Discussion
Infection by SARS-COV-2 virus evokes cytokine storm resulting in liberation of excessive IL-6 and autacoids, these liberated chemicals are responsible for excessive hyper inflammation, excessive coagulation, multiple pulmonary embolism, raised antiphospholipid antibodies, alveolar endothelial damage, hyaline membrane formation, fibrosis due to liberation with nitric oxide and exudation of fluid resulting in alveoli-perfusion defect at times and preserve the lung compliance. Irrespective of severe hypoxia as seen in the present case, the patient did not complain of difficulty in respiration, a condition commonly called dead man walking or happy hypoxia. At the post-mortem, both lungs appear stiff, stony-hard, and ten-times heavier than normal; these are difficult to be cut even by sharp instruments. There is no oxygen transfusion across the lungs despite administration of >20 litres oxygen per minute inhalation and of ventilator support. The oxygen therapy is used to reverse hypoxia, but our case recovered without giving oxygen in spite of having an oxygen saturation of barely 72%. In animal studies, hyperoxia was found to cause alveolar inflammation, fibrosis and loss of diffusion capacity ( 1).Oxygen is routinely available in almost all hospitals. It has been observed that there is a rise in the reactive oxygen species, if supplemental oxygen is administered to a case of chronic obstructive pulmonary disease (COPD) (2). In patients with risk factors such as ARDS, and COPD, oxygen therapy should be started when SpO2 is <88% and stopped when it is >92%. Priestly wrote “excessive oxygen might burn the candle of life too quickly and soon exhaust the animal power within”, thus, oxygen has come to be recognized as both essential and toxic. Inhalation of pure oxygen can lead to convulsions, asphyxiation, blindness and death (3).Hence, it is imperative to have a well balanced and controlled approach towards oxygen administration; the quantity should be sufficient enough to fulfil the tissue requirement of oxygen but not more. RBC free-oxygen carriers more efficiently provide oxygen to tissue. Hyperoxia leads to the formation of reactive oxygen species, enhances the ATP synthesis and vasoconstriction (4) . Tissue oxygen requirement is the deciding factor of auto regulation of local blood flow (1,5). Oxygen toxicity is due to excessive formation of free radicals responsible for causing lung damage such as marked exudation, congestion and edema, accompanied with intra alveolar haemorrhage, necrosis of the alveolar cells and epithelial desquamation, due to damaged capillary endothelium, thickening of the alveolar septum and loss of type-1 pneumocytes, formation of hyaline membranes and fibrosis (appendix) (5).
Fatal pneumonia occurred in animals after only four days of exposure to 73% oxygen(6). Lower concentration of oxygen used for a longer time like 24-48 hours results in pulmonary toxicity including tracheobronchitis, ARDS and pulmonary interstitial fibrosis(1). Thus, hypoxemia requires a careful use of oxygen and awareness of the dangers of oxygen sensitivity and oxygen toxicity.