Project description:PurposeTo determine whether Macklin effect (a linear collection of air contiguous to the bronchovascular sheath) on baseline CT imaging is an accurate predictor for subsequent pneumomediastinum (PMD)/pneumothorax (PNX) development in invasively ventilated patients with COVID-19-related acute respiratory distress syndrome (ARDS).Materials and methodsThis is an observational, case-control study. From a prospectively acquired database, all consecutive invasively ventilated COVID-19 ARDS patients who underwent at least one baseline chest CT scan during the study time period (February 25th, 2020-December 31st, 2020) were identified; those who had tracheal lesion or already had PMD/PNX at the time of the first available chest imaging were excluded.Results37/173 (21.4%) patients enrolled had PMD/PNX; specifically, 20 (11.5%) had PMD, 10 (5.8%) PNX, 7 (4%) both. 33/37 patients with subsequent PMD/PNX had Macklin effect on baseline CT (89.2%, true positives) 8.5 days [range, 1-18] before the first actual radiological evidence of PMD/PNX. Conversely, 6/136 patients without PMD/PNX (4.4%, false positives) demonstrated Macklin effect (p < 0.001). Macklin effect yielded a sensitivity of 89.2% (95% confidence interval [CI]: 74.6-96.9), a specificity of 95.6% (95% CI: 90.6-98.4), a positive predictive value (PV) of 84.5% (95% CI: 71.3-92.3), a negative PV of 97.1% (95% CI: 74.6-96.9) and an accuracy of 94.2% (95% CI: 89.6-97.2) in predicting PMD/PNX (AUC:0.924).ConclusionsMacklin effect accurately predicts, 8.5 days in advance, PMD/PNX development in COVID-19 ARDS patients.
Project description:PurposeEspecially in elderly and multimorbid patients, Coronavirus Disease 2019 (COVID-19) may result in severe pneumonia and secondary complications. Recent studies showed pneumothorax in rare cases, but tension pneumothorax has only been reported once.Case presentationA 47-year-old male was admitted to the emergency department with fever, dry cough and sore throat for the last 14 days as well as acute stenocardia and shortage of breath. Sputum testing (polymerase chain reaction, PCR) confirmed SARS-CoV-2 infection. Initial computed tomography (CT) showed bipulmonary groundglass opacities and consolidations with peripheral distribution. Hospitalization with supportive therapy (azithromycin) as well as non-invasive oxygenation led to a stabilization of the patient. After 5 days, sputum testing was negative and IgA/IgG antibody titres were positive for SARS-CoV-2. The patient was discharged after 7 days. On the 11th day, the patient realized pronounced dyspnoea after coughing and presented to the emergency department again. CT showed a right-sided tension pneumothorax, which was relieved by a chest drain (Buelau) via mini open thoracotomy. Negative pressure therapy resulted in regression of the pneumothorax and the patient was discharged after 9 days of treatment.ConclusionTreating physicians should be aware that COVID-19 patients might develop severe secondary pulmonary complications such as acute tension pneumothorax.Level of evidenceV.
Project description:Purpose of reviewSpontaneous pneumothorax (SP) is a common manifestation of patients with diffuse cystic lung diseases (DCLDs) such as lymphangieoleiomyomatosis (LAM), pulmonary Langerhans cell histiocytosis (PLCH) and Birt-Hogg-Dubé syndrome (BHD). Air travel may pose an additional risk for the development of SP. Here, we summarize the literature pertaining to air travel related SP in DCLDs in order to assist patients and clinicians in appropriate decision-making with regards to air travel.Recent findingsSeveral recent studies have estimated that the per-flight risk of SP in patients with DCLDs is approximately 1%, with disease-specific risk estimates of 1.1-2.6% in LAM, 0-0.63% in BHD, and 0.37% in PLCH.SummaryIn general, it should be safe for most patients with DCLDs to undertake air travel. Patients should be counseled to seek medical attention and not board the airplane in the presence of sudden/new onset chest pain and/or dyspnea prior to boarding the plane.
Project description:SARS-CoV-2 is a novel coronavirus that causes acute respiratory distress syndrome (ARDS), death and long-term sequelae. Innate immune cells are critical for host defense but are also the primary drivers of ARDS. The relationships between innate cellular responses in ARDS resulting from COVID-19 compared to other causes of ARDS, such as bacterial sepsis is unclear. Moreover, the beneficial effects of dexamethasone therapy during severe COVID-19 remain speculative, but understanding the mechanistic effects could improve evidence-based therapeutic interventions. To interrogate these relationships, we developed an scRNAseq atlas that is freely accessible (biernaskielab.ca/COVID_neutrophil). We discovered that compared to bacterial ARDS, COVID-19 was associated with distinct neutrophil polarization characterized by either interferon (IFN) or prostaglandin (PG) active states. Neutrophils from bacterial ARDS had higher expression of antibacterial molecules such as PLAC8 and CD83. Dexamethasone therapy in COVID patients rapidly altered the IFNactive state, downregulated interferon responsive genes, and activated IL1R2+ve neutrophils. Dexamethasone also induced the emergence of immature neutrophils expressing immunosuppressive molecules ARG1 and ANXA1, which were not present in healthy controls. Moreover, dexamethasone remodeled global cellular interactions by changing neutrophils from information receivers into information providers. Importantly, male patients had higher proportions of IFNactive neutrophils and a greater degree of steroid-induced immature neutrophil expansion. Indeed, the highest proportion of IFNactive neutrophils was associated with mortality. These results define neutrophil states unique to COVID-19 when contextualized to other life-threatening infections, thereby enhancing the relevance of our findings at the bedside. Furthermore, the molecular benefits of dexamethasone therapy are also defined. The identified molecular pathways can now be targeted to develop improved therapeutics.
Project description:Severe respiratory sequelae drive morbidity-associated with coronavirus 2019 (COVID-19) disease. We report a case of COVID-19 pneumonia complicated by cavitary lesions and pneumothorax in a young healthy male. Pneumothorax management with catheter thoracostomy and rapid resolution of the cavitary lesions are described. An extensive work-up for other causes a cavitation was negative and the temporal correlation of the cavities with COVID-19 infection plus their rapid resolution suggest a direct relationship. We propose a mechanism for cavitation secondary to microangiopathy, a cause of cavitation in the vasculitides and a known feature of COVID-19.
Project description:BackgroundIn acute respiratory distress syndrome (ARDS), extravascular lung water index (EVLWi) and pulmonary vascular permeability index (PVPI) measured by transpulmonary thermodilution reflect the degree of lung injury. Whether EVLWi and PVPI are different between non-COVID-19 ARDS and the ARDS due to COVID-19 has never been reported. We aimed at comparing EVLWi, PVPI, respiratory mechanics and hemodynamics in patients with COVID-19 ARDS vs. ARDS of other origin.MethodsBetween March and October 2020, in an observational study conducted in intensive care units from three university hospitals, 60 patients with COVID-19-related ARDS monitored by transpulmonary thermodilution were compared to the 60 consecutive non-COVID-19 ARDS admitted immediately before the COVID-19 outbreak between December 2018 and February 2020.ResultsDriving pressure was similar between patients with COVID-19 and non-COVID-19 ARDS, at baseline as well as during the study period. Compared to patients without COVID-19, those with COVID-19 exhibited higher EVLWi, both at the baseline (17 (14-21) vs. 15 (11-19) mL/kg, respectively, p = 0.03) and at the time of its maximal value (24 (18-27) vs. 21 (15-24) mL/kg, respectively, p = 0.01). Similar results were observed for PVPI. In COVID-19 patients, the worst ratio between arterial oxygen partial pressure over oxygen inspired fraction was lower (81 (70-109) vs. 100 (80-124) mmHg, respectively, p = 0.02) and prone positioning and extracorporeal membrane oxygenation (ECMO) were more frequently used than in patients without COVID-19. COVID-19 patients had lower maximal lactate level and maximal norepinephrine dose than patients without COVID-19. Day-60 mortality was similar between groups (57% vs. 65%, respectively, p = 0.45). The maximal value of EVLWi and PVPI remained independently associated with outcome in the whole cohort.ConclusionCompared to ARDS patients without COVID-19, patients with COVID-19 had similar lung mechanics, but higher EVLWi and PVPI values from the beginning of the disease. This was associated with worse oxygenation and with more requirement of prone positioning and ECMO. This is compatible with the specific lung inflammation and severe diffuse alveolar damage related to COVID-19. By contrast, patients with COVID-19 had fewer hemodynamic derangement. Eventually, mortality was similar between groups.Trial registration number and date of registrationClinicalTrials.gov (NCT04337983). Registered 30 March 2020-Retrospectively registered, https://clinicaltrials.gov/ct2/show/NCT04337983 .
Project description:BackgroundProne positioning is recommended for patients with moderate-to-severe acute respiratory distress syndrome (ARDS) receiving mechanical ventilation. While the debate continues as to whether COVID-19 ARDS is clinically different from non-COVID ARDS, there is little data on whether the physiological effects of prone positioning differ between the two conditions. We aimed to compare the physiological effect of prone positioning between patients with COVID-19 ARDS and those with non-COVID ARDS.MethodsWe retrospectively compared 23 patients with COVID-19 ARDS and 145 patients with non-COVID ARDS treated using prone positioning while on mechanical ventilation. Changes in PaO2/FiO2 ratio and static respiratory system compliance (Crs) after the first session of prone positioning were compared between the two groups: first, using all patients with non-COVID ARDS, and second, using subgroups of patients with non-COVID ARDS matched 1:1 with patients with COVID-19 ARDS for baseline PaO2/FiO2 ratio and static Crs. We also evaluated whether the response to the first prone positioning session was associated with the clinical outcome.ResultsWhen compared with the entire group of patients with non-COVID ARDS, patients with COVID-19 ARDS showed more pronounced improvement in PaO2/FiO2 ratio [adjusted difference 39.3 (95% CI 5.2-73.5) mmHg] and static Crs [adjusted difference 3.4 (95% CI 1.1-5.6) mL/cmH2O]. However, these between-group differences were not significant when the matched samples (either PaO2/FiO2-matched or compliance-matched) were analyzed. Patients who successfully discontinued mechanical ventilation showed more remarkable improvement in PaO2/FiO2 ratio [median 112 (IQR 85-144) vs. 35 (IQR 6-52) mmHg, P = 0.003] and static compliance [median 5.7 (IQR 3.3-7.7) vs. - 1.0 (IQR - 3.7-3.0) mL/cmH2O, P = 0.006] after prone positioning compared with patients who did not. The association between oxygenation and Crs responses to prone positioning and clinical outcome was also evident in the adjusted competing risk regression.ConclusionsIn patients with COVID-19 ARDS, prone positioning was as effective in improving respiratory physiology as in patients with non-COVID ARDS. Thus, it should be actively considered as a therapeutic option. The physiological response to the first session of prone positioning was predictive of the clinical outcome of patients with COVID-19 ARDS.
Project description:Veno-venous extracorporeal membrane oxygenation (ECMO) is being more commonly used in patients with acute respiratory distress syndrome (ARDS) due to potentially reversible illnesses. Survival from ARDS using ECMO has been reported even in patients with AIDS. However, the indications for ECMO for ARDS due to immune reconstitution inflammatory syndrome (IRIS) in patients with AIDS are unknown. A 23-year-old man with AIDS and Pneumocystis jirovecii pneumonia was admitted to the intensive care unit with severe ARDS refractory to mechanical ventilator support requiring ECMO. Although ECMO was discontinued, a second treatment with ECMO was necessary due to IRIS-associated ARDS, resulting in an excellent patient outcome. This patient's clinical course suggests two important messages. First, ECMO is a reasonable option for the treatment of patients with ARDS even in a patient with AIDS. Second, ECMO may be effective for the treatment of patients with IRIS.
Project description:ObjectiveTo determine whether the apparent excess incidence of pneumothorax and pneumomediastinum in patients with coronavirus disease 2019 (COVID-19) is explained adequately by iatrogenic causes vs reflecting sequelae of severe acute respiratory syndrome coronavirus 2 infection.Patients and methodsWe retrospectively reviewed patients within our health care system from March 15, 2020, through May 31, 2020, who had a diagnosis of pneumothorax or pneumomediastinum during hospitalization for confirmed COVID-19 infection with attention to timing of pneumothorax and pneumomediastinum; presence, laterality, and placement, or attempts at central lines; and presence of mechanical ventilation before the event.ResultsWe report clinical data and outcomes from 9 hospitalized patients with COVID-19 who developed pneumothorax and/or pneumomediastinum among more than 1200 hospitalized patients admitted within our hospital system early in the pandemic. Many events were inexplicable by iatrogenic needle injury, including 1 spontaneous case without central line access or mechanical ventilation. One occurred before central line placement, 2 in patients with only a peripherally inserted central line, and 1 contralateral to a classic central line. Three of these 9 patients died of complications of COVID-19 during their hospital stay.ConclusionWith COVID-19 affecting the peripheral lung pneumocytes, patients are vulnerable to develop pneumothorax or pneumomediastinum irrespective of their central line access site. We hypothesize that COVID-19 hyperinflammation, coupled with the viral tropism that includes avid involvement of peripheral lung pneumocytes, induces a predisposition to peripheral bronchoalveolar communication and consequent viral hyperinflammatory-triggered pneumothorax and pneumomediastinum.
Project description:ObjectiveTo determine the incidence, predictors, and outcome of pneumothorax (PNX)/pneumomediastinum (PMD) in coronavirus disease 2019 (COVID-19) acute respiratory distress syndrome (ARDS).DesignObservational study.SettingTertiary-care university hospital.ParticipantsOne hundred sixteen consecutive critically ill, invasively ventilated patients with COVID-19 ARDS.InterventionsThe authors collected demographic, mechanical ventilation, imaging, laboratory, and outcome data. Primary outcome was the incidence of PNX/PMD. Multiple logistic regression analyses were performed to identify predictors of PNX/PMD.Measurements and main resultsPNX/PMD occurred in a total of 28 patients (24.1%), with 22 patients developing PNX (19.0%) and 13 developing PMD (11.2%). Mean time to development of PNX/PMD was 14 ± 11 days from intubation. The authors found no significant difference in mechanical ventilation parameters between patients who developed PNX/PMD and those who did not. Mechanical ventilation parameters were within recommended limits for protective ventilation in both groups. Ninety-five percent of patients with PNX/PMD had the Macklin effect (linear collections of air contiguous to the bronchovascular sheaths) on a baseline computed tomography scan, and tended to have a higher lung involvement at intensive care unit (ICU) admission (Radiographic Assessment of Lung Edema score 32.2 ± 13.4 v 18.7 ± 9.8 in patients without PNX/PMD, p = 0.08). Time from symptom onset to intubation and time from total bilirubin on day two after ICU admission were the only independent predictors of PNX/PMD. Mortality was 60.7% in patients who developed PNX/PMD versus 38.6% in those who did not (p = 0.04).ConclusionPNX/PMD occurs frequently in COVID-19 patients with ARDS requiring mechanical ventilation, and is associated with increased mortality. Development of PNX/PMD seems to occur despite use of protective mechanical ventilation and has a radiologic predictor sign.