Anesthesia and analgesia
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Anesthesia and analgesia · Apr 2004
Randomized Controlled Trial Clinical TrialPreoperative oral dextromethorphan attenuated tourniquet-induced arterial blood pressure and heart rate increases in knee cruciate ligament reconstruction patients under general anesthesia.
The precise mechanism of tourniquet-induced arterial blood pressure increase is unknown. We determined the effect of preoperative oral dextromethorphan (DM) on arterial blood pressure and heart rate changes during tourniquet inflation in knee cruciate ligament reconstruction patients under general anesthesia. Patients in the DM group (n = 38) received oral DM 30 mg, and patients in the control group (n = 38) received oral placebo 2 h before the induction of anesthesia. Anesthesia was maintained with sevoflurane 2.0% and N(2)O in 33% oxygen, and the trachea was intubated until the end of surgery. Arterial blood pressure and heart rate were measured at 0, 30, and 60 min after the start of tourniquet inflation. Systolic arterial blood pressure and heart rate at 60 min in the control group were significantly more than those in the DM group (131.1 +/- 15.8 mm Hg versus 123.6 +/- 15.9 mm Hg [P < 0.05] and 74.1 +/- 11.3 bpm versus 67.8 +/- 8.5 bpm [P < 0.01], respectively). The percentage increase in systolic arterial blood pressure and heart rate in the DM group was also attenuated when compared with that in the control group (P < 0.05). In conclusion, preoperative oral DM 30 mg significantly attenuated arterial blood pressure and heart rate increases during tourniquet inflation under general anesthesia. ⋯ We demonstrated that preoperative oral dextromethorphan 30 mg significantly attenuated arterial blood pressure and heart rate increases at 60 min during tourniquet inflation in patients undergoing knee cruciate ligament reconstruction under general anesthesia.
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Anesthesia and analgesia · Apr 2004
Case ReportsUnusually low bispectral index values during emergence from anesthesia.
We observed unusually low BIS values during emergence from anesthesia apparently caused by misanalysis (as "suppression") of low voltage electroencephalogram. ⋯ When BIS values do not adequately correspond with clinical status, it is necessary to check raw electroencephalogram waveforms to more clearly characterize patient status.
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Lumbar epidural anesthesia and analgesia has gained increasing importance in perioperative pain therapy for abdominal and lower limb surgery. The loss-of-resistance technique, used to identify the epidural space, is thought to rely on the penetration of the ligamentum flavum. However, the exact morphology of the ligamentum flavum at different vertebral levels remains controversial. Therefore, in this study, we directly investigated the incidence of lumbar ligamentum flavum midline gaps in embalmed cadavers. Vertebral column specimens were obtained from 45 human cadavers. On each dissected level, ligamentum flavum midline gaps were recorded. The incidence of midline gaps per number of viable specimens at the following levels was: L1-2 = 10 of 45 (22.2%), L2-3 = 5 of 44 (11.4%), L3-4 = 5 of 45 (11.1%), L4-5 = 4 of 43 (9.3%), L5/S1 = 0 of 33 (0%). In conclusion, the present study determined the frequency of lumbar ligamentum flavum midline gaps. Gaps in the lumbar ligamentum flavum are most frequent between L1 and L2 but are more rare below this level. When using the midline approach, the ligamentum flavum may not impede entering the epidural space in all patients. ⋯ The ligamentum flavum is a crucial anatomical landmark for the safe performance of epidural anesthesia. However, the present study demonstrates some failure of the lumbar ligamentum flavum as a landmark. This may mean that, using a midline approach, one cannot always rely on the ligamentum flavum as a perceptible barrier to epidural needle advancement.
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Anesthesia and analgesia · Apr 2004
The antiinflammatory effects of ketamine in endotoxemic rats during moderate and mild hypothermia.
Endotoxemia is a common problem among critically-ill patients. We previously found that ketamine inhibited hypotension, metabolic acidosis, and increase of plasma cytokines during endotoxemia in rats. Although endotoxic patients often develop hypothermia, it has not been determined whether ketamine retains its antiinflammatory effects during hypothermia. We investigated the effects of ketamine on endotoxemic rats subjected to moderate and mild hypothermia. Male Wistar rats (n = 100) were anesthetized intraperitoneally with pentobarbital sodium and assigned to one of two protocols: one representing moderate hypothermia (30 degrees C-32 degrees C) and the other, mild hypothermia (33 degrees C-35 degrees C). Each protocol included 5 equal groups: 1). Escherichia coli endotoxin (15 mg/kg IV) in normothermia, 2). ketamine (10 mg x kg(-1) x h(-1) IV) during and after endotoxin injection in normothermia, 3). saline in hypothermia, 4). endotoxin (15 mg/kg IV) in hypothermia, and 5) ketamine (10 mg x kg(-1) x h(-1) IV) in hypothermia after endotoxin injection. Rats were then warmed or cooled to maintain rectal temperatures as above for 6 h. We assessed hemodynamics, acid-base status, and plasma concentrations of tumor necrosis factor-alpha, and interleukin-6. Endotoxemic rats developed hypotension and metabolic acidosis as well as increased plasma cytokine concentrations. At 6 h after endotoxin injection, the mean systolic arterial blood pressure decreased by 71% in the saline/normothermia/endotoxin group, whereas it decreased by only 6%, 41%, and 29% in the ketamine/normothermia/endotoxin, saline/moderate hypothermia/endotoxin, and ketamine/moderate hypothermia/endotoxin groups, respectively. Ketamine administration to endotoxemic rats with hypothermia, whether moderate or mild, also attenuated hypotension, metabolic acidosis, and cytokine increase, but these effects were not superior to those of hypothermia alone. Our findings suggest that, during hypothermia, ketamine administration may not have additive beneficial antiinflammatory effects. ⋯ Although ketamine administration decreased the severity of hypotension and acidosis in endotoxemic rats, ketamine administration may not have additive beneficial antiinflammatory effects during hypothermia.