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      Risk factors for prolonged intensive care unit stays in patients after cardiac surgery with cardiopulmonary bypass: A retrospective observational study

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          Abstract

          Objectives

          Patients after cardiac surgery with cardiopulmonary bypass (CPB) require a stay in the ICU postoperatively. This study aimed to investigate the incidence of prolonged length of stay (LOS) in the ICU after cardiac surgery with CPB and identify associated risk factors.

          Methods

          The current investigation was an observational, retrospective study that included 395 ICU patients who underwent cardiac surgery with CPB at a tertiary hospital in Guangzhou from June 2015 to June 2017. Data were obtained from the hospital database. Binary logistic regression modeling was used to analyze risk factors for prolonged ICU LOS.

          Results

          Of 395 patients, 137 (34.7%) had a prolonged ICU LOS (>72.0 h), and the median ICU LOS was 50.9 h. Several variables were found associated with prolonged ICU LOS: duration of CPB, prolonged mechanical ventilation and non-invasive assisted ventilation use, PaO 2/FiO 2 ratios within 6 h after surgery, type of surgery, red blood cell infusion during surgery, postoperative atrial arrhythmia, postoperative ventricular arrhythmia (all P < 0.05).

          Conclusions

          These findings are clinically relevant for identifying patients with an estimated prolonged ICU LOS, enabling clinicians to facilitate earlier intervention to reduce the risk and prevent resulting delayed recovery.

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          Clinical review: intensive care unit acquired weakness

          Greet Hermans, Greet Van den Berghe (2015)
          A substantial number of patients admitted to the ICU because of an acute illness, complicated surgery, severe trauma, or burn injury will develop a de novo form of muscle weakness during the ICU stay that is referred to as “intensive care unit acquired weakness” (ICUAW). This ICUAW evoked by critical illness can be due to axonal neuropathy, primary myopathy, or both. Underlying pathophysiological mechanisms comprise microvascular, electrical, metabolic, and bioenergetic alterations, interacting in a complex way and culminating in loss of muscle strength and/or muscle atrophy. ICUAW is typically symmetrical and affects predominantly proximal limb muscles and respiratory muscles, whereas facial and ocular muscles are often spared. The main risk factors for ICUAW include high severity of illness upon admission, sepsis, multiple organ failure, prolonged immobilization, and hyperglycemia, and also older patients have a higher risk. The role of corticosteroids and neuromuscular blocking agents remains unclear. ICUAW is diagnosed in awake and cooperative patients by bedside manual testing of muscle strength and the severity is scored by the Medical Research Council sum score. In cases of atypical clinical presentation or evolution, additional electrophysiological testing may be required for differential diagnosis. The cornerstones of prevention are aggressive treatment of sepsis, early mobilization, preventing hyperglycemia with insulin, and avoiding the use parenteral nutrition during the first week of critical illness. Weak patients clearly have worse acute outcomes and consume more healthcare resources. Recovery usually occurs within weeks or months, although it may be incomplete with weakness persisting up to 2 years after ICU discharge. Prognosis appears compromised when the cause of ICUAW involves critical illness polyneuropathy, whereas isolated critical illness myopathy may have a better prognosis. In addition, ICUAW has shown to contribute to the risk of 1-year mortality. Future research should focus on new preventive and/or therapeutic strategies for this detrimental complication of critical illness and on clarifying how ICUAW contributes to poor longer-term prognosis.
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            Ventilator-induced diaphragm dysfunction: cause and effect.

            Michael P. Wiggs, Kurt J. Sollanek, Ashley J. Smuder … (2013)
            Mechanical ventilation (MV) is used clinically to maintain gas exchange in patients that require assistance in maintaining adequate alveolar ventilation. Common indications for MV include respiratory failure, heart failure, drug overdose, and surgery. Although MV can be a life-saving intervention for patients suffering from respiratory failure, prolonged MV can promote diaphragmatic atrophy and contractile dysfunction, which is referred to as ventilator-induced diaphragm dysfunction (VIDD). This is significant because VIDD is thought to contribute to problems in weaning patients from the ventilator. Extended time on the ventilator increases health care costs and greatly increases patient morbidity and mortality. Research reveals that only 18-24 h of MV is sufficient to develop VIDD in both laboratory animals and humans. Studies using animal models reveal that MV-induced diaphragmatic atrophy occurs due to increased diaphragmatic protein breakdown and decreased protein synthesis. Recent investigations have identified calpain, caspase-3, autophagy, and the ubiquitin-proteasome system as key proteases that participate in MV-induced diaphragmatic proteolysis. The challenge for the future is to define the MV-induced signaling pathways that promote the loss of diaphragm protein and depress diaphragm contractility. Indeed, forthcoming studies that delineate the signaling mechanisms responsible for VIDD will provide the knowledge necessary for the development of a pharmacological approach that can prevent VIDD and reduce the incidence of weaning problems.
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              Clinical review: Ventilator-induced diaphragmatic dysfunction - human studies confirm animal model findings!

              Samir Jaber, Boris Jung, Stefan Matecki … (2011)
              Diaphragmatic function is a major determinant of the ability to successfully wean patients from mechanical ventilation. However, the use of controlled mechanical ventilation in animal models results in a major reduction of diaphragmatic force-generating capacity together with structural injury and atrophy of diaphragm muscle fibers, a condition termed ventilator-induced diaphragmatic dysfunction (VIDD). Increased oxidative stress and exaggerated proteolysis in the diaphragm have been linked to the development of VIDD in animal models, but much less is known about the extent to which these phenomena occur in humans undergoing mechanical ventilation in the ICU. In the present review, we first briefly summarize the large body of evidence demonstrating the existence of VIDD in animal models, and outline the major cellular mechanisms that have been implicated in this process. We then relate these findings to very recently published data in critically ill patients, which have thus far been found to exhibit a remarkable degree of similarity with the animal model data. Hence, the human studies to date have indicated that mechanical ventilation is associated with increased oxidative stress, atrophy, and injury of diaphragmatic muscle fibers along with a rapid loss of diaphragmatic force production. These changes are, to a large extent, directly proportional to the duration of mechanical ventilation. In the context of these human data, we also review the methods that can be used in the clinical setting to diagnose and/or monitor the development of VIDD in critically ill patients. Finally, we discuss the potential for using different mechanical ventilation strategies and pharmacological approaches to prevent and/or to treat VIDD and suggest promising avenues for future research in this area.
              Article 0 comments Cited 61 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Xueying Zhang
                Wenxia Zhang
                Hongyu Lou
                Chuqing Luo
                Qianqian Du
                Ya Meng
                Xiaoyu Wu
                Meifen Zhang
                Journal
                Journal ID (nlm-ta): Int J Nurs Sci
                Journal ID (iso-abbrev): Int J Nurs Sci
                Title: International Journal of Nursing Sciences
                Publisher: Chinese Nursing Association
                ISSN (Print): 2096-6296
                ISSN (Electronic): 2352-0132
                Publication date PMC-release: 07 September 2021
                Publication date Collection: 10 October 2021
                Publication date (Electronic): 07 September 2021
                Volume: 8
                Issue: 4
                Pages: 388-393
                Affiliations
                [a ]School of Nursing, Sun Yat-Sen University, Guangzhou, China
                [b ]Sun Yat-Sen University Cancer Center, Guangzhou, China
                [c ]Digestive Disease Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China
                Author notes
                [∗ ]Corresponding author. zhmfen@ 123456mail.sysu.edu.cn
                [1]

                Both authors contributed equally to this work.

                Article
                Publisher Item ID: S2352-0132(21)00091-0
                DOI: 10.1016/j.ijnss.2021.09.002
                PMC ID: 8488808
                PubMed ID: 34631988
                SO-VID: f0f3ca99-a22c-418a-93df-5af2dab95501
                Copyright © © 2021 The authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 13 May 2021
                Date revision received : 28 August 2021
                Date accepted : 2 September 2021
                Categories
                Subject: Original Article

                Keywords: cardiac surgery,cardiopulmonary bypass,intensive care units,length of stay,risk factors
                Data availability:
                Keywords: cardiac surgery, cardiopulmonary bypass, intensive care units, length of stay, risk factors

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