Biomedical subjects
Publications and source records attributed to Shinn-Long Lin.
We report a case of prominent postoperative macroglossia after posterior fossa surgery in the prone position. The potential risk factors predisposing to its generation, prophylactic measures to avoid it and treatments for its alleviation are reviewed and discussed.
This study was designed to investigate the effect of acute and chronic intrathecal (i.t.) injection of gabapentin (GBP) on the antinociceptive effect of morphine and tolerance development using a tail-flick latency test. Levels of excitatory amino acids (EAA) in i.t. CSF dialysates were also measured by high performance liquid chromatography. Male Wistar rats were implanted with either one or two i.t. catheters for drug injection or pump infusion and with a microdialysis probe for CSF dialysate collection. The effect of acute GBP (10 microg i.t.) injection on the morphine dose response was examined in both naïve rats and rats made tolerant by continuous infusion of morphine (15 microg/h i.t.) for 5 days. At such a low dose (10 microg i.t.), GBP did not enhance morphine's antinociception in naïve rats. In morphine-tolerant rats, however, acute GBP (10 microg i.t.) injection potentiated morphine's antinociception and yielded a 14.6-fold shift in morphine's dose-response curve. When GBP (10 microg/h i.t.) was co-infused with morphine (15 microg/h i.t.) to examine its effect on the development of morphine tolerance, GBP attenuated the development of morphine tolerance. The effect of GBP and morphine on CSF glutamate and aspartate levels was examined in naïve rats, and the effect of morphine challenge on CSF glutamate and aspartate levels was examined in rats previously infused for 5 days with morphine alone or morphine plus GBP. Acute injection of GBP (10 microg i.t.), morphine (50 microg i.t.), or GBP (10 microg i.t.) followed by morphine (50 microg i.t.) 30 min later had no significant effect on CSF EAA concentration in naïve rats; however, in tolerant rats, morphine challenge (50 microg i.t.) increased aspartate and glutamate levels to 221 +/- 22% and 296 +/- 43%, respectively, of those before morphine challenge, and this phenomenon was inhibited by GBP co-infusion. Our results show that GBP, at a dose without enhanced effect on morphine's antinociception in naïve rats, not only potentiates morphine's antinociceptive effect in morphine-tolerant rats but also attenuates the development of morphine tolerance. The mechanism of the effect of GBP on morphine tolerance might be via suppression of the EAA concentration in spinal CSF dialysate.
Naltrexone, an opioid antagonist, has been reported to possess an anti-inflammatory effect via blockade of opioid receptor. The aim of this study is to evaluate the protective effect of naltrexone on LPS-induced septic shock in rats. Sepsis was induced by administration of LPS (10 mg/kg, i.v.) in anesthetized rats. Results demonstrated that pretreatment with naltrexone (10 mg/kg, i.v.) significantly ameliorated hypotension and bradycardia of rats 6 h after LPS administration. In isolated blood vessel, study showed that pretreatment with naltrexone significantly improved norepinephrine-induced vasoconstriction and ACh-induced vasorelaxation in aorta of endotoxemic animals. Naltrexone significantly reduced the elevation of serum glutamate-oxalacetate transaminase and glutamate-pyruvate transaminase (as index of hepatic function) induced by LPS. The infiltration of polymorphonuclear neutrophils into liver 48 h after LPS treatment in mice was also reduced by naltrexone. On the other hand, naltrexone significantly decreased the levels of plasma TNF-alpha and inhibited overproduction of superoxide anions in aortic rings. However, naltrexone did not suppress the overproduction of NO (measured by its metabolites nitrite/nitrate in plasma) and iNOS expression in lungs induced by LPS. In in vitro study, naltrexone did not attenuate non-enzymatic iron-induced lipid peroxidation in rat brain homogenates. In conclusion, pretreatment with naltrexone significantly improved circulatory failure and hepatic dysfunction in sepsis. These effects were associated with reduction of TNF-alpha levels and superoxide anion formation, which may be attributed to antagonism of opioid receptors.
We designed this study to evaluate the effect of injection time and smoking on fentanyl-induced cough. Four-hundred-fifty ASA class I-II patients, aged 18-80 yr and weighing 40-90 kg, scheduled for elective surgery were included. All patients received fentanyl (100 microg for patients weighing 40-69 kg and 150 microg for patients weighing 70-90 kg for clinical convenience) via the proximal port of a peripheral IV line on the forearm. Patients were randomly assigned to 3 groups of 150 patients each. Patients in Group I received fentanyl injection over 2 s, whereas for patients in Groups II and III the fentanyl was injected at a constant rate over 15 s and 30 s, respectively. We recorded the number of coughs of each patient during and 30 s after fentanyl injection. The incidence of cough was 18% in group I, 8% in Group II, and 1.3% in Group III, significantly less (P < 0.05) with a longer injection time. Current smokers had a less frequent incidence of cough than nonsmokers; however, this effect was only significant in light smokers (<10 cigarettes per day or <10 smoking years or <10 pack-years). In conclusion, a longer injection time reduces the incidence of fentanyl-induced cough, and light smoking may be a protective factor against fentanyl-induced cough.
BACKGROUND: In our previous study, we had demonstrated that intramuscular (i.m.) dextromethorphan (DM) could provide a preemptive analgesic effect and improve postoperative pain management. Regrow is a long-duration slow-release oral dextromethorphan available for clinical use with good patient compliance. The present study was designed to examine whether oral regrow may also offer the same preemptive analgesic effect as i.m. DM does in postoperative pain management. METHODS: Seventy-five patients, ASA status I and II, scheduled for hemorrhoidectomy were included and randomly assigned to the control and study groups. In the control group patients received placebo orally 8 h before surgical incision. In the study group, patients received regrow orally either 120 mg (R-120) or 240 mg (R-240) 8 h before skin incision. Pethidine (1 mg/kg, i.m.) was given for postoperative pain relief on demand. The time to first pethidine injection, total pethidine consumption, worst pain score, and pethidine-related side effects were recorded for two days. RESULTS: The times to first pethidine injection were 5.4 +/- 3.1, 6.5 +/- 3.5 and 12.7 +/- 5.7 h in the control, R-120 and R-240 groups, respectively. Total pethidine consumptions were 150 +/- 12, 132 +/- 11.8 and 82 +/- 12.5 mg in the control, R-120 and R-240 groups, respectively. The worst visual analog scale pain scores were respectively 7.2 +/- 0.4, 6.9 +/- 0.2 and 5.5 +/- 0.4 in the control, R-120 and R-240 groups during the 2-day observation. Five and three patients suffered pethidine-related side effects in the control and R-120 groups, respectively. CONCLUSIONS: This study revealed that premedication of oral regrow 240 mg provided a preemptive analgesic effect, thus reducing the severity of postoperative pain and pethidine requirement in post-hemorrhoidectomy patients.
An aged female patient with previous stroke and atrial fibrillation (AF) undertook a dynamic hip screw (DHS) fixation due to femoral fracture. She suffered from a new stroke 6 h after surgery. After emergent evaluation and treatment, the patient regained her consciousness and fully recovered neurologic function before discharge. The etiology and management of stroke after orthopedic surgery are discussed.
Malfunction of either inspiratory or expiratory check valve in a breathing circuit system may allow carbon dioxide (CO2) rebreathing and result in hypercapnia. The subsequent increase of PaCO2 may entail increased sympathetic activity which in turn causes serious problems such as tachyarrhythmia and myocardial ischemia, particularly in patients who have history of coronary artery disease (CAD). Here, we report an incident of rupture of the inspiratory valve in the breathing circuit which happened to a patient during induction of general anesthesia and eventuated in markedly heightened end-tidal CO2 (EtCO2) of the patient. The recognition, related complications and management of the inspiratory valve malfunction are discussed.
BACKGROUND: Anesthetic techniques are known to affect blood hemostasis, which may be responsible for the pathogenesis of postoperative venous thromboembolism. The purpose of this study was to evaluate the effect of general and spinal anesthesias on blood hemostasis using thromboelastography. METHODS: Forty patients undergoing arthroscopic knee surgery were enrolled for study and randomly allocated to one of two groups, to receive either general (GA; n = 20) or spinal anesthesia (SA; n = 20). In addition to thromboelastography, prothrombin and activated partial-thromboplastin time, and haematocrit and platelet count were also examined concurrently. Blood was sampled and examined before anesthesia to provide the baseline data (Time 1). Three more evaluations were performed at different time, i.e., twenty minutes after induction of anesthesia and just prior to skin incision (Time 2), thirty minutes after skin incision (Time 3), and three hours after surgery (Time 4). RESULTS: There were no intra- or inter-group differences noted as comparing the measured parameters obtained prior to, during, or three hours after surgery. CONCLUSIONS: From the present study, we do not find any individual anesthetic technique which would have effect on the hemostasis of patients who received diagnostic arthroscopic surgery.