The outbreak of the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection, responsible for coronavirus disease 2019 (COVID‐19), has rapidly reached a pandemic spreading.

Contagion mainly occurs through the upper respiratory tract that is often involved in early disease, and pulmonary damage is the main cause of death. Nevertheless, SARS‐CoV‐2 can virtually localize in every organ, engendering site‐specific damage.¹

COVID‐19 complications due to the prothrombotic potential associated with SARS‐CoV‐2 infection go beyond deep venous thrombosis and pulmonary thromboembolisms (PTEs).² Additional extrapulmonary tissues, such as heart, brain, and splanchnic organs, may be affected by thromboembolic events, likely originating from large vessels or due to microcirculation damage, across a wide spectrum of clinical severity.³

Here we report the case of a COVID‐19 patient who developed PTEs, multiple floating thrombi in the aorta and splenic infarcts, as well as a large hepatic lesion, suspected for intrahepatic cholangiocarcinoma, turning out to be a sequela of portal vessel damage.

The patient, a 68‐year‐old man, suffered from hypertension, type II diabetes mellitus, and dyslipidemia. He was receiving atorvastatin and metformin as chronic medications. No prior thrombosis or cerebrovascular events were recorded in the past medical history.

In late March 2020, the patient was hospitalized for worsening of dyspnea and oxygen desaturation, in the context of fever and dry cough. High‐resolution computer tomography (HRCT) showed lung bilateral ground‐glass infiltrates, consistent with COVID‐19 interstitial pneumonia (Figure 1A), and the patient tested positive for severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) RNA. High‐flow oxygen therapy was started (reservoir mask at 15 L/min, fraction of inspired oxygen [FiO₂]: 80%). Main therapy consisted of hydroxychloroquine and colchicine, antibiotic and antiviral therapy, cardio aspirin 100 mg daily and enoxaparin 8000 IU daily, both as prophylaxis. Given the respiratory deterioration, a contrast‐enhanced computerized tomography (CT) scan was performed. The pulmonary disease progressed to extensive consolidations in all the lobes, with a prevalent subpleural distribution, bilateral segmental pulmonary embolism was also documented. In addition, some eccentric parietal thrombi at the level of the aortic arch, descending aorta passage, descending aorta, abdominal aorta, and upper mesenteric artery were detected (Figure 1B,C). Collaterally, an irregularly, polylobulate, hypodense lesion, with ill‐defined margins, was reported at the VI hepatic segment (4 × 5 cm), highly evocative for an intrahepatic cholangiocarcinoma (Figure 1D,E). Moreover, the presence of multiple infarcts (hilum and upper pole) in the spleen was recorded (Figure 1C). Given the pulmonary embolism, low‐molecular‐weight heparin (LMWH) posology was augmented to therapeutic dose (enoxaparin 6000 IU + 8000 IU). Liver function tests remained normal during the hospitalization. Due to the progressive clinical improvement, the patient was discharged at home on at the end of April 2020, with the indication to maintain therapy with cardio aspirin and LMWH.

In the post‐hospitalization regimen 1 month after the baseline exam, the patient underwent a novel contrast‐enhanced CT scan. The aortic thrombi and the splenic ischemic foci appeared significantly reduced (Figure 1B,C), while the hepatic lesion was unchanged (Figure 1D,E). As malignancy was suspected, a contrast‐enhanced ultrasonography (CEUS) was performed. CEUS showed mild enhancement in the arterial phase with progressive washout and hypoechoic aspect in the portal and late vascular phase, a behavior that could not exclude a malignant diagnosis (Figure 1F,G). A liver biopsy was performed (Figure 2). The histology showed an inflammatory lesion characterized by portal‐based confluent linpho‐histiocytic and plasma cellular infiltrates. There was no evidence of neoplasia. Alongside the clinical history of the patient, the pattern of damage was suggestive of a resolving abscess likely due to an underlying pylephlebitis, complicated by a portal venular damage sustained by an altered coagulative state.

The peculiar tropism of SARS‐CoV‐2 for the endothelium,⁴ coupled with the perturbation of the thromboembolic homeostasis, is a major determinant in COVID‐19 morbidity and mortality. In our case, we hypothesize that the splenic ischemic lesions were a consequence of the embolic sprouting of floating aortic thrombi.

The manifestations of SARS‐CoV‐2 can mimic a neoplastic disease, as show in the present case and by Efe et al.,⁵ who surgically removed a highly symptomatic temporal mass in a young patient with the suspicion of a glial tumor, turning out to be COVID‐19‐related encephalitis. The clinical stability of our patient allowed a conservative approach, leading to a definitive diagnosis of a portal vasculopathy engendering extensive liver damage and excluding a cholangiocarcinoma, evoked by the radiological aspect of the hepatic lesion. Functional hepatic damage is known in COVID‐19 patients,⁶ while vascular damage, including portal vein thrombosis and gallbladder vasculitis,^7-9 have been described in affecting hepatic circulation.¹⁰

严重急性呼吸系统综合症冠状病毒2（SARS‐CoV‐2）感染的爆发是造成2019年冠状病毒病（COVID‐19）的迅速蔓延。

传染主要通过通常与早期疾病有关的上呼吸道发生，而肺损伤是主要的死亡原因。尽管如此，SARS-CoV-2几乎可以在每个器官中定位，从而造成特定地点的损害。^1个

由SARS-CoV-2感染引起的潜在血栓形成可能导致的COVID-19并发症超出了深静脉血​​栓形成和肺血栓栓塞（PTE）的范围。²其他广泛的肺外组织，例如心脏，大脑和内脏器官，可能受到血栓栓塞事件的影响，这些事件可能来自大血管，也可能是由于微循环损伤，在广泛的临床严重性范围内。³

在此我们报道了一名COVID-19患者，该患者发展为PTE，主动脉多处漂浮的血栓和脾梗塞以及疑似肝内胆管癌的大肝病灶，结果证明是门脉血管损伤的后遗症。

该患者为68岁的男性，患有高血压，II型糖尿病和血脂异常。他正在接受阿托伐他汀和二甲双胍作为慢性药物。在过去的病史中没有记录过先前的血栓形成或脑血管事件。

2020年3月下旬，患者因发烧和干咳而呼吸困难和氧气饱和度下降而住院。高分辨率计算机断层扫描（HRCT）显示肺部双侧毛玻璃样浸润，与COVID-19间质性肺炎一致（图1A），该患者的重症急性呼吸综合征冠状病毒2（SARS-CoV-2）RNA检测呈阳性。开始进行高流量氧气治疗（储气罐面罩以15 L / min的速度吸入氧气[FiO ₂]：80％）。主要治疗方法为预防性治疗，包括羟氯喹和秋水仙碱，抗生素和抗病毒治疗，心肺阿司匹林每天100 mg和依诺肝素每天8000 IU。考虑到呼吸系统恶化，进行了对比增强的计算机断层扫描（CT）扫描。肺部疾病在所有肺叶中均进展为广泛的巩固性病变，伴有广泛的胸膜下分布，也记录了双侧节段性肺栓塞。此外，在主动脉弓，降主动脉通道，降主动脉，腹主动脉和肠系膜上动脉的水平上检测到了一些偏心的顶叶血栓（图1B，C）。附带报道，在VI肝段（4×5 cm）有不规则，多叶，低密度的病灶，边缘不清楚。肝内胆管癌的高度唤起作用（图1D，E）。此外，记录到脾脏中存在多个梗塞（肺门和上极）（图1C）。考虑到发生肺栓塞，低分子量肝素（LMWH）的剂量增加至治疗剂量（依诺肝素6000 IU + 8000 IU）。住院期间肝功能检查保持正常。由于临床上的逐步改善，该患者于2020年4月底在家出院，适应症为继续使用阿司匹林和LMWH进行治疗。住院期间肝功能检查保持正常。由于临床上的逐步改善，该患者于2020年4月底在家出院，适应症为继续使用阿司匹林和LMWH进行治疗。住院期间肝功能检查保持正常。由于临床上的逐步改善，该患者于2020年4月底在家出院，适应症为继续使用阿司匹林和LMWH进行治疗。

在基线检查后1个月的住院后治疗方案中，对患者进行了新的对比增强CT扫描。主动脉血栓和脾缺血灶似乎显着减少（图1B，C），而肝病灶未改变（图1D，E）。由于怀疑为恶性肿瘤，因此进行了超声造影检查（CEUS）。CEUS在动脉期显示轻度增强，在门脉期和晚期血管期逐渐出现冲洗和低回声，这种行为不能排除恶性诊断（图1F，G）。进行了肝活检（图2）。组织学显示炎性病变，其特征是基于门静脉的融合型嗜肝细胞和浆细胞浸润。没有瘤形成的证据。除了患者的临床病史，

内皮的SARS-CoV-2特有的向性⁴以及血栓栓塞稳态的扰动是COVID-19发病率和死亡率的主要决定因素。在我们的案例中，我们假设脾脏缺血性病变是漂浮的主动脉血栓栓塞萌发的结果。

如本例和Efe等人[ ^5]所示，SARS-CoV-2的表现可模仿肿瘤性疾病，他们通过外科手术切除了怀疑患有神经胶质瘤的年轻患者的高度症状性颞骨肿块，结果证明是与COVID-19相关的脑炎。我们患者的临床稳定性允许采取保守的方法，从而导致对门脉血管病变的明确诊断，从而引起广泛的肝损伤，并且排除了由肝病灶的放射学方面引起的胆管癌。功能性肝损害在COVID-19患者中是已知的[ ^6]，而血管损害（包括门静脉血栓形成和胆囊血管炎）[ ^7-9]被描述为影响肝循环。¹⁰