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50
A. Larem et al.
Fig. 3.7 Auricular hematoma
Auricular Pseudocysts
It is endochondral cyst-like degeneration with no
epithelial or endothelial lining of the anterior surface of the auricle also termed idiopathic pseudocystic chondromalacia. It is believed to result
from recurrent minor trauma. It occurs mainly in
young adults as a painless mass and can be confused with auricular hematomas. It may require
treatment which includes aspiration followed by
intralesional steroid injection with a high chance
of recurrence or surgical intervention with incision and drainage, curettage, and obliteration
with a sclerozing agent.
Laceration andAvulsion
Lacerations can be supercial involving skin
only or deep extending into the cartilage, and in
both cases, there is a risk of chondritis. Surgical
reconstruction is required; most of the lacerations
without a signicant tissue loss can be closed primarily after irrigation with conservative debridement, supportive management with tetanus shot,
and appropriate antibiotics coverage should be
given. In the case of exposed cartilage, it can be
covered with wedge excision, local aps, or
burial in a postauricular pocket for later reconstruction. In case of helical rim defect (Fig.3.8),
a small defect may be closed primarily if less
than 2cm, while in larger one (more than 2cm),
Fig. 3.8 Traumatic helical rim defect of right auricle
a chondrocutaneous advancement ap can be
used [9].
Avulsions can be partial or complete, and in
partial with a well-preserved pedicle, it can be
treated by reattachment of the affected part, while
complete avulsion requires urgent replantation
with microvascular anastomosis, which is difcult and challenging to repair.
3.2.2.6 Other
The auricle may be affected by other disorders
such as frostbite, seborrheic dermatitis, allergic
contact dermatitis (Fig.3.9), gout (tophi), chondrodermatitis nodularis chronica helicis, and
psoriasis.
3.3 External Auditory Canal
(EAC)
3.3.1 Congenital Anomalies
oftheExternal Auditory Canal
3.3.1.1 Aural Atresia
Aural atresia is uncommon condition occurring
in 1in 10,000–20,000 patients [10]. It has a high
association with microtia. Although in most of
the time it is a non-syndromic, it can be seen in
syndromes as Treacher Collins, Crouzon, Nager,
3 The External Ear
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Fig. 3.9 Allergic contact dermatitis in the auricle against
bismuth iodoform parafn paste (BIPP) pack post
tympanoplasty
Goldenhar, Klippel–Feil, and Pierre Robin. It
can be bilateral in one-third of the cases [10].
Fusion of malleus and incus is the most common
middle ear anomaly, and footplate is usually normal. The facial nerve is typically displaced more
anterior, superior, and lateral than in the normal
anatomy [11].
The management in unilateral atresia does not
require immediate intervention if the contralateral ear hearing is normal, but in bilateral atresia,
an early amplication is essential in infants with
bilateral signicant hearing loss. The nonsurgical rehabilitative option is achieved by bone
conduction hearing aids such as bone-anchored
hearing aid (BAHA). The surgical repair can be
performed at age 6–7 years old after microtia
repair if present, and patient with a major malformation (poor mastoid pneumatization, abnormal
or absent oval window/footplate, abnormal facial
nerve course, and abnormalities of the inner ear)
is a poor candidate for surgical repair. There are
three surgical approaches for repair of aural atre-
51
sia that include the mastoid, the anterior, and the
modied anterior approaches. The most frequent
complications of the surgical reconstruction are
canal stenosis and failure to achieve an adequate
hearing level [12].
3.3.2 Acquired andInammatory
Conditions oftheExternal
Auditory Canal
3.3.2.1 Cerumen Impaction
Cerumen is a desquamated epithelium mixed
with sebum and watery secretions produced from
sebaceous glands and modied apocrine sweat
glands, respectively. The predisposing factors to
develop cerumen impaction include the use of
hearing aids, cotton buds, earplugs, the presence
of a narrow EAC, and genetic predisposition in
some cases. It is considered as one of the most
common complaints in the ENT clinics, where
the patients present with ear fullness, ear discomfort, tinnitus, autophony, decreased hearing, and
itching.
Cerumen removal is the most performed procedure in ENT clinics and is done through suction, low-pressure irrigation, or using a hook.
Cerumen-softening ear drops are also helpful.
3.3.2.2 Foreign Bodies (FB)
It is one of the common presentations to the ENT
clinic especially in children less than 6years old.
It can be classied into living and no-living foreign bodies. It is more common in the right ears
due to the dominance of right-handedness.
It can be extracted in the ofce if the patient is
cooperative by crocodile forceps, hook, irrigation,
or suction. To avoid injury in non- cooperative
patients, it is advised to be done under general
anesthesia. Living FBs (such as insects) must be
killed before removal. Batteries must be removed
as soon as possible to avoid chemical burns to the
EAC and the drum. Irrigation in the case of seeds
is not recommended as it may cause an increase
in their size. It is always recommended for young
children to examine the ears and the nose after
the FB removal to rule out other FBs.
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A. Larem et al.
3.3.2.3 External Ear Canal Infections
The EAC may give rise to acute or chronic infections, which can result from bacterial or fungal
infections.
Otitis Externa
It is an inammatory condition of the EAC usually caused by an acute bacterial infection (for
fungal otitis externa, see Sect. “Otomycosis”). It
is caused by a break in the protective barrier
(skin) of EAC through direct injury (while cleaning the EAC) or obstruction (e.g., hearing aid,
foreign body, cerumen impaction) or change in
media to a more alkalotic EAC (swimming). The
most common isolated pathogens include
Pseudomonas aeruginosa and Staphylococcus
aureus [2]. Clinical manifestations include severe
pain, itching, and otorrhea, and physical examination reveals tragal tenderness, canal edema,
discharge, erythema, and stenosis. Investigation
including swab culture is generally not indicated
except for treatment failure.
Treatment of otitis externa depends on ear toileting, topical therapy of antibiotics with steroids,
and dry ear precautions. Caution is needed to
avoid ototoxic antimicrobials such as aminoglycosides in the case of tympanic membrane perforation. Systemic antibiotics typically are not
required unless concurrent otitis media, persistent or severe symptoms, cellulitis, or systemic
illness [2].
Chronic infections tend to be related to chronic
ear skin conditions, irritation by a foreign body,
or manifestation of systemic diseases (e.g.,
Psoriasis). Chronic otitis externa needs to be
treated depending on the etiology, in contact dermatitis avoid the offending agent, and in systemic
disease treat the underlying condition [2].
Otomycosis
Otomycosis is a fungal infection of the skin of
EAC.The high-risk group includes immunocompromised patients, hearing aid users, and the
overuse of topical antibiotics. The most common
pathogens include Aspergillus niger (most common) and Candida albicans [2]. Patients primarily complain of pruritus, ear fullness, and reduce
hearing. The clinical examination reveals a white,
black, or dotted gray membrane with an appearance of “tissue-paper”. Treatment includes frequent ear toileting and using acidifying agents or
anti-fungal drops along with dry ear precautions.
Malignant Otitis Externa (MOE)
Malignant otitis externa or necrotizing otitis
externa is a progressive infection of the external
auditory canal (EAC), the adjacent soft tissues,
and the skull base. MOE is usually a disease of
the immunocompromised and elderly diabetic
patients, though it can occur in immunocompetent patients on very rare occasions [2].
Pseudomonas aeruginosa is the most common
causative pathogen. Other species of bacteria,
such as Staphylococcus aureus, and fungal species, including Aspergillus and Candida, have
been reported [2].
The patient commonly presents with longstanding otalgia, described as a severe deep dull
pain, and otorrhea, with a nding of granulation
tissue at the bony cartilaginous junction of the
EAC.Without proper treatment, the infection can
spread and involve the cranial nerves, the facial
nerve being the most common cranial nerve
involved. Other complications include sinus
thrombosis, sepsis, intracranial infections, and
death.
Diagnosis is mainly based on the patient’s history, clinical examination, microbiology, and
radiological ndings. Consider biopsy and culture of EAC, and check for elevated ESR. CT
scan helps in detecting bony erosion, and MRI
has a superior role in bone marrow edema, softtissue abnormalities, and intracranial extension
detection (see Fig.3.10). Technettium-99m bone
scan detects early bone changes and areas of
osteoblastic activity, and it is helpful in detecting
early disease, while follow-up is monitored better
with Gallium-67 citrate and Indium-111 labeled
leukocyte, though cost and false-positive results
limit their use.
Medical management with administration of
prolonged systemic and topical antibiotics, regular EAC toileting, and strict blood sugar control is the cornerstone in the treatment of
malignant otitis externa. Surgical debridement
has a limited role due to complex access to the
3 The External Ear
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53
Fig. 3.10 MRI T1 axial image at the level of ear canal
showing a signicant postcontrast enhancement on the
left temporal bone and skull base as compared to right
side suggestive of an extensive malignant otitis externa
skull base. Hyperbaric oxygen is used as adjuvant therapy [2].
Myringitis
It is an inammatory condition of the tympanic
membrane (TM) that can be primary or secondary to a middle ear or EAC infection. Granular
myringitis is a chronic inammatory condition of
the epidermal layer of the TM.Bullous myringitis occurs when some serous/hemorrhagic bullae
formed on the epithelial surface of the TM.It is
caused by different pathogens including
Streptococcus pneumonia, Mycoplasma (bullous
myringitis), and viral pathogens (inuenza or
herpes) [
2].
The patient presents with acute severe otalgia,
serosanguinous otorrhea, and hearing loss. The
physical examination shows bullae on congested
inamed TM (see Fig.3.11). The audiogram can
show sensorineural hearing loss or mixed hearing
loss in 65% [2].
Decompression of the bulla provides relief to
the pain, topical antibiotic/steroid drop is the
treatment of choice along with proper analgesia,
and oral macrolides or quinolones may be added
to eradicate mycoplasma. Granulation tissue may
Fig. 3.11 Bullous myringitis
be treated with surgical removal, chemical cauterization, or vinegar irrigations [
13].
3.3.2.4 Keratosis Obturans
andExternal Auditory Canal
Cholesteatoma
Both of keratosis obturans and external auditory
canal cholesteatoma are marked by abnormal
accumulation of keratin within the medial portion of EAC.
Keratosis Obturans
It represents an abnormal accumulation of dense
plug of keratin within the EAC without bony erosion. It is usually a bilateral disorder and affects
young adults, and it is associated with bronchiectasis and chronic sinusitis. It presents with severe
ear pain and otorrhea secondary to otitis externa,
and also presents with conductive hearing loss
with a widening of the EAC causing automastoidectomy [
14]. It can be diagnosed with a tem-
poral CT scan showing signicantly diffuse
widening of EAC without boney erosion.
Treatment involves careful, slow, and complete removal of keratin plugs with softening ear
drops. It is usually an ofce-based procedure,
and antibiotics/steroid drops are used if the infection exists [14].
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ab
A. Larem et al.
External Canal Cholesteatoma
It is a rare condition of cholesteatoma in EAC
causing ulceration and erosion of the underlying
bone of the inferior posterior part of the canal. It
is usually unilateral and affects older patients
with focal bony erosion which distinguishes it
from keratosis obturans (see Table3.2). It presents with severe ear pain, otorrhea, and conductive hearing loss and may erode the middle ear or
attic. CT scan shows a soft-tissue lling EAC
with focal bony erosion.
Treatment is with regular cleaning of the canal
from debris, with medications to eradicate otitis
externa, and surgery may be required in refractory cases to remove cholesteatoma matrix and
necrotic bone with canaloplasty [2].
Table 3.2 The differences between keratosis obturans
and external auditory canal cholesteatoma
External auditory
Keratosis
obturans
Age Young adult Elderly
Pain Acute severe pain Chronic dull pain
Lateralization Bilateral Unilateral
Osteonecrosis Absent Present
EAC bony
erosion
Otorrhea Rare Frequent
Circumferentially Focally
canal
cholesteatoma
3.3.2.5 Benign Neoplasms
The EAC may give rise to both benign and malignant neoplasms. Benign processes include exostosis, osteoma, and other lesions.
Exostosis
Multiple acquired benign bony outgrowths
(hyperostosis) at the EAC periosteum usually in
patients have repeated exposure to cold water;
therefore, it is called “surfer’s ear”. Exostosis
growths arise from the medial aspect of bony
EAC near tympanic annulus, along tympanomastoid and tympanosquamous suture lines. Most of
the time it is asymptomatic and appears as narrowing of EAC by multiple, bilateral smooth
broad-based sessile masses (see Fig.3.12).
Treatment is usually unnecessary unless they
are large and intervene with hearing or causing
repeated ear infections due to cerumen and epithelial debris retaining or to allow a proper hearing aid tting [15]. All cases being considered for
surgery must have a hearing test and CT temporal
bone to identify the anatomical landmarks around
the bony lesions. Surgical approaches include
transcanal or postauricular approach, being aware
that facial nerve can be at risk of injury during
drilling of the posteroinferior aspect of the bony
canal; therefore, intraoperative facial nerve monitor is recommended.
Fig. 3.12 (a) Axial CT scan of left ear exostosis, (b) Endoscopic view of exostosis
ab
3 The External Ear
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Fig. 3.13 (a) Axial CT scan of left ear Osteoma, (b) Endoscopic view of Osteoma
Table 3.3 The differences between exostosis and
osteoma
Exostosis Osteoma
Number of
lesion
Predisposing
factor
Site On suture
Lateralization Bilateral Unilateral
Multiple Single
Repeated
exposure to
cold water
lines of
EAC (more
medial)
Not related to specic
exposure
On tympanosquamous
suture near bony
cartilaginous junction
(more lateral)
55
Osteoma
It is a solitary benign bony growth unlike exostosis, mostly at the bony cartilaginous junction,
located more laterally in comparison to exostosis.
Fig. 3.14 Ear polyp covering the attic area with keratin
debris hiding an underlying cholesteatoma
Most of the time it is asymptomatic and appears
as narrowing of EAC by single, unilateral pedunculated mass (see Fig. 3.13). See Table 3.3 to
check the differences between exostosis and
osteoma.
It is usually not treated unless they increase in
size causing decrease hearing, recurrent infection,
impaction of cerumen, and ear secretions [15].
lesteatoma, and malignant tumor (see Fig.3.14).
The treatment includes silver nitrate cauterization and topical steroid/antibiotic drops.
Excisional biopsy is indicated if unclear etiology
or non-resolution polyp, but the surgeon should
be aware of the polyp attachments to deeper
structures (ossicles, the facial nerve) or its origin
Aural Polyp
It is a soft-tissue mass that arises in the EAC due
to underlying inammation process, and it can be
associated with ventilation tubes, foreign bodies,
chronic ear infections, middle ear disease, cho-
if it is coming from intracranial defect (meningoencephalocele, encephalocele); therefore, it
should be investigated with radiologic studies
(CT and/or MRI) to dene the anatomic site of
origin.
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A. Larem et al.
3.3.2.6 Malignant Neoplasms
Primary cancers of the auricle and EAC include
more commonly cutaneous carcinomas (basal cell
carcinoma, squamous cell carcinoma, and melanoma) and rarely ceruminous gland tumors (ceruminous adenoma, ceruminous adenocarcinoma,
pleomorphic adenoma, and adenoid cystic carcinoma). Basal cell carcinoma is the most common
cutaneous carcinoma in the auricle and preauricular area, while squamous cell carcinoma is the
most common cutaneous carcinoma in the EAC.
Take-Home Messages
• Prominent Ear (Bat Ear) surgical corrections are usually performed in preschool
age (4–6 years old) to avoid social
stigmatization.
• Prenatal exposure to isotretinoin, thalidomide, and alcohol can increase the
risk of microtia.
• The surgical repair of aural atresia can
be performed at age 6–7years old as a
second step after microtia repair if present to ensure a eld without scars or
compromised blood supply to avoid
failure of the auricular reconstruction.
• Pseudomonas aeruginosa is considered
the most common pathogen in auricular
perichondritis, bacterial otitis externa,
and malignant otitis externa.
• Keratosis obturans affects mainly young
adults, and it is associated with bronchiectasis and chronic sinusitis.
• Radiologic studies by CT and MRI
should be performed for aural polyps in
case of suspicion of an attachment to
deeper structures (ossicles, the facial
nerve), or if it is coming from intracranial defect (meningoencephalocele,
encephalocele).
References
1. Francis HW. Anatomy of the temporal bone, external ear, and middle ear, Chap. 127. In: Francis
HW, editor. Cummings otolaryngology, head and
neck surgery. 6th ed. Philadelphia: Elsevier; 2015.
p.1977–8.
2. Farkas LG.Anthropometry of normal and anomalous
ears. Clin Plast Surg. 1978;5:401–12.
3. Yotsuyanagi T. Nonsurgical correction of congenital auricular deformities in children older than
early neonates. Plast Reconstr Surg. 2004;114(1):
190–1.
4. Harris J, Källén B, Robert E. The epidemiology of anotia and microtia. J Med Genet. 1996;
33:809.
5. Kountakis SE, Helidonis E, Jahrsdoerfer RA.Microtia
grade as an indicator of middle ear development in
aural atresia. Arch Otolaryngol Head Neck Surg.
1995;121(8):885–6.
6. Sharma A, Gnanapandithan K, Sharma K, Sharma
S. Relapsing polychondritis: a review. Clin
Rheumatol. 2013;32(11):1575–83.
7. Brant JA, Ruckenstein MJ. Infections of the external
ear, Chap. 137. In: Francis HW, editor. Cummings
otolaryngology, head and neck surgery. 6th ed.
Philadelphia: Elsevier; 2015. p.2115–22.
8. Sweeney CJ, Gilden DH.Ramsay Hunt syndrome. J
Neurol Neurosurg Psychiatry. 2001;71:149–54.
9. Krunic AL, Weitzul S, Taylor RS.Chondrocutaneous
advancement ap for reconstruction of helical rim
defects in dermatologic surgery. Australas J Dermatol.
2006;47(4):296–9. Review.
10. Jahrsdoerfer RA. Congenital atresia of the ear.
Laryngoscope. 1978;88(Suppl 13):1–46.
11. Schuknecht HF. Congenital aural atresia.
Laryngoscope. 1989;99:908–17.
12. De la Cruz A, Teufert KB.Congenital aural atresia
surgery: long-term results. Otolaryngol Head Neck
Surg. 2003;129(1):121–7.
13. Neilson L, Hussain S. Management of granular
myringitis: a systematic review. J Laryngol Otol.
2007;25:1–8.
14. Persaud RAP, Hajioff D, Thevasagayam MS, et al.
Keratosis obturans and external ear canal cholesteatoma: how and why we should distinguish between
these conditions. Clin Otolaryngol Allied Sci.
2004;29:577–81.
15. Kemink JL, Graham MD. Osteomas and exostoses of the external auditory canal - medical and
surgical management. J Otolaryngol. 1982;11(2):
101–6.
Otitis Media withEusion (OME)
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AmrA.Elhakeem, Ma’inAliAl Shawabkeh,
andHassanHaidar
4
4.1 Introduction
There are different nomenclatures of Otitis Media
with Effusion (OME)-like serous otitis media,
exudative otitis media, nonsuppurative otitis
media, and seromucous otitis media. It is an
inammatory condition of the middle ear where
middle ear uid forms behind an intact tympanic
membrane (TM). It is called chronic OME if the
uid persists for more than 3 months. Usually,
OME is related to acute otitis media (AOM).
However, it can happen without a previous episode of AOM.Nowadays, OME is considered the
most common cause of hearing impairment in
children.
4.2 Epidemiology
Ninety percent of children have at least one episode of otitis media with effusion by the age of 4.
The prevalence among children below 4 years is
10–17%, and it declines to 2–4% for those between
6 and 8years. It is more common in winter, and
males have a slight increase in risk [1].
A. A. Elhakeem (*) · M. A. Al Shawabkeh
ENT Department, Hamad Medical Corporation,
Doha, Qatar
e-mail: aelhakeem@hamad.qa
H. Haidar
Hamad Medical Corporation, Doha, Qatar
4.3 Pathogenesis
Two theories can explain OME:
1. Ex vacuo theory: Eustachian tube (ET)
obstruction secondary to adenoid hypertrophy
or mucosal edema can lead to negative pressure in the middle ear leading to passive transduction of uid.
2. Inammatory theory: Gas deciency can
cause hypoxia in the middle ear, which can
initiate a mucosal inammation leading to an
active exudation in the middle ear [2].
4.4 Risk Factors (Look atTable
4.1)
1. Age: the incidence of OME decreases as age
increases, which is due to the maturation of
ET and the immune system.
2. ET anatomy: Children have a more horizon-
tal ET, which can make the entry of bacteria
easier to the middle ear.
3. Craniofacial abnormalities: there is an
increased incidence of OME in patients with
cleft lip and palate, as it is believed those
conditions can lead to the immaturity of the
cartilaginous part of ET.
4. Adenoid: adenoid hypertrophy can lead to
ET obstruction and can act as a reservoir for
bacteria that increases the incidence of OME.
© 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_4
AL GRAWANY
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58
Table 4.1 Risk factors of OME
Age
ET anatomy (Horizontal)
Craniofacial abnormalities (cleft lip and palate)
Adenoid hypertrophy
Daycare attendance
Passive smoking
Recurrent middle ear infection
Bacterial biolms
Allergic rhinitis
Gastroesophageal reux
Genetic predisposition
5. Daycare attendance.
6. Smoking exposure (passive smoking).
7. Recurrent middle ear infection: bacterial
endotoxin initiates OME. Haemophilus
inuenzae and Moraxella catarrhalis were
found in more frequency as compared to
AOM where Streptococcus pneumoniae
predominates.
8. Biolms: it plays a vital role in the pathogenesis of OME [3].
9. Allergic rhinitis: it can lead to ET edema and
can reduce the immune system function of
the upper respiratory tract system.
10. Gastroesophageal reux: middle ear uid
shows and elevated Pepsin/pepsinogen [4].
11. Genetic predisposition: Having a sibling in
whom a ventilation tube was placed is an
essential factor in developing OME.Studies
involving twins and triplets show genetic
susceptibility to OME [5].
4.5 Clinical Features
4.5.1 Symptoms
Acute symptoms are typically absent in
OME. Hearing loss is the most common complaint in symptomatic patients; it is conducive
with a hearing level of approximately 25dB [6].
This can affect binaural processing, sound localization, and speech perception. This effect is
more pronounced in patients with underlying
hearing disabilities [7]. Other symptoms like ear
A. Elhakeem et al.
Fig. 4.1 Right ear otomicroscopy: retrotympanic air-
uid level (arrows). (Adapted from Mansour S., Magnan
J., Nicolas K., and Haider H. (2018). Middle ear disease)
fullness, sleep disturbance, and otalgia can be
seen in OME.
4.5.2 Otoscopic Findings
1. Air-uid level, which is the most specic feature. However, it is not the most frequent one
(Figs.4.1 and 4.2).
2. Amber-colored TM (Fig.4.3).
3. TM can be dull, retracted, and yellow, especially in “Glue ear” where the effusion is thick
and looks like glue (Fig.4.4).
4. In retracted TM, the handle of malleus looks
shorter and horizontal with a prominent short
process.
4.5.3 Pneumatic Otoscopy
It will show restricted mobility of TM when positive pressure is applied. In clinical practice, this
test is not easy to be performed in children [8].
4 Otitis Media withEusion (OME)
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59
Fig. 4.2 Left ear with serous effusion. After Valsalva
maneuver, air bubbles appeared anteriorly. (Adapted from
Mansour S., Magnan J., Nicolas K., and Haider H. (2018).
Middle ear disease)
Fig. 4.3 Left ear with abundant serous effusion. (Adapted
from Mansour S., Magnan J., Nicolas K., and Haider H.
(2018). Middle ear disease)
4.5.4 Tympanometry
Fig. 4.4 Left ear with mucoid effusion and retracted
drum. (Adapted from Mansour S., Magnan J., Nicolas K.,
and Haider H. (2018). Middle ear disease)
4.5.5 Hearing Assessment
It is recommended in children who have risk factors of speech or learning disorders, or those who
have persistent OME for more than 3 months.
Important notes while evaluating patients with
OME:
1. The presence of acute signs of infection along
with uid in the middle ear is characteristic of
AOM. So, ear pain with bulging of TM
excludes OME.
2. In cases of unilateral OME in adults, it is
essential to do exible nasopharyngoscopy
to rule out nasopharyngeal mass (see
Fig.4.6).
3. In refractory cases of OME, conditions like
nasopharyngeal mass, adenoid hypertrophy,
ET congenital defect, IgG subclass deciencies, and ciliary dyskinesia should be kept in
mind.
It is the most useful test in diagnosing OME.It is
4.6 The Clinical Course ofOME
a cost-effective and an objective test. Type B
(Flat curved) tympanometry is considered
pathognomonic for OME (see Fig.4.5).
Eighty-ve percent of cases will resolve spontaneously. Thirty to 40% of cases will have recur-
AL GRAWANY
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