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CLINICAL PRACTICE
A Review of Ludwig’s Angina for Nurse Practitioners
Sandra Winters, MSN, APRN, CNA, BC
Purpose
To discuss the causative factors, clinical course,
and current treatment modalities for Ludwig’s
angina, a submandibular cellulitis, and to raise
nurse practitioners’ (NPs’) awareness of this
condition.
Data Sources
Recent clinical articles, research, case studies,
and medical texts.
Conclusions
Ludwig’s angina may be fatal. Early diagnosis,
aggressive antibiotic therapy, and management
involving a multidisciplinary team approach
are imperative for the patient to progress with-
out complications.
Implications for Practice
Education and awareness are crucial for suc-
cessful diagnosis of and management of treat-
ment for Ludwig’s angina. Although NPs have
a limited role in the treatment of Ludwig’s
angina, their ability to recognize the signs and
symptoms will prompt emergency care and
treatment and facilitate better outcomes for
their clients.
Key Words
Ludwig’s angina, odontogenic infection, deep
neck infection.
Author
Sandra Winters, MSN, APRN, CNA, BC is a
Family Nurse Practitioner at Whites Crossing
Medical Center in Carbondale, PA. Contact Ms.
Winters by e-mail at kswinters@pikeonline.net.
546
INTRODUCTION
Although uncommon, Ludwig’s angina can be a potentially life-threaten-
ing infection of the submandibular, sublingual, and submental spaces.
Wilhelm von Ludwig first described this condition in 1836 as a gangrenous
induration of the soft tissues of the neck and floor of the mouth with
“woody” cellulitis (Busch & Shah, 1997; Schreiner & Calhoun, 1999). A
significant decline in the mortality rate has occurred since the preantibiotic
era, but Ludwig’s angina remains a clinical emergency as a result of its intrin-
sic development of airway obstruction (Barakate, Hemli, Jensen, & Graham,
2001). Improved outcomes result from airway protection and aggressive
antimicrobial therapy when instituted early in the course of infection.
A primary care nurse practitioner (NP) may be the first health care
provider a patient consults with complaints of fever, malaise, and painful
neck swelling. Prompt recognition of these and more definitive characteris-
tic signs and symptoms of Ludwig’s angina, combined with a good history
and physical examination, will allow the patient a better chance for a suc-
cessful outcome. NPs must diagnose deep neck infections early and refer
promptly to emergency treatment. Patients are best treated by a team of
providers, including an otolaryngologist, an infectious disease specialist, and
a dentist (Nicklaus & Kelley, 1996). This article discusses the causes and risk
factors, clinical presentation, clinical course, and current treatment of
Ludwig’s angina in order to enhance NPs’ knowledge base and ability to
diagnose this life-threatening condition.
CAUSES AND RISK FACTORS
Patients affected by submandibular space infections are usually young,
previously healthy adults with oral or odontogenic infections, most com-
monly originating in an infected lower molar (Durand, Joseph, & Sullivan-
Baker, 1998; Khanna & Ost, 2002; Schreiner & Calhoun, 1999). Moreland,
Corey, and McKenzie’s (1988) review of 141 cases of Ludwig’s angina
demonstrated that some form of dental disorder was the initiating event in
85% of the cases. Five of the six patients described by Busch and Shah
(1997) sought treatment for infected mandibular teeth. An additional review
of 41 Ludwig’s angina cases (Kurien, Mathew, Job, & Zachariah, 1997)
showed that 52% of the adult cases had associated dental caries; conversely,
the children in the study, ranging in age from 5 months to 12 years, had no
significant associated illness or complication.
Other, less common causes include epiglottitis, oral lacerations, sub-
mandibular sialadenitis, and peritonsillar or parapharyngeal abscesses
(Barakate et al., 2001; Busch & Shah, 1997; Lerner & Troost, 1991). A post-
traumatic infection resulting from a compound mandibular fracture, an
infiltrating injury to the floor of the mouth, or even traumatic intubation
VOLUME 15, ISSUE 12, DECEMBER 2003
have preceded Ludwig’s angina (Ferrera, Busino, & Snyder,
1996; Lerner & Troost; Moreland et al., 1988). Perkins, Meisner,
and Harrison (1997) documented a case of Ludwig’s angina sec-
ondary to a recent tongue piercing. In perhaps the most disturb-
ing scenario, no causative agent or factor could be identified
(Khanna & Ost, 2002).
Although, the majority of Ludwig’s angina cases occur in pre-
viously healthy individuals, there are certain coexisting condi-
tions that may predispose patients to severe submandibular
infection. These include, but are not limited to, diabetes melli-
tus, neutropenia, aplastic anemia, glomerulonephritis, dermato-
myositis, systemic lupus erythematosus, and altered immunode-
ficiency states (Busch & Shah, 1997; Khanna & Ost, 2002;
Pizzo, 1999). Khanna and Ost conceded that because of the low
incidence of Ludwig’s angina, these associations lack convincing
support and are more anecdotal.
The causative organisms are varied and often mixed and
include aerobes and anaerobes. Busch and Shah (1997) report
alpha-hemolytic streptococci, staphylococci, and bacteroides as
the most commonly reported organisms. Besides Bacteroides
melaninogenicus and Bacteroides oralis, anaerobes such as
Peptostreptococcus, Peptococcus, Fusobacterium nucleatum,
Veillonella, and spirochetes are additionally reported (Busch &
Shah; Moreland et al., 1988). Hartmann (1999) documents that
a foul breath odor usually indicates the presence of an anaerobe.
There are also documented cases of gram-negative organisms such
as Neisseria catarrhalis, Escherichia coli, Pseudomonas aeruginosa,
and Haemophilus influenzae (Busch & Shah; Moreland et al.).
CLINICAL PRESENTATION
Subjective characteristics of Ludwig’s angina include a com-
plaint of mouth and/or tooth pain with a possible history of
recent dental extraction or poor dental hygiene (Moreland et al.,
1988). Constitutional symptoms of fever and malaise are com-
mon. Dysphagia and drooling are also common, and some
patients may experience severely painful swallowing (Schreiner
& Calhoun, 1999). Essentially all patients experience severe
neck pain, stiffness, and swelling (Sethi & Stanley, 1994). Some
individuals display dysphonia and/or dysarthria, which
Schreiner and Calhoun describe as a “hot potato” voice.
Physical examination may reveal fever and tachycardia with a
characteristic firm, woody, hard mouth floor (Barakate et al.,
2001; Kurien et al., 1997). Carious molar teeth may also be pre-
sent (Hartmann, 1999). An induration and swelling of the sub-
mandibular space combined with an elevated, protruding tongue
is generally observed. Trismus can also occur and indicates direct
irritation of the masticatory muscles (Barakate et al., 2001;
Schulman & Owens, 1996). Any indication of dyspnea, tachyp-
nea, inspiratory stridor, and cyanosis are signs of impending air-
way obstruction and indicate a medical emergency (Marple,
1999).
Although the diagnosis of Ludwig’s angina is usually clear-cut
based on the history and physical examination, a number of
imaging methods are nonetheless useful in defining the severity
JOURNAL OF THE AMERICAN ACADEMY OF NURSE PRACTITIONERS
of the infection. Khanna and Ost (2002) recommended blood
cultures obtaining for both aerobic and anaerobic organisms.
Although plain radiographs of the neck are limited in diagnos-
ing or defining deep neck abscesses, they may demonstrate the
extent of soft tissue swelling (Barakate et al., 2001; Nicklaus &
Kelley, 1996). Chest radiography can reveal extension of the
infective process into the mediastinum or lungs (Khanna & Ost;
Nicklaus & Kelley). Ultrasonography can distinguish location,
size, and collections of pus and may reveal metastatic abscess for-
mation (Barakate et al., 2001; Nicklaus & Kelley).
Ultrasonography can be particularly helpful in children because
it is noninvasive and involves no radiation; it can also be useful
in localization of abscesses for needle aspiration (Nicklaus &
Kelley). Computed tomography (CT) is probably the most
widely used imaging modality because it can provide the best
radiological evaluation of a deep neck abscess (Healy, 1989).
Areas of fluid collection, spread of infection, and degree of air-
way restriction may be detected with CT (Khanna & Ost).
Miller, Furst, Sandor, and Keller (1999) conducted a study to
determine whether there is a scientific basis for the routine use
of contrast-enhanced CT (CECT) in the evaluation of suspect-
ed deep neck infection. They concluded that CT used alone in
determination of deep neck infections has a high sensitivity and
low specificity; thus, its use may lead to unnecessary surgery for
some patients. Therefore, clinical examination combined with
CECT is the most accurate method to determine the extent of
deep neck infections. Magnetic resonance imaging may provide
superior resolution of soft tissues compared to CECT, but mag-
netic resonance imaging has the disadvantage of lengthy imaging
times, which can be extremely dangerous to a patient with a pos-
sible airway compromise (Nicklaus & Kelley).
CLINICAL COURSE
Ludwig’s angina is a bilateral cellulitis of the submandibular
space that attacks the connective tissue, fascia, and muscles but
not the glandular structures (Nicklaus & Kelley, 1996). The sub-
mandibular space extends from the hyoid bone to the floor of
the mouth and is composed of two spaces, the sublingual space
and the submaxillary space. Clinically, these two spaces function
as one because of their free intercommunication and their com-
mon clinical signs and symptoms (Linder, 1986). The buc-
copharyngeal gap, which is created by the styloglossus muscle
passing between the middle and superior constrictors, is a poten-
tially dangerous connection between the submandibular and lat-
eral pharyngeal spaces (Schreiner & Calhoun, 1999). Ludwig’s
angina infection spreads directly via the buccopharyngeal gap to
the lateral pharyngeal space, where the cellulitis is increasingly
dangerous (Schreiner & Calhoun) and can cause a life-threaten-
ing airway obstruction.
Because the anatomic barriers are relatively unrestricted, the
infection can spread easily to other tissues in the neck, to the
retropharyngeal fascial space, and, infrequently, to mediastinum or
subphrenic space (Barakate et al., 2001). In addition to airway
compromise, which can occur at any time and without warning,
547
complications of Ludwig’s angina can include cavernous sinus
thrombosis from the infection in the facial venous system, aspira-
tion of infected secretions, and subphrenic abscess formation.
Further reported complications include mediastinitis, pericardial
and/or pleural effusion, empyema, infection of the carotid sheath
with possible rupture of the carotid artery, and suppurative throm-
bophlebitis of the internal jugular vein (Barakate et al.; Ferrera et
al., 1996; Furst, Ersil, & Caminiti, 2001; Stewart, 2000).
MANAGEMENT
Management of Ludwig’s angina requires three areas of con-
centration. First and foremost is the maintenance of a patent air-
way. Second, aggressive antibiotic therapy is required to treat and
limit the spread of infection. And third, decompression of the
submandibular, sublingual, and submental spaces should be per-
formed in some cases (Busch & Shah, 1997).
Tracheostomy was once thought to be necessary in most
patients, but with the advent of better intubation techniques and
fiber-optic endotracheal tube placement, the necessity of tra-
cheostomy has decreased (Khanna & Ost, 2002). Intubation
may require nasal intubation using a flexible telescope with the
patient awake and in an upright position (Busch & Shah, 1997).
If this is not possible, cricothyroidotomy or tracheotomy under
local anesthesia may be necessary (Busch & Shah). Since the
aggressive use of antibiotics, airway observation has become a
more popular option, particularly if the patient is in an optimal
facility with skilled and experienced staff available to perform
emergency surgical airway patency (Marple, 1999; Neff, Merry,
& Anderson, 1999).
Khanna and Ost (2002) discussed the use of a trial of heliox
in patients who had early upper airway compromise. Heliox, a
low-density helium-oxygen mixture, reduces the work of breath-
ing by reducing the large pressure drop associated with turbulent
flow across the obstruction. This mixture has been useful in the
treatment of other conditions affiliated with airway compromise,
although no controlled trials exist with the condition of Ludwig’s
angina. Heliox may be a useful temporizing measure in border-
line patients, as long as appropriate intervention is available in
the event of further airway compromise (Khanna & Ost).
The six patients discussed by Busch and Shah (1997) were
initially treated with intravenous dexamethasone for 48 hr, in
addition to receiving antibiotic therapy and surgical decompres-
sion. Dexamethasone use allows intubation to be carried out
under more controlled conditions, often avoiding the need for
tracheotomy or cricothyroidotomy. Additionally, they found
that length of hospital stay was reduced with the use of dexam-
ethasone. They initially administered 10 mg, followed by 4 mg
every 6 hr for 48 hr.
After airway patency is secured, intravenous (IV) antibiotic
should be administered. Historically, high doses of penicillin (2
million to 4 million units IV q4h have been used as the first-line
agent for Ludwig’s angina. With the increasing prevalence of
beta-lactamase production, particularly among Bacteroides
species, the addition of metronidazole or clindamycin should be
548
considered (Khanna & Ost, 2002; Sandor, Low, Judd, &
Davidson, 1998). Blood culture and fluid culture results will
help to optimize treatment regimens (Khanna & Ost).
Decompression of the submandibular, sublingual, and sub-
mental spaces can be accomplished with through-and-through
drains by using a single submental incision (Busch & Shah,
1997) in the setting of suppurative infection (Barakate et al.,
2001). Indications for surgical drainage include fluctuance,
crepitus, and the presence of soft tissue air (Ferrera et al., 1996;
Lerner & Troost, 1991; Patterson, Kelly, & Strome, 1982).
Generally, the incision is made parallel and 3 cm inferior to the
angle of the mandible. Size and location of the initial incision
depend on the specific anatomic spaces involved, and extension
to the midline below the chin may be needed in severe cases
(Barakate et al.). In addition to decompression of all closed fas-
cial spaces of the neck, another goal of surgical drainage is evac-
uation of pus (Barakate et al.). If an infected tooth is the culprit
of the initiating event, it must be extracted to promote complete
drainage (Barakate et al.).
SUMMARY
Ludwig’s angina is a potentially fatal infection. Although seen
with less frequency because of improved dental care and antibi-
otic therapy, it remains a significant threat to those with limited
access or opportunity for dental care (Busch & Shah, 1997). NPs
need to be able to recognize the clinical features of Ludwig’s
angina in order to provide the prompt emergency care required
for these clients. Early diagnosis, airway management, and
appropriate referral are the crucial first actions for NPs; collabo-
rative management by a specialist team with antibiotic therapy,
and surgical drainage if required, is essential for Ludwig’s angina
to resolve without complications.
REFERENCES
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angina: Report of a case and review of management issues. Annals of
Otology, Rhinology and Laryngology, 110, 453–456.
Busch, R. F., & Shah, D. (1997). Ludwig’s angina: Improved treatment.
Otolaryngology—Head and Neck Surgery, 117, S172–S175.
Durand, M., Joseph, M., & Sullivan-Baker, A. (1998). Infections of the oral cavi-
ty and pharynx. In A. S. Fauci, E. Braunwald, K. J. Isselbacher, J. D. Wilson,
J. B. Martin, D. L. Kasper, S. L. Hauser, & D. L. Longo (Eds.), Harrison’s prin-
ciples of internal medicine (pp.182–183). New York: McGraw-Hill.
Ferrera, P. C., Busino, L. J., & Snyder, H. S. (1996). Uncommon complications of
odontogenic infections. American Journal of Emergency Medicine, 14,
317–22.
Furst, I. M., Ersil, P., & Caminiti, M. (2001). A rare complication of tooth abscess:
Ludwig’s angina and mediastinitis. Journal of the Canadian Dental
Association, 67(6), 324–327.
Hartmann, R. W. (1999). Ludwig’s angina in children. American Family
Physician, 60, 109–112.
Healy, G. B. (1989). Inflammatory neck masses in children: A comparison of
computed tomography, ultrasound, and magnetic resonance imaging.
Archives of Otolaryngology, Head and Neck Surgery, 115, 1027–1028.
VOLUME 15, ISSUE 12, DECEMBER 2003
Khanna, D., & Ost, D. (2002). How to identify and manage life-threatening infec-
tions of the upper airway: Part 2. The Journal of Critical Illness, 17(4),
134–140.
Kurien, M., Mathew, J., Job, A., & Zachariah, N. (1997). Ludwig’s angina. Clinical
Otolaryngology, 22, 263–265.
Lerner, D. N., & Troost, T. (1991). Submandibular sialadenitis presenting as
Ludwig’s angina. Ear, Nose, and Throat Journal, 70, 807–809.
Linder, H. H. (1986). The anatomy of the fasciae of the face and neck with par-
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56–66.

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