Several researchers have reported the link between COVID-19 and generalized organ damage, including organs in the abdominopelvic. This association is thought to be because SARS-CoV-2 binds to the angiotensin-converting enzyme 2 (ACE-2) receptor found in alveolar epithelial cells in the lung, and these receptors are also detected in gastrointestinal epithelial cells resulting in infection and local viral replication, and increase cytotoxic effect.(4,5) In addition, some authors also think that organ damage in some COVID-19 patients may be caused by severe systemic inflammation caused by upregulation of cellular and natural immunity. SARS-CoV-2 infection triggers the activation of T lymphocytes and the inflammatory signaling pathway which ultimately results in the release of multiple proinflammatory cytokine, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin (IL) -2, IL-6, IL-7, IL-10, and tumor necrosis factor-α (TNF- α).(6) This cytokine cascade can eventually result in extensive cell damage, necrosis, and injury to multiple organs and may partly explain the different multisystem symptoms in patients with confirmed viral infections, including gastrointestinal necrosis.(6,7)
Intestinal necrosis is a late stage discovery characterized by cell death due to reduced blood flow to the digestive tract. This serious condition is often fatal and can lead to vascular occlusion, colitis, obstruction, or infection. In adults, the most common cause of intestinal necrosis is acute mesenteric occlusion, and, less commonly, perforation, chronic ischemia, inflammatory disease, and other mechanical disorders.(8,9) In our case, the bowel necrosis we found had patent blood vessels and did not involve mesenteric necrosis, therefore, we think that it might be due to microvascular thrombosis and the inflammation associated with hypercoagulability in this patient. Several studies have recently investigated the association between COVID-19 and hypercoagulability which is usually characterized by high D-dimer.(10,11) Some patients may show prolonged thrombin time and prothrombin time, and shortened aPTT. Several other studies have shown aPTT prolongation in patients with confirmed COVID-19.(11)
Bowel necrosis without adequate intervention and proper surgical management will lead to near 100% mortality. The operative mortality rate for acute mesenteric ischemia has been reported to be 47%. Patients who survive the initial event have a high probability of postoperative complications.(12,13) Sepsis can cause hypotension and end-organ damage, especially kidney and liver failure. For those who survive the early intervention, mortality continues to increase from comorbidities.(13)
Although rare, the emergent surgery for bowel necrosis and COVID-19 infection presents unique challenges for clinicians.