(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.