Anaesthetic care of patients undergoing primary hip and knee arthroplasty: consensus recommendations from the International Consensus on Anaesthesia-Related Outcomes after Surgery group (ICAROS) based on a systematic review and meta-analysis.

BACKGROUND: Evidence-based international expert consensus regarding anaesthetic practice in hip/knee arthroplasty surgery is needed for improved healthcare outcomes. METHODS: The International Consensus on Anaesthesia-Related Outcomes after Surgery group (ICAROS) systematic review, including randomised controlled and observational studies comparing neuraxial to general anaesthesia regarding major complications, including mortality, cardiac, pulmonary, gastrointestinal, renal, genitourinary, thromboembolic, neurological, infectious, and bleeding complications. Medline, PubMed, Embase, and Cochrane Library including Cochrane Database of Systematic Reviews, Cochrane Central Register of Controlled Trials, NHS Economic Evaluation Database, from 1946 to May 17, 2018 were queried. Meta-analysis and Grading of Recommendations Assessment, Development and Evaluation approach was utilised to assess evidence quality and to develop recommendations. RESULTS: The analysis of 94 studies revealed that neuraxial anaesthesia was associated with lower odds or no difference in virtually all reported complications, except for urinary retention. Excerpt of complications for neuraxial vs general anaesthesia in hip/knee arthroplasty, respectively: mortality odds ratio (OR): 0.67, 95% confidence interval (CI): 0.57-0.80/OR: 0.83, 95% CI: 0.60-1.15; pulmonary OR: 0.65, 95% CI: 0.52-0.80/OR: 0.69, 95% CI: 0.58-0.81; acute renal failure OR: 0.69, 95% CI: 0.59-0.81/OR: 0.73, 95% CI: 0.65-0.82; deep venous thrombosis OR: 0.52, 95% CI: 0.42-0.65/OR: 0.77, 95% CI: 0.64-0.93; infections OR: 0.73, 95% CI: 0.67-0.79/OR: 0.80, 95% CI: 0.76-0.85; and blood transfusion OR: 0.85, 95% CI: 0.82-0.89/OR: 0.84, 95% CI: 0.82-0.87. CONCLUSIONS: Recommendation: primary neuraxial anaesthesia is preferred for knee arthroplasty, given several positive postoperative outcome benefits; evidence level: low, weak recommendation. RECOMMENDATION: neuraxial anaesthesia is recommended for hip arthroplasty given associated outcome benefits; evidence level: moderate-low, strong recommendation. Based on current evidence, the consensus group recommends neuraxial over general anaesthesia for hip/knee arthroplasty. TRIAL REGISTRY NUMBER: PROSPERO CRD42018099935.

A prospective, randomized, controlled trial comparing ultrasound versus nerve stimulator guidance for interscalene block for ambulatory shoulder surgery for postoperative neurological symptoms.

BACKGROUND: Visualization with ultrasound during regional anesthesia may reduce the risk of intraneural injection and subsequent neurological symptoms but has not been formally assessed. Thus, we performed this randomized clinical trial comparing ultrasound versus nerve stimulator-guided interscalene blocks for shoulder arthroscopy to determine whether ultrasound could reduce the incidence of postoperative neurological symptoms. METHODS: Two hundred thirty patients were randomized to a standardized interscalene block with either ultrasound or nerve stimulator with a 5 cm, 22 g Stimuplex insulated needle with 1.5% mepivacaine with 1:300,000 epinephrine and NaCO3 (1 meq/10 mL). A standardized neurological assessment tool (questionnaire and physical examination) designed by a neurologist was administered before surgery (both components), at approximately 1 wk after surgery (questionnaire), and at approximately 4-6 weeks after surgery (both components). Diagnosis of postoperative neurological symptoms was determined by a neurologist blinded to block technique. RESULTS: Two hundred nineteen patients were evaluated. Use of ultrasound decreased the number of needle passes for block performance (1 vs 3, median, P < 0.001), enhanced motor block at the 5-min assessment (P = 0.04) but did not decrease block performance time (5 min for both). No patient required conversion to general anesthesia for failed block, and patient satisfaction was similar in both groups (96% nerve stimulator and 92% ultrasound). The incidence of postoperative neurological symptoms was similar at 1 wk follow-up with 11% (95% CI of 5%-17%) for nerve stimulator and 8% (95% CI of 3%-13%) for ultrasound and was similar at late follow-up with 7% (95% CI of 3%-12%) for nerve stimulator and 6% (95% CI of 2%-11%) for ultrasound. The severity of postoperative neurological symptoms was similar between groups with a median patient rating of moderate. Symptoms were primarily sensory and consisted of pain, tingling, or paresthesias. CONCLUSIONS: Ultrasound reduced the number of needle passes needed to perform interscalene block and enhanced motor block at the 5 min assessment; however, we did not observe significant differences in block failures, patient satisfaction or incidence, and severity of postoperative neurological symptoms.

Ketamine as an adjunct to postoperative pain management in opioid tolerant patients after spinal fusions: a prospective randomized trial.

Management of acute postoperative pain is challenging, particularly in patients with preexisting narcotic dependency. Ketamine has been used at subanesthetic doses as a N-methyl D-aspartate (NMDA) receptor antagonist to block the processing of nociceptive input in chronic pain syndromes. This prospective randomized study was designed to assess the use of ketamine as an adjunct to acute pain management in narcotic tolerant patients after spinal fusions. Twenty-six patients for 1-2 level posterior lumbar fusions with segmental instrumentation were randomly assigned to receive ketamine or act as a control. Patients in the ketamine group received 0.2 mg/kg on induction of general anesthesia and then 2 mcg kg(-1) hour(-1) for the next 24 hours. Patients were extubated in the operating room and within 15 minutes of arriving in the Post Anesthesia Care Unit (PACU) were started on intravenous patient-controlled analgesia (PCA) hydromorphone without a basal infusion. Patients were assessed for pain (numerical rating scale [NRS]), narcotic use, level of sedation, delirium, and physical therapy milestones until discharge. The ketamine group had significantly less pain during their first postoperative hour in the PACU (NRS 4.8 vs 8.7) and continued to have less pain during the first postoperative day at rest (3.6 vs 5.5) and with physical therapy (5.6 vs 8.0). Three patients in the control group failed PCA pain management and were converted to intravenous ketamine infusions when their pain scores improved. Patients in the ketamine group required less hydromorphone than the control group, but the differences were not significant. Subanesthetic doses of ketamine reduced postoperative pain in narcotic tolerant patients undergoing posterior spine fusions.

Similar analgesic effect after popliteal fossa nerve blockade with 0.375% and 0.75% bupivacaine.

This study tested the hypothesis that increasing the concentration of bupivacaine from 0.375 to 0.75% would increase the duration of postoperative analgesia by 3 h. Seventy patients scheduled for hospital admission after foot or ankle surgery gave consent to enter this prospective randomized trial. Patients were randomly assigned to receive a popliteal fossa block (posterior approach) using 30 cc of either 0.375% or 0.75% bupivacaine, with epinephrine. Patients also received a neuraxial anesthetic and postoperative intravenous patient-controlled analgesia. Patient characteristics, duration of analgesia, pain scores, use of analgesic medications, and side effects of analgesic therapy were determined. Duration of analgesia was similar with both concentrations of bupivacaine (0.375% 14 +/- 8 h, 0.75% 13 +/- 6 h; mean +/- SD). Pain scores were the same for both groups on the first postoperative day (3 of 10 at rest, 5 with therapy). Analgesic use and side effects attributable to pain management did not differ between groups. In conclusion, postoperative analgesia was not affected by the concentration of bupivacaine used for the nerve block. There was no benefit to increasing the concentration of bupivacaine above 0.375% for single-injection popliteal fossa nerve blockade when performed for postoperative analgesia.

Hemodynamic effects of di-sec-butyl phenol, an anesthetic substituted phenol.

Dose- and age-related hemodynamic effects were determined for an anesthetic substituted phenol, 2,6-di-sec-butyl phenol (DSB). DSB, 7.5 mg/kg, induced hypnosis in young rabbits and increased mean blood pressure to 170 +/- 14% and heart rate to 150 +/- 21% of control values. In elderly rabbits, 7.5 mg/kg DSB induced hypnosis, had no effect on blood pressure, but increased the heart rate to 130 +/- 2% of control. After ganglionic blockade with hexamethonium, 7.5 mg/kg DSB caused a decline in mean blood pressure (71 +/- 5% of control) without change in heart rate. DSB increased norepinephrine release from SH-SY5Y cells, a human neuroblastoma cell line (5.4 +/- 1.7% vs. 3.5 +/- 0.3%). DSB produced age-dependent elevation of mean blood pressure in rabbits, probably by causing release of catecholamines from the sympathetic nervous system.

Inhibition by propofol of intracellular calcium mobilization in cultured mouse pituitary cells.

UNLABELLED: Propofol inhibited regulated secretion of the neuropeptide beta-endorphin from AtT-20 cells, a pituitary tumor cell line. Neuropeptide secretion depends on an increase of intracellular calcium (Ca(2+)) levels. We investigated the hypothesis that propofol altered intracellular Ca(2+) levels in AtT-20 cells. Propofol (100 microM) did not inhibit Ca(2+)-induced secretion of beta-endorphin from digitonin-permeabilized cells. Thus, propofol did not inhibit neuropeptide secretion by blocking the effects of increased intracellular Ca(2+). Intracellular Ca(2+) was measured in intact cells using a Ca(2+)-sensitive dye. Ca(2+) transients were generated by depolarization with KCl or by incubation with thapsigargin (an inhibitor of Ca(2+) uptake into the endoplasmic reticulum). Propofol inhibited generation of Ca(2+) transients in intact cells by KCl (half-maximal inhibitory concentration of 14.9 microM; P < 0.05). Nitrendipine also inhibited potassium-induced Ca(2+) peaks. Propofol 50 microM reduced the thapsigargin-induced Ca(2+) peak to 47% of control (P < 0.05). Thapsigargin-induced Ca(2+) peaks were not affected by calcium channel blockade by nitrendipine. Propofol inhibited the stimulus-induced increase in intracellular Ca(2+). Propofol inhibited thapsigargin-induced Ca(2+) transients, but nitrendipine did not, indicating that propofol had effects on intracellular Ca(2+) independent of blockade of L-type Ca(2+) channels. Propofol may inhibit release of Ca(2+) from intracellular stores. These results are consistent with the hypothesis that propofol inhibits neuropeptide secretion by inhibiting the stimulus-induced increase in intracellular Ca(2+). IMPLICATIONS: Propofol may block both entry of calcium into cells and release of calcium from intracellular stores, thereby inhibiting regulated secretion of neuropeptides. Study of the effects of propofol on intracellular calcium metabolism may increase understanding of how propofol alters brain function and may aid development of better IV anesthetics.