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      Effects of theophylline therapy on respiratory muscle strength in patients with prolonged mechanical ventilation : A retrospective cohort study

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          Abstract

          Mechanical ventilation may cause diaphragm weakness an effect termed ventilator-induced diaphragm dysfunction (VIDD). The prevalence of VIDD among patients receiving mechanical ventilation is very high, with the degree of diaphragmatic atrophy being associated with the length of mechanical ventilation. Theophylline is known to increase diaphragmatic contractility and reduce fatigue, so in this study, we evaluated the effect of theophylline in patients with prolonged mechanical ventilation.

          Patients who depended on mechanical ventilation were included in the study. We compared the maximum inspiratory pressure (PImax) values, rapid shallow breathing index (RSBI) values, and successful weaning rates of theophylline-treated and non-theophylline-treated patients.

          Eighty-four patients received theophylline and 76 patients did not. These 2 groups’ clinical characteristics, including their PImax and RSBI at initial admission, were similar. The results showed that the theophylline-treated group had significantly better PImax and RSBI, with a higher last PImax (30.1 ± 9.7 cmH 2O vs 26.9 ± 9.1 cmH 2O; P = .034) and lower last RSBI (107.0 ± 68.4 vs 131.4 ± 77.7; P = .036). The improvements to each respective patient's PImax and RSBI were also significantly higher in the theophylline-treated group (PImax: 20.1 ± 5.7% vs 3.2 ± 1.1%, P = .005; RSBI: 11.2 ± 3.0% vs 2.7 ± 1.6%, P = .015). The weaning success rate of the theophylline-treated group was also higher, but not significantly so.

          Theophylline might improve respiratory muscle strength in patients with prolonged mechanical ventilation and it needs further prospective studies to confirm.

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          Most cited references28

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          Rapidly progressive diaphragmatic weakness and injury during mechanical ventilation in humans.

          Diaphragmatic function is a major determinant of the ability to successfully wean patients from mechanical ventilation (MV). Paradoxically, MV itself results in a rapid loss of diaphragmatic strength in animals. However, very little is known about the time course or mechanistic basis for such a phenomenon in humans. To determine in a prospective fashion the time course for development of diaphragmatic weakness during MV; and the relationship between MV duration and diaphragmatic injury or atrophy, and the status of candidate cellular pathways implicated in these phenomena. Airway occlusion pressure (TwPtr) generated by the diaphragm during phrenic nerve stimulation was measured in short-term (0.5 h; n = 6) and long-term (>5 d; n = 6) MV groups. Diaphragmatic biopsies obtained during thoracic surgery (MV for 2-3 h; n = 10) and from brain-dead organ donors (MV for 24-249 h; n = 15) were analyzed for ultrastructural injury, atrophy, and expression of proteolysis-related proteins (ubiquitin, nuclear factor-κB, and calpains). TwPtr decreased progressively during MV, with a mean reduction of 32 ± 6% after 6 days. Longer periods of MV were associated with significantly greater ultrastructural fiber injury (26.2 ± 4.8 vs. 4.7 ± 0.6% area), decreased cross-sectional area of muscle fibers (1,904 ± 220 vs. 3,100 ± 329 μm²), an increase of ubiquitinated proteins (+19%), higher expression of p65 nuclear factor-κB (+77%), and greater levels of the calcium-activated proteases calpain-1, -2, and -3 (+104%, +432%, and +266%, respectively) in the diaphragm. Diaphragmatic weakness, injury, and atrophy occur rapidly in critically ill patients during MV, and are significantly correlated with the duration of ventilator support.
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            Ventilator-induced diaphragmatic dysfunction.

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              Diaphragm dysfunction on admission to the intensive care unit. Prevalence, risk factors, and prognostic impact-a prospective study.

              Diaphragmatic insults occurring during intensive care unit (ICU) stays have become the focus of intense research. However, diaphragmatic abnormalities at the initial phase of critical illness remain poorly documented in humans. To determine the incidence, risk factors, and prognostic impact of diaphragmatic impairment on ICU admission. Prospective, 6-month, observational cohort study in two ICUs. Mechanically ventilated patients were studied within 24 hours after intubation (Day 1) and 48 hours later (Day 3). Seventeen anesthetized intubated control anesthesia patients were also studied. The diaphragm was assessed by twitch tracheal pressure in response to bilateral anterior magnetic phrenic nerve stimulation (Ptr,stim). Eighty-five consecutive patients aged 62 (54-75) (median [interquartile range]) were evaluated (medical admission, 79%; Simplified Acute Physiology Score II, 54 [44-68]). On Day 1, Ptr,stim was 8.2 (5.9-12.3) cm H2O and 64% of patients had Ptr,stim less than 11 cm H2O. Independent predictors of low Ptr,stim were sepsis (linear regression coefficient, -3.74; standard error, 1.16; P = 0.002) and Simplified Acute Physiology Score II (linear regression coefficient, -0.07; standard error, 1.69; P = 0.03). Compared with nonsurvivors, ICU survivors had higher Ptr,stim (9.7 [6.3-13.8] vs. 7.3 [5.5-9.7] cm H2O; P = 0.004). This was also true for hospital survivors versus nonsurvivors (9.7 [6.3-13.5] vs. 7.8 [5.5-10.1] cm H2O; P = 0.004). Day 1 and Day 3 Ptr,stim were similar. A reduced capacity of the diaphragm to produce inspiratory pressure (diaphragm dysfunction) is frequent on ICU admission. It is associated with sepsis and disease severity, suggesting that it may represent another form of organ failure. It is associated with a poor prognosis. Clinical trial registered with www.clinicaltrials.gov (NCT 00786526).
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                Author and article information

                Journal
                Medicine (Baltimore)
                Medicine (Baltimore)
                MEDI
                Medicine
                Wolters Kluwer Health
                0025-7974
                1536-5964
                January 2019
                11 January 2019
                : 98
                : 2
                : e13982
                Affiliations
                [a ]Department of Pulmonary and Critical Care Medicine, Chang-Gung Memorial Hospital, Keelung
                [b ]Department of Thoracic Medicine, Chang-Gung Memorial Hospital
                [c ]Department of Respiratory Therapy, Chang-Gung University, Taoyuan, Taiwan.
                Author notes
                []Correspondence: Kuo-Chin Kao, Department of Thoracic Medicine, Chang-Gung Memorial Hospital, No. 5, Fuxing St., Guishan Dist., Taoyuan 33305, Taiwan (e-mail: kck0502@ 123456cgmh.org.tw ).
                Article
                MD-D-18-05712 13982
                10.1097/MD.0000000000013982
                6336648
                30633180
                8d198fdb-addb-4f8a-82d0-fc69111242d8
                Copyright © 2019 the Author(s). Published by Wolters Kluwer Health, Inc.

                This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0

                History
                : 13 August 2018
                : 6 December 2018
                : 10 December 2018
                Categories
                3900
                Research Article
                Observational Study
                Custom metadata
                TRUE

                prolonged mechanical ventilation,respiratory muscle,theophylline,vidd

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