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
206
https://t.me/medicina_free
N. Sarı et al.
A Taiwanese study reported by Yang etal. using a case-control design and based
on the general population across the island noted that NOE was associated with
diabetes mellitus. The authors noted that the frequency of diabetes mellitus amongst
patients with NOE was 54.8%, whereas diabetes only occurred in 13.9% of control
subjects. For patients suffering from NOE, the adjusted odds ratio for having a preexisting diagnosis of diabetes was 10.07 [13].
Sylvester and colleagues looked at 8300 cases where NOE was the diagnosis.
These cases were sourced from the National Inpatient Sample database between the
years 2002 and 2013. It was discovered that cases where the patient was an adult or
older adult and diabetic were more likely to suffer from co-morbid conditions,
require a longer in-patient period (5.5days in diabetics compared to 4.0days where
diabetes was not present) and paid more for their care (on average $25,118 compared to $17,039). Despite these differences, the risk of dying as an in-patient did
not differ at the level of statistical signicance between diabetic and nondiabetic
patients (0.6% compared to 0.5%) [14].
15.4 Aetiology
• Diabetes mellitus (present in 90% of cases) [3]:
– The highest risk for NOE is found in those individuals with diabetes.
– Diabetic changes in the small-calibre vessels and less effective immunity in
diabetics explains this association.
– Ear wax in diabetic patients is less acidic than normal and contains less lyso-
zyme. This may lead to less localised bactericidal activity.
– Diabetes mellitus types I and II both predispose equally to NOE.
– There does not appear to be a straightforward relationship between how long
or how severely raised the blood glucose level is.
• Immunodeciency, which may be secondary to a disorder such as a lymphoproliferative condition or may be drug-related.
• AIDS [3]
– Cases of NOE occurring in association with AIDS may differ in their patho-
– The symptomatic presentation is similar to other cases, but the age at onset is
– Granulation tissue may not form within the ear canal.
– There may be a different pathogen responsible, unlike other cases, which are
– The prognosis in this group of patients is worse in general than in patients
• Ear irrigation/washout. Up to half of all cases of NOE have a history of trauma
secondary to ear washing out and are diabetic [3].
.
logical features from non-AIDS-associated cases.
lower, and the patient is not diabetic.
typically due to P. aeruginosa.
who are diabetic.
15 Necrotising (Malignant) Otitis Externa andAuditory Impairment inChildren
https://t.me/medicina_free
207
15.5 Epidemiology
• Although the introduction of antibiotics with activity against a broader range of
micro-organisms has decreased the frequency of NOE, it is still by no means a
rare disorder [1].
• Although cases occur across the entire age range, it is most frequently seen in
older adults (i.e. above the age of 60years [15].
• NOE has a male predilection [16].
• The incidence rises inlocations where the climate is typically humid [17].
• NOE is seldom seen in children [18].
15.6 Signs andSymptomatology ofNOE
Signs of inammation are seen within the ear canal and the soft tissues surrounding
the pinna. The degree of otalgia is greater than would be expected from the physical
ndings alone. The area lying between the ramus of the mandible and the tip of the
mastoid is very tender to palpation. Granulation tissue is visible on the oor of the
external auditory meatus at the junction between the bony and cartilaginous canal.
If granulation tissue is observed at this location, the diagnosis is almost certainly
NOE.There may be bare bone visible on otoscopy [3].
There are several other features in the clinical presentation to look out for, such
as the following [3]
• Presence of diabetes mellitus (in 90% of cases) or a reason for the immune system to be suppressed (either due to another condition or drug-related).
• Ear ache is felt deeply and severely and does not stop. It is especially bothersome
at night.
• Headaches are felt around the temples.
• Pus may be discharged from the ear, with a foul odour.
• Swallowing may be impaired, and there may be dysphonia +/− signs of a seventh
cranial nerve palsy.
15.7 Complications, Including Auditory Impairment, inNOE
NOE may cause auditory impairment of conductive type. It varies in severity. If
NOE is of high severity, a cranial neuropathy may be evident. A seventh cranial
nerve neuropathy is the initial development, but if the condition progresses, the
glossopharyngeal, vagus and accessory nerves may be affected. The basal skull
develops osteomyelitis, stretching from the stylomastoid to the jugular foramen, or
even further [19].
208
https://t.me/medicina_free
N. Sarı et al.
15.8 Physical Examination
• Signs of inammation are seen within the ear canal and the soft tissues surrounding the pinna.
• The degree of otalgia is greater than would be expected from the physical ndings alone.
– The area lying between the ramus of the mandible and the tip of the mastoid
is very tender to palpation.
– Granulation tissue is visible on the oor of the external auditory meatus at the
junction between the bony and cartilaginous canal. If granulation tissue is
observed at this location, the diagnosis is almost certainly NOE.There may
be bare bone visible on otoscopy.
• A neurological examination of the fth to twelfth cranial nerves should be
undertaken.
• Assessment of mental state is needed. Any change in mental state may potentially signify extension of infection into the cranial cavity.
• The ear drum is typically normal.
• Pyrexia is rarely noted [3].
The most effective approach to diagnosing NOE involves the use of the diagnos-
tic criteria rst proposed by Cohen and Friedman [4]. The diagnostic scheme
involves major criteria, which must be present to make the diagnosis, and minor
criteria, which represent features that are sometimes present.
Major Diagnostic Criteria
• Otalgia, which is frequently greater than physical examination might suggest
• Swelling
• Discharge
• Granulation tissue formation within the external auditory meatus
• Microabscess (visible during a surgical procedure)
• Imaging evidence from radioisotopic technetium scan (99Tc)
• Topical treatment does not lead to resolution within 7days
Minor Diagnostic Criteria
• Diabetes mellitus
• Cranial neuropathy
• X-ray evidence
• Debilitation
• Elderly patient
To diagnose NOE, the major diagnostic criteria must apply. The existence of
minor criteria alone is insufcient to conrm the presence of NOE [20, 21].
There should be a neurological examination, focused on the cranial nerves,
which are frequently involved in cases of NOE.
15 Necrotising (Malignant) Otitis Externa andAuditory Impairment inChildren
https://t.me/medicina_free
• The seventh cranial nerve is the most frequently involved.
• The ninth, tenth, and eleventh cranial nerves may also be affected.
• The 12th cranial nerve is not usually affected [11].
The patient’s mental state must also be assessed, as any change in this may indi-
cate that there is involvement of the intracranial cavity [22].
209
15.9 Diagnosis
There is generally either no leucocytosis or at most a mild leucocytosis in NOE.A
left shift is an infrequent nding. However, in every case, the erythrocyte sedimentation rate (ESR) is raised. The mean value is 87mmh−1 [3].
In cases where there is pre-existing diabetes mellitus, a biochemical prole is
required to assess any metabolic effects of the infection. If there is no previous diagnosis of diabetes, testing should be undertaken for impairment of glucose tolerance [3].
Wherever feasible, any otic discharge should be cultured prior to starting antibi-
otic treatment. The pathogen occurring with the highest frequency (95% of cases) is
P. aeruginosa. Radiological investigations are key to assessing whether osteomyelitis is present, and if so, how extensive it is and how it responds to treatment. Suitable
investigations include a bone scan with Tc99m methylene diphosphonate, a gallium- 67 citrate study, scans using indium-111 leucocytic labelling, computed
tomography (CT) or magnetic resonance imaging (MRI) [3]. A histological specimen of the external auditory meatus should be sent for evaluation of potential
malignancy or other conditions [3].
15.9.1 Imaging Investigations
Imaging plays a key role in diagnostic work-up, since it can conrm whether osteomyelitis is present and, if so, how extensive it is and how it responds to treatment [3].
15.9.2
Imaging of the bone using 99mTc methylene diphosphonate works by labelling
osteoblasts. Even if the osteoblasts are only 10% more active than usual, this change
can be seen on the scan. The result lacks specicity, however, as the same appearances may also result from a neoplastic or dysplastic bone lesion, which both
increase osteoblastic activity. Nonetheless, this investigation is helpful in appropriate situations since a positive result conrms the clinical impression [3].
responding to treatment because the osteoblastic activation continues for a considerable period after clinical resolution. It also has limitations in cases where there has
99m
Tc Methylene Diphosphonate Bone Scan
This form of imaging cannot supply information about whether the lesion is
210
https://t.me/medicina_free
been mastoiditis or ear surgery in the past. Historically, the scan suffered from low
spatial resolution, but the advent of single-photon emission computed tomography
(SPECT) has somewhat improved this situation [3].
N. Sarı et al.
15.9.3 Gallium-67 Imaging Scan
Although imaging using a gallium-67 tracer benets from high sensitivity, the specicity is low since this isotope is bound to any actively mitotic cell, whether in
inammation, neoplasia or osteoblastic activation. Thus, a positive scan may be
difcult to interpret diagnostically, since it may represent inammation or another
lesion of the soft or osseous tissues. Its main value lies in the evaluation of response
to therapy. A less active lesion on imaging indicates treatment success in this setting. The usual method is to scan the patient when NOE is rst diagnosed to allow
meaningful comparison with later scans as treatment progresses [3].
If the two ears are compared in a quantitative manner, so that the diseased ear is
compared with the normal ear, imaging may be able to differentiate between acute
otitis externa and NOE and may indicate how successful treatment has been. Once
again, by using SPECT, there can be an improvement in the level of spatial resolution the scan can offer [3].
15.9.4 Imaging Utilising Indium-111 Leucocytic Labelling
Imaging that uses the indium-111 radioisotope to label leucocytes is as sensitive as
the gallium-67 method but offers greater specicity in identifying inammation. It
does not appear to be superior as a nuclear medical technique for diagnosing NOE,
but it is possibly superior in terms of monitoring when therapy has succeeded. Scans
used for other chronic osteomyelitic lesions at other body locations suffer from a
lack of reliability; thus, further investigation is needed into how reliable this technique is in cases of NOE [3].
15.9.5 CT andMR Imaging
Both CT and MRI offer benet inlocating where soft tissue inammation occurs,
identifying an abscess and assessing possible extension into the cranial cavity. CT
has limited ability to highlight osteomyelitis in its initial stages, since it can only
detect the lesion following 30–50% osseous destruction. MRI, on the other hand, is
not the ideal method to image bone. Response of the lesion to treatment is apparent
on CT and MRI as regression of soft tissue changes. The osseous tissues appear
abnormal on CT for more than 1 year. MRI does not reveal these osseous changes
clearly. Accordingly, neither CT nor MRI can determine whether the osteomyelitis
has fully resolved.
15 Necrotising (Malignant) Otitis Externa andAuditory Impairment inChildren
https://t.me/medicina_free
Goh and colleagues [23] examined MR images retrospectively. They ascertained
that there were differences apparent between cases of advanced malignancy of the
nasopharynx and NOE.In the latter, the ndings were that the lesion extends laterally, there is enhancement of the surrounding soft tissues on T2 weighted scans, the
architecture does not become distorted, and the enhanced areas have the same signal
as mucosa or even higher [23].
The majority of the literature is in favour of undertaking CT imaging at the initial
stage of diagnosis. Benecke, however, believes that CT should only be requested
where the cranial nerves are involved, the Tc99m scan indicates osteoblastosis, or
the lesion does not show a clinical response to therapy. According to both Grandis
etal. and Okpala etal. CT imaging should be undertaken at an early stage in management. Peleg etal. found that the size of the lesion on CT imaging performed at
the beginning of treatment correlated with the clinical progression [24].
Whilst MRI and CT have the same associated sensitivity for detecting soft tissue
involvement, MRI has superior sensitivity for evaluating spread into the cranial
cavity [3].
211
15.10 Therapy
The management of NOE may involve scrupulous control of blood sugar, manual
cleaning of the ear, both topical and systemic antibiotics and hyperbaric oxygen
administration [25, 26]. Currently, operative intervention is indicated where there is
an area to be debrided, there are sequestrated lesions in the bone or an abscess needs
to be drained [3].
15.10.1 Antimicrobial Treatment
• Pharmacotherapy consists of systemic antibiotics using agents that are active
against Pseudomonas spp. One of the uoroquinolone agents is usually chosen if
the pathogen is P. aeruginosa. Since ciprooxacin is very widely used in cases of
upper respiratory tract infection, drug-resistant organisms have been extensively
documented [7]. This agent may be given by mouth to patients in the community
provided there is no cranial neuropathy, and they do not require hospitalisation
for analgesia and stabilisation of diabetes mellitus. In cases of treatment resistance, antibiotics of beta lactams which are active against Pseudomonas +/− an
aminoglycoside can be administered intravenously [4].
• Whilst P. aeruginosa is the pathogen responsible in the majority of cases of
NOE, there are other microbes that may cause the condition, and thus, treatment
selection should be guided by identication of the pathogen.
• How long treatment goes on for is dictated by how well the lesion responds to
treatment. Progress should be monitored by means of a gallium-67 scan each
4–6weeks whilst therapy continues.
212
https://t.me/medicina_free
N. Sarı et al.
• Pharmacotherapy continues for 7 days after the last normal result from a gallium- 67 scan [4].
15.10.2 Hyperbaric Oxygen Administration
• The use of hyperbaric oxygen in treating NOE is common, but multiple researchers have demonstrated that it adds no additional benet to pharmacotherapy with
or without operative intervention [26, 27].
15.10.3 Operative Interventions
• Surgical interventions are only used where pharmacotherapy alone does not
result in resolution of the lesion. Operative interventions consist of debriding a
particular area, excising sequestered lesions in bone and draining of abscesses.
Decompression of the seventh cranial nerve is not required in cases of facial
neuropathy since it has no effect upon the outcome [28, 29].
References
1. Karaman E, Yilmaz M, Ibrahimov M, Haciyev Y, Enver O.Malignant otitis externa. J Craniofac
Surg. 2012;23(6):1748–51.
2. Chandler JR.Malignant external otitis. Laryngoscope. 1968;78(8):1257–94.
3. Nussenbaum B. Malignant otitis externa. In: Meyers AD, editor. Medscape; 2020. https://
emedicine.medscape.com/article/845525- overview. Accessed 10 Feb 2022.
4. Al Aaraj MS, Cecylia KC. Malignant otitis externa. Treasure Island (FL): StatPearls
Publishing; 2022.
5. van Kroonenburgh AMJL, van der Meer WL, Bothof RJP, van Tilburg M, van Tongeren J,
Postma AA.Advanced imaging techniques in skull base osteomyelitis due to malignant otitis
externa. Curr Radiol Rep. 2018;6(1):3.
6. Kwon BJ, Han MH, Oh SH, Song JJ, Chang KH.MRI ndings and spreading patterns of
necrotizing external otitis: is a poor outcome predictable? Clin Radiol. 2006;61(6):495–504.
7. Rubin Grandis J, Branstetter BF, Yu VL.The changing face of malignant (necrotising) external
otitis: clinical, radiological, and anatomic correlations. Lancet Infect Dis. 2004;4(1):34–9.
8. Chandler JR. Malignant external otitis: further considerations. Ann Otol Rhinol Laryngol.
1977;86(4 Pt 1):417–28.
9. Franco-Vidal V, Blanchet H, Bebear C, Dutronc H, Darrouzet V.Necrotizing external otitis: a
report of 46 cases. Otol Neurotol. 2007;28(6):771–3.
10. Soudry E, Joshua BZ, Sulkes J, Nageris BI.Characteristics and prognosis of malignant external otitis with facial paralysis. Arch Otolaryngol Head Neck Surg. 2007;133(10):1002–4.
11. Mani N, Sudhoff H, Rajagopal S, Moffat D, Axon PR.Cranial nerve involvement in malignant
external otitis: implications for clinical outcome. Laryngoscope. 2007;117(5):907–10.
12. Nawas MT, Daruwalla VJ, Spirer D, Micco AG, Nemeth AJ.Complicated necrotizing otitis
externa. Am J Otolaryngol. 2013;34(6):706–9.
13. Yang TH, Xirasagar S, Cheng YF, etal. Malignant otitis externa is associated with diabetes: a
population-based case-control study. Ann Otol Rhinol Laryngol. 2020;129(6):585–90.
15 Necrotising (Malignant) Otitis Externa andAuditory Impairment inChildren
https://t.me/medicina_free
14. Sylvester MJ, Sanghvi S, Patel VM, Eloy JA, Ying YM.Malignant otitis externa hospitalizations: analysis of patient characteristics. Laryngoscope. 2017;127(10):2328–36.
15. Kaya İ, Sezgin B, Eraslan S, Öztürk K, Göde S, Bilgen C, Kirazlı T. Malignant otitis
externa: a retrospective analysis and treatment outcomes. Turk Arch Otorhinolaryngol.
2018;56(2):106–10.
16. Mills R.Malignant otitis externa. Br Med J (Clin Res Ed). 1986;292(6518):429–30.
17. Walton J, Coulson C.Fungal malignant otitis externa with facial nerve palsy: tissue biopsy
AIDS diagnosis. Case Rep Otolaryngol. 2014;2014:192318.
18. Wiegand S, Berner R, Schneider A, Lundershausen E, Dietz A.Otitis externa. Dtsch Arztebl
Int. 2019;116(13):224–34.
19. Kesser BW. Malignant external otitis (necrotizing Otitis externa; skull base osteomyelitis).
MSD Manual Professional Version. 2020. https://www.msdmanuals.com/professional/ear,-
nose,- and- throat- disorders/external- ear- disorders/malignant- external- otitis. Accessed 10
Feb 2022.
20. Cohen D, Friedman P. The diagnostic criteria of malignant external otitis. J Laryngol Otol.
1987;101(3):216–21.
21. Illing E, Zolotar M, Ross E, Olaleye O, Molony N.Malignant otitis externa with skull base
osteomyelitis. J Surg Case Rep. 2011;2011(5):6.
22. Manso MC, Rodeia SC, Rodrigues S, Cavilhas P, Domingos R.Malignant otitis externa and
stroke. Eur J Case Rep Intern Med. 2016;3(4):000387.
23. Goh JPN, Karandikar A, Loke SC, Tan TY.Skull base osteomyelitis secondary to malignant
otitis externa mimicking advanced nasopharyngeal cancer: MR imaging features at initial presentation. Am J Otolaryngol. 2017;38(4):466–71.
24. Peleg U, Perez R, Raveh D, Berelowitz D, Cohen D.Stratication for malignant external otitis.
Otolaryngol Head Neck Surg. 2007;137(2):301–5.
25. Ling SS, Sader C.Fungal malignant otitis externa treated with hyperbaric oxygen. Int J Infect
Dis. 2008;12(5):550–2.
26. Phillips JS, Jones SE.Hyperbaric oxygen as an adjuvant treatment for malignant otitis externa.
Cochrane Database Syst Rev. 2013;2013(5):CD004617.
27. Phillips JS, Jones SE.Hyperbaric oxygen as an adjuvant treatment for malignant otitis externa.
Cochrane Database Syst Rev. 2005;2005(2):CD004617.
28. Raines JM, Schindler RA.The surgical management of recalcitrant malignant external otitis.
Laryngoscope. 1980;90(3):369–78.
29. Lee SK, Lee SA, Seon SW, Jung JH, Lee JD, Choi JY, Kim BG.Analysis of prognostic factors
in malignant external otitis. Clin Exp Otorhinolaryngol. 2017;10(3):228–35.
213
Acute Otitis Media andHearing Loss
https://t.me/medicina_free
inChildren
BilalSizer, CemalCingi, andGabrielaKopacheva-Barsova
16.1 Introduction
For children below the age of 5 years living in the United States, acute otitis media
(AOM) is the most frequently occurring indication for pharmacotherapy. AOM is
dened as acute inammation of the middle ear resulting in typical signs and symptoms and having a maximum duration of 3 weeks [1–4].
Although AOM and the related otitis media with effusion (OME) each cost the
American economy billions of dollars every year and have been intensively investigated, both in terms of how they can be prevented and how best treated, the incidence has not fallen signicantly, and the cost keeps going up [1].
Whereas AOM by denition refers to a disorder of maximum 3-week duration
with signs and symptoms consistent with an acute inammatory process, the denition of OME stipulates that uid be found in the middle ear, and there should be
auditory impairment of conductive type but no signs or symptoms indicating an
acute process. If the period for which OME exists is between 3weeks and 3months
16
B. Sizer (*)
Section of Otorhinolaryngology, Memorial Diyarbakır Hospital, Diyarbakır, Türkiye
e-mail: bilalsizer@arel.edu.tr
C. Cingi
Department of Otorhinolaryngology, Faculty of Medicine, Eskişehir Osmangazi University,
Eskişehir, Türkiye
e-mail: cemal@ogu.edu.tr; ccingi@gmail.com
G. Kopacheva-Barsova
Department of Otorhinolaryngology, Faculty of Medicine, Cyril and Methodius University of
Skopje, Skopje, Republic of North Macedonia
e-mail: gabrielak70@yahoo.com
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
A. E. Arısoy et al. (eds.), Hearing Loss in Congenital, Neonatal and Childhood
Infections, Comprehensive ENT, https://doi.org/10.1007/978-3-031-38495-0_16
215
216
https://t.me/medicina_free
after the beginning of AOM, it is described as ‘subacute’, whereas OME lasting
beyond this time is termed ‘chronic’ [2, 3].
Conventionally, AOM has been treated by antibiotic therapy, and this still remains
the rst line of therapy, despite concerns arising from the growing numbers of
antibiotic- resistant bacterial pathogens isolated. In cases where operative interventions are required, there are three alternative techniques used: tympanocentesis,
myringotomy and myringotomy with grommet placement [1].
B. Sizer et al.
16.2 Pathophysiology
The key triggering event for the development of AOM seems to be blockage of the
auditory tube. By far, the most common cause is an upper respiratory tract infection
that affects the nasopharyngeal region [1].
16.2.1 Infections by Bacteria andViruses
Although the upper respiratory tract infection is typically caused by a virus, other
pathological processes that affect the patency of the auditory tube, such as an allergic reaction or other cause of inammation, may result in a similar pathology.
Nasopharyngeal inammation affects the medial portion of the auditory tube, provoking stasis and an inammatory response. The middle ear pressure is changed by
these events, being, in most cases, lower than the surrounding pressure, although
sometimes higher.
Since stasis develops, this sets up the necessary conditions for bacterial pathogens to colonise the middle ear cavity, an area which is usually sterile. Nasopharyngeal
bacteria may enter through being reuxed, aspirated or insufated into the auditory tube.
There develops an acute inammatory response to the presence of the pathogen.
This consists of dilation of blood vessels, formation of an exudate, recruitment of
white cells to the area, phagocytosis of the offending organism and localised
immune responses in the middle ear cavity. This response accounts for the way
AOM presents clinically [1].
16.2.2 Immunological Factors
There may be an important immunological component to how commonly AOM
occurs and its eventual outcome. There has been a greater research focus on immunological factors in OME than in AOM; however, there are also demonstrable effects
of the patient’s immunocompetence on AOM, too. These include the following [1]:
• The ability to synthesise immunoglobulins can ensure the middle ear is cleared
of the pathogen following the initial invasion.
Соседние файлы в папке Библиотека им академика М.И. Перельмана