Ludwig's Angina
Roger G. Finch, MD; George E. Snider, Jr, MD; Philip M. Sprinkle, MD
LUDWIG'S angina is a life-threatening infection of the
sublingual and submandibular spaces, first described by
Von Ludwig in 1836. Before the widespread use of
antibiotics, the disease seems to have occurred relatively
frequently, as evidenced by several large series.1,2 In recent
years, scattered case reports makeup most of the
available information,3,4 suggesting that the disease is now
either less commonly seen or recognized.
Mortality has exceeded 50%,2 and fatalities are still
reported.5 Our recent experience with six cases of Ludwig's
angina seen over a 32-month period has prompted this
review. Despite the critical nature of their illness, all of
our patients showed a prompt and complete response to
treatment. Table 1 summarizes some clinical features
present on admission, while Table 2 outlines the roentgen-
ographic, surgical, and antibiotic aspects of the manage-
ment of these six cases.
Pathogenesis
Ludwig's angina may arise de novo, but this is uncom-
mon. Poor dental hygiene and its associated problems of
gingivitis and dental sepsis the most common predis¬
are
posing conditions1 and were seen in all but one of our
patients. Dental extractions, most frequently of the
mandibular second or third molars, for either impaction
or periodontal disease, may also trigger the disease,3 and
did so in case 1. Other local orodental causes include
compound fractures of the mandible, traumatic lacera¬
tions of the floor of the mouth, and peritonsillar abscess.3
On the other hand, several systemic diseases such as
neutropenia, combined immunodeficiency disease, aplastic
anemia, systemic lupus erythematosus, diabetes mellitus,
glomerulonephritis, and hypersensitivity states have been
complicated by Ludwig's angina.35
From the Division of Infectious Diseases, Department of Medicine (Dr
Finch), and the Division of Otolaryngology, Department of Surgery (Drs
Snider and Sprinkle), West Virginia University Medical Center, Morgantown.
Dr Finch is now with the Department of Microbial Diseases, City Hospital,
Nottingham, England.
Reprint requests to Morgantown ENT Clinic, Inc, 3334 University Ave,
Morgantown, WV 26505 (Dr Snider).
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The following case reports illustrate several aspects of
the pathogenesis, clinical, and roentgenographic features
and management of Ludwig's angina and will be used as a
basis for discussion.
Report of Cases
Case 1.—Six days after a routine extraction of both mandibular
third molars, a 20-year-old woman had notable trismus, bilateral
submandibular swelling and tenderness, dysphagia, and difficulty
with breathing when supine. On admission she was febrile and
appeared ill and toxic, with crepitus of the submandibular tissues
and restriction of neck movements secondary to the pain and
swelling. The mouth could be opened only 2 cm, and the tongue
was greatly elevated. The floor of the mouth and submental
region were firm and tender. She had received penicillin V
potassium, 500 mg orally, every six hours from the time of
surgery. Roentgenograms of the neck and jaw showed marked
soft-tissue swelling, with gas and anterior displacement of the
trachea. Shortly after admission the patient was given anesthesia
locally, and 50 mL of foul-smelling green pus was drained through
a right external submandibular incision, which resulted in a
prompt improvement in the patient's airway and well-being.
Tracheotomy was thought to be unnecessary. She was treated
with penicillin G potassium, 1 million units every four hours
intravenously (IV), and gentamicin sulfate, 80 mg three times
daily. The next day there was reaccumulation of the abscess on
the right side of the neck, which was explored and drained. The
fascial planes of the submandibular, sublingual, and left lateral
pharyngeal spaces contained copious amounts of foul-smelling
pus, which subsequently grew Bacteroides fragilis. The patient
then made a prompt and uneventful recovery.
Case 2.—After a four-day history of progressive submental
fullness and pain, this patient noted rapid progression of trismus
and odynophagia: He had a long history of poor dental hygiene.
Examination showed moderate enlargement and elevation of the
tongue, "woody" firmness of the floor of the mouth, but only
minimal submental swelling and no evidence of airway obstruc¬
tion. He had chronic gingivitis and a moderate degree of calculus
but no evidence of gross dental decay. The plain roentgenograms
confirmed the soft-tissue swelling, but indicated some impinge¬
ment on the posterior pharynx. He was given penicillin G
potassium, 4 million units IV every four hours. Difficulty
speaking and swallowing developed overnight, and the patient
became tachypneic and restless, with a pulse rate of 130 beats per
minute. In the operating room, attempts at awake intubation
 Table 1.—Clinical Details of Patients With Ludwig's Angina
Case/Sex/ Temperature on Total WBCs, Antibiotic Before
Age, yr Initiating Event Admission, °C No./cu mm(% PMN)* Admission
1/F/20 Extraction of molar 39.3 17.6(86) Penicillin V potassium for 3 days
2/M/22 Chronic
3/M/25
gingivitis_38.6_17.4 (85)_None_
Advanced periodontal disease 38.0 18.0(84) None
4/M/26 Advanced periodontal disease 39.5 11.0(73) Penicillin G potassium, single dose
Mild
5/M/35 gingivitis_36.8_12.3 (70)_Cephradine, orally, for 4 days
6/F/23 Right mandibular abscess; chronic gingivitis 38.6 13.0(80) None
*PMN indicates neutrophil polymorphonuclear leukocytes.

Table 2.—Roentgenographic Investigations and Treatment of Ludwig's Angina

Roentgenographic View
,_, Antibiotic
Case Lateral Mandible Panorex, Mandible Tracheostomy Drainage Therapy
1 Soft-tissue swelling, gas in floor of Not done Not done Right submandibular Penicillin G potas-
mouth, and retropharyngeal space sium, gentamicin
2 Intralingual soft-tissue swelling and No bony abnormalities Emergency Sublingual abscess Penicillin G potas-
slight narrowing of posterior pharynx sium
3 Intralingual soft-tissue swelling Multiple periapical erosions Not done Not done Clindamycin
4 Soft-tissue swelling; no bony Generalized loss of alveolar Emergency Not done Clindamycin
abnormalities crest bone
5 Submandibular soft-tissue swelling Not done Emergency Sublingual abscess Clindamycin
6 Soft-tissue swelling with slight narrowing Cystic area beneath
right in- Not done Periapical abscess Penicillin G potassium
of pharynx; several carious teeth cisor with pulpal decay

failedowing to the severe swelling of the base of the tongue. An
emergency tracheotomy was performed with the patient in a
semi-sitting position under local anesthesia, followed by drainage
through a midline submental incision of a large sublingual
abscess. The pus failed to yield a pathogen on culture, but on
Gram's stain showed numerous pus cells, Gram-positive cocci,
and Gram-negative rods. The patient made an uneventful recov¬
ery, with removal of the tracheostomy tube and drains after six
days.
Clinical Features
The clinical features of Ludwig's angina reflect the
degree and rate of involvement of the sublingual and
submandibular spaces by the spreading gangrenous cellu-
litis of the deep cervical fascia.'
These spaces are in anatomic continuity, although
separated by the mylohyoid muscle. Involvement of the
sublingual space produces elevation and, later, backward
displacement and protrusion of the tongue, while the floor
of the mouth is tender and edematous and has a charac¬
teristic "woody" consistency. Involvement of the subman¬
dibular space produces tense brawny swelling of the neck,
usually confined to the suprahyoid region. There is little
evidence of fluctuation, lymph node, salivary gland, or
skin involvement. However, the infection may track along
fascial planes to involve the pharynx, retropharynx, and,
on rare occasions, the mediastinum.3
The symptoms are progressive trismus, drooling of
secretions, and dysphonia, resulting in the aptly described
"hot pototo" voice. Fever is usual and is often high. It was
present on admission in all but one of our patients. Chills
and sweats are common, and tachycardia almost univer¬
sal. The progressive soft-tissue swelling of the suprahyoid
region, the elevation, swelling, and posterior displacement
of the tongue, and the frequent presence of laryngeal
edema all result in increasing tachypnea, dyspnea, stridor,
and cyanosis, and can prove fatal. Obstruction of the
airway can progress with frightening rapidity and may be
aggravated in the supine position.
Examination of the neck may show crepitus of the
tissues and marked restriction of neck movements from
pain and swelling. The degree of trismus may make
adequate assessment of the oropharynx and larynx diffi¬
cult; the epiglottis can appear horizontal and the larynx
narrowed from the extensive soft-tissue swelling. How¬
ever, it is vital to assess the patency of the airway
frequently and as accurately as possible to determine the
need for tracheotomy.
Investigations
Plain roentgenograms of the head and neck will reflect
the degree of soft-tissue swelling and should be carefully
examined for evidence of airway narrowing. The tissues
may also contain gas arising from bacterial fermentation.
To appreciate the presence of periodontal disease of the
mandible, wide-angled panorex views are more helpful
than the plain roentgenograms." As can be seen from
Table 2, three of the four patients who had panorex films
done showed evidence of periodontal disease, which
included periapical erosions, loss of alveolar crest bone,
and multiple cystic areas.
The peripheral WBC count is usually elevated (Table 1),
with a preponderance of neutrophil polymorphonuclear
leukocytes and the presence of immature forms. The ESR
is accelerated.
Management
The essential aspects of caring for these patients
include maintenance of the airway, antimicrobial therapy
for systemic effect, and evaluating the need for surgical
incision and drainage of purulent material. However, of
these three, the most important is the frequent and
accurate assessment and maintenance of the airway. The

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 rapidity with which airway obstruction can develop is well
illustrated by case 2.
From Table 2 it can also be seen that three of our
patients required tracheostomy
a as an emergency proce¬
dure. Tracheostomy is best performed with anesthesia
given locally,3 as in two of our patients, since general
anesthesia or neuromuscular blockade with agents such as
curare or succinylcholine chloride may worsen the degree
of airway obstruction from laxity of the pharyngeal
musculature. Intubation using either endotracheal or
nasotracheal tube has been found useful in controlling the
airway and preventing aspiration, although the procedure
is often difficult or dangerous owing to extreme trismus
and airway obstruction and potential for causing laryn-
gospasm. Intubation under direct vision, with the patient
awake, using the fiberoptic laryngoscope has also been
successfully employed.3 Prophylactic tracheostomy also
has its advocates, owing to the speed with which airway
obstruction can develop. In any event, a tracheotomy set
should be available at the bedside in case the need for
emergency intervention arises.
In selecting antimicrobial therapy, it is important to
appreciate the variety of microbes that have been associ¬
ated with Ludwig's angina. Infections have been reported
most frequently with Staphylococcus aureus and the
viridans groups of streptococci.3 Pseudomonas aeruginosa,
Escherichia coli, Haemophilus influenzae, and Candida
albicans have also been noted.5 Unless the pathogen is
isolated from the blood there is always the concern that
samples may be contaminated by the normal oropharyn-
geal flora. Aspiration of pus may prove helpful if cultured.
The foul odor characteristic of anaerobic bacterial infec¬
tions may be apparent and was recognized in case 1, whose
cultures yielded B fragilis. Anaerobic bacteria are now
recognized as causing, or as being associated with, a wide
variety of orodental sepsis and should be strongly consid¬
ered when selecting initial antimicrobial therapy in
Ludwig's angina.
It is often difficult to obtain meaningful culture results,
since patients may have received antibiotics before admis¬
sion or drainage of pus. Nevertheless, all cultures should
be set up in media appropriate for the isolation of aerobic
and anaerobic bacteria.
Use of antibiotics for systemic treatment is mandatory,
and in fact may be curative once the airway is protected.
This was seen in case 3 (Table 2). Penicillins and
clindamycin are active against the majority of oral
anaerobic bacteria and were found effective in our experi¬
ence. Chloramphenicol also seems to be an appropriate
choice of agent for this life-threatening infection. The
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presence of Bfragilis in one of our patients suggests that
penicillin alone may not always be appropriate, although
most B fragilis infections above the diaphragm are
sensitive to penicillin G. The antibiotic regimen may be
modified once laboratory information becomes available.
The need for surgical drainage procedures in patients
with Ludwig's angina has remained a point of controver¬
sy.4 Some authors think that modern chemotherapy
renders the need for drainage uncommon. However, the
presence of frank pus has varied from 2% to 81% in some
large series.u Fluctuation may not be apparent owing to
the deep-seated nature of the infection. In our experience
four patients had evidence of frank suppuration (Table 2),
including one patient who had dramatic relief of com-
pressive symptoms after the drainage of 50 mL of pus. It is
therefore appropriate to consider the possible need for
drainage and not to reply entirely orí antibiotic therapy.
Complications
The complications associated with Ludwig's angina are
related to the extent and speed of the suppurative process.
Airway compression and the problems associated with
intubation have been discussed. Asphyxiation remains a
leading cause of death. Aspiration pneumonia and occa¬
sional lung abscess may occur but may be preventable by
the use of a cuffed tracheostomy tube.3
Blood-borne spread of infection can produce metastatic
sepsis. However, contiguous spread along fascial planes is
more usual and can involve the pharynx, retropharyngeal
area, and mediastinum, with erosion of vital structures
such as the carotid vessels.
Careful management, including close observation and
maintenance of the airway and the judicious use of
surgical drainage, can avoid many of these complications.
Hospitalization for this therapeutic emergency need not
be prolonged. The six patients discussed made complete
recoveries and were discharged after an average stay of
eight days (range, four to 13 days).
Nonproprietary Names and Trademarks of Drugs
Clindamycin—Cleocin.
Gentamicin sulfate—Garamycin.
1. Taffel M, Harvey SC: Ludwig's angina: An analysis of 45 cases.
Surgery 11:841-850, 1942.
2. Williams AC, Guralnick WC: The diagnosis and treatment of Ludwig's
angina. N Engl J Med 228:443-450,1943.
3. Meyers BR, Lawson W, Hirschman SZ: Ludwig's angina: Case report
with review of bacteriology and current therapy. Am J Med 53:257-260,
1972.
4. Holland CS: The management of Ludwig's angina. Br J Oral Surg
13:153-159,1975.
5. Barkin RG, Bovis SL, Elghammer RM, et al: Ludwig's angina in
children. J Pediatr 87:563-565,1975.