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6 Surgery oftheFace
149
66. Malhotra R, Huilgol SC, Huynh NT, Selva D. The
Australian Mohs database, part II: periocular
basal cell carcinoma outcome at 5-year follow-up.
Ophthalmology. 2004;111(4):631–6.
67. Cherian P, Gunson T, Borchard K, Tai Y, Smith
H, Vinciullo C. Oral antibiotics versus topical
decolonization to prevent surgical site infection after
Mohs micrographic surgery-a randomized, controlled trial. Dermatol Surg. 2013;39(10):1486–93.
68. Alam M, Ibrahim O, Nodzenski M, Strasswimmer
JM, Jiang SI, Cohen JL, etal. Adverse events associated with Mohs micrographic surgery: multicenter
prospective cohort study of 20? 821 cases at 23 centers. JAMA Dermatol. 2013;149:1378.
69. Kaur S, Thami GP, Kanwar AJ. Basal cell carcinoma—treatment with cryosurgery. Indian J
Dermatol Venereol Leprol. 2003;69(2):188–90.
70. Nakuçi M, Bassukas ID. Ofce-based treatment
of basal cell carcinoma with immunocryosurgery:
feasibility and efcacy. Acta Dermatovenerol Alp
Panonica Adriat. 2013;22(2):35–8.
71. Mendenhall WM, Amdur RJ, Hinerman RW,
Cognetta AB, Mendenhall NP. Radiotherapy
for cutaneous squamous and basal cell carcinomas of the head and neck. Laryngoscope.
2009;119(10):1994–9.
72. Arits AH, Mosterd K, Essers BA, Spoorenberg
E, Sommer A, De Rooij MJ, etal. Photodynamic
therapy versus topical imiquimod versus topical uorouracil for treatment of supercial basal-cell carcinoma: a single blind, non-inferiority, randomised
controlled trial. Lancet Oncol. 2013;14(7):647–54.
73. Aldara cream 5% (imiquimod) [package insert].
Graceway Pharmaceuticals; 2007.
74. Geisse J, Caro I, Lindholm J, Golitz L, Stampone P,
Owens M. Imiquimod 5% cream for the treatment
of supercial basal cell carcinoma: results from two
phase III, randomized, vehicle-controlled studies. J
Am Acad Dermatol. 2004;50(5):722–33.
75. Sapijaszko MJ. Imiquimod 5% cream (Aldara) in
the treatment of basal cell carcinoma. Skin Therapy
Lett. 2005;10(6):2–5.
76. Micali M, Nasca MR, Musumeci ML.Treatment of
an extensive supercial basal cell carcinoma of the
face with imiquimod 5% cream. Int J Tissue React.
2005;27(3):111–4.
77. Bilu D, Sauder DN.Imiquimod: modes of action. Br
J Dermatol. 2003;149(Suppl 66):5–8.
78. Wuest M, Dummer R, Urosevic M.Induction of the
members of notch pathway in supercial basal cell
carcinomas treated with imiquimod. Arch Dermatol
Res. 2007;299(10):493–8.
79. Von Hoff DD, LoRusso PM, Rudin CM, Reddy JC,
Yauch RL, Tibes R, etal. Inhibition of the hedgehog
pathway in advanced basal-cell carcinoma. N Engl J
Med. 2009;361(12):1164–72.
80. Patel MS, Thigpen JT, Vance RB, Elkins SL, Guo
M.Basal cell carcinoma with lung metastasis diagnosed by ne-needle aspiration biopsy. South Med J.
1999;92(3):321.
81. Akinci M, Aslan S, Markoç F, Cetin B, Cetin
A.Metastatic basal cell carcinoma. Acta Chir Belg.
2008;108(2):269–72.
82. Mc Loone NM, Tolland J, Walsh M, etal. Follow-up
of basal cell carcinomas: an audit of current practice.
J Eur Acad Dermatol Venereol. 2006;20(6):698–701.
83. Pieh S, Kuchar A, Novak P, Kunstfeld R, Nagel
G, Steinkogler FJ. Long-term results after surgical
basal cell carcinoma excision in the eyelid region. Br
J Ophthalmol. 1999;83(1):85–8.
84. Elad S, Zadik Y, Zeevi I, etal. Oral cancer in patients
after hematopoietic stem-cell transplantation: longterm follow-up suggests an increased risk for recurrence. Transplantation. 2010;90(11):1243–4. https://
doi.org/10.1097/TP.0b013e3181f9caaa.
85. Freedberg IM, et al. Fitzpatrick’s dermatology in
general medicine. 6th ed. McGraw-Hill; 2003.
ISBN: 0-07-138076-0.
86. Rapini RP, Bolognia JL, Jorizzo JL. Dermatology:
2-volume set. St. Louis: Mosby; 2007. ISBN:
1-4160-2999-0.
87. Gross KG, et al. Mohs surgery, fundamentals and
techniques. Mosby; 1999.
88. Chollet A, Hohl D, Perrier P.Risk of cutaneous squamous cell carcinomas: the role of clinical and pathological reports. 2012.
89. Brantsch KD, Meisner C, Schönsch B, Trilling
B, Wehner-Caroli J, Röcken M, Breuninger
H.Analysis of risk factors determining prognosis of
cutaneous squamous-cell carcinoma: a prospective
study. Lancet Oncol. 2008; https://doi.org/10.1016/
S1470- 2045(08)70178- 5.
90. WHO disease and injury country estimates. World
Health Organization; 2009.
91. O’Bryant CL, Poust JC.Melanoma. In: DiPiro JT,
Talbert RL, Yee GC, etal., editors. Pharmacotherapy:
a pathophysiologic approach. 8th ed. New York:
McGraw-Hill Medical; 2011.
92. Kazerooni R, Madden T.Melanoma. In: Schumock
GT, Brundage DM, Richardson M, editors.
Pharmcotherapy self-assessment program: hematology/oncology I and II (Book 10). 5th ed. Kansas
City, MO: American College of Clinical Pharmacy;
2006. p.55–80.
93. American Cancer Society. What are the key statistics about melanoma? 2012. www.cancer.org/
Cancer/SkinCancer- Melanoma/Detailed- Guide/
melanoma- skin- cancer- key- statistics.
94. Urba WJ, Washington CV, Nadiminti H. Cancer
of the skin. In: Longo DL, Fauci AS, Kasper
DL, etal., editors. Harrison’s principles of internal medicine. 18th ed. New York: McGraw-Hill
Medical; 2012.
95. Goldstein AM, Tucker MA. Genetic epidemiology
of cutaneous melanoma: a global perspective. Arch
Dermatol. 2001;137:1493–6.
96. American Cancer Society. Melanoma skin
cancer. 2012. www.cancer.org/Cancer/
SkinCancer- Melanoma/Detailed- Guide/
melanoma- skin- cancer- prevention.
t.me/Dr_Mouayyad_AlbtousH
150
M. Sakr
97. Robinson JK. Sun exposure, sun protection, and
vitamin D.JAMA. 2005;294:1541–3.
98. American Academy of Dermatology. Be Sun
Smart. 2012. www.aad.org/skin- care- and- safety/
skin- cancer- prevention/be- sun- smart/be- sun- smart.
99. Slinluff CL Jr, Flaherty K, Rosenberg SA, Read
PW. Cutaneous melanoma. In: DeVita Jr VT,
Lawrence TS, Rosenberg SA, editors. DeVita,
Hellman, and Rosenberg’s cancer: principles
& practice of oncology. 8th ed. Philadelphia,
PA: Lippincott Williams & Wilkins; 2008.
p.1897–951.
100. CDC. United States Cancer Statistics (USCS).
1999–2007 incidence and mortality data. 2012.
www.cdc.gov/uscs.
101. Molife R, Hancock BW. Adjuvant therapy of
malignant melanoma. Crit Rev Oncol Hematol.
2002;44:81–102.
102. PegIntron (peginterferon alfa-2b) product information. Whitehouse Station, NJ: Schering Corp; 2011.
103. Intron A (interferon alfa-2b, recombinant) product information. Whitehouse Station, NJ: Schering
Corp; 2011.
104. Eggermont AM, Robert C. New drugs in melanoma: it’s a whole new world. Eur J Cancer.
2011;47:2150–7.
105. National Comprehensive Cancer Network. NCCN
clinical practice guidelines in oncology melanoma,
version 3. 2012.
106. Zhang J, Stringer MD). Ophthalmic and facial
veins are not valveless. Clin Experiment
Ophthalmol. 2010;38(5):502–10. https://doi.
org/10.1111/j.1442- 9071.2010.02325.x.
107. Munckhof WJ, Krishnan A, Kruger P, Looke
D. Cavernous sinus thrombosis and meningitis from community-acquired methicillinresistant Staphylococcus aureus infection.
Intern Med J. 2008;38(4):283–7. https://doi.
org/10.1111/j.1445- 5994.2008.01650.x.
108. Bhatia K, Jones NS.Septic cavernous sinus thrombosis secondary to sinusitis: are anticoagulants indicated? A review of the literature. J Laryngol Otol.
2002;116:667–76.
109. Coutinho J, de Bruijn SF, Deveber G, Stam
J. Anticoagulation for cerebral sinus thrombosis.
Cochrane Database Syst Rev. 2011:CD002005.
110. Southwick FS, Richardson EP Jr, Swartz MN.Septic
thrombosis of the dural venous sinuses. Medicine.
1986;65:82–106.
111. Gallagher RM, Gross CW, Phillips CD.Suppurative
intracranial complications of sinusitis.
Laryngoscope. 1998;108:1635–42.
112. Clifford-Jones RE, Ellis CJ, Stevens JM, et al.
Cavernous sinus thrombosis. J Neurol Neurosurg
Psychiatry. 1982;45:1092–7.
113. Igarashi H, Igarashi S, Fujio N, et al. Magnetic
resonance imaging in the early diagnosis of cavernous sinus thrombosis. Ophthalmologica.
1995;209:292–6.
114. Silver HS, Morris LR. Hypopituitarism secondary to cavernous sinus thrombosis. South Med J.
1983;76:642–6.
115. Sahjpaul RL, Lee DH.Infratentorial subdural empyema, pituitary abscess, and septic cavernous sinus
thrombophlebitis secondary to paranasal sinusitis:
case report. Neurosurgery. 1999;44:864–6.
t.me/Dr_Mouayyad_AlbtousH
Deep Neck Space Infections
MahmoudSakr
7
7.1 Introduction
Deep neck space infections (DNSIs) most commonly arise from a septic focus of the mandibular
teeth, tonsils, parotid gland, deep cervical lymph
nodes (LNs), middle ear, or sinuses. Before the
widespread use of antibiotics, nearly 70% of
DNSIs were caused by spread from tonsillar and
pharyngeal infections. Currently, tonsillitis
remains the most common cause of DNSI in children, whereas infection of an odontogenic origin
is the most common cause in adults [1–4]. These
DNSIs often have a rapid onset and can progress
to life-threatening complications. Clinicians
must thus be aware of such infections and should
not underestimate their signicant risks of morbidity and mortality, particularly now that they
have become relatively uncommon in the postantibiotic era. Moreover, with the widespread use
of antibiotics and/or profound immunosuppression, the classic local and/or constitutional manifestations of these infections may be absent [5].
Infections of the deep neck spaces present a
challenging problem for several reasons: (1) the
complex anatomy of the deep neck spaces renders localization of infection difcult, (2) the surgical access for infections of these deep locations
makes the intervening neurovascular and soft tis-
M. Sakr (*)
Department of Surgery, Faculty of Medicine,
Alexandria University, Alexandria, Egypt
sue structures prone to injury, (3) the possible
involvement of the vital surrounding tissues
(bones, nerves, vessels, and other soft tissues) in
the inammatory process subjects the patient to
more complicated sequelae such as neural dysfunction, vascular erosion, thrombosis, and
osteomyelitis, and (4) the real and potential avenues of communication of the deep neck spaces
with each other and with other regions such as the
mediastinum allow infection to gain access to
increasingly larger portions of the neck and other
parts of the body.
Anatomically, within the deep neck are 11
spaces created by planes of greater and lesser
resistance between the fascial layers. These
include the submandibular space, parapharyngeal
space (PPS), retropharyngeal space, peritonsillar
space, danger space, prevertebral space, pretracheal space, carotid space, masticator space, temporal space, and the parotid space.
7.2 Ludwig’s Angina
The term “Ludwig’s angina” was originally
described in 1836, by Karl Friedrich Willhelm
von Ludwig (a German physician and physiologist, 1790–1865). It describes inammation
and cellulitis of the submandibular space (primary site) that can result in life-threatening airway compromise and spread to other cervical
spaces [6].
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
M. Sakr (ed.), Head and Neck and Endocrine Surgery,
https://doi.org/10.1007/978-3-031-64102-2_7
t.me/Dr_Mouayyad_AlbtousH
151
152
ular gland
M. Sakr
7.2.1 Surgical Anatomy
The submandibular space is bounded inferiorly
by the supercial layer of the deep cervical fascia
that extends from the hyoid to the mandible, laterally by the body of the mandible and superiorly
by the mucosa of the oor of mouth. It is divided
by the mylohyoid muscle into two subdivisions:
the sublingual space inferiorly and the submaxillary space superiorly. The sublingual space contains the sublingual gland, hypoglossal nerve,
and Wharton’s duct. It is in continuity with the
submaxillary space through the posterior margin
of the mylohyoid muscle around which pus can
readily tract (Fig.7.1). Infection may also spread
to the para- or retropharyngeal space.
7.2.2 Etiology
Infection in the submandibular space may be
odontogenic in origin (90%), usually from the
second and third molars, or non-odontogenic
(10%) from mandibular fracture, tongue piercing, neoplasms, neck trauma, or sialadenitis.
Infection usually starts in the submaxillary space
and spreads to the sublingual space via the fascial
planes rather than the lymphatics. The organisms
most often isolated in patients with Ludwig’s
angina are Streptococcus viridans and
Staphylococcus aureus. Anaerobes, including
Bacteroides, are also frequently involved. Gram-
negative organisms that have been isolated
include Neisseria, Escherichia coli, Pseudomonas,
Haemophilus inuenzae, and Klebsiella species.
7.2.3 Clinical Manifestations
There is usually a history of recent dental procedure and dental pain. As the submandibular space
is expanded by cellulitis or abscess, the oor of
the mouth becomes indurated (Fig.7.2) and the
tongue is forced upward and backward, causing
airway obstruction. There is typically a bilateral
submandibular edema, with marked tenderness
and, occasionally, subcutaneous emphysema.
The swelling of the anterior soft tissues of the
neck above the hyoid bone sometimes leads to a
characteristic appearance known as “bull’s neck.”
Lymphadenopathy and uctuance are not usually
seen in patients with Ludwig’s angina. Typically,
the patient also presents with drooling, trismus,
neck pain, dysphagia, and dysphonia or, more
specically, a mufed tone at higher registers
(“hot potato” voice) caused by edema of the
vocal apparatus. Hoarseness, stridor, respiratory
distress, decreased air movement, cyanosis, and a
“snifng” position (upright posture with the neck
thrust forward and the chin elevated) are all signs
of impending airway obstruction.
In addition to airway compromise, complications of Ludwig’s angina may include cavernous
sinus thrombosis and brain abscess. Other
Fig. 7.1 Anatomy of
the submandibular
space. It has two
subdivisions separated
by the mylohyoid
muscle: the sublingual
space inferiorly and the
submaxillary space
superiorly
t.me/Dr_Mouayyad_AlbtousH
Sublingual gland
Submandib
Mylohyoid muscle
Digastric muscle
7 Deep Neck Space Infections
153
helpful if extension into the mediastinum is suspected. Although an MRI scan provides an excellent soft tissue resolution to help localize the
region of involvement, it is not considered to be
the initial modality of choice because of the
increased time and expense [12].
Differential diagnosis of Ludwig’s angina
includes angioneurotic edema, lingual carcinoma, sublingual hematoma (following anticoagulation), salivary gland abscess, lymphadenitis,
cellulitis, and peritonsillar abscess (PTA).
7.2.5 Treatment
Fig. 7.2 Ludwig’s angina (inammation and cellulitis of
the submandibular space)
reported complications include carotid sheath
infection and arterial rupture, suppurative thrombophlebitis of the internal jugular vein (IJV),
osteomyelitis of the mandible, mediastinitis,
pericardial and/or pleural effusion, empyema,
subphrenic abscess, and aspiration pneumonia
[7–11].
7.2.4 Diagnosis
Plain X-rays (PXRs) of the neck and chest often
show the soft tissue shadow, the presence of gas,
and the extent of airway narrowing. Panoramic
radiographic views of the jaw may show a dental
focus of infection. Ultrasonography (US) does
not reveal anatomical details but has been used to
identify uid collections in the soft tissues, as has
gallium citrate Ga-67 scanning. Moreover, US
can help distinguish between phlegmon and
abscess, provide information about the surrounding vessels, and guide ne-needle aspiration
(FNA) attempts.
Computed tomography (CT) scanning with
contrast is the gold standard in the evaluation of
deep neck infections. It indicates the location,
boundaries, and relation of the infection with the
surrounding neurovascular structures. It also
shows the presence of gas, uid collection, and
airway compromise. A Chest CT scan may be
7.2.5.1 Medical Treatment
The airway is the rst priority of treatment [13].
Airway management is accomplished by immediate orotracheal or beroptic nasotracheal
intubation. If the patient is not intubated, then a
tracheostomy or a cricothyroidotomy should be
performed for airway control. Tracheostomy
should be performed before any attempts at surgical drainage in these patients [14]. Intravenous
(IV) broad-spectrum antibiotics should be
started before culture results are obtained based
on the local resistance patterns and most common etiologies. Oral antibiotics are administered after completion of an IV course of
antibiotics and the patient shows clinical
improvement and has been afebrile for at least
48 h [15]. Corticosteroids have also been
recently added to the therapeutic regimen to
reduce edema [16].
7.2.5.2 Surgical Therapy
Surgical drainage is required in case of suppuration, which takes place in nearly 65% of cases,
and in patients with no improvement after
48–72 h of IV antibiotics. Separation of the
supercial lobes of the submandibular gland and
division of the mylohyoid muscles are usually
necessary to decompress the fascial spaces [17].
The most important preoperative considerations
are stabilization of a secure airway, volume and
metabolic resuscitation, and initiation of antibiotics. Needle aspiration under CT or US guidance
may be used in patients with small, easily
t.me/Dr_Mouayyad_AlbtousH
154
M. Sakr
reachable abscesses or in patients who are too
unstable to undergo general anesthesia. It may
also provide preliminary culture specimens
before formal incision and drainage (I&D).
Postoperatively, the patient should be closely
monitored for signs of response to therapy, reaccumulation or impending complications, and
for culture and sensitivity results for appropriate
tailoring of antibiotics. The patient’s airway must
also be monitored closely for any signs of
obstruction.
7.2.5.3 Prognosis
The prognosis of Ludwig’s angina depends primarily on immediate protection of the airway and
then on prompt antibiotic—and possibly surgical—treatment of the infection. In the pre-antibiotic era, the mortality rate of Ludwig angina was
50%, but with the advent of modern antimicrobial and surgical therapies, the mortality rate has
been markedly reduced to less than 5% [8–10].
7.3 Peritonsillar Abscess (PTA)
A peritonsillar abscess (PTA), also known as
quinsy or quinsey, occurs in the peritonsillar
space, which is bounded by the tonsil medially
and the superior constrictor laterally. The remaining borders are formed by the anterior and posterior tonsillar pillars. It is the most common DNSI
that presents to the otorhinolaryngological emer-
gency department and may spread to the parapha-
ryngeal space if not managed promptly [18].
osis (IMN), smoking, chronic lymphocytic leu-
kemia (CLL), and stones or calcium deposits in
the tonsils (tonsilloliths).
7.3.2 Clinical Presentation
Progressive unilateral sore throat and pain during
swallowing are usually the earliest symptoms. As
the abscess develops, persistent peritonsillar
pain, pyrexia, malaise, headache, mufed voice,
and distortion of vowels (hot potato voice) may
appear. Neck pain associated with tender,
enlarged LNs, otalgia, halitosis, dysphagia, and
trismus are also common.
General physical signs include mild-tomoderate distress, fever, tachycardia, and dehydration. Locally, there is erythema and edema in
the tonsillar area of the affected side (Fig.7.3)
with displacement of the uvula toward the unaffected side as well as enlargement and tenderness
of the jugulodigastric LNs.
Complications of PTA include septicemia, retropharyngeal abscess (RPA), and extension of
the abscess in other deep neck spaces, leading to
airway compromise. The severity of complications depends on the timing of management,
7.3.1 Etiology
A peritonsillar abscess usually arises as a complication of an untreated or inadequately treated
acute tonsillitis but may also occur de novo. The
commonly involved aerobic pathogens include
Streptococcus, Staphylococcus, and
Haemophilus. Anaerobic pathogens including
Bacteroides have also been incriminated [19–24].
Dental infection (such as periodontitis and
gingivitis) may be a risk factor. Other risk factors
include chronic tonsillitis, infectious mononucle-
t.me/Dr_Mouayyad_AlbtousH
Fig. 7.3 A peritonsillar abscess in the left peritonsillar
space. The erythema and edema in the tonsillar area of the
affected side should be noted
7 Deep Neck Space Infections
155
rapidity of illness progression, and characteristics of the affected fascial spaces.
7.3.3 Diagnosis
A peritonsillar abscess is usually diagnosed
based on history taking and careful physical
examination. Laboratory tests and imaging are
not used often. The monospot test may be ordered
to rule out infectious mononucleosis (IMN),
which is associated with up to 20% of PTAs. Pus
from the abscess may be sent for culture and sensitivity analysis to select the appropriate antibiotic. Ultrasound, both lateral and intraoral, and
even CT scanning with contrast (Fig.7.4) may be
ordered to delineate the abscess and determine its
extent.
Differential diagnosis of PTA includes peritonsillar cellulitis, tonsillar abscess, dental infections, cervical adenitis, IMN, salivary gland
infection, mastoid infection, foreign body aspiration, and neoplasms (lymphoma, leukemia).
7.3.4 Treatment
7.3.4.1 Medical Therapy
Patients with PTAs who are dehydrated require IV
uid administration until the inammation resolves
and they are able to resume an adequate oral uid
Peritonsillar
Abcess
Fig. 7.4 A computed tomographic image showing a peritonsillar abscess (arrow)
intake. Antipyretics and analgesics are used to
relieve fever and pain. Antibiotic therapy should
begin after cultures of pus have been obtained.
Infection is frequently penicillin- resistant, so it is
now common to treat with clindamycin [25] or
metronidazole in combination with penicillin G
benzathine [26]. Oral antibiotics may be prescribed
once the patient is able to tolerate oral intake and
should be continued for 7–10days.
The use of steroids has been controversial.
Ozbek etal. reported that the addition of a single
dose of IV dexamethasone to parenteral antibiotics signicantly lowered the length of hospital
stay, throat pain, fever, and trismus as compared
to only parenteral antibiotics [27].
7.3.4.2 Surgical Treatment
Needle aspiration can be carried out in children
as young as 7years, especially if conscious sedation is used. The uid aspirated may be sent for
culture and, in some cases, it may not need to be
followed by an incision and drainage (I&D).
Intraoral I&D is performed after localizing the
abscess, the opening is left open, and the patient
is asked to gargle with saline solution. Successful
aspiration or drainage leads to dramatic relief of
the patient’s symptoms.
Tonsillectomy with open I&D (quinsy tonsillectomy) is controversial. Many studies have
reported its safety, whereas others have shown
that immediate or delayed tonsillectomy may not
be necessary because of the high rate of success
and low rates of recurrence and morbidity associated with intraoral drainage. However, when the
abscess is located in an area that is difcult to
access, a tonsillectomy may be the only means to
drain it [28].
7.3.4.3 Prognosis
Most patients treated with antibiotics and adequate drainage of their abscess cavity recover
within a few days. Patients presenting with recurrent abscess or chronic sore throat after proper
I&D may require a tonsillectomy. Wang et al.
reported that the risk of PTA recurrence increases
with higher frequencies of previous tonsillitis in
patients of all ages and in children managed with
only aspiration [29].
t.me/Dr_Mouayyad_AlbtousH
156
space
M. Sakr
7.4 Parapharyngeal Abscess
7.4.1 Surgical Anatomy
The parapharyngeal space (PPS) is shaped like an
inverted pyramid, with the skull base superiorly
and the greater horns of the hyoid bone inferiorly.
The posterior border is formed by the prevertebral fascia and by the posterior aspect of the
carotid sheath, whereas the anterior boundary is
the interpterygoid fascia and the pterygomandibular raphe. The PPS can be subdivided into anterior and posterior compartments by a line
extending from the medial aspect of the medial
pterygoid plate to the styloid process (Fig.7.5).
The anterior (prestyloid) compartment contains the internal maxillary artery, inferior alveolar nerve, lingual nerve, and auriculotemporal
nerve (ATN). Infections in this compartment
often results in signicant trismus.
The posterior (poststyloid) compartment contains the carotid artery, internal jugular vein
(IJV), the last four cranial nerves, sympathetic
chain, and lymphatics. This space provides a cen-
tral connection for all other deep neck spaces. It
connects posteromedially with the retropharyngeal space, inferiorly with the submandibular
space, and laterally with the masticator space. It
is directly involved by the lateral extension of
PTA, and the carotid sheath courses through this
space into the chest.
7.4.2 Etiology
Infections in the PPS usually originate in the tonsils or pharynx. Spread is by direct continuity or
by lymphatic drainage. Thus, a parapharyngeal
abscess may be secondary to tonsillitis or bursting of a PTA.Other sources include dental infection (usually from the lower last molar tooth),
periostitis, other deep head and neck spaces, and
penetrating trauma of the neck [30]. A parapharyngeal abscess may be also iatrogenic, from
injection of a local anesthetic for tonsillectomy
or a mandibular nerve block.
7.4.3 Clinical Presentation
Retropharyngeal
space
Parapharyngeal
Fig. 7.5 Anatomy of the parapharyngeal space
The rst symptoms are identical to those of
uncomplicated acute pharyngitis or tonsillitis
(fever, sore throat, nasal voice, dysphonia,
enlarged cervical LNs). Progression of the signs
and symptoms pertains to inammation and
obstruction of the upper airways and/or gastrointestinal tract (GIT). There may be dysphagia,
dyspnea, stridor, neck stiffness, trismus, and/or
chest pain. General physical signs are those of
septicemia and toxemia. Locally, there is tenderness and swelling below the angle of the mandible, indicating the presence of pus [31].
Infections of the PPS are important causes of
morbidity and mortality because of the possible
complications, which include acute edema of the
larynx with respiratory compromise,
thrombophlebitis of the IJV with septicemia
(Lemierre’s syndrome), spread of infection to the
retropharyngeal space or mediastinum (along the
carotid space). Mycotic aneurysm with possible
subsequent rupture of the internal carotid artery
t.me/Dr_Mouayyad_AlbtousH
7 Deep Neck Space Infections
157
(ICA) and massive hemorrhage may also occur
[32, 33].
7.4.4 Diagnosis
Diagnosis is primarily based on classical signs
and symptoms and is conrmed using a CT scan
with contrast (Fig.7.6), which is considered the
radiologic test of choice. It provides details of the
size, location, and relations of the abscess to
large vessels and other deep spaces of the neck.
These details aid in determining the appropriate
mode of management [34].
7.4.5 Treatment
Treatment may require airway control. Parenteral
broad-spectrum antibiotics (e.g., ceftriaxone,
clindamycin) and surgical drainage are generally
required.
Posterior abscesses are drained externally
through the submaxillary fossa, whereas anterior
abscesses may often be drained via an intraoral
incision. Several days of parenteral culturedetermined antibiotics are necessary after drainage, followed by a 10–14-day course of oral
antibiotics. Occasionally, small abscesses can be
treated with IV antibiotics alone [32, 33]. Surgical
drainage carries its own inherent risks and potential complications. Consequently, percutaneous
aspiration under US or CT guidance has been
suggested as an alternative to conventional surgical I&D.Nutritional support needs special attention, particularly in the presence of septicemia.
Nasogastric (NG) feeding may be required.
7.5 Retropharyngeal Abscess
(RPA)
7.5.1 Surgical Anatomy
The retropharyngeal space is sometimes considered the third medial compartment within the
parapharyngeal space (PPS) because both communicate laterally (Fig.7.5). This space lies posterior to the pharynx, bound by the
buccopharyngeal fascia anteriorly, the prevertebral fascia posteriorly (Fig.7.7), and the carotid
sheaths laterally. It extends superiorly to the base
of the skull and inferiorly to the mediastinum. It
primarily contains retropharyngeal lymphatics.
An infection may enter this space directly
from traumatic perforations of the posterior pharyngeal wall or esophagus or indirectly from the
PPS.Infections of this space may drain into the
prevertebral space and consequently into the
chest, resulting in mediastinitis and empyema.
An abscess in this space may push forward,
Fig. 7.6 A contrast-enhanced axial computed tomography (CT) scan image showing a parapharyngeal abscess
(blue arrow)
t.me/Dr_Mouayyad_AlbtousH
Fig. 7.7 Location of the retropharyngeal abscess (RPA)
between the pharynx anteriorly and the prevertebral fascia
posteriorly (arrow)
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