TITLE: Deep Neck Abscesses and Life-Threatening Infections of the Head and
Neck
SOURCE: Grand Rounds, Dept of Otolaryngology UTMB
DATE: February 25, 1998
RESIDENT: Carl Schreiner, MD
FACULTY PHYSICIAN: Francis B. Quinn, MD
SERIES EDITOR: Francis B. Quinn, Jr. MD
"This material was prepared by resident physicians in partial fulfillment of
educational requirements established for Postgraduate Medical Education activities
and was not intended for clinical use in its present form. It was prepared for
the purpose of stimulating group discussion in a conference setting. No warranties,
either express or implied, are made with respect to its accuracy, completeness,
or timeliness. The material does not necessarily reflect the current or past opinions
of subscribers or other professionals and should not be used for purposes of diagnosis
or treatment without consulting appropriate literature sources and informed professional
opinion."
INTRODUCTION
Life-threatening infections of the head and neck are much less
common since the introduction of antibiotics and mortality rates
are lower. The widespread use of antibiotics has not only
lowered the incidence of life-threatening infections but has
also altered their clinical presentation. Obvious signs of
systemic toxicity, such as chills and spiking fevers and classic
presentations of infectious syndromes may be lacking in patients
with partially treated infections. This, combined with the
increasing number of patients with severe immunosupression makes
it worthwhile for the physician to review these syndromes and
the unique anatomic features of the head and neck which can lead
to life-threatening complications.
HEAD AND NECK ANATOMIC CONSIDERATIONS
The most common sources of life-threatening soft tissue
infections of the head and neck are the dentition and tonsils.
Most infections are polymicrobial and the responsible bacteria
are often normal flora (Bacteroides, Peptostreptococcus,
Actimomyces, Fusobacterium and microaerophilic strep.) that
become virulent and invasive when normal barriers are broken
(ie. tonsillitis, dental abscess, trauma). Obligate anaerobes
frequently outnumber the anaerobes by a factor of 10:1 and
synergistic effects often promote invasiveness. From these
sites, infection may spread along facial planes, which serve to
either separate or connect distant sites by limiting or
directing the spread of infection. The most common sources for
intracranial complications are the nose, sinuses and ear, which
all have unique pericranial and periorbital locations.
Infection from these sites may spread either through direct
extension through bone or through retrograde venous spread. The
following discussion will review the clinical patterns of deep
neck space infections and summarize the parameningeal or
intracranial complications of head and neck infections.
DEEP NECK SPACE AND SOFT-TISSUE INFECTIONS
Deep neck space infections are most commonly odontogenic in
origin. The vast majority of dental infections are treated with
root canal, extraction or periodontal therapy before they become
serious. However, a small number of infections follow a
fulminant course and may become life-threatening either through
airway compromise, necrotizing fascitis, or rapid spread to
involve the orbit, cranium or chest. Dierks et. al. found, in
their review of fulminant odontogenic infections, that most
cases involved delayed treatment of molar infections. Anaerobic
infections predominated and most patients were young and without
debilitating medical conditions.
Before discussing individual fascial compartments of the neck, a
brief review of the cervical fascial layers is necessary (2,3).
Fascial compartments of the neck are potential spaces between
layers of fascia. The cervical fascia is divided into two main
compartments; the superficial cervical fascia and the deep
cervical fascia. The superficial cervical fascia lies just
below the skin, envelopes the platysma and muscles of facial
expression, and completely surrounds the neck. The deep
cervical fascia is subdivided into superficial, middle, and deep
layers. The superficial (investing) layer of the deep cervical
fascia invests the sternocleidomastoid, trapezius, strap
muscles, parotid and submandibular glands. The middle
(visceral) layer surrounds the thyroid gland, esophagus and
trachea. Its upper limit attaches to the hyoid bone and it
extends inferiorly into the mediastinum. The deep layer of the
deep cervical fascia splits into prevertebral and alar layers.
The prevertebral layer lies immediately adjacent to the
vertebral bodies and extends from the skull base to the coccyx.
The alar layer is located just anterior to the prevertebral
layer but extends only to the level of the second thoracic
vertebra. All three layers of the deep cervical fascia
contribute to the carotid sheath so that infection of any layer
may spread directly to involve the great vessels of the neck,
whick have direct communication to the chest.
Submandibular Space
The prototypical infection of this space was described by
Wilhelm von Ludwig in 1836. He described a gangrenous
infection of the neck with woody cellulitis without
suppuration and insidious asphyxiation. With minor changes, his
definition still holds today although the term Ludwigs angina
implies bilateral submandibular space involvement.
The submandibular space extends from the hyoid bone to the
mucosa of the floor of the mouth. It is bound anteriorly and
laterally by the mandible and inferiorly by the superficial
layer of the deep cervical fascia. The mylohyoid muscle acts as
a sling across the mandible and divides the submandibular space
into sublingual and submylohyoid spaces. Because these spaces
communicate freely around the posterior border of the mylohyoid,
some feel they should be considered as a single unit, the
submandibular space. Again, the definition of Ludwigs angina
requires bilateral submandibular (including sublingual) space
involvement.
The mylohyoid muscle also plays a key role in determining the
direction of spread of dental infections. It attaches to the
mandible at an angle, leaving the apices of the second and third
molars below the mylohyoid line and the apex of the first
molar above. Most apical molar infections perforate the
mandible on the lingual side, so if the tooth apex is above the
mylohyoid line it will involve the sublingual space. If it
perforates below the mylohyoid line is involves the
submylohyoid space.
The bucopharyngeal gap is a potentially dangerous connection
between the submandibular and lateral pharyngeal spaces that is
created by the styloglossus muscle as is passes between the
middle and superior constrictors. Due to this connection,
cellulitis of the submandibular space can directly spread to the
lateral pharyngeal space, which, as will be discussed, is a more
dangerous space for infection.
Most patients with submandibular space infections are young,
healthy adults with an odontogenic infection. Patients usually
present with mouth pain, dysphagia, drooling and stiff neck. In
the case of Ludwigs angina, massive tongue and floor of mouth
edema can rapidly lead to posterior and superior displacement of
the tongue as well as anterior displacement out the mouth. The
patient often maintains the neck in an extended position and may
have a muffled or "hot potato" voice. The neck shows a
characteristic erythematous woody swelling but fluctuance is
usually absent. Trismus, which indicates lateral pharyngeal or
masticator space involvement, should be absent in isolated
submandibular space infections.
The most common cause of death in Ludwigs angina is asphyxia.
Airway control is the first priority of treatment, followed by
intravenous antibiotics and timely surgical drainage. The
method of controlling the airway in Ludwigs angina is
controversial and may include close observation, tracheotomy,
fiberoptic intubation or cricothyroidotomy. Airway control is
not always needed with close observation in an ICU. Blind oral
or nasotracheal intubation or attempts with neuromuscular
paralysis is contraindicated in Ludwigs angina as they may
precipitate an airway crisis. Tracheotomy is still the most
widely used method of airway control but some authors feel the
risk of aspiration pneumonia (from close proximity of the trach
site to open neck wounds)and the risk of mediastinal infection
as reasons to avoid tracheotomy if possible. Cricothyroidotomy
is usually not a good option with in patients with massive neck
edema.
Penicillin has long been the drug of choice in the treatment of
deep neck space infections but there appears to be a trend of
increasing beta-lactamase producing organisms (particularly
Bacteroides) so broader spectrum antibiotics are needed. In
cases of critically ill patients or a poor response to therapy,
clindamycin or metronidazole may be added, but neither drug
should be used alone. Antibiotic therapy alone may be curative
in the cellulitic phase but failure to respond to intravenous
antibiotics may ether be due to undrainied purulent collections
or extension into adjacent spaces.
Surgical drainage was once universally required but now may be
reserved for cases where antibiotic treatment fails or when soft
tissue air or pus is noted. Intraoral drainage may be adequate
in a few cases of limited sublingual involvement but drainage
through submandibular incisions with splitting of the mylohyoid
muscle is usually required. If the infection is odontogenic,
the offending tooth should also be removed.
Lateral Pharyngeal Space
This space (also called the parapharyngeal space) occupies a
critical area in the neck, as it communicates with all other
fascial spaces. It sits as an inverted cone with its base at
the base of skull and apex at the hyoid bone. Its posterior
boundary is the prevertebral fascia and its anterior boundary is
the raphe junction of the buccinator and superior constrictor
muscles. It is bound laterally by the mandible and the parotid
fascia, which is often noncontiguous over the parotid, allowing
communication between the parotid and the lateral pharyngeal
space. The lateral pharyngeal space can be divided into
anterior (prestyloid) and posterior (retrostyloid) compartments
by the styloid process. The anterior compartment contains only
fat, lymph nodes and muscle. The posterior compartment contains
the carotid and internal jugular vessels, as well as cranial
nerves IX through XII.
Infections of the anterior space present with pain, fever, neck
swelling below the mandible and trismus. The source if the
infection is again most often dental, but may arise from
numerous sources, including the tonsils, parotid, and
submandibular, peritonsilar, masticator, or retropharyngeal
spaces. Rotation of the neck away from the side of swelling
causes severe pain from tension on the ipsilateral
sternocleidomastoid muscle. Ominous signs of posterior
involvement include Horners syndrome, CN IX through XII palsies
and complications include septic jugular thrombophlebitis (most
common) and carotid artery erosion or thrombosis. Sentinel
bleeds, or recurrent bleeding from the nose, mouth or ear should
always alert the physician of the possibility of an impending
carotid rupture. Hematogenous dissemination can also occur with
major vessel involvement. Airway impingement due to medial
bulging of the pharyngeal wall and supraglottic edema can
occasionally occur but is much less likely than in Ludwigs
angina.
The treatment of lateral pharyngeal abscess is similar to the
treatment of Ludwigs angina except that surgical drainage is
usually required and frank purulence is more often encountered
in lateral pharyngeal abscesses. CT scanning is the imaging
modality of choice and is helpful in confirming which
compartments are involved. In complicated cases such as septic
jugular vein thrombosis, several weeks of intravenous
antibiotics may be required. Resection of the thrombosed
internal vein is now rarely performed except in refractory
cases.
Retropharyngeal, Danger, And Prevertebral Spaces
The retropharyngeal, danger and prevertebral spaces all lie
between the deep cervical fascia surrounding the pharynx
anteriorly and the spine posteriorly. The retropharyngeal space
is bordered anteriorly by the constrictor muscles and
posteriorly by the alar layer of the deep cervical fascia.
Infections of this space can extend down to the superior
mediastinum. These infections most commonly occur in children
as a complication of suppurative adenitis. Presenting symptoms
include fever, stiff neck, drooling and dysphagia. Bulging of
the posterior pharyngeal wall is often difficult to appreciate.
Properly performed lateral neck films in extension will show
thickened prevertebral soft tissue but a CT scan is essential to
determine the inferior limits of involvement. Retropharyngeal
abscesses should be considered the most dangerous deep neck
space abscess because complications include supraglottic edema
with airway obstruction, aspiration pneumonia due to rupture of
the abscess and acute mediastinitis. Mediastinitis is the most
feared complication and may result in empyema or pericardial
effusions. If the infection perforates the alar layer
posteriorly, it enters the danger space, which extends down the
entire mediastinum to the level of the diaphragm. Further
extension posteriorly enters the prevertebral space, which
extends down to the coccyx. Treatment involves intravenous
antibiotics and timely surgical drainage. Recent reports have
shown good responses to conservative therapy so a trial of
antibiotics prior to surgical drainage may be indicated.
Surgical drainage should be performed in the operating room via
a transoral approach with the head down to prevent rupture
during intubation and septic aspiration.
Masticator Space
The masticator (or masseteric space) contains the pterygoid and
masseter muscles as well as the insertion of the temporalis
muscle on the coronoid process of the mandible. It communicates
freely with the temporal space superiorly but not usually to the
adjacent more dangerous spaces. Most masticator space
infections are caused by molar teeth and trismus is the most
pronounced clinical feature and often precludes intraoral
examination. CT is invaluable in the assessment of masticator
space infections as it can often influence the surgical approach
and distinguish abscess from cellulitis. Intraoral approaches
are often sufficient for simple masticator space abscesses but
an external approach may be required cases with extension to
other spaces.
Peritonsillar Abscess
Peritonsillar abscess is a complication of acute tonsillitis
that is rarely life- threatening in itself but, as previously
discussed, can spread to involve the lateral pharyngeal space.
Ther peritonsillar space is a potential space of loose areolar
tissue that surrounds the tonsil and is bounded laterally by the
superior constrictors. Most abscesses occur in younger patients
who present with fever, sore throat and dysphagia. Treatment
options include serial aspiration, local incision and drainage
or surgical drainage with tonsillectomy. Local incision and
drainage in the emergency room after intravenous fluid
replacement and intravenous antibiotics is our method of
treatment. Unless severely dehydrated or unable to tolerate
fluids, the patient usually does not require admission.
Necrotizing Fasciitis
Necrotizing fasciitis of the head and neck is a progressive,
polymicrobial, synergistic infection of the superficial layer of
the deep cervical fascia. Devastating facial necrosis and
severe systemic toxicity and death can rapidly occur if left
untreated. In general, due to its abundant vascular supply, the
head and neck is rarely (compared to the trunk and extremities)
involved and is often associated with diabetes or severe
vascular disease. Again, dental infections are the most common
source. Spankus, in his review of craniocervical necrotizing
fascitis, found that involvement of the galea aponeurotica
following trauma with extension into the neck to be relatively
common. Most infections spread along fascial planes without any
obvious skin involvement initially, but crepitance, skin
anesthesia, purple discoloration and bullae may later form. The
presence of necrosis is a key diagnostic point and is suggested
by air or creptance in the soft tissues, failure of the
infection to respond to antibiotics and dusky blue skin over the
effected area. It is also important to realize that skin
changes are a late sign of necrosis and significant soft tissue
necrosis can occur with normal overlying skin Radical surgical
resection of all necrotic skin and soft tissue with intravenous
antibiotics are essential, along with correction of any
underlying systemic abnormalities. Skin grafting is often
required initially to promote wound closure. Antibiotic
coverage should include a pencillinase-resistant penicillin (to
cover emerging resistant strains of Bacteroides) plus an
aminoglycoside or third generation cephalosporin. The most
commonly isolated organisms include anaerobes, streptococcus
sp., S. aureus, bacteroides and occasionally clostridia. Gas
formation is characteristic of clostridial infections but
involvement of the neck is actually very rare and the presence
of air in the neck does not always indicate infection. Air in
the neck can be caused by surgical manipulation, trauma or air
dissection from adjacent sites (i.e. chest) In general,
necrotizing fasciitis of the head and neck is a surgical
emergence with a mortality rate of 22% in the head and neck if
not treated aggressively.
Acute Supraglottitis
Although not a deep neck space infection, supraglottitis, is
obviously considered life-threatening due to potential airway
compromise. Supraglottitis is a more appropriate term than
epiglottis because isolated involvement of the epiglottis is
rare. Although much less common after the development of H.
influenzae type b vaccines, acute supraglottitis in children
does still occur and prompt treatment can be life-saving. The
typical child presents with a muffled (not hoarse) voice, fever,
drooling and stridor. The stridor is usually most pronounced on
inspiration and the child tends to maintain an upright position
with the neck extended. Rapid inspiration tends to collapse the
already edematous epiglottis so respirations are usually slow
and deliberate. Once the diagnosis is suspected, further
attempts to examine the child, especially fiberoptic examination
should be avoided and the child should be taken to the operating
room for airway control. Plain films of the neck will show an
enlarged epiglottis but radiologic examination should not
precede airway control in suspected cases. The child should
escorted to the operating room with a skilled physician present
at all times as the clinical course can rapidly worsen without
warning. Controlled intubation should be performed in the
operating room with available bronchoscopic and tracheotomy
equipment. Conversion to a nasotracheal tube is usually felt to
be a lower risk for extubation in the intensive care unit.
Treatment should then include intubation and intravenous
antibiotics in an ICU setting with controlled extubation in the
operating room following the resolution of the infection and
edema.
LIFE THREATENING SINONASAL INFECTIONS
Rhinocerebral Mucormycosis
Rhinocerebral Mucormycosis is a rapidly progressive invasive
infection of the paranasal sinuses by fungi from the Mucoraceae
family, which includes Absidia, Mucor, Rhizomucor and Rhizopus.
These organisms ore ubiquitous and disseminated by aerosolized
spores. Fulminant infections occur primarily in severe
diabetics and the immunocompromized. The relationship of
hyperglycemia and macrophage dysfunction has been proposed as an
explanation for the involvement of diabetics. The fungi are
vasculotropic an tend to grow along vessels, causing severe
necrosis. Infection may extent intracranially through the thin
cribiform plate, leading to meningitis or intracranial abscess
formation. Clinically, the initial lesions appear as black
necrotic areas involving the nasal mucosa or palate. Orbital
involvement is characterized by ophthalmoplegia, proptosis,
chemosis and eventual visual loss. Intracranial extension is
suggested by headache, cranial nerve palsies, seizures or
meningeal signs. Computerized tomography often shows
opacificatioin of the involved sinuses and bone erosion or
destruction. Early surgical debridement to normal bleeding
tissues is mandatory and the diagnosis is confirmed by the
presence of broad, nonseptate hyphae branching at right angles.
Once invasion is confirmed, high dose amphotercin is also
administered. Early recognition and surgical debridement has
greatly improved the mortality rates fir this once almost
uniformly fatal disease.
Complications of Paranasal Sinusitis
The anterior cranial fossa forms the roof of the ethmoid sinuses
and the posterior wall of the frontal sinuses. This unique
parameningeal location leads to several potential intracranial
complications from sinusitis. Due to its location, direct
extension from the maxillary sinus to vital structures is rare.
Frontal or ethmoid sinusitis can lead to meningitis, epidural
abscess, subdural empyema, or frontal lobe abscess. Frontal
sinusitis can lead to thrombosis of the superior sagital venous
sinus. The sphenoid sinus is surrounded by the pituitary gland,
optic nerve and chiasm, internal carotid artery and cavernous
sinus. Sphenoid sinusitis can spread to cause cavernous sinus
thrombosis, meningitis, temporal lobe abscess, and the superior
fissure symdrome. The superior orbital fissure syndrome is
characterized by orbital pain, proptosis and ophthalmoplegia
(cranial nerves III, IV and VI) and numbness of the ophthalmic
division of the trigeminal nerve. Cavernous sinus thrombosis
has similar findings but signs of venous congestion (chemosis,
proptosis, eyelid edema and retinal findings) are more prominent
and vision loss due to involvement of the ophthalmic vein may
occur. Less life-threatening but severe complications can arise
from periorbital or retroorbital eye involvement (through
penetration of the paper-thin lamina paprycia) or frontal
osteomyelitis (Potts puffy tumor). In Clayman's review of
intracranial complications of paranasal sinusitis, frontal lobe
abscess was the most common complication, followed by
meningitis, subdural empyema and cavernous sinus thrombosis.
The most common presenting symptoms were related to increased
intracranial pressure and included fever, headache, lethargy and
seizure. Negative cultures for both anaerobes and anaerobes
were common, likely reflecting prior antibiotic treatment. High
resolution CT is the imaging study of choice and treatment
requires gram-positive and anaerobic antibiotic coverage and
timely surgical intervention.
Complications of Otologic infections
Infections the middle ear and mastoid can extend into the middle
cranial fossa to involve the temporal lobe or the posterior
cranial fossa to involve the cerebellum. Although the incidence
of intracranial complications in patients with chronically
draining ears is likely extremely low, Schwaber et. al. found
the presence of purulent malodorous ear drainage, fever and
headache to be warning signs of an impending intracranial
complication in a patient with a "chronic ear." Half of the
patients had a visible cholesteatoma on exam. The most common
complication was epidural abscess, followed by meningitis and
brain abscess. Lateral sinus septic thrombosis can also occur
and should be suspected if persistent spiking fevers occur
postoperatively. Other warning signs of an intracranial
complication include vestibular symptoms or hearing loss and
facial paralysis. The management of subdural empyema can be
particularly challenging, as it can occur as a complication of
meningitis, sinusitis or otomastoiditis. The treatment often
requires a combined otolaryngology and neurosurgical approach
for proper drainage.
Malignant otitis externa is a necrotizing pseudomonal infection
of the external ear canal that occurs almost exclusively in the
severely debilitated or diabetic. An external ear infection
spreads through the junction of the cartilaginous and bony
junction of the ear canal to the base of the skull. Clinically,
it presents as severe otalgia, purulent ear drainage and the
formation of granulation tissue or a polyp at the junction of
the bony and cartilaginous ear canal. Multiple cranial nerve
palsies including facial paralysis may ensue. The diagnosis is
confirmed with positive technetium (bone) and gallium scans and
treatment includes local debridement and long-term antibiotic
therapy until the gallium scan clears.
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