GI symptoms such as nausea, anorexia, vomiting and diarrhea are common among SARS-CoV-2 infected patients(1, 2). Viral shedding with stools is well established and prospects as one etiology behind the GI symptoms(3). Further, the virus had been found in other specimens, such as gall bladder, during the cholecystectomy(4, 5). Acute replication in the GI tract is shown in some studies(6).
Liver enzyme abnormalities are a common finding. However, acute cholecystitis, acute pancreatitis, ileus, pseudo-colonic obstruction and mesenteric ischemia and bowel necrosis have unusual presentations with higher Morbidity and mortality. Mortality is 50% in bowel necrosis.
Mesenteric ischemia is usually reported by critically ill patients(7–12). Abdominal pain, nausea, vomiting and per-rectal bleeding are usual signs and distension and tenderness features of peritonism are usual signs(13). Laboratory findings and their importance are still not validated. However, Leukocyte count s found to be elevated in more than 90% of patients. High lactate levels with acidosis were found in 88% of the cases(14). Lactate levels of more than 2mmol/l were associated with intestinal ischemia with poor prognosis(15).
It should be emphasized that the presence of lactic acidosis in combination with abdominal pain when the patient may not otherwise appear clinically ill should lead to consideration for early CTA. Further, D-dimer > 0.9 mg/L had a specificity, sensitivity, and accuracy of 82, 60, and 79%, respectively. As D- dimer is released from the fibrinolysis. Thus, D-dimer may be helpful in early assessment(16). Elevated amylase, intestinal fatty acid binding protein (I-FABP), serum alpha-glutathione S-transferase (alpha–GST), and cobalt-albumin binding assay (CABA) have been suggested for initial diagnosis. Nevertheless, it needs further validation.
CTA is the gold standard test to identify the thrombus or embolus in the MSA with a sensitivity of 93%, specificity of 100%, and positive and negative predictive values of 100 and 94%, respectively(17, 18).
If mesenteric ischemia is probable, operative intervention is often considered for bowel examination and resection. In addition, endovascular or open angiography and thrombectomy are required when proximal arterial thromboembolic disease is suspected.
On intraoperative examination of the bowel in these patients, many surgeons reported unusual findings with patchy areas of well-demarcated yellow discolouration involving the antimesenteric bowel wall(19). However, in our case, there were multiple patches varying from 0.5-2 cm. We did not disturb those areas as the bowel wall was so thin during the surgery. The terminal ileum is the most active area of intestinal necrosis, as in our case. Sometimes, the bowel will appear pale or ischemic but not frankly necrotic(19).
On the contrary, the bowel in our patient was plethoric. In those cases, leaving the abdomen temporarily open for a planned second-look laparotomy within 12 to 24 hours is recommended, as ischemia can often quickly evolve into transmural necrosis. However, we decided close at that time due to clinical judgment. Second look laparoscopy instead of laparotomy can be considered as a novel option(20).
The pathological examination of the resected bowel is reported to demonstrate extensive mucosal ulceration, congestion with areas of extensive transmural inflammation, and transmural infarction. In addition, fibrin microthrombi were occasionally noted in the capillaries underlying areas of necrosis, again raising the possibility of thrombosis at the submucosal vessel level, which is compatible with our patients.
Despite these observations, the pathophysiology of bowel ischemia in these critically ill patients with SARS-COV-2 remains uncertain. It has been reported that mesenteric ischemia occurs with mean arterial pressure less than 45mmHg(21). It is well established that patients who are admitted to the ICU can develop mesenteric ischemia simply due to high doses of vasopressors, hemodynamic instability, and metabolic derangements that compromise intestinal blood flow(7–10, 22). At the same time, this may contribute to the high rate of bowel ischemia observed in patients with SARS-COV-2. In our case, the patient has no symptoms of severe SARS-COV-2 before the onset of abdominal pain. Hence, SARS-COV-2 triggers a direct mechanism leading to bowel ischemia. Further, the atypical features of the mesenteric ischemia and the rare involvement of the watershed areas strongly suggest alternative mechanisms that are specific to SARS-COV-2.
Inflammatory coagulopathy has been assumed to be linked to worse pulmonary disease, deep vein thrombosis, cerebrovascular accidents, and renal failure. The authors believe that the exact mechanism may potentially promote mesenteric ischemia. However, at the time of writing, sparse evidence to recommend empiric therapeutic anticoagulation to SARS-CoV-2 patients. Potential markers such as D-dimer can be suggested but need further validation.
The mortality rate of SARS-COV-2 patients who develop mesenteric ischemia is currently reported to be as high as 40 per cent, with more than 92 per cent of the deaths occurring within the immediate postoperative days due to multiorgan failure or refractory septic shock.
Since we are dealing with a novel disease whose clinical manifestations are partly unknown, we are learning about possible rare expressions of the infection and its complications. Global participation is needed in the identification of complications. Forming risk algorithms for the prevention of severe morbid complications is mandatory. This case highlights severe extrapulmonary complications that can occur in the asymptomatic population.