Percutaneous Tracheostomy in Respiratory Failure Due to COVID-19.

BACKGROUND: Coronavirus disease 2019 (COVID-19) can lead to hypoxemic respiratory failure resulting in prolonged mechanical ventilation. Typically, tracheostomy is considered in patients who remain ventilator dependent beyond 2 weeks. However, in the setting of this novel respiratory virus, the safety and benefits of tracheostomy are not well-defined. Our aim is to describe our experience with percutaneous tracheostomy in patients with COVID-19. MATERIALS AND METHODS: This is a single center retrospective descriptive study. We reviewed comorbidities and outcomes in patients with respiratory failure due to COVID-19 who underwent percutaneous tracheostomy at our institution from April 2020 to September 2020. In addition, we provide details of our attempt to minimize aerosolization by using a modified protocol with brief periods of planned apnea. RESULTS: A total of 24 patients underwent percutaneous tracheostomy during the study. The average body mass index was 33.0±10.0. At 30 days posttracheostomy 17 (71%) patients still had the tracheostomy tube and 14 (58%) remained ventilator dependent. There were 3 (13%) who died within 30 days. At the time of data analysis in November 2020, 9 (38%) patients had died and 7 (29%) had been decannulated. None of the providers who participated in the procedure experienced signs or symptoms of COVID-19 infection. CONCLUSION: Percutaneous tracheostomy in prolonged respiratory failure due to COVID-19 appears to be safe to perform at the bedside for both the patient and health care providers in the appropriate clinical context. Morbid obesity did not limit the ability to perform percutaneous tracheostomy in COVID-19 patients.

Cell-Type-Specific Immune Dysregulation in Severely Ill COVID-19 Patients.

Recent studies have demonstrated immunologic dysfunction in severely ill coronavirus disease 2019 (COVID-19) patients. We use single-cell RNA sequencing (scRNA-seq) to analyze the transcriptome of peripheral blood mononuclear cells (PBMCs) from healthy (n = 3) and COVID-19 patients with moderate disease (n = 5), acute respiratory distress syndrome (ARDS, n = 6), or recovering from ARDS (n = 6). Our data reveal transcriptomic profiles indicative of defective antigen presentation and interferon (IFN) responsiveness in monocytes from ARDS patients, which contrasts with higher responsiveness to IFN signaling in lymphocytes. Furthermore, genes involved in cytotoxic activity are suppressed in both natural killer (NK) and CD8 T lymphocytes, and B cell activation is deficient, which is consistent with delayed viral clearance in severely ill COVID-19 patients. Our study demonstrates that COVID-19 patients with ARDS have a state of immune imbalance in which dysregulation of both innate and adaptive immune responses may be contributing to a more severe disease course.

Cell type-specific immune dysregulation in severely ill COVID-19 patients.

Coronavirus disease 2019 (COVID-19) has quickly become the most serious pandemic since the 1918 flu pandemic. In extreme situations, patients develop a dysregulated inflammatory lung injury called acute respiratory distress syndrome (ARDS) that causes progressive respiratory failure requiring mechanical ventilatory support. Recent studies have demonstrated immunologic dysfunction in severely ill COVID-19 patients. To further delineate the dysregulated immune response driving more severe clinical course from SARS-CoV-2 infection, we used single-cell RNA sequencing (scRNAseq) to analyze the transcriptome of peripheral blood mononuclear cells (PBMC) from hospitalized COVID-19 patients having mild disease (n = 5), developing ARDS (n = 6), and recovering from ARDS (n = 6). Our data demonstrated an overwhelming inflammatory response with select immunodeficiencies within various immune populations in ARDS patients. Specifically, their monocytes had defects in antigen presentation and deficiencies in interferon responsiveness that contrasted the higher interferon signals in lymphocytes. Furthermore, cytotoxic activity was suppressed in both NK and CD8 lymphocytes whereas B cell activation was deficient, which is consistent with the delayed viral clearance in severely ill COVID-19 patients. Finally, we identified altered signaling pathways in the severe group that suggests immunosenescence and immunometabolic changes could be contributing to the dysfunctional immune response. Our study demonstrates that COVID-19 patients with ARDS have an immunologically distinct response when compared to those with a more innocuous disease course and show a state of immune imbalance in which deficiencies in both the innate and adaptive immune response may be contributing to a more severe disease course in COVID-19.

Rapid Response and Cardiac Arrest Teams: A Descriptive Analysis of 103 American Hospitals.

Despite improvements in the management of in-hospital cardiac arrest over the past decade, in-hospital cardiac arrest continues to be associated with poor prognosis. This has led to the development of rapid response systems, hospital-wide efforts to improve patient outcomes by centering on prompt identification of decompensating patients, expert clinical management, and continuous quality improvement of processes of care. The rapid response system may include cardiac arrest teams, which are centered on identification and treatment of patients with in-hospital cardiac arrest. However, few evidence-based guidelines exist to guide the formation of such teams, and the degree of their variation across the United States has not been well described. DESIGN: Descriptive cross-sectional, internet-based survey. SETTING: Cohort of preidentified clinicians involved in their hospital's adult rapid response system across the United States. SUBJECTS: Clinicians who had been identified by study team members using personal and professional contacts over a 7-month period from June 2018 to December 2018. INTERVENTIONS: An 80-item survey was developed by the investigators. It sought information on the afferent (identification and notification of providers) and efferent (response of providers to patient) limbs of the rapid response system, as well as management of patients post in-hospital cardiac arrest. MEASUREMENTS AND MAIN RESULTS: One-hundred fourteen surveys were distributed. Of these, 109 (96%) were completed. Six were duplicates and were excluded, leaving a total of 103 surveys from 103 hospitals in 30 states. Seventy-six percent of hospitals were academic, 30% were large hospitals (> 750 inpatient beds), and 58% had large ICUs (> 50 ICU beds). We found wide variation in the structure and function in both the afferent and efferent limbs of the rapid response system. The majority of hospitals had a rapid response team and a cardiac arrest team. Most rapid response teams contained a provider, a critical care nurse, and a respiratory therapist. In hospitals with training programs in internal medicine, anesthesia, emergency medicine, or critical care, 45% of rapid response teams and 75% of cardiac arrest teams were led by trainees, with inconsistent attending presence. Targeted temperature management and coronary catheterization were widely used post in-hospital cardiac arrest, but indications varied considerably. CONCLUSIONS: We have demonstrated substantial variation in the structure and function of rapid response systems as well as in management of patients during and after in-hospital cardiac arrest.

Epidemiology, Pathophysiology, and Natural History of Pulmonary Embolism.

Pulmonary embolism (PE) is a common and potentially deadly form of venous thromboembolic disease. It is the third most common cause of cardiovascular death and is associated with multiple inherited and acquired risk factors as well as advanced age. The prognosis from PE depends on the degree of obstruction and hemodynamic effects of PE and understanding the pathophysiology helps in risk-stratifying patients and determining treatment. Though the natural history of thrombus is resolution, a subset of patients have chronic residual thrombus, contributing to the post-PE syndrome.

Multidisciplinary approach to the management of pulmonary embolism patients: the pulmonary embolism response team (PERT).

Pulmonary embolism (PE) is a potentially fatal disease with a broad range of treatment options that spans multiple specialties. The rapid evolution and expansion of novel therapies to treat PE make it a disease process that is well suited to a multidisciplinary approach. In order to facilitate a rapid, robust response to the diagnosis of PE, some hospitals have established multidisciplinary pulmonary embolism response teams (PERTs). The PERT model is based on existing multidisciplinary teams such as heart teams and rapid response teams. A PERT is composed of clinicians from the range of specialties involved in the treatment of PE, including pulmonology critical care, interventional radiology, cardiology, and cardiothoracic surgery among others. A PERT is a 24/7 consult service that is able to provide expert advice on the initial management of PE patients and convene in real time to develop a consensus treatment plan specifically tailored to the needs of a particular patient and consistent with the capabilities of the institution. In this review, we discuss the rationale for establishing a PERT and its potential benefits. We discuss considerations in forming a PERT and present case studies of several PERTs currently in operation at different institutions. We also discuss potential difficulties in forming a PERT and review evidence that has been generated by some of the PERTs that have been in operation the longest.

A pulmonary embolism response team's initial 20 month experience treating 87 patients with submassive and massive pulmonary embolism.

Pulmonary Embolism Response Teams (PERTs) have emerged to provide rapid multidisciplinary assessment and treatment of PE patients. However, descriptive institutional experience and preliminary outcomes data from such teams are sparse. PERT activations were identified through a retrospective review. Only confirmed submassive or massive PEs were included in the data analysis. In addition to baseline variables, the therapeutic intervention, length of stay (LOS), in-hospital mortality, and bleeding rate/severity were recorded. A total of 124 PERT activations occurred over 20 months: 43 in the first 10 months and 81 in the next 10. A total of 87 submassive (90.8%) and massive (9.2%) PE patients were included. The median age was 65 (51-75 IQR) years. Catheter-directed thrombolysis (CDT) was administered to 25 patients, systemic thrombolysis (ST) to six, and anticoagulation alone (AC) to 54. The median ICU stay and overall LOS were 6 (3-10 IQR) and 7 (4-14 IQR) days, respectively, with no association with any variables except a brain natriuretic peptide (BNP) >100 pg/mL ( p=0.008 ICU LOS; p=0.047 overall LOS). Twelve patients (13.7%) died in the hospital, nine of whom had metastatic or brain cancer, with a median overall LOS of 13 (11-17 IQR) days. There were five major bleeds: one in the CDT group, one in the ST group, and three in the AC group. Overall, (1) PERT activations increased after the first 10 months; (2) BNP >100 pg/mL was associated with a longer LOS; (3) rates of mortality and bleeding did not correlate with treatment; and (4) the majority of in-hospital deaths occurred in patients with advanced cancer.

Successful catheter-directed thrombolysis of a massive pulmonary embolism in a patient after recent pneumonectomy.

Massive pulmonary embolism (PE) after major thoracic surgery is an uncommon but life-threatening event that is challenging to manage. At present, the treatment of acute PE is either anticoagulation with or without systemic thrombolytic therapy. We report a case of a 65-year-old female with recent left pneumonectomy who developed a massive PE. The patient was successfully and safely treated with catheter-directed thrombolysis. To our knowledge, this is the first patient treated in this fashion.

Prolonged hypothermia for neurological protection.

Treatment with mild hypothermia induced after cardiopulmonary resuscitation has become a standard of care, but optimal timing and duration of hypothermia remains unclear. We present a 66-year-old man admitted after an out-of-hospital cardiac arrest. Because of his severe hypoxemia, cardiopulmonary instability, and respiratory acidosis after resuscitation, he was continued on therapeutic hypothermia until his hypoxia resolved. As a result, the patient was kept at the goal hypothermic temperature of 33°C for a total of 48 hours, compared with the usual 24-hour standard, with excellent sustained neurological recovery. This case documents the usefulness of extending hypothermia when applied to severely unstable patients and suggests that a sliding-target approach may be applied on a patient-by-patient basis.