Table 2

Multiorgan histopathological alterations and clinicopathological correlation

Pulmonary tissueLymphoid tissue
(patient 2)
Cardiac tissue
(patient 3)
Hepatic tissue
(patient 3)
Patient 1Patient 2
Histopathological alterationsAlveolar collapse,
exudates, hyaline membrane,
widened alveolar septa and
few lymphocytic infiltrates
Pneumocyte hyperplasia,
early fibrosis,
residual hyaline membrane,
suspected viral inclusions and
neutrophilic infiltrates
Primary lymphoid follicles,
scattered T lymphocytes,
focal necrosis,
nuclear fragmentation and negative viral RNA
Hypertrophic myocytes,
fatty infiltration,
nuclear pyknosis,
interstitial oedema, and fibrosis
Coagulative necrosis,
microvesicular steatosis,
canalicular cholestasis and negative viral RNA
Pathological diagnosisEarly DADLate DAD combined with bacterial pneumoniaNon-specific acute lymphadenitisOMIIschaemic hepatic injury with mild lobular hepatitis
Clinicopathological correlationDAD results in chest tightness, dry cough and decline in SaO2 and exudates caused the chest CT to show patchy shadows.DAD causes extensive destruction of alveolar epithelium and increases the chance of secondary bacterial infection. Pulmonary organisation caused the chest CT to show ground-glass and plaque shadows.Lymphocytic degeneration of lymph nodes leading to a decrease in peripheral lymphocyte count.Acute exacerbation of OMI; and rise in serum levels of creatine kinase.Hepatocyte necrosis caused by hepatic ischaemia and lobular hepatitis may caused by drug-induced hepatic injury.
  • DAD, diffuse alveolar damage; OMI, old myocardial infarction.