Chih-Ping Yang

The interaction effect of perioperative cotreatment with dextromethorphan and intravenous lidocaine on pain relief and recovery of bowel function after laparoscopic cholecystectomy

Both dextromethorphan (DM) and IV lidocaine improve postoperative pain relief. In the present study, we evaluated the interaction of DM and IV lidocaine on pain management after laparoscopic cholecystectomy (LC). One-hundred ASA physical status I or II patients scheduled for LC were randomized into four equal groups to receive either: (a) chlorpheniramine maleate (CPM) intramuscular injection (IM) 20 mg and IV normal saline (N/S) (group C); (b) DM 40 mg IM and IV N/S (group DM); (c) CPM 20 mg IM and IV lidocaine 3 mg · kg−1 · h−1 (group L); or (d) DM 40 mg IM and IV lidocaine (group DM+L). All treatments were administered 30 min before skin incision. Analgesic effects were evaluated using visual analog scale pain scores at rest and during coughing, time to meperidine request, total meperidine consumption, and the time to first passage of flatus after surgery. Patients of the DM+L group exhibited the best pain relief and fastest recovery of bowel function among groups. Patients in the DM and L groups had significantly better pain relief than those in the C group. The results showed an additional effect on pain relief and a synergistic effect on recovery of bowel function when DM was combined with IV lidocaine after LC.

Preincisional intravenous pentoxifylline attenuating perioperative cytokine response, reducing morphine consumption, and improving recovery of bowel function in patients undergoing colorectal cancer surgery

Cytokine release during surgery can produce a long-lasting hyperalgesia. Thus, preoperatively-administered cytokine inhibitors might reduce the production of cytokines, decreasing central nervous system sensitization and improving the quality of postoperative pain relief. We investigated the hypothesis that preincisional IV pentoxifylline (PTX) treatment could attenuate the release of proinflammatory (tumor necrosis factor, interleukin (IL)-1&bgr;, IL-6, and IL-8) and antiinflammatory (IL-1 receptor antagonist) cytokines in patients who underwent elective colorectal cancer surgery. Forty patients were randomly assigned to 1 of 2 groups of 20 each: the PTX group received a PTX 5 mg/kg IV infusion before the induction of anesthesia, whereas the control group received an equal volume of normal saline. Venous blood samples were obtained at frequent intervals. After surgery, all patients received patient-controlled analgesia (PCA) morphine for postoperative pain relief. Patients in the PTX group exhibited longer PCA trigger times, less morphine consumption, and a faster return of bowel function compared with patients in the control group. Moreover, the plasma levels of IL-6, IL-8, and IL-1 receptor antagonist were less in the treatment group, and there was no significant difference in wound infections, tumor recurrence, or metastatic rates between groups during a 2-yr follow-up.

Early use of small-dose vasopressin for unstable hemodynamics in an acute brain injury patient refractory to catecholamine treatment: a case report.

IMPLICATIONS Small-dose IV vasopressin infusion may be beneficial in acute brain injury patients with unstable hemodynamics who are refractory to fluid resuscitation and catecholamine vasopressors.

Intrathecal ultra-low dose naloxone enhances the antinociceptive effect of morphine by enhancing the reuptake of excitatory amino acids from the synaptic cleft in the spinal cord of partial sciatic nerve-transected rats.

BACKGROUND: In this study, we examined the effects of ultra-low dose naloxone on the antinociceptive effect of morphine and on spinal cord dorsal horn glutamate transporter expression in rats with neuropathic pain. METHODS: Neuropathic pain was induced in male Wistar rats by partial transection of the left sciatic nerve and an intrathecal catheter was implanted for drug administration; in some rats, an intrathecal microdialysis probe for cerebrospinal fluid (CSF) dialysate collection was also implanted. Nociception was assessed using the plantar test, a Hargreaves radiant heat apparatus, and by the von Frey test, using a dynamic plantar anesthesiometer. Glutamate transporter protein expression in the left spinal cord dorsal horn was examined by Western blotting and immunohistochemistry. Levels of the excitatory amino acids (EAAs) glutamate and aspartate in the CSF dialysate were measured using high-performance liquid chromatography. RESULTS: Reduced astrocyte expression of glutamate transporters (GLT-1 and GLAST levels were 55% and 53%, respectively, of that in sham-operated rats) in laminae I and II of the spinal cord dorsal horn ipsilateral to the partial sciatic nerve transection (PST), and hyperalgesia and allodynia in the PST hindlimb were observed. High-dose naloxone (15 &mgr;g) attenuated the antihyperalgesia and antiallodynia effects of the morphine (10 &mgr;g). In contrast, ultra-low dose (15 ng) naloxone enhanced the antinociceptive effect of morphine (10 &mgr;g), with an increase in the paw withdrawal threshold to thermal stimulus (from 19% to 35%) and to tactile stimulus (from 33% to 55%) compared with morphine treatment alone, and this was associated with restoration of GLAST and GLT-1 expression to control levels (102% and 114%, respectively) in the astrocytes of laminae I and II in the spinal cord dorsal horn ipsilateral to the PST hindlimb and a decrease in EAA levels in the CSF dialysate (glutamate: 10.0 &mgr;M; aspartate: 1.1 &mgr;M). CONCLUSIONS: Ultra-low dose naloxone enhanced the antinociceptive effect of morphine in PST rats, possibly by restoration of GLAST and GLT-1 expression in astrocytes, which inhibited the accumulation of EAAs in the synapses, resulting in a neuroprotective effect.

Correlation between changes in regional cerebral blood flow and pain relief in complex regional pain syndrome type 1.

Objective: Analyzing changes in regional cerebral blood flow (rCBF) with SPECT in complex regional pain syndrome type 1 (CRPS 1), formerly known as reflex sympathetic dystrophy, is an optimal method for evaluating effective pain relief. We attempted to investigate the correlation of changes in rCBF with pain relief during treatments of sympathetic blockade and multimodal epidural pain control. Case Report: We describe a patient with severe CRPS 1 in whom conventional treatment failed to relieve the pain. Combined repeated lumbar sympathetic blocks and long-term epidural morphine, bupivacaine, and ketamine administration provided satisfactory pain relief and functional activity recovery. Six normal control subjects having one Tc-99m HMPAO scan each and the patient with CRPS having 3 Tc-99m HMPAO scans (once before treatment and twice at 4 months and 6 months after treatment, respectively). The patient with CRPS showed lower rCBF than normal controls in the left thalamus and higher rCBF than normal controls in the right parietal lobe and left frontal lobe. After subsequent treatment, the subtraction images showed increased rCBF in the left thalamus and decreased rCBF in the right parietal and left frontal lobes. Conclusions: Tc-99m HMPAO SPECT showed a relationship of rCBF in the thalamus, parietal lobe, and frontal lobe with pain relief. rCBF alterations may provide an indicator for the quality of pain management for neuropathic pains. Subtraction analysis between pre- and posttreatment, by using statistical parametric mapping (version 2), can be used as an objective indicator for the effectiveness of therapy.

Epidural fentanyl speeds the onset of sensory and motor blocks during epidural ropivacaine anesthesia

In this study we examined the onset times of sensory and motor block during epidural ropivacaine anesthesia with and without the addition of fentanyl to the epidural solution. Forty-five young male patients undergoing knee arthroscopic surgery were randomly allocated into 3 groups of 15 patients each: epidural fentanyl (EF; epidural administration of 15 mL of 1% ropivacaine plus 100 &mgr;g fentanyl followed by IV injection of 2 mL of normal saline); IV fentanyl (IF; epidural administration of 15 mL of 1% ropivacaine plus 2 mL of normal saline followed by IV injection of 100 &mgr;g fentanyl); and control (C; epidural administration of 15 mL of 1% ropivacaine plus 2 mL of normal saline followed by IV injection of 2 mL of normal saline). The sensory and motor blocks were assessed by pinprick and modified Bromage scale, respectively. The hemodynamic changes, postepidural shivering, and side effects of epidural fentanyl were also recorded. There was no difference in the distribution of age, weight, and height among the 3 groups. The onset time of sensory block to the T10 dermatome was significantly more rapid in the EF group (13.0 ± 3.0 min) than in the IF group (16.2 ± 3.5 min, P < 0.05) or C group (17.7 ± 3.6 min, P < 0.05). The onset times of motor block up to Bromage scale 1 and 2 were significantly more rapid in the EF group (11.9 ± 4.6 and 24.4 ± 5.9 min) than in the IF group (16.9 ± 4.7 and 30.8 ± 5.6 min, P < 0.05) or C group (18.3 ± 4.9 and 32.7 ± 5.7 min, P < 0.05). There was no difference in the incidence of shivering among the three groups. Pruritus was observed in three patients of the EF group and one patient of the IF group. No nausea, vomiting, respiratory depression, urinary retention, or hypotension was observed in any patient. We conclude that epidural administration of the mixture of 100 &mgr;g fentanyl and 1% ropivacaine solution accelerated the onset of sensory and motor blocks during epidural ropivacaine anesthesia without significant fentanyl-related side effects.

Intrathecal ultra-low dose naloxone enhances the antihyperalgesic effects of morphine and attenuates tumor necrosis factor-α and tumor necrosis factor-α receptor 1 expression in the dorsal horn of rats with partial sciatic nerve transection.

BACKGROUND: Glutamate homeostasis and microglia activation play an important role in the development and maintenance of neuropathic pain. We designed this investigation to examine whether ultra-low dose naloxone administered alone or in combination with morphine could alter the concentration of the excitatory amino acids (EAAs) glutamate and aspartate, as well as the expression of tumor necrosis factor-&agr; (TNF-&agr;) and its receptors (TNFR1 and TNFR2) in the spinal cord dorsal horn of rats with partial sciatic nerve transection (PST). METHODS: Male Wistar rats underwent intrathecal catheter implantation for drug delivery and were divided in 7 groups: sham-operated + saline (sham), PST + saline (S), PST + 15 ng naloxone (n), PST + 15 µg naloxone (N), PST + 10 µg morphine (M), PST + 15 ng naloxone + 10 µg morphine (Mn), PST + 15 µg naloxone + 10 µg morphine (MN). Thermal withdrawal latency and mechanical withdrawal threshold, TNF-&agr; and TNFR expression in the spinal cord and dorsal root ganglia, and EAAs glutamate and aspartate concentration in cerebrospinal fluid dialysates were measured. RESULTS: Ten days after PST, rats developed hyperalgesia (P < 0.0001) and allodynia (P < 0.0001), and increased TNF-&agr; (P < 0.0001) and TNFR1 expression (P = 0.0009) were measured in the ipsilateral spinal cord dorsal horn. The antihyperalgesic and antiallodynic effects of morphine (10 &mgr;g) were abolished by high-dose naloxone (15 &mgr;g; P = 0.0031) but enhanced by ultra-low dose naloxone (15 ng; P = 0.0015), and this was associated with a reduction of TNF-&agr; (P < 0.0001) and TNFR1 (P = 0.0009) expression in the spinal cord dorsal horn and EAAs concentration (glutamate: P = 0.0001; aspartate: P = 0.004) in cerebrospinal fluid dialysate. Analysis of variance (ANOVA) or Student t test with Bonferroni correction were used for statistical analysis. CONCLUSIONS: Ultra-low dose naloxone enhances the antihyperalgesia and antiallodynia effects of morphine in PST rats, possibly by reducing TNF-&agr; and TNFR1 expression, and EAAs concentrations in the spinal dorsal horn. Ultra-low dose naloxone may be a useful adjuvant for increasing the analgesic effect of morphine in neuropathic pain conditions.

Cerebrospinal fluid rhinorrhea after thermometer insertion through the nose.

Cerebrospinal fluid (CSF) rhinorrhea is a rare clinical condition. Most leaks either are caused by traumatic head injury or are a complication of surgical procedures on the base of the skull. CSF rhinorrhea from nasal tube placement has been reported previously. We report a case of nasal thermometer placement during anesthesia complicated by a CSF leakage. We reemphasize that any material—including thermometers, nasogastric tubes, and endotracheal tubes—should be directed posteriorly after introduction into the external naris.