The interaction of temperature with thiopental and etomidate on extracellular dopamine and glutamate levels in Wistar-Kyoto rats subjected to forebrain ischemia.

BACKGROUND: Many studies demonstrate an association between brain damage and the extracellular release of catecholamines and amino acids during cerebral ischemia. While the clinical value of hypothermia during periods of compromised cerebral blood flow and oxygen delivery is well established, the role of anesthetic agents is less clear. Furthermore, the interaction between these agents and hypothermia remains to be elucidated. The purpose of this study was to examine the interactive effects of temperature, sodium thiopental (STP) and etomidate (ETOM) on extracellular neurotransmitter accumulation in the rat corpus striatum during cerebral ischemia. METHODS: Animals were randomly assigned to one of six subgroups: normal saline (NS-norm, pericranial t approximately equal to 37 degrees C, and NS-hypo, t=30 degrees C), etomidate (ETOM-norm and ETOM-hypo), and sodium thiopental (STP-norm and STP-hypo). Microdialysis probes were inserted into the corpus striatum. Dopamine (DA), glutamate, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) levels were measured. At zero minutes, animals received a 10-min infusion of STP (3 mg x kg(-1) x min(-1)), ETOM (0.6 mg x kg(-1) x min(-1)), or NS. Prior to ischemia, animals were given either intravenous STP (10 mg x kg(-1)), ETOM (3 mg x kg(-1)), or NS in bolus form. Each animal was then subjected to 10 min of forebrain ischemia (Is1) followed by a reperfusion interval (Rep1). The entire sequence was then repeated. RESULTS: There were significant interactions between temperature and drug for DA (Is1, P=0.006, Is2, P=0.032) and its metabolites (DOPAC, Is1 P=0.01, HVA, Is1 P=0.03), and for glutamate (Is1, P=0.03, Is2 P=0.06). The nature of this interaction differed for DA and glutamate. The reduction in DA accumulation seen during hypothermia was offset by the addition of either STP or ETOM, whereas the addition of these drugs did not affect the reduced glutamate levels seen with hypothermia. During normothermia, STP and ETOM resulted in diminished DA accumulation compared to controls, yet they increased the accumulation of extracellular glutamate. CONCLUSIONS: Consistent with other studies, hypothermia was associated with diminished extracellular DA concentrations during forebrain ischemia. However, depending on the temperature condition, the addition of STP or ETOM in our forebrain ischemia model led to unexpected findings. The administration of these agents during normothermia diminished ischemia-induced DA accumulation yet resulted in significantly higher concentrations of extracellular glutamate. In contrast, STP and ETOM during hypothermia were noted to significantly offset the DA-reducing effects of hypothermia.

The practice of peripheral nerve blocks in the United States: a national survey [p2e comments].

BACKGROUND AND OBJECTIVES: A nationwide survey was conducted in order to describe practice patterns surrounding the use of peripheral nerve blocks (PNBs). METHODS: Questionnaires were mailed to 805 anesthesiologists selected systematically from the 1995 ASA and ASRA membership directories. Responses from 409 attending anesthesiologists (response rate 56.5%) were analyzed. RESULTS: While almost all respondents (97.8%) regularly use at least some regional anesthesia techniques in their practices, significantly fewer use PNBs, with most anesthesiologists (59.7%) performing less than five PNBs monthly. Peripheral nerve blocks of the lower extremity (femoral 32 %, sciatic 22 %, popliteal 11%) were less frequently used than PNB of the upper extremity (axillary 88%, interscalene 61%) (McNemar chi-square test = 215.2; P < .001). Anesthesiologists who rated their training in PNBs as adequate (50.8%) devoted a larger percentage of their practice to PNBs than anesthesiologists who rated their training as inadequate (P = .02). Despite the infrequent use of PNBs, 176 respondents (42.6%) predicted that their use of PNBs would increase in the future. CONCLUSIONS: Although this survey indicates that regional anesthesia is frequently practiced in the United States, PNBs and particularly PNBs of the lower extremities remain underutilized.

Laudanosine and atracurium concentrations in a patient receiving long-term atracurium infusion.

OBJECTIVE: Atracurium is sometimes used for muscle relaxation in patients undergoing mechanical ventilation. Use of atracurium in high doses or for a long period of time has raised the possibility of the accumulation of laudanosine, a breakdown product known to cause seizure activity in animals. The objective of this report was to see if laudanosine accumulation and seizure activity had occurred in a patient who had received a long-term, relatively high-dose infusion of atracurium. DESIGN: Case report. The patient received atracurium for 38 days, at rates ranging from 0.3 to 0.96 mg/kg/hr. An electroencephalogram (EEG) was done before the discontinuation of the infusion, and plasma concentrations of atracurium and laudanosine were measured at, and after, the termination of the atracurium infusion. The laudanosine elimination half-life was calculated. SETTING: Intensive care unit. PATIENT: A 23-yr-old woman admitted with sickle cell crisis, complicated by acute chest syndrome, acute respiratory distress syndrome, and hepatic and renal failure. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: As expected, laudanosine concentrations were increased but were below the level reported to cause seizure activity in animals. Laudanosine elimination half-life was prolonged to 617 mins, which was consistent with previously reported values. The patient's EEG was normal, with no ictal pattern. CONCLUSIONS: Despite long-term use of high doses of atracurium infusion and the increased elimination half-life of laudanosine, only moderate accumulation of laudanosine occurred, and the EEG was normal. Hence, it appears unlikely that toxic concentrations of laudanosine would be reached, even in a critically ill patient.

Combined popliteal and posterior cutaneous nerve of the thigh blocks for short saphenous vein stripping in outpatients: an alternative to spinal anesthesia.

STUDY OBJECTIVE: To compare a combination of peripheral nerve blocks with spinal anesthesia in ambulatory patients undergoing short saphenous vein stripping. DESIGN: Prospective, randomized study. SETTING: University hospital. PATIENTS: 28 ASA physical status l and II ambulatory surgery patients undergoing short saphenous vein stripping. INTERVENTIONS: 14 patients received a popliteal block (sciatic nerve block at the popliteal fossa) using 30 ml of alkalinized 3% chloroprocaine and a posterior cutaneous nerve of the thigh block with 10 ml of 1% lidocaine. The 14 patients who were randomized to the spinal anesthesia group received 65 mg of 5% hyperbaric lidocaine. MEASUREMENTS AND MAIN RESULTS: There were no significant differences in age and gender between the two groups (mean age 53 +/- 13 years, 8 men and 20 women). Patients in the peripheral nerve block group recovered significantly faster in phase 1 of the postanesthesia care unit (PACU) (67 +/- 10 min vs. 122 +/- 50 min, p < 0.01) and were discharged home sooner (222 +/- 53 min vs. 294 +/- 69 min, p < 0.01) than the patients in the spinal anesthesia group. CONCLUSIONS: The combination of popliteal and posterior cutaneous nerve of the thigh blocks provided adequate anesthesia and a faster recovery profile with a similar subjective acceptance of both anesthetic techniques in ambulatory patients undergoing short saphenous vein stripping in the prone position.

Supine approach to the sciatic nerve in the popliteal fossa.

PURPOSE: Sciatic nerve block in the popliteal fossa (popliteal nerve block, PNB) is an anaesthetic technique well-suited for operations below the knee. However, difficulty with positioning the patient in the prone position often precludes the classical, posterior approach to the block. In this report, an alternative approach to PNB that can easily be performed with a patient in the supine position is described. CLINICAL FEATURES: Three patients in whom the clinical circumstances precluded the use of the classical approach to PNB are described. In each case, PNB was performed using the alternative, supine approach. With a patient in the supine position, the leg is flexed at both the hip and knee, and supported by an assistant. After the anatomical landmarks of the popliteal fossa are identified, an insulated needle attached to a peripheral nerve stimulator is inserted 7 cm above the popliteal crease, 1 cm laterally to the midline and directed 45 degrees cephalad. Upon obtaining either dorsal or plantar flexion of the foot at the output current of 0.5 mAmp or less. 30-40 ml of local anaesthetic solution are injected. CONCLUSION: The supine approach to PNB allows the use of the block in patients that cannot be positioned in the prone position. Flexion of the leg at the knee greatly facilitates identification of the anatomical landmarks. When combined with a block of the femoral or saphenous nerve, this technique provides excellent anaesthesia for patients undergoing foot and ankle surgery.

Effect of etomidate on in vivo ischemia-induced dopamine release in the corpus striatum of the rat: a study using cerebral microdialysis.

Dopamine (DA) is released in large quantities into the corpus striatum during cerebral ischemia and may exacerbate tissue damage. Using cerebral microdialysis, we studied the effect of etomidate on in vivo ischemia-induced DA release in rat corpus striatum. Reversible cerebral ischemia was induced by using carotid ligatures and hypovolemic hypotension, and monitored with laser Doppler flowmetry. After baseline measurements, 20 normothermic, anesthetized rats were subjected to three separate periods of cerebral ischemia, interrupted by 45- to 75-min periods of reperfusion. The rats were randomized into two groups. All rats received 400 mg/kg of intraperitoneal chloral hydrate for induction of anesthesia. In Group I (n = 10) anesthesia was maintained using additional intraperitoneal chloral hydrate 100 mg/kg every 2 h. Group II received etomidate 0.6 mg/kg 10 min before the first episode of cerebral ischemia, followed by an infusion of 60 micrograms.kg-1 x min-1. Before each subsequent period of induced ischemia, an additional dose of etomidate (0.6 mg/kg) was administered. DA levels were approximately 350 times above baseline in Group I during the three ischemic episodes (IS1, IS2, and IS3). In Group II, ischemia-induced DA release was significantly attenuated (by 79%) during IS1, IS2, and IS3 compared to Group I (P < 0.01). DA levels did not significantly change in magnitude during the three ischemic episodes in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of isoflurane and halothane on in vivo ischemia-induced dopamine release in the corpus striatum of the rat. A study using cerebral microdialysis.

BACKGROUND: Dopamine is released in large quantities into the corpus striatum during cerebral ischemia and may exacerbate tissue damage. METHODS: Using cerebral microdialysis, the effect of isoflurane on in vivo ischemia-induced dopamine release was studied in rat corpus striatum. Reversible cerebral ischemia was induced using carotid ligatures and induced hypovolemia and was monitored with laser-Doppler flowmetry. Following baseline measurements, 28 normothermic, anesthetized rats were subjected to cerebral ischemia followed by reperfusion. The rats were divided into four groups. Group 1 (n = 10) was anesthetized using chloral hydrate. Groups 2 and 3 received 1.5% end-tidal isoflurane. In group 2 (n = 6), hypotension was left untreated during the reperfusion period, and in group 3 (n = 6), mean arterial pressure was maintained using phenylephrine. Group 4 (n = 6) received 1-1.2% end-tidal halothane. RESULTS: Compared with pre-ischemic levels, large quantities of dopamine (350 x baseline levels) were released in group 1 animals during cerebral ischemia. Compared with group 1, ischemia-induced dopamine release was significantly reduced in group 2 (by 58%) and in group 3 (by 56%), but not in group 4. Group 2 animals were uniformly hypotensive during reperfusion and continued to release substantial amounts of dopamine (8 x baseline levels). In groups 1, 3, and 4, dopamine release decreased to near baseline levels during reperfusion. In group 3, dopamine metabolite production was significantly increased during ischemia, suggesting that enzymatic function and neuronal reuptake of dopamine was preserved. CONCLUSIONS: Isoflurane, compared with chloral hydrate and halothane, inhibits the release of the neurotransmitter dopamine during cerebral ischemia.

Role of two-dimensional transoesophageal echocardiography in the management of a right ventricular tumour.

Right ventricular outflow tract tumours are rarely reported. The perioperative management of a patient presenting for excision of an obstructing right ventricular outflow tract myxoma is described. Two-dimensional transoesophageal echocardiography was performed intraoperatively and was found to be of considerable value in understanding the pathophysiology of the tumour. Following excision of the tumour, right ventricular function improved and tricuspid regurgitation resolved.