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Biomedical subjects

R Tempelhoff

Publications and source records attributed to R Tempelhoff.

At least 19 recordsLinked to original sources
PubMed2001

The effects of clonidine premedication and scalp infiltration of lidocaine on hemodynamic responses to laryngoscopy and skull pin head-holder insertion during skull base procedures.

This study was designed to determine if oral clonidine or lidocaine, injected into the scalp before head-holder (H-H) insertion, would attenuate the hemodynamic effects associated with intubation and H-H placement. Thirty-four patients undergoing skull base procedures were randomized to four groups. Group 1 received clonidine 5 mcg/kg po before surgery with 10 to 15 ml of 1% lidocaine infiltrated at pin insertion sites; Group 2 received clonidine with saline infiltration; Group 3 received a placebo preoperatively and had lidocaine infiltrated at pin sites; and Group 4 received a placebo with saline infiltrated. All patients had a standard anesthetic titrated to a 10 to 14 Hz EEG endpoint during laryngoscopy and H-H placement. Mean arterial pressure (MAP) was similar between groups during intubation, but heart rate (HR) increased in patients who did not receive clonidine. H-H application increased HR and MAP in Group 4. HR also increased after H-H placement in patients who received oral clonidine, while patients receiving scalp lidocaine or both clonidine and scalp lidocaine had little change in either value. Clonidine attenuated HR increases after laryngoscopy but not after H-H placement. Lidocaine injected at the pin sites reduced HR, and MAP increased after H-H insertion. The combination of oral clonidine and scalp lidocaine blunted hemodynamic responses to both intubation and H-H placement.

Journal Article↗
PubMed2001

The effect of prone positioning on intraocular pressure in anesthetized patients.

BACKGROUND: Ocular perfusion pressure is commonly defined as mean arterial pressure minus intraocular pressure (IOP). Changes in mean arterial pressure or IOP can affect ocular perfusion pressure. IOP has not been studied in this context in the prone anesthetized patient. METHODS: After institutional human studies committee approval and informed consent, 20 patients (American Society of Anesthesiologists physical status I-III) without eye disease who were scheduled for spine surgery in the prone position were enrolled. IOP was measured with a Tono-pen XL handheld tonometer at five time points: awake supine (baseline), anesthetized (supine 1), anesthetized prone (prone 1), anesthetized prone at conclusion of case (prone 2), and anesthetized supine before wake-up (supine 2). Anesthetic protocol was standardized. The head was positioned with a pinned head-holder. Data were analyzed with repeated-measures analysis of variance and paired t test. RESULTS: Supine 1 IOP (13 +/- 1 mmHg) decreased from baseline (19 +/- 1 mmHg) (P < 0.05). Prone 1 IOP (27 +/- 2 mmHg) increased in comparison with baseline (P < 0.05) and supine 1 (P < 0.05). Prone 2 IOP (40 +/- 2 mmHg) was measured after 320 +/- 107 min in the prone position and was significantly increased in comparison with all previous measurements (P < 0.05). Supine 2 IOP (31 +/- 2 mmHg) decreased in comparison with prone 2 IOP (P < 0.05) but was relatively elevated in comparison with supine 1 and baseline (P < 0.05). Hemodynamic and ventilatory parameters remained unchanged during the prone period. CONCLUSIONS: Prone positioning increases IOP during anesthesia. Ocular perfusion pressure could therefore decrease, despite maintenance of normotension.

Adolescent↗
PubMed2000

Visual loss after spine surgery: a survey.

OBJECTIVE: To survey a large number of neurosurgical spine surgeons for data regarding the presence of risk factors in patients experiencing visual loss after spine surgery. METHODS: A survey was sent to current members (as of 1997) of the American Association of Neurological Surgeons/Congress of Neurological Surgeons, Section on Disorders of the Spine and Peripheral Nerves, with questions focusing on intraoperative factors that may predispose patients to perioperative visual loss. RESULTS: Two hundred ninety surveys were returned, and 24 patients with visual loss after spine surgery were reported by 22 surgeons. Although many of these patients had probable causative factors for visual loss after surgery (e.g., hypotension, low hematocrit level, coexisting disease), some did not (n = 8). CONCLUSION: These results suggest the necessity of a high index of suspicion for evolving perioperative visual loss even in the absence of risk factors.

Adolescent↗
PubMed1999

Anesthesia and epilepsy.

The patient with epilepsy is an anesthetic challenge. New drugs and surgical procedures are being used to treat epilepsy. Certain anesthetics have been reported to cause perioperative seizures. This discussion will focus on advances in the treatment of epilepsy, as well as the pro- and anti-convulsant effects of the newer anesthetic agents.

Journal Article↗
PubMed1997

Intravenous agents and intraoperative neuroprotection. Beyond barbiturates.

The authors discuss the role of intravenous anesthetic agents in brain protection. The newer intravenous anesthetics, etomidate and propofol, have been proposed as neuroprotective agents. Thiopental remains the drug of choice, however, for use prior to intraoperative ischemic events. The anesthetic ketamine presents surprising similarities to other N-methyl-D-aspartate receptor inhibitors, but remains controversial in its use in neurologically compromised patients.

Anesthetics, Intravenous↗
PubMed1997

Etomidate and thiopental-based anesthetic induction: comparisons between different titrated levels of electrophysiologic cortical depression and response to laryngoscopy.

STUDY OBJECTIVE: To determine whether etomidate-based induction can provide better hemodynamics than a standard thiopental sodium-based anesthetic induction. DESIGN: Prospective, single-blind clinical trial. SETTING: Multicenter university neurosurgical operating room. PATIENTS: 66 ASA physical status II and III inpatients undergoing neurosurgical procedures for intracranial tumor or other pathology. INTERVENTIONS: Patients were divided into two groups for anesthetic induction. The first group (control) was divided into two subgroups, with the first subgroup receiving "low-dose" etomidate (LET) 0.4 to 0.6 mg/kg titrated to an electroencephalographic (EEG) spectral edge frequency (SEF) of 10 to 12 Hz. The second subgroup received thiopental sodium (THIO) 3 to 6 mg/kg titrated to the same EEG endpoint. The study group was given high-dose etomidate (HET) 0.5 to 1.7 mg/kg titrated to an early burst suppression pattern. MEASUREMENTS AND MAIN RESULTS: Baseline (awake) measurements of mean arterial pressure (MAP) heart rate (HR), and SEF were obtained prior to anesthetic induction that was accomplished using a small bolus plus an infusion of the induction drug titrated to the EEG target. MAP, HR, and SEF were recorded just prior to laryngoscopy and intubation (T1), 30 seconds after laryngoscopy and intubation (T2), and 90 seconds after (T3) laryngoscopy and intubation. Times to reach EEG endpoint, along with total dose of anesthetic given, were also recorded. Compared with baseline values, the THIO group had the highest increase in both HR (22.9 +/- 4.4 bpm.) and MAP (16.8 +/- 4.2 mmHg) (P < 0.05) after laryngoscopy and intubation. The LET group also had significant increases compared with the HET group that demonstrated the least hemodynamic variability. No correlations could be made between age and dose of induction drug. CONCLUSIONS: Etomidate-based anesthetic induction, titrated to EEG burst suppression, produced stable hemodynamics during laryngoscopy and intubation as compared with lower dose, more "classic" inductions with etomidate or thiopental.

Adult↗
PubMed1997

Anesthesia for carotid endarterectomy: a survey.

Indications for carotid endarterectomy (CEA) have been expanded recently, and a consensus statement has been made regarding these changes. However, the debate regarding the "ideal" anesthetic for CEA remains on-going. This study was designed to evaluate the actual anesthetic techniques used by anesthesiologists for CEA. A total of 426 1-page questionnaires were mailed to all current (1995) members of the Society of Neurosurgical Anesthesia and Critical Care (SNACC). Of these, 216 (50.7%) were completed and returned. The majority of these respondents (84.7%) administered general anesthesia (GA) for CEA. Regional anesthesia (RA) was the anesthetic method of choice for 16.7%, whereas 2.8% each chose either local anesthesia (LOC) or a combined regional/general (RA/GA) technique. Despite the controversial role of nitrous oxide in neuroanesthesia, 74.6% of those returning the survey use nitrous oxide during CEA. Intraoperative neuromonitoring use was reported by 90% of the respondents, with the electroencephalography (EEG) the favored modality (67.5%). Specific intraoperative neuroprotective measures were provided by only 22.2% of all respondents, with barbiturates as the favorite method (50.0%). The technique of intraoperative hypertension is practiced by a majority of those surveyed (61.1%), with the most common target blood pressures being either preoperative baseline or preoperative baseline plus 20%. Although there is some trend towards nonintensive care setting for postoperative care, the intensive care remains the location of choice for overnight care of CEA patients (71.8%). The results of this study show that despite arguments for RA over GA, the majority of anesthesiologists surveyed choose GA for CEA.

Anesthesia↗
PubMed1997

Convection versus conduction cooling for induction of mild hypothermia during neurovascular procedures in adults.

Hypothermia for cerebral protection is usually achieved by administration of intravenous fluids at room temperature, cooling ambient air, ice packs, and a temperature-adjustable circulating water mattress. We compared cooling by conduction by using a water mattress to cool by convection by using a forced-air cooling device. Twenty patients were prospectively randomized to two groups: 10 patients cooled by convection (CC) and 10 patients cooled by traditional methods (TC). Two patients in the CC group were withdrawn from the study and excluded from the analysis; one patient for failure to cool despite the use of both techniques, and the other for the abrupt onset of arrhythmias and myocardial depression during hypothermia. Temperature was measured at the tympanic membrane, pulmonary artery, and esophageal probe sites and recorded every 15 min. The time required to reach the target temperature range of 33-34 degrees C was recorded. We found no differences in the temperatures measured at the three sites during cooling and rewarming. Baseline temperatures recorded from the pulmonary artery catheter before beginning "active cooling" were similar in both groups (TC, 35.0 +/- 0.2 degrees C vs. CC, 35.3 +/- 0.1 degrees C). We found no difference in the time to target temperature between TC and CC (TC, 178 +/- 25 min vs. CC, 142 +/- 21 min). One patient had some arrhythmias on cooling in the convective group, but her preoperative condition may have been responsible. In conclusion, cooling by convection appears to be a safe alternative to conduction cooling.

Adult↗
PubMed1997

Anesthetic implications of epilepsy, status epilepticus, and epilepsy surgery.

Epilepsy is a clinical paroxysmal disorder of recurring seizures, excluding alcohol or drug withdrawal seizures or such recurring exogenous events as repeated insulin-induced hypoglycemia. Epilepsy has a profound impact on each individual diagnosed with this disease. Seizures have been and are thought to arise as a result of abnormalities in (a) neural circuits, (b) excitation/inhibition balance, (c) potassium, and (d) genetic abnormalities. Therapy for epilepsy is either medical, entailing the use of a variety of antiepileptic drugs, or surgical. An urgent approach to seizure control is indicated when status epilepticus occurs. When all standard therapy fails, general anesthesia can be used to control status epilepticus. Surgery is an option in the treatment of epilepsy and requires extensive preoperative evaluation. The primary concerns for the neuroanesthesiologist anesthetizing the patient with epilepsy are the capacity of anesthetics to modulate or potentiate seizure activity and the interaction of anesthetic drugs with antiepileptic drugs. Proconvulsant and anticonvulsant properties have been reported for nearly every anesthetic. If seizure spikes are to be evoked during seizure surgery, then light anesthesia with a proconvulsant anesthetic is used. Conscious analgesia can be used for awake seizure surgery. However, if electrocorticography is not planned, then a general anticonvulsant anesthetic maintenance regimen is used. The latter technique also may be useful in patients whose anesthetic management is complicated by an incidental history of epilepsy.

Anesthesia↗
PubMed1996

Large-dose propofol alone in adult epileptic patients: electrocorticographic results.

The primary objective of this study was to evaluate the electrophysiologic effects of large-dose propofol, used as the sole anesthetic in patients with epilepsy. Nine patients with medically intractable complex partial epilepsy undergoing a three-stage approach to the surgical management of epilepsy were recruited. State I involved placement of the intracranial electrode array, while Stage II consisted of extraoperative localization of the seizure focus. The patients were studied during induction of anesthesia for Stage III (removal of electrodes and resection of seizure focus). Unpremedicated patients were induced with a propofol infusion (0.5 mg.kg-1.min-1) until one of the following occurred: 1) electrical seizure activity, 2) burst suppression, or 3) total dose of 10 mg/mg. Electrocorticography (ECoG) was recorded continuously during this period. Two patients were excluded from the study after experiencing delayed awakening after the Stage I procedure. Both had received propofol along with other anesthetics. No ECoG evidence of seizure activity was detected in the seven patients completing the study. Burst suppression was attained in six patients using a mean dose of 5.7 mg/kg +/- 2.6. We conclude that large dose propofol alone does not trigger electrical epileptiform activity on the ECoG of seizure patients.

Adolescent↗
PubMed1996

Recovery from mivacurium-induced neuromuscular blockade is not affected by anticonvulsant therapy.

Long-term chronic anticonvulsant therapy produces a resistance to the effects of all nondepolarizing neuromuscular blocking agents studied to date. Since the metabolism of mivacurium is unique among the nondepolarizing neuromuscular blocking agents, the effect of anticonvulsants on its recovery parameters was examined. Forty-five patients were separated into three groups based on the number of chronic anticonvulsant medications the subjects were taking: subjects in group 1, the control group, took no anticonvulsant medication; group 2 subjects took one medication; and group 3 subjects took two medications. Mivacurium, 0.15 mg/kg i.v., was administered after induction of general anesthesia with thiopental sodium, 4-6 mg/kg, and fentanyl 2-4 micrograms/kg i.v. Maintenance anesthesia consisted of N2O in O2. 0.2-0.3% end-tidal isoflurane, and a fentanyl infusion. The evoked compound electromyograph (ECEMG) of the adductor pollicis-brevis muscle was measured for time of onset, T-1 (time at which ECEMG signal reaches 5, 25, 50, and 75% of baseline), TR (TOF ratio), and recovery index. T-1 at 25% was 18.2 +/- 1.8, 20.7 +/- 1.9, and 21.5 +/- 1.4 min for groups 1, 2, and 3, respectively, with TR at 25% being 23.7 +/- 2.3, 26.9 +/- 2.4, and 27.3 +/- 2.3 min. No significant differences were noted in neuromuscular recovery between groups at any time point. These results fail to demonstrate the resistance to the nondepolarizing neuromuscular blockade of mivacurium that has been observed with other nondepolarizing agents.

Adolescent↗
PubMed1996

Jugular bulb temperature: comparison with brain surface and core temperatures in neurosurgical patients during mild hypothermia.

Blood temperature at the jugular bulb was monitored in 10 patients undergoing neurovascular procedures that used induced mild hypothermia, and its correlation with surface brain, core, and peripheral temperatures was determined. The study was motivated by the difficulty encountered in directly measuring global brain temperature and the poor correlations between various core and peripheral sites temperatures and brain temperature, particularly during deep hypothermia. Although not statistically significant, previous studies have suggested a trend toward higher brain temperatures. Temperatures from the jugular bulb (collected using a No. 5 French Swan-Ganz catheter) as well as from subdural, pulmonary artery, esophagus, tympanic membrane, and bladder sites were analyzed during three surgical conditions: prior to incision, with the dura open, and after closure of the dura. No complications related to placement of the jugular bulb catheter, induced hypothermia, or temperature monitoring were seen. The authors found that jugular bulb temperature was similar to pulmonary artery and esophageal temperatures; although prior to incision it tended to be higher than that found at the pulmonary artery, most commonly by 0.2 degrees C. Surface brain temperature was cooler than all other temperatures (p < 0.05), except that of the tympanic membrane, and was particularly sensitive to environmental variations. Finally, as has been shown by others, bladder temperature lagged substantially behind core temperatures particularly during rapid cooling and rewarming of the patient. In summary, monitoring of jugular bulb temperature is a feasible technique, and temperatures measured in the jugular bulb are similar to core temperatures.

Adult↗
PubMed1995

[Cerebral protection: contribution of intravenous anesthetic agents].

The administration of an intravenous anaesthetic agent before experimental cerebral ischaemia in animals improves the functional and histological outcome. Cerebral ischaemia may be global or focal, complete or incomplete. Intravenous anaesthetic agents reduce the cerebral metabolic demand for oxygen (CMRO2) and abolish electrophysiological activity. This reflects a discontinuation of the functional neuronal activity with maintenance of its basic metabolic activity. The oxygen spared by the decrease in consumption, while reducing the functional activity, might be used by the neurons to sustain longer periods of ischaemia. This protective effect is also observed after pretreatment with either lidocaine or volatile agents, but their potentially deleterious vasodilating effect must be considered. Ketamine has recently been shown to antagonize NMDA receptors. The protective effect of barbiturates was experimentally demonstrated more than 30 years ago. They are still used as a reference. They reduce CMRO2, optimise the ratio between oxygen consumption and oxygen delivery and thus reduce cerebral blood flow and cerebral blood volume, as a result of the decrease of the metabolic demand. This might explain why a protective effect is seen in case of global or focal hypoxia with increased intracranial pressure, while no protection is documented in case of global cerebral ischaemia, such as after cardiac arrest, where EEG is immediately flat and ICP low. However, at doses required to obtain a protective effect, barbiturates induce deleterious side effects such as severe arterial hypotension, which limits their use. Cerebrovascular and cardiac surgery or surgery of the carotids are characterised by potentially ischaemic episodes which can be predicted.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics, Intravenous↗