Effects of spinal anesthesia and sedation with dexmedetomidine or propofol on cerebral regional oxygen saturation and systemic oxygenation a period after spinal injection.

PURPOSE: To evaluate changes in cerebral regional oxygen saturation (rSO2) after spinal anesthesia and compare the changes in rSO2 and systemic oxygenation between dexmedetomidine sedation and propofol sedation. METHODS: Thirty-six patients scheduled to undergo transurethral surgery under spinal anesthesia were randomly assigned to the dexmedetomidine (n = 18) and propofol groups (n = 18). We used near-infrared spectroscopy sensors to measure rSO2, and obtained data from each side were averaged. After oxygen insufflation, baseline measurements of mean arterial blood pressure (MAP), heart rate, rSO2, pulse oximetry saturation (SpO2), bispectral index, and body temperature were made. After spinal anesthesia, we measured these parameters every 5 min. Twenty minutes after spinal injection, dexmedetomidine or propofol administration was started. We measured each parameter at 10, 25, and 40 min after the administration of dexmedetomidine or propofol. RESULTS: The baseline rSO2 in the dexmedetomidine group was 71.3 ± 7.3%, and that in the propofol group was 71.8 ± 5.6%. After spinal anesthesia, rSO2 in both groups decreased significantly (dexmedetomidine group: 65.4 ± 6.9%; propofol group: 64.3 ± 7.4%). After administering sedatives, rSO2 was equivalent after spinal anesthesia. rSO2 was comparable between the two groups. MAP and SpO2 were significantly higher in the dexmedetomidine group than in the propofol group. CONCLUSION: Spinal anesthesia decreased rSO2; however, the decline was not severe. Dexmedetomidine and propofol did not compromise cerebral oxygenation under spinal anesthesia. Nevertheless, MAP and SpO2 were more stable in dexmedetomidine sedation than in propofol sedation. Dexmedetomidine may be suitable for spinal anesthesia.

[Anesthetic Management of Hardy's Operation in a Patient with Acromegalic Heart Disease].

We report the successful anesthetic management of Hardy's operation in a patient with acromegalic heart failure. A 43-year-old man, weighing 98 kg, 182 cm in height, was scheduled for Hardy's operation under general anesthesia. He was admitted 'to our hospital with acute heart failure. At admission, the left ventric- ular ejection fraction (EF) decreased to 20% ; however, the angiography revealed no evidence of coronary artery stenosis. His physical features (enlargement of hand, feet, lips and ears, expansion of the skull at the fontanel) and a high level of growth hormone indicated acromegaly. Thus, we concluded that heart failure was due to acromegaly (acromegaly cardiomyopathy : AHD). The patient was scheduled for Hardy's opera- tion. Anesthesia was induced with midazolam, fentanyl, ketamine, propofol and rocuronium, and maintained with desflurane, remifentanil and intermittent doses of fentanyl. We used FlotracTM/VigileoTM monitor(Edwards Lifesciences) to check cardiac output and stroke vol- ume variation during operation. Intraoperative and postoperative hemodynamic variables remained stable. At follow-up 6 months after operation, he was clinically stable with no recurrence of heart failure, and repeat echocardiography demonstrated resolution of the myo- cardial dysfunction (EF 50%). Although acromegaly is well known as being associated with difficult laryngos- copy and intubation, we should pay attention to the presence of acromegalic heart disease. Improvement of cardiac function is expected after surgical therapy.

Epidural Hematoma related to lower limb pain and massive liver bleeding in Gorham-Stout disease: A case report.

RATIONALE: Gorham-Stout disease (GSD) is a rare disease that causes massive osteolysis and proliferation of abnormal lymphangiomatous tissues. Patients with GSD often experience pain associated with bone fractures and chylothorax. However, bleeding caused by abnormal lymphangiomatous tissue or hematological dysfunction rarely occurs. PATIENT CONCERNS: A 22-year-old female patient with GSD presented with severe left hip and lower limb pain. The GSD had disappeared her right pelvic bone and femur, but no abnormalities were found in the bones at the site of the pain. DIAGNOSES: The patient presented with a chylothorax and cerebrospinal fluid leakage. She was treated with sirolimus and an epidural blood patch, and her symptoms resolved. Computed tomography and magnetic resonance imaging revealed an epidural hematoma extending from L3 to the caudal region, and blood results revealed a consumption coagulopathy. INTERVENTIONS: We presumed that the hematoma caused pain and prescribed pregabalin and morphine. The pain gradually subsided. OUTCOMES: An unexpected liver subcapsular hemorrhage occurred 4 months later, and the patient went into hemorrhagic shock. Transcatheter arterial embolization was promptly performed, and the patient recovered. LESSONS: GSD infrequently causes bleeding related to abnormal lymphangiomatous tissues and coagulopathy, yet it can lead to serious events if it occurs.

Amiodarone Provides Long-Lasting Local Anesthesia and Analgesia in Open-State Mouse Nociceptors.

Local anesthetics with long-lasting effects and selectivity for nociceptors have been sought over the past decades. In this study, we investigated whether amiodarone, a multiple channel blocker, provides long-lasting local anesthesia and whether adding a TRPV1 channel activator selectively prolongs sensory anesthetic effects without prolonging motor blockade. Additionally, we examined whether amiodarone provides long-lasting analgesic effects against inflammatory pain without TRPV1 channel activator co-administration. In the sciatic nerve block model, 32 adult C57BL/6J mice received either bupivacaine, amiodarone with or without capsaicin (a TRPV1 agonist), or vehicle via peri-sciatic nerve injection. Sensory and motor blockade were assessed either by pinprick and toe spread tests, respectively. In another set of 16 mice, inflammatory pain was induced in the hind paw by zymosan injection, followed by administration of either amiodarone or vehicle. Mechanical and thermal sensitivity and paw thickness were assessed using the von Frey and Hargreaves tests, respectively. The possible cardiovascular and neurological side effects of local amiodarone injection were assessed in another set of 12 mice. In the sciatic nerve block model, amiodarone produced robust anesthesia, and the co-administration of TRPV1 agonist capsaicin prolonged the duration of sensory blockade, but not that of motor blockade [complete sensory block duration: 195.0 ± 9.8 min vs. 28.8 ± 1.3 min, F (2, 21) = 317.6, p < 0.01, complete motor block duration: 27.5 ± 1.6 min vs. 21.3 ± 2.3 min, F (2, 22) = 11.1, p = 0.0695]. In the zymosan-induced inflammatory pain model, low-dose amiodarone was effective in reversing the mechanical and thermal hypersensitivity not requiring capsaicin co-administration [50% withdrawal threshold at 8 h (g): 0.85 ± 0.09 vs. 0.25 ± 0.08, p < 0.01, withdrawal latency at 4 h (s) 8.5 ± 0.5 vs. 5.7 ± 1.4, p < 0.05]. Low-dose amiodarone did not affect zymosan-induced paw inflammation. Local amiodarone did not cause cardiovascular or central nervous system side effects. Amiodarone may have the potential to be a long-acting and nociceptor-selective local anesthetic and analgesic method acting over open-state large-pore channels.

[Patient-controlled epidural analgesia combined with patient-controlled intravenous analgesia for postoperative analgesia after Miles' operation for rectal cancer].

A 69-year-old woman (156 cm, 53 kg) underwent a Miles' operation, total hysterectomy, resection of vagina, and thigh flap to vulva for rectal cancer. Before general anesthesia, an epidural catheter was inserted at T11-12 interspace, and 1.5% mepivacaine 7ml was administered. Sensory block level spread from T4 to L1. Anesthesia was induced with propofol and maintained with sevoflurane in air oxygen mixture. Operation was performed uneventfully. After the operation, postoperative analgesia was achieved with patient-controlled epidural analgesia (PCEA). The epidural solution of 0.06% ropivacaine with 4 microg x ml(-1) fentanyl and 20 microg x ml(-1) was connected to a PCA pump (i-Fuser, JMS, Japan) that was programmed as an 8 ml initial bolus, 4 ml x hr(-1) basal infusion, 2 ml bolus dose, and 10-min lockout interval. Although abdominal pain was well controlled by PCEA, intractable pain in the pelvic nerve region existed. Patient-controlled intravenous analgesia (IV-PCA) with fentanyl, ketamine, and lidocaine was added to PCEA. Then excellent pain relief was obtained without any side effects such as nausea, vomiting, drowsiness, and respiratory depression. It could be useful to use IV-PCA together with PCEA when wide spread postoperative analgesia is necessary.

Clonazepam for pain due to muscle spasm in a patient with vertebral compression fractures caused by multiple myeloma: a case report.

BACKGROUND: Vertebral compression fractures can cause severe back pain. Although many types of analgesics and interventional treatments are available, they are sometimes ineffective in mitigating the pain. We encountered a case where clonazepam was effective for the management of severe low back pain caused by lumbar vertebral compression fractures. CASE PRESENTATION: A 44-year-old male was diagnosed with multiple myeloma and had vertebral compression fractures of the first and second lumbar vertebrae. He had been suffering from severe low back pain on movement with muscle spasm and pain-associated anxiety. We considered this breakthrough low back pain to be caused by facet joint pain; thus, we prescribed clonazepam as a muscle relaxant and anxiolytic. Following this treatment, the intractable breakthrough pain was dramatically relieved. CONCLUSION: Clonazepam, which has both muscle relaxant and anxiolytic effects, might be helpful in mitigating pain, associated anxiety, and muscle spasms due to vertebral compression fractures.

Tapentadol Safety and Patient Characteristics Associated with Treatment Discontinuation in Cancer Therapy: A Retrospective Multicentre Study in Japan.

INTRODUCTION: Tapentadol has analgesic effects comparable to those of conventional opioids and is associated with fewer side effects, including gastrointestinal symptoms, drowsiness, and dizziness, than other opioids. However, the safety of tapentadol in the Japanese population remains unclear; the present multicentre study aimed to examine the safety of tapentadol and the characteristics of patients likely to discontinue this treatment owing to adverse events. METHODS: The safety of tapentadol was assessed retrospectively in patients with any type of cancer treated between August 18, 2014 and October 31, 2019 across nine institutions in Japan. Patients were examined at baseline and at the time of opioid discontinuation. Multivariate analysis was performed to identify factors associated with tapentadol discontinuation owing to adverse events. RESULTS: A total of 906 patients were included in this study, and 685 (75.6%) cases were followed up until tapentadol cessation for any reason. Among patients who discontinued treatment, 119 (17.4%) did so because of adverse events. Among adverse events associated with difficulty in taking medication, nausea was the most common cause of treatment discontinuation (4.7%), followed by drowsiness (1.8%). Multivariate analysis showed that those who were prescribed tapentadol by a palliative care physician (odds ratio [OR] 2.60, 95% confidence interval [CI] 1.36-4.99, p = 0.004), patients switching to tapentadol due to side effects from previous opioids (OR 2.19, 95% CI 1.05-4.56, p = 0.037), and patients who did not use naldemedine (OR 5.06, 95% CI 2.47-10.37, p < 0.0001) had an increased risk of treatment discontinuation owing to adverse events. CONCLUSIONS: This study presents the safety profile of tapentadol and the characteristics of patients likely to discontinue this treatment owing to adverse events in the Japanese population. Prospective controlled trials are required to evaluate the safety of tapentadol and validate the present findings. TRIAL REGISTRATION NUMBER: UMIN 000044282 (University Hospital Medical Information Network).

Analgesic effects of amiodarone in mouse models of pain.

Purpose: Although amiodarone is classified as a Vaughan-Williams class Ⅲ antiarrhythmic drug, it has inhibitory effects on voltage-gated sodium and calcium channels and on ß-adrenergic receptors. Given these pharmacological profiles, amiodarone may have analgesic properties. Most patients who are prescribed amiodarone possess multiple cardiovascular risk factors. Despite the fact that pain plays a crucial role as a clinical indicator of cardiovascular events, the effects of amiodarone on pain have not been investigated. The aim of the current study was to investigate the analgesic effects of amiodarone by using mouse models of pain in an effort to elucidate underlying mechanisms. Methods: Adult male C57B6 mice received single bolus intraperitoneal injections of amiodarone at doses of 25, 50, 100, and 200 mg/kg, while the mice in the control group received only normal saline. The analgesic effects of amiodarone were evaluated using the acetic acid-induced writhing test, formalin test, and tail withdrawal test. In addition, the potassium channel opener NS1643, voltage-gated sodium channel opener veratrine, calcium channel opener BAYK8644, and selective ß-adrenergic agonist isoproterenol were used to uncover the underlying mechanism. Results: During the acetic acid-induced writhing test, formalin test, and tail withdrawal test, amiodarone induced analgesic responses in a dose-dependent manner. The analgesic effects of amiodarone were abolished by veratrine but not by NS1643, BAYK8644, or isoproterenol. Conclusion: Amiodarone induced analgesic responses in a dose-dependent manner, likely by blocking voltage-gated sodium channels. These results indicate that clinical doses of amiodarone can affect nociception and may mask or attenuate pain induced by acute cardiovascular events.