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_4446_Библиотеки_им_академика_М_И_Перельмана
.pdf
198
H. Haidar and S. Mohamed
It can be adequately treated with wide myrin-
gotomy and systemic antibiotics.
18.6.6 Chronic Otitis Media
Facial nerve dysfunction associated with chronic
suppurative otitis media (mucosal inammation
or cholesteatoma) reects a toxic neuritis, external compression, or intraneural compression
from edema or abscess.
18.6.6.1 Treatment
Treatment includes mastoidectomy as soon as
possible with surgical removal of irreversible
disease in the middle ear and mastoid, as well as
decompression of the involved segment.
18.6.7 Malignant Otitis Externa
It affects elderly patients with uncontrolled diabetes
mellitus or in others who are immunocompromised
and typically present with symptoms of otorrhea
and progressive disabling otalgia lasting few weeks.
The pathognomonic signs are otoscopic evidence of ear canal inammation or granulation
tissue at the bony–cartilaginous junction.
Facial palsy reects advanced skull base
extension of the osteomyelitis.
Less than 5% of facial palsy is caused by a
neoplasm [7].
Despite the rarity of facial nerve tumors, the
presence of a progressive, persistent, or recurrent facial nerve function decit should always
arouse suspicion of a facial nerve lesion and warrants MRI with gadolinium. Other clues for facial
nerve tumors are hemifacial spasm antecedent
to the palsy, associated dysfunction of regional
cranial nerves, prolonged otalgia or facial pain,
mass in the middle ear, external ear canal, digastric region, or parotid gland.
Schwannomas are the most commonly identied histopathologically, followed by hemangiomas and meningiomas.
Facial nerve schwannomas can arise from
any segment of the facial nerve and are usually
located in a multisegment manner, intratemporally and particularly in the geniculate ganglion
(Fig.18.4).
The number of cases with isolated intraparotid
locations is limited [8].
18.6.7.1 Diagnosis
– MRI is very helpful for establishing extent of
disease and monitoring response to therapy.
18.6.7.2 Treatment
– Systemic antipseudomonal antibiotics
– Operative debridement of the tympanic bone,
the mastoid, and the skull base is indicated
only when medical treatment fails
18.6.8 Facial Nerve Neoplasms
Facial nerve tumors are rare lesions.
Fig. 18.4 Postcontrast T1 MRI showing right sided
enhancing lesion with cystic change suggestive of facial
nerve schwannoma involving the cerebellopontine angle,
meatus, labyrinthine segment, and geniculate ganglion
18 The Facial Nerve
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Facial Nerve Schwannomas
• Most common primary neoplasm of
facial nerve.
• Slowly growing tumors, average 1m per
year.
• Multisegmental involvement with geniculate ganglion most commonly affected [9].
• Iso to hypointense on T1, iso to
hyperintense on T2 with homogenous
enhancement.
• Cystic change in 20% of cases
(Fig.18.4) [9].
• CT may show bone remodeling and
scalloping if intratemporal in location.
• Management: Observation, Radiosurgey,
rarely excision (see algorithm Fig.18.5).
Facial Nerve Hemangioma
• Venous vascular malformation of the
facial nerve.
• Predilection for the geniculate ganglion.
• Facial palsy out of proportion to the size
of the lesion.
• Heterogeneously hyperintense T2 mass
with punctuate foci of hypointensity
which enhances.
• CT scan: honey comb appearance.
199
18.6.8.1 Management Plan
Preoperative facial nerve function is the most
important factor determining the treatment
approach (see algorithm Fig.18.5):
• Normal nerve function or weakness HB III or
less → Clinical and radiological follow-up.
• Growing facial nerve tumors → Radiosurgery.
• Facial palsy HB grade IV or more → Surgical
excision+ reconstruction.
• Symptomatic facial nerve tumors → surgical
excision.
18.6.8.2 Surgery
In most cases, excision of the involved facial
nerve segment is required for total tumor resection. In such cases, reconstruction with a nerve
graft is required. Postoperative facial nerve function is usually not better than HB Grade 3 [10].
The most important factor determining postop-
erative facial nerve function is the grade and duration of facial nerve paralysis before surgery [11].
Long-standing complete facial palsy implies very
bad prognosis for postoperative facial nerve function.
18.6.9 Iatrogenic Facial Paralysis
The facial nerve can be injured by direct mechanical disruption from a rotating burr, transection
with a sharp instrument, accidental evulsion (eg,
Fig. 18.5 Algorithm
showing management
plan for facial nerve
schwannoma
Wait and scan
Facial Nerve Shwannoma
HB Grade < IV
Growth in size or HB grade
became ≥IV
AL GRAWANY
HB Grade ≥ IV
Small growing tumors
Radiosurgery
Intervention
and HB grade ≤IV
Large tumors or
HB grade V-VI
Surgical resection + grafting
200
H. Haidar and S. Mohamed
from traction), or a crushing injury. A rotating
surgical burr can produce thermal injury without directly contacting the facial nerve. Thermal
injury is more likely when diamond burrs are
used than when cutting burrs are employed.
18.6.9.1 Parotid Surgery
• Most common surgery with iatrogenic FN
injury.
• The likelihood of facial weakness correlates
with tumor location deep to the plane of the
facial nerve, previous parotid surgery, and previous sialadenitis.
• All parotid surgery is best undertaken with
facial nerve monitoring, and at the end of the
procedure, the main trunk should be stimulated to conrm continuity.
• If there is no response, the nerve and its
branches should be closely inspected for
areas of discontinuity and repaired
immediately.
18.6.9.2 Ear Surgery
• The incidence of FN palsy is less than 1%.
• Most commonly during mastoidectomy followed by cochlear implantation.
• Very rare in tympanoplasty or stapedectomy
• Mechanism—direct mechanical injury or heat
generated from drilling
• Most common area of injury: second genu,
followed by mastoid segment
• Management: (Fig.18.6)
– Recognized at surgery:
Complete or more than 50% transaction
→ Primary repair
Less than 50% disruption: decompression (1cm from each side of injury)
No return of function should be anticipated before 4months
– Recognized immediate postoperatively:
Remove the mastoid dressing and ear
pack and wait for few hours for LAinduced weakness to wear off
Paralysis persists and surgeon unsure
about integrity of facial nerve → Reexplore as soon as possible
Sure about integrity of facial nerve →
High-dose steroids ×10 days
Facial Palsy after Ear Surgery
Damage recognized intraoperatively
Complete transaction
or
> 50% fibers interruption
Primary
anastomosis
or cable graft if
not possible
Sheath Injury
or
<50% disruption
Decompression
(1 cm from each
side of injury)
Immediate Postop facial palsy
Remove dressing and ear pack &
wait few hours for LA to wear off
Paralysis persist
Surgeon sure about
Surgeon NOT sure
about nerve integrity
Re-explore as soon
as possible
nerve integrity
Fig. 18.6 Algorithm for management of iatrogenic facial palsy after ear surgery
Delayed facial palsy
Prednisone and
High dose steroids x10 days
Worsening paralysis or
72 hrs ENoG : >90% denervation
acyclovir
18 The Facial Nerve
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
201
72 h—ENoG to assess degree of degeneration: >90% degeneration → re-explore
<90% degeneration—monitor
If worsening paralysis occurs, re-explore
– Delayed palsy
Incidence of 1%
Reactivation of HSV or VZV is postulated as the underlying mechanism
Combined use of prednisone and acyclovir should be considered
Overall prognosis appears to be good
IntraoperativeFacial Nerve Monitoring
• Intraoperative monitoring uses facial
electromyography, with or without a
stimulating probe.
• Muscle relexants must be avoided to
permit muscle stimulation and neural
monitoring, and this fact must be communicated to the anesthesiologist.
• Intraoperative monitoring is not a substitute for anatomic knowledge and
good surgical technique. Facial nerve
monitoring is cost effective and benecial for neurotologic, mastoid, amd
parotid surgery, and its use can reduce
the risk of iatrogenic facial nerve injury.
• Intraoperative monitoring is not a substitute for anatomic knowledge and good
surgical technique. Improper set up,
equipment failure, or misuse may lead to
worse outcomes than if facial monitoring
was not used.
18.7 Bilateral Facial Nerve
Paralysis (Fig.18.7)
18.7.1 Melkersson–Rosenthal
Syndrome
pathic disease, but there may be a genetic predisposition. Crohn’s disease or sarcoidosis can have
similar manifestations.
Diagnosis is mainly based on clinical features.
Biopsy of the lip is useful in diagnosis as well as
in differentiating between the different types of
the disease.
Treatment is symptomatic and may include
NSAIDs and corticosteroids to reduce swelling.
18.8 Facial Nerve Reanimation
Strategies
The aims of facial nerve reanimation strategies are
to protect the eye, restore facial symmetry, facilitate a spontaneous, dynamic smile, and improve
speech. Operative procedures may be static or
dynamic (Fig. 18.8). The patinet should wait at
least 12 months for the rst sign of facial movment after any kind of facila nerve surgery. At the
end of this period, failure to have any sign of facial
movment imposes the need for another facial
reanimation strategy (dynamic or static).
18.8.1 Static Procedures
Static procedures do not reproduce the dynamic
movement of the face, although it may be
ameliorated. Static procedures may be very benecial to provide corneal protection, improve the
nasal airway, prevent drooling, and improve facial
asymmetry at rest. They are potentially indicated
in the elderly, the unt, those unwilling or unt
to undergo prolonged surgery, and those with
established paralysis without viable facial musculature. Static procedures to correct functional
disabilities include temporary or permanent tarsorrhaphy; insertion of gold weights, brow lift
or suspension; forehead skin excision; unilateral
facelift type procedures; and static slings.
Melkersson–Rosenthal syndrome is a rare disease of childhood and early adolescence characterized by recurrent facial paralysis, swelling
of the face and lips (usually the upper lip), and
ssured tongue.
Melkersson–Rosenthal syndrome is idio-
18.8.2 Dynamic Procedures
Dynamic procedures attempt to improve facial
symmetry at rest and to provide synchronous
AL GRAWANY
202
Fig. 18.7 Most
common causes of
bilateral facial paralysis
H. Haidar and S. Mohamed
Guillain-Barré
syndrome
Primary anastomosis:
- Best outcome
- Involves microsurgical anatomosis of
epineurim
Sarcoidosis
Facial Nerve Reanimation
Strategies
Bilateral
facial nerve
paralysis
Melkersson−
Rosental
syndrome
Infectious:
Lyme disease,
HIV, syphilis,
meningitis
Cable (interpoistion) graft:
- If need < 10 cm → greater auricular nerve
- If need > 10 cm → sural nerve
Hypoglossal-facial anatomosis:
- Indicated when proximal stump unavailable
but distal segment intact
- Sacrifices ipsilateral hypoglossal function
Facial nerve crossover graft:
- Use graft to connect branches of opposite
facial nerve to
distal segment of injured nerve
Fig. 18.8 Facial nerve reanimation strategies
< 1 year
> 1−2 years
(EMG shows facial muscle atrophy)
(EMG still shows evidence of muscle activity)
Static procedure:
- Gold weight, lat. canthoplasty, brow lift
- Alloderm or tensor fascia lata graft
Dynamic procedures:
T-Temporalis or masseter muscle
transpoition
Gracilis muscle free flap
Nerve impulses
18 The Facial Nerve
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
facial movement, preferably in a spontaneous
manner.
18.9 Hemifacial Spasm
Hemifacial spasm is a movement disorder of
muscles innervated by the facial nerve, which
is almost always unilateral. The cause in most
cases is a compression of the facial nerve in
the cerebellopontine angle by an artery, most
commonly by PICA (postero-inferior cerebellar artery) (Fig.18.9). The root exit zone of the
facial nerve (REZ) corresponds to a junctional
area between central and peripheral myelin.At
this level, the facial nerve is sensitive to compression from a vascular loop; vascular compression at the REZ of the facial nerve is the
most acceptable underlying physiopathology of
a hemifacial spasm.
18.9.1 Diagnosis
203
Fig. 18.10 CISS T2 sequence MRI showing vascular
loop (red arrow) in contact with facial nerve exit zone
By the clinical features.
Magnetic resonance imaging using CISS
artery and to rule out other intracranial cause
(Fig.18.10).
sequence is helpful to identify the offending
18.9.2 Treatment
Local injection of botulinum toxin masks the
symptoms for few months.
Microvascular decompression surgery via retrosigmoid approach with interposition of an insulating material (Teon pad) between the nerve
and the offending artery. The cure rate is above
95% with very low morbidity.
Take Home Massages
• Facial nerve is one of the complex cranial nerve due to his complex function
Artery
Nerve fibres
Fig. 18.9 Left CPA endoscopy showing compression of
the facial nerve(VII) by PICA (postero-inferior cerebellar
nerve)
and anatomical course.
• Facial nerve palsy can be unilateral or
bilateral; cases can vary from idiopathic,
infectious, neoplastic, or iatrogenic.
• Prognosis of facial nerve recovery
depends on primary pathology, type of
injury, and duration of palsy.
• Facial nerve function test can give an idea
about the type of injury and help to plan the
appropriate nerve reanimation strategy.
AL GRAWANY
204
H. Haidar and S. Mohamed
References
1. May M, Schaitkin BM, editors. The facial nerve. 2nd
ed. NewYork: Thieme; 2000.
2. Fisch U, Esslen E.Total intratemporal exposure of the
facial nerve. Pathologic ndings in Bell’s palsy. Arch
Otolaryngol. 1972;95(4):335–41.
3. Willand MP, Nguyen MA, Borschel GH, Gordon
T. Electrical stimulation to promote peripheral
nerve regeneration. Neurorehabil Neural Repair.
2016;30(5):490–6.
4. Sullivan FM, Swan IR, Donnan PT, etal. Early treatment with prednisolone or acyclovir in Bell’s palsy.
N Engl J Med. 2007;357(16):1598–607. https://doi.
org/10.1056/NEJMoa072006.
5. Peitersen E.The natural history of Bell’s palsy. Am J
Otol. 1982;4(2):107–11.
6. Murakami S, Hato N, Horiuchi J, Honda N, Gyo
K, Yanagihara N. Treatment of Ramsay Hunt syn-
drome with acyclovir-prednisone: signicance
of early diagnosis and treatment. Ann Neurol.
1997;41(3):353–7.
7. Jackson CG, Glasscock ME, Hughes F, etal. Facial
paralysis of neoplastic origin, diagnosis and management. Laryngoscope. 1980;90:1581–95.
8. Caughey RJ, May M, Schaitkin BM. Intraparotid
facial nerve schwannoma: diagnosis and management.
Otolaryngol Head Neck Surg. 2004;130:586–92.
9. Thompson AL, et al. Magnetic resonance imaging of facial nerve schwannoma. Laryngoscope.
2009;119(12):2428–36.
10. Falcioni M, Russo A, Taibah A, Sanna M.Facial nerve
tumors. Otol Neurotol. 2003;24:942–7.
11. Chao WC, Liu TC, Ng SH, Wu CM. Facial nerve
schwannoma. Otolaryngol Head Neck Surg.
2009;141:146–7.
External Ear Malignancies
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
AishaLarem, Ma’inAliAl Shawabkeh,
andZeynelA.Dogan
19
19.1 Introduction
Generally speaking, malignant neoplasms of the
auricle are common, and that can be attributed to
sun exposure, especially in men. It constitutes
5% of all other cutaneous malignancies. Fair
skin, chronic immunosuppressive therapies,
radiotherapy, and certain skin conditions are
examples of risk factors that can increase the
individual susceptibility to this type of malignancies. Cutaneous malignancies are considered the
most common malignant tumor of the ear canal.
Primary malignancies of the external auditory
canal (EAC) are rare; they are usually an extension of the cutaneous malignancies of the sunexposed area of the auricle.
A. Larem (*)
Hamad Medical Corporation, Doha, Qatar
HMC, Doha, Qatar
e-mail: alarem@hamad.qa
M. A. Al Shawabkeh
HMC, Doha, Qatar
e-mail: MAIGhshoum@hamad.qa
Z. A. Dogan
ENT(ORL-HNS), Head and Neck Department,
St. Anna Hospital—University of Dusseldorf,
Dusseldorf, Germany
19.2 Malignancy ofAuricle
19.2.1 Actinic Keratosis
• Solar keratosis and senile keratosis are other
terms for this condition.
• It is premalignant [1].
• It is caused by sun exposure.
• Risk factors: Fair skin, chronic immunosup-
pressive therapies, and increasing age [1].
• Appearance: erythematous raised patch that
has at top with sandpaper [2].
• It has 5% of malignant transformation into
squamous cell carcinoma (SCC) [2].
• Treatment: curettage, cryotherapy, topical
tretinoin, 5-uorouracil, laser, dermabrasion,
or excision [2].
19.2.2 Lentigo Maligna
• Hutchinson’s freckle is another term for this
condition.
• It is a melanoma in situ [2].
• Appearance: macular spot, which is brown to
black with irregular boundaries that enlarge
overtime slowly [3].
• It has 5% of malignant transformation into an
invasive melanoma [2].
• It has high recurrence rates [2].
• Treatment: Surgical excision. Moh’s tech-
nique can be utilized in anatomically essential
regions [2].
© Springer Nature Switzerland AG 2021
A. Al-Qahtani et al. (eds.), Textbook of Clinical Otolaryngology,
https://doi.org/10.1007/978-3-030-54088-3_19
AL GRAWANY
205
206
A. Larem et al.
19.2.3 Keratoacanthoma
• Appearance: a volcano-like bump that is affecting an area of the pinna and grows rapidly,
reaching maximum size in 1–2months [2].
• Risk factors: sun exposure, male, and fair
skin [4].
• Common in male, middle-age to elderly
patients [4].
• Treatment: excision [4].
19.2.4 Basal Cell Carcinoma (BCC)
• The least aggressive skin cancer, with a low
incidence of metastasis (below 0.1%)
• The most common skin cancer in the head and
neck area [5]
• Risk factors: Sun exposure, radiotherapy,
immunosuppression therapy, and specic conditions like:
– Xeroderma Pigmentosum, which is an
autosomal-recessive genetic disease. The
patient has a defect in the DNA repair
mechanism after UV damage; he will have
multiple BCC.In addition, they will have
corneal opacication and neurological deficits [2, 6].
– Nevoid basal cell carcinoma syndrome: It
is an autosomal-dominant disorder. Patients
will have multiple BCC along with odontogenic keratocyte formation, intracranial
calcication, palmar pitting, and ribs
abnormalities [2, 7].
• Appearance: a pearly skin lesion with rolled
borders and telangiectasias [8].
• Histology: It has different subtypes like supercial, nodular, pigmented, inltrative, morpheaform (sclerosis), and basal squamous.
Morpheaform (sclerosis) and basal squamous
have a more aggressive clinical course than
the others. Basal squamous has the worst clinical picture [8].
• Treatment: Surgical excision with 4–5 mm
margins. Radiotherapy can also be used. Moh’s
micrographic mapping can be utilized [5].
• BCC and SCC have the same staging.
• Look at Fig.19.1:
19.2.5 Squamous Cell Carcinoma
• It is considered the most common malignancies for auricle [2].
• It has a capacity for metastasis and local
destruction.
• The high metastasis and recurrence rates can be
related to its close relation to structures underneath it, which will make the resection more difcult. Some believe that this is due to its close
approximation to the external auditory canal [2].
• Risk factors: sun exposure, fair skin, radiation
exposure, immunosuppression therapy, preexisting lesions, scars, and burns [9].
• Appearance: An indurated erythematous
patch, its border cannot be distinguished. It
has an area of an ulceration that can bleed easily (see Fig.19.2) [9].
Fig. 19.1 Patient with BCC of upper part of helix of the right ear
19 External Ear Malignancies
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Fig. 19.2 Patients with SCC of the left auricle, note the ulcerative lesion
207
• Most common location: Helix then posterior
pinna, antihelix, and triangular fossa [2].
• Can spread through the lymphatic system. For
lesion in the auricle, it can spread to preauricular within parotid and postauricular
LN.Level II–V lymph nodes can be involved
as well [2].
• Staging system: see Table19.1.
• Treatment: Excision with 6mm margins circumferentially, which might require auriculectomy. Radiotherapy might be indicated
postoperatively. Close follow-up of the patient
is required to monitor the resected area and to
detect any new lesion in sun-exposed areas.
See Figs.19.3 and 19.4 [2,10].
Table 19.2 shows a comparison between BCC
and SCC.
19.2.6 Melanoma
• It arises from the melanocytes.
• It can arise from the sun-exposed area, lentigo
maligna lesion, or even from a nevus.
• Twenty to 30% of melanoma are located in the
head and neck region, and 10–15% are in the
auricle [2].
•
It occurs mainly in the elderly, especially on
the left side of the face due to sun exposure
during driving [2, 5].
• The most common location in auricle is the
helix followed by the lobule [11].
• Histology: It has four subtypes: supercial
spreading, nodular, lentigo maligna, and acral
lentiginous. Supercial spreading is the most
common type [5].
• It has 12–36% chance of lymph node spread.
The lymphatic drainage is determined by sentinel lymph node sample [2].
Treatment: some believe a total auriculectomy
•
with parotidectomy and neck dissection is
required for all auricular lesions [12].
• Excisional margins:
In situ 5mm
Depth less than 1cm 1cm
Depth between 1 and 2cm Between 1 and 2cm
Depth more than 2cm 2cm
• In general, auricle has a worse prognosis than
other parts of the body [11].
• Staging: there are three staging systems available, TNM from AJCC, Clark, and Breslow.
AL GRAWANY
Соседние файлы в папке Библиотека им академика М.И. Перельмана