Anesthesia and analgesia
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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 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
Chloral hydrate sedation: the additive sedative and respiratory depressant effects of nitrous oxide.
The combination of chloral hydrate and nitrous oxide (N2O) is often used for sedation in pediatric dentistry. The purpose of this study was to determine the extent to which N2O increases the level of sedation and respiratory depression in children sedated with chloral hydrate. Thirty-two children, 1-9 yr, received chloral hydrate, 70 mg/kg (maximum 1.5 g), and then received N2O (30% and 50%). Hypoventilation (maximal PETCO2 > 45 mm Hg) occurred in 23 (77%) children during administration of chloral hydrate alone, in 29 (94%) breathing 30% N2O (P = 0.08 versus control), and in 29 (97%) breathing 50% N2O (P = 0.05 versus control). Mean PETCO2 was increased during 30% (P = 0.007) and 50% (P = 0.02) N2O administration. Using chloral hydrate alone, 8 (25%) children were not sedated, 10 (31%) were consciously sedated, and 14 (44%) were deeply sedated. Using 30% N2O, 2 children (6%) were not sedated, 0 were consciously sedated, and 29 (94%) were deeply sedated (P < 0.0001). Using 50% N2O, 1 child (3%) was not sedated, 0 were consciously sedated, 27 (94%) were deeply sedated, and 1 (3%) had no response to a painful stimulus (P < 0.0001). We conclude that the addition of 30% or 50% N2O to chloral hydrate often causes decreases in ventilation and usually results in deep, not conscious, sedation in children. ⋯ Pediatric sedation in the dental office often consists of nitrous oxide (N2O) after chloral hydrate premedication. We found that the addition of 30% or 50% N2O to chloral hydrate often causes decreases in ventilation and usually results in deep, not conscious, sedation in children.
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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.
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Anesthesia and analgesia · Apr 1998
Inhaled prostaglandin E1 for treatment of acute lung injury in severe multiple organ failure.
Acute lung injury is characterized by hypoxemia due to pulmonary ventilation/perfusion-mismatching. I.v. administered prostaglandin E1 (PGE1), a vasodilator with a high pulmonary clearance, has been studied in acute lung injury. Inhalation of the vasodilators nitric oxide and prostacyclin improved oxygenation by selective dilation of the pulmonary vasculature in ventilated lung areas. In the present study, PGE1 inhalation was used for treatment of acute lung injury. Fifteen patients with acute lung injury defined as PaO2/fraction of inspired oxygen (FIO2) <160 mm Hg were treated with PGE1 inhalation in addition to standard intensive care. The drug was continuously delivered via a pneumatic nebulizer. Acute physiology and chronic health evaluation system II and multiple organ failure scores were (mean +/- SEM) 33 +/- 2 and 10 +/- 0.3, respectively. Inhaled PGE1 was administered for 103 +/- 17 h at a dose of 41 +/- 2 microg/h. The PaO2/FIO2 ratio increased from 105 +/- 9 to 160 +/- 17 mm Hg (P < 0.05) and to 189 +/- 25 mm Hg (P < 0.05) after 4 h and 24 h, respectively. PGE1 inhalation decreases in mean pulmonary artery pressure and central venous pressure were not statistically significant. Mean arterial pressure, pulmonary capillary wedge pressure, cardiac output, and heart rate remained unchanged. Intensive care unit mortality was 40%. The present data suggest that inhaled PGE1 is an effective therapeutic option for improving oxygenation in patients with acute lung injury. Whether inhaled PGE1 will increase survival in acute lung injury should be investigated in a controlled prospective trial. ⋯ In patients with severe acute lung injury and multiple organ failure, inhaled prostaglandin E1 improved oxygenation and decreased venous admixture without affecting systemic hemodynamic variables. Controlled clinical trials are warranted.