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10 Lateral Cervical Swellings
217
Fig. 10.9 Biphasic appearance of Schwannoma due to
the presence of Antoni A and B patterns, which are the
hyper-cellular and hypo-cellular portions, respectively.
H&E stain
Fig. 10.8 A Schwannoma appearing as a homogenous,
encapsulated mass. Cut-section is light tan and glistening
and shows some yellow patches
10.4.5.4 Clinical Presentation
Schwannoma usually presents as a painless
(asymptomatic) slowly growing lump in the neck
[54]. However, it may reach a large size and
cause pressure effects, as on the RLN causing
hoarseness of voice, or on the esophagus causing
dysphagia [24]. Involvement of the sympathetic
nerve will cause Horner’s syndrome, which is
characterized by ptosis, meiosis, and/or mydriasis on the affected side [41, 42, 55].
Physical examination usually reveals a deeply
seated mass, 3–5cm in size, at about the middle
of the neck, characterized by being smooth, wellencapsulated, round in shape, and rm in consistency. It is non-pulsatile and moves in the
transverse direction but is relatively immobile
longitudinally due to its nested intra-neural location. The primary nerve of origin may be entirely
encompassed within the tumor [56, 57].
Rarely (<1%) Schwannoma may undergo
malignant transformation, which is primarily
associated with neurobromatosis Type 1 [58,
59]. Clinical suspicion of malignant transforma-
tion may be derived from its difference in the rate
of progression and the associated pain and neuro-
logical decit. The occurrence of metastases
indicates a malignant tumor [60].
10.4.5.5 Investigations
Imaging Studies
Computed tomography (CT) scans and magnetic
resonance imaging (MRI) may be very helpful in
the diagnosis of schwannomas.
Computed Tomography (CT) Scan
Computed Tomography (CT) scan with contrast
enhancement should be routinely done preoperatively as some of the Schwannomas are very vascular [40, 57]. Shoss etal. (1985) [59] have also
recommended high-resolution CT scan to determine the size and extent of the tumor, to demonstrate a degree of tumor vascularity and to help
differentiate between benign and malignant
lesions. On CT scan, Schwannoma usually
appears as a spherical or ovoid soft tissue mass
and may show moderate to marked contrast
enhancement; cystic component may be apparent
and fatty degeneration may be seen.
Magnetic Resonance Imaging (MRI)
On MRI, Schwannomas commonly present as a
well-encapsulated, round, or ovoid mass that is
isointense to muscle on T1-weighted images,
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218
M. Sakr
hyper-intense on T2-weighted images, and
enhances following contrast administration [61,
62].
Cytology/Histology
Fine-Needle Aspiration Cytology (FNAC)
FNAC is usually very effective in differentiating
benign and malignant tumors of soft tissue.
Although FNAC is very useful in most neck
masses, it has a low accuracy in the diagnosis of
neural tumors [63].
Tissue Biopsy
The nal diagnosis of Schwannoma is conrmed
by a tissue biopsy, but it is not usually favored as
it can give rise to complications such as bleeding,
hematoma, and hoarseness of voice [55].
10.4.5.6 Dierential Diagnosis
The differential diagnosis of cervical Schwannoma
must include metastatic or reactive lymphadenopathy, soft tissue neoplasms such as broma, leiomyoma, and lipoma, paraganglioma, carotid
artery aneurysm, branchial cleft cyst, angioma,
and other neurogenic tumors [55, 64, 65].
10.4.5.7 Treatment
Management ofResectable Schwannoma/
Surgery
Treatment of resectable cervical Schwannoma is
complete surgical excision [66–70]. Recurrence
after successful en-bloc removal of the tumor is
rare [71]. Surgery is particularly indicated in
symptomatic cases with progressive disease, and
in case of suspicion of malignancy.
With the patient placed in the spine position
with slight neck extension and head turn to the
contralateral side, a transcervical skin incision is
performed and skin aps are raised superiorly
and inferiorly. The anterior border of the SCM
muscle is skeletonized exposing the mass deep to
the muscle. The carotid artery is then identied
and is retracted laterally. The IJV is visualized
deep and medial to the mass and carefully
retracted medially. The vagus nerve and sympathetic trunk are identied and the mass is observed
arising directly from the peri-neurium of the
nerve. With gentle and meticulous dissection, the
nerve is separated from the mass, which is completely excised leaving the intact nerve behind.
Good hemostasis is achieved, and the wound is
then closed in two layers with a small drain
secured in situ [39].
Management ofUnresectable
Schwannoma
Radiotherapy (RT)
Schwannoma is radio-resistant, and the possibility of the malignant degeneration of the benign
tumor is extremely rare [59]. Unresectable
Schwannomas are those rare cases involving the
skull base when multiple cranial nerves are
affected precluding surgery due to morbidity.
Such cases can be treated with RT along with
symptomatic treatment for pain.
Pharmacotherapy
Medications such as calcium-channel alpha-2
delta ligands such as gabapentin, serotoninnorepinephrine re-uptake inhibitors such as venlafaxine, and tricyclic anti-depressants such as
amitriptyline can be used for pain relief [72].
Watchful Waiting (Wait andScan)
A new strategy of watchful waiting with serial
imaging has also been successfully employed.
Generally, most of the lesions remain radiologically stable. In a few cases, development and progression of neuropathy were observed. Watchful
waiting with its advantages of preventing surgery
and its potential complications is especially valuable in asymptomatic, older patients [73–75]. The
strategy can be changed to active treatment in case
of signicant tumor growth. Even though the tumor
is small, it can be found to be malignant; thus, the
best treatment remains surgical excision [45].
10.4.5.8 Prognosis
Overall, the prognosis of benign tumors is good,
with no effect on the lifespan. However, it
depends on the size of the tumor, its location, the
surgical procedure performed, and underlying
condition. Recurrence after total resection is
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10 Lateral Cervical Swellings
219
uncommon. Malignant changes may occur in
long-standing Schwannomas, and the prognosis
of is poor regardless of the treatment modality,
with overall 5-year survival of 15% [76]. Worse
prognosis is mainly associated with large size,
high grade, metastases, and location.
10.4.6 Sternocleidomastoid (SCM)
Tumor
10.4.6.1 Denition
A SCM tumor is dened as “a growth of tissue
that is not coordinated with the normal surrounding tissue and persists in growing even if the
original trigger for its growth is removed.” It is a
benign growth that may cause disgurement but
is not malignant and does not metastasize [77].
10.4.6.2 Etiology/Pathogenesis
The different theories proposed to explain the
pathogenetic mechanism of SCM tumors include
birth trauma, fetal malposition, ischemic necrosis
following vascular compression during birth,
infection, and presence of endogenous factor
[78–80]. It has been postulated in the past that
SCM itself is a remnant of a hematoma caused by
tissue injury during delivery [81]. The tumor has
also been suggested to be an “ischemic contracture of a segment of the SCM muscle resulting
from an arterial insult of the sternomastoid artery,
a branch of the superior thyroid artery that supplies mainly the middle third of the muscle.”
It has also been postulated that venous outow
obstruction occurring in the fetus in-utero or during delivery leads to degeneration of SCM muscle
bers and subsequent brosis of the damaged
areas [82]. Finally, it has been suggested that an
injury due to poor fetal head positioning in the
uterus produces a compartment syndrome-like
pressure-induced injury to the SCM muscle that
results in muscle cell death followed by brosis
and SCM tumor [77].
bers [82], and, in some cases, regenerating skeletal muscle bers [81]. The broblasts have a
completely normal appearance with no evidence
suggesting malignancy [82].
FNAC shows scant to moderately cellular,
scattered, oval-shaped to spindle-shaped broblasts, naked nuclei, wisps of collagen, atrophic,
degenerating muscle bers, regenerating muscle
bers, and intact skeletal muscle cells containing
multiple nuclei. The cells are usually scattered
singly and also in clusters of varying sizes
(Fig.10.10). There is no evidence of inammation, hemorrhage, cell necrosis, or rapidly dividing and/or proliferating cells [78–81, 83–86].
10.4.6.4 Clinical Picture
The SCM tumor is more common in males and
the right SCM muscle [77] although very rare
cases present with bilateral tumors [87]. These
tumors most commonly present as slow-growing,
rm, mobile, non-tender, spindle-shaped masses
[82] in the middle or lower two-thirds of the
SCM muscle [88] of infants at birth or in the rst
8weeks of delivery [87]. The mother may notice
the lump or that the child keeps his head turned to
one side due to SCM contracture [82]. Attempts
to turn the head straight may cause pain or
distress. As the child grows, the head becomes
turned to one side and tilted toward the other
side. The swelling is usually 1–3cm across, fusiform in shape with its long axis along the line of
10.4.6.3 Pathology
Microscopically, SCM tumors consist of spindleshaped broblasts located in a background of
collagen bers, decomposing skeletal muscle
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Fig. 10.10 Fine-needle aspiration cytology (FNAC) of
sternocleido-mastoid (SCM) tumor showing bundles of
broblasts and myo-broblasts intermixed with a collagenous stroma and entrapped myocytes. H&E stain
220
M. Sakr
the SCM muscle (Fig.10.11), has a smooth surface, and not xed to the overlying skin. The
anterior and posterior edges are distinct but the
superior and inferior edges, where the lump
becomes continuous with normal muscle, are
indistinct.
Because each SCM muscle rotates the head to
the contralateral side and tilts the head to the ipsilateral side, so in the presence of a SCM tumor,
shortening of the left muscle, for example, turns
the head toward the right but tilts the head to the
left. Both these deformities may be present and
the resulting disease is called “congenital torticollis” (torticollis=wry-neck) [82] (Fig.10.12).
Untreated, it may cause face asymmetry, unilateral amblyopia, and cervical vertebral deformities. Torticollis can be a means of correcting a
squint. Move the head into a vertical and central
position and watch the eyes. If the torticollis is
secondary to a squint and not a SCM tumor, the
squint will appear as the head is straightened.
10.4.6.5 Investigations
Imaging Studies
US is the imaging modality of choice. The SCM
muscle is seen diffusely enlarged but most
involves the muscle belly, to assume a fusiform/
ellipsoid shape (Fig.10.13) [88]. If these imaging
ndings are not diagnostic, CT scan typically
shows a diffusely enlarged SCM that is isoattenuating to normal neighboring musculature.
Adjacent fat planes are well preserved. At times,
calcication may be present [89].
MRI may be useful in patients with nonmuscular causes of torticollis; however, it is not recommended in asymptomatic patients with
infantile torticollis [90]. Evaluation of MRI
results in correlation with histopathology has
demonstrated that if multiple or large low-signal
intensities that represent increased brosis and
aberrant dense connective tissue within the SCM
are noted, then a surgical release should be considered [91].
Cytology/Histology
When combined with imaging ndings, the
lesion’s natural history, and its clinical presentation, FNAC likely conrm the diagnosis of SCM
tumor in almost all cases [81, 82, 85]. Surgical
diagnostic biopsy may result in complications
such as cosmetic defect due to contracture band
and is usually reserved for difcult cases [79].
Histopathological ndings include brous
replacement of skeletal muscle bers that
Fig. 10.11 Neck torticollis due to right SCM tumor.
Fusiform mass of the middle third of the right SCM muscle (arrow)
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Fig. 10.12 Neck torticollis due to left sternocleidomastoid (SCM) tumor
10 Lateral Cervical Swellings
Fig. 10.13 Ultrasound of the neck showing fusiform/
ellipsoid swelling involving the sternocleidomastoid
(SCM) muscle
undergo atrophy. The degree of brosis and its
extent or distribution may vary. Even in neonates,
the brous tissue is mature. This nding indicates
that the disease began before birth.
10.4.6.6 Dierential Diagnosis
It is important to differentiate muscular from
nonmuscular torticollis. Congenital muscular torticollis is benign; missing a case of nonmuscular
torticollis is potentially life-threatening [92]. The
“clinical” differential diagnosis includes (1) congenital lesions such as branchial cyst, (2) inammatory conditions like tuberculous lymphadenitis,
(3) benign neoplastic condition like hemangioma,
(4) malignant neoplasm like neuroblastoma,
rhabdomyosarcoma and lymphoma, and (5) other
forms of infantile bromatosis [83, 85, 93].
The “cytological” differential diagnosis
includes all types of benign proliferation of
infancy. Nodular fasciitis can be excluded by the
absence of inammatory cells and pleomorphic
proliferating broblasts. Infantile bromatosis
shows inltrative pattern affecting adjacent muscle [79]. On the other hand, low-grade brosarcoma/infantile brosarcoma rarely affect the
neck region and always show considerable cellularity and atypia [79, 86].
221
head such as permanent facial asymmetry, attened head, loss of neck mobility, and scoliosis.
Infants presenting with SCM tumors should also
be examined for the presence of associated hip
dysplasia [87].
Conservative Treatment
Active Home Stimulation Program
Sternocleidomastoid brosis spontaneously
resolves in the vast majority of infants. About
95% of infants with minimal limitations in their
head’s mobility show improvements in this
mobility after 4weeks of an “active home stimulation program” that entails observation, massage, and active and passive stretching [82].
Passive stretching of SCM before the age of
12month is the most effective mode of physical
therapy [94–96].
Targeted Physiotherapy
Physiotherapy may be recommended; however,
there is little evidence to indicate that this alters
the course of the condition if the patient is older
than 1year. Approximately, 91% of infants with
more severe movement limitations show good
results after three sessions of “targeted
physiotherapy” over a 3–4 month period [97].
Patients with a thicker SCM, a lower birth weight,
and a history of breech delivery have a longer
rehabilitation duration [98, 99].
Other Physical Treatments
Other physical treatments include massage of
tight neck muscles and subcutaneous tissues,
which increases pain-free range of motion, joint
mobilization, and therapeutic taping [100].
Kinesiology taping is an approach that is sometimes adopted in conservative management [101].
When applied on the affected side, it has an
immediate effect on the muscle function scores
for the muscular imbalance in the lateral exors
of the neck [101].
10.4.6.7 Treatment
Prompt diagnosis and treatment of SCM tumors
are crucial for avoiding the impairments that may
follow long-term mal-positioning of infant’s
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Botulinum Toxin (BTX) Type A
Botulinum toxin (BTX) type A has been injected
into the SCM for the treatment of congenital
muscular torticollis in pediatric and adult patients
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M. Sakr
[102]. Recently, in a study of 39 children with
treatment-resistant congenital muscular torticollis, Limpaphayom et al. (2019) evaluated the
adjunctive use of BTX injection into the SCM,
followed by physical therapy. None of the
patients required tendon-lengthening surgery
[103].
In a systematic review and meta-analysis of
one non-randomized experimental study and nine
cases or case series (n=411), Qiu etal. (2020)
assessed the effectiveness and safety of BTX
injections for congenital muscular torticollis and
found an 84% overall effective rate, a 9% rate of
conversion to surgery, and a 1% adverse reaction
rate (primarily injection-site erythema and transient dysphagia) [104].
Surgical Treatment
Currently, surgical treatment of SCM tumor
involves mainly soft tissue correction, which
includes unipolar or bipolar SCM release, and
partial SCM muscle resection. The aim of surgical treatment is to correct the deformity, maintain
the correction, and prevent recurrence. Most children with SCM tumor can improve with nonoperative treatment before 1 year of age, and
surgical treatment should be considered if the
efcacy is poor. Since the SCM muscle is enveloped by the investing fascia, the pathological
changes associated with SCM tumor include not
only contracture of the SCM muscle but also contracture of its fascial sheath. Depending on the
severity and duration of the disease, contracture
of the posterior carotid sheath and scalene muscle may be involved. Therefore, SCM tumor correction may require management of the above
structures in addition to division of the SCM
muscle [105–109]. The optimal timing for surgery is believed to be at an age between 1 and
4years [77, 80–82, 110, 111]. Follow-up should
be continued until the torticollis resolves completely, until head and neck movement normalize, and until cervical and thoracic scoliosis is
resolved in older children.
Unipolar Tenotomy
The most popular treatment for infants who show
no improvements in mobility after 1 year of
physical therapy or who initially present at
>12months of age is surgical tenotomy (cutting)
of one of the tendons (unipolar tenotomy) of the
involved SCM muscle [112]. Tenotomy may be
performed through the open surgical approach or
endoscopic approach [87]. It is followed by the
use of a collar for a few weeks and subsequent
physiotherapy.
Bipolar Tenotomy
Bipolar SCM tenotomy may be necessary in
selected cases and entails open tenotomy of the
mastoid and clavicular attachments, release of
the cervical fascia, and Z-plasty of the sternal
head. In 2014, Ekici etal. described the approach
to surgical management of congenital muscular
torticollis that used the Z-plasty technique [113].
Complications of surgery may include hematomas that may develop because of inadequate
hemostasis during surgery, injury of the IJV during subcutaneous tenotomy and injury of the spinal accessory nerve during division of the upper
end of the muscle.
10.4.6.8 Prognosis
In general, the overall prognosis of SCM tumors
is good using the adequate treatment measures
[112]. Recurrent torticollis after surgery is rare
(approximately 5%) [114]. Even in patients older
than school age and those who have nished
growth, sufcient unipolar or bipolar release of
the SCM, and intensive postoperative care can
generally be expected to yield satisfactory treatment results [106].
10.5 Cystic Swellings
oftheAnterior Triangle
10.5.1 Cervical Abscess
10.5.1.1 Pyogenic Abscess
Denition
A pyogenic cervical abscess is a collection of pus
from an infection in spaces between the structures of the neck. As the amount of pus increases,
the soft tissue spaces expand and push against the
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10 Lateral Cervical Swellings
223
structures in the neck, such as the throat, tongue,
and, in extreme cases, the trachea [115].
Etiology
A neck abscess occurs during or just after a bacterial or viral infection in the head or neck such as
a tonsillitis, sinus infection, or otitis media. As an
infection worsens, it can spread down into the
deep tissue spaces in the neck. Pus collects and
builds up in these spaces forming a mass.
Sometimes, a neck abscess occurs following an
inammation or infection of a congenital neck
mass such as a branchial cyst or an acquired cyst
such as a dermoid cyst. A cervical abscess may
also result from infection of a cyst or enlarged
LN in the neck (Fig. 10.14). Epidermal (sebaceous) cysts (often referred to as sebaceous cysts)
rarely become infected.
Clinical Presentation
Symptoms may include neck pain or stiffness,
dysphagia, dyspnea, and potentially fatal airway
obstruction in case of deep cervical infections. A
pyogenic abscess is painful and tender, and the
overlying skin is red and hot. There may be signs
of toxemia (fever, chills, and body aches). In pyo-
genic abscess of the submandibular region, pus
may collect under the tongue, pushing it upwards
and toward the back of the throat, which can
explain the dyspnea and dysphagia. It is not common in young children but may occur in older
adolescents, especially after a dental infection.
Diagnosis
In general, diagnosis is made by a complete medical history and physical examination. Culture
from the pus is recommended, primarily to identify Methicillin-resistant Staphylococcus aureus
(MRSA). In addition, diagnostic procedures for a
neck abscess may include (1) throat culture, (2)
blood tests including CBC, ESR, and CRP, (3)
US to determine consistency of the mass (cystic
or solid), and (4) CT scan—it shows detailed
images of the mass and its relations to surrounding structures, and (5) biopsy—samples are taken
(with a needle or during surgery) for histological
examination.
Treatment
Generally, treatment includes incision and drainage (I&D) drainage under sterile conditions, preferably under general anesthesia, and appropriate
antibiotics. Hospitalization may be required in
some cases. Some small abscesses resolve without draining. Warm compresses help accelerate
the process. I&D are indicated when signicant
pain, tenderness, and swelling are present; it is
unnecessary to wait for uctuance [116, 117].
Antibiotics have traditionally been considered
unnecessary unless the patient has signs of systemic infection, cellulitis, multiple abscesses,
immunocompromise, or a facial abscess in the
area drained by the cavernous sinus. In these
cases, empiric therapy should be started with a
drug active against MRSA such as trimethoprim/
sulfa-methoxazole, clindamycin; for severe
infection, Vancomycin until the results of bacterial culture become available [118].
Fig. 10.14 Right cervical abscess (infected lymph
nodes) in the anterior triangle of the lateral side of the
neck
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10.5.1.2 Cold (Tuberculous) Abscess
Etiology
A cold (TB) abscess is caused by mycobacterium
TB that does not tend to stimulate acute inammation. It is commonly seen in the upper part of
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the neck but may occur in any group of cervical
LNs. Other causes include actinomycosis, leprosy, fungal infections such as Blastomycosis,
and hyper-immunoglobulin E (IgE) syndrome
(Job’s syndrome) characterized by recurrent
staphylococcal cold abscess, eczema, and high
levels of IgE.
Clinical Picture
Locally, patients usually present with a painless, enlarging, or persistent neck mass of a
variable duration [119–121]. The affected LNs
are enlarged (3–10cm in diameter) but remain
discrete [122]. Node tenderness is noted in
only 10–35% of cases [119, 122, 123]. The
LNs then coalesce and breakdown to form TB
pus, which may perforate the deep fascia (DF)
and form a “cold abscess.” If the abscess bursts
through the DF into the subcutaneous tissues,
it will have two compartments, one on either
side of the DF connected by a small central
track (Collar-stud Abscess). In 4–11% of cases,
the skin overlying may show breakdown and
form a sinus [119, 122, 123]. Cord-like structures (lymphatics) may be felt between the
enlarged LNs due to TB lymphangitis. Multiple
masses are encountered in approximately twothirds of patients, and bilateral nodes in onethird [120, 122, 123]. Symptoms of tuberculosis
(TB) toxemia (night fever, night sweating, loss
of appetite, and loss of weight), or other TB
lesions may be present.
Diagnosis/Dierential Diagnosis
Tests that aid in reaching the proper diagnosis
include Mantoux/Tuberculin skin test, ESR (elevation is not specic), ELISA (for antibodies to
mycobacterial antigen, sensitivity 60–80%), and
PCR assay. Aspiration reveals the characteristic
caseous material. Plain X-ray may show calcication. Other studies include US, CT scan, and
US-guided FNAC.A cold abscess should be differentiated from pyogenic abscess, lipoma, cysts,
and soft tissue tumors.
Treatment
Treatment of a cold abscess includes the following [124–126]:
– Anti-tuberculous drugs: Small cold abscesses
may heal with anti-TB drugs alone.
– Aspiration: Nondependent valvular (zig-zag)
aspiration should be performed to avoid sinus
formation plus installation of 1g Streptomycin
± INH solution to avoid recurrence.
– Percutaneous drainage: US-guided pig-tail
catheter drainage.
– Surgical management: Open I&D if aspiration
fails. It should be performed through a nonde-
pendent incision and without insertion of a
drain to avoid sinus formation. Correction of
any underlying bony lesion, if present, should
also be performed.
10.5.1.3 Ludwig’s Angina Suppuration
Denition
Ludwig’s angina is a rapidly progressive gangrenous cellulitis of soft tissues of the neck and oor
of the mouth [127], often caused by bacterial
sources [128]. The primary site is the submandibular space.
Etiology
The most common cause of Ludwig’s angina is
dental-related (odontogenic) [129] accounting
for approximately 75–90% of cases [129–132].
Infections of the lower second and third molars
are usually implicated due to their roots extending below the mylohyoid muscle [129, 133].
Other causes are “non-odontogenic” and include
oral ulcerations, tongue piercing, infections secondary to oral malignancy, mandible fractures,
sialolithiasis-related submandibular gland infections, and penetrating injuries of the oor of the
mouth [129]. Patients with alcoholism, obesity,
and systemic illness, such as diabetes mellitus,
malnutrition, compromised immune system, and
organ transplantation, are also commonly predisposed to Ludwig’s angina [132].
Clinical Presentation
Ludwig’s angina presents with an acute onset and
spreads very rapidly; thus, early diagnosis and
emergency treatment are vital and could be lifesaving [127]. Symptoms include dental aches,
painful neck swelling, dysphonia, dysphagia,
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10 Lateral Cervical Swellings
225
dysarthria, drooling, shortness of breath, fever,
and general malaise [134].
External signs may include bilateral submandibular or lower facial swelling around the jaw
and upper neck, characteristically brawny, tense,
and eryhtematous. The swelling of the soft tissues of the anterior neck above the hyoid bone
often leads to the characteristic “bull’s neck”
appearance of affected patients. Intraoral signs
may include elevated or protruding tongue and
elevation of the oor of mouth due to sublingual
space involvement and posterior displacement of
the tongue, creating the potential for a compromised airway distress with dyspnea, tachypnea,
or stridor [127].
Complications of Ludwig’s angina include
suffocation, suppuration, and spread of infection
to the para-pharyngeal space, carotid sheath, and
pterygo-palatine space. Serious complications
may include cavernous sinus thrombosis descending necrotizing mediastinitis, which occurs
through the retro-pharyngeal space (71%) and
carotid sheath (21%) [134].
Diagnosis
Imaging
Infections originating in the roots of teeth can be
identied with a dental X-ray [135–137]. Cervical
CT scan with contrast material is considered the
image of choice and is used to identify deep neck
space infections [138].
Microbiology
Traditionally, a cultural sample is collected
although it is time-consuming and sometimes
unreliable if not processed correctly [139].
Ludwig’s angina is most often found to be caused
multiple microbes (poly-microbial) and anaerobes [127].
Dierential Diagnosis
Differential diagnosis includes angioneurotic
edema, cellulitis, lingual carcinoma, sublingual
hematoma following anti-coagulation, peritonsillar abscess, salivary gland abscess, and
lymphadenitis [138].
Treatment
The main principles that guide the treatment of
Ludwig’s Angina include immediate hospital
admission, proper airway management, early and
aggressive antibiotic therapies, and corticosteroids, I&D in case of suppuration, which is seen
in approximately 65% of patients, and adequate
nutrition and hydration support [132, 140].
10.5.2 Branchial Cyst
Paired branchial arches originally appear as
mesodermal condensations in the walls of the
primitive pharynx in the fourth gestational week.
Between the six branchial arches lie, ve branchial grooves or clefts externally, and ve pharyngeal pouches internally. The fth arch fails to
develop due to early degeneration of its blood
supply. The branchial clefts are lined by ectoderm, the pouches by endoderm, and in between
there is a thin layer of mesoderm between each
pouch and groove. The mesoderm of each arch
differentiates then into cartilage and muscle
(Table10.2) [141–144].
During the seventh week of gestation, the second branchial arch grows more caudally to fuse
with the fourth branchial arch thus covering the
third and 4th. Fusion of the ectodermal lining of
the sinus occurs, and now the sinus is a buried
space lined by squamous epithelium. It then disappears completely. Persistence of the cervical
sinus results in a branchial cyst, while failure of
the operculum between the second and fourth
arches to fuse gives rise to a branchial sinus or
stula. Accordingly, the branchial cyst will be
existing deep to the structures originating from
the second arch that is hyoid bone, external
carotid artery, and facial nerve, and supercial to
the structures originating from the third arch that
is stylohyoid and stylo-pharyngeus muscles,
internal carotid artery, internal jugular vein, glossopharyngeal, and hypoglossal nerves.
A stula is seen most commonly with the second branchial cleft and extends from the anterior
border of the SCM muscle inferiorly, inward
through the bifurcation of the carotid artery, and
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Table 10.2 Neck branchial apparatus and its derivatives
Arch Derivative Muscles Nerve Artery
First arch – Maxilla
– Malleus and its anterior
ligament
– Incus
– Spheno-mandibular
ligament
– Mandible
Second arch – Stapes
– Styloid process
– Stylohyoid ligament
– Lesser cornu and upper
body of hyoid bone
Third arch Rest of hyoid bone. Glossopharyngeal Part of ICA
Fourth arch Laryngeal cartilages. – Pharynx
Sixth arch Inferior laryngeal
Mastication Trigeminal Maxillary
Facial
expression
– Larynx
Facial Stapedial
Superior laryngeal
nerve of vagus
nerve of vagus
– Denitive aorta on
the left side
– Subclavian artery
on the right side
Denitive pulmonary
trunk
M. Sakr
enters the posterolateral pharynx just below the
tonsillar fossa. The third branchial cleft remnant
courses posterior to the common carotid artery,
ending in the pyriform sinus region. Surgical
excision is preferred to establish the denitive
diagnosis of a branchial cleft cyst and to avoid
nontreatment of a masquerading head and neck
regional metastasis [141–144].
10.5.2.1 Epidemiology
Branchial cysts are the most common congenital
cause of a neck mass, representing approximately
17% of all pediatric cervical masses. An estimated 2–3% of cases are bilateral. A tendency
exists for cases to cluster in families [145]. No
ethnic or gender predilection has been reported
for branchial cleft cysts. Branchial cysts are congenital in nature, but they may not present clinically until later in life, usually by early adulthood
at the age of 15–25years or even later on. Cysts
occur more commonly than stulae with a ratio
of 10:1 [145].
10.5.2.2 Types ofBranchial Cleft Cysts
Four branchial clefts (grooves) form during the
development of a human embryo. The rst cleft
normally develops into the external auditory
canal, but the remaining three arches are obliter-
ated and have no persistent structures in normal
development. Persistence or abnormal formation
of these four clefts can all result in branchial cleft
cysts, which may or may not drain via sinus
tracts.
First branchial cleft cysts account for 8% of
the sinuses and cysts of the neck. The cysts are
usually located in the preauricular area (type I
cyst) or below the angle of mandible (type II
cyst). Cysts are rarely malignant [146].
Second branchial cleft cysts account for
90–95% of the neck cysts. The cyst is located
medial to the facial nerve, at the anterior neck,
anterior to the SCM muscle, and above the hyoid
bone. Skin pit can be found in this location.
Infection of the cysts in this region can compress
trachea causing dyspnea or the esophagus caus-
ing dysphagia, and irritating the SCM muscle,
causing torticollis [146].
Third and fourth branchial cleft cysts are rare,
usually accounting for 2% of all branchial arch
abnormalities. They are located below the second
branchial arc and may be misdiagnosed as bronchogenic cyst. They are usually left-sided and
associated with neck infection [146].
10.5.2.3 Clinical Picture oftheSecond
Branchial Arch Cyst
The patient usually complains of a painless, lateral neck mass that may become tender and/or
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