Anesthesia and analgesia
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Anesthesia and analgesia · Apr 1998
The impact of postoperative pain on the development of postoperative delirium.
We performed a prospective observational study to examine the role of postoperative pain and its treatment on the development of postoperative delirium. Pain was measured in direct patient interviews using a visual analog scale (VAS) and was assessed for pain at rest, pain with movement, and maximal pain over the previous 24 h. Postoperative delirium was diagnosed during these interviews by using the confusion assessment method (CAM) and/or by using data from the medical record and the hospital's nursing intensity index. The method of postoperative analgesia, type of opioid, and cumulative opioid dose were also recorded. After controlling for known preoperative risk factors for delirium (age, alcohol abuse, cognitive function, physical function, serum chemistries, and type of surgery), higher pain scores at rest was associated with an increased risk of delirium over the first 3 postoperative days (adjusted risk ratio 1.20, P = 0.04). Pain with movement and maximal pain were not associated with delirium. Method of postoperative analgesia, type of opioid, and cumulative opioid dose were not associated with an increased risk of delirium. We conclude that more effective control of postoperative pain reduces the incidence of postoperative delirium. ⋯ We performed daily interviews in a large population of patients undergoing noncardiac surgery to measure their level of pain and development of delirium. We found an association between higher pain levels at rest and the development of delirium. Our results suggest that better control of postoperative pain may reduce this serious complication.
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Anesthesia and analgesia · Apr 1998
The relationship of soluble adhesion molecule concentrations in systemic and jugular venous serum to injury severity and outcome after traumatic brain injury.
Adhesion molecules control the migration of leukocytes into tissue after injury. This may result in further cellular damage. We hypothesized that altered serum concentrations of soluble intercellular adhesion molecule (sICAM)-1 and soluble L-selectin (sL-selectin) after traumatic brain injury would correlate with injury severity and neurological outcome. We investigated serum concentrations of sICAM-1 and sL-selectin in 22 patients with traumatic brain injury admitted to the intensive care unit. The Glasgow Coma Scale (GCS) score and Injury Severity Score were recorded. Paired arterial and jugular venous blood samples were taken on admission and 24, 48, and 96 h after injury. Mean systemic and jugular venous concentrations of sICAM-1 were normal on admission but became significantly increased by 96 h (P = 0.018). sL-selectin concentrations of injured patients were markedly below those of controls at all time points (P < 0.001). There were no significant differences between jugular venous and arterial concentrations of either sICAM-1 or sL-selectin. Serum sICAM-1 was significantly related to neurological outcome (P < 0.001) and to the GCS score (P < 0.001). These changes in adhesion molecule expression after acute brain injury may be important in the pathophysiology of secondary injury. The highly significant relationship between serum sICAM-1 and neurological outcome suggests that the inflammatory response to injury may be detrimental. Drugs that antagonize the actions of the adhesion molecules may have a role in therapy after traumatic brain injury. ⋯ This observational study shows that there is a strong association between soluble intercellular adhesion molecule-1 in serum and poor neurological outcome after traumatic brain injury. This suggests that inflammation after brain injury may worsen the prognosis and that therapies directed against this inflammation may prove useful.
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Anesthesia and analgesia · Apr 1998
Comparative StudySuccessful strategies for improving operating room efficiency at academic institutions.
In this prospective study, we evaluated the etiology of operating room (OR) delays in an academic institution, examined the impact of multidisciplinary strategies to improve OR efficiency, and established OR timing benchmarks for use in future OR efficiency studies. OR times and delay etiologies were collected for 94 cases during the initial phase of the study. Timing data and delay etiologies were analyzed, and 2 wk of multidisciplinary OR efficiency awareness education was conducted for the nursing, surgical, and anesthesia staff. After the education period, timing data were collected from 1787 cases, and monthly reports listing individual case delays and timing data were sent to the Chiefs of Service. For the first case of the day, patient in room, anesthesia ready, surgical preparation start, and procedure start time were significantly earlier (P < 0.01) in the posteducation period compared with the preeducation period, and the procedure start time for the first case of the day occurred, on average, 22 min earlier than all other procedures. For all cases combined, turnover time decreased, on average, by 16 min. Unavailability of surgeons, anesthesiologists, and residents decreased significantly (P < 0.05) as causes of OR delays. Anesthesia induction times were consistently longer for the vascular and cardiothoracic services, whereas surgical preparation time was increased for the neurosurgical and orthopedic services (P < 0.05). Identification of the etiology of OR inefficiency, combined with multidisciplinary awareness training and personal accountability, can improve OR efficiency. The time savings realized are probably most cost-effective when combined with more flexible OR staffing and improved OR scheduling. ⋯ We achieved significant improvements in operating room efficiency by analyzing operating room data on causes of delays, devising strategies for minimizing the most common delays, and subsequently measuring delay data. Personal accountability, streamlining of procedures, interdisciplinary team work, and accurate data collection were all important contributors to improved efficiency.
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Anesthesia and analgesia · Apr 1998
Comparative StudyIsoflurane and pentobarbital reduce the frequency of transient ischemic depolarizations during focal ischemia in rats.
Repetitive transient ischemic depolarizations (IDs) during focal cerebral ischemia are thought to contribute to ischemic damage. Isoflurane and pentobarbital reduce injury (versus the nonanesthetized state) after focal cerebral ischemia. The mechanism by which these drugs reduce injury is not known. This protective effect might be mediated by a reduction in the number of IDs. We measured the frequency of IDs during focal cerebral ischemia in animals anesthetized with isoflurane or pentobarbital and compared it with that in N2O/fentanyl anesthetized animals and in animals in which the N-methyl-D-aspartate receptor antagonist MK801 (dizocilpine) was given. Focal cerebral ischemia was induced by the occlusion of the middle cerebral artery for a period of 2 h. Cortical infarct volumes were determined after 3 h of reperfusion by image analysis of 2,3,5-triphenyl tetrazolium-stained coronal brain sections. The infarct volume was significantly greater in the N2O/fentanyl group than in the other three groups. Infarct volumes in the isoflurane, pentobarbital, and MK801 groups were similar. The frequency of IDs was significantly greater in the N2O/fentanyl group than in the other three groups, and was the least in the MK801 group. There was a direct correlation between the number of IDs and the volume of tissue injury. The data indicate that the protective effect of isoflurane and pentobarbital might, in part, be determined by their ability to reduce IDs during focal ischemia. However, the observation that the infarct volume was similar in the MK801, isoflurane, and pentobarbital groups, despite a greater frequency of IDs in the latter two groups, suggests that mechanisms other than a simple reduction in the number of IDs probably also play a role in anesthetic-mediated cerebral protection. ⋯ Transient ischemic depolarizations during focal ischemia contribute to brain injury. Both isoflurane and pentobarbital reduced the frequency of these depolarizations. Isoflurane- and pentobarbital-mediated reduction in the frequency of depolarizations might, in part, mediate the previously documented neuroprotective effect of these drugs.
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Anesthesia and analgesia · Apr 1998
The dose-response relationship of ketorolac as a component of intravenous regional anesthesia with lidocaine.
Ketorolac (K) is a useful addition to lidocaine for i.v. regional anesthesia (IVRA). However, the minimal dose of K that is effective for this purpose has not been established. We added 0, 5, 10, 15, 20, 30, and 60 mg of K to 0.5% lidocaine IVRA for either carpal tunnel release or tenolysis. Pain was assessed in the postanesthesia care unit by using a visual analog scale. The duration of analgesia (time to first request for pain relief) and the use of Tylenol No. 3 tablets (T3) were measured. A linear dose-response relationship was observed between the dose of K and the duration of analgesia (r = 0.988) up to 20 mg of K. Similarly, the number of T3 tablets used was inversely related to the dose of K (r = 0.960) over the same range. There were no significant differences among the groups who received 20, 30, or 60 mg of K. We conclude that 20 mg of K is the optimal dose for inclusion with 0.5% lidocaine for IVRA under the conditions of our study. ⋯ The antiinflammatory drug ketorolac is a useful addition to lidocaine for i.v. regional anesthesia. This study showed that 20 mg of ketorolac is equally effective as 60 mg in this context. However, smaller doses provided less effective pain relief, and a linear dose-response relationship was demonstrated.