To our knowledge, there is a paucity of literature on sonographic abdominal imaging features of COVID-19 patients, by continuously increasing in number of the confirmed COVID-19 patients all over the world (exceeding 9,700,000 patients at the time of writing), there are increasing frequency of GIT symptoms and ICU admission with the limitation in possible CT examinations for isolated and mechanically ventilated patients, the most common indications for sonographic studies in the ICU were elevated liver function tests (n, 21/41; 51.2%), this matches with the COVID-19 frequent abdominal imaging study indications in Bhayana R et al. study [9], this study was done on both ICU and non-ICU patients with more frequent indications in their study like abdominal pain [9].
Up to date, the most acceptable pathogenesis of COVID-19 infection is that SARS-COV2 virus can gain access to the respiratory alveolar epithelial cells by binding to angiotensin-converting enzyme 2 (ACE2) receptors [10], leading to cytokine-mediated immune response and inflammation, imaging findings, and disease course are further affected by severity of the cytokine-mediated inflammation (e.g., cytokine storm syndrome). Circulating cytokines can impact multiple other organ systems, causing secondary diseases and complications [11].
ACE2 receptors are also found in the brain, arterial, and venous vascular endothelial cells, kidney, liver (hepatocytes and cholangiocytes), GIT, and gall bladder epithelial cells. This offers a chance for direct viral invasion of theses organs with variable clinical presentations and imaging spectrum [11, 12].
In our study, male to female ratio was 6.5:1, while in Bhayana et al.’s study [9], male to female ratio was 1.4:1, with similarity in increase male to female ratio in both studies.
Hepatomegaly was the most common findings in sonographic examinations with bright echo patterns reflecting diffuse hepatic parenchymal disease (n, 23/41; 56.1%) followed by biliary system disease (n, 17/41; 41.4%). Hepatic dysfunction could be noted in about 50% of COVID-19 patients [13].
Ji et al. [14] demonstrated that COVID19 patients with high body mass index and non-alcoholic fatty liver disease (NAFLD) have a greater risk for both progressions in liver damage and COVID-19, in similarity to our study, these patients show increase liver function tests with hepatomegaly. Progression in liver damage related to NAFLD (and potentially other chronic liver disorders) will complicate COVID-19 presentation, clinical course, and the role of imaging, with the potential for hepatic failure, hepatic encephalopathy, and gastrointestinal bleeding [14].
Sonographic findings of biliary disease were noted in 41.4% in our study sample, biliary system disease was noted in 54% in Bhayana et al.’s study [9] spectrum of gall bladder pathology was noted in our study including luminal mud, stone, mural thickening, signs of inflammation with edematous wall, mural hyperemia, and thin rim pericholecystic fluid could be noted, this spectrum of findings is similar to Bhayan et al.’s study with their population sample in their study including ICU and non-ICU patients. SARS-COV2 can bind to the gall bladder epithelial cells leading to mucosal inflammation and this can explain the sonographic observations [14].
SARS-CoV-2 has a direct inflammatory effect on vascular endothelium [15]. Further, systemic coagulopathy is common in critically ill patients with COVID-19 [16, 17]. Tang et al. [16] found that next to an increased risk of thrombosis, patients seem to have an increased risk of bleeding as well, due to imbalances in platelet production and disruption, and disorders of the coagulation system. Coagulopathy sequel in our study was noted in four examinations (9.7%) including spontaneous hematomas noted in two examinations as well as vascular thrombotic sequel noted in two examinations. Major bleeding sequel to COVID-19 was noted in two patients only in Conti C et al.’s published study [17].
Nephropathy was the 3rd most common sonographic observation (n, 7/41; 17%) in our study, associated increase in renal function tests was noted. Few studies focused mainly on renal histopathology in COVID-19 patients were published [18, 19]. Further dedicated imaging studies are needed for more clarification.
The authors recommend dealing with COVID-19 as a systemic disease possibly due to possible direct viral cytopathic effect on the ACE-2 receptors rich organs and/or harmful systemic immune-mediated response to SARS-COV 2 infection.
The limitation of this study was that of a single-center retrospective study, which limits its generalizability. Pathologic correlation was not available for many patients with imaging abnormalities.