Background

Mechanical ventilation (MV) via tracheostomy is performed commonly for patients who are in long-term acute care hospitals (LTACHs) after respiratory failure. However, the outcome of MV in COVID-19-associated respiratory failure in LTACHs is not known.

Research question

What is the ventilator liberation rate of patients who have received tracheostomy with COVID-19-associated respiratory failure compared with those with respiratory failure unrelated to COVID-19 in LTACHs?

Study design and methods

In this retrospective cohort study, we examined mechanically ventilated patients discharged between June 2020 and March 2021. Of 242 discharges, 165 patients who had undergone tracheostomy arrived and were considered for ventilator liberation. One hundred twenty-eight patients did not have COVID-19 and 37 patients were admitted for COVID-19.

Results

The primary outcome of the study was ventilator liberation; secondary outcomes were functional recovery, length of stay (LOS) at the LTACH, and discharge disposition. After controlling for demographics, the number of comorbidities, hemodialysis, vasopressor need, thrombocytopenia, and the LOS at the short-term acute care hospital, our results indicated that patients with COVID-19 showed a higher adjusted ventilator liberation rate of 91.4% vs 56.0% in those without COVID-19. Functional ability was assessed with the change of Functional Status Score for the Intensive Care Unit (FSS-ICU) between admission and discharge. The adjusted mean change in FSS-ICU was significantly higher in the COVID-19 group than in the non-COVID-19 group: 9.49 (95% CI, 7.38-11.6) vs 2.08 (95% CI, 1.05-3.11), respectively (P < .001). Patients with COVID-19 experienced a shorter adjusted LOS at the LTACH with an adjusted hazard ratio of 1.57 (95% CI, 1.0-2.46; P = .05) compared with patients without COVID-19. We did not observe significant differences between the two groups regarding discharge location, but a trend toward need for lower level of care was found in patients with COVID-19.

Interpretation

Our study suggests that patients with COVID-19 requiring MV and tracheostomy have a higher chance for recovery than those without COVID-19.

Background: Survivors of COVID-19 pneumonia often suffer from chronic critical illness (CCI) and require long-term hospitalization. Long-term acute care (LTAC) hospitals are vital in the care of CCI patients, but their role for patients post COVID-19 infection is not known. Barlow Respiratory Hospital (BRH) is a 105-bed, LTAC hospital network serving ventilator-dependent and medically-complex patients transferred from the ICUs of hospitals in southern California. We report patient characteristics of our first series of COVID-19 survivors admitted to the post-acute venue of an LTAC hospital. Methods: Single-center observational descriptive report of patients recovering from acute infectious complications of COVID-19 pneumonia requiring long-term respiratory support. Results: From 28 April to 7 September 2020, 41 patients were admitted to BRH for continued recovery from COVID-19 pneumonia. Median age: 68 [44-94] years, 25/41 (61%) male, 33/41 (80.5%) with tracheostomy, 21/41 (51.2%) on invasive mechanical ventilation, 9/41 (22%) receiving hemodialysis. All mechanical ventilation and hemodialysis interventions were initiated at the transferring hospital. Conclusions: To our knowledge, this is the first report to characterize CCI and medically complex COVID-19 patients transferred to the post-acute venue of an LTAC hospital. Patients on average spent over six weeks in the transferring hospital mostly in the ICU, are largely elderly, carry the known risk factors for COVID-19 infection, and experienced respiratory failure necessitating prolonged mechanical ventilation via tracheostomy. Our findings suggest that these patients will continue to require considerable medical interventions and treatments, including weaning from mechanical ventilation, owing to the numerous sequelae of the infection and the burden of acute-on-chronic diseases. As ICU survival rates improve, this research further emphasizes the important role of the LTAC hospital in responding to the COVID-19 crisis.

Patients requiring mechanical ventilation (MV) beyond 21 days, usually referred to as prolonged MV, represent a unique group with significant medical needs and a generally poor prognosis. Research suggests that approximately 10% of all MV patients will need prolonged ventilatory care, and that number will continue to rise. Although we have extensive knowledge of MV in the acute care setting, less is known about care in the post-ICU setting. More than 50% of patients who were deemed unweanable in the ICU will be liberated from MV in the post-acute setting. Prolonged MV also presents a challenge in care for medically complex, elderly, socioeconomically disadvantaged and marginalized individuals, usually at the end of their life. Patients and their families often rely on ventilator weaning facilities and skilled nursing homes for the continuation of care, but home ventilation is becoming more common. The focus of this review is to discuss recent advances in the weaning strategies in prolonged MV, present their outcomes and provide insight into the complexity of care.

Background Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury commonly associated with pneumonia, including coronavirus disease-19 (COVID-19). The resultant effect can be persistent lung damage, but its extent is not known. We used quantitative high resolution computed tomography (QHR-CT) lung scans to radiographically characterize the lung damage in COVID-19 ARDS (CARDS) survivors. Methods Patients with CARDS (N=20) underwent QHR-CT lung scans 60 to 90 days after initial diagnosis, while hospitalized at a long-term acute care hospital (LTACH). QHR-CT assessed for mixed disease (QMD), ground glass opacities (QGGO), consolidation (QCON) and normal lung tissue (QNL). QMD was correlated with respiratory support on admission, tracheostomy decannulation and supplementary oxygen need on discharge. Results Sixteen patients arrived with tracheostomy requiring invasive mechanical ventilation. Four patients arrived on nasal oxygen support. Of the patients included in this study 10 had the tracheostomy cannula removed, four remained on invasive ventilation, and two died. QHR-CT showed 45% QMD, 28.1% QGGO, 3.0% QCON and QNL=23.9%. Patients with mandatory mechanical ventilation had the highest proportion of QMD when compared to no mechanical ventilation. There was no correlation between QMD and tracheostomy decannulation or need for supplementary oxygen at discharge. Conclusions Our data shows severe ongoing lung injury in patients with CARDS, beyond what is usually expected in ARDS. In this severely ill population, the extent of mixed disease correlates with mechanical ventilation, signaling formation of interstitial lung disease. QHR-CT analysis can be useful in the post-acute setting to evaluate for interstitial changes in ARDS.

Circadian rhythms are a hallmark of physiology, but how such daily rhythms organize cellular catabolism is poorly understood. Here, we used proteomics to map daily oscillations in autophagic flux in mouse liver and related these rhythms to proteasome activity. We also explored how systemic inflammation affects the temporal structure of autophagy. Our data identified a globally harmonized rhythm for basal macroautophagy, chaperone-mediated autophagy, and proteasomal activity, which concentrates liver proteolysis during the daytime. Basal autophagy rhythms could be resolved into two antiphase clusters that were distinguished by the subcellular location of targeted proteins. Inflammation induced by lipopolysaccharide reprogrammed autophagic flux away from a temporal pattern that favors cytosolic targets and toward the turnover of mitochondrial targets. Our data detail how daily biological rhythms connect the temporal, spatial, and metabolic aspects of protein catabolism.

Introduction

Transbronchial lung cryobiopsy (TBLC) has emerged as a promising alternative to surgical lung biopsy for the diagnosis of interstitial lung disease. However, uncertainty remains regarding its overall complications due to a lack of procedural standardization including the size of cryoprobe utilized.

Methods

This is a prospective cohort study of a protocolized transbronchial cryobiopsy program utilizing a 2.4 mm cryoprobe. 201 consecutive subjects were enrolled at a single academic center.

Results

The average biopsy size was 106.2 ± 39.3 mm². Complications included a total pneumothorax rate of 4.9% with 3.5% undergoing chest tube placement. Severe bleeding defined by the Nashville Working Group occurred in 0.5% of cases. There were no deaths at 30-days.

Discussion

A protocolized transbronchial cryobiopsy program utilizing a 2.4 mm cryoprobe in can achieve a high diagnostic yield with a favorable safety profile.

Background

Acute respiratory distress syndrome (ARDS) is a severe form of lung injury characterized by damage to the epithelial barrier with subsequent pulmonary edema and hypoxic respiratory failure. ARDS is a significant medical problem in intensive care units with associated high care costs. There are many potential causes of ARDS; however, alveolar injury associated with mechanical ventilation, termed ventilator-induced lung injury (VILI), remains a well-recognized contributor. It is thus critical to understand the mechanism of VILI. Based on our published preliminary data, we hypothesized that the endoplasmic reticulum (ER) stress response molecule Protein Kinase R-like Endoplasmic Reticulum Kinase (PERK) plays a role in transmitting mechanosensory signals the alveolar epithelium.

Methods

ER stress signal responses to mechanical stretch were studied in ex-vivo ventilated pig lungs. To explore the effect of PERK inhibition on VILI, we ventilated live rats and compared lung injury parameters to non-ventilated controls. The effect of stretch-induced epithelial ER Ca²⁺ signaling on PERK was studied in stretched alveolar epithelial monolayers. To confirm the activation of PERK in human disease, ER stress signaling was compared between ARDS and non-ARDS lungs.

Results

Our studies revealed increased PERK-specific ER stress signaling in response to overstretch. PERK inhibition resulted in dose-dependent improvement of alveolar inflammation and permeability. Our data indicate that stretch-induced epithelial ER Ca²⁺ release is an activator of PERK. Experiments with human lung tissue confirmed PERK activation by ARDS.

Conclusion

Our study provides evidences that PERK is a mediator stretch signals in the alveolar epithelium.