Biomedical subjects

C J Kalkman

Publications and source records attributed to C J Kalkman.

At least 37 records · Page 2Linked to original sources

PubMed2002

Validation of a clinical prediction rule to reduce preoperative type and screen procedures.

BACKGROUND: We have developed a prediction rule for the occurrence of perioperative red blood cell transfusion to help to reduce the number of unnecessary preoperative type and screen procedures. We evaluated the robustness of this prediction rule in patients from another hospital. METHODS: The rule was retrospectively applied to 1282 consecutive patients ('validation set') who underwent similar surgical procedures to the patients in the derivation study. The outcome was similarly defined as any allogeneic transfusion on the day of surgery or during the first postoperative day. The predictive value of the rule was assessed using a Receiver Operating Characteristic curve (ROC) and compared with the results of the derivation study. Subsequently, the number of correctly predicted transfusions was compared. RESULTS: The patient characteristics did not differ between the two sets, except for the incidence of transfusion (derivation study: 18%; present study: 8%). In the validation set, the ROC area of the prediction rule was 0.78 (95% confidence intervals [CI]: 0.73-0.82), which was within the CI of the ROC area found in the derivation study (0.75; 95% CI: 0.72-0.79). In total, 35% of the type and screen procedures could be omitted (derivation study: 50%), with 13% missed transfused patients (derivation study: 20%). CONCLUSIONS: After comparing the results of this validation study with that of the derivation study, the prediction rule was robust and may work in other clinics as well.

Adolescent↗

PubMed2001

Neuropathic pain: a possible role for the melanocortin system?

In humans, damage to the nervous system can lead to a pain state referred to as neuropathic pain. Here, we give a short overview of the clinical picture and classification of neuropathic pain and highlight some of the currently known pathophysiological mechanisms involved, with special emphasis on neuropeptide plasticity. In this context, we discuss a specific group of neuropeptides, the melanocortins. These peptides have been demonstrated to play a role in nociception and to functionally interact with the opiate system. Recently, we demonstrated that spinal melanocortin receptors are upregulated in a rat model of neuropathic pain and that blockade of the melanocortin MC(4) receptor has anti-allodynic effects in this condition, suggesting that the melanocortin system plays a role in neuropathic pain. A natural agonist of melanocortin receptors is alpha-melanocyte-stimulating hormone (alpha-MSH), derived from the precursor molecule pro-opiomelanocortin (POMC). Cleavage of this precursor also yields beta-endorphin, which is co-released with alpha-MSH in nociception-associated areas of the spinal cord. We hypothesise that melanocortin receptor blockade attenuates a tonic influence of alpha-MSH on nociception, thus allowing the analgesic effects of beta-endorphin to develop, resulting in the alleviation of allodynia. In this way, treatment with melanocortin receptor antagonists might enhance opioid efficacy in neuropathic pain, which would be of great benefit in clinical practice.

Animals↗

PubMed2001

Long-term propofol infusion and cardiac failure in adult head-injured patients.

Five adult patients with head injuries inexplicably had fatal cardiac arrests In our neurosurgical intensive-care unit after the introduction of a sedation formulation containing an increased concentration of propofol. To examine the possible relation further, we did a retrospective cohort analysis of head-injured adults admitted to our unit between 1996 and 1999 who were sedated and mechanically ventilated. 67 patients met the inclusion criteria, of whom seven were judged to have died from propofol-infusion syndrome. The odds ratio for the occurrence of the syndrome was 1.93 (95% CI 1.12-3.32, p=0.018) for every mg/kg per h increase in mean propofol dose above 5 mg/kg per h. We suggest that propofol infusion at rates higher than 5 mg/kg per h should be discouraged for long-term sedation in the intensive-care unit.

Adolescent↗

PubMed2001

Spinal cord monitoring: somatosensory- and motor-evoked potentials.

Monitoring myogenic motor EPs after transcranial electrical stimulation is effective in detecting spinal cord ischemia. During thoracoabdominal aortic aneurysm surgery, this technique is sufficiently rapid to allow timely interventions aimed at correcting ischemic conditions and preserving spinal cord blood flow. If strategies are applied to protect the spinal cord during thoracoabdominal aortic aneurysm repair (e.g., distal bypass, cerebrospinal fluid drainage, reattachment of segmental arteries), motor EP monitoring should be included in this protocol to improve neurologic outcome further. Although SSEPs provide information regarding the adequacy of spinal cord blood flow, monitoring SSEPs during thoracoabdominal aortic aneurysm repair has serious limitations. The response time is too slow to be of practical use. SSEPs also do not provide information regarding anterior horn motor function and supply, whereas the motor neurons in the anterior horn are most likely to sustain ischemic injury.

Evoked Potentials, Motor↗

PubMed2001

Biphasic EEG changes in relation to loss of consciousness during induction with thiopental, propofol, etomidate, midazolam or sevoflurane.

The time course of four EEG effect variables, amplitude in the 2-5 Hz and in the 11-15 Hz band, spectral edge frequency 95% (SEF95), and bispectral index (BIS), in response to increasing concentrations of thiopental, propofol, etomidate, midazolam, or sevoflurane during a 10 min induction of anaesthesia was studied in 25 patients to determine the existence of a biphasic effect and to study the relationship of the EEG effect to the moment of loss of consciousness. A biphasic effect, that is, an initial increase of the effect variable followed by a decrease at higher concentrations, during the transition from consciousness to unconsciousness was found in EEG amplitude (both frequency bands) and in SEF95 for all anaesthetics except midazolam. There was a concentration-related decrease in BIS for all anaesthetics. There was no consistent relationship between the time of occurrence of the peak EEG effect, or the value of the EEG variable and the moment of loss of consciousness. With rapidly changing drug concentrations during the induction of anaesthesia, none of these EEG effect variables could be correlated to the moment of loss of consciousness.

Adolescent↗

PubMed2001

Predictability of processed electroencephalography effects on the basis of pharmacokinetic-pharmacodynamic modeling during repeated propofol infusions in patients with extradural analgesia.

BACKGROUND: Pharmacokinetic-pharmacodynamic (PKPD) modeling can be used to characterize the concentration-effect relation of drugs. If the concentration-effect relation of a hypnotic drug is stable over time, an effect parameter derived from the processed electroencephalographic signal may be used to control the infusion for hypnosis. Therefore, the stability of the propofol concentration-electroencephalographic effect relation over time was investigated under non-steady state conditions. METHODS: Three propofol infusions (25 mg x kg(-1) x h(-1) for 10 min, 22 mg x kg(-1) x h(-1) for 10 min, and 12.5 mg x kg(-1) x h(-1) for 20 min) were administered to 10 patients during extradural analgesia. Each successive infusion was started immediately after the patient had regained responsiveness after termination of the preceding infusion. Electroencephalography was recorded from bilateral prefrontal to mastoid leads. Electroencephalographic amplitude in the 11- to 15-Hz band and the Bispectral Index were used as electroencephalographic effect variables. PKPD parameters were calculated with use of parametric and nonparametric models based on electroencephalographic data and arterial propofol concentrations derived during the initial infusion, and these were used to predict electroencephalographic effect during the subsequent infusions. The predictability of the electroencephalographic effects was determined by the coefficient of determination (R2) and of the -2 log likelihood of the sequential infusions. RESULTS: The direction of electroencephalographic changes in response to the infusions was reproducible. Although PKPD parameters could be estimated well during the initial infusion (median [range] parametric R2 = 0.74 [0.56-0.95] for electroencephalographic amplitude and 0.90 [0.27-0.99] for Bispectral Index), none of the modeling techniques could predict accurately the electroencephalographic effect during subsequent infusions (R2 = 0.00 [-0.31-0.46] for electroencephalographic amplitude and 0.15 [-.46-0.57] for Bispectral Index; P < 0.01). CONCLUSIONS: The relation between blood propofol concentrations and the electroencephalographic effect under non-steady state conditions is not stable over time and is too complex to be modeled by any of the applied PKPD models.

Adult↗

PubMed2001

Randomized controlled trial of total intravenous anesthesia with propofol versus inhalation anesthesia with isoflurane-nitrous oxide: postoperative nausea with vomiting and economic analysis.

BACKGROUND: To assess the incidence of postoperative nausea and vomiting after total intravenous anesthesia (TIVA) with propofol versus inhalational anesthesia with isoflurane-nitrous oxide, the authors performed a randomized trial in 2,010 unselected surgical patients in a Dutch academic institution. An economic evaluation was also performed. METHODS: Elective inpatients (1,447) and outpatients (563) were randomly assigned to inhalational anesthesia with isoflurane-nitrous oxide or TIVA with propofol-air. Cumulative incidence of postoperative nausea and vomiting was recorded for 72 h by blinded observers. Cost data of anesthetics, antiemetics, disposables, and equipment were collected. Cost differences caused by duration of postanesthesia care unit stay and hospitalization were analyzed. RESULTS: Total intravenous anesthesia reduced the absolute risk of postoperative nausea and vomiting up to 72 h by 15% among inpatients (from 61% to 46%, P < 0.001) and by 18% among outpatients (from 46% to 28%, P < 0.001). This effect was most pronounced in the early postoperative period. The cost of anesthesia was more than three times greater for propofol TIVA. Median duration of stay in the postanesthesia care unit was 135 min after isoflurane versus 115 min after TIVA for inpatients (P < 0.001) and 160 min after isoflurane versus 150 min after TIVA for outpatients (P = 0.039). Duration of hospitalization was equal in both arms. CONCLUSION: Propofol TIVA results in a clinically relevant reduction of postoperative nausea and vomiting compared with isoflurane-nitrous oxide anesthesia (number needed to treat = 6). Both anesthetic techniques were otherwise similar. Anesthesia costs were more than three times greater for propofol TIVA, without economic gains from shorter stay in the postanesthesia care unit

Adult↗

PubMed2001

Wavelet analysis of middle latency auditory evoked responses: calculation of an index for detection of awareness during propofol administration.

BACKGROUND: Middle latency auditory evoked responses (MLAER) as a measure of depth of sedation are critically dependent on data quality and the analysis technique used. Manual peak labeling is subject to observer bias. This study investigated whether a user-independent index based on wavelet transform can be derived to discriminate between awake and unresponsive states during propofol sedation. METHODS: After obtaining ethics committee approval and written informed consent, 13 volunteers and 40 patients were studied. In all subjects, propofol was titrated to loss of response to verbal command. The volunteers were allowed to recover, then propofol was titrated again to the same end point, and subjects were finally allowed to recover. From three MLAER waveforms at each stage, latencies and amplitudes of peaks Pa and Nb were measured manually. In addition, wavelet transform for analysis of MLAER was applied. Wavelet transform gives both frequency and time information by calculation of coefficients related to different frequency contents of the signal. Three coefficients of the so-called wavelet detail level 4 were transformed into a single index (Db3d4) using logistic regression analysis, which was also used for calculation of indices for Pa, Nb, and Pa/Nb latencies. Prediction probabilities for discrimination between awake and unresponsive states were calculated for all MLAER indices. RESULTS: During propofol infusion, subjects were unresponsive, and MLAER components were significantly depressed when compared with the awake states (P < 0.001). The wavelet index Db3d4 was positive for awake and negative for unresponsive subjects with a prediction probability of 0.92. CONCLUSION: These data show that automated wavelet analysis may be used to differentiate between awake and unresponsive states. The threshold value for the wavelet index allows easy recognition of awake versus unresponsive subjects. In addition, it is independent of subjective peak identification and offers the advantage of easy implementation into monitoring devices.

Adult↗

PubMed2001

Pharmacologic neuroprotection in experimental spinal cord ischemia: a systematic review.

Various surgical procedures may cause temporary interruption of spinal cord blood supply and may result in irreversible ischemic injury and neurological deficits. The cascade of events that leads to neuronal death following ischemia may be amenable to pharmacological manipulations that aim to increase the tolerable duration of ischemia. Many agents have been evaluated in experimental spinal cord ischemia (SCI). In order to investigate whether an agent is available that justifies clinical evaluation, the literature on pharmacological neuroprotection in experimental SCI was systematically reviewed to assess the neuroprotective efficacy of the various agents. In addition, the strength of the evidence for neuroprotection was investigated by analyzing the methodology. The authors used a systematic review to conduct this evaluation. The included studies were analyzed for neuroprotection and methodology. In order to be able to compare the various agents for neuroprotective efficacy, relative risks and confidence intervals were calculated from the data in the results sections. A total of 103 studies were included. Seventy-nine different agents were tested. Only 14 of the agents tested did not afford protection at all. A large variation was observed in the experimental models to produce SCI. This variation limited comparison of the individual agents. In 48 studies involving 31 single agents, the relative risks and confidence intervals could be calculated. An analysis of the methodology revealed poor temperature management and lack of statistical power in the majority of the 103 studies. The results suggest that numerous agents may protect the spinal cord from transient ischemia. However, poor temperature management and lack of statistical power severely weakened the evidence. Consequently, clinical evaluation of pharmacological neuroprotection in surgical procedures that carry a risk of ischemic spinal cord damage is not justified on the basis of this study.

Animals↗

PubMed2000

Epidural versus subdural spinal cord cooling: cerebrospinal fluid temperature and pressure changes.

BACKGROUND: Regional spinal cord cooling can increase the tolerable duration for spinal cord ischemia resulting from aortic clamping. We compared the efficacy of epidural and subdural cooling and the effect of the resulting cerebrospinal fluid-pressure (CSF) increases on spinal cord motor neuron function. METHODS: In 8 pigs, CSF temperature and pressure were assessed in the subdural space at L4, T15, and T7. Saline was infused at 333, 666, and 999 ml/h at four consecutive locations: L4 subdural, L4 epidural, T15 subdural, and T15 epidural. First, the influence of CSF-pressure increases during normothermic infusion on transcranial motor evoked potentials (tc-MEPs) was assessed. Then, hypothermic infusion (4 degrees C) was performed to assess CSF-temperature changes. RESULTS: During normothermic infusion, baseline CSF pressures increased uniformly from 6 +/- 4 mm Hg to 34 +/- 18, 42 +/- 17, and 50 +/- 18 mm Hg with increasing infusion rates (p < 0.001), and did not differ between epidural or subdural infusion. Tc-MEPs indicated spinal cord ischemia in 6 animals when CSF pressures reached 65 +/- 11 mm Hg. During hypothermic infusion, CSF temperatures decreased from 37 degrees to 35 +/- 1.2 degrees, 31 +/- 2.2 degrees, and 28 +/- 2.8 degrees C, but increasing CSF-temperature gradients were observed between the infusion location and distant segments. Subdural cooling resulted in lower CSF temperatures (p < 0.001), but caused larger CSF-pressure increases (p < 0.001). CONCLUSIONS: Subdural and epidural infusion cooling produce localized spinal cord hypothermia in pigs. The concurrent pressure increases, however, are uniformly distributed and can result in tc-MEP evidence of ischemia.

Animals↗

PubMed2000

Effect of ischemic pretreatment on heat shock protein 72, neurologic outcome, and histopathologic outcome in a rabbit model of spinal cord ischemia.

OBJECTIVE: In the present study, we investigated the effect of ischemic pretreatment on heat shock protein 72 concentration and neurologic and histopathologic outcome after transient spinal cord ischemia. METHODS: In 28 New Zealand White rabbits, an aortic occlusion device was placed infrarenally. The animals were randomly assigned to 2 groups: ischemic pretreatment (n = 14 animals) and control (n = 14 animals). The duration of ischemic pretreatment was 6 minutes. After 24 hours, the aorta was occluded for 26 minutes in both groups of animals. Neurologic function was assessed 24 and 48 hours after the definite ischemic insult. At 48 hours, the animals were killed for histopathologic evaluation of the spinal cord. In a separate set of animals, heat shock protein 72 levels were determined in the lumbar spinal cord after both a 6- and 10-minute ischemic period, with the use of a Western blot analysis. RESULTS: No significant difference in neurologic outcome between the groups was observed at 24 and 48 hours. The incidence of paraplegia and severe paresis at 48 hours was 79% in the control group and 92% in the ischemic pretreatment group. There was no difference in histopathologic scores between the groups. Heat shock protein 72 could be clearly detected 1 and 2 days after 6- or 10-minute periods of spinal cord ischemia. CONCLUSIONS: In the present rabbit study, ischemic pretreatment could not induce tolerance against a moderately severe spinal cord ischemic insult, despite increased heat shock protein 72 levels after the preconditioning stimulus.

Animals↗

PubMed2000

Prevention of paraplegia in pigs by selective segmental artery perfusion during aortic cross-clamping.

PURPOSE: During thoracoabdominal aortic aneurysm repair, a prolonged interruption of the spinal cord blood supply can result in irreversible spinal cord damage. The aim of this study was to investigate whether selective segmental artery perfusion during aortic clamping could prevent paraplegia in pigs. METHODS: Specially designed segmental artery perfusion catheters, which could be attached to an extracorporeal bypass graft system, were used. In experiment I (n = 10), it was assessed whether selective segmental artery perfusion could reverse electrophysiologic evidence of spinal cord ischemia and maintain transcranial motor evoked potentials (tc-MEPs) during 60 minutes of aortic cross-clamping. The abdominal aorta, containing critical segmental arteries, was bypassed through use of an aortoaortic bypass graft system. After the disappearance of tc-MEPs, an aortotomy was followed by selective segmental artery perfusion. In experiment II (n = 10), the aim was to determine whether selective segmental artery perfusion could prevent paraplegia. In five animals (group A), aortic cross-clamping was followed by selective segmental artery perfusion; five control animals (group B) underwent segmental artery blockade only. Postoperative hind limb function and spinal cord histopathology were evaluated on the third postoperative day. RESULTS: In experiment I, tc-MEPs disappeared within 3.7 +/- 3.7 minutes after cross-clamping and returned in all animals in 8.5 +/- 5.3 minutes after selective perfusion. During the study period, tc-MEP amplitudes recovered to a median of 49% (range, 28%-113%) of baseline values. Total bypass graft flow was 880 +/- 294 mL/min, of which 184 +/- 54 mL/min was directed to the selective perfusion catheters. The flow in individual catheters was 52 +/- 13 mL/min. In experiment II, all perfused animals demonstrated normal hind limb function, whereas four of five control animals were paraplegic on day 3 (P =.04) In the perfused animals, histopathologic examination showed either no spinal cord damage or eosinophilic neurons only, whereas in paraplegic controls there was infarction in large areas of the cord (P <.0001). CONCLUSION: In pigs, selective segmental artery perfusion can provide sufficient spinal cord blood flow to prevent paraplegia resulting from 60 minutes of aortic clamping, as shown by clinical outcomes and histopathologic examination.

Animals↗

PubMed2000

Neuroprotective effects of riluzole and ketamine during transient spinal cord ischemia in the rabbit.

BACKGROUND: Massive release of central excitatory neurotransmitters is an important initial step in ischemic neuronal injury, and modification of this process may provide neuroprotection. We studied the protective effects of the voltage-dependent sodium channel antagonist riluzole and the N-methyl-d-aspartate receptor antagonist ketamine on hind limb motor function and histopathologic outcome in an experimental model of spinal cord ischemia. METHODS: Temporary spinal cord ischemia was induced by 29 min of infrarenal balloon occlusion of the aorta in 60 anesthetized New Zealand white rabbits. Animals were randomly assigned to one of four treatment groups (n = 15 each): group C, saline (control); group R, riluzole, 8 mg/kg intravenously; group K, ketamine, 55 mg/kg intravenously; group RK, riluzole and ketamine. After reperfusion, riluzole treatment was continued with intraperitoneal infusions. Normothermia (38 degrees C) was maintained during ischemia, and rectal temperature was assessed before and after intraperitoneal infusions. Neurologic function, according to Tarlov's criteria, was evaluated every 24 h, and infarction volume and the number of eosinophilic neurons and viable motoneurons in the lumbosacral spinal cord was evaluated after 72 h. RESULTS: Neurologic outcome was better in groups R and RK than in groups C and K. All animals in group C (100%) and all animals but one in group K (93%) were paraplegic 72 h after the ischemic insult versus 53% in group R and 67% in group RK (P < 0.01 each). More viable motoneurons were present in groups R and RK than in controls (P < 0.05). CONCLUSIONS: The data indicate that treatment with riluzole can increase the tolerance of spinal cord motoneurons to a period of normothermic ischemia. Intraischemic ketamine did not provide neuroprotection in this model.

Animals↗

PubMed2000

Assessment of spinal cord ischemia by means of evoked potential monitoring during thoracoabdominal aortic surgery.

Besides renal failure and mesenteric infarction, spinal cord ischemia is the most dreaded complication after thoracoabdominal aortic surgery. Several techniques have been developed to improve neurologic outcome of these massive surgical procedures, including pharmacologic adjuncts, epidural cooling, distal aortic perfusion, cerebrospinal fluid drainage, and reattachment of segmental arteries. The authors developed a technique to assess spinal cord integrity as part of the surgical protocol, dictating operative strategies to restore blood supply to the endangered grey matter. Monitoring motor evoked potentials (MEPs) was performed in experimental studies and in 170 patients with a thoracoabdominal aortic aneurysm. The surgical protocol included left heart bypass and cerebrospinal fluid drainage, and MEP monitoring was applied to identify critical intercostal and lumbar arteries. Based on MEPs, the aggressive surgical approach resulted in a significant reduction of neurologic complications (2.3%).

Animals↗

PubMed1999

Development of spinal cord ischemia after clamping of noncritical segmental arteries in the pig.

BACKGROUND: Blood flow to the thoracolumbar spinal cord is thought to be critically dependent on the arteria radicularis magna. We investigated whether spinal cord blood supply becomes dependent on other, noncritical, segmental arteries if spinal cord perfusion pressure (SCPP) is decreased. The SCPP is equal to the mean arterial pressure (MAP) minus the cerebrospinal fluid (CSF) pressure (SCCP = MAP - CSF). METHODS: The thoracoabdominal aorta was exposed in 10 pigs. Functional integrity of spinal cord motor pathways was assessed with myogenic motor-evoked potentials after transcranial electrical stimulation (tc-MEPs). Using this technique, a group of segmental arteries not critical for spinal cord blood supply was identified. Before, during, and after clamping of the noncritical segmental arteries, spinal cord ischemia was produced by decreasing SCPP by means of increasing CSF pressure, and the SCPP threshold at which tc-MEPs showed evidence of spinal cord ischemia was determined. Ischemic SCPP thresholds, obtained during and after clamping of the noncritical segmental arteries, were compared with the ischemic threshold obtained before clamping (control value). RESULTS: Before noncritical segmental arteries were clamped, ischemic tc-MEP changes occurred when the SCPP was below 15 +/- 5 (SD) mm Hg. With a total of 9 +/- 3 (SD) segmental arteries clamped, the ischemic SCPP threshold was 48 +/- 14 mm Hg (p < 0.01). After the release of all clamps, ischemia occurred at a SCPP of 15 +/- 5 (SD) mm Hg. CONCLUSIONS: In this porcine experiment, clamping of originally noncritical segmental arteries significantly reduced the tolerance of the spinal cord to a decrease in SCPP.

Animals↗

PubMed1999

The influence of regional spinal cord hypothermia on transcranial myogenic motor-evoked potential monitoring and the efficacy of spinal cord ischemia detection.

OBJECTIVE: Myogenic motor-evoked responses to transcranial electrical stimulation (transcranial myogenic motor-evoked potentials) can rapidly detect spinal cord ischemia during thoracoabdominal aortic aneurysm repair. Recent evidence suggests that regional spinal cord hypothermia increases spinal cord ischemia tolerance. We investigated the influence of subdural infusion cooling on transcranial myogenic motor-evoked potential characteristics and the time to detect spinal cord ischemia in 6 pigs. METHODS: Regional hypothermia was produced by subdural perfusion cooling. A laminectomy and incision of the dura were performed at L2 to advance 2 inflow catheters at L4 and L6, to cool the lumbar subdural space with saline solution. Two temperature probes were advanced at L3 and L5, and 1 cerebrospinal fluid pressure line was advanced at L4. Spontaneous cerebrospinal fluid outflow was allowed. Spinal cord ischemia was produced by clamping a set of critical lumbar arteries, previously identified by transcranial myogenic motor-evoked potentials and lumbar artery clamping. The time between the onset of ischemia and detection with transcranial myogenic motor-evoked potentials (amplitude < 25%) was determined at cerebrospinal fluid temperatures of 37 degrees C and 28 degrees C. Thereafter, the influence of progressive cerebrospinal fluid cooling on transcranial myogenic motor-evoked potential amplitude and latency was determined. RESULTS: The time necessary to produce ischemic transcranial myogenic motor-evoked potentials, after the clamping of critical lumbar arteries, was not affected at moderate subdural hypothermia (3.8 +/- 0.9 min) compared with subdural normothermia (3.2 +/- 0.5 min; P =.6). Thereafter, progressive cooling resulted in a transcranial myogenic motor-evoked potential amplitude increase at 28 degrees C to 30 degrees C and was followed by a progressive decrease. Response amplitudes decreased below 25% at 14.0 degrees C +/- 1.1 degrees C. The influence of cerebrospinal fluid temperature on transcranial myogenic motor-evoked potential amplitude was best represented by a quadratic regression curve with a maximum at 29.6 degrees C. In contrast, transcranial myogenic motor-evoked potential latencies increased linearly with decreasing subdural temperatures. CONCLUSIONS: Detection of spinal cord ischemia with transcranial myogenic motor-evoked potentials is not delayed at moderate subdural hypothermia in pigs. At a cerebrospinal fluid temperature of 28 degrees C, transcranial myogenic motor-evoked potential amplitudes are increased. Further cerebrospinal fluid temperature decreases result in progressive amplitude decreases and latency increases.

Animals↗

PubMed1999

Strategies to prevent neurologic deficit based on motor-evoked potentials in type I and II thoracoabdominal aortic aneurysm repair.

PURPOSE: Motor-evoked potentials (MEPs) were monitored during thoracoabdominal aortic aneurysm (TAAA) repair to assess spinal cord ischemia and evaluate the subsequent protective strategies to prevent neurologic deficit. METHODS: Between January 1996 and December 1997, 52 consecutive patients with type I (n = 24) and type II (n = 28) TAAA underwent surgery (mean patient age, 60 years; range, 21-78 years). The surgical protocol included left heart bypass, cerebrospinal fluid drainage, and monitoring transcranial myogenic MEPs. When spinal cord ischemia was detected, distal aortic pressure and mean arterial pressure were increased. By means of sequential crossclamping, MEPs were used to identify critical intercostal or lumbar arteries. RESULTS: Reproducible MEPs could be recorded in all patients, and spinal cord ischemia was detected within 2 minutes. During distal aortic perfusion, 14 patients (27%) showed rapid decrease in the amplitude of MEPs to less than 25% of baseline, indicating spinal cord ischemia, which could be corrected by increasing distal aortic pressure. The mean distal aortic pressure to maintain adequate cord perfusion was 66 mm Hg; however, it varied among individuals between 48 and 110 mm Hg. In 24 patients (46%), MEPs disappeared after segmental clamping and returned after reattachment of intercostal arteries. In 9 patients (17%), MEPs disappeared completely, but no intercostal arteries were found. After aortic endarterectomy, 6 or 8 mm Dacron grafts were anastomosed to intercostal arteries, and MEPs returned after reperfusion. Using this aggressive surgical approach based on MEPs, no early or late paraplegia occurred in this series. CONCLUSION: Monitoring of MEPs is an effective technique to assess spinal cord ischemia. Operative strategies based on MEPs prevented neurologic deficits in patients treated for type I and II TAAA.

Adult↗

PubMed1999

Advanced pulse oximeter signal processing technology compared to simple averaging. II. Effect on frequency of alarms in the postanesthesia care unit.

STUDY OBJECTIVE: To determine the effect of a new pulse oximeter (Nellcor Symphony N-3000, Pleasanton, CA) with signal processing technique (Oxismart) on the incidence of false alarms in the postanesthesia care unit (PACU). DESIGN: Prospective study. SETTING: Nonuniversity hospital. PATIENTS: 603 consecutive ASA physical status I, II, and III patients recovering from general or regional anesthesia in the PACU. INTERVENTIONS: We compared the number of alarms produced by a recently developed "third"-generation pulse oximeter (Nellcor Symphony N-3000) with Oxismart signal processing technique and a conventional pulse oximeter (Criticare 504, Waukesha, WI). Patients were randomly assigned to either a Nellcor pulse oximeter or a Criticare with the signal averaging time set at either 12 or 21 seconds. For each patient the number of false (artifact) alarms was counted. MEASUREMENTS AND MAIN RESULTS: The Nellcor generated one false alarm in 199 patients and 36 (in 31 patients) "loss of pulse" alarms. The conventional pulse oximeter with the averaging time set at 12 seconds generated a total of 32 false alarms in 17 of 197 patients [compared with the Nellcor, relative risk (RR) 0.06, confidence interval (CI) 0.01 to 0.25] and a total of 172 "loss of pulse" alarms in 79 patients (RR 0.39, CI 0.28 to 0.55). The conventional pulse oximeter with the averaging time set at 21 seconds generated 12 false alarms in 11 of 207 patients (compared with the Nellcor, RR 0.09, CI 0.02 to 0.48) and a total of 204 "loss of pulse" alarms in 81 patients (RR 0.40, CI 0.28 to 0.56). The lower incidence of false alarms of the conventional pulse oximeter with the longest averaging time compared with the shorter averaging time did not reach statistical significance (false alarms RR 0.62, CI 0.3 to 1.27; "loss of pulse" alarms RR 0.98, CI 0.77 to 1.3). CONCLUSIONS: To date, this is the first report of a pulse oximeter that produced almost no false alarms in the PACU.

Anesthesia Recovery Period↗