Controlling pain in cancer patients is important for several reasons including patient quality of life (QOL). In moderate-to-severe cancer-pain management, opioid analgesics are indispensable. Among these, morphine is the most representative. Unfortunately, many studies have shown that morphine is potentially associated with cancer growth, recurrence, and metastasis. Specifically, in animal as well as in vivo and in vitro studies, morphine has been demonstrated to have possibly positive effects on cancer progression. However, those effects have not yet been confirmed as entirely harmful, for several reasons: the results of animal and laboratory research have not been subjected to clinical trials; there are as yet no well-designed clinical studies, and indeed, some studies have shown that morphine can have negative, suppression effects on tumor growth. This review paper will present some of the data on the potentially positive relationships between morphine and cancer. It should not be forgotten, though, that such relationships remain controversial, and that pain itself promotes cancer progression.
Analgesics, Opioid ; Animals ; Humans ; In Vitro Techniques ; Morphine* ; Neoplasm Metastasis ; Quality of Life ; Recurrence

Background: Postoperative pain is affected by preoperative depression. If the risk of postoperative pain associated with depression can be predicted preoperatively, anesthesiologists and/or surgeons can better manage it with personalized care. The objective of this study was to determine the efficacy of Patient Health Questionnaire-2 (PHQ-2) depression screening tool as a predictor of postoperative pain. Methods: A total of 50 patients scheduled for elective laparoscopic cholecystectomy with an American Society of Anesthesiologists grade of 1 or 2 were enrolled. They answered the PHQ-2, which consists of two questions, under the supervision of a researcher on the day before the surgery. The numerical rating scale (NRS) scores were assessed at post-anesthesia care unit (PACU), at 24, and 48 postoperative hours, and the amount of intravenous patient-controlled analgesia (IV-PCA) administered was documented at 24, 48, and 72 postoperative hours. At 72 h, the IV-PCA device was removed and the final dosage was recorded. Results: The NRS score in PACU was not significantly associated with the PHQ-2 score (correlation coefficients: 0.13 [P = 0.367]). However, the use of analgesics after surgery was higher in patients with PHQ-2 score of 3 or more (correlation coefficients: 0.33 [P = 0.018]). Conclusions We observed a correlation between the PHQ-2 score and postoperative pain. Therefore, PHQ-2 could be useful as a screening test for preoperative depression. Particularly, when 3 points were used as the cut-off score, the PHQ-2 score was associated with the dosage of analgesics, and the analgesic demand could be expected to be high with higher PHQ-2 scores.

Background: The STOP-BANG questionnaire is a simple screening tool with high sensitivity for the detection of severe obstructive sleep apnea (OSA). Predicting airway obstruction would allow the safe management of sedative patients to prevent intraoperative hypoxia. This study was designed to check the correlation between the STOP-BANG score and oxygen saturation (SpO2) during sedation and confirm the availability of the STOP-BANG questionnaire as a preoperative exam for predicting the incidence of hypoxia in sedative patient management. Methods: This study included 56 patients who received spinal anesthesia. The pre-anesthesia evaluation was conducted using the STOP-Bang questionnaire. The patients were under spinal anesthesia with an average block level of T10. Dexmedetomidine was infused with a loading dose of 1 μg/kg over 10 min and a maintenance dose of 0.5 μg/kg/h until the end of the procedure. The SpO2 of the patients was recorded every 5 min. Results: The STOP-Bang score was negatively correlated with the lowest SpO2 (coefficient = –0.774, 95% confidence interval [CI]: –0.855 to –0.649, standard error [SE] = 0.054, P < 0.001). The item of “observed apnea” was the most correlated one with hypoxic events (odds ratio = 6.00, 95% CI: 1.086 to 33.145). Conclusions The STOP-BANG score was significantly correlated with the lowest SpO2 during spinal anesthesia, which enabled the prediction of meaningful hypoxia before it occurred in the sedated patients.

BACKGROUND: Sedation by dexmedetomidine, like natural sleep, often causes bradycardia. We explored the nature of heart rate (HR) changes as they occur during natural sleep versus those occurring during dexmedetomidine sedation. METHODS: The present study included 30 patients who were scheduled to undergo elective surgery with spinal anesthesia. To assess HR and sedation, a pulse oximeter and bispectral index (BIS) monitor were attached to the patient in the ward and the operating room. After measuring HR and BIS at baseline, as the patients slept and once their BIS was below 70, HR and BIS were measured at 5-minute intervals during sleep. Baseline HR and BIS were also recorded before spinal anesthesia measured at 5-minute intervals after dexmedetomidine injection. RESULTS: During natural sleep, HR changes ranged from 2 to 19 beats/min (13.4 ± 4.4 beats/min), while in dexmedetomidine sedation, HR ranged from 9 to 40 beats/min (25.4 ± 8.5 beats/min). Decrease in HR was significantly correlated between natural sleep and dexmedetomidine sedation (R2 = 0.41, P < 0.001). The lowest HR was reached in 66 min during natural sleep (59 beats/min) and in 13 min with dexmedetomidine sedation (55 beats/min). The time to reach minimum HR was significantly different (P < 0.001), but there was no difference in the lowest HR obtained (P = 0.09). CONCLUSIONS: There was a correlation between the change in HR during natural sleep and dexmedetomidine sedation. The bradycardia that occurs when using dexmedetomidine may be a normal physiologic change, that can be monitored rather than corrected.
Anesthesia, Spinal ; Bradycardia ; Dexmedetomidine ; Heart Rate ; Heart ; Humans ; Hypnotics and Sedatives ; Operating Rooms

BACKGROUND: Sedation by dexmedetomidine, like natural sleep, often causes bradycardia. We explored the nature of heart rate (HR) changes as they occur during natural sleep versus those occurring during dexmedetomidine sedation. METHODS: The present study included 30 patients who were scheduled to undergo elective surgery with spinal anesthesia. To assess HR and sedation, a pulse oximeter and bispectral index (BIS) monitor were attached to the patient in the ward and the operating room. After measuring HR and BIS at baseline, as the patients slept and once their BIS was below 70, HR and BIS were measured at 5-minute intervals during sleep. Baseline HR and BIS were also recorded before spinal anesthesia measured at 5-minute intervals after dexmedetomidine injection. RESULTS: During natural sleep, HR changes ranged from 2 to 19 beats/min (13.4 ± 4.4 beats/min), while in dexmedetomidine sedation, HR ranged from 9 to 40 beats/min (25.4 ± 8.5 beats/min). Decrease in HR was significantly correlated between natural sleep and dexmedetomidine sedation (R2 = 0.41, P < 0.001). The lowest HR was reached in 66 min during natural sleep (59 beats/min) and in 13 min with dexmedetomidine sedation (55 beats/min). The time to reach minimum HR was significantly different (P < 0.001), but there was no difference in the lowest HR obtained (P = 0.09). CONCLUSIONS There was a correlation between the change in HR during natural sleep and dexmedetomidine sedation. The bradycardia that occurs when using dexmedetomidine may be a normal physiologic change, that can be monitored rather than corrected.