ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveSubjective scales to assess agitation and sedation in adult intensive care unit (ICU) patients have rarely been tested for validity or reliability. We revised and prospectively tested the Sedation-Agitation Scale (SAS) for interrater reliability and compared it with the Ramsay scale and the Harris scale to test construct validity.DesignA convenience sample of ICU patients was simultaneously and independently examined by pairs of trained evaluators by using the revised SAS, Ramsay, and Harris Scales.SettingMultidisciplinary 34-bed ICU in a nonuniversity, academic medical center.PatientsForty-five ICU patients (surgical and medical) were examined a total of 69 times by evaluator pairs.Measurements and Main ResultsThe mean patient age was 63.2 yrs, 36% were female, and 71% were intubated. When classified by using SAS, 45% were anxious or agitated (SAS 5 to 7), 26% were calm (SAS 4), and 29% were sedated (SAS 1 to 3). Interrater correlation was high for SAS (r2= .83; p < .001) and the weighted kappa score for interrater agreement was 0.92 (p < .001). Of 41 assessments scored as Ramsay 1, 49% scored SAS 6, 41% were SAS 5, 5% were SAS 4, and 2% each were SAS 3 or 7. SAS was highly correlated with the Ramsay (r2= .83; p < .001) and Harris (r2= .86; p < .001) scales.ConclusionsSAS is both reliable (high interrater agreement) and valid (high correlation with the Harris and Ramsay scales) in assessing agitation and sedation in adult ICU patients. SAS provides additional information by stratifying agitation into three categories (compared with one for the Ramsay scale) without sacrificing validity or reliability. (Crit Care Med 1999; 27:1325-1329)

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectivesTo determine whether the allele frequencies and genotype distribution of an interleukin (IL)-1 beta TaqI polymorphism and an interleukin-1 receptor antagonist polymorphism are associated with susceptibility to and outcome of severe sepsis. In addition, we analyze a possible linkage disequilibrium between a previously described NcoI polymorphism within the tumor necrosis factor (TNF) locus and the two IL-1 gene family polymorphisms.DesignProspective, consecutive entry study of patients with diagnosis of severe sepsis.SettingIntensive care unit (ICU) of a university hospital.PatientsNinety-three patients with diagnosis of severe sepsis admitted to the ICU between June 1993 and June 1996.InterventionsNone.Measurements and Main ResultsThe polymorphic region within intron 2 of the IL-1ra gene containing variable numbers of a tandem repeat of 86 base pairs was amplified by means of the polymerase chain reaction. Alleles A1-5 are identified according to the size of the amplified DNA product. The region that contains the biallelic TaqI site within exon 5 of the IL-1 beta gene was analyzed by polymerase chain reaction amplification and subsequent digestion using the TaqI restriction enzyme. A NcoI TNF-beta polymorphism was determined.The allele frequency of the allele IL-1raA2 was increased in 93 patients with severe sepsis compared with normal individuals (p < .01). No association with patients' outcome was observed. Allele frequencies or genotype distribution of the IL-1 beta TaqI polymorphism did not differ between patients and controls. In addition, the allele TNFB2 of the NcoI TNF-beta polymorphism was associated with nonsurvival. Occurrence of the TNFB1 and TNFB2 alleles and genotypes was unrelated to alleles and genotypes of the two IL-1 gene family polymorphisms.ConclusionIn contrast to the TNF-beta NcoI polymorphism, which has been associated with patients' nonsurvival, the allele IL-1raA2 of the polymorphism within the intron 2 of IL-1ra may contribute to susceptibility to sepsis. (Crit Care Med 1999; 27:1330-1334)

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectivesTo test the hypothesis that greater cerebral perfusion pressure (CPP) is required to restore cerebral blood flow (CBF), oxygen metabolism, adenosine triphosphate (ATP), and intracellular pH (pHi) levels after variable periods of no-flow than to maintain them when cardiopulmonary resuscitation (CPR) is started immediately.DesignProspective, randomized, comparison of three arrest times and two perfusion pressures during CPR in 24 anesthetized dogs.SettingUniversity cerebral resuscitation laboratory.InterventionsWe used radiolabeled microspheres to determine CBF and magnetic resonance spectroscopy to derive ATP and pHi levels before and during CPR. Ventricular fibrillation was induced, epinephrine administered, and thoracic vest CPR adjusted to provide a CPP of 25 or 35 mm Hg after arrest times of 0, 6, or 12 mins.Measurements and Main ResultsWhen CPR was started immediately after arrest with a CPP of 25 mm Hg, CBF and ATP were 57 +/- 10% and 64 +/- 14% of prearrest (at 10 mins of CPR). In contrast, CBF and ATP were minimally restored with a CPP at 25 mm Hg after a 6-min arrest time (23 +/- 5%, 16 +/- 5%, respectively). With a CPP of 35 mm Hg, extending the no-flow arrest time from 6 to 12 mins reduced reflow from 71 +/- 11% to 37 +/- 7% of pre-arrest and reduced ATP recovery from 60 +/- 11% to 2 +/- 1% of pre-arrest. After 6- or 12-min arrest times, brainstem blood flow was restored more than supratentorial blood flow, but cerebral pHi was never restored.ConclusionsA CPP of 25 mm Hg maintains supratentorial blood flow and ATP at 60% to 70% when CPR starts immediately on arrest, but not after a 6-min delay. A higher CPP of 35 mm Hg is required to restore CBF and ATP when CPR is delayed for 6 mins. After a 12-min delay, even the CPP of 35 mm Hg is unable to restore CBF and ATP. Therefore, increasing the arrest time at these perfusion pressures increases the resistance to reflow sufficient to impair restoration of cerebral ATP. (Crit Care Med 1999; 27:1335-1342)

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveIn rodent models, enhanced formation of nitric oxide and formation of peroxynitrite have been implicated in the pathogenesis of various forms of shock. Here we examined the effect of mercaptoethylguanidine (MEG), an inducible nitric oxide synthase inhibitor and peroxynitrite scavenger, in a severe hemorrhagic shock model.DesignRandomized, placebo-controlled trial.SettingAnimal laboratory.SubjectsTwenty-one anesthetized immature Yorkshire pigs.InterventionsMechanical ventilation, sternotomy, continuous cardiac output (pulmonary artery flowmetry), and systemic and intracardial pressure measurements were taken. Pigs were bled to a cardiac index of 40 mL/kg/min for 2 hrs, which was followed by saline resuscitation (20 mL/kg). MEG was administered in the resuscitation fluid (15 mg/kg bolus plus 15 mg/kg/hr infusion).Measurements and Main ResultsHemodynamic variables, systemic and mixed venous blood gas tensions and oxygenation, arterial lactate concentration, myeloperoxidase activity, malondialdehyde content, and histologic injury in the lung and intestine were measured. Reduction of cardiac output to 40 mL/kg/min led to the following changes during hypovolemia: decreases in mean arterial blood pressure (to 30-35 mm Hg), both atrial pressures, systemic oxygen consumption (by 35%), mixed venous saturation (by 65%), and lactic acidosis (5.5-6.0 mM). Fluid replacement failed to restore blood pressure and cardiac output during resuscitation and was followed by gradual hemodynamic decompensation. Hemorrhagic shock induced lipid peroxidation, neutrophil deposition, and severe histologic alterations in the lung and intestine. MEG significantly ameliorated the decrease in blood pressure and cardiac output during resuscitation, improved survival rate, reduced lipid peroxidation in the intestine, and ameliorated neutrophil accumulation in the lung and intestine. MEG prevented the reduction in oxygen consumption during resuscitation.ConclusionsWhen given during resuscitation, MEG exerted beneficial effects in a porcine model of severe hemorrhagic shock. We propose that the mode of MEG's action is related to improved cardiac contractility. (Crit Care Med 1999; 27:1343-1350)

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectivesBrain-injured patients are susceptible to secondary brain damage related to decreased cerebral perfusion pressure associated with edema formation and increased intracranial pressure (ICP). Whenever conventional therapy fails to reduce elevated ICP, barbiturate coma represents an additional intervention that may control ICP. In patients suffering from severe traumatic brain injury, cerebrospinal fluid levels of glutamate, hypoxanthine, and lactate were measured during barbiturate coma and correlated to electroencephalographic recordings and ICP.DesignProspective, descriptive study.SettingTen-bed surgical intensive care unit in a university hospital.PatientsTwenty-one patients with severe traumatic brain injury (Glasgow Coma Scale score <or=to9); 11 required barbiturate coma because of refractory intracranial hypertension, and 10 were manageable with continuous administration of fentanyl and midazolam.InterventionsThiopental was administered continuously for increased ICP within the first 24 hrs after trauma and adjusted to the burst-suppression pattern (four to six bursts per minute) on continuous electroencephalographic monitoring.Measurements and Main ResultsGlutamate and hypoxanthine were analyzed using high-performance liquid chromatography, whereas lactate was measured enzymatically. Patients requiring thiopental presented with significantly higher ICP, glutamate, and hypoxanthine levels than patients receiving fentanyl and midazolam (p < .05). Within the first 24 hrs, thiopental significantly reduced cerebrospinal fluid glutamate and hypoxanthine levels in all patients, i.e., the burst-suppression pattern was successfully induced (p < .001). Interestingly, in five patients cerebrospinal fluid glutamate increased to initial values again despite unchanged neuronal activity. In these patients, ICP, hypoxanthine, and lactate remained significantly elevated compared with the six patients with steadily decreasing cerebrospinal fluid glutamate, hypoxanthine, lactate, and ICP values (p < .02).ConclusionsBarbiturate coma does not unequivocally preserve energetic stability despite successful suppression of neuronal activity. Despite the use of barbiturate coma in patients with refractory intracranial hypertension, persistent release or impaired uptake of glutamate may be associated with continuous anaerobic metabolism, as shown by increases in cerebrospinal fluid hypoxanthine and lactate levels. (Crit Care Med 1999; 27: 1351-1357)

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo review the pharmacology of neuromuscular blocking drugs (NMBDs), their use in critically ill or injured infants and children, and the relevance of developmental changes in neuromuscular transmission.Data SourcesComputerized search of the medical literature.Study SelectionStudies specifically examining the following were reviewed: a) the developmental changes in neuromuscular transmission; b) the pharmacokinetics and pharmacodynamics of all clinically available NMBDs in neonates, infants, children, and adults; and c) clinical experience with NMBDs in the critical care setting. Particular attention was directed toward studies in the pediatric population.Data SynthesisNeuromuscular transmission undergoes maturational changes during the first 2 months of life. Alterations in body composition and organ function affect the pharmacokinetics and pharmacodynamics of the NMBDs throughout active growth and development. Numerous NMBDs have been developed during the last two decades with unique pharmacologic profiles and potential clinical advantages. The NMBDs are routinely used in critically ill or injured patients of all ages. This widespread use is associated with rare but significant clinical complications, such as prolonged weakness.ConclusionsSignificant gaps in our knowledge of the pharmacokinetics and pharmacodynamics of NMBDs in infants and children continue to exist. Alterations in electrolyte balance and organ-specific drug metabolism may contribute to complications with the use of NMBDs in the critical care arena. (Crit Care Med 1999; 27:1358-1368)

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID