Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4466_Библиотеки_им_академика_М_И_Перельмана
.pdf
23 Focal Suppurative Infections of the Central Nervous System in Children…
https://t.me/medicina_free
Fig. 23.9 Right transverse
sinus thrombosis. A
coronal 3D reconstruction
image from contrastenhanced MR venography
shows a lack of ow in the
proximal portion of the
right transverse sinus
(thick arrow). (Right
sigmoid sinus [thin arrow],
left transverse sinus
[double arrow], left
sigmoid sinus
[arrowhead]). (Courtesy
Zeynep Yazıcı, MD)
319
23.4.1 Microbiology
In most cases of septic LST, bacteria cannot be isolated in culture. One review
reported that the culture isolated rate was 46% [22]. The most commonly isolated
bacteria are S. pyogenes, S. pneumoniae, S. aureus, H. inuenza, P. aeruginosa,
E. coli, and upper respiratory tract anaerobes, including Fusobacterium) [23]. While
there is primarily polymicrobial (aerobic and anaerobic bacteria) growth in adults,
the rate of polymicrobial growth in children has been reported as 6%. When it
occurs as a complication of chronic otitis media, the main pathogens are the microorganisms that cause chronic otitis media [1, 22].
23.4.2 Epidemiology
Septic LST is a rare condition in the pediatric age group. It has a high mortality rate
(5–10%) and can be associated with severe clinical morbidities if not diagnosed and
treated early [23]. Septic LST accounts for 2–20% of intracranial complications of
AOM, but the probability of LST being associated with AOM is around 67% (autogenic LST) [22]. In one study, 13 (2.7%) of 475 patients with mastoiditis and AOM
had MR-identiable autogenic LST [20]. It occurs twice as often in boys as in girls
and occurs at a mean age of 7.7years [21, 22, 24]. It is most commonly seen on the
right side. It has been reported that the prevalence of thrombophilia as a risk factor
for LST in children varies between 10% and 78% [1, 16]. However, in one study, in
320
https://t.me/medicina_free
25 cases with pediatric autogenic LST, at least one of the thrombophilia-specic
laboratory tests was positive in a signicant proportion (96%). Among them,
MTHFR (80%), protein S deciency (44%), and heterozygote or homozygous FV
Leiden mutation (24%) were found most frequently [1, 19].
T. Çelik et al.
23.4.3 Pathogenesis
Although different factors contribute to the development of autogenic LST, it most
often occurs as a complication of acute or chronic otitis media. If AOM is not treated
appropriately, the infection may spread to the mastoid and the lateral sinus [1, 23].
Due to the anatomical proximity of the lateral and sigmoid sinuses to the mastoid
part of the temporal bone, the spread of infection in the mastoid and middle ear cavity to the lateral sinus through the veins draining into the sinuses is facilitated [20,
24]. Secondary to infection or inammation of adjacent tissue, intravascular mural
thrombus may develop due to cytokine release and activation of the coagulation
pathway, activating the formation of thrombocytes and brin. This thrombus may
spread or embolize into cerebral transverse, inferior, or superior petrosal venous
sinuses and internal jugular veins [1, 19, 20, 23, 24]. In mastoiditis, the infection
may reach the perisinus region from the mastoid air cell system and result in perisinus abscess and then spread to the dura and intimal layer of the sinuses, causing the
formation of a mural thrombus, organized clot particle in the vein or venous sinus
wall. If adequate treatment is not initiated promptly, the mural thrombus enlarges,
necroses, and an intramural abscess occurs [21]. In addition, embolization of the
disseminated infected thrombus into the systemic circulation causes septicemia.
Thus, septic pulmonary embolism may occur as a rare complication of lateral sinus
thrombosis [1, 21]. Disruption of regional venous drainage in LST, causing cochlear
blood ow insufciency and acute cochlear dysfunction, may result in hearing and
balance problems. This condition is usually reversible, improves with the resolution
of the disease, and the prognosis is generally good [6]. With untreated or inadequate
treatment, progression of thrombosis, impaired venous circulation, and increased
intracranial pressure may result in impaired absorption/drainage of CSF and, consequently, hydrocephalus [1, 20, 23]. Since thrombus formation is a protective mecha-
nism that tries to localize the infection, a tendency to heal in thrombus is observed
when the source of infection is removed [25]. Susceptibility to hypercoagulopathy
in children appears to be an additional risk factor. Although the magnitude of this
risk has not been systematically measured, a prothrombotic state was found in more
than 70% of cases in an AOM-related series [1].
23.4.4 Clinical Manifestations
Septic LST often has a subacute onset. Symptoms usually begin a few weeks before
the presentation and are associated with developing septic LST and the underlying
infection [1]. The most common reason for admission is symptoms due to benign
intracranial hypertension or pseudotumor cerebri [24].
23 Focal Suppurative Infections of the Central Nervous System in Children…
https://t.me/medicina_free
321
In almost all patients, ear complaints such as ear pain suggestive of AOM, which
started and persisted several weeks before the onset of headache, are usually the rst
symptom and may continue up the presentation [1, 20, 24]. In cases associated with
chronic otitis media, ear discharge may be a presenting symptom [21]. The headache is usually severe, persistent, and localized on the side of the ear infection. The
headache is thought to be due to intracranial hypertension related to LST, irritation
of the CN-V, or a developing epidural abscess complication. Nausea and vomiting
develop in about half of the cases. Other symptoms include vertigo, diplopia, photophobia, and neck pain or stiffness. Less frequently, patients may present with
headache and neurologic symptoms without earache and may have radiological
ndings consistent with chronic otitis media that may be accompanied by cholesteatoma. In some patients, hemoptysis may develop due to septic pulmonary embolism [1].
Fever is present in approximately 80% of the cases, and the cases often appear
ill. However, fever may not be evident in those associated with chronic otitis media.
Most patients have an abnormal tympanic membrane examination; e.g., it is perforated in 40% and hyperemic in 20%. In more than half of the cases, posterior auricular swelling, edema, hyperemia, and sometimes tenderness are present, resulting
from occlusion of the mastoid veins. This nding is called the Griesinger1 sign and
is considered clinically pathognomonic for septic LST.The most common ndings
in the neurological examination are papilledema, cranial nerve palsy (most commonly CN-VI), cerebellar ndings (ataxia), and HL [1, 20, 24]. Bilateral papilledema due to high CSF pressure is present in half of the cases. In addition, a 15%
loss of visual acuity develops. Unilateral CN-VI palsy has been reported in more
than one-third of patients. Acute otitis media, CN-VI palsy, and CN-V irritation;
temporoparietal and retroorbital pain in the trigeminal nerve region is known as
Gradenigo2 syndrome. It is rare, but LST should be considered when this symptom
complex is detected. Nuchal rigidity is present in one-third to half of the patients
and is likely the result of meningeal inammation. Mental status is depressed in
14% of cases [1]. In a study in which 11 (73%) male and four (27%) female LST
patients aged 9–60years were evaluated over 5 years, it was reported that all patients
had hearing difculties, 11 (73%) conductive HL, and four (27%) mixed-type
HL [20].
23.4.5 Laboratory
Computed tomography or MR can conrm otomastoid infection. Mastoid imaging
ndings are abnormal in all patients with septic LST and present with mastoid trabeculae loss, bone sclerosis, and lytic lesions of the temporal and parietal bones [1].
On contrast-enhanced CT or MR venography, lling defects due to thrombus and
absence of ow in the dural sinus can be detected in patients with septic LST.In a
1
Wilhelm Griesinger (1817–1868); German neurologist and psychiatrist.
2
Guiseppe Gradenigo (1859–1926); Italian physician.
322
https://t.me/medicina_free
study evaluating 46 cases with surgically conrmed LST, contrast-enhanced CT had
a sensitivity of 87%; MR was found to be 100% sensitive in 30 surgically conrmed
cases [1, 22].
Round inltrates caused by septic embolism that migrates from the sinus to the
internal jugular vein and into the pulmonary venous circulation may rarely be seen
on chest radiographs [1].
Two sets of blood cultures should be sent before starting antibiotic therapy. In
CSF evaluation, CSF pressure increases due to impaired CSF absorption, and ndings showing parameningeal inammation may be detected for the cases considered
as CNS infection. Gram stain and culture should also be sent from CSF [1]. There
may be an increase in acute phase reactants such as leukocytosis, CRP, and ESR
elevation for infection, supporting uncontrolled otitis and mastoid infection.
Children with LST may have underlying prothrombotic tendencies that cause
thrombosis [20]. In a retrospective and 10-year study, acute unilateral HL due to
ipsilateral LST developed in three cases out of 38 cases with CST.Oral contraceptive intake was found in two of them, and heterozygous factor V Leiden mutation
was found in one [7]. Although some authors do not recommend routine evaluation
for hypercoagulopathy, it should be kept in mind that in case series, 1/3–1/2 of children may have hypercoagulopathy, especially in the presence of AOM and chronic
otitis media with evidence of thrombosis [1]. Therefore, it would be prudent to
perform laboratory tests to evaluate hypercoagulopathy in these patients [20].
T. Çelik et al.
23.4.6 Differential Diagnosis
Septic LST should be suspected in a patient with acute/chronic otitis media who
develops neurological ndings such as headache, vertigo, CN-VI palsy, papilledema, and diplopia. Imaging methods such as contrast-enhanced MR and CT, MR,
and CT venography should be performed to conrm the diagnosis and make a differential diagnosis [1, 22]. Lateral sinus thrombosis should be suspected in children
with high intracranial pressure, previously diagnosed with acute/chronic otitis
media, even if they do not have typical otomastoid complaints such as ear discharge
or ear pain. The neuroradiological diagnosis of CST and LST can be difcult, given
that anatomical variants of the dural venous sinus may be common in individuals.
Some normal variants may mimic CST, such as prominent arachnoid granulations,
hypoplasia, or aplasia of the intrasinus septum and dural sinuses [20].
23.4.7 Treatment
Antibiotics form the basis of the treatment approach in managing septic LST.If
there is any indication, mastoidectomy and placement of the ventilation tube should
be considered. Therefore, the necessity of mastoid surgery for eradication of the
disease with antibiotics should be discussed in all these cases with LST.The presence of hypercoagulopathy may predispose to LST. Although the role of
23 Focal Suppurative Infections of the Central Nervous System in Children…
https://t.me/medicina_free
anticoagulation in treatment is controversial, it is generally recommended. In
patients with evidence of increased intracranial pressure, acetazolamide therapy is
recommended [1, 20, 25].
323
23.4.7.1 Antibiotics
Intravenous antibiotics should be started immediately. The empirical antibiotic
approach chosen is the same as in septic CavST.Methicillin-resistant S. aureus is
rare in patients with septic LST compared to CavST.Therefore, the most appropriate initial empirical parenteral regimen is cefotaxime or ceftriaxone plus metronidazole. If Pseudomonas is suspected (e.g., patients with chronic otitis media and
known Pseudomonas colonization), cefepime should be preferred instead of cefotaxime or ceftriaxone. Alternatively, meropenem may be preferred due to its effectiveness against Pseudomonas. There is no need to add metronidazole initially in
patients who will be given meropenem. Empirical addition of vancomycin to routine therapy is recommended in patients with MRSA in previous cultures of the
mastoid and critically ill patients until culture results are available. If microorganisms are identied in the samples taken, therapy should be modied to target organisms identied based on antibiotic susceptibility [1].
Since mastoiditis is the most common primary infection, antibiotics are usually
recommended for at least 3–4weeks or longer in the presence of mastoiditis, following clinical signs. A shorter period may be sufcient if the infection site has
been surgically resected and the clinical signs have completely regressed [1].
23.4.7.2 Surgery
Although patients diagnosed with LST are considered an emergency in terms of
surgery, it is a common opinion that surgical treatment is not a critical outcome
determinant, and it would be prudent to consider it individually according to the
patient [1, 19, 24]. A mastoidectomy may not be required in all cases of LST.In a
pediatric series, three out of ve patients had underlying otitis; he responded rapidly
to antibiotic therapy and myringotomy and was shown to recover entirely without
aggressive surgical intervention [1]. If surgery is planned, the lateral sinus should be
evaluated beforehand. Although sometimes removing the thrombus from the lateral
sinus can be considered, once the infection is under control, recanalization or collateral venous drainage may occur without additional surgical intervention [1, 23].
Therefore, it is generally recommended that mastoidectomy be planned, independent of LST, only in patients with erosive or coalescent mastoiditis, subperiosteal abscess, and erosion of the mastoid or internal cortical bone [19]. In a study
evaluating 13 cases of mastoiditis with LST, surgery (nine mastoidectomies) was
performed in 10, antibiotics were given only in three, and no mortality was detected
in any of the cases. In addition, sigmoid sinus or internal jugular vein exploration
was not performed in any patient in this study [20]. More aggressive options for
thrombus removal, such as surgical lateral sinus drainage, are not routinely recommended. Internal jugular vein ligation is limited to cases of persistent septicemia or
septic pulmonary embolism [22]. Surgeries such as external ventricular drainage,
serial lumbar punctures, intracranial pressure monitoring, and endovascular
324
https://t.me/medicina_free
T. Çelik et al.
thrombectomy may be considered individually in patients with neurological deterioration despite maximal medical therapy [23].
23.4.7.3 Anticoagulation
Anticoagulation is not a major part of the routine management of septic LST in
children [1]. Anticoagulation may be benecial in preventing thrombus growth,
maintaining intracranial drainage, and thus limiting increased intracranial pressure
[23]. Although the indications for anticoagulation therapy are well-dened in adults,
the role of anticoagulation in children is controversial [1, 24]. Indeed, thrombotic
vessels often recanalize without anticoagulation when the infection that induces
and/or accelerates thrombosis is resolved with appropriate antibiotic therapy [1].
Fifteen LST cases in children and adults (9–70years old) were evaluated between
2010 and 2015in India [20]. No coagulation defects were detected in any of them,
none of them were given anticoagulant treatment, and no mortality was detected
with antibiotic treatment alone. However, on the contrary, in another study, between
2006 and 2017, 25 pediatric cases (mean age 6, 68% male) were evaluated [19].
This study found positive genetic studies supporting thrombophilia in 96% (24/25)
cases, and the authors recommended anticoagulant therapy in all cases. However,
even if the risk is low, anticoagulant therapy may cause serious complications such
as bleeding, drug interactions, thrombocytopenia, osteoporosis, and hemorrhagic
skin necrosis [23]. In one study, anticoagulant treatment was initiated in 57.4%
(39/68) of the cases. Postoperative imaging showed partial or complete recanalization of the sinuses in 84% of patients who received anticoagulant therapy and 75%
of those who did not [21]. Studies suggest that anticoagulant therapy should primarily be used in “aseptic” patients with non-autogenic sigmoid sinus disease, but its
role in septic LST is unclear [1, 19]. In addition to antibiotic treatment, anticoagulation treatment is recommended in the case of progressive thrombosis and lack of
clinical improvement despite antibiotics and surgical drainage (persistent fever,
etc.), detection of thrombus spreading to other regions (such as a proximal jugular
vein, transverse sinus, and cavernous sinus) according to the rst admission, neurological ndings, and/or embolic events in the clinical picture, and patients with
pre- existing hypercoagulopathy [1, 20]. In the authors’ clinic, in septic LST, anticoagulant therapy is initiated as a supplement to antibiotics, and clinical and neurological ndings are closely monitored until complete recovery is achieved and
recanalization and blood ow are achieved in the thrombotic area on imaging. In
cases with risk factors for thrombophilia, anticoagulant therapy can be extended
with the recommendation of pediatric hematology.
Low molecular weight heparin is preferred in patients scheduled for anticoagulant therapy and should be started immediately after diagnosis [19]. If anticoagulant
therapy is initiated, a standard duration has not been established [1]. Serial imaging
with MR and MR venography is important to follow the spread of thrombus, especially in children who respond poorly to initial treatment [20]. In patients with clinical improvement, the rst cranial imaging control should be performed at least
2months later to decide the duration of LMWH treatment [19]. In one study, early
recanalization was observed in approximately half of the cases (48%) after
23 Focal Suppurative Infections of the Central Nervous System in Children…
https://t.me/medicina_free
appropriate treatment in the rst 2 months, while the rate of recanalization at
6months was reported to be 68–87% [19]. In another study on children, the mean
recanalization time was 6months (2–12months) [20]. If hypercoagulopathy is documented, it is recommended to continue anticoagulant therapy for at least 6 months.
In pediatric patients whose lateral sinus is not recanalized, prolonged anticoagulation should be continued. For other cases, anticoagulant therapy may be continued
until symptoms and signs of infection, as well as LST, resolve or signicantly
improve (2–12months) [1, 19, 20].
325
23.4.7.4 Treatment ofElevated Intracranial Pressure
In patients with elevated intracranial pressure, treatment with acetazolamide may be
considered to reduce CSF pressure and relieve papilledema. In rare cases, patients
whose intracranial pressure cannot be reduced may require serial lumbar punctures
and/or ventricular drainage every 48h. In the presence of hydrocephalus, permanent
ventricular shunt placement may be necessary [1, 20].
23.4.8 Outcome
Mortality rates for LST today are lower than they used to be but still range from 5%
to 10%, even in advanced centers [20]. Most patients recover completely, but
chronic sequelae occur in 10–15%, including hydrocephalus, decreased visual acuity, hearing impairment, and rarely residual hemiparesis [1]. In one study, children
with early recanalization of thrombosis were, on average, younger than children
with persistent thrombosis [19]. In another study, persistent mild lateral gaze diplopia in one (7%) patient, severe unilateral SNHL in three (20%) patients, and prolonged papilledema (3years) in one (7%) patient were reported [21]. In another
study, 104 patients were evaluated. It was reported that 10% of the patients had
morbidities such as papilledema, cranial nerve palsy, SNHL, paralysis, and hip septic arthritis at discharge; however, all complications were resolved in long-term
follow-up [22]. In another study, the most common sequelae were visual eld
defects, headaches, HL, and seizures [24].
23.4.9 Hearing Loss
Lateral sinus thrombosis is the type of CST in which HL is most common at admission and after discharge. In a review evaluating 104 pediatric LSTs between 1993
and 2011, HL was seen in 10% of admission associated with otitis, improved with
treatment, and did not draw attention to the prognosis [22]. In another review evaluating approximately 200 pediatric autogenic CSTs in the literature, HL was detected
in six cases (3%) [23]. In another study in which 12 patients were evaluated, with a
follow-up period of 3months to 5years (mean 19months), 10 of 12 patients underwent formal audiological evaluation in the early follow-up period; HL was detected
in 50% (ve cases) cases (unilateral mild–moderate conduction type in three patients
326
https://t.me/medicina_free
and mixed-type HL in two patients). Hearing loss was reported to be temporary in
four and permanent in one after long-term follow-up [20]. In another 10-year retrospective study, 3% (approximately 8) of 38 patients with CST developed acute unilateral HL due to ipsilateral LST with MR.Concurrent tinnitus and headache were
also detected in two of them [7].
T. Çelik et al.
23.5 Septic Superior Sagittal Sinus Thrombosis
The superior sagittal sinus is the giant venous duct in the brain. Many cortical veins
eventually empty into the superior sagittal sinus. Septic thrombotic occlusion is
very rare because of the large size of the superior sagittal sinus. The most common
infection associated with complete obstruction of the superior sagittal sinus is bacterial meningitis. Anterior segment thrombosis has sometimes been associated with
frontal bacterial sinusitis. It may develop less frequently after facial plastic surgery
and oral surgery [1].
Septic thrombosis of the superior sagittal sinus can lead to communicating
hydrocephalus and hemorrhagic infarctions due to cortical vein thrombosis. When
associated with meningitis, massive cerebral infarction, which can develop if complicated by meningitis-associated cerebral edema, rapidly leads to transtentorial
brainstem herniation.
Diagnosis is made by demonstrating thrombus formation and decreased venous
ow by cranial MR and MR venography.
If the superior sagittal sinus is completely occluded, the result is fatal. Anterior
segment occlusion with frontal sinusitis presents with mild-to-moderate headache
and resolves spontaneously following the development of collateral venous ducts.
Although anticoagulants and thrombolytic therapy are generally applied in aseptic
superior sagittal sinus thrombosis, their role in septic disease has not been dened [1].
23.6 Conclusion
In conclusion, although CST is rare in children, complications that impair quality of
life, such as HL, are substantial. In particular, the LST is the most common type of
CST with hearing loss. In cavernous sinus thrombosis, however, conductive type or
SNHL may develop due to accompanying otitis media, although HL rarely causes
it. The role of anticoagulant therapy in children is controversial; however, it is generally recommended because the infection that induces and/or accelerates thrombosis resolves with appropriate antibiotic therapy, and thrombotic vessels are often
re-channeled. In general, anticoagulant therapy is recommended in patients with
progression of thrombosis and clinical failure to resolve despite antibiotics and surgical drainage when indicated, detection of thrombus dissemination to other sites,
clinical presentation accompanied by neurological ndings, and/or embolic events,
and pre-existing hypercoagulopathy. Pediatricians should consider the approaches
for early detection and optimal treatment of complicated infections that may cause
23 Focal Suppurative Infections of the Central Nervous System in Children…
https://t.me/medicina_free
327
septic CST, close follow-up of children with hypercoagulopathy for thrombosis, and
early detection and/or treatment of adverse outcomes such as HL when CST
develops.
References
1. Southwick FS.Septic dural sinus thrombosis. In: Tunkel AR, Tung GA, editors. UpToDate.
Waltham, MA: UpToDate; 2022. Updated 20 Nov 2020; literature review: Sep 2022. https://
www.uptodate.com/contents/septic- dural- sinus- thrombosis. Accessed 17 Oct 2022.
2. Ichord R.Cerebral sinovenous thrombosis. Front Pediatr. 2017;5:163.
3. Dlamini N, Billinghurst L, Kirkham FJ. Cerebral venous sinus (sinovenous) thrombosis in
children. Neurosurg Clin N Am. 2010;21:511–27.
4. Crassard I, Biousse V, Bousser MG, Meyer B, Marsot-Dupuch K.Hearing loss and headache revealing lateral sinus thrombosis in a patient with factor V Leiden mutation. Stroke.
1997;28:876–8.
5. Ishak MN, Nik-Abdul-Ghani NM, Mohamad I.Sudden bilateral sensorineural hearing loss
secondary to cerebral venous thrombosis. Iran J Otorhinolaryngol. 2018;30:113–6.
6. Park JW, Kim DH, Kang TK, Sunwoo W.Relationship between the drainage pattern of the
dural venous sinuses and hearing recovery in patients with sudden sensorineural hearing loss.
Sci Rep. 2020;10:6013.
7. Gattringer T, Enzinger C, Birner A, etal. Acute unilateral hearing loss as an early symptom of
lateral cerebral sinus venous thrombosis. Arch Neurol. 2012;69:1508–11.
8. Oh JH, Park K, Lee SJ, Shin YR, Choung YH.Bilateral versus unilateral sudden sensorineural
hearing loss. Otolaryngol Head Neck Surg. 2007;136:87–91.
9. Press CA, Lindsay A, Stence NV, Fenton LZ, Bernard TJ, Mirsky DM.Cavernous sinus thrombosis in children: imaging characteristics and clinical outcomes. Stroke. 2015;46:2657–60.
10. Smith DM, Vossough A, Vorona GA, Beslow LA, Ichord RN, Licht DJ.Pediatric cavernous
sinus thrombosis: a case series and review of the literature. Neurology. 2015;85:763–9.
11. Sweis R, Biller J.Cavernous sinus thrombosis in children. Pediatr Neurol Briefs. 2016;30:4.
12. Levine SR, Twyman RE, Gilman S.The role of anticoagulation in cavernous sinus thrombosis.
Neurology. 1988;38:517–22.
13. Khatri IA, Wasay M. Septic cerebral venous sinus thrombosis. J Neurol Sci. 2016;362:
221–7.
14. American Academy of Pediatrics. Antimicrobial agents and related therapy. In: Kimberlin
DW, Barnett ED, Lyneld R, Sawyer MH, editors. Red Book: 2021–2024 report of the committee on infectious diseases. 32nd ed. Itasca, IL: American Academy of Pediatrics; 2021.
p.863–1002.
15. Southwick FS, Richardson EP Jr, Swartz MN.Septic thrombosis of the dural venous sinuses.
Medicine (Baltimore). 1986;65:82–106.
16. Chalmers E, Ganesen V, Liesner R, etal., British Committee for Standards in Haematology.
Guideline on the investigation, management and prevention of venous thrombosis in children.
Br J Haematol. 2011;154:196–207.
17. Zuurbier SM, Coutinho JM, Stam J, etal. Clinical outcome of anticoagulant treatment in head
or neck infection-associated cerebral venous thrombosis. Stroke. 2016;47:1271–7.
18. van der Poel NA, Mourits MP, de Win MML, Coutinho JM, Dikkers FG.Prognosis of septic
cavernous sinus thrombosis remarkably improved: a case series of 12 patients and literature
review. Eur Arch Otorhinolaryngol. 2018;275:2387–95.
19. Scorpecci A, Massoud M, Giannantonio S, etal. Otogenic lateral sinus thrombosis in children: proposal of an experience-based treatment owchart. Eur Arch Otorhinolaryngol.
2018;275:1971–7.
328
https://t.me/medicina_free
20. Ghosh PS, Ghosh D, Goldfarb J, Sabella C.Lateral sinus thrombosis associated with mastoiditis and otitis media in children: a retrospective chart review and review of the literature. J
Child Neurol. 2011;26:1000–4.
21. Raja K, Parida PK, Alexander A, Surianarayanan G.Otogenic lateral sinus thrombosis: a
review of fteen patients and changing trends in the management. Int Arch Otorhinolaryngol.
2018;22:208–13.
22. Au JK, Adam SI, Michaelides EM. Contemporary management of pediatric lateral sinus
thrombosis: a twenty year review. Am J Otolaryngol. 2013;34:145–50.
23. Castellazzi ML, di Pietro GM, Gaffuri M, et al. Pediatric otogenic cerebral venous sinus
thrombosis: a case report and a literature review. Ital J Pediatr. 2020;46:122.
24. Scherer A, Jea A.Pediatric otogenic sigmoid sinus thrombosis: case report and literature reappraisal. Glob Pediatr Health. 2017;4:2333794X17738837.
25. Singh GB, Arora R, Garg S, Kumar D, Ranjan S.Septic lateral sinus thrombosis: sinus exploration is unnecessary. Case Rep Otolaryngol. 2016;2016:4349538.
T. Çelik et al.
Соседние файлы в папке Библиотека им академика М.И. Перельмана