Objective: Pulmonary thrombosis is observed in severe acute respiratory syndrome coronavirus 2 pneumonia. Aim was to investigate whether subpopulations of platelets were programmed to procoagulant and inflammatory activities in coronavirus disease 2019 (COVID-19) patients with pneumonia, without comorbidities predisposing to thromboembolism. Approach and Results: Overall, 37 patients and 28 healthy subjects were studied. Platelet-leukocyte aggregates, platelet-derived microvesicles, the expression of P-selectin, and active fibrinogen receptor on platelets were quantified by flow cytometry. The profile of 45 cytokines, chemokines, and growth factors released by platelets was defined by immunoassay. The contribution of platelets to coagulation factor activity was selectively measured. Numerous platelet-monocyte (mean±SE, 67.9±4.9%, n=17 versus 19.4±3.0%, n=22; P <0.0001) and platelet-granulocyte conjugates (34.2±4.04% versus 8.6±0.7%; P <0.0001) were detected in patients. Resting patient platelets had similar levels of P-selectin (10.9±2.6%, n=12) to collagen-activated control platelets (8.7±1.5%), which was not further increased by collagen activation on patient platelets (12.4±2.5%, P =nonsignificant). The agonist-stimulated expression of the active fibrinogen receptor was reduced by 60% in patients ( P <0.0001 versus controls). Cytokines (IL [interleukin]-1α, IL-1β, IL-1RA, IL-4, IL-10, IL-13, IL, 17, IL-27, IFN [interferon]-α, and IFN-γ), chemokines (MCP-1/CCL2 [monocyte chemoattractant protein 1]), and growth factors (VEGF [vascular endothelial growth factor]-A/D) were released in significantly larger amounts upon stimulation of COVID-19 platelets. Platelets contributed to increased fibrinogen, VWF (von Willebrand factor), and factor XII in COVID-19 patients. Patients (28.5±0.7 s, n=32), unlike controls (31.6±0.5 s, n=28; P <0.001), showed accelerated factor XII–dependent coagulation. Conclusions: Platelets in COVID-19 pneumonia are primed to spread proinflammatory and procoagulant activities in systemic circulation.

Background/Aims: To report a case of bleeding after pancreatoduodenectomy in a patient with pancreatic leak and portal thrombosis who was successfully treated with an endovascular approach. Methods: A 58-year-old male, suffering from neoplasm of the distal bile duct, underwent a pylorus-preserving Whipple procedure. On the 18th day, following a sudden drop in pressure and low haematocrit values, the patient underwent surgery. The source of the bleeding was not found. Six days later, following the appearance of bleeding from the abdominal drainage and haematemesis with shock, the patient had an immediate angiography. Bleeding from the gastroduodenal artery stump was evident, the portography showed no portal flow. With respect to the shortness of the stump, safe embolisation with coils, while preserving the common hepatic artery patency, was difficult to obtain. Results: By transcatheter placement of covered stents into the hepatic artery and thereby occluding the origin of the gastroduodenal artery, the bleeding was stopped. After 2 months, CT angiography showed patency of both the common and proper hepatic arteries. Nine months after the procedure the patient is in good health. Conclusions: Percutaneous placement of covered stents can be the solution in cases where transcatheter embolisation is not recommendable because of portal vein thrombosis.

To assess the technical and clinical success of endovascular treatment of arterial bleeding in pancreatitis. From 1992 to 2005, 28 patients with pancreatitis underwent endovascular treatment of associated arterial lesions. Fifteen patients were affected by acute pancreatitis and 13 by chronic pancreatitis. The diagnosis was obtained according to medical history and clinical and laboratory evidence of disease. Arterial involvement was diagnosed by non-invasive imaging and angiography. After treatment, all patients underwent CT scanning at a minimum of 15, 30 and 90 days. We evaluated the feasibility of embolization and patients' survival at 90 days. Transcatheter embolization was feasible in 26/28 patients (93%). In 2 patients with acute pancreatitis, selective catheterization failed so we could not proceed with the angiographic approach. After treatment, there were 3/26 rebleeds (11.5%), all of whom died within the first week. At 90 days' follow-up, 21/26 patients (81%) were alive. Two of 26 patients (8%) suffered splenic complications. Among the 13 patients with acute pancreatitis, 8 (61.5%) were alive after 90 days. All 13 patients with chronic pancreatitis were alive after 90 days. Comparing our results with the surgical literature, we found that embolization is less invasive and, at least, as successful as surgery. Thus, it should be considered the first choice in pancreatitis arterial complications.

Cross-sectional imaging of the upper abdomen, especially if intravenous contrast has been administered, will most likely reveal any acute or chronic disease harbored in the spleen. Unless imaging is performed with the specific purpose of evaluating the spleen or characterizing a known splenic lesion, incidentally discovered splenic lesions pose a small challenge. Solitary benign splenic lesions include cysts, hemangiomas, sclerosing angiomatous nodular transformation (SANT), hamartomas, and abscesses, among others. Sarcoidosis and tuberculosis, although predominantly diffuse micronodular disease processes, may also present as a solitary splenic mass lesion. In addition, infarction and rupture, both traumatic and spontaneous, may take place in the spleen. This review aims to describe the imaging features of the most common benign focal splenic lesions, with emphasis on the imaging findings as these are encountered on routine cross-sectional imaging from a multicenter pool of cases that, coupled with clinical information, can allow a definite diagnosis.