Table 2.

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.