摘要:

ObjectiveTo evaluate the feasibility and outcome results of noninvasive mechanical ventilation (NIV) in daily clinical practice outside any prospective protocol-driven trial.DesignAn observational retrospective cohort study.SettingA 22-bed medical intensive care unit in a university hospital.PatientsA consecutive cohort of 124 patients who underwent 143 NIV trials, regardless of the indication, over two consecutive years (1997–1998).InterventionsNone.ResultsA total of 604 acute respiratory failure patients underwent mechanical ventilation, and 143 NIVs were performed in 124 patients. The overall prevalence of NIV use was 143 of 604 patients (24%) in three groups: hypoxemic acute respiratory failure (29.5%), hypercapnic acute respiratory failure (41%), and weaning/postextubation (29.5%). Intubation was avoided in 92 of 143 of the NIVs performed (64%), 19 (13%) after changing the initial NIV mode (i.e., a success rate of 62%, 51%, and 86% in the three groups, respectively). A total of 35 of 51 intubated patients (69%) required intubation during the first 24 hrs of NIV. Intensive care unit stay was 12 ± 10 days for the overall population, and mortality, when NIV failed, was 13 of 124 patients (10.5%). Arterial pH (p= .0527) and the Pao2/Fio2ratio (p= .0482) after 1 hr were the only independent predictive factors for NIV failure by multivariate analysis.ConclusionsThis study confirms the results of controlled trials and demonstrates the feasibility and efficacy of NIV applied in daily clinical practice. These results suggest that NIV should be considered as a first-line ventilatory treatment in various etiologies of acute respiratory failure and as a promising weaning technique and postextubation ventilatory support. However, NIV should certainly be performed by a motivated and sufficiently trained care team.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveTo evaluate effects of lipopolysaccharide (endotoxin) on protein and fluid permeability in a whole organ skeletal muscle preparation.DesignControlled, prospective laboratory study.SettingUniversity research laboratory.SubjectsEleven adult male cats.InterventionsThe study was performed on the autoperfused and denervated calf muscles of the cat hindlimb placed in a fluid-filled plethysmograph. The endotoxin-induced change in the osmotic reflection coefficient for albumin was used as a measure of alteration in protein permeability of the microvascular wall, and the simultaneous change in capillary filtration coefficient was used as a measure of alteration in fluid permeability. Endotoxin as a bolus infusion (1 mg/kg iv) was given to six cats, and another five cats given only the vehicle (NaCl) were used as control.Measurements and Main ResultsArterial blood flow, arterial and venous blood pressures, total vascular resistance, and tissue volume changes were measured continuously. The ratio between the osmotic reflection coefficients for albumin on two occasions (before and about 1.5 hr after endotoxin infusion) was calculated from the Starling fluid equilibrium equation. This was performed by measurement of the maximum absorption rate from an isovolumetric state by an intravenous bolus infusion of 20% human albumin (0.6 g/kg) and the capillary filtration coefficient. Albumin concentrations were measured before and after the albumin infusion to correct for effects of difference in plasma volume on the induced increase in colloid osmotic pressure. We found that the osmotic reflection coefficient for albumin was reduced by 30% (p< .05), and the capillary filtration coefficient was increased by 31% (p< .05) by endotoxin. No changes were seen in the vehicle experiments.ConclusionEndotoxin causes a significant increase in both protein and fluid microvascular wall permeability. These effects may explain the marked leakage of plasma to the interstitium that is often seen in critically ill patients with sepsis and systemic inflammatory response syndrome.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveThe reduced pressure response to norepinephrine in septic patients has directed our interest to the regulation of &agr;1-adrenergic receptorsin vitroandin vivoduring conditions mimicking acute sepsis.DesignProspective animal trial followed by a controlled cell culture study.SettingLaboratory of the Department of Anesthesiology.SubjectsMale Sprague-Dawley rats weighing 200 to 250 g and a mesangial cell line.InterventionsExperimental endotoxemia was induced in rats with lipopolysaccharide, and blood pressure dose-response studies with norepinephrine were performed. &agr;1-Receptor gene expression was determined in various organs by a specific RNase protection assay, and tissue concentrations of the proinflammatory cytokines interleukin-1&bgr; and tumor necrosis factor-&agr; were measured. Rat renal mesangial cells were incubated with these cytokines or with nitric oxide donors to investigate the regulation of &agr;1-adrenergic receptors during severe inflammation on a cellular level.Measurements and Main ResultsThe pressor effect of norepinephrine was markedly diminished during endotoxemia. The animals showed down-regulated mRNA levels of &agr;1A-, &agr;1B- and &agr;1D-receptors in all organs investigated, and the tissue concentrations of interleukin-1&bgr; and tumor necrosis factor-&agr; were highly increased during experimental endotoxemia. Incubation of cultured rat renal mesangial cells with the cytokines resulted in diminished &agr;1B-receptor gene expression and [H]prazosin binding capacity, whereas incubation of the cells with nitric oxide donors did not affect &agr;1B-receptor expression. In line, blocking of cytokine-induced nitric oxide synthesis by coincubation of mesangial cells withNG-nitro-l-arginine methyl ester did not influence cytokine-induced down-regulation of &agr;1B-receptors.ConclusionsOur data show that endotoxemia causes a systemic down-regulation of &agr;1-receptors on the level of gene expression and suggest that this effect is likely mediated by proinflammatory cytokines in a synergistic but nitric oxide-independent fashion. We propose that this down-regulation of &agr;1-adrenergic receptors contributes to the attenuated blood pressure response to norepinephrine and, therefore, to septic circulatory failure in patients.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveArginine vasopressin was established recently as a drug of choice in the treatment of cardiac arrest and in retractable ventricular fibrillation; however, the hemodynamic effect of vasopressin following endotracheal drug administration has not been fully elucidated. We compared the effects of endotracheally administered vasopressin vs. adrenaline on hemodynamic variables in a canine model, and we investigated whether vasopressin produces the same deleterious immediate blood pressure decrease as did endotracheal adrenaline in the canine model.DesignProspective controlled study.SettingAnimal laboratory in Tel-Aviv University, Israel.SubjectsFive adult mongrel dogs weighing 6.5–20 kg.InterventionsDogs were anesthetized; each dog was intubated orally, and both femoral arteries were cannulated for the measurement of arterial pressure and for sampling blood gases. Each dog was studied four times, 1 wk apart, by using the same protocol for injection and anesthesia: endotracheal placebo (10 mL NaCl 0.9%,), endotracheal vasopressin (1 units/kg), endobronchial adrenaline (0.1 mg/kg), and endotracheal adrenaline (0.1 mg/kg). Following placebo, vasopressin, and adrenaline instillation, five forced manual ventilations were delivered with an Ambu bag. Each dog was its own control.Measurements and Main ResultsFollowing placebo or drug administration, heart electrocardiography and arterial pressures were continuously monitored with a polygraph recorder for 1 hr. Endotracheal vasopressin produced an immediate increase of diastolic blood pressure (from 83 ± 10 mm Hg [baseline] to 110 ± 5 mm Hg at 1 min postinjection). This response lasted >1 hr. In contrast, both endotracheal and endobronchial administration of adrenaline produced an early and significant (p< .05) decrease in diastolic and mean blood pressures. The diastolic blood pressure increase from 85 ± 10 mm Hg to 110 ± 10 mm Hg took an ill-afforded 55 secs following endotracheal adrenaline. Diastolic blood pressure was significantly (p< .05) higher following vasopressin compared with adrenaline administration in both routes.ConclusionsVasopressin accomplishes its hemodynamic effect, particularly on diastolic blood pressure, more rapidly, vigorously, and protractedly and to a significant degree compared with both endotracheal and endobronchial adrenaline. Evaluation of the effects of endotracheal vasopressin in a closed chest cardiopulmonary resuscitation model is recommended.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveThe interaction between coagulation and inflammation has become one of the major topics in critical care medicine. In the present study, we investigated the effect of posttreatment of sepsis with recombinant human antithrombin.DesignExperimental laboratory in a university hospital.SettingUniversity laboratory.SubjectsFemale merino ewes (n = 16).InterventionsAfter 1 wk of recovery from the surgical preparation, a tracheotomy was performed followed by insufflation of 48 breaths of cotton smoke (<40°C). Afterward, a stock solution of livePseudomonas aeruginosa(5 × 1011colony-forming units) was instilled in the both lung lobes through a bronchoscope. All sheep were mechanically ventilated employing 100% oxygen. An infusion of recombinant human antithrombin (100 units·kg−1·24 hrs−1, intravenously; n = 6) or saline (n = 6) was started 1 hr after injury. Sham control animals (n = 4) were surgically prepared but not insufflated with smoke and bacteria. Lung histologic changes were evaluated by a scoring system.Measurements and Main ResultsThe infusion of recombinant human antithrombin maintained the baseline antithrombin activity throughout the study; in the saline-treated group, antithrombin activity decreased significantly. The lung wet/dry weight ratio and the histology score (combined scores for congestion, edema, inflammation, and hemorrhage) were significantly increased by the insult, but recombinant human antithrombin attenuated these responses. More than 30% of both bronchi and bronchioles were obstructed by cast formation after smoke inhalation and pneumonia. The cast was composed of epithelial cells, neutrophils, mucus, and fibrin. The obstruction was significantly improved by recombinant human antithrombin infusion. Arterial pressure and urine output were also attenuated in recombinant human antithrombin-treated animals. The increases in plasma nitrate/nitrite concentrations and pulmonary shunt fraction after the injury were not attenuated by recombinant human antithrombin.ConclusionPosttreatment by recombinant human antithrombin was effective in treating acute lung injury after smoke inhalation and pneumonia in sheep. We hypothesize that the decrease in antithrombin activity during sepsis might induce severe airway obstruction and that supplementation with antithrombin inhibits this decrease.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveMannitol is widely used in hospitals worldwide to treat patients with high intracranial pressure and/or cerebral edema. One of the mechanisms by which mannitol is thought to affect intracranial pressure is by increasing the patient’s serum osmolarity, but not the osmolarity in the brain or cerebrospinal fluid. In this way, mannitol is thought to increase the osmolarity gap between the brain and the blood, which in turn leads to removal of excess water from the brain. However, relatively little is known regarding long-term effects of mannitol on osmolarity of cerebrospinal fluid. We therefore sought to determine the effects of mannitol administration on the osmolarity of cerebrospinal fluid.DesignControlled trial.SettingUniversity teaching hospital.PatientsPatients with severe head injury and patients with subarachnoid bleeding who required insertion of an intracranial probe.Measurements and Main ResultsSerum and cerebrospinal fluid osmolarity were measured before and during mannitol administration in ten patients treated with mannitol for ≥72 hrs (group 1), ten patients treated for 24 to 48 hrs (group 2), and ten controls (group 3). Serum osmolarity increased quickly in all patients receiving mannitol (groups 1 and 2), whereas remaining constant in controls. Average cerebrospinal fluid osmolarity slowly increased in all patients receiving mannitol; cerebrospinal fluid osmolarity increased from (mean ± sd) 291.5 ± 4.0 to 315.5 ± 4.5 mOsm/kg after 96 hrs in group 1 (p< .01), and from 288.9 ± 3.5 to 296.9 ± 6.2 mOsm/kg after 48 hrs in group 2 (p< .01). Cerebrospinal fluid osmolarity remained constant in controls (p< .01 for group 1 vs. group 3 and for group 2 vs. group 3, respectively). In group 1, the gap between serum and cerebrospinal fluid osmolarity initially increased (which was the desired effect), but later decreased first to baseline values and then to below-normal levels.ConclusionsLong-term administration of mannitol can induce significant increases in cerebrospinal fluid osmolarity in patients with subarachnoid hemorrhage or severe head injury. This may be an undesirable and potentially dangerous effect. Therefore, cerebrospinal fluid osmolarity should be measured regularly in all patients receiving mannitol for longer than 24 hrs. If cerebrospinal fluid osmolarity increases, discontinuation or tapering of mannitol therapy should be considered.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveTo investigate whole body,in vivoarginine metabolism and nitric oxide synthesis rates in septic, critically ill pediatric patients.DesignProspective study.SettingPediatric intensive care unit at a general hospital.PatientsTen consecutive septic patients age 6–16 yrs.InterventionsSeptic patients received an 8-hr primed, constant intravenous tracer infusion of l-[guanidino-15N2]arginine, l-[1-13C]leucine, and [13C]urea. A 24-hr urine collection was obtained for determination of [15N]nitrate enrichment (15NO3−) and urinary nitrogen. The next day they received an infusion of l-[5-13C]arginine and l-[5-13C-ureido, 5,5,2H2]citrulline. Blood samples were obtained for determination of plasma isotopic enrichment of the tracers given and of derived [15N]citrulline (nitric oxide synthesis), l-[13C-guanidino 5,5,2H2]arginine (M+3 arg) (arginine synthesis), and [15N2]urea (urea formation). Data are compared with historic controls from studies in healthy young adults.Measurements and Main ResultsPlasma arginine fluxes were 67 ± 21 and 72 ± 17 &mgr;mol·kg−1·hr−1, respectively, for the [15N2guanidino] and the [13C] arginine labels, which were not different from reported adult values. The rates of arginine oxidation were 22.9 ± 10.8 &mgr;mol·kg−1·hr−1and were higher thande novoarginine synthesis rates of 9.6 ± 4.2 &mgr;mol·kg−1·hr−1(p< .01); therefore, these patients were in a negative arginine balance. The rates of nitric oxide synthesis as estimated by the [15N]citrulline method were 1.58 ± 0.69 &mgr;mol·kg−1·hr−1for septic patients and higher (p< .05) than values of 0.96 ± 0.1 &mgr;mol·kg−1·hr−1in healthy adults. Septic patients were in a negative protein (leucine) balance of about −1.00 ± 0.40 g·kg−1·day−1.ConclusionsHomeostasis of plasma arginine in septic patients was impaired compared with reported adult values. The rates of arginine oxidation were increased whereasde novonet arginine synthesis was unchanged, leading to a negative arginine balance. The rates of nitric oxide synthesis and the fraction of plasma arginine used for nitric oxide and urea formation were increased. These findings suggest that under condition of sepsis, arginine becomes essential in critically ill children.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Severe and prolonged states of catabolic stress have been shown to have profound effects on the intestinal tract microflora and intestinal function. Gut-derived sepsis is a term used to describe a state of systemic inflammation with organ dysfunction after severe catabolic stress hypothesized to be initiated and perpetuated by the intestinal tract microflora. Popular notions of the mechanism of this process have suggested that stress promotes the translocation of intestinal bacteria or their toxins into the systemic compartment resulting in the release of proinflammatory cytokines which participate in the systemic inflammatory response syndrome. This review is an attempt to redefine the mechanism of gut-derived sepsis by focusing on molecular events that result from host-pathogen interactions within the intestinal tract itself. This evidence-based review posits that gut-derived bacteremia, even with potent nosocomial pathogens, is an event of low proinflammatory potential and, itself, is an insufficient stimulus for the systemic inflammatory response and organ failure state typically seen after severe and prolonged catabolic stress. Mechanisms of this apparent paradox are discussed.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

The use of inadequate empirical antimicrobial therapy is common in intensive care unit patients and contributes to a number of poor outcomes. Selecting appropriate antimicrobial therapy is complicated by many factors, including the large number of agents available, the presence of resistant organisms, and the general desire among practitioners to use the most focused therapy available. An important aspect of appropriate antimicrobial use is prompt initiation of adequate empirical therapy, which has been shown to improve mortality rates in hospitalized patients with pneumonia and other serious infections. Other key strategies include streamlining antimicrobial therapy when a pathogen is identified and switching from intravenous to oral therapy when clinically indicated. In addition, antibiotic rotation (or cycling) has been evaluated in several trials as a means to minimize resistance. Promoting appropriate antimicrobial therapy ultimately will require a multidisciplinary, system-oriented, institution-specific approach because each intensive care unit has its own unique flora and antimicrobial resistance patterns.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectivePatients with a hemispheric infarct accompanied by massive edema have a poor prognosis; the case fatality rate may be as high as 80%, and most survivors are left severely disabled. Various treatment strategies have been proposed to limit brain tissue shifts and to reduce intracranial pressure, but their use is controversial. We performed a systematic search of the literature to review the evidence of efficacy of these therapeutic modalities.Data SourcesLiterature searches were carried out on MEDLINE and PubMed.Study SelectionStudies were included if they were published in English between 1966 and February 2002 and addressed the effect of osmotherapy, hyperventilation, barbiturates, steroids, hypothermia, or decompressive surgery in supratentorial infarction with edema in animals or humans.Data SynthesisAnimal studies of medical treatment strategies in focal cerebral ischemia produced conflicting results. If any, experimental support for these strategies is derived from studies with animal models of moderately severe focal ischemia instead of severe space-occupying infarction. None of the treatment options have improved outcome in randomized clinical trials. Two large nonrandomized studies of decompressive surgery yielded promising results in terms of reduction of mortality and improvement of functional outcome.ConclusionsThere is no treatment modality of proven efficacy for patients with space-occupying hemispheric infarction. Decompressive surgery might be the most promising therapeutic option. For decisive answers, randomized, controlled clinical trials are needed.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID