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Covid-19 has the maximal impact on the lungs and respiratory symptoms of a person. It can have short & long-term impact. With the evaluation of thousands and thousands of patients, every passing day is giving us a deeper insight in the Covid-19 infection and its effects on the lungs. Below are few of the effects seen in the patients suffering and recovering from Covid-19 infection.


A large proportion of cases have been reported to be asymptomatic and have been diagnosed only through contact tracing and surveillance.

Upper respiratory tract

  • Mild cases may only present with upper respiratory tract symptoms like sore throat, rhinorrhea, nasal congestion.
  • Fever being another common symptom.
  • Anosmia- olfactory dysfunction in 20-60% of patients. Majority of anosmia is temporary and full gain of smell within few days of recovery. Due to conductive olfactory loss.
  • Ageusia- loss of taste, commonly accompanies anosmia.


Lower respiratory tract symptoms commonly comprise of

  • Fever- by far the most common symptom
  • Dry cough
  • Shortness of breath
  1. Pneumonia-
  • Once the virus moves down into the lower respiratory tract, its pike surface glycoprotein attaches itself to ACE-2 receptors present on type 2 pneumocytes.
  • Inflamed lungs with fluid buildup is observed with bilateral involvement of lungs affecting the ability of lung to take up oxygen. Pulmonary involvement is usually without generalized lymphoid organ hyperplasia.
  • This results in cough and difficulty in breathing.
  • Patients require oxygen therapy and may cause long lasting breathing difficulties
  • Radiologically, B/L round multifocal glassgow opacities are seen termed as “COVID balls”

2 .  Acute respiratory Distress Syndrome (ARDS)

  • Seen as a complication of Pneumonia. Patient presents with breathlessness and tachycardia in Type 2 respiratory failure.
  • This is due to diffuse alveolar damage to ty2 pneumocytes.
  • ARDS in Covid-19 has been observed as a two stage process a) Inflammatory Stage b) Fibrotic Stage.
  • Hyaline membrane formation is followed by fibroblast proliferation and pulmonary edema. This leaves the patient into severe hypoxic state.
  • The patient’s sPo2 drops significantly causing tissue hypoxia and may require invasive mechanical ventilatory support.

3. Cytokines storm

  • The virus causes activation of Pro-inflammatory cytokines like Tumour necrosis factor (TNF) α, Interleukin 1β (IL-1β), IL-6, Granulocyte-colony stimulating factor, monocyte chemoattractant protein-1, and macrophage inflammatory proteins 1-α to name a few which contributes to the multiple organ dysfunction (MODS) in severe COVID-19 patients.

4. Pulmonary intravascular coagulopathy

  • In cases of severe acute respiratory distress syndrome (ARDS), the inflammation stage is followed by the fibrotic stage.
  • Fibrin clots form in the alveoli, platelet-fibrin microthrombi pepper the small pulmonary capillaries in the lung that are responsible for gas exchange with the alveoli.
  • This is termed as Diffuse pulmonary intravascular coagulopathy.
  • Thrombus is mainly seen in lungs while CNS and peripheral involvement is less likely. Also, lymphoid organ hyperplasia is absent diffentiating it from Disseminated Intravascular coagulopathy (DIC).