Fascial Space Infection

When dental infection spreads deeply into soft tissue rather than exiting superficially through
oral or cutaneous routes, fascial spaces can be affected (Box 12-1). Following the path of least
resistance through connective tissue and along fascial planes, infection can spread distantly from
its dental source, causing considerable morbidity and occasionally death. A thorough knowledge
of the anatomy of the face and neck is necessary to predict the pathways of spread of these
infections accurately and to drain these deep spaces adequately.

Spread of infection through deep fascial spaces is determined by the presence and
patterns of loose connective tissue. Fasciae develop in planes of connective tissue subjected to
muscular movement and contraction. Surrounding or separating muscles, the fasciae and fascial
planes offer an anatomically defined highway for infection to spread from superficial to deep
parts of the face and neck. A description of deep fascial spaces essentially is an anatomic
discussion of the various fasciae that surround or separate the anatomic boundaries of a given
space. The concept of fascial “spaces” is based on the anatomist’s knowledge that all spaces exist
only potentially until fasciae are separated by pus, blood, drains, or a surgeon’s finger.

Infections of fascial spaces are discussed here primarily in terms of their odontogenic
origins. Teeth are the most common cause of these infections, and therapy is incomplete without
definitive dental treatment. However, deep fascial space infections of the neck also can occur as
a result of pharyngeal and tonsillar infections, trauma, reconstructive surgery, cancer surgery,
and sialadenitis of major salivary glands.

Each fascial space infection described in this chapter is a clinical entity; case reports
appearing in Appendix I illustrate the unique characteristic of each situation. In the treatment of
infections of fascial spaces, including surgical treatment, the principles discussed earlier should
always be considered. The following points also are germane:

1. Diffusion of antibiotics into close fascial spaces is limited because of poor vascularity.
Penetration of antibiotics through thick-walled abscesses is minimal. “Average” doses may be
inadequate.

2. Therapy of fascial space infections depends on adequate, open, and dependent drainage.
3. Large surgical incisions may be necessary to obtain adequate exposure of deep compartments.

4. Fascial spaces are contiguous, and infection spreads readily from one space to another.
Multiple incisions may be necessary because frequently more than one space is involved in the
infection.

5. Primary and secondary spaces must be drained.

6. The anatomy of the face or neck may be severely distorted by the swelling of the infectious
process.

7. Repeated surgical drainage may be necessary.

8. The fascial spaces most commonly involved in odontogenic infections are the submandibular,
submental, and buccal spaces. Less common are the masticator space compartments, lateral
pharyngeal, and temporal spaces. Least common are the retropharyngeal and canine spaces.

Although observation and palpation can elicit the presence of superficial dentoalveolar
and fascial space infections (i.e., buccal, canine, submental spaces), the presence of deep
infections must always be a suspicion. The presence of dysphagia, dyspnea, prolonged white
blood cell and temperature elevation, and unresolved trismus suggests the need for repeated
imaging (CT, magnetic resonance imaging) of deep spaces, inasmuch as the presence of or even
surgical drainage of superficial infection may obscure a concomitant or secondary deep space
involvement.

Canine Space

The canine space is infrequently involved in odontogenic infections and is implicated even less
frequently in nasal infections. Infections of the maxillary canine teeth usually appear as labial
sulcus swelling and less commonly as palatal swelling (Figure 12-7). However, the levator
muscle of the upper lip overlies the apex of the canine root. The origin of the muscle is high in
the canine fossa of the maxillary wall, whereas its insertion is the angle of the mouth,
intermingling with the fibers of the orbicularis oris muscle of the mouth and the zygomatic
muscle.
 If the canine infection perforates the lateral cortex of maxillary bone superior to the
origin of the muscle, the potential canine space is affected. Whether this represents a true fascial
space or simply a muscular compartment is debatable, but abscess of this space requires surgical
intervention. Canine space infections can cause marked cellulitis of the eyelids. Drainage is
accomplished best through an intraoral approach, high in the maxillary labial vestibule by sharp
and blunt dissection. This approach is an extension of that used for fenestration or apicoectomy
of the canine root apex. Percutaneous drainage may be performed lateral to the nose, but this
procedure does not afford dependent drainage and results in a visible scar.

See Appendix I for an illustrative case.

Cavernous Sinus Thrombosis

Although ascending infection (venous sinus thrombosis) is not a fascial space infection, it can be
of odontogenic origin. Cavernous sinus infection, ascending from the maxillary teeth, upper lip,
nose, or orbit through the valveless anterior and posterior facial veins, carries an extremely high
mortality rate. Any patient with initial signs of proptosis, fever, obtunded state of consciousness,
ophthalmoplegia, or paresis of the oculomotor, trochlear, and abducens nerves, especially after
maxillary infections and exodontia, should have an emergency neurosurgical consultation (see
Chapter 21)

Buccal Space

Mandibular and maxillary premolar and molar teeth tend to drain in a lateral and buccal
direction. The relation of the root apices to the origins of the buccinator muscle (the outer
surfaces of the alveolar process of the maxilla and mandible) determines whether infection exits
intraorally in the buccal vestibule or extends deeply into the buccal space. Molar infections
exiting superiorly to the maxillary origin of the muscle or inferiorly to the mandibular origin of
the muscle enter the buccal space.

The buccal space contains the buccal fat pad, the Stensen (parotid) duct, and the facial
(external maxillary) artery. Infection of this space is diagnosed easily because of marked cheek
swelling associated with a diseased molar or premolar tooth. When fluctuance occurs, it should
be drained percutaneously. Attempts to direct fluctuance intraorally by warm rinses are futile,
and intraoral drainage through mucosa, submucosa, and buccinator muscle may be difficult.

Cutaneous drainage should be performed inferior to the point of fluctuance with blunt
dissection into the depth and extreme boundaries of the space. The purulent contents can expand
the space to a surprising volume (Figures 12-8 and 12-9). The branches of the facial nerve should
be avoided. The usual incision and drainage site is quite inferior to Stensen’s duct. Aspiration of
this space is performed easily.

Of special interest, and far from uncommon, is nonodontogenic buccal space infection or
buccal cellulitis caused by Haemophilus influenzae. This infection, usually seen in infants or
children younger than 3 years, is characterized by high fever for at least 24 hours before the
appearance of clinical signs. The rapid onset of dark red swelling can be easily confused with an
odontogenic infection or erysipelas. Otitis media frequently is also present or has occurred
recently. Now commonly resistant to ampicillin, H. influenzae infection may respond well to
amoxicillin-clavulanate (Augmentin) or a cephalosporin such as cefaclor. This process can occur
in older children (Figure 12-10).

Recurrent buccal space abscesses can occur as a complication of Crohn’s disease. This
segmental transmural intestinal disease, whose clinical course includes intermittent abdominal
pain, fever, weight loss, and diarrhea, is characterized by inflammatory granulomas, which can
occur throughout the entire length of the gastrointestinal tract, from the mouth to the anus.
Granulomatous lesions and ulcerations of the buccal mucosa can progress to true buccal space
abscesses. A high recurrence rate of the granulomas or new abscess formation is possible despite
antibiotic, corticosteroid, or surgical therapy.

See Appendix I for an illustrative case.

Masticator Spaces

The masticator spaces (masseteric, pterygoid, and temporal) are well differentiated, but
communicate with each other and with the buccal, submandibular, and parapharyngeal spaces.
Infection may be confined to any one of these compartments or may spread rather readily to any
or all the other compartments.

Of the muscles of mastication, only the outer surface of the masseter and the inner
surface of the medial (internal) pterygoid are covered by true fascia. Sicher21 states that the
temporal fascia is really the suspensory bracing of the zygomatic arch, rather than a muscle
sheath. Although little space exists between the fibers of the masseter and temporalis muscles,
considerable space is present between the temporalis muscle and the pterygoid muscles. The
fatty connective tissue in this space extends anteriorly to the border of the buccinator muscle at
the pterygomandibular raphe.

The masticator space as a unit is bound by fascia. It contains the muscles of mastication,
the internal maxillary artery, and the mandibular nerve. If subdivided, the boundaries of the
masseteric compartment are the masseter muscle laterally and the mandibular ascending ramus
medially, whereas the pterygoid compartment is bounded medially by the pterygoid muscles and
laterally by the mandible. Both compartments communicate freely with the superficial and deep
temporal pouches superiorly, the buccal space anteriorly, and the lateral pharyngeal spaces
posteriorly. Extension of infection into parotid and submandibular spaces can also occur.

Infection of the masticator space occurs most frequently from molar teeth, and infections
of the third molars (wisdom teeth) are implicated most commonly as the cause. Pericoronitis of
the gingival flap of third molars or cariesinduced dental abscesses usually can be found in cases
of masticator space infection. Infections of this space also have been reported as a result of
contaminated mandibular block anesthetic injections, or infection may spread to this space from
nearby contiguous spaces. Infection of the masticator space also can result from direct trauma to
or through the muscles of mastication or surgery in the area (e.g., after temporal cranial flaps are
made for neurosurgery or following orthognathic surgery).

Infratemporal space infections also can occur as a result of temporomandibular joint

surgery or arthroscopy. The postulated mechanism is contamination from the external auditory
canal flora (streptococci, staphylococci, Haemophilus, Proteus, and Pseudomonas organisms).

Clinically the hallmark of masticator space infection is trismus, the sine qua non of
masticator space infection. If trismus is not present, these spaces are uninvolved with the
infectious process. An exception would be infection in a patient who is immunosuppressed, who
might not exhibit the classic signs of inflammation or the unique signs of deep space infection.

Swelling may not be a prominent sign of masticator space infection, especially in the
masseteric compartment. In this area, the infectious process exists deep to large muscle masses
that obscure or prevent much observable swelling. This process distinctly contrasts with
infections of the buccal space, in which swelling is the cardinal sign of infection.

Surgical access to the various compartments of the masticator space is complicated by the
containment of the infectious process by the muscle masses. Although drainage of the entire
masticator space from the intraoral space is possible and occasionally practical, access from an
extraoral incision is easier technically and more prudent. Some suggest an approach to all
compartments through an incision along the pterygomandibular raphe. This incision is
technically possible in a cadaver, but is less feasible in an infected patient with trismus. In such
patients, the oral approach could compromise the airway postoperatively because of persistent
bloody or purulent oozing, and intraoral drains may be difficult to maintain and can be aspirated
if loosened inadvertently.

The masseteric and pterygoid compartments can be entered by superficial sharp and deep
blunt dissection at the external angle of the mandible, avoiding the mandibular branch of the
facial nerve. This approach allows dependent drainage of both spaces at the insertion of the
muscle sling on the inferior border at the mandibular angle. Adequate local anesthesia can be
accomplished at the mandibular angle (Figures 12-11 and 12-12).

The temporal spaces, although accessible through Sicher’s intraoral incision, also can be
drained percutaneously through an incision slightly superior to the zygomatic arch. The incision
should be made parallel to the zygomatic arch and therefore parallel to the zygomatic branch of
the facial nerve rather than perpendicular to it.

See Appendix I for an illustrative case.

Submandibular and Sublingual Spaces

The submandibular (submaxillary) and sublingual spaces, although distinct anatomically, should
be considered as a surgical unit because of their proximity and frequent dual involvement in
odontogenic infection. Some confusion in nomenclature exists because some anatomists describe
these spaces as compartments of the “submandibular space.”

The mylohyoid muscle, which forms the floor of the oral cavity, is the key to the
diagnosis and surgical management of these space infections. Separating the sublingual space
above from the submandibular space below is the mylohyoid muscle, which attaches to the
lingual surface of the mandible in an obliquely downward line from posterior to anterior. Thus,
the root apices of the premolar and first molar teeth usually are superior to this attachment. As a
result, lingual perforations of infections from these teeth penetrate into the more superior
(sublingual) compartment (see Figure 12-3). Only loose connective tissue rather than true fascia
actually separates one side of the floor of the mouth from the other, an anatomic situation that
permits infection to spread bilaterally with ease.

Anteriorly, the sublingual space communicates with the submental space. In this area the
sublingual space can be invaded by infection from incisor teeth, especially from periodontal
infection. Posteriorly, the sublingual space communicates with the lateral pharyngeal spaces, in
the neighborhood of the posterior edge of the mylohyoid muscle and the lesser wings of the
hyoid bone.

Infection of the sublingual space appears clinically as brawny, erythematous, tender

swelling of the floor of the mouth, beginning close to the mandible and spreading toward the
midline or beyond. Some elevation of the tongue may be noted in late cases (Figure 12-13).
Infection must be differentiated from the cellulitis that might accompany an impacted sialolith in
the Wharton duct.

Surgical drainage of the sublingual space should be performed intraorally by an incision

through the mucosa parallel to the Wharton duct bilaterally. If the submandibular space is to be
drained, both spaces can be reached through a submandibular approach.

The submandibular space is separated from the overlying sublingual space by the fibers
of the mylohyoid muscle. Odontogenic infections of this space are commonly caused by the
second and third molar teeth (and, rarely, the first molar), inasmuch as their root apices lie
inferior to the mylohyoid line of muscle attachment. The space is bounded laterally by the
submandibular skin, superficial fascia, platysma muscle, superficial layer of deep cervical fascia,
and the lower border of the mandible. The contents of the submandibular space include the
submandibular salivary gland and its lymph nodes, the facial (external maxillary) artery, the
proximal portion of the Wharton duct, and the lingual and hypoglossal nerves as they course
deep to the submandibular gland on the inferior surface of the mylohyoid muscle (Figures 12-14
and 12-15).

Diagnosis of submandibular space infection is made by finding the typical swelling of the
space, either brawny or soft, and correlating it with the presence of a diseased mandibular molar.
Infection can be related to sepsis in an adjoining space, such as the sublingual, the submental, or
the masticator space. Conversely, infection can spread from the submandibular space into any
contiguous space, including the pharyngeal spaces. The infectious process commonly spreads
across the midline into the contralateral submandibular space. If spread is bilateral and involves
all submandibular and sublingual spaces and the submental space, the result is the well-known
Ludwig’s angina.

Differential diagnosis should include acute sialadenitis, sublingual trauma or foreign

body, and submandibular lymphadenitis; these can produce a secondary overlying cellulitis that
further confuses the diagnosis.

Therapy for submandibular space odontogenic infection includes surgical drainage,

antibiotics, and definitive care of the primary dental infection. Incision is performed through the
skin below and parallel to the mandible. Blunt dissection is carried to the depths of the space and
to its anterior and posterior margins. Deep abscess loculations should be entered with a small
closed clamp, probing in all directions while attempting to avoid damage to the submandibular
gland, the facial artery, and the lingual nerve. The contralateral space should not be entered
unless it is involved in the infection; if necessary, however, drains can be placed into both sides,
as in the treatment of Ludwig’s angina.

See Appendix I for an illustrative case.

Submental Space
A potential fascial space exists in the chin and occasionally becomes infected, either directly
from a mandibular incisor or indirectly from the submandibular space. The submental space is
located below the chin and is bound above by the skin and the chin (mentalis) muscles, laterally
by the anterior bellies of the digastric muscles, deeply by the mylohyoid muscle, and superiorly
by the deep cervical fascia, the platysma muscle, the superficial fascia, and the skin. Submental
infection can spread easily to either or both submandibular spaces.

If infection from the incisors exits labially through the mandibular bone, inferior to the
muscle attachments, then the submental space becomes involved. The chin appears grossly
swollen and is firm and erythematous (Figure 12-16). Percutaneous surgical drainage is the most
effective approach. A horizontal incision in the most inferior portion of the chin, in a natural skin
crease, provides dependent drainage and the most cosmetically acceptable scar. The space can be
drained orally through the mentalis muscle through the labial vestibule, but dependent drainage
cannot be established from this approach.

See Appendix I for an illustrative case.

Infections Associated with Impacted Third Molar Teeth

Lower third molars are a frequent cause of infection, even in otherwise healthy patients. In
Western society, where contemporary dental care and the widespread use of fluoridated drinking
water have resulted in the remarkable decrease in dental caries and prevention of early loss of
first and second molar teeth, a high rate of impacted third molars has resulted. Impaction is often
associated with pericoronal infection (Figure 12-17). Bacteriologically the profuse colonization
under the moist, poorly oxygenated pericoronal flap consists of the usual mixed aerobic-
anaerobic flora, but can result in tissue destruction and pain to a level similar to that of acute
necrotizing ulcerative gingivitis.22 The use of antibiotics is recommended for third molar
pericoronitis if body temperature is elevated or if trismus or adenopathy are present. Initially,
gentle mechanical irrigation and debridement can be useful, as are incision and drainage, with
extraction of the maxillary third molar (or cuspal reduction) if it is in occlusion with the
edematous mandibular flap. Lower extraction usually is delayed until the trismus has resolved
sufficiently to permit surgical access.
 Pericoronitis occasionally spreads rapidly because of the anatomic location of the
mandibular third molar at the crossroads of the masticator, submandibular, and buccal fascial
spaces with adjacent anatomic access to contiguous parapharyngeal, parotid, submandibular, and
other spaces (Figure 12-18).23 Unfortunately, the same potentially serious sequelae exist as
postextraction complications, which is an important issue in the risk/benefit ratio and
medicolegal areas of surgery.

The role of prophylactic antibiotics in third molar surgery is controversial. If pericoronitis

is present at the time of surgery or has been present recently, antibiotic therapy is indicated.
However, removal of the truly asymptomatic and completely impacted third molar fits the
category of clean-contaminated rather than contaminated surgery, and data exist to support the
efficacy of both the use and nonuse of prophylactic antibiotics. If the mandibular marrow space
has been widely exposed, especially during a lengthy extraction, “prophylactic” postoperative
antibiotics would seem prudent. However, for true prophylaxis, the antibiotic ideally should be
administered preoperatively.24 The use of antibiotics after third molar extraction has not altered
the infection rate. Advocates and dissenters continue the ongoing clinical debate.

Penicillin (or amoxicillin) remains the antibiotic of choice, administered as 2 g of

amoxicillin orally 1 hour before the procedure and a second dose 2 hours after the initial dose,
with no further doses given. Alternatively, 2 g of penicillin G can be given intravenously as a
single dose. In patients who are allergic to penicillin, clindamycin, 600 mg orally or
intravenously as a single dose, is suggested. The overall third molar postoperative infection rate
ranges from 4.2 to 6.3% with or without antibiotics, but most studies are subject to challenge
because they fail to differentiate which patients have a history of pericoronitis and whether the
extraction sites are profusely irrigated.

Ludwig’s Angina

Ludwig’s angina is a firm, acute, toxic cellulitis of the submandibular and sublingual spaces
bilaterally and of the submental space. As early as 1796, extraction of abscessed teeth was
considered contraindicated because “it might give rise to extensive inflammation and angina, in a
dangerous degree.” Three F’s became evident even before the first written description of the
disease: it was to be feared, it rarely became fluctuant, and it often was fatal. A sensation of
choking and suffocation (angina) often was combined with the name of the author (Ludwig) who
fully described it in 1836.

The original description of the disease has not been improved since the observations of
Wilhelm Friedrich von Ludwig were published while he was court physician to the King of
Wurttemberg and president of that kingdom’s medical association. His descriptive phrases ring
true today, despite considerable improvements in therapy and mortality:

. . . amidst the symptoms which herald the approach—an erysepalous angina, temperature swings
. . . discomfort upon swallowing, there develops on one or both sides of the neck a firm
connective tissue with which it comes in contact . . . it extends uniformly about the periphery of
the neck . . . to a marked degree. It advances in similar fashion to involve the tissues which cover
the small muscles between the larynx and the floor of the mouth . . . the tongue rests upon a red,
indurated mass which feels like a hard ring adjacent to the inner surface of the jaw bone. It
becomes difficult and painful to open the mouth . . . speech is impaired and hoarse . . . this is
because the tongue is pressed backward and upwards, there is pressure upon the larynx . . . as the
disease progresses . . . externally certain areas become, at times, softer . . . at other times more
prominent and apparently fluctuant. Fever increases with morning exacerbations . . . swallowing
continues to be difficult and the patient opens the mouth only with effort; dyspnea appears
usually in paroxysms . . . and on the tenth to twelfth day of the disease, death occurs, with the
patient in a comatose state with evidence of respiratory paralysis . . . there are nuances in the
typical picture of the disease . . . particularly the onset and severity of the local lesion. . . .
Among the cases in which autopsy was permitted . . . there were found abscess cavities whose
walls were made up of gangrenous partly decomposed masses of muscle . . . the periosteum of
the inner surface of the jaw was loosened from the bone and was discolored.

Ludwig refrained from suggesting a “scientifically valid” hypothesis of the cause of the disease,
but stated that “it differentiates itself from other neck inflammations with symptomatic or
idiopathic swelling of the salivary glands.”25a As therapy, he recommended local and general
bloodletting, softening poultices, and external and internal use of mercurials, vesicants,
cathartics, and diuretics. He described the case of Fraulein N.N., who suffered both the disease
and the therapy, including leeches, bran poultices, tartar emetic, dry heat, a gargle of althea and
honey, almond oil, ipecac, and finally, “a piece of silver nitrate the size of a six Krenzer coin
over the middle of the swelling . . . which had created a splendid necrosis.” Because of or despite
the therapy (chemical incision and drainage), N.N. survived, and “three weeks after the onset,
when the last traces of the induration could still be felt, the patient felt well and strong.”

Almost 60 years passed before the causative relationship between dental disease and
Ludwig’s angina was established. Carious rotten teeth were ubiquitous in Ludwig’s era, whereas
his eponymous angina was comparatively uncommon; hence, he never recognized the
association. Considering that the germ theory of disease had yet to be postulated, antibiotics were
undiscovered, anesthesia did not exist, and contemporary surgeons were reluctant to incise
without the certainty of finding “laudable pus,” N.N. was indeed fortunate to have survived.
Curiously, Ludwig did not survive a throat inflammation and he died in 1865 at the age of 75.

Today, Ludwig’s angina is a disease primarily of dental origin. Dental infection has been
reported as the causative factor in 90% of cases in some series, either as primary dental infection
or as a postextraction phenomenon. As was stated in 1943, “The dentist who is unfortunate
enough to have performed extraction on a patient who subsequently develops Ludwig’s angina is
more likely to have been incidental to the train of events than to have been the responsible
agent.”

Other causative factors include submandibular gland sialadenitis, compound mandibular

fracture, oral soft tissue lacerations, puncture wounds of the oral floor, and secondary infections
of oral malignancies. Ludwig’s angina infection has been reported in a newborn. The term
pseudo-Ludwig’s angina has been applied to these cases of nondental origin; they also are
referred to as pseudo-Ludwig’s phenomena.

Fortunately, the incidence of Ludwig’s angina remains low in this modern era of
preventative dental care and antibiotic therapy. In the preantibiotic era, a mortality rate greater
than 50% was reported, but this was reduced to approximately 5% with the use of penicillin.
Most early cases probably are aborted by the use of antibiotics before rapid, deep spread of
infection occurs. Representing less than 1% of all admissions to oral-maxillofacial services,
Ludwig’s angina is observed most frequently in the contemporary compromised host. If the
disease is untreated, the mortality rate is close to 100%. A true Ludwig’s angina is an obligatory
hospital admission.

Bilateral infection of the sublingual and submandibular spaces with brawny edema, an
elevated tongue, airway obstruction, and a paucity of pus are the clinical hallmarks of Ludwig’s
angina. The submental space also is swollen, and sepsis can spread rapidly to involve the
masticator and pharyngeal spaces.

A veritable host of organisms have been implicated as the causative agents of this
disease. Because Ludwig’s angina is commonly of dental origin, streptococci or mixed oral flora
are the most commonly reported organisms from cultures of whatever exudate can be obtained
after surgical drainage. Contemporary reports of Ludwig’s angina have demonstrated the
presence of staphylococci, gram-negative enteric organisms such as E. coli and Pseudomonas,
and anaerobes, including Bacteroides and Peptostreptococcus species. The isolation of these
organisms may indicate the changing oral flora of the antibiotic era or reflect more sophisticated
modern culture techniques. Prevotella melaninogenicus, Prevotella oralis, and Prevotella
corrodens also have been isolated from patients with Ludwig’s angina or other odontogenic
infections. Experimental data from studies of cutaneous infections similar to the ulcer of
Meleney suggest that a synergistic or obligatory synergistic relationship may exist among
anaerobes such as Prevotella (P. melaninogenicus), anaerobic streptococci, and fusospirochetes,
all common organisms. Mixtures of oral organisms that did not include Prevotella could not
create transmissible subcutaneous infections in experimental animals, whereas an infection was
produced by the addition of that organism. Whatever the role of anaerobes, primary or
synergistic, a search for them should not be omitted when culturing specimens from Ludwig’s
angina or other serious odontogenic infections (see Geisler et al27 and Chow et al28).

Treatment of Ludwig’s angina includes early diagnosis of the incipient cases,

maintenance of a patent airway, intense and prolonged antibiotic therapy, extraction of the
affected teeth, hydration, and early surgical drainage (with a life in the balance, a quick
extraction is more rational than timeconsuming tooth salvage). Empirical antibiotic therapy
(intravenous) for Ludwig’s angina should be intense; choices include penicillin plus
metronidazole or clindamycin or imipenem used as single agents.
 Establishment and maintenance of an adequate airway are the sine qua non of therapy.
Death is more likely to occur early from airway obstruction than from sepsis. Tracheostomy has
been almost routine during most of the twentieth century, but may prove difficult to perform in
the late stage of the disease because of massive neck edema and tissue distortion. Attempts at
blind endotracheal intubation can be time consuming, unsuccessful, and fraught with danger,
especially if attempted by an inexperienced anesthesiologist, because of the swollen elevated
tongue and glottic edema. The danger of rupturing a bulging lateral pharyngeal or
retropharyngeal abscess exists if the infection involves these fascial spaces. Cervical soft tissue
plain radiographs and CT scanning should be done before attempted tracheostomy, if time
permits. Fiberoptic laryngoscopy is useful in the airway management of Ludwig’s angina but
requires an anesthesiologist skilled in its use, and the patient must be cooperative and
premedicated. Tracheal intubation with the patient under deep inhalation anesthesia may be
successful, usually obviating the need for tracheostomy. The use of sedative and narcotic agents,
which can cause more rapid respiratory deterioration, is not recommended (see Chapter 32).

Although some authorities advocate high doses of antibiotics without surgery until
fluctuance develops, in most surgeons’ experience, fully developed Ludwig’s angina requires
prompt and deep surgical incision because fluctuance is uncommon and late. Ludwig’s angina is
a diffuse cellulitis of deep fascia. Seventy percent of cases still require surgical intervention and
drainage. The submandibular and sublingual spaces and secondarily involved spaces must be
explored bilaterally. The masticator spaces must be drained if trismus is present. The prudent and
experienced surgeon recognizes the wisdom of the maxim “a chance to cut is a chance to cure”
when confronted with Ludwig’s angina.

A horizontal incision midway between the chin and the hyoid bone was the classic
approach to the surgical drainage of Ludwig’s angina, but this “cut-throat” incision has proved
unnecessary and unaesthetic. Bilateral incision into the submandibular spaces with blunt
dissection to the midline suffices if bilateral drains meeting in the midline are placed. This
maneuver, combined with drainage of the sublingual spaces, relieves the intense pressure of
edematous tissue on the airway and provides specimens for Gram staining and culture (Figure
12-19).
 The platysma muscle and suprahyoid fasciae are incised by this approach, and the fascia
of the submandibular gland is also entered. The mylohyoid muscle should be divided and the
sublingual spaces entered. A closed clamp should be inserted through the median raphe of the
mylohyoid muscle and advanced to the hyoid bone at the base of the tongue. Generally, little pus
is obtained because the infection often represents cellulitis of the fascial spaces rather than true
abscess formation. In some cases, especially late or fully developed ones, purulent flow is
produced.

Needle aspiration of deep fascial space infections has been attempted, sometimes
obviating open drainage procedures. However, Ludwig’s angina, basically a rapidly spreading,
deep cellulitis without localization of pus or formation of fluctuance is not amenable to this
technique, even if the needle is CT guided.

Sequelae after adequate drainage and antibiotic therapy are uncommon. However,
inadequate drainage or premature closure of the surgical wounds can lead to reinfection. Late
spread to other fascial spaces or generalized sepsis can occur and are ever-present dangers.
Failure to extract the offending tooth could cause reinfection. Secondary revision of scarring may
be necessary for cosmetic reasons or to repair stenosis of the Wharton duct.

The mortality rate for Ludwig’s angina has decreased since the advent of prompt surgical
intervention, airway maintenance techniques, and antibiotic therapy. However, three fatal cases
are discussed in Appendix I to illustrate the potential or actual lethality of this disease.

Pharyngeal Space Infection

The lateral pharyngeal space (pharyngomaxillary space) is a lateral neck space shaped like an
inverted cone, with its base at the skull and its apex at the hyoid bone. Its medial wall is
contiguous with the carotid sheath, and it lies deep to the pharyngeal constrictor muscle. It is
divided, for surgical and anatomic purposes, into anterior and posterior compartments.

Infections of the lateral pharyngeal space can result from pharyngitis, tonsillitis, parotitis,
otitis, mastoiditis, and dental infection, especially if the masticator spaces are primarily infected.
Herpetic gingivostomatitis involving pericoronal tissue has also been reported as a cause of the
lateral pharyngeal abscess. If the anterior compartment becomes infected, the patient exhibits
pain, fever, chills, medial bulging of the lateral pharyngeal wall with deviation of the palatal
uvula from the midline, dysphagia, swelling below the angle of the mandible, and usually
trismus (Figure 12-20). Infection of the posterior compartment is noted for absence of trismus
and visible swelling, but respiratory obstruction, septic thrombosis of the internal jugular vein,
and carotid artery hemorrhage can occur in patients at a late stage of infection. CT and magnetic
resonance imaging may prove useful in diagnosing lateral pharyngeal infections and may reveal
confluence with other deep space infections and septic erosion of the wall of the great vessels.

Therapy consists of antibiotics, surgical drainage, and tracheostomy if indicated. The

surgical approach may be oral, by incision of the lateral pharyngeal wall, or external, by
exposure of the carotid sheath near the lateral tip of the hyoid bone after retraction of the
sternocleidomastoid muscle. Blunt dissection along the posterior border of the digastric muscle
leads to the lateral pharyngeal space. In the combined intraoral and extraoral approach, a
mucosal incision is made lateral to the pterygomandibular raphe, and a large curved clamp is
passed medial to the medial pterygoid muscle in a posterior-inferior direction. The tip of the
clamp is delivered through the skin by a cutaneous incision between the angle of the mandible
and the sternocleidomastoid muscle.

See Appendix I for an illustrative case.

Retropharyngeal Space

The esophagus and trachea are enclosed by the middle layer of the deep cervical fascia. A thick
strand of connective tissue extends laterally from the esophagus to the carotid sheath, thus
creating an anterior neck compartment known as the pretracheal (previsceral) space and a
posterior or retropharyngeal (retrovisceral) space. The posterior space lies behind the esophagus
and pharynx and extends inferiorly to the upper mediastinum and superiorly to the base of the
skull.

Clinically, retropharyngeal space infections can result most commonly from nasal and
pharyngeal infections in children (tonsillitis), dental infection diffusing through contiguous
spaces, esophageal trauma or foreign bodies, and tuberculosis. Infection can also reach this space
through the lymphatics to involve the retropharyngeal lymph nodes. Dysphagia, dyspnea, nuchal
rigidity, esophageal regurgitation, and fever characterize infections of the retropharyngeal space.
If the pharynx can be visualized, a bulging of the posterior wall may be observed and is usually
more prominent unilaterally because of the adherence of the median raphe of the prevertebral
fascia. Lateral soft tissue radiographs of the neck are extremely useful and may reveal
considerable widening of the retropharyngeal space, well beyond the 3- to 6-mm width in normal
adults at the second vertebra (or >14 mm in children; Figure 12-21). In adults, the space width/
vertebra ratio is 6 mm at C2 and 20 mm at C6. The presence of gas in the prevertebral soft
tissues and the loss of the normal lordotic curvature of the cervical spine also may be observed
on plain radiographs and CT scans. CT scans reveal the presence of the infection in the
retropharyngeal space and its inferior extent.

Although some reports indicate that 10 to 40% of retropharyngeal infections resolve with
only medical management, these cases reflect early diagnosis and antibiotic therapy. Infection of
the retropharyngeal space usually requires prompt surgical drainage and allows little time for
delay, debate, or decision by committee. Because many anesthesiologists are reluctant to risk
aspiration or airway obstruction by pus pouring from the ruptured space during passage of an
endotracheal tube, tracheostomy may be indicated. However, drainage has been performed
transorally with the patient under local anesthesia in the extreme Trendelenburg position and
with constant suctioning. In the transoral technique, an incision is made through the midline of
the posterior pharyngeal mucosa, and the abscess is opened by blunt dissection.

An external approach generally provides more dependent drainage. An incision is made

along the anterior border of the sternocleidomastoid muscle and parallel to it, inferior to the
hyoid bone. This muscle and the carotid sheath are retracted laterally, and blunt finger dissection
is carried deeply, avoiding the hypoglossal nerve, to the level of the hypopharynx. Blunt finger
dissection deep to the inferior constrictor muscles opens the retropharyngeal space abscess. Deep
drains are placed and maintained until all clinical and laboratory signs of infection are no longer
apparent. Needle aspiration with CT scan guidance has avoided open surgical drainage in a few
cases. The overall mortality rate for retropharyngeal infections of all causes is approximately
10%. See Appendix I for an illustrative case.
Mediastinitis

Extension of infection from deep neck spaces into the mediastinum is heralded by chest pain and
severe dyspnea, unremitting fever, and radiographic demonstration of mediastinal widening.
Rarely, mediastinitis can be caused by odontogenic infection that spreads directly along the great
vessels in the perivascular space of the carotid sheath (Figure 12-22). Intravenous drug abusers
who inject into the major blood vessels of the neck are at risk for deep neck infections, including
the carotid space, and may have septic thrombosis of the jugular veins.

Spread of an odontogenic infection to the mediastinum also is noteworthy because it is

preceded by infection of other fascial spaces that may have been drained adequately. Therefore,
mediastinitis may be a late complication and should be suspected in patients with exacerbation of
fever associated with substernal pain. Progressive septicemia, mediastinal abscesses, pleural
effusion, empyema, compression of mediastinal veins with decreased venous return to the heart,
and pericarditis can occur, with death as the final outcome.

Necrotizing mediastinitis of dental origin may be related to the synergistic effect of

aerobic and anaerobic bacteria invading susceptible tissue far from their normal oral
environment.29-32 Passively commensal in the mouth, the bacteria can become synergistically
aggressive and invasive elsewhere.

Treatment of suppurative mediastinitis consists of extensive, long-term antibiotic therapy

and surgical drainage of the mediastinum. Specimens for culture should be obtained regularly
during long-term therapy. See Appendix I for an illustrative case.

Infection-Induced Osteomyelitis

Osteomyelitis is an inflammatory process of the medullary portion of the bone in which a

bacterial source causes bony destruction. The process may extend to cortical bone, as well as the
periosteum. Because of the availability of antibiotics the incidence of osteomyelitis has
decreased.2-4

The literature contains a variety of ways to classify osteomyelitis. In the final analysis,
however, osteomyelitis can be broken into two primary categories: acute and chronic. Acute
osteomyelitis is characterized by fever, malaise, facial cellulitis, trismus, and leukocytosis. Most
commonly, chronic osteomyelitis is secondary to acute osteomyelitis. The dividing point
between acute and chronic has been established at the 4-week point. This secondary chronic
osteomyelitis is characterized by swelling, deep pain, purulence, intraoral or extraoral fistulae,
nonhealing bone, and overlying soft tissue wounds. A primary form of chronic osteomyelitis has
also been described in which there was no preceding acute phase.

The key to treatment of osteomyelitis is early detection, which means early suspicion.
Identification of the causative organism may be difficult, but is important for appropriate
antibiotic selection. Surgical treatment is almost always part of the treatment plan.