15 results on '"Dries DJ"'
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2. Paradoxical Positioning: Does "Head Up" Always Improve Mechanics and Lung Protection?
- Author
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Selickman J, Crooke PS, Tawfik P, Dries DJ, Gattinoni L, and Marini JJ
- Subjects
- Humans, Lung, Prospective Studies, Respiratory Mechanics physiology, Tidal Volume physiology, Positive-Pressure Respiration methods, Respiratory Distress Syndrome therapy
- Abstract
Objectives: Head-elevated body positioning, a default clinical practice, predictably increases end-expiratory transpulmonary pressure and aerated lung volume. In acute respiratory distress syndrome (ARDS), however, the net effect of such vertical inclination on tidal mechanics depends upon whether lung recruitment or overdistension predominates. We hypothesized that in moderate to severe ARDS, bed inclination toward vertical unloads the chest wall but adversely affects overall respiratory system compliance (C rs )., Design: Prospective physiologic study., Setting: Two medical ICUs in the United States., Patients: Seventeen patients with ARDS, predominantly moderate to severe., Intervention: Patients were ventilated passively by volume control. We measured airway pressures at baseline (noninclined) and following bed inclination toward vertical by an additional 15°. At baseline and following inclination, we manually loaded the chest wall to determine if C rs increased or paradoxically declined, suggestive of end-tidal overdistension., Measurements and Main Results: Inclination resulted in a higher plateau pressure (supineΔ: 2.8 ± 3.3 cm H 2 O [ p = 0.01]; proneΔ: 3.3 ± 2.5 cm H 2 O [ p = 0.004]), higher driving pressure (supineΔ: 2.9 ± 3.3 cm H 2 O [ p = 0.01]; proneΔ: 3.3 ± 2.8 cm H 2 O [ p = 0.007]), and lower C rs (supine Δ: 3.4 ± 3.7 mL/cm H 2 O [ p = 0.01]; proneΔ: 3.1 ± 3.2 mL/cm H 2 O [ p = 0.02]). Following inclination, manual loading of the chest wall restored C rs and driving pressure to baseline (preinclination) values., Conclusions: In advanced ARDS, bed inclination toward vertical adversely affects C rs and therefore affects the numerical values for plateau and driving tidal pressures commonly targeted in lung protective strategies. These changes are fully reversed with manual loading of the chest wall, suggestive of end-tidal overdistension in the upright position. Body inclination should be considered a modifiable determinant of transpulmonary pressure and lung protection, directionally similar to tidal volume and positive end-expiratory pressure., Competing Interests: The authors have disclosed that they do not have any potential conflicts of interest., (Copyright © 2022 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the Society of Critical Care Medicine and Wolters Kluwer Health, Inc.)
- Published
- 2022
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3. Paradoxical response to chest wall loading predicts a favorable mechanical response to reduction in tidal volume or PEEP.
- Author
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Selickman J, Tawfik P, Crooke PS, Dries DJ, Shelver J, Gattinoni L, and Marini JJ
- Subjects
- Humans, Positive-Pressure Respiration, Prospective Studies, Tidal Volume, Respiratory Distress Syndrome therapy, Thoracic Wall
- Abstract
Background: Chest wall loading has been shown to paradoxically improve respiratory system compliance (C
RS ) in patients with moderate to severe acute respiratory distress syndrome (ARDS). The most likely, albeit unconfirmed, mechanism is relief of end-tidal overdistension in 'baby lungs' of low-capacity. The purpose of this study was to define how small changes of tidal volume (VT ) and positive end-expiratory pressure (PEEP) affect CRS (and its associated airway pressures) in patients with ARDS who demonstrate a paradoxical response to chest wall loading. We hypothesized that small reductions of VT or PEEP would alleviate overdistension and favorably affect CRS and conversely, that small increases of VT or PEEP would worsen CRS ., Methods: Prospective, multi-center physiologic study of seventeen patients with moderate to severe ARDS who demonstrated paradoxical responses to chest wall loading. All patients received mechanical ventilation in volume control mode and were passively ventilated. Airway pressures were measured before and after decreasing/increasing VT by 1 ml/kg predicted body weight and decreasing/increasing PEEP by 2.5 cmH2 O., Results: Decreasing either VT or PEEP improved CRS in all patients. Driving pressure (DP) decreased by a mean of 4.9 cmH2 O (supine) and by 4.3 cmH2 O (prone) after decreasing VT , and by a mean of 2.9 cmH2 O (supine) and 2.2 cmH2 O (prone) after decreasing PEEP. CRS increased by a mean of 3.1 ml/cmH2 O (supine) and by 2.5 ml/cmH2 O (prone) after decreasing VT. CRS increased by a mean of 5.2 ml/cmH2 O (supine) and 3.6 ml/cmH2 O (prone) after decreasing PEEP (P < 0.01 for all). Small increments of either VT or PEEP worsened CRS in the majority of patients., Conclusion: Patients with a paradoxical response to chest wall loading demonstrate uniform improvement in both DP and CRS following a reduction in either VT or PEEP, findings in keeping with prior evidence suggesting its presence is a sign of end-tidal overdistension. The presence of 'paradox' should prompt re-evaluation of modifiable determinants of end-tidal overdistension, including VT , PEEP, and body position., (© 2022. The Author(s).)- Published
- 2022
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4. Variation in Early Management Practices in Moderate-to-Severe ARDS in the United States: The Severe ARDS: Generating Evidence Study.
- Author
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Qadir N, Bartz RR, Cooter ML, Hough CL, Lanspa MJ, Banner-Goodspeed VM, Chen JT, Giovanni S, Gomaa D, Sjoding MW, Hajizadeh N, Komisarow J, Duggal A, Khanna AK, Kashyap R, Khan A, Chang SY, Tonna JE, Anderson HL 3rd, Liebler JM, Mosier JM, Morris PE, Genthon A, Louh IK, Tidswell M, Stephens RS, Esper AM, Dries DJ, Martinez A, Schreyer KE, Bender W, Tiwari A, Guru PK, Hanna S, Gong MN, and Park PK
- Subjects
- Adult, Aged, Cohort Studies, Early Medical Intervention, Extracorporeal Membrane Oxygenation statistics & numerical data, Female, Glucocorticoids therapeutic use, Humans, Male, Middle Aged, Neuromuscular Blockade statistics & numerical data, Patient Positioning, Positive-Pressure Respiration, Practice Guidelines as Topic, Prone Position, Quality of Health Care, Severity of Illness Index, United States, Vasodilator Agents, Guideline Adherence statistics & numerical data, Hospital Mortality, Practice Patterns, Physicians' statistics & numerical data, Respiration, Artificial methods, Respiratory Distress Syndrome therapy, Ventilator-Induced Lung Injury prevention & control
- Abstract
Background: Although specific interventions previously demonstrated benefit in patients with ARDS, use of these interventions is inconsistent, and patient mortality remains high. The impact of variability in center management practices on ARDS mortality rates remains unknown., Research Question: What is the impact of treatment variability on mortality in patients with moderate to severe ARDS in the United States?, Study Design and Methods: We conducted a multicenter, observational cohort study of mechanically ventilated adults with ARDS and Pao
2 to Fio2 ratio of ≤ 150 with positive end-expiratory pressure of ≥ 5 cm H2 O, who were admitted to 29 US centers between October 1, 2016, and April 30, 2017. The primary outcome was 28-day in-hospital mortality. Center variation in ventilator management, adjunctive therapy use, and mortality also were assessed., Results: A total of 2,466 patients were enrolled. Median baseline Pao2 to Fio2 ratio was 105 (interquartile range, 78.0-129.0). In-hospital 28-day mortality was 40.7%. Initial adherence to lung protective ventilation (LPV; tidal volume, ≤ 6.5 mL/kg predicted body weight; plateau pressure, or when unavailable, peak inspiratory pressure, ≤ 30 mm H2 O) was 31.4% and varied between centers (0%-65%), as did rates of adjunctive therapy use (27.1%-96.4%), methods used (neuromuscular blockade, prone positioning, systemic steroids, pulmonary vasodilators, and extracorporeal support), and mortality (16.7%-73.3%). Center standardized mortality ratios (SMRs), calculated using baseline patient-level characteristics to derive expected mortality rate, ranged from 0.33 to 1.98. Of the treatment-level factors explored, only center adherence to early LPV was correlated with SMR., Interpretation: Substantial center-to-center variability exists in ARDS management, suggesting that further opportunities for improving ARDS outcomes exist. Early adherence to LPV was associated with lower center mortality and may be a surrogate for overall quality of care processes. Future collaboration is needed to identify additional treatment-level factors influencing center-level outcomes., Trial Registry: ClinicalTrials.gov; No.: NCT03021824; URL: www.clinicaltrials.gov., (Copyright © 2021. Published by Elsevier Inc.)- Published
- 2021
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5. Finding Best PEEP: A Little at a Time.
- Author
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Dries DJ and Marini JJ
- Subjects
- Humans, Positive-Pressure Respiration, Prospective Studies, Pulmonary Gas Exchange, Respiratory Distress Syndrome
- Abstract
Competing Interests: The authors have disclosed no conflicts of interest.
- Published
- 2020
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6. Acute Respiratory Distress Syndrome and Lung Protection.
- Author
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Dries DJ
- Subjects
- Acute Lung Injury, Humans, Respiration, Artificial, Lung, Respiratory Distress Syndrome
- Published
- 2016
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7. PEEP titration: new horizons.
- Author
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Keenan JC and Dries DJ
- Subjects
- Female, Humans, Male, Lung Compliance, Positive-Pressure Respiration methods, Respiratory Distress Syndrome therapy
- Published
- 2013
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8. Time course of physiologic variables in response to ventilator-induced lung injury.
- Author
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Dries DJ, Adams AB, and Marini JJ
- Subjects
- Animals, Disease Models, Animal, Female, Male, Pressure, Respiratory Distress Syndrome etiology, Severity of Illness Index, Swine, Pleural Cavity physiopathology, Pulmonary Gas Exchange physiology, Respiration, Artificial adverse effects, Respiratory Distress Syndrome physiopathology, Respiratory Mechanics physiology
- Abstract
Background: The time course of the physiological derangements that result from ventilator-induced lung injury has not been adequately described. Similarly, the regional topographies of pleural pressure and tissue edema have not been carefully mapped for this injury process., Methods: Lung injury was induced in 9 normal pigs by ventilating for 6 hours at a transpulmonary pressure of 35 cm H(2)O, with the animals in the supine position. Eight additional normal pigs received right thoracotomy to place pleural-surface-pressure sensors prior to an identical period and intensity of injurious ventilation. Gas exchange and lung mechanics were tracked in all the animals. Cytokines (tumor necrosis factor alpha, interleukin 6, and interleukin 8) in peripheral blood were assayed at 2 hour intervals, beginning at the onset of mechanical ventilation, from all the animals., Results: After a brief "induction" period, P(aO(2)) and tidal volume declined steadily in the animals that were ventilated to induce lung injury. The rate of decline was greater in the animals that received thoracotomy. The pleural pressure gradient steadily increased from ventral to dorsal. The serum cytokine levels did not evolve with developing injury, but cytokines were elevated at the onset of ventilation. Tissue edema, as assessed by the ratio of wet weight to dry weight, was greater in the thoracotomized animals than in the nonthoracotomized animals, and tissue edema tended to be greater in the caudal lung regions than in the cephalad lung regions., Conclusions: Following the induction period, the development of ventilator-induced lung injury progressed steadily and then plateaued, as assessed by quantitative physiology variables during 6 hours of ventilation at a transpulmonary pressure of 35 cm H(2)O. Greater injury developed in animals that had a coexisting potential insult (thoracotomy). Injury development was not paralleled by bloodborne inflammatory cytokines.
- Published
- 2007
9. Absence of alveolar tears in rat lungs with significant alveolar instability.
- Author
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Pavone LA, Dirocco JD, Carney DE, Gatto LA, McBride NT, Norton JA, Hession RM, Boubert F, Hojnowski KA, Lafollette RL, Dries DJ, and Nieman GF
- Subjects
- Animals, Disease Models, Animal, Male, Microscopy, Electron, Scanning, Microscopy, Video, Pulmonary Alveoli ultrastructure, Pulmonary Gas Exchange physiology, Rats, Rats, Sprague-Dawley, Respiration, Artificial adverse effects, Respiratory Distress Syndrome etiology, Respiratory Distress Syndrome physiopathology, Rupture, Pulmonary Alveoli injuries, Respiratory Distress Syndrome pathology
- Abstract
Background: Lung injury associated with the acute respiratory distress syndrome can be exacerbated by improper mechanical ventilation creating a secondary injury known as ventilator-induced lung injury (VILI). We hypothesized that VILI could be caused in part by alveolar recruitment/derecruitment resulting in gross tearing of the alveolus., Objectives: The exact mechanism of VILI has yet to be elucidated though multiple hypotheses have been proposed. In this study we tested the hypothesis that gross alveolar tearing plays a key role in the pathogenesis of VILI., Methods: Anesthetized rats were ventilated and instrumented for hemodynamic and blood gas measurements. Following baseline readings, rats were exposed to 90 min of either normal ventilation (control group: respiratory rate 35 min(-1), positive end-expiratory pressure 3 cm H(2)O, peak inflation pressure 14 cm H(2)O) or injurious ventilation (VILI group: respiratory rate 20 min(-1), positive end-expiratory pressure 0 cm H(2)O, peak inflation pressure 45 cm H(2)O). Parameters studied included hemodynamics, pulmonary variables, in vivo video microscopy of alveolar mechanics (i.e. dynamic alveolar recruitment/derecruitment) and scanning electron microscopy to detect gross tears on the alveolar surface., Results: Injurious ventilation significantly increased alveolar instability after 45 min and alveoli remained unstable until the end of the study (electron microscopy after 90 min revealed that injurious ventilation did not cause gross tears in the alveolar surface)., Conclusions: We demonstrated that alveolar instability induced by injurous ventilation does not cause gross alveolar tears, suggesting that the tissue injury in this animal VILI model is due to a mechanism other than gross rupture of the alveolus., (Copyright (c) 2007 S. Karger AG, Basel.)
- Published
- 2007
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10. Transient hemodynamic effects of recruitment maneuvers in three experimental models of acute lung injury.
- Author
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Lim SC, Adams AB, Simonson DA, Dries DJ, Broccard AF, Hotchkiss JR, and Marini JJ
- Subjects
- Analysis of Variance, Animals, Disease Models, Animal, Female, Hemodynamics physiology, Lung Volume Measurements, Male, Oleic Acid, Pneumonia, Pneumococcal, Probability, Pulmonary Gas Exchange, Respiration, Artificial, Respiratory Distress Syndrome physiopathology, Risk Factors, Sensitivity and Specificity, Swine, Cardiac Output physiology, Positive-Pressure Respiration methods, Respiratory Distress Syndrome therapy
- Abstract
Objective: Elevated lung volumes and increased pleural pressures associated with recruitment maneuvers (RM) may adversely affect pulmonary vascular resistance and cardiac filling or performance. We investigated the hemodynamic consequences of three RM techniques after inducing acute lung injury., Design: Prospective, randomized, controlled experimental study., Setting: Hospital research laboratory., Subjects: Thirteen anesthetized, mechanically ventilated pigs., Interventions: We induced three types of acute lung injury: oleic acid injury (n = 4); ventilator-induced lung injury (n = 4); and pneumonia (n = 5). All three models were designed to initiate a similar severity of oxygenation impairment. RM methods tested were sustained inflation, incremental positive end-expiratory pressure (PEEP) with a limited peak pressure, and pressure-controlled ventilation with increased PEEP and a fixed driving pressure. From a baseline PEEP of 8 cm H2O, all interventions were tested using post-RM PEEP levels of 8, 12, and 16 cm H2O. Cardiac output by thermodilution and systemic and pulmonary artery pressures were measured frequently during the RM and for 15 mins after its completion., Measurements and Main Results: During the RM, cardiac output decreased to a greater extent in the pneumonia model (0.49 of baseline cardiac output) than in the oleic acid injury (0.67 of baseline) or ventilator-induced lung injury (0.79 of baseline) models. Cardiac output recovered to the baseline value by 5 mins post-RM in oleic acid injury and ventilator-induced lung injury models. However, cardiac output remained decreased 15 mins post-RM in the pneumonia model. There were no differences in hemodynamic parameters among RM methods in oleic acid injury and ventilator-induced lung injury models. In the pneumonia model, however, cardiac output decreased to a greater extent during the RM with sustained inflation (to 0.33 of baseline cardiac output) compared with pressure-controlled ventilation (to 0.68 of baseline)., Conclusions: We conclude that RM transiently but profoundly depressed cardiac output in three models of acute lung injury. The results imply that a lung recruiting maneuver should be used with caution, especially when using sustained inflation in the setting of pneumonia.
- Published
- 2004
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11. Intercomparison of recruitment maneuver efficacy in three models of acute lung injury.
- Author
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Lim SC, Adams AB, Simonson DA, Dries DJ, Broccard AF, Hotchkiss JR, and Marini JJ
- Subjects
- Analysis of Variance, Animals, Disease Models, Animal, Lung Compliance, Lung Volume Measurements, Oleic Acid, Pneumonia, Pneumococcal, Probability, Pulmonary Gas Exchange, Respiration, Artificial, Respiratory Distress Syndrome physiopathology, Respiratory Function Tests, Risk Factors, Sensitivity and Specificity, Swine, Positive-Pressure Respiration methods, Respiratory Distress Syndrome therapy, Respiratory Mechanics physiology
- Abstract
Objective: To compare the relative efficacy of three forms of recruitment maneuvers in diverse models of acute lung injury characterized by differing pathoanatomy., Design: We compared three recruiting maneuver (RM) techniques at three levels of post-RM positive end-expiratory pressure in three distinct porcine models of acute lung injury: oleic acid injury; injury induced purely by the mechanical stress of high-tidal airway pressures; and pneumococcal pneumonia., Setting: Laboratory in a clinical research facility., Subjects: Twenty-eight anesthetized mixed-breed pigs (23.8 +/- 2.6 kg)., Interventions: The RM techniques tested were sustained inflation, extended sigh or incremental positive end-expiratory pressure, and pressure-controlled ventilation., Primary Measurements: Oxygenation and end-expiratory lung volume., Main Results: The post-RM positive end-expiratory pressure level was the major determinant of post-maneuver PaO2, independent of the RM technique. The pressure-controlled ventilation RM caused a lasting increase of PaO2 in the ventilator-induced lung injury model, but in oleic acid injury and pneumococcal pneumonia, there were no sustained oxygenation differences for any RM technique (sustained inflation, incremental positive end-expiratory pressure, or pressure-controlled ventilation) that differed from raising positive end-expiratory pressure without RM., Conclusions: Recruitment by pressure-controlled ventilation is equivalent or superior to sustained inflation, with the same peak pressure in all tested models of acute lung injury, despite its lower mean airway pressure and reduced risk for hemodynamic compromise. Although RM may improve PaO2 in certain injury settings when traditional tidal volumes are used, sustained improvement depends on the post-RM positive end-expiratory pressure value.
- Published
- 2004
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12. Ventilator-induced lung injury.
- Author
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Adams AB, Simonson DA, and Dries DJ
- Subjects
- Animals, Disease Models, Animal, Humans, Lung physiopathology, Lung Injury, Positive-Pressure Respiration adverse effects, Respiratory Distress Syndrome therapy
- Abstract
Ventilator-induced lung injury has been established as a significant risk to patients receiving PPV. Animal studies have provided definitive experimental data that support the existence of VILI. Clinical studies have implied the role of VILI in ARDS and ALI patients. In patients who have ARDS or ALI, however, VILI cannot be distinguished from exacerbation of the primary condition. Animal and clinical studies that clearly show elevated levels of cytokines when PPV is applied beyond certain limits support the concept that an inflammatory process is activated by PPV. Whether the induction of inflammatory mediators contributes to the mortality or morbidity of the ventilated patient has not been established. A potential role for anti-inflammatory therapeutic agents is promising. Therefore, the following considerations can guide the clinical care of ventilator patients: Alveolar pressure exposure (plateau pressure) should be limited to less than 32 cm H2O. Positive end-expiratory pressure should be applied to avoid end-expiratory collapse and reopening. Tidal volume should be set at approximately 6 mL/kg or further guided by plateau pressure limitation. Although studies suggest that reducing Ti, flow, and f may be important in avoiding VILI, there are no current guidelines. The results of preliminary studies investigating the preventative potential of respiratory acidosis, prone positioning, or careful vascular pressure management seem promising. Inflammatory response in VILI has been established, but a role for intervention, such as general or specific suppression of the response, has not been established.
- Published
- 2003
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13. A rationale for lung recruitment in acute respiratory distress syndrome.
- Author
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Dries DJ and Marini AJ
- Subjects
- Humans, Respiratory Distress Syndrome physiopathology, Tidal Volume, Respiration, Artificial adverse effects, Respiratory Distress Syndrome therapy
- Published
- 2003
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14. Pulmonary microvascular fracture in a patient with acute respiratory distress syndrome.
- Author
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Hotchkiss JR, Simonson DA, Marek DJ, Marini JJ, and Dries DJ
- Subjects
- Aged, Capillaries diagnostic imaging, Female, Humans, Microscopy, Electron, Scanning, Pulmonary Alveoli diagnostic imaging, Respiratory Distress Syndrome therapy, Ultrasonography, Pulmonary Alveoli blood supply, Respiration, Artificial adverse effects, Respiratory Distress Syndrome pathology
- Abstract
Objective: To present electron micrographs of lung tissue obtained from a patient exposed to high ventilatory pressures in the context of pulmonary dysfunction and pulmonary hypertension., Design: Case report., Setting: Adult intensive care unit of a university-affiliated teaching hospital., Patients: A patient exposed to high-pressure mechanical ventilation during support for acute respiratory distress syndrome; the acute respiratory distress syndrome in this case was secondary to septic shock., Measurements and Main Results: Scanning electron micrographs of lung tissue, focusing on the internal alveolar surfaces., Findings: Multiple gross disruptions of the alveolar walls, suggestive of stress fractures., Conclusion: High-pressure mechanical ventilation may promote fracturing of the alveolar blood:airspace barrier.
- Published
- 2002
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15. Urine hydrogen peroxide during adult respiratory distress syndrome in patients with and without sepsis.
- Author
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Mathru M, Rooney MW, Dries DJ, Hirsch LJ, Barnes L, and Tobin MJ
- Subjects
- Adolescent, Adult, Aged, Bacterial Infections complications, Female, Humans, Injury Severity Score, Lung Injury, Male, Middle Aged, Prognosis, Respiratory Distress Syndrome complications, Shock, Septic complications, Shock, Septic urine, Survival Rate, Time Factors, Bacterial Infections urine, Hydrogen Peroxide urine, Respiratory Distress Syndrome urine
- Abstract
Background: The lung injury in adult respiratory distress syndrome (ARDS) has been associated with increased expiratory hydrogen peroxide (H2O2) concentrations. Furthermore, patients with sepsis and ARDS are reported to have greater serum scavenging of H2O2 than patients with ARDS only. We hypothesized that the systemic presence of H2O2 would be detectable in the urine of these two groups of patients and that, in the case of ARDS sepsis, the relative contribution of each disease to the production this analyte would be discernible. Accordingly, we used an in vitro radioisotope assay to follow the weekly course of urine H2O2 levels in ARDS patients with and without sepsis, and in samples from control non-ARDS patients with sepsis with indwelling urinary catheters and in samples provided by healthy volunteers., Methods: Thirty patients with ARDS were included in the study: 23 had sepsis and 7 were sepsis free. An indwelling catheter was used to collect urine from each patient over a 24-h period, first within 48 h of ICU admission and then every seventh day over the course of their illness. Urine H2O2 was measured by competitive decarboxylation of 1-14C-alpha-ketoglutaric acid by H2O2. Urine samples were provided by 20 healthy volunteers while, in 10 non-ARDS patients with sepsis, urine was collected over one 24-h period following a 5-day minimum with an indwelling urinary catheter., Results: Urine H2O2 concentration in healthy control subjects (88 +/- 4 mumol/L) and non-ARDS patients with urinary catheters (96 +/- 5 mumol/L) was not significantly different. During the first 48 h in the ICU, urine H2O2 in patients with ARDS only (295 +/- 29 mumol/L) was significantly lower (p < 0.05) than patients with ARDS and sepsis (380 +/- 13 mumol/L); however, the lung injury scores of these two groups did not differ. Furthermore, within the first 48 h, the urine H2O2 of the patients with ARDS and sepsis who did not survive (427 +/- 19 mumol/L; n = 7) was significantly higher than that in patients who survived sepsis (352 +/- 14 mumol/L; n = 15). Thereafter, the lung injury scores and urine H2O2 levels of the nonsurvivor ARDS-sepsis group remained significantly higher compared with the other two groups. At lung injury scores of 3 and 2, regardless of days in ICU, the patients with ARDS only had significantly lower urine H2O2 (266 +/- 30 mumol/L and 167 +/- 24 mumol/L, respectively) compared with the survivor ARDS-sepsis group (376 +/- 19 mumol/L and 250 +/- mumol/L). When the patients with ARDS (both ARDS only and with sepsis) recovered, their urine H2O2 concentration did not differ from the control groups (healthy donors and patients without ARDS)., Conclusion: Lung injury scores did not differentiate patients with ARDS and sepsis from patients with ARDS only during the first 10 days in the ICU; however, urine H2O2 levels were significantly greater in the patients with ARDS and sepsis. Moreover, despite no initial difference in lung injury, patients who did not survive ARDS and sepsis had consistently greater urine H2O2 concentration than patients who survived sepsis. The urine H2O2 level in the ARDS-only group was about 70 percent of the level in the survivor ARDS and sepsis group, suggesting that ARDS alone is the major contributor to the H2O2 oxidant processes during combined ARDS and sepsis. Furthermore, these studies demonstrate that urine H2O2 may be a useful analyte to differentiate the severity of oxidant processes in patients with ARDS and sepsis albeit the prognosis appears to be survival or nonsurvival.
- Published
- 1994
- Full Text
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