The virus is spread in humans primarily through respiratory droplets entering the nose and mouth. Direct and indirect contact and aerosol particles are also means for viral transmission. Once inside the respiratory tract, SARS-Cov-2 may gain access to nasopharyngeal, tracheobronchial, and/or alveolar epithelial cells by binding to angiotensin converting enzyme 2 (ACE2) receptors, leading to cytokine-mediated immune response and inflammation.
The COVID-19 incubation period is up to two weeks. Common presenting symptoms include fever, cough, shortness of breath, myalgia, and fatigue. Hypertension, cardiovascular disease, diabetes, chronic pulmonary disorders, and chronic liver disease are comorbidities that may exacerbate the extent of disease. Clinical presentation, radiologic findings, and disease course are further affected by severity of the cytokine-mediated inflammation (eg, cytokine storm syndrome). Circulating cytokines can impact multiple other organ systems, causing secondary diseases and complications.
ACE2 receptors are also found in the brain, heart, arterial and venous endothelial cells, kidneys, liver (hepatocytes and cholangiocytes), gastrointestinal tract, and gallbladder. This also offers the potential for SARS-Cov-2 to impact multiple organ systems, leading to atypical COVID-19 clinical presentations and the need for a wider range of radiologic imaging, with variable radiologic findings. In our experience and as reported in the literature, less common symptoms and presentations include headaches (7-23%), syncope, seizures, altered mental status, chest pain, acute cardiovascular events, abdominal pain, vomiting, and diarrhea
With regard to liver involvement, up to approximately 50% of COVID-19 patients may present with liver dysfunction, evidenced by elevated ALT and AST. Most dysfunction is mild, with prevalence varying with severity of COVID-19. Liver dysfunction is likely secondary to the virus binding hepatic ACE2 receptors causing an immune cytokine storm, leading to hepatocellular inflammation and damage (eg, hepatitis).
Ji et al demonstrated that COVID-19 patients with high body mass index and nonalcoholic fatty liver disease (NAFLD) have a greater risk for both progression in liver damage and COVID-19. 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.
Definitive COVID-19 diagnosis is made with viral antigen (RT-PRC) and antibody testing. Chest radiography and CT are also key diagnostic tools, with higher sensitivity and specificity demonstrated by CT. Common chest radiologic findings include bilateral, multilobar, multifocal nodular and coalescent GGO in a peripheral distribution. Diffuse GOOs, consolidation, and reticular densities may also be found, simulating other infectious and inflammatory diseases.8
The spectrum of radiologic findings for COVID-19 pneumonia will vary with the duration and severity of disease and presence of comorbid cardiopulmonary disease. Chest imaging may be performed in patients with suspected COVID-19 and respiratory symptoms. Recognition of typical pulmonary findings would lead to a presumed diagnosis of active COVID-19. For other patients, neck, chest, and/or abdominal CT may be performed to evaluate symptoms not thought to be related to COVID-19. In these instances, evaluating the complete or partially imaged lungs may reveal unsuspected COVID-19 pneumonia.
In our case, the patient presented only with abdominal symptoms. Liver transaminases were slightly elevated; all other laboratory parameters were normal. Despite the patient’s recent exposure, active COVID-19 was not clinically suspected given the absence of respiratory symptoms. Obtaining an abdominal-pelvic CT was an appropriate diagnostic approach.
The fluid-filled bowel loops identified on CT were consistent with the clinical diarrhea; the intermittent small-bowel mucosa hyperemia and thickening were consistent with active inflammation. Once COVID-19 was suspected based upon the typical lung abnormalities, bowel observations could be attributed to the presence of COVID-19 in the gastrointestinal tract. ACE2 receptors are found throughout the gastrointestinal tract, with greatest functional role in the small bowel and colon. SARS-Cov-2 binding to bowel epithelial cells leads to mucosal inflammation (eg, enteritis). Viral alterations in intestinal microbial flora and cellular regulation of fluid and electrolytes can lead to diarrhea.
The fatty liver could have been interpreted as an incidental, isolated finding. However, once COVID-19 pneumonia was identified at the lung bases, hepatic steatosis became a significant finding. The elevated ALT and AST indicated mild liver dysfunction. The presence of hepatic steatosis indicated our patient was at risk for progression in liver dysfunction and COVID-19.
The gallbladder-wall hyperemia without gallstones, sludge, or pericholecystic fluid also became a significant finding when interpreted in conjunction with lung observations. To date, gallbladder-wall hyperemia in the setting of COVID-19 has not been reported. We propose that SARS-Cov-2 binding to gallbladder epithelial cells, leading to mucosal inflammation, can explain the radiologic observations.
Yes maybe. Sometimes infection is swallowed from the intestinal form of Covid-19. However, it should be noted that the respiratory form is one of the most typical for the virus. Regards, Sergey Viktorovich Pushkin
Even it is rare, it is possible. If coronavirus after entering the respiratory system can arrive to the gastro-intestinal organs, perhaps can appear abdominal symptoms before respiratory ones.
This fenomen is determined by distribution of ACE-2 receptors, thus more common is respiratory tract infection also gastrointestinal, especially abdominal pain, with Covid 19.
YES. In the few cases, gastrointestinal symptoms, especially abdominal pain , can to be isolated in Covid 19, thus, non associated with respiratory symptoms.