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.