Within a very short period, outbreaks of a novel coronavirus disease (COVID-19) have affected 183 countries worldwide. COVID-19 resolves acutely, but it has resulted in thousands of deaths, with an overall fatality rate of 2% to 5% (1). Among the fatal cases, over 50% of patients died from respiratory failure with massive alveolar damage due to virus-activated “cytokine storm syndrome” (2). Of these patients, 67% developed adult respiratory distress syndrome (ARDS), 29% developed acute kidney injury, 23% developed cardiac injury, and 29% experienced liver dysfunction (3). The intensive care unit (ICU) mortality rate among those who required invasive mechanical ventilation was 86% (4), and the mortality of patients who received extracorporeal membrane oxygenation was also extremely high (5). Until now, there have been no proven effective specific treatment strategies and so methylprednisolone may be the best option for COVID-19 patients who develop ARDS (6). Although interferon alfa-2b, antiviral therapy, antibiotics for the prevention of secondary infection, and methylprednisolone were all administered to attenuate lung inflammation, histological examination still revealed bilateral diffuse alveolar damage with hyaline membrane formation in an autopsy of a patient (7). According to the imaging changes and pathological findings associated with ARDS, a tubular and enlarged appearance of the pulmonary vessels with a sudden caliber reduction seen within ground glass opacity lesions showing partial consolidation and fibrosis should be expected in severe cases of COVID-19 (8, 9). Fortunately, corticosteroids have a greater anti-inflammatory effect when administered intrapleurally, rather than via the intravenous route, because the permeability of the damaged visceral pleural membrane increases during pulmonary edema and steroid treatment, with the characteristic of fat-solubility, further permits infiltration into the lung parenchyma. Glucocorticoids can easily pass through the visceral pleura and bind to steroid hormone receptors, thereby allowing them to reach the injured areas and avoiding the problems of a ventilation–perfusion mismatch and the need for a shunt via intratracheal instillation or intravenous instillation. Glucocorticoids can normalize the ion pump (Na-K pump) and increase the synthesis of Na+/K+-ATPase, thus contributing to reductions in lung edema and optimization of oxygenation because alveolar fluid clearance is impaired in the majority of patients with ARDS (10). In COVID-19 severe refractory ARDS, more aggressive management is required to reduce the inflammatory reaction and consequent lung injury. The results of our study provide more evidence supporting the efficacy of intrapleural steroid instillation (IPSI) in the treatment of ARDS with multiple organ failure (11). This alternative treatment resulted in significant improvement in oxygenation and survival benefits after 5 days of treatment. The dosing schedule of intrapleural methylprednisolone was initially 40 mg q6 h in both pleural cavities, but the dose was reduced on the basis of chest radiography appearance, inspired oxygen concentration demand, and positive end-expiratory pressure of the ventilator. Thoracic catheterization was easily performed because COVID-19 patients usually had significant pleural effusion. Although managing COVID-19 pneumonia is currently a major issue for ICU healthcare providers around the world, IPSI will greatly improve the ability to respond effectively to current needs. Our recommendation in this severe case of COVID-19 might help physicians implement suitable therapeutic strategies for similar severe patients and reduce mortality.
Read full abstract
Jul 1, 2021
Open Access
