Jitsu Kato

Effects of presurgical local infiltration of bupivacaine in the surgical field on postsurgical wound pain in laparoscopic gynecologic examinations: a possible preemptive analgesic effect.

OBJECTIVE A randomized, double-blind, controlled study was designed to evaluate the effect of presurgical local infiltration of bupivacaine in the surgical field on postsurgical wound pain relief and analgesic requirements in 28 healthy patients scheduled for laparoscopic gynecologic examinations. INTERVENTIONS After induction of general anesthesia by routine methods, the patients were randomly divided into two groups. In the bupivacaine (B) group (n = 15), patients were injected with 5 ml of 0.25% bupivacaine at each incisional area (four sites, total of 20 ml) approximately 15 minutes before skin incision. In the control (C) group (n = 13), the surgical field was injected with an equal volume of physiologic saline solution (four sites, total of 20 ml). OUTCOME MEASURES Postsurgical wound pain at rest was evaluated by a 10-cm visual analog pain scale at 1, 10, 24, and 72 hours and 1 month after surgery. The patients were interviewed via telephone 1 month after hospital discharge for re-evaluation of resting pain. RESULTS The results indicated that the incidence of postsurgical wound pain for up to 10 hours after surgery in group B was significantly lower (p < 0.05) than in group C. Pain intensity ranged from mild to moderate (2-5 cm). In addition, the mean visual analog pain scale pain intensity was significantly less for group B (0.31 +/- 0.85 cm) than for group C (2.62 +/- 2.06 cm) for up to 10 hours after surgery (p < 0.05). The number of patients who requested analgesics and complained of sleep disturbances was significantly higher in group C (p < 0.05). The mean cumulative dose of diclofenac sodium at 24 hours was significantly (p < 0.05) lower in group B (6.67 +/- 17.6 mg) than in group C (30.8 +/- 25.3 mg). Prolonged postsurgical wound pain persisting 1 month after surgery was observed in one patient in group C. CONCLUSIONS It is concluded that presurgical infiltration of 0.25% bupivacaine in the surgical field is a useful method for decreasing postsurgical wound pain for up to 10 hours and analgesic consumption for up to 24 hours after laparoscopic gynecologic examination.

Reversibility of rocuronium-induced profound neuromuscular block with sugammadex in younger and older patients

BACKGROUND This study compared the reversibility of rocuronium-induced profound neuromuscular block with sugammadex in younger and older patients. METHODS Fifteen younger (20-50 yr) and 15 older (≥70 yr) patients were sequentially enrolled in this study. After induction of anaesthesia and laryngeal mask insertion, contraction of the adductor pollicis muscle in response to ulnar nerve stimulation was quantified using acceleromyography during 1.0-1.5% end-tidal sevoflurane and remifentanil anaesthesia. All patients initially received rocuronium 1 mg kg(-1), followed by 0.02 mg kg(-1) when a post-tetanic count (PTC) of 1 or 2 was observed. After completion of surgery, at reappearance of 1-2 PTC, the time required for a single bolus dose of 4 mg kg(-1) sugammadex to produce recovery to a train-of-four (TOF) ratio of 0.9 was recorded. RESULTS There were no differences in the total dose of rocuronium administered between the younger [mean (sd): 93.4 (17.5) mg] and the older [97.5 (32.2) mg] groups. In all patients, adequate recovery of the TOF ratio to 0.9 was achieved after administration of sugammadex, although it was significantly slower in the older [3.6 (0.7) min, P<0.0001] than in the younger group [1.3 (0.3) min]. There were no clinical events attributable to recurarization. CONCLUSIONS Sugammadex can adequately restore neuromuscular function in older patients, although a longer time is required to recover from profound rocuronium-induced neuromuscular block than in younger patients.

Central Hypervolemia with Hemodilution Impairs Dynamic Cerebral Autoregulation

BACKGROUND:Frequent changes in the perioperative central blood volume could affect cerebral autoregulation through alterations in sympathetic nerve activity, cardiac output, blood viscosity, and cerebral vasomotor tone. However, the effect of dynamic cerebral autoregulation has not been studied during acute wide-ranging changes in central blood volume, especially with respect to central hypervolemia with hemodilution. METHODS:We evaluated dynamic cerebral autoregulation during central hypovolemia and central hypervolemia with hemodilution using spectral and transfer function analysis between mean arterial blood pressure (MBP) and cerebral blood flow (CBF) velocity variability in 12 individuals. Rapid changes in central blood volume were achieved using two levels of lower body negative pressure (−15 and −30 mm Hg) and two discrete infusions of normal saline (15 mL/kg and total 30 mL/kg). We then estimated changes in central blood volume as central venous pressure (CVP) and/or cardiac output using impedance cardiography. RESULTS:Steady-state CBF velocity and cardiac output decreased at −30 mm Hg lower body negative pressure (changes of CVP approximately −4 mm Hg) or were increased by each saline infusion (changes of CVP 4–6 mm Hg), without a significant change in MBP. However, transfer function gain (magnitude of transfer) between MBP and CBF velocity variability significantly increased only after saline infusion, suggesting an increased magnitude of transfer from MBP oscillations to CBF fluctuations during central hypervolemia with hemodilution. CONCLUSION:Our results suggest that, although steady-state CBF velocity changes under both central hypervolemia and hypovolemia, only hypervolemic hemodilution impairs dynamic cerebral autoregulation.

Dexmedetomidine Weakens Dynamic Cerebral Autoregulation as Assessed by Transfer Function Analysis and the Thigh Cuff Method

Background:Dexmedetomidine, which is often used in intensive care units in patients with compromised circulation, might induce further severe decreases in cerebral blood flow (CBF) with temporal decreases in arterial pressure induced by various stimuli if dynamic cerebral autoregulation is not improved. Therefore, the authors hypothesized that dexmedetomidine strengthens dynamic cerebral autoregulation. Methods:Fourteen healthy male subjects received placebo, low-dose dexmedetomidine (loading, 3 &mgr;g · kg−1 · h−1 for 10 min; maintenance, 0.2 &mgr;g · kg−1 · h−1 for 60 min), and high-dose dexmedetomidine (loading, 6 &mgr;g · kg−1 · h−1 for 10 min; maintenance, 0.4 &mgr;g · kg−1 · h−1 for 60 min) infusions in a randomized, double-blind, crossover study. After 70 min of drug administration, dynamic cerebral autoregulation was estimated by transfer function analysis between arterial pressure variability and CBF velocity variability, and the thigh cuff method. Results:Compared with placebo, steady state CBF velocity and mean blood pressure significantly decreased during administration of dexmedetomidine. Transfer function gain in the very-low-frequency range increased and phase in the low-frequency range decreased significantly, suggesting alterations in dynamic cerebral autoregulation in lower frequency ranges. Moreover, the dynamic rate of regulation and percentage restoration in CBF velocity significantly decreased when a temporal decrease in arterial pressure was induced by thigh cuff release. Conclusion:Contrary to the authors’ hypothesis, the current results of two experimental analyses suggest together that dexmedetomidine weakens dynamic cerebral autoregulation and delays restoration in CBF velocity during conditions of decreased steady state CBF velocity. Therefore, dexmedetomidine may lead to further sustained reductions in CBF during temporal decreases in arterial pressure.

The Different Effects of Midazolam and Propofol Sedation on Dynamic Cerebral Autoregulation

BACKGROUND: Although midazolam and propofol reduce cerebral blood flow (CBF) similarly, they generate different effects on the autonomic nervous system and endothelium-induced relaxation. Midazolam induces sympathetic dominance, whereas propofol induces parasympathetic dominance. Midazolam has no effect on endothelium-dependent relaxation, whereas propofol suppresses endothelium-dependent relaxation. Moreover, midazolam apparently constricts cerebral arterioles. We therefore hypothesized that midazolam and propofol have different effects on dynamic cerebral autoregulation. METHODS: Ten healthy male subjects received midazolam, propofol, and placebo administrations in a randomized, single-blind, crossover study. The modified Observers Assessment of Alertness/Sedation scale was used to assess sedation depth. After reaching a target depth of sedation (Observers Assessment of Alertness/Sedation scale score 3, responds only after name is called loudly and/or repeatedly) or after 15 minutes of normal saline administration as placebo, dynamic cerebral autoregulation was evaluated by spectral and transfer function analyses between mean arterial blood pressure variability in the radial artery measured by tonometry, and CBF velocity variability in the middle cerebral artery measured by transcranial Doppler ultrasonography. RESULTS: Steady-state CBF velocity decreased significantly with midazolam and propofol administration (significant interaction effects, P = 0.024). However, transfer function gain in the low-frequency range decreased significantly only with midazolam administration (significant interaction effects, P = 0.015), suggesting a reduced magnitude of transfer from mean arterial blood pressure oscillations to CBF fluctuations during midazolam sedation. CONCLUSION: Our results suggest that midazolam and propofol sedation have different effects on dynamic cerebral autoregulation despite causing equivalent decreases in steady-state CBF velocity. Only midazolam sedation is likely to improve dynamic cerebral autoregulation.

The effect of sevoflurane on dynamic cerebral blood flow autoregulation assessed by spectral and transfer function analysis

Sevoflurane reduces autonomic neural control, which plays a significant role in cerebral autoregulation. Therefore, we hypothesized that sevoflurane influences cerebral autoregulation. We investigated the effects of sevoflurane on dynamic cerebral blood flow (CBF) autoregulation by using spectral and transfer function analysis between blood pressure variability and CBF velocity variability. Eleven healthy male subjects received 0.5%, 1.0%, and 1.5% sevoflurane via facemask. Dynamic cerebral autoregulation was evaluated by transfer function gain, phase, and coherence between CBF velocity in the middle cerebral artery measured by transcranial Doppler, and blood pressure in the radial artery. Coherence in the very low-frequency range (0.02–0.07 Hz) increased above 0.5 during administration of 0.5% and 1.0% sevoflurane. Transfer function gain in this frequency range (0.02–0.07 Hz), as an index of dynamic cerebral autoregulation, increased significantly with 0.5% and 1.0% sevoflurane. Transfer function gain and coherence in the low- and high-frequency ranges, however, remained unchanged during administration of sevoflurane. These results suggest that sevoflurane impairs dynamic cerebral autoregulation in the very-low-frequency range even with small concentrations, whereas dynamic cerebral autoregulation in the low- and high-frequency ranges remained unchanged.

Successful Pain Management of Primary and Independent Spread Sites in a Child with CRPS Type I Using Regional Nerve Blocks

Dear Editor, A 14-year-old girl reported severe pain of the left first toe after a sprain of the left ankle joint when she was 9 years old. She complained of continuous pain in her chest, back, abdomen, and left first toe. The pain at all the sites was of a burning type with intensity of 6 on the numerical rating pain scale. She was unable to walk due to pain. Mechanical allodynia was present. Redness and swelling were recognized over the left first toe. …

Bell-shaped relationship between central blood volume and spontaneous baroreflex function

Spontaneous baroreflex function can be altered by acute changes in central blood volume. Both a reduction in spontaneous baroreflex function at central hypovolemia and augmentation at hypervolemia suggest a dose-effect relationship between central blood volume and spontaneous baroreflex function. However, this relationship has not been quantified over stepwise widespread changes in central blood volume. Twelve individuals underwent central hypovolemia at two levels of lower body negative pressure (LBNP) (-15 mm Hg, LBNP15; -30 mm Hg, LBNP30) and hypervolemia with two discrete infusions of normal saline (NS) (15 ml kg(-1), NS15; total 30 ml kg(-1), NS30). Spontaneous baroreflex function was assessed using transfer function analysis and the sequence method between blood pressure and R-R interval. Both central venous pressure (-0.6-7.9 mm Hg) and left ventricular end-diastolic volume (72.4-133.1 ml) decreased during LBNP and increased after saline infusion. Both spontaneous baroreflex indices of high-frequency transfer function gain (LBNP30, 17.4+/-3.2; LBNP15, 22.3+/-3.8; baseline, 25.6+/-4.1; NS15, 28.5+/-4.2 ms mm Hg(-1), ANOVA P=0.001) and of the sequence slope (LBNP30, 14.4+/-2.2; LBNP15, 17.2+/-2.5; baseline, 20.5+/-2.8; NS15, 24.5+/-3.1 ms mm Hg(-1), ANOVA P=0.001) increased stepwise from hypovolemia of LBNP30 to hypervolemia of NS15. However, these indices were lower at NS30 (high-frequency transfer function gain, 22.0+/-2.2 ms mm Hg(-1), post-hoc P=0.071; sequence slope, 17.7+/-1.7 ms mm Hg(-1), post-hoc P<0.05) than NS15 during hypervolemia. These results indicated that the relationship between central blood volume and spontaneous baroreflex function is apparently bell-shaped, with maximal augmentation at moderate hypervolemia.

Effects of low-dose ketamine on neuropathic pain : An electroencephalogram-electrooculogram/behavioral study

Abstract The aim of the present study was to clarify the neurophysiological changes associated with analgesic and behavioral effects of low‐dose ketamine HCl in patients suffering from chronic neuropathic pain. Ten in‐patients with neuropathic pain participated in this single‐blind, placebo‐controlled study after giving written informed consent. Following intravenous injections of a saline solution (placebo), three bolus injections of 5 mg ketamine HCl were administered at 5 min intervals. Changes in pain perception were assessed using a numerical rating scale for pain. Behavioral changes, including psychotomimetic effects, were assessed using the Brief Psychiatric Rating Scale (BPRS). Electroencephalograms (EEG) and electrooculograms (EOG) were recorded continuously throughout the testing period. One minute EEG and closed‐eye eye movements were quantified. The effects of ketamine were evaluated by comparing the neurophysiological and behavioral parameters obtained from the placebo and ketamine trials. Pain reduction was significantly correlated with ketamine‐induced changes in hallucinatory behavior and excitement as measured by the BPRS. Ketamine injections caused a significant decrease in the EEGα amplitude without an accompanying reduction in EEG frequency. The EEGα amplitude reduction at the right central electrode was significantly related to subjective pain relief. Subanesthetic doses of ketamine significantly decreased rapid eye movements, but did not initiate slow eye movements. In conclusion, the present EEG‐EOG/behavioral results indicate that ketamine‐induced failure of neural integration between cortical–subcortical regions induces psychotic symptoms and alters pain perception on neuropathic pain.

Cardiovascular reflex responses to temporal reduction in arterial pressure during dexmedetomidine infusion: a double-blind, randomized, and placebo-controlled study

BACKGROUND The low and moderate doses of dexmedetomidine reduce arterial pressure and heart rate (HR), suggesting attenuation of sympathetic activity and dominance of cardiac-vagal activity. These autonomic responses under dexmedetomidine sedation may attenuate cardiovascular reflex responses to temporal reduction in arterial pressure, inducing a severe hypotension. We therefore investigated the effects of dexmedetomidine on cardiovascular reflex responses to temporal reduction in arterial pressure induced by the thigh cuff method. METHODS Twelve healthy men received placebo, low-dose (loading 3 microg kg(-1) h(-1) for 10 min; maintenance 0.2 microg kg(-1) h(-1) for 60 min), and moderate-dose (loading 6 microg kg(-1) h(-1) for 10 min; maintenance 0.4 microg kg(-1) h(-1) for 60 min) dexmedetomidine infusions in a randomized, double-blind, crossover study. After 70 min of drug infusion, systolic arterial pressure (SAP) and HR responses after thigh cuff deflation were evaluated as indices of cardiovascular reflex. RESULTS Reduction in SAP (Delta SAP) [placebo 8 (4), low 12 (4), moderate 19 (5) mm Hg] after thigh cuff deflation was significantly greater in dexmedetomidine than placebo infusions, in a dose-dependent manner. The change in HR (Delta HR), Delta HR/Delta SAP, and the percentage restoration of SAP were lower with dexmedetomidine compared with placebo. CONCLUSIONS The present results indicated that dexmedetomidine weakens arterial pressure preservation and HR responses after thigh cuff deflation, suggesting attenuated cardiovascular reflexes. Therefore, it must be cautioned that dexmedetomidine can lead to further and sustained reduction in arterial pressure during transient hypotension induced by postural changes, haemorrhage, and/or other stresses.