Biomedical subjects

William E Hoffman

Publications and source records attributed to William E Hoffman.

13 recordsLinked to original sources

PubMed2006

Response entropy is more reactive than bispectral index during laparoscopic gastric banding.

OBJECTIVE: There is a potential use for spectral entropy or bispectral index (BIS) for controlling level of anesthesia, but it is not known how these EEG monitors relate during steady state anesthesia. We compared Response Entropy (RE) and BIS during anesthesia for laparoscopic gastric banding with RE targeted to 45. METHODS: Forty patients undergoing laparoscopic gastric banding were randomly assigned to receive either fentanyl or dexmedetomidine infusion, with desflurane concentration adjusted to maintain RE at 45. During anesthesia the average RE and BIS was determined in each patient and the RE-BIS difference plotted as a function of RE every 10 seconds. Fifteen of 40 patients showed activation of RE above 60 during surgery. In these patients RE, BIS and the electromyogram (EMG) were evaluated for the period 10 minutes before and including the peak change in RE. RESULTS: In fentanyl and dexmedetomidine treated patients the average RE was 44-47 with no statistical difference between anesthesia groups or between RE and BIS. In each patient there was a linear relationship between the RE-BIS difference and RE during anesthesia. RE and BIS were similar at a level of 41-44 and RE showed a greater range at higher and lower values compared to BIS. When RE activation was identified during surgery in 15 patients, it was associated with an increase in BIS and EMG. CONCLUSION: Within the range of 41-44, RE and BIS are equal but the gain of RE is 0.5 greater than BIS with deeper or lighter anesthesia. This is not likely due to increased smoothing with BIS. Identifying periods of RE activation show that BIS, EMG and RE increase together.

Adult↗

PubMed2006

Fentanyl or dexmedetomidine combined with desflurane for bariatric surgery.

STUDY OBJECTIVE: Because fentanyl has ventilatory depressing effects, alternative methods for analgesia may be beneficial for management of bariatric surgery. We evaluated whether dexmedetomidine infusion could replace fentanyl for facilitation of open gastric bypass surgery. DESIGN: Randomized, single blinded, open label. SETTING: University teaching hospital. PATIENTS: Twenty bariatric patients with an average body mass index of 54 to 61 kg/m2 undergoing surgery for open gastric bypass. INTERVENTIONS: Patients were randomized to receive either fentanyl (0.5-microg/kg bolus, 0.5 microg.kg(-1).h(-1), n = 10) or dexmedetomidine (0.5-microg/kg bolus, 0.4 microg.kg(-1).h(-1), n = 10) for intraoperative analgesia. In both groups, end-tidal desflurane was adjusted to maintain the bispectral index at 45 to 50. MEASUREMENTS: In the operating room, blood pressure and heart rate were measured at 5-minute intervals. Bispectral index and end-tidal desflurane concentration were measured every hour. During recovery in the postanesthesia care unit, patient-evaluated pain scores and morphine use by patient-controlled analgesia pump were determined. MAIN RESULTS: During surgery, desflurane concentrations necessary to maintain the bispectral index at 45 to 50 were decreased, and blood pressure and heart rate were lower with in the dexmedetomidine compared with fentanyl group. In the postanesthesia care unit, pain scores and morphine use were decreased in the dexmedetomidine group. CONCLUSIONS: Dexmedetomidine, when used to substitute for fentanyl during gastric bypass surgery, attenuates blood pressure and provides postoperative analgesia.

Adrenergic alpha-Agonists↗

PubMed2005

Recovery from paralysis with succinylcholine increased Response entropy and EMG but not State entropy.

OBJECTIVE: It is reported that the electromyogram is an indicator of patient arousal during pain stimulation if anesthesia is inadequate. This may not be true during recovery from succinylcholine induced paralysis. We evaluated State entropy of the electroencephalogram (EEG, 0.8-32 Hz) and Response entropy, a combined measure of the electromyogram (EMG) and EEG (0.8-47 Hz), during recovery from paralysis with succinylcholine. METHODS: Twenty patients were randomized to receive either 0.8% (n = 10) or 1.4% isoflurane (n = 10), with 2 mg/kg succinylcholine administered for paralysis in all patients. State entropy and Response entropy were evaluated using a Datex-Ohmeda Entropy module. Frontal EMG was measured separately by an EEG module. State entropy, Response entropy, and EMG were measured in awake patients, during isoflurane anesthesia and paralysis, and after 100% recovery to train of four stimulation. RESULTS: Response entropy and State entropy decreased from awake levels in a dose related manner during 0.8% or 1.4% isoflurane and succinylcholine. Recovery from succinylcholine significantly increased Response entropy and EMG in 5 of 10 patients with 0.8% isoflurane and 8 of 10 with 1.4% isoflurane without a change in State entropy. CONCLUSION: Although RE and EMG increased during recovery from paralysis with succinylcholine, SE, an indicator of EEG, was not stimulated. EMG activity may not be an indicator of patient arousal after succinylcholine treatment.

Anesthetics, Inhalation↗

PubMed2005

Response entropy increases during painful stimulation.

Frontal electromyography (FEMG) may increase during painful stimulation and indicate patient arousal. The Datex-Ohmeda Entropy Module calculates state entropy (SE) of the electroencephalogram (EEG; 0.8-32 Hz) and response entropy (RE) of EEG and FEMG (0.8-47 Hz). We determined whether RE increases above SE (RE--SE), an indication of FEMG, increase during painful stimuli and if this is related to paralysis or level of anesthesia. With the unanesthetized baseline measurement, SE was 89 +/- 2 and RE was 98 +/- 2. During paralysis and anesthesia with either 0.8% (n = 10) or 1.4% (n = 10) isoflurane, SE decreased to 63 +/- 7 and 34 +/- 14, respectively, and the RE--SE difference decreased 90%. Before recovery from paralysis, arterial catheter or head pin placement increased RE--SE above unanesthetized levels in eight patients (five treated with 0.8% and three with 1.4% isoflurane), consistent with an increase in FEMG. The elevated RE--SE difference was related to a significant increase in SE, blood pressure, and heart rate. After recovery from paralysis, tetanic stimulation of the ulnar nerve increased the RE--SE difference above unanesthetized levels in 8 of 20 patients (6 treated with 0.8% and 2 with 1.4% isoflurane). In these patients, SE increased significantly. The remaining 12 patients did not show an increase in RE--SE during tetanic stimulation and SE did not increase. We conclude that increased RE during painful stimulation was not dependent on recovery from paralysis but was seen more often in patients anesthetized with 0.8% compared with 1.4% isoflurane. This suggests that RE reflects FEMG and may be useful to identify inadequate anesthesia and patient arousal during painful stimuli.

Aged↗

PubMed2005

Clip readjustment in aneurysm surgery after flow evaluation using the ultrasonic perivascular probe: case report.

Occlusion or stenosis of a parent vessel or its distal branches is a major cause of poor patient outcome after cerebral aneurysm surgery. Despite great attempts to preserve patency at the time of clip application, intraoperative visual observation may not reveal arterial compromise or occlusion. Quantitative measurement of blood flow in cerebral vessels during aneurysm surgery can help prevent ischaemia and improve patient outcome. We report a case of a large complex middle cerebral artery (MCA) aneurysm in which perivascular microflow probes were used to measure blood flow quantitatively in MCA and its branches before and after aneurysm clipping. Following aneurysm clipping, blood flow in the MCA branches were significantly reduced to less than its initial baseline value with occlusion of the inferior M2 segment. Prompt detection of compromised blood flow gave the surgeon the opportunity to adjust the clip. This adjustment was performed several times until restore MCA flow to its preclipping values. Intraoperative quantitative vessel-flow measurements were safe and may have prevented cerebral ischaemia and neurological deficit to this patient.

Adult↗

PubMed2004

Jet injector compared with oral midazolam for preoperative sedation in children.

BACKGROUND: This study compared onset of sedation and satisfaction with two needleless jet injectors with the oral route for the administration of midazolam. METHODS: Forty-five children ages 1-6 years were randomly assigned to receive either 0.5 mg kg(-1) oral midazolam, 0.2 mg kg(-1) subcutaneous midazolam by J-Tip injector or 0.2 mg kg(-1) intramuscular midazolam by Bioject injector. After midazolam administration the children were monitored for oxygen saturation, heart rate and level of sedation (0, alert; 1, calm; 2, drowsy; 3, dozing; 4, asleep) every 2 min for 20 min by a physician blinded to the route of administration. Patient satisfaction, resistance to treatment, success of delivery, problems with separation, and acceptance of mask at the time of induction were evaluated after midazolam treatment. RESULTS: The Bioject showed a faster onset of sedation than either the J-Tip injector or the oral midazolam (P < 0.05). The children were significantly less satisfied with the Bioject and J-Tip administration vs oral midazolam (P < 0.05). There were no differences in resistance, success of delivery, problems with separation, mask acceptance, arterial oxygen saturation or heart rate. CONCLUSION: Despite children being less satisfied with Bioject injection of midazolam, the procedure is safe, effective and provides a more rapid onset of preoperative sedation in children than either the J-Tip injection or oral route.

Administration, Oral↗

PubMed2003

Non-opioid analgesia improves pain relief and decreases sedation after gastric bypass surgery.

PURPOSE: Several non-opioid drugs have been shown to provide analgesia during and after surgery. We compared sevoflurane anesthesia with fentanyl analgesia to sevoflurane and non-opioid drug treatment for gastric bypass surgery and recovery. METHODS: Thirty obese patients (body mass index > 50 kg.m(-2)) undergoing gastric bypass were randomized to receive sevoflurane anesthesia with either fentanyl or a non-opioid regimen including ketorolac, clonidine, lidocaine, ketamine, magnesium sulfate, and methylprednisolone. Morphine use by patient-controlled analgesia (PCA) pump and pain score measured by visual analogue scale were determined in the postanesthesia care unit (PACU) and for the first 16 hr after surgery. Sedation was evaluated in the PACU. Investigators assessing patient outcomes were blinded to the study group. RESULTS: Fentanyl treated patients were more sedated in the PACU compared to the non-opioid group. Non-opioid treated patients required 5.2 +/- 2.6 mg.hr(-1) morphine by PCA during their stay in the PACU while patients anesthetized with fentanyl used 7.8 +/- 3.3 mg.hr(-1) (P < 0.05). Fentanyl and non-opioid treated patients showed no difference in pain score one or 16 hr after surgery. CONCLUSION: Our results show that non-opioid analgesia produced pain relief and less sedation during recovery from gastric bypass surgery compared to fentanyl.

Adult↗

PubMed2003

Comparison of adenosine, isoflurane, and desflurane on myocardial tissue oxygen pressure during coronary artery constriction in dogs.

OBJECTIVE: To compare adenosine-, isoflurane-, or desflurane-induced hypotension with and without left anterior descending (LAD) coronary artery constriction for the effects on myocardial tissue oxygen pressure (PmO(2)) in dogs. DESIGN: Prospective, randomized, nonblinded. SETTING: University teaching hospital. PARTICIPANTS: Male nonpurpose-bred dogs (n = 18). INTERVENTIONS: Dogs were anesthetized with 1.5% isoflurane (n = 12) or 8% desflurane (n = 6). A flow probe and balloon occluder were placed on the LAD artery. A probe that measured myocardial oxygen pressure was inserted into the middle myocardium in the LAD region. Myocardial oxygen consumption (MVO(2)) was calculated as LAD flow x arterial minus coronary sinus oxygen content. MEASURES AND MAIN RESULTS: Measures were made during hypotension produced by adenosine infusion, 2.8% isoflurane, or 14% desflurane with and without LAD constriction to decrease blood flow 30%. Without LAD artery constriction, adenosine infusion increased LAD flow 90% and MVO(2) 70%, 2.8% isoflurane produced no change in MVO(2), and 14% desflurane decreased MVO(2) 25%, but no treatment changed PmO(2). LAD artery constriction decreased PmO(2) 50% by itself. Adenosine infusion during LAD constriction decreased tissue oxygen pressure an additional 60%, 2.8% isoflurane produced no change, and 14% desflurane increased PmO(2) 100%. CONCLUSION: There was an inverse relationship between the effect of adenosine, 2.8% isoflurane, and 14% desflurane on MVO(2) and PmO(2) during ischemia. This is consistent with reports that increasing oxygen demand worsens myocardial ischemia.

Adenosine↗

PubMed2003

Loss of SSEP during sitting craniotomy.

A 54-year-old woman with a past medical history of asthma and depression presented with right side hearing loss and ataxia. She was scheduled for a sitting craniotomy for cerebellopontine angle tumor resection. Somatosensory evoked potential, brainstem auditory evoked response, and facial nerve EMG were monitored intraoperatively. Approximately 30 minutes into the case, there was an episode of air embolism, which resolved after the source was identified and treated. Near the conclusion of the case, there was an abrupt loss of the right cortical somatosensory evoked potential signal, which never returned to baseline. A postoperative CT scan showed a substantial amount of subarachnoid air and intraventricular air in the frontal and temporal regions. The patient awakened in the ICU with no new neurologic deficit besides preoperative hearing loss on the right side. Despite the high specificity of somatosensory evoked potential change associated with postoperative neurodeficit when the change never returns to the baseline, there was no postoperative neurologic deficit in this patient. This case indicates the false-positive somatosensory evoked potentials caused by pneumocephalus in the sitting position.

Cerebellar Neoplasms↗

PubMed2003

The effect of sevoflurane and propofol on cerebral neurotransmitter concentrations during cerebral ischemia in rats.

UNLABELLED: Sevoflurane and propofol are neuroprotective possibly by attenuating central or peripheral catecholamines. We evaluated the effect of these anesthetics on circulating catecholamines and brain neurotransmitters during ischemia in rats. Forty male Sprague-Dawley rats were randomly assigned to one of the following treatment groups: fentanyl and N(2)O/O(2) (control), 2.0% sevoflurane, 0.8-1.2 mg x kg(-1) x min(-1) of propofol, and sham-operated rats with fentanyl and N(2)O/O(2). Ischemia (30 min) was produced by unilateral common carotid artery occlusion plus hemorrhagic hypotension to a mean arterial blood pressure of 32 +/- 2 mm Hg. Pericranial temperature, arterial blood gases, and pH value were maintained constant. Cerebral catecholamine and glutamate concentrations, sampled by microdialysis, and plasma catecholamine concentrations were analyzed using high-pressure liquid chromatography. During ischemia, circulating catecholamines were almost completely suppressed by propofol but only modestly decreased with sevoflurane. Sevoflurane and propofol suppressed brain norepinephrine concentration increases by 75% and 58%, respectively, compared with controls. Intra-ischemia cerebral glutamate concentration was decreased by 60% with both sevoflurane and propofol. These results question a role of circulating catecholamines as a common mechanism for cerebral protection during sevoflurane and propofol. A role of brain tissue catecholamines in mediating ischemic injury is consistent with our results. IMPLICATIONS: During incomplete cerebral ischemia, the neuroprotective anesthetics sevoflurane and propofol suppressed cerebral increases in norepinephrine and glutamate concentrations. In contrast, propofol, but not sevoflurane, suppressed the ischemia-induced increase in circulating catecholamines to baseline levels. The results question a role for plasma catecholamines in cerebral ischemic injury.

Anesthetics, Inhalation↗

PubMed2002

GABA alpha6 receptors mediate midazolam-induced anxiolysis.

STUDY OBJECTIVE: To compare the ability of midazolam to produce sedation and anxiolysis and attenuate memory in 100 patients aged 20 to 70 years. The effect of a point mutation (Pro385Ser) for the gamma amino-butyric acid (GABA) alpha6 receptor on the sedative, anxiolytic, and memory effects of midazolam was determined. SETTING: University hospital. DESIGN: Prospective, randomized, double-blind study. PATIENTS: 100 ASA physical status I and II patients scheduled for surgery. INTERVENTIONS: Two midazolam dose groups, 20 microg/kg and 40 microg/kg, with 40 patients per group and 20 control patients receiving saline as a sham control. Treatments were randomly assigned. Blood was collected at the beginning of each study. MEASUREMENTS: Patient sedation and anxiolysis were measured using a visual analog scale and explicit and implicit memory of a word task determined before and six minutes after midazolam or saline. A 365-base pair fragment of the GABA alpha6 receptor gene was amplified by polymerase chain reaction (PCR) from patient blood DNA and digested with the restrictase Fok I. Restriction fragments were visualized by ethidium bromide staining after electrophoresis to evaluate the GABA alpha6 receptor subunit mutation. MAIN RESULTS: Midazolam produced dose-related sedation and anxiolysis. Explicit (recall) memory was attenuated with high-dose midazolam but implicit (recognition) memory remained intact. The GABA alpha6 receptor mutation did not affect baseline sedation, anxiety, or memory but significantly attenuated the anxiolytic effect of low-dose midazolam. Sedation and explicit memory were not affected by the mutation. CONCLUSIONS: A Pro385Ser mutation of the GABA alpha6 receptor subunit decreased the anxiolytic effect of low-dose midazolam.

Adult↗

PubMed2002

Myocardial tissue oxygen during coronary artery constriction and hypotension in dogs.

BACKGROUND: Sodium nitroprusside (SNP) may decrease myocardial tissue oxygenation in dogs with normal coronary arteries. We compared SNP- with desflurane-induced hypotension on myocardial tissue oxygen and pH in dogs with left anterior descending artery constriction. METHODS: Twenty-four dogs were anesthetized with 8% desflurane for baseline anesthesia. Catheters were inserted into the femoral artery and vein and the coronary sinus. A flow probe and flow restriction device was placed on the left anterior descending (LAD) artery. A probe that measured myocardial oxygen pressure was inserted into the middle myocardium in the LAD region. Baseline measures were made of LAD artery flow, arterial and coronary sinus blood gases, and myocardial tissue gases. A 30% decrease in blood pressure was induced with SNP with unrestricted LAD flow (n=6) or when LAD artery flow was restricted by 30% from baseline (n=6). In separate dogs, a 30% decrease in blood pressure was produced with 14 +/- 1% desflurane with unrestricted LAD flow (n=6) or with baseline LAD artery flow restricted by 30% (n=6). RESULTS: During SNP-induced hypotension with no LAD constriction, LAD artery flow and coronary sinus oxygen tension increased but myocardial tissue oxygen tension (PmO2) decreased by 40%. When baseline artery flow was decreased by 30% by LAD constriction, SNP-induced hypotension decreased tissue oxygen pressure by 80%, and ischemic acidosis was produced. During unrestricted LAD artery flow or with a 30% flow restriction, desflurane-induced hypotension produced no significant change from baseline myocardial tissue oxygen tension or pH. CONCLUSION: During coronary artery constriction, desflurane-induced hypotension maintained myocardial tissue oxygenation and pH better than did SNP-induced hypotension. The divergence between tissue and coronary sinus oxygen tension during SNP suggests that arteriovenous shunting may occur.

Anesthetics, Inhalation↗

PubMed2002

Sodium nitroprusside-induced, but not desflurane-induced, hypotension decreases myocardial tissue oxygenation in dogs anesthetized with 8% desflurane.

OBJECTIVE: To compare sodium nitroprusside (SNP)-induced hypotension with desflurane-induced hypotension for the effects on myocardial blood flow and tissue oxygenation in dogs. DESIGN: Prospective, randomized, crossover, nonblinded. SETTING: University teaching hospital. PARTICIPANTS: Male nonpurpose-bred hounds (n = 8). INTERVENTIONS: Dogs were anesthetized with 8% desflurane. Catheters were inserted into the femoral artery and coronary sinus. A flow probe was placed in the left anterior descending (LAD) branch of the coronary artery. A sensor that measured myocardial oxygen pressure (PmO(2)) was inserted into the myocardium of the left ventricle. Myocardial oxygen consumption (MVO(2)) was calculated as LAD flow x arterial - coronary sinus oxygen content. MEASUREMENTS AND MAIN RESULTS: Measurements were made at baseline blood pressure levels of 99 mmHg (measure 1), during hypotension to 62 to 66 mmHg using intravenous SNP or 14% desflurane (measure 2), and during SNP or 14% desflurane with blood pressure support using phenylephrine (measure 3). Each dog randomly received both hypotensive treatments, separated by 1 hour. Baseline measures were PmO(2) = 46 +/- 9 mmHg, LAD flow = 43 +/- 11 mL/min, and MVO(2) = 2.47 +/- 0.73 mL O(2)/min. During hypotension induced with SNP, PmO(2) decreased 30% (p < 0.05), LAD flow increased 40% (p < 0.05), and MVO(2) did not change. During hypotension induced with 14% desflurane, PmO(2) did not change, and LAD flow and MVO(2) decreased 25% and 40% (p < 0.05). Blood pressure support with phenylephrine increased LAD flow and MVO(2) but did not change PmO(2) during SNP or 14% desflurane treatment. CONCLUSION: SNP-induced hypotension produced myocardial vasodilation, but tissue oxygenation was impaired. PmO(2) was maintained during desflurane-induced hypotension.

Anesthesia↗