A 35-year-old male presented with upper abdominal pain of one week's duration, characterized as intermittent dull pain with episodic exacerbation, occurring without obvious inciting factors. The pain worsened after eating but was unaffected by positional changes. There was no radiation, referred pain, acid reflux, belching, hematemesis, or melena. Initial upper endoscopy revealed chronic atrophic gastritis (C1) with erosions and bile reflux; testing for Helicobacter pylori (HP) was positive. A diagnosis of chronic gastritis was made, and treatment with acid suppression, gastric mucosal protection, prokinetics, and HP eradication was initiated. However, the abdominal pain intensified three days later, prompting hospital admission. Physical examination revealed epigastric tenderness without rebound tenderness or palpable masses; Murphy's sign was negative. Laboratory findings included: D-dimer 3.32 mg/L, prothrombin time 21.1 s, fibrinogen 4.426 g/L; potassium 3.15 mmol/L, alanine aminotransferase (ALT) 168 U/L, aspartate aminotransferase (AST) 63 U/L, gamma-glutamyl transferase (GGT) 182 U/L, alkaline phosphatase (ALP) 167 U/L, total bile acids 27.0 μmol/L, blood glucose 9.55 mmol/L. On the third hospital day, the patient experienced worsening hemorrhoids. The patient was admitted for further evaluation. An upper abdominal Doppler ultrasound was performed on hospital day 2, which revealed hepatic steatosis but failed to identify the portal vein thrombosis. Consequently, a contrast-enhanced CT scan was obtained on hospital day 7, which confirmed the diagnosis.

A 45-year-old male presented with continuous, distending abdominal pain of three days' duration, primarily localized periumbilically and in the upper abdomen, without apparent cause, radiation, or positional relief. The pain intensified one day prior to presentation. Symptomatic treatment at a community clinic provided no relief; he subsequently developed nausea and vomited gastric contents once, without hematemesis or coffee-ground material. Physical examination revealed tenderness in the right and lower abdomen with mild rebound tenderness, no significant guarding, no visible peristalsis, no costovertebral angle tenderness, negative Murphy's sign, and active bowel sounds. Laboratory results showed: D-dimer 7.32 mg/L, prothrombin time 15.7 s, fibrinogen 5.160 g/L; ALT 51 U/L, GGT 434 U/L, ALP 219 U/L, albumin 39.0 g/L, direct bilirubin 8.3 μmol/L. An abdominal contrast-enhanced CT scan was performed on the day of admission to establish the etiology of his acute abdomen.

APVT is defined by the recent formation of thrombi within the portal vein and other mesenteric veins, in the absence of pre-existing cavernous transformation or portal hypertension (6). Its pathogenesis aligns with Virchow's triad: venous stasis, endothelial injury, and hypercoagulability (7). Risk factors for APVT (6, 8) encompass acquired or hereditary thrombophilia, myeloproliferative neoplasms, paroxysmal nocturnal hemoglobinuria, systemic conditions (malignancy, autoimmune diseases, pregnancy), and local inflammatory or traumatic factors [appendicitis, diverticulitis (9), inflammatory bowel disease, pancreatitis, trauma, surgery]. Case 1 exemplifies hereditary thrombophilia associated with the *PAI-1* 4G/5G genotype. Type 1 plasminogen activator inhibitor (PAI-1) is the primary inhibitor of tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA) in the body's plasma, and it is responsible for regulating the balance between coagulation and fibrinolysis. Elevated levels of PAI-1 predispose the body to thrombus formation. Studies have shown that several polymorphisms in the PAI-1 gene are associated with the level of PAI-1 activity in plasma. It has been identified that a guanosine insertion/deletion polymorphism exists in the promoter region of the PAI-1 gene at the −675 bp position, and this polymorphism is referred to as the 4G/5G polymorphism. in vitro studies indicate that the 4G allele exhibits higher activity than the 5G allele; it can increase the plasma PAI-1 concentration by upregulating the expression of the PAI-1 gene. This places patients with the *PAI-1* 4G/5G genotype in a hypercoagulable state, which is manifested as a thrombotic tendency (10). Although APVT is less common than chronic portal vein thrombosis in cirrhosis, over half of patients have at least one identifiable risk factor; local factors are present in about one-fifth, while approximately one-quarter have no discernible cause (“idiopathic”). Case 2 in our study is consistent with this clinical pattern—after systematic evaluation, no acquired, local, or hereditary risk factors were detected, and it was therefore classified as idiopathic APVT. Notably, SARS-CoV-2 infection impacts all components of Virchow's triad, making venous thromboembolism (VTE), including splanchnic vein thrombosis, a recognized complication of COVID-19, with reported prevalence up to 8% in hospitalized patients (11). Thromboembolic events like APVT can occur weeks after resolution of acute COVID-19 symptoms and have also been associated with COVID-19 vaccination; several cases of APVT linked to SARS-CoV-2 infection have been documented (12, 13). Therefore, in the context of the ongoing pandemic, obtaining relevant SARS-CoV-2 exposure and vaccination history is crucial.

Non-specific abdominal pain is the predominant symptom, occurring in up to 90% of APVT patients, often accompanied by nausea, fever, or diarrhea. Thrombosis extending into mesenteric veins can precipitate intestinal ischemia, manifesting as vomiting, diarrhea, rectal bleeding, or splenomegaly, potentially progressing to sepsis. Untreated vascular occlusion risks catastrophic complications like intestinal perforation (14), peritonitis, shock, and multi-organ failure (2); mortality associated with bowel necrosis can reach 50%–75% (15). Elevated C-reactive protein (CRP) is observed in approximately 80% of patients (16). Based on thrombus extent and vascular occlusion severity, APVT can be classified (6): Grade 1 (portal vein involvement only, occlusion <50%, minimal/no SMV involvement); Grade 2 (portal vein occlusion ≥50%); Grade 3 (complete occlusion of portal vein and proximal SMV); Grade 4 (complete occlusion of portal vein and SMV). Systemic anticoagulation is the first-line treatment (8). Endovascular interventions (mechanical thrombectomy—balloon, rheolytic, or aspiration—and catheter-directed thrombolysis) (17) are indicated for patients with signs of impending bowel ischemia or contraindications to anticoagulation.

Contrast-enhanced CT is highly accurate, reliable, sensitive, and specific for diagnosing APVT (18). Key direct findings include: venous dilation secondary to acute thrombus; iso- or hyperdense thrombus on unenhanced scans (varying with thrombus composition) (19); perivascular fat stranding due to edema/inflammation (20); and non-enhancing filling defects within the opacified venous lumen on contrast-enhanced scans. Peripheral rim enhancement of the vein may sometimes be seen, attributed to perithrombotic flow or venous wall inflammation (21). CT precisely delineates thrombus location and extent (22). APVT can be categorized based on involved vessels (23): intrahepatic portal vein, extrahepatic portal vein, combined intra/extrahepatic portal vein, or mesenteric/splenic vein. Indirect signs vary: intrahepatic involvement often causes perfusion abnormalities (e.g., transient hepatic attenuation differences); mesenteric vein involvement typically manifests as bowel wall thickening, edema, and luminal dilation, potentially progressing to hemorrhage in severe cases. Other indirect signs include ascites, mesenteric edema/stranding, luminal fluid, and (rarely) portal venous gas or bowel wall pneumatosis. CT also aids in identifying potential underlying causes (e.g., inflammation, malignancy) and complications (e.g., bowel ischemia, portal hypertension features like ascites, splenomegaly, collaterals). Untreated APVT may progress to cavernous transformation of the portal vein, observable within 15–30 days of symptom onset; linear thrombus calcification and established collaterals suggest chronicity (19).

CT is invaluable for post-treatment follow-up. Attali et al. (24) classified outcomes on follow-up CT (within the first year of anticoagulation) as: “Recanalization” (no residual thrombus), “Intermediate” (stable or partially recanalized thrombus), or “Worsening” (increased/extended or new thrombus). Their cohort showed 30%, 52%, and 18% in these groups, respectively. Standardized imaging reporting is essential. The American Association for the Study of Liver Diseases (AASLD) recommends descriptions include (25): Thrombus site/extent: Specify involvement of intrahepatic portal veins, main portal vein trunk, splenic vein, mesenteric veins; describe thrombus length and segmental relationships. Luminal obstruction: Characterize as complete (100% occlusion), partial (>50% occlusion), mild (<50% occlusion), or cavernous transformation. Chronicity/Dynamics: Note chronic features or changes from prior imaging.

Beyond contrast-enhanced computed tomography, ultrasonography and MRI also serve as crucial imaging tools for the diagnosis and follow-up of APVT. In APVT, two-dimensional ultrasonography can demonstrate dilation of the portal vein lumen. The thrombus itself typically appears isoechoic or hypoechoic. Some fresh thrombi, due to a higher red blood cell content, may present as slightly hyperechoic, creating a marked contrast against the surrounding anechoic blood (26). If the thrombus extends to the superior mesenteric or splenic veins, dilation of these respective veins with heterogeneous intraluminal echogenicity can be observed. Color Doppler Ultrasonography (CDU) further enables the assessment of portal venous hemodynamic changes. In complete APVT, the portal vein lumen shows an absence of color flow signals, and pulsed-wave Doppler fails to detect a flow spectrum. Conversely, incomplete APVT is characterized by color flow filling defects within the lumen, accompanied by decreased flow velocity and potentially turbulent signals (18). It is important to note that the diagnostic accuracy of CDU can be influenced by operator expertise, patient body habitus (e.g., obesity), and interference from bowel gas (27).

MRI offers the advantages of being radiation-free and utilizing multi-parametric imaging, making it particularly suitable for pregnant women, pediatric patients, and individuals with contraindications to iodinated contrast media. The MRI appearance of APVT has characteristic features. On T1-weighted imaging (T1WI), acute thrombus (<30 days), rich in deoxyhemoglobin, usually appears isointense or slightly hypointense. On T2-weighted imaging (T2WI), it typically presents as hyperintense; this signal can be more pronounced in fresh thrombi due to their high water content. Magnetic Resonance Venography (MRV), a non-invasive vascular imaging technique, can directly visualize filling defects within the portal vein lumen, clearly defining the extent of thrombus involvement (21).