摘要:

ObjectivesTo determine whether acute cardiogenic pulmonary edema is associated with damage to the alveolocapillary barrier, as evidenced by increased leakage of surfactant specific proteins into the circulation, to document the duration of alveolocapillary barrier damage in this setting, and to explore the role of pulmonary parenchymal inflammation by determining if circulating tumor necrosis factor-&agr; is increased after acute cardiogenic pulmonary edema.DesignProspective, observational study.SettingCritical care, cardiac intensive care, and cardiology wards of a tertiary-care university teaching hospital.PatientsA total of 28 patients presenting with acute cardiogenic pulmonary edema and 13 age-matched normal volunteers.InterventionsCirculating surfactant protein-A and -B and tumor necrosis factor-&agr; were measured on days 0 (presentation), 1, 3, 7, and 14. Clinical markers of pulmonary edema were documented at the same times.Measurements and Main ResultsSurfactant protein-A and -B were elevated on day 0 compared with controls (367 ± 17 ng/mL vs. 303 ± 17 and 3821 ± 266 ng/mL vs. 2747 ± 157 [mean ± sem],p< .05), and although clinical, hemodynamic and radiographic variables improved rapidly (p< .001), surfactant protein-A and -B rose further until day 3 (437 ± 22,p< .001, 4642 ± 353,p< .01). Tumor necrosis factor-&agr; was elevated at presentation (p< .05), doubled by day 1 (6.98 ± 1.36 pg/mL,p< .05), remained elevated on day 3 (5.72 ± 0.96 pg/mL,p< .05), and peak levels were related to chest radiograph extravascular lung water score (rp= 0.64,p= .003).ConclusionsAlthough the initial increase in plasma surfactant protein-A and -B may represent hydrostatic stress failure of the alveolocapillary barrier, the prolonged elevation, when hemodynamic abnormalities have resolved, and the delayed elevation of tumor necrosis factor-&agr; are consistent with pulmonary parenchymal inflammation, which may further damage the alveolocapillary barrier. This prolonged physiologic defect at the alveolocapillary barrier after acute cardiogenic pulmonary edema may partly account for the vulnerability of these patients to recurrent pulmonary fluid accumulation.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveSevere systemic inflammation with a vasodilatory syndrome occurs in about one third of all patients after cardiac surgery with cardiopulmonary bypass. Hydrocortisone has been used successfully to reverse vasodilation in septic patients. We evaluated if stress doses of hydrocortisone attenuate severe systemic inflammatory response syndrome in a predefined risk group of patients after cardiac surgery with cardiopulmonary bypass.DesignRandomized, nonblinded, controlled trial.SettingAnesthesiologic intensive care unit for cardiac surgical patients of an university hospital.PatientsAfter a risk analysis, we enrolled 91 patients into a prospective randomized trial. Patients were included according to the evaluated criteria (preoperative ejection fraction, duration of cardiopulmonary bypass, type of surgery).InterventionsThe treatment group received stress doses of hydrocortisone perioperatively: 100 mg before induction of anesthesia, then 10 mg/hr for 24 hrs, 5 mg/hr for 24 hrs, 3 × 20 mg/day, and 3 × 10 mg/day.Measurements and Main ResultsWe measured various laboratory (e.g., lactate) and clinical variables (e.g., duration of ventilation and length of stay in the intensive care unit), characterizing the patients’ outcome. The two study groups did not differ regarding age, preoperative medication, duration of the cardiopulmonary bypass, and type of surgery. The patients in the treatment group had significantly lower concentrations of IL-6 and lactate, higher antithrombin III concentration, lower need for circulatory and ventilatory support and for transfusions, lower Therapeutic Intervention Scoring System values, and shorter length of stay in the intensive care unit and in the hospital. The mortality rate did not differ significantly between the groups.ConclusionsAlthough we acknowledge the limitations of a nonblinded interventional trial, stress doses of hydrocortisone seem to attenuate systemic inflammation in a predefined risk group of patients after cardiac surgery with cardiopulmonary bypass and improve early outcome.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveTo ascertain the prevalence, predictors, and prognostic significance of microalbuminuria in critically ill patients.DesignProspective cohort study.SettingMedical intensive care unit of a community teaching hospital.PatientsAdmitted critically ill patients.Measurements and Main ResultsWe measured serial spot urine albumin-creatinine ratios in 104 critically ill patients, with a median age of 64.5 yrs and median Acute Physiology and Chronic Health Evaluation (APACHE) II and Sequential Organ Failure Assessment (SOFA) scores of 20.5 and 5.0, respectively. Sixty-nine percent of the patients had microalbuminuria or clinical proteinuria and 43.3% had an albumin-creatinine ratio ≥100 mg/g at admission. The acuity of illness, being non-White, and having diabetes mellitus were independent predictors of albumin-creatinine ratio ≥100 mg/g. The overall mortality rate was 26.9% (28/104). Patients with an albumin-creatinine ratio ≥100 mg/g were 2.7 times as likely to die compared with those with an albumin-creatinine ratio <100 mg/g, even after simultaneous adjustments for age, and APACHE II and SOFA scores (odds ratio, 2.7; 95% confidence interval, 1.1–7.2,p= .04). The association of albumin-creatinine ratio ≥100 mg/g with death was consistent across age, ethnicity, renal function, acuity of illness, and comorbid conditions. Among survivors, patients with an albumin-creatinine ratio ≥100 mg/g stayed approximately 5 days longer in the hospital (p= .0007). Overall, the albumin-creatinine ratio shared similar predictive characteristics with APACHE II and SOFA scores.ConclusionsThis study confirms a high prevalence of microalbuminuria in critically ill patients and suggests that an albumin-creatinine ratio ≥100 mg/g is an independent predictor of mortality and hospital stay.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectivePrevious studies have shown a wide variation in the prevalence of total serum hypomagnesemia in intensive are unit (ICU) patients and in associated mortality rates. As the ionized part of magnesium is the active portion, we sought to define the prevalence of ionized hypomagnesemia in critically ill patients and to evaluate its relationship with organ dysfunction, length of stay, and mortality.DesignProspective observational study.SettingA 31-bed, medical-surgical, university hospital ICU.PatientsA total of 446 consecutive patients admitted to the ICU over a 3-month period.InterventionsNone.Measurements and Main ResultsThe ionized magnesium level (normal value, 0.42–0.59 mmol/L) was measured at admission and then every day until discharge from the ICU. At admission, 18% of patients had ionized hypomagnesemia, 68% had normal ionized magnesium levels, and 14% had ionized hypermagnesemia. There was no significant difference in the length of stay or in the mortality rate between these three groups of patients. Hypomagnesemic patients more frequently had total and ionized hypocalcemia, hypokalemia, and hypoproteinemia. A total of 23 patients developed ionized hypomagnesemia during their ICU stay; these patients had higher Acute Physiology And Chronic Health Evaluation II (14.9 ± 5.4 vs. 11.0 ± 6.2) and Sequential Organ Failure Assessment (SOFA; 7.1 ± 5.4 vs. 3.9 ± 2.8) scores at admission (p< .01 for both), a higher maximum SOFA score during their ICU stay (10.0 ± 5.6 vs. 4.4 ± 3.2,p< .01), a higher prevalence of severe sepsis and septic shock (57 vs. 11%,p< .01), a longer ICU stay (15.4 ± 15.5 vs. 2.8 ± 4.7 days,p< .01), and a higher mortality rate (35% vs. 12%,p< .01) than the other patients. The major risk factors for developing hypomagnesemia during the ICU stay were a prolonged ICU stay, treatment with diuretics, and sepsis.ConclusionDevelopment of ionized hypomagnesemia during an ICU stay is associated with a worse prognosis. It is often associated with the use of diuretics and the development of sepsis. Monitoring of ionized magnesium levels may have prognostic, and perhaps therapeutic, implications.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveTo determine the effect of restriction of third-generation cephalosporin use on antibiotic resistance and the outcome of patients with infection.DesignA prospective, before–after comparative study.SettingA general intensive care unit with 14 beds at a university-affiliated teaching hospital.PatientsAll patients admitted to the intensive care unit within 2 yrs.InterventionsA new antibiotic treatment strategy was implemented during phase II. All patients with confirmed or suspected Gram-negative bacterial infections were treated mainly with antibiotics other than third-generation cephalosporins.Measurements and Main ResultsAntibiotic resistance among common Gram-negative bacilli and infection-related hospital mortality during phase I were compared with phase II. A 26.6% reduction in third-generation cephalosporin use (from 168.2 ± 48.0 to 123.5 ± 39.3 g/month,p= .021), accompanied by a 277.7% increase in cefepime use (from 10.3 ± 19.2 to 38.9 ± 31.7 g/month,p= .014) occurred in phase II compared with phase I. This was accompanied by a significant decrease in reduced susceptibility of Gram-negative bacilli to third-generation cephalosporins (p< .05), mainly because of the improved susceptibility ofEscherichia coliandKlebsiellaspecies (p< .05). Infection-related hospital mortality was significantly lower in phase II (19.3% vs. 36.3%,p= .014). Multiple logistic regression analysis demonstrated lower respiratory tract infection, the status of immunocompromise, and continuous veno-venous hemofiltration as independent risk factors for infection-related hospital mortality (p< .05), whereas infection withE. coliorKlebsiellaspecies (p= .039) and restriction of third-generation cephalosporin use (p= .025) were associated with a significantly lower mortality rate.ConclusionsRestriction of third-generation cephalosporin use may improve the antibiotic susceptibility and reduce infection-related hospital mortality in critically ill patients.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveTo determine health-related quality of life in medical intensive care patients with multiple organ dysfunction.DesignProspective, observational study.SettingA 12-bed, noncoronary, medical intensive care unit of a university hospital.PatientsBetween June 1998 and May 1999, 318 consecutively admitted adult patients with an intensive care unit stay of >24 hrs were studied.Measurements and Main ResultsHealth-related quality of life was assessed using a generic instrument, the Medical Outcomes Study Short Form-36 Health Survey, at admission and at 6-month follow-up. Patients who developed multiple organ dysfunction (n = 170) consumed 85% of the therapeutic activity provided in the intensive care unit. Compared with age- and sex-adjusted general population controls, multiple organ dysfunction patients had a worse preadmission health-related quality of life than other intensive care unit patients, predominantly due to a higher burden of comorbid disease. In a multivariate analysis, multiple organ dysfunction was the only variable independently associated with deteriorated physical health domains at follow-up (odds ratio, 4.4; 95% confidence interval, 1.3–14.6;p= .015), but it had no impact on dimensions of mental health. Analyzing the impact of different organ system failures, respiratory failure (odds ratio, 4.1; 95% confidence interval, 1.6–10.3;p= .002) and acute renal failure (odds ratio, 3.3; 95% confidence interval, 1.0–11.5;p= .05) increased the risk of deteriorated physical health at follow-up. No impact of the various organ system failures on mental health was noted. At 6-month follow-up, 83–90% of survivors had regained their previous health-related quality of life, and 94% were living at home with their families.ConclusionsThis study has shown that preadmission health-related quality of life of our medical, noncoronary patients was substantially reduced compared with a matched general population. This demonstrates the need to take prehospitalization health-related quality of life into account when examining the outcomes of intensive care unit survivors. Multiple organ dysfunction was the major determinant of poor physical health at follow-up, but it had no impact on mental health domains.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveTo determine the factors associated with ventilator-associated pneumonia recurrence in patients alive after 8 days of treatment for a first episode.DesignA 16-month, prospective, observational cohort study of patients diagnosed with a first ventilator-associated pneumonia episode. Predictors of recurrence were assessed by logistic regression analysis.SettingTwo intensive care units in a university hospital.PatientsBronchoscopy was performed in 124 patients with clinically or radiologically suspected ventilator-associated pneumonia. Ventilator-associated pneumonia was confirmed by the presence of at least two of the following criteria: ≥2% of cells with intracellular bacteria found on direct examination of bronchoalveolar lavage fluid, protected specimen brush sample culture ≥103colony-forming units/mL, or bronchoalveolar lavage culture ≥104colony-forming units/mL. Ventilator-associated pneumonia recurrence was confirmed using the same microbiological criteria. Antibiotic treatment for ventilator-associated pneumonia lasted 14 days.Measurements and Main ResultsClinical, radiologic, and biological data at intensive care unit admission, on the day of bronchoscopy (D1) and on D8, and outcome variables were prospectively recorded. Ventilator-associated pneumonia recurred in 28 patients (all of them still on mechanical ventilation on D8), 21 ± 9 days after the first episode (82% after D14). Factors significantly associated with recurrence were: acute respiratory failure as initial reason for mechanical ventilation, D1 radiologic score >7, D8 radiologic score >8, adult respiratory distress syndrome on D8, mechanical ventilation persistence on D8, D8 temperature >38°C, and D8 temperature >D1 temperature, but not disease-severity scores at inclusion and D8, or first-episode pathogen(s). Multivariate analysis identified D1 radiologic score >7 (odds ratio = 3.9; 95% confidence interval, 1.3–11.6), D8 temperature >38°C (odds ratio = 4.4; 95% confidence interval, 1.4–13.4), and adult respiratory distress syndrome on D8 (odds ratio = 14.6; 95% confidence interval, 1.5–143.5) as predictors of recurrence.ConclusionsFactors of ventilator-associated pneumonia recurrence evaluated on D8 of a 14-day course of antibiotics are linked to the severity of lung injury and persistence of fever, but not to first-episode pathogen(s).

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveCytokines and adhesion molecules have a decisive role in the development of early inflammatory response as well as the late sequelae of sepsis. Because L-selectin-deficient mice are protected from lethal endotoxemia, blockade of L-selectin may provide a useful therapeutic option in human sepsis. Heparin has immunomodulatory properties and effectively inhibits L- and P-selectin bindingin vitro. We therefore investigated whether clinically applied doses of unfractionated or low-molecular-weight heparin affect early inflammatory response in human endotoxemia.DesignThe study was randomized, double-blinded, placebo-controlled, in three parallel groups consisting of 30 healthy male volunteers.SettingUniversity medical center.InterventionsAll subjects received a 2-ng/kg intravenous bolus of lipopolysaccharide and 10 mins later unfractionated heparin, low-molecular-weight heparin, or placebo as bolus primed continuous infusion for 6 hrs.Measurements and Main ResultsLipopolysaccharide infusion induced similar increases of tumor necrosis factor-&agr;, interleukin-6, interleukin-8, C-reactive protein, and soluble E-selectin levels in all treatment groups. CD11b expression increased by approximately 400%, but L-selectin decreased by 41% in the placebo arm 6 hrs after lipopolysaccharide infusion. Interestingly, both heparins (in particular unfractionated heparin) decreased L-selectin down-regulation as compared with placebo. Similarly, the decrease in lymphocyte counts was significantly less in the unfractionated heparin group during the first 24 hrs (p< .05 vs. placebo)ConclusionsHeparins displayed little effects on cytokine production and endothelial cell activation in endotoxemia. Of note, however, unfractionated heparin reduced L-selectin down-regulation and lymphocytopenia. These could present novel mechanisms of action of unfractionated heparin.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveTo investigate the adrenocortical function in brain-dead patients, potential organ donors.DesignProspective study.SettingIntensive care units in two teaching hospitals.PatientsA total of 37 patients (28 men, nine women) with severe brain injury, having a mean age of 42 ± 18 yrs, were included in the study. Group A consisted of 20 brain-injured patients who did not deteriorate to brain death. Group B included 17 brain-injured patients who were brain dead; of these, ten patients developed brain death during ICU stay and seven patients were admitted to the ICU after clinical brain death.InterventionsIn all patients (group A and group B), a morning blood sample was obtained at admission to the ICU to determine baseline plasma cortisol. Subsequently, 1 &mgr;g of corticotropin (adrenocorticotropic hormone, Synacthen) was administered intravenously, and a blood sample was taken 30 mins after the injection. In group B patients who became brain dead while being treated in the ICU (n = 10), the same procedure was repeated the morning after the confirmation of brain death. Patients having a cortisol level of at least 18 &mgr;g/dL after the administration of adrenocorticotropic hormone were defined as responders.Measurements and Main ResultsAfter the occurrence of brain death, group B patients had significantly lower values for baseline (8.5 ± 6.2 vs. 17.0 ± 6.6 &mgr;g/dL,p< .001) and stimulated (16.9 ± 6.3 vs. 23.9 ± 5.7 &mgr;g/dL,p= .001) plasma cortisol compared with group A patients. Thirteen group B patients (76%) and two group A patients (10%) were nonresponders to adrenocorticotropic hormone (p< .001). In group B patients, baseline and stimulated cortisol concentrations were significantly related (r= .71,p= .001), whereas there was no correlation between baseline cortisol and the increment in cortisol (r= −.37,p= .15). Mean hormonal data of the ten brain-dead patients studied at admission in the ICU and after the occurrence of brain death were the following: baseline plasma cortisol (23.5 ± 11.4 vs. 6.8 ± 4.2 &mgr;g/dL,p= .003) and stimulated serum cortisol (28.8 ± 9.9 vs. 16.3 ± 4.3 &mgr;g/dL,p= .008).ConclusionsAdrenal cortisol secretion after dynamic stimulation is deficient in a substantial proportion of brain-dead potential organ donors.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveTo investigate the effects of total parenteral nutrition administration on intestinal ion transport and intestinal epithelial permeability. Additionally, to assess the role of interferon-&ggr; on the total parenteral nutrition-induced loss of epithelial barrier function.DesignRandomized, controlled study.SettingExperimental laboratory, University of Michigan Medical School, Ann Arbor.SubjectsAdult wild-type and interferon-&ggr; knockout mice.InterventionsWild-type mice received total parenteral nutrition or enteral diet (control group) for 7 days. Segments of small bowel from the mice were mounted in Ussing chambers. Short circuit current, as an indictor of active ion transport, was constantly monitored. Epithelial barrier function was assessed by measuring transepithelial resistance and transmural passage of51Cr-EDTA and3H-mannitol. Intestinal intraepithelial lymphocyte-derived interferon-&ggr; protein expression was detected with enzyme-linked immunosorbent assay and confirmed by using intracellular staining and flow cytometry. To investigate the effect of total parenteral nutrition on intestinal ion transport, we used a secretory agonist, carbachol, and an absorptive agent, glucose.Measurements and Main ResultsTotal parenteral nutrition significantly increased small-bowel permeability. Ion transport in the total parenteral nutrition group was significantly increased. To stimulate ion transport, we found that increases in short circuit current induced by carbachol and glucose were higher in the total parenteral nutrition group compared with the control group. Intestinal intraepithelial lymphocyte interferon-&ggr; protein expression significantly increased with the administration of total parenteral nutrition. Intestinal permeability in interferon-&ggr; knockout total parenteral nutrition mice was significantly lower than in wild-type mice receiving total parenteral nutrition.ConclusionTotal parenteral nutrition has significant effects on intestinal epithelial physiology, stimulating ion secretion and reducing epithelial barrier function. Interferon-&ggr; appears to play an important role in the loss of the epithelial barrier function that is associated with total parenteral nutrition.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID