(Table 2)
Spontaneous rupture of a macroscopically and microscopically normal spleen is a debated entity with an unclear mechanism. In fact, it could be a delayed break on a trauma that may have been forgotten by the patient or even not noticed [6].
Several hypotheses concerning the pathophysiology of spontaneous rupture have been put forward: the spleen presents a diseased focus which disappears during the rupture and is no longer found during the anatomopathological analysis; anatomical variations make the spleen more mobile, which undergoes repeated twisting that leads to congestion and eventually rupture; the congestion can also come from a reflex spasm of the splenic vein; the splenic artery may rupture on localized vascular anomaly [6]. Physiological activities that increase intra-abdominal pressure may result in repeated injury to the capsule [10]. Indeed, the trauma may be minor such as lifting a heavy weight, coughing, vomiting, or defecating [10][11].
The classic symptomatology is a pain in the left hypochondrium that can radiate to the homolateral shoulder [12]. Clinical features such as tenderness, muscle guarding on the palpation and signs of hemodynamic shock are often present [6]. However, the pain can be described as crampy or sharp [13]. Sometimes the symptomatology may be more confusing and may mimic a myocardial infarction or pulmonary embolism in the setting of chest pain with hemodynamic instability [14]. It can also be confused with a gastric ulcer, acute appendicitis, ectopic pregnancy or diverticulitis [6]. In fact, in the face of abdominal pain and hypotension, ASR remains a diagnosis of exclusion [11].
The diagnostic procedure is based on the hemodynamic status of the patient. Thus, in the unstable patient, the extended focused assessment sonography for trauma (E-FAST) is the technique of choice for rapid demonstration of free fluid. While the intravenous contrast computed tomography scan of the abdomen remains the gold standard for the stable or well stabilized patient [15].
Hemodynamically unstable patients (transfusion dependent or on vasopressors) should have an emergency laparotomy for splenectomy [15].
At the end of the first decade of the 21st century, DOACs arrived on the market for the prevention of stroke and systemic thrombus in non-valvular atrial fibrillation and for the treatment of deep vein thrombosis and pulmonary embolism. They are increasingly prescribed because, unlike vitamin K antagonists, they do not require close monitoring and are safer in terms of major bleeding with less intracranial bleeding [16]. As a result, the physician is increasingly confronted with its complications. Although DOACs have fewer drug interactions than vitamin K antagonists, molecules can interfere with their metabolism and increase the risk of bleeding. Those molecules are the permeability glycoprotein (P-gp) inhibitors and enzyme 3A4 of cytochrome P450 (CYP3A4) inhibitors. Co-medication with antiplatelet therapy also increases de bleeding risk [17][18].
DOAC intake should be adjusted or even avoided in case of renal or hepatic impairment [17].
The two reviews mentioned above were conducted up to 2008 [4] and 2011 [3] and do not mention the type of anticoagulant. We therefore searched the literature for cases of RSA related to DOACs.
We therefore searched Pubmed and Google scholar for cases of ASR related to DOACs with the keywords ”rivaroxaban” ”apixaban” ”dabigatran” ”betrixaban” ”edoxaban” and ”splenic rupture”. Abstracts and full texts written in French and English until June 2022 were included in our research. We found 13 other cases in addition to ours [19][20] [21] [22] [23] [24] [25] [26] [27] [28] [29] [30]. We have summarized them in Table 3.