Tso-Chou Lin

Intra-articular ketamine for pain control following arthroscopic knee surgery.

BACKGROUND In an attempt to demonstrate the peripheral effect of ketamine on the synovia of knee joint and to smoothen the recovery from arthroscopic knee surgery, this study was designed to evaluate the analgesic effect of intra-articular ketamine injection after knee arthroscopy. METHODS In a double blind randomized study, 60 patients were assigned to three groups. Group A patients received saline 5 mL intra-articularly after closure of the surgical wound to serve as control; group B patients received ketamine 0.5 mg/kg of body weight intra-muscularly to rule out the systemic effect and group C patients received ketamine 0.5 mg/kg of body weight diluted with saline up to 5 mL intra-articularly. After surgery, patients were evaluated for pain with visual analogue scale (VAS 0 to 10) for 24 h with the operated leg in the position of extension rest and active flexion of the knee joint to 60 degree angle. Rescue pethidine (1 mg/kg of body weight) was given intra-muscularly for pain relief at request every 4 h postoperatively if necessary. The time to first rescue analgesic request was recorded, and the total doses of pethidine were calculated. RESULTS The results showed no difference in the VAS pain scores at rest and during active motion in the range of 60 degree among three groups during a 24 h observation. CONCLUSIONS Ketamine had been reported to have peripheral analgesic effects with variable duration on measurements of pain and hyperalgesia. However, in the present study, we failed to demonstrate that ketamine could provide a clinically relevant peripheral analgesic effect for postoperative arthroscopic pain.

Glucose Reduces the Effect of Water to Promote Orthostatic Tolerance

BACKGROUND Recent studies have shown that ingestion of glucose water lowers blood pressure (BP) in patients with perturbed autonomic control and more modestly lowers BP in elderly normal subjects. Whether glucose water affects cardiovascular control during orthostatic stress in normal young healthy subjects is unknown. We hypothesized that glucose water ingestion will reduce orthostatic tolerance in young healthy volunteers. METHODS In a randomized, controlled, within-subject study, 15 healthy male subjects (21-28 years of age) ingested water or 10% glucose water 5 min before tilt-table testing. We measured finger BP, brachial BP, heart rate, and peripheral vascular resistance. Orthostatic tolerance was measured as the time to presyncope during a 70 degrees head-up tilt, in which the head was tilted for 45 min or until presyncopal symptoms were observed. RESULTS During the first 45 min of tilt, 8 of 15 subjects who ingested 10% glucose water experienced presyncope, but only 2 of 15 who ingested water (P = 0.029) experienced presyncope. Ingestion of 10% glucose water increased the heart rate significantly more than pure water during head-up tilt (P = 0.026). Ingestion of water increased the peripheral vascular resistance significantly >10% glucose water during the head-up tilt test (P = 0.013). CONCLUSIONS Ingestion of 10% glucose water impairs head-up tilt tolerance relative to water ingestion. The contrasting effect of 10% glucose water vs. pure water on orthostatic tolerance is associated with increased heart rate and attenuation of the increase in peripheral vascular resistance in head-up tilt testing.

Midazolam attenuates adenosine diphosphate-induced P-selectin expression and platelet–leucocyte aggregation

Background and objective: The expression of P-selectin on the surface of platelets and platelet-leucocyte conjugate formation are considered to be an indicator of platelet activation in thrombotic and inflammatory disease. Midazolam is a widely used sedative and anaesthetic induction agent. It may inhibit platelet aggregation and suppress interleukin-6 and -8 response in human leucocytes, but any effect on the adhesion of activated platelets to leucocytes remains obscure. We have examined the influence of midazolam on adenosine diphosphate (ADP)-induced platelet surface P-selectin expression and platelet-leucocyte aggregation in whole blood. Methods: Human whole blood was stimulated with 2 × 10−5 M ADP in the presence of midazolam (3 × 10−4 to 3 × 10−6 M). Samples were stained with a fluorochrome-conjugated CD62P and CD41a antibody for detecting human platelet P-selectin antigens. The leucocyte subpopulations were separately gated and platelet-leucocyte aggregates were defined as cells found positive for CD45 and CD62P. All samples were analysed and were electronically separated into specific cell types (platelets, neutrophils, monocytes and lymphocytes) according to their typical forward/side scattering by flow cytometry. Results: Midazolam significantly inhibited ADP-induced platelet P-selectin expression and attenuated platelet-leucocyte aggregation (mainly in neutrophils and monocytes) in a dose-dependent manner with a maximum inhibitory effect at 3 × 10−4 M (P < 0.01). Conclusions: This study demonstrated that midazolam decreases the ADP-induced expression of platelet surface P-selectin and platelet-leucocyte aggregation.

Eclampsia Following Cesarean Section with HELLP Syndrome and Multiple Organ Failure

We present a rare case of postpartum eclampsia with overt acute heart and renal failure, in the absence of any precursive signs of preeclampsia. A 41-year-old parturient underwent elective cesarean section for the delivery of twins under spinal anesthesia. Prior to the procedure, preoperative laboratory examination revealed only traceable proteinuria but she had hypertension perioperatively. Approximately 8 hours after the cesarean section, she developed seizures, followed by evident acute heart and renal failure. The diagnosis of postpartum eclampsia with HELLP (hemolysis, elevated liver enzymes and low platelets) syndrome was established and she was admitted to the surgical intensive care unit for close care. Fortunately, the patient recovered fully and was discharged 26 days later. From this illustrative example, unexplainable and sustained hypertension following cesarean section should serve as a signal to warn the health care staff concerned about the possibility of impending life-threatening postpartum eclampsia.

Analysis of anesthesia-controlled operating room time after propofol-based total intravenous anesthesia compared with desflurane anesthesia in gynecologic laparoscopic surgery: A retrospective study

Background: Anesthesia technique may contribute to the improvement of operation room (OR) efficiency by reducing anesthesia-controlled time (ACT). We compared the difference between propofol-based total intravenous anesthesia (TIVA) and desflurane (DES) anesthesia for gynecologic laparoscopic surgery undergoing general anesthesia. Materials and Methods: We performed a retrospective study using data collected in our hospital to compare the ACT of gynecologic laparoscopic surgery using either TIVA via target-controlled infusion (TCI) with propofol/fentanyl or DES/fentanyl-based anesthesia between January 2010 and December 2011. The various time intervals (waiting for anesthesia, operation time, anesthesia time, emergence time, exit from OR after extubation, total OR time and postanesthesia care unit stay time) and the incidence of prolonged extubation (≥15 min) were compared between the two anesthetic techniques. Results: We included data from 926 patients, with 377 patients receiving TIVA and 549 patients receiving DES. The only significant difference is emergence time, TIVA was faster than the DES group (7.3 ± 3.3 min vs. 8.3 ± 3.1 min; P < 0.001). The factors of prolonged extubation are DES anesthesia, body mass index, surgical time, and anesthesia time. Conclusion: In our hospital, propofol-based TIVA by TCI provide faster emergence compared with DES anesthesia in gynecologic laparoscopic surgery.

Intrapleural Misplacement of a Thoracic Epidural Catheter in an Anesthetized Patient

Thoracic epidural analgesia provides adequate postoperative pain relief and favorable outcomes in major operations. However, a small number of devastating complications have been reported. Here we present a case of asymptomatic but potentially life-threatening intrapleural insertion of a thoracic epidural catheter intended for postoperative analgesia. A 39-year-old male diagnosed with esophageal carcinoma was scheduled for esophageal reconstruction. After induction of general anesthesia, a thoracic epidural catheter was inserted with a paramedian approach at the T8-9 interspace, using loss of resistance to ensure correct placement. The administration of a test dose of 2% lidocaine with epinephrine was unremarkable. After right thoracotomy, the epidural catheter was found in the right pleural cavity and was instantly removed. The patient underwent the operation smoothly and was discharged 10 days later without any sequelae. We recommend practitioners estimate the depth from the skin to the epidural space by computed tomography scan before operation and perform the placement of thoracic epidural catheter while the patient is awake to avoid accidental intrapleural misplacement.

Single Vital-capacity and Successive Tidal-volume Breathing of Sevoflurane in Induction of Anesthesia for Tracheal Intubation in Gynecologic Patients

BACKGROUND The optimal end-tidal concentrations of sevoflurane in induction of anesthesia for tracheal intubation have been widely studied and discussed. Single vital-capacity breathing of a high concentration of inspiratory sevoflurane rapidly elevates the end-tidal concentration to cause loss of consciousness, although it does not bear relation to proportional body or brain uptake. This study was designed to investigate the time effect of fast wash-in of alveolar sevoflurane in induction of anesthesia for tracheal intubation with single vital-capacity and ensuing tidal-volume breathing in gynecologic patients. METHODS Thirty-six ASA I-II patients undergoing gynecologic surgeries under general anesthesia were included in the study. Prior to anesthesia, they were instructed on the vital capacity technique for induction with prior primed 7.2% inspiratory sevoflurane in 6 L/min oxygen in the breathing circuit. Immediately after loss of consciousness, assisted ventilation with fixed 3.5% sevoflurane in oxygen was applied to patients in groups 1 and 2 for 3 minutes, and for 4.5 minutes in group 3. Patients in group 2 received fentanyl 1.5 mug/kg before induction. In all patients, tracheal intubation was performed following succinylcholine 1.5 mg/kg. Inspiratory and end-tidal concentrations of sevoflurane, blood pressure and heart rate were recorded. RESULTS All patients achieved vital capacity induction uneventfully, of whom two-thirds needed a second or third breath. The induction time was 60.6 +/- 19.2 seconds and could be reduced to 48.3 +/- 17.9 seconds with fentanyl pretreatment. The end-tidal concentration of sevoflurane was 2.68 +/- 0.20% after 4.5 minutes of ventilation with 3.5% sevoflurane, at which concentration the intubation-induced hemodynamic responses could not be suppressed. CONCLUSION This study demonstrated that vital-capacity induction with a high concentration of sevoflurane is a safe and feasible technique for our female patients. The end-tidal 1.5 minimum alveolar concentration sevoflurane following 4.5 minutes of tidal-volume ventilation did not suppress intubation-induced hemodynamic responses. Pretreatment with fentanyl helped to shorten the induction time and provide better hemodynamic control for tracheal intubation.

Extreme Hyperlactatemia After Heart Transplantation: One Center's Experience.

INTRODUCTION Hyperlactatemia may occur early after cardiac surgery and is correlated with prognosis. This study was conducted to analyze the perioperative variables and postoperative outcomes among heart transplant recipients with extremely high lactate levels (>15 mmol/L). METHODS The single-center medical records of heart transplantation from June 2006 to May 2013 were retrospectively reviewed for patient characteristics, perioperative hemodynamic variables, arterial blood gas analysis data, and postoperative mortality. RESULTS Among 58 consecutive heart transplant recipients, lactate levels over the detectable upper limit (>15 mmol/L) were identified in 12 patients after intensive care unit admission, with peak time at 1.9 ± 2.0 (range 0-6.1) hours. The maximal preoperative lactate level was 3.1 mmol/L, and most (11/12) postoperative lactate levels returned to <4 mmol/L at 27.5 ± 12.8 hours after surgery (range 15-58, median 24), displaying a trend toward delayed extubation time in 10 recipients (P < .01). Blood glucose levels elevated significantly from preoperative 148.9 ± 45.2 to 375.7 ± 96.9 mg/dL at peak lactate level (P < .01). Four patients died in the ICU (range 5-32 days), 4 died after discharge (range 5-57 months), with 6 in total surviving over 1 year. CONCLUSION Extreme hyperlactatemia commonly occurred early after heart transplantation and mostly recovered within 30 hours; however, with delayed extubation time after operation.

Duration effect of desflurane anesthesia and its awakening time and arterial concentration in gynecologic patients

OBJECTIVES: To determine the awakening arterial blood concentration of desflurane and its relationship with the end-tidal concentration during emergence from various durations of general anesthesia. METHOD: In total, 42 American Society of Anesthesiologists physical status class I-II female patients undergoing elective gynecologic surgery were enrolled. General anesthesia was maintained with fixed 6% inspiratory desflurane in 6 l min-1 oxygen until shutoff of the vaporizer at the end of surgery. One milliliter of arterial blood was obtained for desflurane concentration determination by gas chromatography at 20 and 10 minutes before and 0, 5, 10, 15, and 20 minutes after the discontinuation of desflurane and at the time of eye opening upon verbal command, defined as awakening. Concentrations of inspiratory and end-tidal desflurane were simultaneously detected by an infrared analyzer. RESULTS: The mean arterial blood concentration of desflurane was 1.20% at awakening, which correlated with the awakening end-tidal concentration of 0.96%. The mean time from the discontinuation of desflurane to eye opening was 5.2 minutes (SD = 1.6, range 3-10), which was not associated with the duration of anesthesia (60-256 minutes), total fentanyl dose, or body mass index (BMI). CONCLUSIONS: The mean awakening arterial blood concentration of desflurane was 1.20%. The time to awakening was independent of anesthetic duration within four hours. Using well-assisted ventilation, the end-tidal concentration of desflurane was proven to represent the arterial blood concentration during elimination and could be a clinically feasible predictor of emergence from general anesthesia.

Lower Body Negative Pressure–Induced Vagal Reaction: Role for the Osmopressor Response?

BACKGROUND Water ingestion elicits an osmopressor response in patients with impaired baroreflexes. In young, healthy subjects, water elicits sympathetic vasoconstriction. This study investigated the effect of water on the lower body negative pressure (LBNP)-induced vasovagal reaction and also analyzed its effect on the change of regional cerebral blood flow during LBNP. METHODS Twelve young healthy subjects underwent LBNP (40 mm Hg) tolerance testing for 45 minutes or until presyncopal symptoms occurred. Subjects received either LBNP or no LBNP with or without prior water ingestion. The severity of vasovagal reaction was determined by participant self-report rating of orthostatic symptoms during the LBNP test. Changes of regional cerebral blood flow (rCBF) between LBNP and water ingestion with LBNP groups were assessed using statistical parametrical mapping analyses. RESULTS Water ingestion attenuated the severity of symptomatic scores during LBNP (P = 0.004). Water ingestion increased Total peripheral vascular resistance (P < 0.001) and attenuated the blood pressure drop (P < 0.001) at the cessation of study. LBNP decreased rCBF over the left superior prefrontal gyrus, limbic-parahippocampal gyrus, left sublobar-caudate body, and hypothalamus (P < 0.001). Water increased rCBF significantly over the right frontal lobe, including the inferior and medial prefrontal gyrus, subcallosal, and sublobar insula, during LBNP stimulation (P < 0.001). CONCLUSIONS Water ingestion strongly reduces symptomatic burden of the vasovagal reaction induced by LBNP stimulation. The cortical activation of limbic and prefrontal cortex likely indicates the involvement of osmopressor response in central autonomic cardiovascular physiology. The central cortical activation of osmopressor response might provide insight into the mechanisms by which water ingestion reduces the vasovagal reaction.