The coagulopathy that goes with COVID-19 has gained increasing interest recently. The International Society of Thrombosis and Haemostasis reported that patients with severe coronavirus disease 2019 (COVID-19) have fulminant activation of coagulation and consumption of coagulation factors [13].
In our study, we found 124 patients (about 10%) with thromboembolic manifestations out of 1245 Covid-19-positive patients, 68.5% of them were admitted to the ICU. The rate of thromboembolism reported in the literature is variable. Some studies have reported thromboembolic rates in the range of 20–30% while others have reported rates as high as 40–70% [14]. The number of patients with thromboembolic manifestations in our study was less than that of Klok et al. [3] who observed thrombotic complications in 31% of ICU patients in a multicenter cohort of 180 patients admitted to the ICU of three Dutch hospitals, and that difference was due to the specific group of patients that they studied as all patients were in the ICU.
The presence of hypercoagulation and thromboembolic complications had been noted to correlate with disease severity and ICU admission [14]. In our study, 85 patients (68.5%) were admitted to the ICU.
In the current study, pulmonary embolism was the most common complication presented in 56 patients (45.2%) that was similar to Grillet et al. [15] who stated that pulmonary embolism is the most common thromboembolic complication of COVID-19; it has been presented radiologically in up to 30% of patients with COVID-19 on pulmonary CT angiography and in 14% of ICU patients diagnosed with COVID-19 pneumonia Figs. 3, 4 and 5.
In a meta-analysis conducted by Xiong et al. [16], they found that prothrombin time and d-dimer levels were significantly higher in patients with severe COVID-19 than in those with the mild disease. Lorant et al. [17] stated that COVID-19 patients with pulmonary embolism have higher d-dimer levels than those without pulmonary emboli and are more likely to be admitted to the ICU. They also reported that d-dimer > 2660 ng/mL has 100% sensitivity and 67% specificity for pulmonary embolism diagnosis prediction in COVID-19 patients, and that was the same in our study which found that highest d-dimer average value was found in patients with pulmonary embolism (average 2765.45 ± 169.11).
As a complication of pulmonary embolism, the lung infarction is rare due to the dual arterial supply of the lung, but it has been described in COVID-19 patients. On CT, lung infarction appears as ground-glass opacities in the early phases in unobstructed lung zones that represents pulmonary haemorrhage and peripheral wedge-shaped pulmonary consolidation [18, 19].
Therefore, the radiological findings of lung infarction from pulmonary embolism should be differentiated from GGO as well as consolidations of the COVID-19 pneumonia that may also show reverse a halo sign in about 4% of patients as this will positively impact the patient management. In non-enhanced CT, the presence of peripheral lung opacities with a reverse halo sign, dilatation of pulmonary trunk, and/or increased cardiac volume (particularly, enlargement of the right cardiac chamber) indicate risk of PE and may aid in the decision to perform CT pulmonary angiography to confirm or exclude pulmonary embolism [20]. Clinical parameters including highly elevated d-dimer levels, haemoptysis, and/or sudden worsening of respiratory function or chest pain should also be considered [21].
We have identified 14 patients with radiological findings that favor the evidence of lung infarction more than the classic GGO and consolidations of COVID-19. These patients had higher d-dimer levels with dilatation of the affected segment of the pulmonary artery. The peripheral wedge-shaped consolidation was associated with thrombus of the related subsegmental artery (Figs. 6 and 7).
In the current study, we reported 32 patients with acute cerebrovascular manifestations, 27 (65.6%) of them had evidence of vascular occlusion (arterial in 18 patients Fig. 8 and venous sinus thrombosis in 9 patients Fig. 9) and 7 (21.88%) had haemorrhagic stroke. These results are close to those of Li et al. [22] who reported cerebrovascular manifestations for (6%) of 221 COVID-19 patients in a retrospective case series from Wuhan: 5% patients developed ischaemic strokes, < 1% intracerebral haemorrhage, and < 1% cerebral venous sinus thrombosis. However, the number of patients in our results was much less than the patients of Benussi et al. [23] who reported that (77%) of 55 COVID-19 patients admitted to one neurology unit with cerebrovascular disease, 35 of them had ischaemic stroke, three patients had haemorrhagic stroke, and five had transient ischaemic attacks. This difference is likely due to specific patient’s group that they studied as it was specialized neurology unit.
In our study, five patients (12.5%) presented with small infarcts identified only on MRI with no definite vascular involvement. Figures 10 and 11 Kandemirli et al. [24] reported that 44% of ICU COVID-19 patients with neurological symptoms showed abnormal findings on brain MRI studies.
In a study done by Wichmannet et al. [25] on autopsy series, they found unsuspected deep vein thrombosis in the majority of COVID-19 patients, and that pulmonary embolism was the cause of death; also, Goldman et al. [26] stated that there is high incidence of arterial thrombosis in COVID-19 patients presenting with ischaemic leg symptoms (100% of cases in their cohort). They found that lower extremity arterial thrombosis associated with COVID-19 is characterized by greater thrombus burden and increased rate of amputation and death. In our study, 17 patients had peripheral thromboembolic manifestations, 9 patients (52.9%) had deep venous thrombosis of the lower limb, 2 patients (11.8%) had deep venous thrombosis of the upper limb, 5 patients (29.4%) had lower limb ischaemia Fig. 12, and one patient (5.9%) had upper limb ischaemia.
Bhayana et al. [27], in their study, described radiological abnormalities detected on abdominal CT in about 42% of COVID-19 patients as large or small bowel thickening, pneumatosis intestinale, portal vein gas, or bowel perforation, and also bowel ischaemia or necrosis was demonstrated in some of these patients who underwent surgery. In addition, acute infarction in abdominal solid organs was demonstrated in 4.8% of patients.
In the current study, we reported 19 cases with gastrointestinal thromboembolic complications, 17 venous thrombosis (89.5%) and 2 arterial embolism (10.5%). The most presenting symptom was abdominal pain in 18 patients (94.7%). Isolated superior mesenteric vein thrombosis was detected in 4 patients (21%), isolated portal vein thrombosis occurred in 3 patients (15.8%), isolated inferior vein thrombosis was detected in 1 patients (5.3%), and combination of more than one vein thrombosis was detected in 9 patients (47.4%) Fig. 13. Arterial thrombosis was detected in the superior mesenteric artery in 2 patients (10.5%) and both of them presented with bowel ischaemia and intestinal obstruction.