Steroids for COVID-19 treatment

 PATHOPHYSIOLOGY OF AKI IN COVID- 19 PATIENTS. AKI appears to involve a complex process driven by virus-mediated injury, cytokine storm, AngII pathway activation, dysregulation of complement, hypercoagulation, and microangiopathy interacting with common and known risk factors for AKI . There is paucity of data regarding clinical and laboratory characteristics of AKI in patients with COVID-19. We urge that further studies describing and analyzing the clinical course of patients with COVID-19 include appropriate indices of kidney function and diagnosis of AKI in their analyses, including kidney injury markers, urine microscopy, quantified urine protein, urine output, and urine electrolytes. Markers of macrophage activation, coagulation, microangiopathy, and complement activation, as well as kidney imaging and need for KRT (with relevant details), are important data needed to further our understanding of AKI pathophysiology associated with COVID-19. Rates of reversibility of, or partial improvement in, kidney function and any kidney biopsy results (including immunofluorescence and electron microscopy) should be reported. In the rush to report medical complications of COVID-19, we are missing valuable clinical information. Speculation about specific interventions would not be appropriate until we obtain appropriate information. We advocate for a complete and standardized appraisal of the clinical and laboratory picture so that preventative and therapeutic strategies for AKI can be appropriately designed and implemented.

#its_time. x ray of Covid 19 patient 35yrs old taken in serial from day 1 to 7 trying to show pathological changes in the Lung. #Expert_opinion on this

This patient was admitted to the ICU with COVID pneumonia a few weeks ago and due to a very high D-dimer level, empiric anticoagulation was initiated. The night prior to extubation, the patient's oxygen saturation plummeted, fresh blood appeared in the ventilator tubing, and the second X-ray was obtained.

Confirmed #covid-19 crp >300, WBC 11, temperature 38.8, spo2 90% room air, RR 30, terrible wheeze, SOB, sweaty. Rapid deterioration in breathing, intubated and ventilated 24 hours later.

Treatment for severe acute respiratory distress syndrome from COVID-19 In The Lancet Respiratory Medicine, Kollengode Ramanathan and colleagues provide excellent recommendations for the use of extracorporeal membrane oxygenation (ECMO) for patients with respiratory failure from acute respiratory distress syndrome (ARDS) secondary to coronavirus disease 2019 (COVID-19). The authors describe pragmatic approaches to the challenges of delivering ECMO to patients with COVID-19, including training health-care personnel, resolving equipment and facilities issues, implementing systems for infection control and personal protection, providing overall support for health-care staff, and mitigating ethical issues. For patients with COVID-19 who require endotracheal intubation, use of low tidal volume (6 mL/kg per predicted bodyweight) with a plateau airway pressure of less than 30 cm H2O, and increasing the respiratory rate to 35 breaths per min as needed, is the mainstay of lung-protective ventilation. If the hypoxaemia progresses to a PaO2:FiO2 ratio of less than 100–150 mm Hg, there are several therapeutic options. The level of positive end-expiratory pressure can be increased by 2–3 cm H2O every 15–30 min to improve oxygen saturation to 88–90%, with the goal of maintaining a plateau airway pressure of less than 30 cm H2O. Lower driving pressures (plateau airway pressure minus positive end-expiratory pressure) with a target of 13–15 cm H2O can also be used. To read more- https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30127-2/fulltext Source- The Lancet Authors- Michael A Matthay, J Matthew Aldrich, Jeffrey E Gotts