\documentclass[10pt]{article}

\usepackage{fullpage}
\usepackage{setspace}
\usepackage{parskip}
\usepackage{titlesec}
\usepackage[section]{placeins}
\usepackage{xcolor}
\usepackage{breakcites}
\usepackage{lineno}
\usepackage{hyphenat}





\PassOptionsToPackage{hyphens}{url}
\usepackage[colorlinks = true,
            linkcolor = blue,
            urlcolor  = blue,
            citecolor = blue,
            anchorcolor = blue]{hyperref}
\usepackage{etoolbox}
\makeatletter
\patchcmd\@combinedblfloats{\box\@outputbox}{\unvbox\@outputbox}{}{%
  \errmessage{\noexpand\@combinedblfloats could not be patched}%
}%
\makeatother


\usepackage{natbib}




\renewenvironment{abstract}
  {{\bfseries\noindent{\abstractname}\par\nobreak}\footnotesize}
  {\bigskip}

\titlespacing{\section}{0pt}{*3}{*1}
\titlespacing{\subsection}{0pt}{*2}{*0.5}
\titlespacing{\subsubsection}{0pt}{*1.5}{0pt}


\usepackage{authblk}


\usepackage{graphicx}
\usepackage[space]{grffile}
\usepackage{latexsym}
\usepackage{textcomp}
\usepackage{longtable}
\usepackage{tabulary}
\usepackage{booktabs,array,multirow}
\usepackage{amsfonts,amsmath,amssymb}
\providecommand\citet{\cite}
\providecommand\citep{\cite}
\providecommand\citealt{\cite}
% You can conditionalize code for latexml or normal latex using this.
\newif\iflatexml\latexmlfalse
\providecommand{\tightlist}{\setlength{\itemsep}{0pt}\setlength{\parskip}{0pt}}%

\AtBeginDocument{\DeclareGraphicsExtensions{.pdf,.PDF,.eps,.EPS,.png,.PNG,.tif,.TIF,.jpg,.JPG,.jpeg,.JPEG}}

\usepackage[utf8]{inputenc}
\usepackage[ngerman,english]{babel}



\usepackage{float}








\begin{document}

\title{Clinical features of otogenic cerebral sinovenous thrombosis: our
experience and review of literature}



\author[1]{Abir Meherzi}%
\author[1]{Amal Gdissa}%
\author[1]{Habiba Ben sghaier}%
\author[1]{Malika Omri}%
\author[1]{Mouna  Bellakhdhar}%
\author[1]{Jihen Houass}%
\author[1]{Wassim Kermani}%
\author[1]{Mohamed Abdelkefi}%
\affil[1]{Farhat Hached University Hospital of Sousse}%


\vspace{-1em}



  
  \date{June 09, 2024}


\begingroup
\let\center\flushleft
\let\endcenter\endflushleft
\maketitle
\endgroup





\selectlanguage{english}
\begin{abstract}
We aimed to focus on clinical features, on diagnosis of this pathology
and to review the most controversial aspect of management. We reviewed
10 in patients between 1995 and 2020. All patients were treated with
broad-spectrum antibiotherapy, anticoagulation in 9 patients, and
surgery required in 9 patients.%
\end{abstract}%



\sloppy


\textbf{Introduction:}

Otogenic cerebral thrombophlebitis is a rare intracranial complication
of otitis media in the modern age of antibiotics. It poses a danger that
requires immediate diagnosis and urgent medical and surgical treatment.
Complications are now more likely to arise from chronic ear disease or
cholesteatoma rather than acute otitis media.(1) The mortality has
significantly decreased but still range from 5 to 10\%.(2)

This study aims to focus on clinical features, on diagnosis of this
pathology and to review the most controversial aspect of management.

\textbf{Patients and Methods:}

We conducted a retrospective study on 10 patients with otogenic cerebral
thrombophlebitis diagnosed and treated in patients admitted in the ENT
Department of Farhat Hached Hospital over a period of the period of 25
years (1995 to 2020). Our series included 10 patients; they were 8men
and 2 women with a sex ratio (M/F) = 4. The mean age was 35 years
(11year old- 77years old). Neurologic signs (headache) were present in 5
patients and fever was noted in 3 other patients. All patients were
assessed by cerebral CT scan, 3 among them benefits from a cerebral MRI
also. The diagnosis was confirmed by radiographic examination in all
cases. 90\% of patients were anticoagulated.

\textbf{Results:}

A total of 10 inpatients were identified. Four patients (40\%) had
poorly controlled diabetes. All patients had a history of otitis, either
recurrent acute or chronic otitis media. The mean delay of consultation
was 27 days (extremes: from 7 days to 3 months).

The most commonly reported symptoms were headache in 5patients (50\%),
otalgia in all patients, otorrhea in 9 patients (90\%), and fever in 3
patients (30\%).

The etiology was related to an acute otitis media (AOM) in 4 cases
(40\%), cholesteatoma otitis media (COM) in 3 cases (30\%), and
necrotizing external otitis (NEO) in 3 cases (30\%) (Table 1).

All patients had positive otoscopic findings, which included purulent
ear discharge. Retraction pockets with cholesteatoma debris were present
in 2 patients. Congested and retracted pars tensa was found in one
patient (Table 2). The decreased visual acuity was found in one case.
And conductive hearing decrease was noted in one other case.

All patients were assessed by cerebral CT scan with contrast
(contrast-enhanced computed tomography (CECT)) of the brain and temporal
bones. The ``empty delta sign'' (central non-enhancing clot surrounded
by enhancing dural sinus wall) which is related to the presence of
thrombus which has been objectified in 7 patients (70\%) (Fig1a,b). 3
patients (30\%) underwent a MRI.

The thrombus was confined only to the lateral sinus in 5 patients
(50\%), extended to the internal jugular vein in 4 patients (40\%)
(fig2), and extended to the cavernous sinus in 1 patient (10\%) (Fig3).

Regarding the case extension to the cavernous sinus, CT scan showed
low-intensity cavernous sinus, with bulging of its lateral margins,
dilatation of the ophthalmic veins, and bilateral exophthalmia more
marked in the left eye.

The thrombophlebitis was on the right side in 3 cases, on the left side
in 6 cases, and bilateral in 1 case. The occlusion was total in 4 cases
and partial in 6 cases.

Imaging had objectified other associated signs like mastoiditis which
was identified in 5 patients (50\%) (fig4), swelling neck in one case,
and a retropharyngeal abscess in one case (fig5).

70\% of patients presented other cranial complications associated: such
as frank cerebellar abscess (3 patients) and extradural empyema in two
patients (20\%) (fig6), and meningitis in one patient (\%).

Complete blood counts showed concentration of hemoglobin \textless{} 10
g /dL in 2 (20 \%) patients, leukocytosis in 7 (70 \%) patients. All
patients had normal plated counts. All patients had normal coagulation
profiles.

Microbiologic cultures were produced from the middle ear of all patients
and 3 of them had negative cultures. Among the positive cultures,
Pseudomonas aeruginosa was isolated in 2 cases, Proteus mirabilis in one
case, Streptococcus in one case, and streptococcus pneumonia in one
case. Mycological cultures were positive in 2 cases: lichetmiae
corymbiform in one case and Candida Albicans in the other case.

All patients received initially a broad-spectrum antibiotherapy,
subsequently adapted according to the isolated germ. Duration of
antibiotic therapy was for 15 days to 3 months (Table 3 \&4).

90\% of patients were anti coagulated: 6 patients were treated with
subcutaneous low molecular weight heparin (enoxaparin) for an average
period of 60 days, and 3 patients had intravenous unfractionated heparin
for 15 days, then relayed with Sintrom (Acenocoumarol), for a mean
period of 90 days.

Surgical management was completed in 5 cases. It was exclusive in 4
cases (Table 5).

All patients recovered satisfactorily; with complete resolution of their
symptoms and complications except one patient who had a loss of visual
acuity. The middle ear infection was controlled in 9 cases. The
mortality rate was 0\%. 4 patients showed recanalization, and one
patient had a significant decrease of the thrombus. The average length
of the follow-up was 16 months (range: 30 days to 36 months).

\textbf{Discussion:}

Since the advent of antibiotics, the incidence of cerebral sinovenous
thrombosis has been remarkably decreased and it has rarely been reported
in the few last decades(3).This rare condition has been more frequently
reported in the pediatric population (3)(4), with an incidence of 0.7
per 100000 children per year (5).

A clear male predominance has been documented in most
studies(2)(4)(6)(7). We also found the same predominance in our series.

The anatomic proximity of the middle ear cavity and mastoid air cells to
the dural venous sinuses makes them vulnerable to thrombophlebitis
secondary to infection and inflammation in the middle ear and
mastoid(8). Two pathogenic mechanisms of infection spread were
suggested: the direct spread of infection by erosive osteitis and
retrograde thrombophlebitis (9)(10).Edema, increase in local vascular
pressure, and hyper-coagulability stateis caused by the inflammatory
process. Therefore it leads to venous stasis and subsequent thrombosis
(11).

Severe frontal and occipital headache, otalgia,nausea, vomiting,
diplopia, loss of visual acuity, sixth nerve palsy, hemiparesis, and
spiking fever, were the most common signs and symptoms found in cases of
lateral sinus thrombosis before the era of antibiotics(1).Nowadays, the
most commonly reported symptom was a headache. The clinical presentation
was reported by Raja.K in her series ``Otogenic Lateral Sinus
Thrombosis : A Review of Fifteen Patients and Changing Trends in the
Management~\selectlanguage{ngerman}»was made also of otorrhea, hard of hearing, and fever(2).
This finding was reproduced in Bales's study and Sherer's series as
well(4)(12).

Otalgia and vomiting were the commonest presenting features (63\%)
followed by fever (57\%) and headache (43\%) in Krishnan's study(11).
Exophthalmos, loss of visual acuity, ophthalmoplegia, ptosis, and
palpebral edema associated with headaches and fever were the major signs
and symptoms of cavernous sinus thrombosis(13)(14)(15). Zanoletti and
al. argues that the absence of typical clinical signs of mastoiditis
does not exclude the presence of otogenic lateral sinus thromboses (16).
In our series headache was present in 50\% of cases and fever in 30\% of
cases.

The bacteriology of cerebral sinovenous thrombosishas changed with the
use of antibiotics. Before the age of antibiotics, B-haemolytic
streptococcus and Pneumococcus were the most cultured organisms.
Pseudomonas and proteus species used to be common too(1).

The microbiological profiles are changing. Culture from the middle ear
discharge characteristically yields mixed flora, including Pseudomonas,
Proteus, Bacteroides, Staphylococcus, Enterobacteriaceae, and other
species. It is might be frequently negative due to previous antibiotic
treatment. (2)(1).In Raja's study, 6 (40\%) patients had negative
cultures. In patients with positive cultures, Proteus mirabilis (4
cases; 44\%) and Pseudomonas aeruginosa (4 cases; 44\%), followed by
Enterococcus fecal (1 case; 11\%) and Escherichia coli (1 case;
11\%).(2). In our series, the culture was positive in 7 patients.5 one
was related to a bacterial infection and 2 were related to mycologic
infection which caused the external ear infection. Among the positive
bacterial culture, we isolated Pseudomonas aeruginosa was isolated in 2
cases, Proteus mirabilis in one case, Streptococcus in one case, and
streptococcus pneumonia in one case.

The diagnosis of cerebral thrombophlebitis is based on radiographic
imaging techniques. Contrast enhancing computed tomography of the head
and neck is performed to investigate intra cranial complications of
otitis media, especially the cerebral sinovenous thrombosis (5), (9).

Lateral Sinus thrombosis may be diagnosed by the presence of the
pathognomonic empty delta sign which consists of an empty triangle
appearance created by the thrombus within the sinus surrounded by
contrast-enhanced dura (9)(17)(14)(5). In our study, the lateral sinus
was the most common location in our patients. It was confined in 70\% of
cases and spread to the jugular vein in 4 cases and the cavernous sinus
in only one case.

Cavernous sinus thrombosis may be initially explored with non-contrast
CT of the head which can show subtle abnormalities such as bulging of
the lateral margins of the cavernous sinus, heterogeneous filling
defect, and engorgement of the superior and/or inferior ophthalmic
veins. In addition to the above-mentioned signs, contrast-enhanced
CT/MRI, shows the presence of asymmetric filling defects, thrombosis in
the superior ophthalmic vein, other venous tributaries, dural venous
sinuses, and cerebral veins(18). In our case, a CT scan was able to
diagnose the thrombus in the cavernous sinus by showinglow-intensity
cavernous sinus, with bulging of its lateral margins, dilation of the
ophthalmic veins, and bilateral exophthalmos more marked in the left
eye.

CT scan can misdiagnose the thrombus pathology because of bone-related
artifacts(1). Therefore, M R I / M R V is more sensitive in detecting
this complication (2).

MRI/MRV is valuable to exclude other intracranial complications like
adjacent subdural empyema, cerebritis, or cerebralabscess. It can also
eliminate the risk ofradiation compared with CT scans, especially for
children(2). The MRI does not require contrast injection to showthe
thrombuswhich seems isointense on T1-weighted images and hypointense on
T2-weighted images, with increased intraluminal sign intensity onboth T1
and T2 sequences (17). The MRV remains the gold standard in diagnosing
cerebral sinovenus thrombosis because it is a non-invasivetechnique;it
offers the advantage of precising the patency of the central venous
sinuses. Besides, itenables the distinction between a slow venous flow
and an occlusive thrombus and can be performed simultaneously with
cerebral MRI(17)(11). In our study, the MRI revealed the thrombus in 3
cases where the scanner was negative.

Additional intracranial complications must be investigated in the
presence of cerebral sinus thrombosis. The high association of cerebral
sinus thrombosis with other cranial complications is well documented
(8).

In the pre-antibiotic era, concurrent complications were present in 80\%
of cases. The advent of antibiotics has reduced the incidence of
complications to 20\%. Concomitant intracranial and extracranial
complications included meningitis, otitis hydrocephalus, internal
jugular vein thrombosis, and intracranial abscesses(8).

Syms and al reported a series of patients who all had concurrent
intracranial complications: 4 patients had a cerebral abscess and 3
patients had hydrocephalus(19). In the series of Kaplan et al, Twelve of
the 13 patients suffered concurrent complications, including meningitis,
cerebral abscesses, epidural abscess, and progression of the thrombus to
the transverse sinus and the internal jugular vein(3).

We have objectified70\% of a cranial complication associated: such as
cerebellar abscess (3 patients) and extradural empyema in two patients,
and meningitis in one patient.

Broad-spectrum intravenous antibiotics should be started at the earliest
and must be adjusted later according to bacterial cultures. Antibiotics
have led to a reduction of incidence of complications from 80\% to
20\%(1). The duration of the antibiotic treatment ranged from four to
eight weeks(2). In our cases, we treated first with broad-spectrum
antibiotics then adapted to the culture result.

The role of anticoagulation therapy in the treatment of LST is unclear.
The clinician should weigh the risks and benefits of anticoagulation
therapy in cases of cerebral sinovenous thrombosis. Au. JKet al reported
a trend in the use of anticoagulation therapy, but lack the statistical
difference(20). Anticoagulation has been advanced to offer the advantage
of preventing the extension of the thrombus to distal sinuses. Thus, it
might be indicated in particular cases of thrombus propagation, embolic
events, and neurological changes(1)(21).LMWH in children with CSVTis
recommended by The American Stroke Association, outside the neonatal
period, even if there is evidence of intracranial hemorrhage(5)(22).It
is preferred to other anticoagulants(17)(5), because it preventsthrombus
propagation, improves recanalization rates, and preventslong-term
neurological sequels. But, on the other hand, it can cause
thrombocytopenia, bleeding, hemorrhagic skin necrosis, and risk of
septic emboli (11).74\% of patients after, showed complete recovery with
complete resolution of the symptoms and recanalization after
antibiotherapy associated with anticoagulation (23).

Anticoagulation was administrated in all of the patients, along with
antibiotics and surgical treatment, with an excellent outcome; 9
patients recovred and only one patient had sequelae.

Surgery is an essential part of the management of this entity. It
assures a better prognosis. However, controversies persist about the
most appropriate surgical management (11). A cortical mastoidectomy is
used successfully to treat noncholesteatoma ear disease. It confirms the
diagnosis of L ST and allows the drainage of the initiating infection. A
modified radical mastoidectomy is sufficient treatment for
cholesteatomatous ears presenting acutely with cerebral sinus
thrombosis(1). Nowadays, routine ligation of the internal jugular vein
is no longer performed. It is usually reserved for unresponsive cases
with persistent septicemia,lung thromboembolism, and deep neck
infection(2)(9).

In our study, we realize a mastoidectomy isolated in 4 patients (40\%),
it was associated to an internal jugular vein ligation in one case, and
to an extradural empyema evacuation in 2 patients (20\%). We recommended
an antro-mastoidectomy with incision of the sinus and evacuation in 2
cases (20\%).

\textbf{Conclusion:}

Otogenic cerebral sinovenous thrombosis is a rare complication of otitic
pathology. It is associated with significant morbidity and mortality. In
the era of antibiotics, classic clinical signs of mastoiditis (pain,
swelling, and erythema posterior to the pinna) are not always present at
the presentation. A clinical presentation might be subtle, which
requires clinicians to maintain a high index of suspicion of this
entity. Imaging (CT, MRI) is a key component in diagnosing and managing
this complication. Treatment of otogenic CSVT consists of conservative
surgery, antibiotics, and anticoagulation.

List of abbreviation:

AOM: acute otitis media

COM: chronic otitis media

NEO: necrotizing external otitis

PFP: peripheral facial paralysis

IVJ: internal jugular vein\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

Figure 1a : lateral sinus thrombosis\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

Figure2: internal jugular vein thrombosis\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image4/image4}

\end{center}
\end{figure}

Figure3: cavernous sinus thrombosis\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image5/image5}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image6/image6}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image7/image7}

\end{center}
\end{figure}

Figure5: retropharyngeal abcess

Figure4: mastoiditis Figure6: cerebral empyeme

Table 1: Table1: The aetiology was acute otitis media in 4 cases,
cholesteatoma otitis media in 3 cases and necrotizing external otitis in
3 cases .\selectlanguage{english}
\begin{longtable}[]{@{}lll@{}}
\toprule
\begin{minipage}[b]{0.30\columnwidth}\raggedright\strut
aetiologiy\strut
\end{minipage} & \begin{minipage}[b]{0.30\columnwidth}\raggedright\strut
Numbre of patients\strut
\end{minipage} & \begin{minipage}[b]{0.30\columnwidth}\raggedright\strut
Affected sinus\strut
\end{minipage}\tabularnewline
\midrule
\endhead
\begin{minipage}[t]{0.32\columnwidth}\raggedright\strut
AOM\strut
\end{minipage} & \begin{minipage}[t]{0.32\columnwidth}\raggedright\strut
4\strut
\end{minipage} & \begin{minipage}[t]{0.32\columnwidth}\raggedright\strut
Lateral sinus: 3 cases Cavernous sinus: 1case\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
COM\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
3\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Lat\selectlanguage{ngerman}éral sinus :3 cases\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
NEO\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
3\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Sinus lat\selectlanguage{ngerman}éral: 3 cas\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}\selectlanguage{ngerman}

Table2: clinical examination findings\selectlanguage{english}
\begin{longtable}[]{@{}ll@{}}
\toprule
Signs & Numbre of patients\tabularnewline
\midrule
\endhead
Fever & 3\tabularnewline
PFP (peripheral facial paralysis) & 1\tabularnewline
Exophtalmos with palpebral oedema & 1\tabularnewline
Torticollis & 1\tabularnewline
Cervical swelling & 1\tabularnewline
Retroauricular tenderness with swelling of the ear lobe &
5\tabularnewline
otorreha & 5\tabularnewline
Retracted tympanic membrane & 1\tabularnewline
Narrowed external auditory canal & 2\tabularnewline
\bottomrule
\end{longtable}

Table3: repartition according to the antibiotic therapy administered and
the causal pathology\selectlanguage{english}
\begin{longtable}[]{@{}lll@{}}
\toprule
Cefotaxime + fosfomycin+m\selectlanguage{ngerman}étronidazole & 4 & 2 AOM 2 COM\tabularnewline
\midrule
\endhead
Cefotaxime+ofloxacin & 1 & AOM\tabularnewline
Cefotaxime+vancomycin+m\selectlanguage{ngerman}étronidazole & 1 & COM\tabularnewline
Ciprofloxacin +ceftazidime & 1 & NEO\tabularnewline
\bottomrule
\end{longtable}

Table4: treatment of the necrotizing otitis externa\selectlanguage{english}
\begin{longtable}[]{@{}lll@{}}
\toprule
\begin{minipage}[b]{0.30\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[b]{0.30\columnwidth}\raggedright\strut
Nbre of patients\strut
\end{minipage} & \begin{minipage}[b]{0.30\columnwidth}\raggedright\strut
Anti fungal treatment\strut
\end{minipage}\tabularnewline
\midrule
\endhead
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Fungal NEO (candida)\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
1\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Voriconazole IV then relay per os\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.32\columnwidth}\raggedright\strut
Fungal NEO (mucorales)\strut
\end{minipage} & \begin{minipage}[t]{0.32\columnwidth}\raggedright\strut
1\strut
\end{minipage} & \begin{minipage}[t]{0.32\columnwidth}\raggedright\strut
Amphot\selectlanguage{ngerman}éricin B: 1mg/kg/day IV (rupture Caspofungin)\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}\selectlanguage{ngerman}

Table5: Surgical treatment\selectlanguage{english}
\begin{longtable}[]{@{}ll@{}}
\toprule
Surgical treatment & Numbre of patients\tabularnewline
\midrule
\endhead
Mastoidectomy & 4\tabularnewline
Mastoidectomy+ internal jugular vein ligation & 1\tabularnewline
Mastoidectomy+ extradural empyema evacuation & 2\tabularnewline
Antro mastoidectomy+ incision of the sinus and evacuation of the clot &
2\tabularnewline
\bottomrule
\end{longtable}

Refereneces:

1. Adhikari P, Guragain RPS. Lateral Sinus Thrombophlebitis : Review of
Literature. Intl Arch Otorhinolaryngol. 2007;11:477--80.

2. Raja K, Kumar Parida P, Alexender A, Surianarayanan G. Otogenic
Lateral Sinus Thrombosis : A Review of Fifteen Patients and Changing
Trends in the Management. Int Arch Otorhinolaryngol. 2018;22:208--13.

3. Kaplan DM, Kraus M, Puterman M, Niv A, Leiberman A, Fliss DM.
Otogenic lateral sinus thrombosis in children. Int J Pediatr
Otorhinolaryngol. 1999;49:177--83.

4. Bales CB, Sobol S, Wetmore R, Elden LM. Lateral Sinus Thrombosis as a
Complication of Otitis Media : 10-Year Experience at the Children ' s
Hospital. Pediatrics. 2015;123(2):709--13.

5. Salloum S, Belzer K. Cerebral sinovenous thrombosis as a complication
of otitis media. Clin Case Reports. 2019;7:186--8.

6. Seven H, Ozbal AE, Turgut S. Management of Otogenic Lateral Sinus
Thrombosis. Am J Otolaryngol. 2004;25(5):329--33.

7. Fergoug I, Latroche M, Mehadji M. Thrombophl\selectlanguage{ngerman}ébite du sinus latéral d
' origine otogène , prise en charge et pronostic. Ann françaises
d'Oto-rhino-laryngologie Pathol Cervico-faciale. 2012;129:110.

8. B. Viswanatha MS and KN. Lateral Sinus Thrombosis in Otology\selectlanguage{english} : a
Review. Mediterr J Hematol Infect Dis. 2010;3:027--33.

9. Doyle KJO. Otogenic cavernous sinus thrombosis. Otolaryngol Neck
Surg. 1990;873--7.

10. JUILLAND N, VINCKENBOSCH, PAULINE et RICHARD C. Otite moyenne aigue
et complications a court terme. Rev Medicale Swisse. 2016;12:338--43.

11. Krishnan M, Walijee H, Jesurasa A, De S, Sinha A, Sharma R.
International Journal of Pediatric Otorhinolaryngology Clinical outcomes
of intracranial complications secondary to acute mastoiditis\selectlanguage{english} : The Alder
Hey experience. Int J Pediatr Otorhinolaryngol. 2019;128(June
2019):1--5.

12. Scherer A, Jea A. Pediatric Otogenic Sigmoid Sinus Thrombosis\selectlanguage{english} : Case
Report and Literature Reappraisal. Glob Pediatr Heal. 2017;4:1--8.

13. Bouslama M, Belcadhi M, Harzallah M, Mani R, Zeglaoui I, Ali MBEN,
et al. THROMBOPHLEBITE DU SINUS CAVERNEUX D ' ORIGINE OTOGENE\selectlanguage{english} : A PROPOS
D'UN CAS. J tun ORL. 2007;37--40.

14. Gobron C, Guichard J, Chabriat H. Thrombose du sinus caverneux. Sang
Thromb Vaiss. 2004;16:130--8.

15. BABIN, E\selectlanguage{english} ; NDYAYE, M\selectlanguage{english} ; BEQUIGNON, A\selectlanguage{english} ; VADILLO, M\selectlanguage{english} ; MOREAU, S\selectlanguage{english} ;
VALZADO, A\selectlanguage{english} ; JOKIC, M\selectlanguage{english} ; COSKUN, O\selectlanguage{english} ; HAMON M. Thrombose otogenes du sinus
caverneux: a propos d'un cas. Ann d'oto-laryngologie Chir
cervico-faciale. 2003;120:237--43.

16. E. Zanoletti, D. Cazzador, C. Faccioli, M. Sari, R. Bovo AM.
Intracranial venous sinus thrombosis as a complication of otitis media
in children: critical review of diagnosis and management,. Int J Pediatr
Otorhinolaryngol. 2015;79:2398--403.

17. Iseri M, Ayd N, Emre U, Alma A. Management of Lateral Sinus
Thrombosis in Chronic Otitis Media. Otol Neurol. 2006;27:1098--103.

18. Bhatia H, Kaur R, Bedi R. MR imaging of cavernous sinus thrombosis.
Eur J Radiol Open {[}Internet{]}. 2020;7(February):100226. Available
from: https://doi.org/10.1016/j.ejro.2020.100226

19. Syms MJ, Tsai PD HM. Management of lateral sinus thrombosis.
Laryngoscope. 1999;109:1616--20.

20. Au JK, Adam SI ME. Contemporary management of pediatric lateral
sinus thrombosis: a twenty year review. Am J Otolaryngol.
2013;34(2):145--50.

21. Ireo E, Gupta P, Dhanasekar G. Otogenic lateral sinus Thrombosis\selectlanguage{english} : a
rare complication of chronic Otitis media. Heighpubs Otolaryngol Rhinol.
2017;1:046--52.

22. Saposnik G, Barinagarrementeria F, Brown RD Jr et al. Diagnosis and
management of cerebral venous thrombosis: a statement for healthcare
professionals from the American Heart Association/ American Stroke
Association. Stroke. 2011;42(4):1158--92.

23. Wong, Ian; Kozak, Frederick K.; Poskitt, Ken; Ludernann, Jeff P.;
Harriman M. Pediatric Lateral Sinus Thrombosis: Retrospective Case
Series and Literature Review. J Otolaryngol. 2005;34(2):79--85.

\selectlanguage{english}
\FloatBarrier
\end{document}

