scholarly journals Lung ultrasound assessment of acute respiratory distress syndrome caused by coronavirus disease 2019: An observational study

2020 ◽  
pp. 102490792096932
Author(s):  
Ruiting Li ◽  
Hong Liu ◽  
Hong Qi ◽  
Yin Yuan ◽  
Xiaojing Zou ◽  
...  

Background: An outbreak of coronavirus disease 2019 (COVID-19) took place in Wuhan, China, by the end of 2019, and the disease continues to spread all over the world. The number of patients is increasing rapidly, a large number of infected patients is critically ill, and the mortality is high. However, information on COVID-19 patients is limited, and its clinical characteristics have not been fully studied. Objectives: To compare the performances of point-of-care lung ultrasound (LUS) and bedside chest X-ray in assessing the condition of COVID-19 patients with acute respiratory distress syndrome (ARDS). Methods: This observational study enrolled 42 COVID-19 patients with ARDS who were admitted to the Department of Critical Care Medicine of the Wuhan Union Hospital from February to April 2020. The point-of-care LUS characteristics of the COVID-19 patients with ARDS were summarized, and the performances of LUS and bedside chest X-ray in assessing the patient’s condition were compared. Results: Most of the 42 patients were elderly individuals with chronic clinical diseases. The proportion of patients older than 60 years old was 85.7%. All patients were given invasive mechanical ventilation; eight (19.0%) of them received venovenous extracorporeal membrane oxygenation support. LUS has evident advantages in detecting lung consolidation, patchy shadows, and pleural thickening, and pleural line changes in particular. The receiver operating characteristic analysis indicated that the sensitivity, Youden index, and kappa value for detecting COVID-19 patients with ARDS were higher for LUS than the chest X-ray. Conclusion: LUS has better diagnostic accuracy and sensitivity in COVID-19 patients with ARDS than the chest X-ray.

2021 ◽  
Vol 14 (3) ◽  
pp. e240891
Author(s):  
Chris Lock ◽  
Catherine M Nix

A 64-year-old man was intubated and ventilated for COVID-19-associated acute respiratory distress syndrome. He had a background history of chronic obstructive pulmonary disease and ischaemic heart disease. His oxygen saturations dropped rapidly to 80% on day 9 of ICU admission. Chest auscultation revealed absent breath sounds over the left upper chest which raised suspicions for pneumothorax, of which a small stable left apical pneumothorax was documented on a recent CT scan of the thorax. Point-of-care ultrasonography was performed prior to attempting chest drain insertion which demonstrated sliding pleura on the left side (GE Healthcare model: Vscan Extend—display: 5 inches, 720×1280 pixels resolution, sector probe—broad bandwidth: 1.7–3.8 MHz, 24 cm penetration and linear probe—broad bandwidth: 3.3–8 MHz, 8 cm penetration). A portable chest X-ray was obtained which demonstrated left upper lobe collapse secondary to mucus plugging. The mucus plug was successfully suctioned from the patient’s airway using bedside bronchoscopy subsequently improving the patient’s oxygen saturation. A follow-up chest X-ray and CT scan of the thorax demonstrated interval resolution of the left upper lobe collapse. While expansion of his existing pneumothorax was first on the list of differential diagnoses, the use of ultrasonography early in the patient’s assessment ensured it was ruled out prior to attempting chest drain insertion, thus prompting the acquisition of the chest X-ray which subsequently demonstrated the left upper lobe collapse as the correct diagnosis.


2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Johannes Herrmann ◽  
Quirin Notz ◽  
Tobias Schlesinger ◽  
Jan Stumpner ◽  
Markus Kredel ◽  
...  

Abstract Background Coronavirus disease 2019 (COVID-19) associated coagulopathy (CAC) leads to thromboembolic events in a high number of critically ill COVID-19 patients. However, specific diagnostic or therapeutic algorithms for CAC have not been established. In the current study, we analyzed coagulation abnormalities with point-of-care testing (POCT) and their relation to hemostatic complications in patients suffering from COVID-19 induced Acute Respiratory Distress Syndrome (ARDS). Our hypothesis was that specific diagnostic patterns can be identified in patients with COVID-19 induced ARDS at risk of thromboembolic complications utilizing POCT. Methods This is a single-center, retrospective observational study. Longitudinal data from 247 rotational thromboelastometries (Rotem®) and 165 impedance aggregometries (Multiplate®) were analysed in 18 patients consecutively admitted to the ICU with a COVID-19 induced ARDS between March 12th to June 30th, 2020. Results Median age was 61 years (IQR: 51–69). Median PaO2/FiO2 on admission was 122 mmHg (IQR: 87–189), indicating moderate to severe ARDS. Any form of hemostatic complication occurred in 78 % of the patients with deep vein/arm thrombosis in 39 %, pulmonary embolism in 22 %, and major bleeding in 17 %. In Rotem® elevated A10 and maximum clot firmness (MCF) indicated higher clot strength. The delta between EXTEM A10 minus FIBTEM A10 (ΔA10) > 30 mm, depicting the sole platelet-part of clot firmness, was associated with a higher risk of thromboembolic events (OD: 3.7; 95 %CI 1.3–10.3; p = 0.02). Multiplate® aggregometry showed hypoactive platelet function. There was no correlation between single Rotem® and Multiplate® parameters at intensive care unit (ICU) admission and thromboembolic or bleeding complications. Conclusions Rotem® and Multiplate® results indicate hypercoagulability and hypoactive platelet dysfunction in COVID-19 induced ARDS but were all in all poorly related to hemostatic complications..


2013 ◽  
Vol 2 (5) ◽  
pp. 24
Author(s):  
Hawa Edriss ◽  
Marie Pfarr

We report a 53-year-old man who ingested 2400 mg of citalopram and presented to the emergency department three hours post-ingestion with altered mental status, somnolence, and a blood pressure of 67/45 mmHg. He failed to respond to three boluses of normal saline (1000 ml each) and required vasopressors. The patient developed serotonin syndrome with hyper-reflexia, rigidity, and ankle myoclonus. He had a tonic-clonic seizure in the ER requiring intravenous lorazepam and phenytoin. An ECG showed QT prolongation. Chest x-ray on presentation was normal. Within 32 hours the patient developed acute respiratory distress, hypoxemia, a wide A-a gradient, PaO2/FiO2< 200, and chest x-ray changes compatible with acute respiratory distress syndrome (ARDS). He had normal central venous pressures, normal cardiac biomarkers, normal systolic and diastolic functions on echocardiography, and no acute ST/T wave changes. His ABG showed a metabolic acidosis and a respiratory acidosis. The patient required intubation and ventilation. Citalopram has been associated with seizures and ECG abnormalities after overdoses. The respiratory complications and metabolic acidosis have been reported only a few times in the literature.  We are reporting the second case of ARDS and the fifth case of metabolic acidosis due to citalopram overdose and suggest that the metabolic acidemia is explained by propionic acid. The respiratory acidosis seen in this patient has not been reported previously.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Premila D. Leiphrakpam ◽  
Hannah R. Weber ◽  
Andrea McCain ◽  
Roser Romaguera Matas ◽  
Ernesto Martinez Duarte ◽  
...  

Abstract Background Acute respiratory distress syndrome (ARDS) is multifactorial and can result from sepsis, trauma, or pneumonia, amongst other primary pathologies. It is one of the major causes of death in critically ill patients with a reported mortality rate up to 45%. The present study focuses on the development of a large animal model of smoke inhalation-induced ARDS in an effort to provide the scientific community with a reliable, reproducible large animal model of isolated toxic inhalation injury-induced ARDS. Methods Animals (n = 21) were exposed to smoke under general anesthesia for 1 to 2 h (median smoke exposure = 0.5 to 1 L of oak wood smoke) after the ultrasound-guided placement of carotid, pulmonary, and femoral artery catheters. Peripheral oxygen saturation (SpO2), vital signs, and ventilator parameters were monitored throughout the procedure. Chest x-ray, carotid, femoral and pulmonary artery blood samples were collected before, during, and after smoke exposure. Animals were euthanized and lung tissue collected for analysis 48 h after smoke inhalation. Results Animals developed ARDS 48 h after smoke inhalation as reflected by a decrease in SpO2 by approximately 31%, PaO2/FiO2 ratio by approximately 208 (50%), and development of bilateral, diffuse infiltrates on chest x-ray. Study animals also demonstrated a significant increase in IL-6 level, lung tissue injury score and wet/dry ratio, as well as changes in other arterial blood gas (ABG) parameters. Conclusions This study reports, for the first time, a novel large animal model of isolated smoke inhalation-induced ARDS without confounding variables such as cutaneous burn injury. Use of this unique model may be of benefit in studying the pathophysiology of inhalation injury or for development of novel therapeutics.


Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Chiara Robba ◽  
◽  
Lorenzo Ball ◽  
Denise Battaglini ◽  
Danilo Cardim ◽  
...  

Abstract Background In COVID-19 patients with acute respiratory distress syndrome (ARDS), the effectiveness of ventilatory rescue strategies remains uncertain, with controversial efficacy on systemic oxygenation and no data available regarding cerebral oxygenation and hemodynamics. Methods This is a prospective observational study conducted at San Martino Policlinico Hospital, Genoa, Italy. We included adult COVID-19 patients who underwent at least one of the following rescue therapies: recruitment maneuvers (RMs), prone positioning (PP), inhaled nitric oxide (iNO), and extracorporeal carbon dioxide (CO2) removal (ECCO2R). Arterial blood gas values (oxygen saturation [SpO2], partial pressure of oxygen [PaO2] and of carbon dioxide [PaCO2]) and cerebral oxygenation (rSO2) were analyzed before (T0) and after (T1) the use of any of the aforementioned rescue therapies. The primary aim was to assess the early effects of different ventilatory rescue therapies on systemic and cerebral oxygenation. The secondary aim was to evaluate the correlation between systemic and cerebral oxygenation in COVID-19 patients. Results Forty-five rescue therapies were performed in 22 patients. The median [interquartile range] age of the population was 62 [57–69] years, and 18/22 [82%] were male. After RMs, no significant changes were observed in systemic PaO2 and PaCO2 values, but cerebral oxygenation decreased significantly (52 [51–54]% vs. 49 [47–50]%, p < 0.001). After PP, a significant increase was observed in PaO2 (from 62 [56–71] to 82 [76–87] mmHg, p = 0.005) and rSO2 (from 53 [52–54]% to 60 [59–64]%, p = 0.005). The use of iNO increased PaO2 (from 65 [67–73] to 72 [67–73] mmHg, p = 0.015) and rSO2 (from 53 [51–56]% to 57 [55–59]%, p = 0.007). The use of ECCO2R decreased PaO2 (from 75 [75–79] to 64 [60–70] mmHg, p = 0.009), with reduction of rSO2 values (59 [56–65]% vs. 56 [53–62]%, p = 0.002). In the whole population, a significant relationship was found between SpO2 and rSO2 (R = 0.62, p < 0.001) and between PaO2 and rSO2 (R0 0.54, p < 0.001). Conclusions Rescue therapies exert specific pathophysiological mechanisms, resulting in different effects on systemic and cerebral oxygenation in critically ill COVID-19 patients with ARDS. Cerebral and systemic oxygenation are correlated. The choice of rescue strategy to be adopted should take into account both lung and brain needs. Registration The study protocol was approved by the ethics review board (Comitato Etico Regione Liguria, protocol n. CER Liguria: 23/2020).


2003 ◽  
Vol 121 (3) ◽  
pp. 121-124 ◽  
Author(s):  
Francisco Garcia Soriano ◽  
Elcio dos Santos Oliveira Vianna ◽  
Irineu Tadeu Velasco

CONTEXT: A case of neuroleptic malignant syndrome and acute respiratory distress syndrome is presented and discussed with emphasis on the role of muscle relaxation, creatine kinase, and respiratory function tests. CASE REPORT: A 41-year-old man presented right otalgia and peripheral facial paralysis. A computed tomography scan of the skull showed a hyperdense area, 2 cm in diameter, in the pathway of the anterior intercommunicating cerebral artery. Preoperative examination revealed: pH 7.4, PaCO2 40 torr, PaO2 80 torr (room air), Hb 13.8 g/dl, blood urea nitrogen 3.2 mmol/l, and creatinine 90 mmol/l. The chest x-ray was normal. The patient had not eaten during the 12-hour period prior to anesthesia induction. Intravenous halothane, fentanyl 0.5 mg and droperidol 25 mg were used for anesthesia. After the first six hours, the PaO2 was 65 torr (normal PaCO2) with FiO2 50% (PaO2/FiO2 130), and remained at this level until the end of the operation 4 hours later, maintaining PaCO2 at 35 torr. A thrombosed aneurysm was detected and resected, and the ends of the artery were closed with clips. No vasospasm was present. This case illustrates that neuroleptic drugs can cause neuroleptic malignant syndrome associated with acute respiratory distress syndrome. Neuroleptic malignant syndrome is a disease that is difficult to diagnose. Acute respiratory distress syndrome is another manifestation of neuroleptic malignant syndrome that has not been recognized in previous reports: it may be produced by neuroleptic drugs independent of the manifestation of neuroleptic malignant syndrome. Some considerations regarding the cause and effect relationship between acute respiratory distress syndrome and neuroleptic drugs are discussed. Intensive care unit physicians should consider the possibility that patients receiving neuroleptic drugs could develop respiratory failure in the absence of other factors that might explain the syndrome.


Anaesthesia ◽  
2010 ◽  
Vol 65 (3) ◽  
pp. 294-297 ◽  
Author(s):  
A. Peris ◽  
G. Zagli ◽  
F. Barbani ◽  
L. Tutino ◽  
S. Biondi ◽  
...  

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