarbonate to local anesthetics enhances the depth of epidural blockade. Repeated electrical stimulation is a reliable test for assessing epidural analgesia and evokes temporal summation. We used this test to investigate the analgesic effect of lidocaine, with or without CO2 or bicarbonate. Twenty-four patients undergoing epidural blockade with 20 mL lidocaine 2% at L2-3 were randomly divided into three groups: lidocaine hydrochloride, lidocaine CO2, and lidocaine plus 2 mL sodium bicarbonate 8.4%. Pain threshold after repeated electrical stimulation (five impulses at 2 Hz), pinprick, and cold test were performed at S1 and L4. Motor block was assessed. The addition of bicarbonate resulted in higher pain thresholds (P < 0.0001), faster onset of action (P = 0.009), and higher degree of motor block (P = 0.004) compared with lidocaine hydrochloride. We found no significant differences between lidocaine CO2 and hydrochloride. Most of these results were not confirmed by pinprick and cold tests. We conclude that the addition of sodium bicarbonate to lidocaine enhances the depth of epidural blockade, increases inhibition of temporal summation, and hastens the onset of block. Pinprick and cold are inadequate tests for comparing drugs for epidural anesthesia. ⋯ We measured pain perception during epidural anesthesia by delivering electrical stimuli to the knee and foot. We found that the addition of sodium bicarbonate to the local anesthetic lidocaine enhances analgesia. We observed no effect of adding carbon dioxide to lidocaine.
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Anesthesia and analgesia · Feb 1998
Randomized Controlled Trial Clinical TrialIntraarticular morphine in the multimodal analgesic management of postoperative pain after ambulatory anterior cruciate ligament repair.
Reconstruction of the anterior cruciate ligament (ACL) is associated with a considerable degree of postoperative pain. Our customary multimodal approach to postoperative analgesia after ambulatory ACL surgery includes perioperative nonsteroidal antiinflammatory drugs, pre- and postincisional intraarticular (I.A.) bupivacaine (B), and postoperative cryotherapy using an external cooling system. This study was designed to determine whether the addition of I.A. morphine (MS) provides improved postoperative analgesia. One hundred patients scheduled for elective ambulatory ACL repair received our standard multimodal therapy. After surgery, patients were randomized to one of four study groups. Group 1 received 30 mL of 0.25% B I.A. Group 2 received 30 mL of normal saline I.A. and 5 mg of MS I.A. Group 3 received 30 mL of 0.25% bupivacaine I.A. and 5 mg of MS I.V.. Group 4 received 30 mL of 0.25% B I.A. and 5 mg of MS I.A. The addition of I.A. B postoperatively provided prolonged analgesia and decreased postoperative pain and analgesic requirements. The addition of MS to I.A. B did not provide additional postoperative analgesia. We conclude that patients undergoing ambulatory ACL repair using our standard multimodal analgesic regimen failed to receive additional postoperative analgesia when MS was added to the I.A. B. ⋯ Patients receiving a multimodal analgesic regimen of perioperative nonsteroidal antiinflammatory drugs, intraarticular bupivacaine, and external cooling did not receive any additional analgesia from intraarticular morphine.
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Anesthesia and analgesia · Feb 1998
The effect of halothane and sevoflurane on fatigue-induced changes in hamster diaphragmatic contractility.
The purpose of this study was to examine the effect of halothane and sevoflurane on fatigue-induced changes in diaphragmatic contractility. Forty-two hamster diaphragm strips were randomly allocated according to anesthetics (no anesthesia control, 1%-3% halothane, 2%-6% sevoflurane) and stimulated directly in an organ bath. Under the influence of the anesthetics, muscle fatigue was induced by repetitive tetanic contraction, and diaphragmatic contractilities (i.e., peak twitch and tetanic tension, twitch contraction time, and half-relaxation time) were measured before and after fatigue. Neither halothane nor sevoflurane changed tension generation before or after fatigue, but each anesthetic significantly enhanced fatigue-induced prolongations of the contraction time and half-relaxation time after fatigue. Specifically, the half-relaxation times after fatigue in the 3% halothane, 4% sevoflurane, and 6% sevoflurane groups (225.6 +/- 37.6, 236.0 +/- 76.5, and 287.3 +/- 55.5 ms, respectively) were more than twice as long as those of the control group (104.7 +/- 19.7 ms, P < 0.05). We conclude that halothane and sevoflurane augment fatigue-induced prolongations of the contraction and relaxation times. Diaphragmatic function may deteriorate when there is a fatiguing task during the clinical administration of halothane or sevoflurane anesthesia. ⋯ This study implicates diaphragmatic fatigue during anesthesia. An in vitro hamster diaphragm muscle preparation was used to study the effect of halothane and sevoflurane on fatigue-induced change in contractility. Our findings suggest that increased load on the diaphragm during volatile anesthesia may lead to impaired diaphragmatic contractility.
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Anesthesia and analgesia · Feb 1998
Catecholamine activation in the vasomotor center on emergence from anesthesia: the effects of alpha2 agonists.
The rostral ventrolateral medulla (RVLM) controls the vascular system and may contribute to postoperative hypertension. It comprises adrenergic cardiovascular neurons, a site for action of alpha2-adrenergic agonists. Because alpha2 agonists minimize perioperative circulatory activation, we asked the following question: do alpha2 agonists, such as clonidine and mivazerol, blunt the catecholamine activation observed in the RVLM on emergence from anesthesia? Halothane-anesthetized, paralyzed rats had their ventilatory, circulatory, and acid-base stability controlled. All pressure points and incisions were infiltrated with local anesthetics. With in vivo electrochemistry, a catechol signal was recorded in the RVLM during 150 min of stable halothane anesthesia (saline-halothane group); for 120 min after halothane discontinuation (saline-emergence group); after emergence and administration of the reference alpha2 agonist, clonidine 7 microg/kg or 21 microg/kg I.V. (50% or 90% effective dose [ED50 or ED90], respectively); and after emergence and administration of a new alpha2 agonist, mivazerol 20 microg/kg or 150 microg/kg I.V. (ED50 or ED90). Under halothane, dose-response curves for the RVLM catecholamine signal were constructed for mivazerol and an alpha2 antagonist, idazoxan (ED50 2.3 mg/kg I.V.). Stable halothane anesthesia (n = 5) led to no change in mean arterial pressure (MAP), heart rate (HR), or catechol signal (CAOC). During emergence from anesthesia, the MAP, HR, and CAOC increased (n = 5). Clonidine led to a near total suppression of the RVLM catecholamine activation noticed on emergence from anesthesia (n = 5). Hypertension was partially blunted with clonidine 7 microg/kg (n = 5). Tachycardia was partially blunted with mivazerol 20 microg/kg (n = 5). Pretreatment with idazoxan suppressed all the effects of mivazerol (n = 5). ⋯ On emergence from anesthesia, alpha2 agonists modify the activity of adrenergic cardiovascular neurons located within the vasomotor center, as assessed by in vivo electrochemistry. We provide a rationale for the use of alpha2 agonists on emergence from anesthesia in coronary/hypertensive patients.