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\begin{document}

\title{Atraumatic splenic rupture in a patient treated with rivaroxaban: a case
report and a narrative review.}



\author[1]{Marie-Laure Labaki}%
\author[1]{Marc De Kock}%
\affil[1]{Centre Hospitalier de Wallonie Picarde}%


\vspace{-1em}



  
  \date{June 18, 2024}


\begingroup
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\selectlanguage{english}
\begin{abstract}
A narrative review based on the case of a patient presenting an atypical
symptomatology of an atraumatic splenic rupture induced by rivaroxaban.
An emergency splenectomy had to be performed. This complication is rare
but increasing since the popularity of direct oral anticoagulants and
the diagnosis is often delayed.%
\end{abstract}%



\sloppy


Atraumatic splenic rupture in a patient treated with rivaroxaban: a case
report and a narrative review.

Authors: Labaki M.-L.*; De Kock M.**

*Department of Intensive Care, Centre Hospitalier de Wallonie Picarde
(CHwapi), Tournai, Belgium. E-mail:\emph{labaki.ml@gmail.com}

**Department of Intensive Care, Centre Hospitalier de Wallonie Picarde
(CHwapi), Tournai, Belgium. E-mail:\emph{marcdekock1888@gmail.com}

Abstract:

\emph{Introduction} : Atraumatic splenic rupture (ASR) is rare, mostly
associated with neoplastic, infectious and inflammatory diseases. ASR
related to drug treatment is infrequent. In this case report we
highlight an unusual complication of the direct oral anticoagulant
rivaroxaban.

\emph{Case presentation} : A 64-year-old male patient was admitted in
the emergency department for lipothymic illness on diffuse abdominal
cramps. There is no history of recent trauma. The clinical examination
showed hemodynamic instability with moderate response to filling and a
mild abdominal discomfort on palpation. His medical history included
chronic hypertension, chronic constipation and a recent atrial flutter
ablation. He was taking amiodarone, bisoprolol, atorvastatin, and
rivaroxaban 20 mg. The diagnosis of splenic rupture was made several
hours later with an abdominal CT scan with contrast injection. A massive
blood transfusion and an emergency laparotomy for splenectomy were
performed. The anatomopathological analysis did not reveal any cause of
neoplastic, inflammatory or infectious cause. The patient was
successfully discharged from intensive care unit 3 days later.

\emph{Conclusion} : Clinicians must remember the potential ASR as
complication due to direct oral anticoagulants when they are confronted
to a patient with abdominal tenderness and hemodynamical instability.
Unfortunately, the clinical presentation is not always typical of a
ruptured spleen. Delayed diagnosis can be life-threatening and fatal.
Splenectomy by laparotomy remain the best therapeutic option in case of
splenic rupture in unstable patients on direct oral anticoagulants.

Keywords: atraumatic splenic rupture, rivaroxaban, direct oral
anticoagulant, spontaneous splenic rupture, apixaban, dabigatran,
betrixaban, edoxaban.

Introduction:

The abdominal trauma is a well-known cause of splenic rupture {[}1{]}.
The major problem in atraumatic splenic rupture (ASR) is the missed or
delayed diagnosis and consequently, delayed management leading to fatal
outcome. In case of ASR, the mortality rate is around 12,2\%. {[}2{]}
Several systematic reviews of the literature reported that the main
etiologies are infectious, neoplastic and inflammatory. The drug-related
cause is even more rare {[}3{]}{[}4{]}. Since the emergence of direct
oral anticoagulants (DOAC) at the beginning of the 21st century,
physicians are increasingly confronted with their adverse effects and
complications. In this article we describe a case of ASR in a patient
treated with rivaroxaban according to CARE guidelines {[}5{]}. Then, we
made a narrative review of the literature by searching until June 2022
other similar cases in the \emph{Pubmed} and \emph{Google
scholar}databases with relevant keywords. Only cases written in French
and English were retained. We compared them and looked for factors
promoting splenic rupture and bleeding in patients taking rivaroxaban
and other DOAC.

Case presentation:

A 64-years-old male patient was admitted in the emergency department for
lipothymic illness on diffuse abdominal cramps. His medical history
included chronic hypertension, chronic constipation and an atrial
flutter ablation 6 days before. He was taking amiodarone, bisoprolol,
atorvastatin, and rivaroxaban 20 mg. There is no history of trauma or
infections in the previous months. Moreover, the patient has limited
contact with the outside world because of the covid-19 pandemic. His
parameters were a blood pressure at 85/55 mmHg, a sinusal cardiac rate
at 76 beats per minute, an oxygen saturation level of 99\% on room air
and a normal body temperature. The physical examination highlighted a
normal cardiopulmonary auscultation, a mild diffuse abdominal tenderness
at the palpation without guarding or irradiation.

He underwent several complementary tests. His blood tests (hemoglobin,
white blood cells, coagulation, ionogram, liver and kidney functions)
came back normal (Table 1). There was no increase in lactate on the
arterial blood gases. The urine spot is without particularity. The PCR
test for covid 19 is negative. The electrocardiogram shows a sinusal
rythm with a frequence around 70 beats per minute and no repolarisation
troubles.\selectlanguage{english}
\begin{longtable}[]{@{}llll@{}}
\toprule
\begin{minipage}[b]{0.22\columnwidth}\raggedright\strut
Variables\strut
\end{minipage} & \begin{minipage}[b]{0.22\columnwidth}\raggedright\strut
Value\strut
\end{minipage} & \begin{minipage}[b]{0.22\columnwidth}\raggedright\strut
Unit\strut
\end{minipage} & \begin{minipage}[b]{0.22\columnwidth}\raggedright\strut
Normal values\strut
\end{minipage}\tabularnewline
\midrule
\endhead
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Hemoglobin Hematocrit\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
13.6\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
g/dL\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
13.1-17.2\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Platelets\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
302\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
10e3/\selectlanguage{greek}µ\selectlanguage{english}L\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
168-411\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
White blood cells count Neutrophils Lymphocytes Monocytes Eosinophils
Basophils\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
10.15 6.12 3.025 0.548 0.061 0.071\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
10e3/\selectlanguage{greek}µ\selectlanguage{english}L 10e3/\selectlanguage{greek}µ\selectlanguage{english}L 10e3/\selectlanguage{greek}µ\selectlanguage{english}L 10e3/\selectlanguage{greek}µ\selectlanguage{english}L 10e3/\selectlanguage{greek}µ\selectlanguage{english}L 10e3/\selectlanguage{greek}µ\selectlanguage{english}L\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
3.7-9.5 1.5-6.5 1.2-3.9 0.2-0.8 \textless{} 0.500 \textless{}
0.190\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
A.P.T.T. P.T.T. I.N.R. Fibrinogen\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
26.0 \textgreater{}100 1.00 382\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Sec \% mg/dL\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
20-30 75-100 \textless{} 1.2 200-400\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
CRP\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
8.7\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
mg/dL\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\textless{} 5\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Urea Creatinine Sodium Potassium Chloride\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
37 0.98 139 3.8 104\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
mg/dL mg/dL mmol/L mmol/L mmol/L\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
16.6-48.5 0.70-1.20 135-145 3.5-5.1 97-110\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Total bilirubin Direct bilirubin Gamma glutamyl transferase Alkaline
phosphatase Alanine aminotransferase Asparate aminotransferase Lactate
dehydrogenase\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.49 0.17 37 56 33 36 143\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
mg/dL mg/dL U/L U/L U/L U/L U/L\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
[?] 1.2 \textless{} 0.3 15-85 40-129 15-37 16-61 87-241\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
HS Troponin\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
19.8\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
pg/mL\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\textless{} 78.5\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

Table 1: shows normal blood tests

Abbreviations: \emph{A.P.T.T.} : \emph{activated partial thromboplastin
time; P.T.T.: Partial thromboplastin time} ; \emph{I.N.R.: international
normalized ratio; CRP: C-reactive protein; HS Troponin: high-sensitivity
troponin}

Because of his recent flutter removal, a transthoracic cardiac
ultrasound is performed by the cardiologist on call and showed: a normal
cardiac function, no valvular disease, no ventricular overload and no
pericardial effusion.

He received as a treatment a painkiller and a filling of one litter of
crystalloid. After that, his blood pressure goes up slightly, but the
patient still has orthostatic discomfort. The cardiologist admitted him
in his cardiac service under telemetry for orthostatism on medications
and vagal illness on abdominal pain due to his chronic constipation.

During the night, the patient presented agitation, dyspnea and cutaneous
pallor. His blood pressure was low at 75/55 mmHg with a cardiac rate at
80 beats/minute. His pulsated blood oxygen saturation was unmeasurable.
Clinical examination showed signs of low capillary perfusion.
Considering the rivaroxaban intake and the recent atrial flutter
ablation, an intravenous contrast computed tomography scan of the
abdomen was performed and showed a splenic rupture with a subcapsular
hematoma (10 cm x 15 cm x 13 cm) and diffuse hemoperitoneum (Figure 1.).\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

\textbf{Figure 1:} Axial (A) and coronal (B) CT-scan showing subcapsular
hematoma (empty arrows), diffuse hemoperitoneum (arrow heads) and
residue or the ruptured spleen (full arrows).

A massive blood transfusion and an emergency laparotomy for splenectomy
were performed. In total, the patient received seven packed red blood
cells, six fresh frozen plasma and one pool of platelets. During the
laparotomy, the surgeon sucked out more than two liters of fresh blood
and clots. Hemostasis was rapidly obtained by ligation of the splenic
vessels and total removal of the spleen that had a large parenchymal
laceration. The anatomopathological analysis did not reveal any cause of
neoplastic, inflammatory or infectious cause. The patient was
successfully discharged from intensive care unit 3 days later. He
remained in the surgical ward for another week before going home.
Rivaroxaban has been permanently discontinued. The vaccines
against~encapsulated organisms have been administered. A holter monitor
was performed by the cardiologist at 1 and 4 months after surgery and
showed no recurrence of rhythm disorders. 10 months later, the patient
is morally and physically well and has completely resumed his daily
activities.

Discussion:

The abdominal trauma is the first and well-known cause of splenic
rupture {[}1{]}. Because ASR is rare, its diagnosis is often delayed,
and mortality is estimated at 12,2\% {[}2{]}. Mortality is increased in
cases of delayed diagnosis, splenomegaly, underlying neoplastic disease
and an age above 40 years {[}2{]} {[}4{]}.

The ASR can be classified into 2 categories: a pathological rupture (ASR
occurred on a diseased spleen) and idiopathic rupture (ASR occurred on a
healthy spleen), also called ``spontaneous rupture'' {[}6{]}. According
to Orloff and Peskin, an idiopathic rupture must meet 4 criteria: no
trauma history; no other diseased organs that can cause the splenic
rupture; no peri-splenic adhesions or pre-existing scars; a
macroscopically and histologically normal spleen {[}7{]}. Later, Crate
and Payne proposed a 5\textsuperscript{th} criterion: no increase in
serological antibody titer in the acute and convalescent phase
suggesting a recent viral infection known to be involved in splenic
rupture {[}8{]}.

In a systematic review, F Kris Aubrey-Bassler and Nicholas Sowers showed
that most of the time spleen rupture was the first symptom of an unknown
underlying disease. Indeed, due to its important vascularization, if the
spleen is afflicted by disease, the risk of rupture after a trivial
stress is increased {[}9{]}. In the literature, many authors misuse the
word ''spontaneous'' instead of the term ''pathological'' or
''atraumatic'' {[}3{]}. ``True spontaneous'' splenic rupture is very
rare. In this same review, 47 cases out of 613 (7,6\%) were associated
with drugs, 21 of which were associated with anticoagulants {[}3{]}. In
another review, P. Renzulli et al. identified 845 patients with ASR and
divided them into 6 etiological groups (Table 2). They showed a ratio
male : female of 2 : 1 and a mean age of 45. Of the 845 cases, 67 were
associated with drugs, 22 of which were anticoagulants. Only 59 patients
(7\%) had a spleen described as normal and no causal factor was found.
465 patients (55\%) had splenomegaly. 84\% underwent total splenectomy
as first-line treatment. 14.9\% of the patients with a conservative
treatment had splenectomy for rebleeding. The percentage of surgical
management is much higher than in the case of traumatic rupture. This is
explained by a higher rate of conservative treatment failure associated
with an abnormal spleen and by an older population {[}4{]}.\selectlanguage{english}
\begin{longtable}[]{@{}l@{}}
\toprule
Atraumatic rupture spleen etiologies\tabularnewline
\midrule
\endhead
Neoplastic disorders 30.3\%\tabularnewline
Infectious disorders 27.3\%\tabularnewline
Inflammatory non infectious disorders 19.9\%\tabularnewline
Drug and treatment related 9.1\%\tabularnewline
Mechanical disorder 6.8\%\tabularnewline
Normal spleen, no etiological factors 6.3\%\tabularnewline
\bottomrule
\end{longtable}

(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 \emph{Pubmed} and \emph{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.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

Table 3 provides interesting informations:

\begin{itemize}
\tightlist
\item
  Several authors, such as Gonzva, use the term ''spontaneous splenic
  rupture'' in the title of their article without mentioning whether
  they had previously looked for diseases affecting the spleen
  {[}19{]}{[}20{]}{[}21{]}{[}22{]}{[}23{]}{[}24{]}{[}25{]}{[}26{]}{[}27{]}.
  Spontaneous splenic rupture in the literature is more frequent than in
  real life due to the abuse of language.
\item
  The population with ruptured spleen associated with DOAC is much older
  than the all-cause population. Their respective mean ages are 72.2
  versus 44.
\item
  The ratio male : female is 1,33 : 1 if we include our own case.
\item
  There are many more cases described with rivaroxaban and apixaban. We
  did not find any cases described in the literature with edoxaban and
  betrixaban
\item
  The failure rate of non-operative treatment by embolization of the
  splenic artery is 71\%.
\end{itemize}

In our patient, the symptomatology was unclear, the pain was crampy and
diffuse without muscle guarding. Given his recent history of atrial
fibrillation ablation, we wanted to exclude a tamponade or another
cardiac problem first. Moreover, the biology and arterial blood gases
were reassuring on admission. A posteriori we hypothesized that the
patient first injured his spleen consecutive to the multiple efforts of
defecation. Then rivaroxaban led to a painful subcapsular hematoma that
eventually tore the capsule and parenchyma. Our diagnosis was delayed.
Moreover, the patient being on bisoprolol and amiodarone never presented
with tachycardia. We did not make the diagnosis in the cardiology unit
with the E-FAST because the computed tomography scan of the abdomen was
directly available at a standard procedure in our institution. Splenic
rupture was most likely spontaneous based of the lack of evidence for
neoplastic, inflammatory or infectious etiologies. Moreover, the
anatomopathological examination of the spleen was macro and
microscopically normal.

Conclusion

We will remember that the symptomatology of a ruptured spleen can be
very atypical. The diagnosis can be difficult. Facing a patient
presenting with unspecific abdominal pain and hypotension, an E-FAST
should be performed. Even though ruptured spleen remains a diagnosis of
exclusion, it can be favoured using DOAC. Often, splenic rupture is
associated with an underlying disease and should be defined as
''atraumatic'' and not ''spontaneous''. Splenectomy remains the gold
standard for an unstable patient.

Patient perspective

The patient does not remember the hours before the surgery and being
taken to the operating room. With his median laparotomy and his
constipation problems in spite of an adapted diet and treatment, he is
anxious when he has to go to the stool even 10 months later. For the
rest, he is happy to have been able to resume his daily activities as
usual.

Consent

The patient has given consent for his medical data and images to be
described in this article.

Conflict of interest disclosure

Non declared.

Funding statement

none

References

{[}1{]} Shamim SM, Razzak JA, Umer SM, Chawla T. Splenic injury after
blunt abdominal trauma: an unusual presentation. \emph{J Emerg Med} .
2011;41(5):489-491.

{[}2{]} Pinar Cigdem Kocael, Osman Simsek, Ismail Ahmet Bilgin, Onur
Tutar, Kaya Saribeyoglu, Salih Pekmezci, Ertugrul Goksoy;
Characteristics of Patients With Spontaneous Splenic Rupture. \emph{Int
Surg} 1 November 2014; 99 (6): 714--718

{[}3{]} Aubrey-Bassler FK, Sowers N. 613 cases of splenic rupture
without risk factors or previously diagnosed disease: a systematic
review. \emph{BMC Emerg Med} . 2012;12:11.

{[}4{]} Renzulli P, Hostettler A, Schoepfer AM, Gloor B, Candinas D.
Systematic review of atraumatic splenic rupture. Br J Surg. 2009
Oct;96(10):1114-21

{[}5{]} Riley, D. S., Barber, M. S., Kienle, G. S., Aronson, J. K., von
Schoen-Angerer, T., Tugwell, P., Kiene, H., Helfand, M., Altman, D. G.,
Sox, H., Werthmann, P. G., Moher, D., Rison, R. A., Shamseer, L., Koch,
C. A., Sun, G. H., Hanaway, P., Sudak, N. L., Kaszkin-Bettag, M.,
Carpenter, J. E., \ldots{} Gagnier, J. J. (2017). CARE guidelines for
case reports: explanation and elaboration document. \emph{Journal of
clinical epidemiology} , \emph{89} , 218--235.

{[}6{]} Debnath D, Valerio D. Atraumatic rupture of the spleen in
adults. \emph{J R Coll Surg Edinb} . 2002;47(1):437-445.

{[}7{]} Dunphy L, Abbas SH, Patel A, Tebala G. Spontaneous splenic
rupture: a rare first presentation of diffuse large B cell
lymphoma.\emph{BMJ Case Rep} . 2019;12(8)

{[}8{]} Crate ID, Payne MJ. Is the diagnosis of spontaneous rupture of a
normal spleen valid?. \emph{J R Army Med Corps} . 1991;137(1):50-51.

{[}9{]} Amonkar SJ, Kumar EN. Spontaneous rupture of the spleen: three
case reports and causative processes for the radiologist to
consider.\emph{Br J Radiol} . 2009;82(978):e111-e113.

{[}10{]} Deol D, Wu H, Lasso-Pirot A, Robinett KS, Diaz-Abad M.
Atraumatic Splenic Rupture Associated with Influenza A (H1N1) Pneumonia:
Case Report and Review of the Literature.~\emph{Case Rep Med} .
2021;2021:6516064

{[}11{]} Wehbe E, Raffi S, Osborne D. Spontaneous splenic rupture
precipitated by cough: a case report and a review of the
literature.~\emph{Scand J Gastroenterol} . 2008;43(5):634-637.

{[}12{]} Sikka R. Unsuspected internal organ traumatic injuries. Emerg
Med Clin North Am. 2004 Nov;22(4):1067-80

{[}13{]} Gedik E, Girgin S, Aldemir M, Keles C, Tuncer MC, Aktas A.
Non-traumatic splenic rupture: report of seven cases and review of the
literature.~\emph{World J Gastroenterol} . 2008;14(43):6711-6716

{[}14{]} Lieberman ME, Levitt MA. Spontaneous rupture of the spleen: a
case report and literature review.~\emph{Am J Emerg Med} .
1989;7(1):28-31.

{[}15{]} Coccolini, F., Montori, G., Catena, F., Kluger, Y., Biffl, W.,
Moore, E. E., \ldots{} \& Ansaloni, L. (2017). Splenic trauma: WSES
classification and guidelines for adult and pediatric
patients.~\emph{World Journal of Emergency Surgery} ,~\emph{12} (1),
1-26.

{[}16{]} Liew A, O'Donnell M, Douketis J. Comparing mortality in
patients with atrial fibrillation who are receiving a direct-acting oral
anticoagulant or warfarin: a meta-analysis of randomized trials.~\emph{J
Thromb Haemost} . 2014;12(9):1419-1424.

{[}17{]} Hellwig T, Gulseth M. Pharmacokinetic and pharmacodynamic drug
interactions with new oral anticoagulants: what do they mean for
patients with atrial fibrillation?.~\emph{Ann Pharmacother} .
2013;47(11):1478-1487.

{[}18{]} Roberti R, Iannone LF, Palleria C, et al. Direct Oral
Anticoagulants: From Randomized Clinical Trials to Real-World Clinical
Practice.~\emph{Front Pharmacol} . 2021;12:684638.

{[}19{]} Gonzva J, Patricelli R, Lignac D. Spontaneus splenic rupture in
a patient treated with rivaroxaban.~\emph{Am J Emerg Med} .
2014;32(8):950.e3. doi:10.1016/j.ajem.2014.01.049

{[}20{]} Hattab, Yousef A., Daniel Speredelozzi, and Omar Bajwa. ''C52
ILLUSTRATIVE DISEASE PRESENTATIONS IN CRITICAL CARE I: Rivaroxaban
Causing Spontanuos Splenic Rupture.''~\emph{American Journal of
Respiratory and Critical Care Medicine} ~191 (2015): 1.

{[}21{]} Naseem, Zainab, Muslim Mustaev, and Boris Strekozov.
''Spontaneous splenic rupture secondary to rivaroxaban: Rare but
raising.''~\emph{IJSM} ~2 (2016): 134-6.

{[}22{]} Amin, Arpit, et al. ''Hemorrhagic shock from spontaneous
splenic rupture requiring open splenectomy in a patient taking
rivaroxaban.''~\emph{The American Surgeon} ~82.2 (2016): E54.

{[}23{]} Nagaraja V, Cranney G, Kushwaha V. Spontaneous splenic rupture
due to rivaroxaban.~\emph{BMJ Case Rep} . 2018;2018:bcr2017223237.

{[}23{]} Pietsch, Ekkehard. ''Spontaneous Splenic Rupture Under
Xarelto.''~\emph{EC Gastroenterology and Digestive System} ~8 (2021).

{[}24{]} Moore CH, Snashall J, Boniface K, Scott J. Spontaneous splenic
hemorrhage after initiation of dabigatran (Pradaxa) for atrial
fibrillation.~\emph{Am J Emerg Med} . 2012;30(9):2082.e1-2082.e20822.

{[}25{]} Lowry, Lacy E, and Jonathan A Goldner. ``Spontaneous splenic
rupture associated with apixaban: a case report.''~\emph{Journal of
medical case reports} ~vol. 10,1 217. 9 Aug. 2016.

{[}26{]} Abdelhady, A et al. ``Apixaban-Associated Spontaneous Splenic
Rupture-A Case Report.''~\emph{Irish medical journal} ~vol. 111,7 792.
13 Aug. 2018

{[}27{]} Janke, Alexander et al. ``Spontaneous splenic hemorrhage in a
patient on apixiban.''~\emph{The American journal of emergency medicine}
~vol. 38,5 (2020): 1044.e1-1044.e2.

{[}28{]} Basnet, Sijan et al. ``Atraumatic splenic rupture associated
with apixaban.''~\emph{SAGE open medical case reports} ~vol. 7
2050313X19832490. 21 Feb. 2019

{[}29{]} Yau, Ho-Cing Victor et al. ``Atraumatic splenic rupture in a
patient treated with apixaban: A case report.''~\emph{International
journal of surgery case reports} ~vol. 71 (2020): 270-273.

{[}30{]} Natarajan, Piruthiviraj et al. ``Atraumatic Splenic Rupture in
a Patient on Apixaban and Dual Antiplatelet Therapy.''~\emph{Journal of
investigative medicine high impact case reports} ~vol. 9 (2021):
23247096211026492.

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