CASE REPORT

A Case of Ludwig Angina

A Case Report and Review of the Literature
Bradley J. Marcus, MD, Jennifer Kaplan, MD, and Kim A. Collins, MD

the Latin word angere, which means “to strangle.”2 Ludwig

Abstract: Ludwig angina is a rapidly progressing submaxillary,
angina originates in the oropharynx and spreads by continuity
submandibular, and sublingual necrotizing cellulitis of the floor of
the mouth that can have lethal consequences due to airway obstruc-
rather than by lymphatic or hematogenous spread.4 The
tion. Various aerobic and anaerobic microorganisms, and less often
continuous spread of this infection is a result of the complex
fungi, have been implicated to cause Ludwig angina, including oral
anatomy of the neck.6,14 Ludwig angina can frequently be
flora such as streptococci and staphylococci. Early recognition and
fatal as a result of airway compromise if not recognized and
the use of parenteral antibiotics can prevent mortality and morbidity.
treated with antibiotics.4
We report a case of a 25-year-old white man who was admitted to
The usual cause of Ludwig angina is a mixture of
the hospital by his dentist after being diagnosed with Ludwig angina
aerobic and anaerobic bacteria including predominately nor-
secondary to periodontal abscesses involving teeth #17 and #32.
mal oral flora.3 Common bacteria that cause Ludwig angina
Although antibiotics were administered, while in the hospital, the
include: Streptococcus viridans, Staphylococcus aureus,
decedent had difficulty swallowing and was drooling. He suddenly
B-hemolytic streptococcus species, Staphylococcus epidermi-
began to have seizure-like activity thought to be anoxic myoclonus.
dis, Bacteroides genus, Fusobacterium nucleatum, Pep-
The decedent was aggressively resuscitated and taken to the oper-
tostreptococcus, and Enterobacter aerogenes.1,8 Rare organ-
ating room for neck exploration and a tracheostomy. Neck explora-
isms that have been implicated as a cause include: Proteus,
tion revealed severe necrotizing acute inflammation of the deep soft
Pseudomonas, Escherichia coli, Haemophilus influenza,
tissues and musculature of the neck. He remained on life support for
Neisseria catarrhalis, Borellia vincenti, and Morganella mor-
7 days until he was declared brain dead. Ludwig angina is a
ganii.3,8,13 Klebsiella pneumoniae in one study was identified
progressive cellulitis that often results in death by asphyxia. Ludwig
in greater than 50% of diabetic patients with Ludwig angina.7
angina can be complicated by subsequent deep neck infection. The
Candida albicans has also been reported.8,13 Early recogni-
underlying etiologies and common scenarios are examined, and
tion of this disease process can prevent a lethal outcome due
significant autopsy findings and dissecting procedures are discussed.
to airway compression and obstruction.4
The pathophysiology of Ludwig angina is studied with a review of
The most common victim of Ludwig angina is a male,
the current literature.
age 20 to 40 years.1 Most cases are associated with a preceding
odontogenic infection, peritonsillar abscess, mandibular fracture,
Key Words: Ludwig angina, neck abscess, airway obstruction, or other facial trauma.4,13 Other predisposing conditions include
asphyxia, neck anatomy, autopsy, cellulitis poor dental hygiene, dental caries, intravenous drug abuse,
(Am J Forensic Med Pathol 2008;23: 255–259)
malnutrition, diabetes mellitus, AIDS, immunosuppression, and
systemic lupus erythematosus.2– 4 In children, Ludwig angina
can occur without any predisposing conditions.4,6
We report a case of Ludwig angina, discuss the autopsy
procedure, and describe the anatomy and pathophysiology
L udwig angina was first described by German surgeon Karl
Friedrich Wilhelm von Ludwig in 1836, as a rapidly
progressive deep gangrenous cellulitis of the soft tissues of
including the progression of the disease and how it can result
in fatal airway obstruction.
the neck and floor of the mouth involving the submandibular
and sublingual glands.1–15 The term angina is derived form CASE HISTORY
The decedent was a 25-year-old white man who was
referred to his dentist by his primary care physician. When
Manuscript received July 5, 2006; accepted October 2, 2006. examined by the dentist, the decedent was found to have
From the Department of Pathology and Laboratory Medicine, Division of
Forensic Pathology, Medical University of South Carolina, Charleston, Ludwig angina secondary to an odontogenic abscesses in-
South Carolina. volving teeth #17 and #32. At this time, he had an oral
Reprints: Bradley J. Marcus, MD, Professional Pathology Services, One Science temperature of 104°F. He was admitted to a local hospital for
Court, Suite 200, Columbia, SC 29203. E-mail: bradley.marcus@ intravenous fluids, antibiotics, and analgesics. Physical ex-
palmettohealth.org.
Copyright © 2008 by Lippincott Williams & Wilkins amination, at the time of admission revealed an oriented,
ISSN: 0195-7910/08/2303-0255 ambulatory white man in moderate distress. He had no
DOI: 10.1097/PAF.0b013e31817efb24 evidence of airway compromise, although his tongue pro-

The American Journal of Forensic Medicine and Pathology • Volume 23, Number 3, September 2008 255
Marcus et al The American Journal of Forensic Medicine and Pathology • Volume 23, Number 3, September 2008

truded in the midline. Significant swelling was in the sub-

mandibular and sublingual regions bilaterally with cervical
lymphadenopathy.
During the evening of admission, the decedent woke
and arose from his hospital bed. He was drooling, had
difficulty swallowing, and had shortness of breath. He sud-
denly became unresponsive, and witnesses stated that he
experienced an episode of “seizure-like” activity. A code was
called secondary to respiratory compromise. The seizure
activity was defined as anoxic myoclonus. After the resusci-
tation, an electroencephalogram was consistent with anoxic
encephalopathy. Cerebrospinal fluid lumbar puncture was
within normal limits. The patient remained unresponsive on a
ventilator and was subsequently taken to the operating room
for a tracheostomy, neck exploration with incision/drainage,
and debridement of the deep neck region.
Postsurgical computed tomography scan of the neck
FIGURE 1. Pus dissecting through the tissue planes of the
and chest revealed residual soft tissue edema as well as a soft neck.
tissue density in the substernal region. The right lower pul-
monary lobe was consolidated, and the left pulmonary base
demonstrated atelectasis. Multiloculated fluid collections
were present in the neck. A nuclear medicine brain scan
revealed no cerebral activity consistent with brain death. Life
support measures were then withdrawn.

AUTOPSY GROSS FINDINGS

The body was that of a well-developed, well-nourished,
adult white man who weighed approximately 280 pounds and
was 74 inches in length. The neck region was markedly
indurated, firm, edematous, and erythematous bilaterally. The
tracheostomy site was identified as well as a horizontal
surgical incision across the neck with a drain in place con-
sistent with the decedent’s surgical history.
Dissection of the skin, subcutaneous soft tissue, and
neck musculature revealed marked induration, edema, and
purulent inflammation. Areas of pus accumulation were
within the neck musculature and soft tissues. The inflamma- FIGURE 2. Boggy gingival mucosa around teeth #31 and
tion and pockets of pus dissected through tissue planes #32.
bilaterally (right greater than left) to the underside of the
sternum (Fig. 1). Further neck dissection revealed the process
extending around the right submandibular gland, beneath the
mandible, and into the sublingual region. A continuous tract
of inflammation connected the right neck, right submandib-
ular gland, right sublingual region, and the right mandibular
gingival regions. The gingiva was boggy around teeth #17,
#31, and #32, (Fig. 2) and a pocket of pus surrounded tooth
and root of #32. Approximately 10 mL of purulent exudate
easily exuded into the oral cavity from this region of the
gingiva.
Deep neck dissection revealed areas of pus accumula-
tion around the thyroid cartilage, dissecting between the neck
strap muscles giving a multiloculated appearance. Removal
of the tongue-larynx-trachea en bloc revealed marked soft
tissue edema (Fig. 3). The epiglottis was markedly edematous
as were the true and false vocal cords and the aryepiglottic
folds. The marked edema with external compression second-
ary to inflammation and induration resulted in narrowing of
the laryngeal cavity. The laryngeal ventricle protruded FIGURE 3. Marked edema of the epiglottis.

256 © 2008 Lippincott Williams & Wilkins

The American Journal of Forensic Medicine and Pathology • Volume 23, Number 3, September 2008
slightly into the airway. Collections of purulent material were
around the thyroepiglottic muscle, thyroarytenoid, and crico-
arytenoid muscles indicative of a deep neck infection.
AUTOPSY MICROSCOPIC FINDINGS
Microscopic examination of tissue around the right and
left pharyngeal tonsils revealed acute inflammation, edema,
focal hemorrhage, peritonsillar soft tissue acute inflamma-
tion, and abscess formation with necrosis. The bilateral sub-
mandibular glands revealed marked interstitial edema and
acute inflammation; the glandular architecture was virtually
obliterated by marked acute inflammation and large regions
of hemorrhage and necrosis. The left perilaryngeal muscula-
ture showed massive acute inflammation and reactive fibro-
blasts, marked necrosis, and edema. Within the anterior neck,
large areas of abscess formation with necrosis were identified
as well as coagulative necrosis of peripherally located muscle
fibers. Hemorrhage, panniculitis, and fat necrosis were also
present. Areas of presumable bacterial colonies were identi-
fied. The epiglottis was edematous. The right and left ster-
nocleidomastoid muscles showed interstitial edema with fo-
cal muscle fiber necrosis and acute inflammation (Fig. 4). The
soft tissue beneath the sternum and the associated skeletal
musculature showed acute inflammation with reactive fibro-
blasts. The inflammation splayed the muscle fibers and ex-
tended into the fat with resulting acute panniculitis. Infiltrat-
ing macrophages were identified within large areas of
necrosis. The tongue showed inflammatory cells, predomi-
nantly lymphocytes and plasma cells, dissecting between the
individual muscle fibers.
ANCILLARY STUDIES
Anaerobic and aerobic cultures were obtained from the
blood, lung, neck soft tissue, substernal soft tissue, and right
mandibular regions of pus confluence. Blood culture revealed
no growth of microorganisms. Lung culture grew Bacteroides
thetaiotaomicron and presumptive Enterococcus species.
FIGURE 4. Acute inflammation and necrosis of strenocleido-
mastoid skeletal muscle fibers (hematoxylin and eosin,
200⫻).
© 2008 Lippincott Williams & Wilkins
A Case of Ludwig Angina
Neck fluid culture grew Bacteroides fragilis. The teeth/
gingival exudates culture grew light growth of mixed Gram
negative bacilli and/or Gram positive cocci with light growth
of yeast, consistent with oral flora. Consultation with a
microbiologist revealed that the culture results of the above
sites were consistent with oral flora.
DISCUSSION
Ludwig angina usually presents in patients with poor
dental hygiene, which accounts for approximately 75% to
95% of cases.8,10,14 The clinical presentation consists of
malaise, dysphagia, bilateral cervical swelling, neck tender-
ness, dysphonia, elevation and swelling of the tongue, pain in
the floor of the mouth, sore throat, restricted neck movement,
and stridor suggestive of impending airway obstruc-
tion.4,6,10,14 Originally, Ludwig proposed a mortality rate of
60% and the mechanism of death was attributed to sepsis.11
However, in the 1900s it was realized that death is due to
airway obstruction that resulted in asphyxia.11 Another factor
implicated is neck swelling resulting in hypersensitivity of the
carotid sinus receptors.11 Mortality from Ludwig angina
dropped significantly from 60% to around 10% with the wide-
spread use of antibiotics and good oral hygiene.11
In 1939, Grodinsky proposed the following criteria to
diagnose Ludwig angina: the process occurs bilaterally in
more than one space; produces gangrenous, serosanguinous,
putrid infiltration with little or no pus; involves connective
tissue, fascia, muscle, and rarely involves glandular struc-
tures; and spreads by continuity not by lymphatics or hemat-
ogenously.2,10,14
The anatomy of the neck is crucial to the understanding
of the pathophysiology of Ludwig angina.11 A complication
of Ludwig angina is deep neck infection, which is the infec-
tion of the fascial planes of the neck and or spaces with
abscess formation and cellulits.7 The head and neck are
encompassed in and protected by several different layers of
cervical fascia.11,14 The relationships of these different layers
are important in the understanding of Ludwig angina and
subsequent deep neck infection because these spaces can
communicate freely with one another.14 The superficial fascia
extends from the head and neck to the thorax, shoulders, and
axilla.14 Deep to the superficial fascia lays the deep cervical
fascia, which is made up of 3 layers: the superficial layer; the
middle layer; and the deep layer. The deep layer is made up
of the prevertebral and alar layers.14 The alar layer extends
from the base of the skull to the posterior mediastinum, lies
posterior to the middle layer and pharynx, and fuses with the
periosteum of the transverse process of the spine.14 The
superficial layer of the deep cervical fascia extends from
the hyoid bone to the mandible and upward towards the
cranium.14 This fascia passes along the superficial muscle on
the floor of the mouth and forms the floor of a potential space
(muscles below and a fascia above) known as the subman-
dibular space.14
Because of the fascial anatomy in the lower face and
neck, many potential spaces exist, where infections, cellu-
lites, and abscesses can spread by continuity rather than by
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Marcus et al The American Journal of Forensic Medicine and Pathology • Volume 23, Number 3, September 2008
lymphatics or blood vessels.6,11 In Ludwig angina, the ana-
tomic space of concern is the submandibular space.6,11,12,14
The submandibular space actually consists of 2 spaces,
the sublingual space which is superior to the mylohyoid
muscle and the submaxillary space which is inferior to the
mylohyoid muscle and is bound superficially by the superfi-
cial layer of the deep cervical fascia.6,11,14 These 2 spaces can
be considered as 1 because the free border of the mylohyoid
muscle allows them to communicate freely.1,6,11,14 The sub-
maxillary space can be further divided into submental, lateral,
and posterior divisions by the anterior belly of the digastric
muscle that can allow spread of infection from 1 division of
the submaxillary space to the other.1,14
Odontogenic infections are the most common cause of
Ludwig angina especially when the second and third lower
molars are involved.13 The roots of these teeth extend infe-
riorly to the mandibular insertion of the mylohyoid muscle.
Abscesses of these molars are believed to erode and perforate
into the mandible and then expand into the submandibular
space.6,11,13,14 Once the submandibular space is penetrated,
infection of this region ensues. Edema and swelling of this
space will cause superior and posterior displacement of the
floor of the mouth and tongue causing airway compro-
mise.6,9,11 This represents a “compartment syndrome” and
has been grossly described as a “bull neck appearance.”6
Infection in the submandibular space may extend to the
lateral pharyngeal and retropharyngeal spaces because these
lie below the level of the deep superficial cervical fascia.14
Infections in the retropharyngeal space can travel downward
to the mediastinum and cause acute mediastinitis, empyema,
or pericarditis.14
In the forensic setting, anyone who sustains facial
trauma can die of Ludwig angina and be referred to the
forensic pathologist for a postmortem examination. When
approaching a case of Ludwig angina, obtaining the proper
history can prove essential. A detailed neck dissection is also
required although it might be challenging because of the
swelling and gangrenous necrosis of the deep soft tissues of
the neck. No published criteria exist explaining the approach
to neck dissection in a case of Ludwig angina.
At autopsy, when doing a neck dissection the prosector
should try to track the infection from the original source,
which is most likely to be in the submandibular space.
Careful bilateral examination of this space should be per-
formed. Subsequent layer by layer dissection of the strap
muscles should follow. Next, the thyroid gland and surround-
ing soft tissues should be examined. The trachea-larynx-
tongue is then removed en bloc, opened from the posterior
aspect exposing the true and false vocal cords, and aryepi-
glottic folds. If the hyoid bone appears soft and necrotic, a
section can be obtained for histologic evaluation. The tongue
should be sectioned. The gingival mucosa and periodontal
spaces should be carefully inspected and histologic sections
obtained. Photographic documentation is strongly recom-
mended. While doing the neck dissection, specimens for
cultures (aerobic and anaerobic organisms) should be taken of
exudate and infected tissue (Table 1). Fungal cultures should
258
TABLE 1. Ludwig Angina
Risks
Odontogenic infection due to poor dental hygiene
Peritonsillar abscess
Facial trauma
Intravenous drug use
Diabetes mellitus
Malnutrition
Immunosuppression, AIDS
Etiologic agents
Streptococcus viridans
Staphylococcus aureus
B-hemolytic streptococcus species
Staphylococcus epidermidis
Bacteroides genus
Fusobacterium nucleatum
Peptostreptococcus
Enterobacter aerogenes
Cause of death
Asphyxia because of airway obstruction/compression
Sepsis
Autopsy (in order of dissection/examination)
Examination of submandibular space
Layer by layer examination of the neck strap muscles
Examination of thyroid gland and surrounding soft tissues
Trachea-larynx-tongue removed en bloc
Examination of true and false vocal cords and aryepiglottic folds
Examination of the gingival mucosa and periodontal spaces
Sectioning of tongue
Examination of hyoid bone and mandible
Cultures of exudates and infected tissue
be procured in immunocompromised patients. In addition,
blood cultures should be performed.
CONCLUSIONS
Ludwig angina is a rapidly progressing and potentially
fatal disease, which may present as sudden death and be seen
by forensic pathologists. Without the proper understanding of
the pathophysiology of the disease and anatomy of the neck
and surrounding deep tissues, the postmortem dissection can
be challenging as the infection tract may not be clearly
visualized. Performing a detailed neck dissection, identifying
the source of infection, and obtaining appropriate microbio-
logical cultures can enable one to make the accurate diagnosis
of Ludwig angina and determine the proper cause and manner
of death.
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