Multiorgan histopathological alterations and clinicopathological correlation
| Pulmonary tissue | Lymphoid tissue (patient 2) | Cardiac tissue (patient 3) | Hepatic tissue (patient 3) | ||
| Patient 1 | Patient 2 | ||||
| Histopathological alterations | Alveolar 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, apoptosis, canalicular cholestasis and negative viral RNA |
| Pathological diagnosis | Early DAD | Late DAD combined with bacterial pneumonia | Non-specific acute lymphadenitis | OMI | Ischaemic hepatic injury with mild lobular hepatitis |
| Clinicopathological correlation | DAD 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.