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Critical Care
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Jaimie Maines, Lauren A. Plante
The acute respiratory distress syndrome (ARDS) is a nonspecific response of the lung to a variety of inciting events. It is the extreme form of a spectrum of acute lung injury (ALI) and has been defined as “a syndrome of inflammation and increased permeability that is associated with a constellation of clinical, radiology, and physiologic abnormalities that cannot be explained by, but may coexist with, left atrial or pulmonary capillary hypertension” [103]. In other words, ARDS is a type of non-cardiogenic pulmonary edema. Inflammation due to activation of neutrophils is thought to be the responsible mechanism of the pathophysiology of ARDS. Pro-inflammatory mediators function to increase vascular permeability which then further leads to disruption of normal lung vasculature and resultant increased inflammation and ultimate lung damage. The increased capillary permeability results from damage to the capillary and alveolar epithelium. Fluid removal from the alveolar space is impaired, leading to alveolar damage and further inflammation [104]. As a result of the inflammation and increased vascular permeability, there is a reduction in the remaining physical size of the lungs, leading to poor compliance and resistance to expansion.
Extracorporeal Membrane Oxygenation
Published in Stephen M. Cohn, Alan Lisbon, Stephen Heard, 50 Landmark Papers, 2021
Ronny Munoz-Acuna, Ameeka Pannu
Currently, severe ARDS treatment continues to be a lung-protective ventilation strategy combined with other maneuvers like prone positioning and neuromuscular blockade. VV ECMO has now been established as a safe rescue modality in patients with severe hypoxemia refractory to the above, especially at centers that frequently use ECMO. While ECMO potentially offers a mortality benefit [1, 8], clinicians must individualize therapy to minimize adverse outcomes. Unanswered questions about the routine use of VV-ECMO include its impact on patient-centered outcomes such as: quality of life and long-term functional status, both of which are gravely impacted in severe ARDS [9]. Given the significant use of VV-ECMO during the COVID 19 pandemic [10], evidence from this experience will likely shed light on optimal patient selection and cannulation timing.
Review on Imaging Features for COVID-19
Published in S. Prabha, P. Karthikeyan, K. Kamalanand, N. Selvaganesan, Computational Modelling and Imaging for SARS-CoV-2 and COVID-19, 2021
The COVID-19 clinical features vary from an asymptomatic state to ARDS and multi-organ dysfunction. The important clinical properties are fatigue, myalgia, headache, cough, breathlessness, sore throat and fever. Generally, COVID-19 patients have fever (85%), cough (70%) and shortness of breath (43%); however, abdominal and other asymptomatic symptoms are often appropriate. Conjunctivitis has also been defined as indistinguishable from other respiratory infections. Finally, the disease may progress to respiratory failure, pneumonia and death. These progressions are associated with a marked increase in inflammatory cytokines (Chen et al., 2020). The intermediate time of symptoms is dyspnea: fifth day, hospitalization: seventh day and eighth day: ARDS. In the disease progression, 25–30% of affected patients require intensive care. Complications includes ARDS, acute lung injury, acute kidney injury and other complications, namely, cardiac, cardiovascular or acute stroke. During the second and third week, patients start recovering; such recovery may be extensive. Unfavourable outcomes and death are more common for elderly people (Coronavirus Outbreak, 2020).
The immunologic aspects of cytokine release syndrome and graft versus host disease following CAR T cell therapy
Published in International Reviews of Immunology, 2022
Vahid Mansouri, Niloufar Yazdanpanah, Nima Rezaei
CRS can present with a variety of symptoms, from mild flu-like symptoms to life-threatening manifestations. CRS usually involves fever, fatigue, anorexia, nausea, vomiting, headache, arthralgia, myalgia, and rash. Moreover, CRS could be accompanied by tachypnea, tachycardia, hypotension, and hypoxia, which can proceed to severe systemic inflammatory response presenting with vasopressor-requiring hypotensive shock, vascular leakage, disseminated intravascular coagulation, and eventually multi-organ failure. In addition, CRS-associated laboratory abnormalities include cytopenia, elevated creatinine, and liver enzymes, high levels of CRP, ferritin, IL-6, and interferon-γ (IFN-γ) and disturbed coagulation parameters. Besides, there are some CRS organ-specified signs and symptoms. Respiratory symptoms could be as mild as having solely tachypnea and cough or as high as developing acute respiratory distress syndrome (ARDS) with bilateral lung involvements. Less commonly, patients with CRS could develop renal insufficiency or cardiac dysfunction with reduced ejection fraction [71] (Figure 2).
Predictors of invasive mechanical ventilation in hospitalized COVID-19 patients: a retrospective study from Jordan
Published in Expert Review of Respiratory Medicine, 2022
Suad Kabbaha, Sayer Al-Azzam, Reema A. Karasneh, Basheer Y. Khassawneh, Abdel-Hameed Al-Mistarehi, William J. Lattyak, Motasem Aldiab, Syed Shahzad Hasan, Barbara R. Conway, Mamoon A. Aldeyab
The coronavirus disease 2019 (COVID-19) caused by the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is a rapidly emerging disease. The initial cases of COVID-19 disease were reported in December 2019 in Wuhan, China. In March 2020, the World Health Organization (WHO) declared the novel coronavirus (COVID-19) outbreak to be a global pandemic [1]. As of 6 March 2022, there were more than 440 million confirmed cases of COVID-19 globally, leading to more than 5 million deaths [2]. Although many cases appear to be mild, severe consequences such as pulmonary infection, acute respiratory distress syndrome (ARDS), and multi-organ failure may occur. Epidemiological studies have shown that around 14% of patients develop a severe form of the COVID-19 disease, while 5% of patients develop a critical form of the disease [3].
Protective effect of oxytocin through its anti-inflammatory and antioxidant role in a model of sepsis-induced acute lung injury: Demonstrated by CT and histological findings
Published in Experimental Lung Research, 2021
I. H. Sever, B. Ozkul, D. Erisik Tanriover, O. Ozkul, C. S. Elgormus, S. G. Gur, I. Sogut, Y. Uyanikgil, E. O. Cetin, O. Erbas
Acute respiratory distress syndrome (ARDS) is a life-threatening condition mostly caused by sepsis, pneumonia, pancreatitis and trauma which trigger the immune system.1 It is characterized by increased permeability of pulmonary capillary endothelial cells and alveolar epithelial cells, massive accumulation of inflammatory cells and pulmonary microvascular coagulopathy.2–4 Despite developments in patient management and pharmacological interventions, ARDS has been one of the most common causes of mortality in critically ill patients with a mortality rate greater than 40%.5–7 Although its pathophysiological mechanism is still unclear, increased pro-inflammatory cytokines and NO release are considered to be responsible in the development of sepsis induced acute lung injury (ALI). Therefore, decreasing the pro-inflammatory response and oxidative stress may protect the endothelial barrier in the lungs and the development of edema was counteracted.8