Biomedical subjects

Jacques T YaDeau

Publications and source records attributed to Jacques T YaDeau.

4 recordsLinked to original sources

PubMed2006

Nerve localization techniques for interscalene brachial plexus blockade: a prospective, randomized comparison of mechanical paresthesia versus electrical stimulation.

Postoperative neurologic symptoms (PONS) are relatively common after upper extremity orthopedic surgery performed under peripheral neural blockade. In this study, we prospectively compared the incidence of PONS after shoulder surgery under interscalene (IS) block using the electrical stimulation (ES) or mechanical paresthesia (MP) techniques of nerve localization. For patients randomized to the MP group, a 1-in, 23-g long-beveled needle was placed into the IS groove to elicit a paresthesia to the shoulder, arm, elbow, wrist, or hand. For patients randomized to the ES group, a 5-cm, 22-g short-beveled insulated needle was placed into the IS groove to elicit a motor response including flexion or extension of the elbow, wrist, or fingers or deltoid muscle stimulation at a current between 0.2 and 0.5 mA. Each IS block was performed with 50-60 mL of 1.5% mepivacaine containing 1:300,000 epinephrine and 0.1meq/L sodium bicarbonate. Two-hundred-eighteen patients were randomized between the two groups. One patient was lost to follow-up. Twenty-five patients (23%) in the ES group experienced paresthesia during needle insertion. The incidence of PONS using the ES technique was 10.1% (11/109), whereas the incidence with the MP technique was 9.3% (10/108) (not significant). The PONS lasted a median duration of 2 mo, and symptoms in all patients resolved within 12 mo. The success rate, onset time, and patient satisfaction were also comparable between groups. We conclude that the choice of nerve localization technique can be made based on the patient's and anesthesiologist's comfort and preferences and not on concern for the development of PONS.

Adult↗

PubMed2005

The effects of femoral nerve blockade in conjunction with epidural analgesia after total knee arthroplasty.

Either epidural analgesia or femoral nerve blockade improves analgesia and rehabilitation after total knee arthroplasty. No study has evaluated the combination of femoral nerve blockade and epidural analgesia. In this prospective, randomized, blinded study we investigated combining femoral nerve blockade with epidural analgesia. Forty-one patients received a single-injection femoral nerve block with 0.375% bupivacaine and 5 microg/mL epinephrine; 39 patients served as controls. All patients received combined spinal-epidural anesthesia and patient-controlled epidural analgesia with 0.06% bupivacaine and 10 microg/mL hydromorphone. Average duration of epidural analgesia was 2 days. All patients received the same standardized physical therapy intervention. Median visual analog scale (VAS) scores with physical therapy were significantly lower for 2 days among patients who received a femoral nerve block versus controls: 3 versus 4 (day 1), 2.5 versus 4 (day 2); P < 0.05. Median VAS pain scores at rest were 0 in both groups on days 1 and 2. Flexion range of motion was improved on postoperative day 2 (70 degrees versus 63 degrees ; P < 0.05). No peripheral neuropathies occurred. We conclude that the addition of femoral nerve blockade to epidural analgesia significantly improved analgesia for the first 2 days after total knee arthroplasty.

Aged↗

PubMed2005

The incidence of transient neurologic symptoms after spinal anesthesia with mepivacaine.

We prospectively evaluated 1273 patients who received spinal (or combined spinal-epidural [CSE]) anesthesia with 1.5% mepivacaine (plain, no glucose) for ambulatory surgery. We hypothesized that analysis of a large series of patients would confirm previous findings that isobaric 1.5% mepivacaine is not frequently associated with transient neurologic symptoms (TNS). Patients were contacted twice after the anesthetic, at days 1-4 and days 6-9. One-thousand-two-hundred-ten patients were successfully contacted postoperatively (95% follow-up rate). None of the patients had permanent neurologic sequelae from the anesthetic. None of the 372 CSE anesthetics was inadequate for surgery. Fourteen of 838 (1.7%) of the spinal anesthetics were inadequate. TNS, defined as the new onset of back pain that radiated bilaterally to buttocks or distally, occurred in 78 patients (6.4%; 95% confidence intervals 5.1%-8%). The mean age of patients who developed TNS (48 +/- 14 yr) was older than that of patients without TNS (41 +/- 16 yr) (P < 0.001). TNS was not influenced by gender or intraoperative position. The frequent success rate and infrequent rates of complications such as TNS and postdural puncture headache suggest that spinal anesthesia with mepivacaine is likely to be a safe and effective anesthetic for ambulatory patients.

Adolescent↗

PubMedDate not supplied

Ketamine stimulates secretion of beta-endorphin from a mouse pituitary cell line.

BACKGROUND AND OBJECTIVES: beta-endorphin is an endogenous opioid that mediates pain-induced analgesia. Propofol inhibits in vitro secretion of beta-endorphin from a mouse pituitary cell line (AtT-20). We hypothesized that ketamine would also alter secretion of beta-endorphin. METHODS: AtT-20 cells were exposed to the intravenous anesthetic ketamine (10 to 40 micromol/L). Secretion of beta-endorphin was determined by enzyme-linked immunosorbent assay. Long-term effects were determined by exposing the cells to ketamine, allowing the cells to recover overnight, then stimulating the secretion of beta-endorphin. AtT-20 cells were stimulated with secretagogues to induce secretion of beta-endorphin. The effect of ketamine on stimulated secretion was determined. Cultures of AtT-20 cells were grown for 5 days in the presence of ketamine. Cell numbers were determined on each day. RESULTS: Ketamine increased secretion of beta-endorphin to levels that were up to 3 times greater than baseline secretion. Stimulation of beta-endorphin secretion by ketamine persisted into the subsequent day. Ketamine caused increased secretion from cells stimulated with secretagogues. Ketamine was not toxic to these cells; AtT-20 cells grew normally for 5 days in the presence of up to 40 micromol/L ketamine. CONCLUSIONS: Clinically relevant concentrations of ketamine stimulated both immediate and delayed secretion of beta-endorphin. This suggests that the prolonged analgesia observed in some clinical situations with ketamine could be in part caused by increased release of an endogenous opioid.

8-Bromo Cyclic Adenosine Monophosphate↗