Ludwig's Angina

Introduction: Ludwigs angina is described as rapidly

spreading cellulitis involving the floor of the mouth. It was
first described by Wilhelm Friedrich von Ludwig in 1836. This
disorder has a potential for airway obstruction.
Synonyms: Cynanche, Carbuculus gangraenosus, Morbus
strangulatorius, and Angina maligna.
Anatomy:
This infection involves the submandibular space. The
submandibular space can be divided into two spaces:
submaxillary and sublingual space. These two spaces are
separated from each other by the mylohyoid muscle. These
two spaces are connected posteriorly through a cleft known
as the mylohoid cleft. The mylohyoid cleft contains the
following structures:
1. Tail of submandibular gland
2. wharton's duct
3. Lingual nerve
4. Hypoglossal nerve
5. Lymphatics
6. Arteries and veins
The floor of the submandibular space is formed by the
superficial layer of deep cervical fascia. It is attached from
the hyoid bone to the mandible. This space communicates
across the midline with that of the space on the opposite
side.
Clinical photograph of a patient with Ludwig's angina

Figure showing submaxillary and sublingual spaces

Boundaries of submandibular space:
The submandibular space is bounded by the oral mucosa
and tongue superiorly and medially, the mandible superiorly,
the superfical layer of deep cervical fascia with its tight
attachment to the mandible and hyoid bone laterally, and the
hyoid bone inferiorly.
Since the mandible and superficial layer of deep cervical
fascia provide unyielding barriers superiorly and laterally, the
tongue is forced upward and posteriorly giving rise to airway
obstruction. This is the most important danger in Ludwig's
angina.

Diagram showing neck spaces

Pathophysiology:
Commonest cause of Ludwig's angina is dental infections.
One important factor to be considered is the relationship of
mandibular dentition to the attachment of mylohoid muscle
(mylohyoid ridge). The anterior teeth and first molars
regularly attach superior to this line, and infections arising
from these roots commonly result in a limited sublingual
abscess. The second and third molar roots are attached
routinely below this line. Infections involving these roots
cause infections of submaxillary space. One other important
relationship is that the roots of the anterior teeth and first
molar approximate the lateral mandibular surface, whereas
the second and third molar roots approach the lingual
surface of the mandible.

Image showing the relationship with tooth to the mylohyoid

line
Criteria for diagnosing Ludwig's angina:
To diagnose Ludwig's angina the following features should
be present:
1. Rapidly spreading cellulitis with no specific tendency to
form abscess.
2. Involvement of both submaxillary and sublingual spaces,
usually bilaterally
3. Spread by direct extension along facial planes and not
through lymphatics
4. Involvement of muscle and fascia but not submandibular
gland or lymph nodes
5. Originates in the submaxillary space with progression to
involve the sublingual space and floor of the mouth.
Etiology:
1. Ludwigs angina is commonly caused as a sequlae to
dental infections. In fact it is very common in young adults
with periodontal disease. Dental causes account for 75% to
80% of these cases.
2. Penetrating injuries involving the floor of the mouth (stab
wounds, gun shot wounds etc)
3. Mandibular fractures
CT scan of a patient with Ludwig's angina
Bacteriology of Ludwig's angina:
Since a majority of cases of Ludwig's angina are caused by
dental infections, cultures from this infected area show oral
cavity flora. The most common aerobes isolated are alpha
haemolytic streptococci followed by staphylococci. Anaerobic
cultures are difficult to interpret. The anaerobes isolated are
peptostreptococcus, peptococcus, fusobacterium nucleatum,
and bacteroids. The combination of aerobic and anaerobic
organisms has a synergistic effect due to production of
endotoxins like collagenase, hyaluranidase, and proteases.
These endotoxins contribute to the rapidly spreading
cellulitis.
Clinical features:
1. Patient has c/o increasing oral cavity and neck pain.
2. These patients have poor oral hygiene
3. Symptoms are at first unialteral but soon become bilateral
4. The soft tissues of the floor of the mouth swells
5. Tongue gets pushed posteriorly causing air way
obstruction
6. These patients are usually febrile
On examination:
These patients have tachycardia, fever, and variable
degrees of respiratory obstruction with dysphagia and
drooling. The submandibular and submental regions are
tense, swollen and tender. The floor of the mouth may
become tense swollen and indurated. Fluctuation is not
present. The tongue is seen to be pushed backwards.
Diagnosis of Ludwigs angina is based on the clinical features
enumerated above. These patients may show leukocytosis.
X ray soft tissue neck may show soft tissue oedema. CT
scan neck is to be considered in all persistent cases to rule
out complications. Xray chest must also be considered to
rule out mediastinitis.

Management:
Airway management: Since the airway is threatened
insertion of oral airway is to be considered. If the patient
does not tolerate an oral airway then tracheostomy is to be
considered.
Intravenous antibiotics with broad spectrum features
(chloramphenicol)may be administered. The drug of choice
is amoxycillin with clavulanic acid. Metronidazole must also
be administered. Clindamycin can be administered in
resistant cases.
Role of surgical drainage: Wide decompression of the supra
hyoid region may be considered. The approach is through a
median horizontal incision three to four finger breadths below
the mandibular margin. The mylohoid muscle is split in the
midline, and drainage is established both medially and
laterally. Pus is very rarely encountered during this
procedure, but starts to drain several days after the
procedure.
Complications:
1. Airway compromise
2. Extension to mediastinum causing mediastinitis. This can
be suspected if there is persistent swelling in the neck with
pain, spiking fever and persistent leukocytosis.
3. Extension into the carotid sheath and retropharyngeal

space.

Etiology:

1. Ludwigs angina is commonly caused as a sequlae to dental infections. In fact it

is very common in young adults with periodontal disease. Dental causes account
for 75% to 80% of these cases.

2. Penetrating injuries involving the floor of the mouth (stab wounds, gun shot
wounds etc)

3. Mandibular fractures

CT scan of a patient with Ludwig's angina

Bacteriology of Ludwig's angina:

Since a majority of cases of Ludwig's angina are caused by dental infections,

cultures from this infected area show oral cavity flora. The most common aerobes
isolated are alpha haemolytic streptococci followed by staphylococci. Anaerobic
cultures are difficult to interpret. The anaerobes isolated are peptostreptococcus,
peptococcus, fusobacterium nucleatum, and bacteroids. The combination of
aerobic and anaerobic organisms has a synergistic effect due to production of
endotoxins like collagenase, hyaluranidase, and proteases. These endotoxins
contribute to the rapidly spreading cellulitis.

Clinical features:

1. Patient has c/o increasing oral cavity and neck pain.

2. These patients have poor oral hygiene

3. Symptoms are at first unialteral but soon become bilateral

4. The soft tissues of the floor of the mouth swells

5. Tongue gets pushed posteriorly causing air way obstruction

6. These patients are usually febrile

On examination:

These patients have tachycardia, fever, and variable degrees of respiratory

obstruction with dysphagia and drooling. The submandibular and submental
regions are tense, swollen and tender. The floor of the mouth may become tense
swollen and indurated. Fluctuation is not present. The tongue is seen to be
pushed backwards.

Diagnosis of Ludwigs angina is based on the clinical features enumerated above.

These patients may show leukocytosis. X ray soft tissue neck may show soft
tissue oedema. CT scan neck is to be considered in all persistent cases to rule
out complications. Xray chest must also be considered to rule out mediastinitis.

Management:

Airway management: Since the airway is threatened insertion of oral airway is to

be considered. If the patient does not tolerate an oral airway then tracheostomy
is to be considered.

Intravenous antibiotics with broad spectrum features (chloramphenicol)may be

administered. The drug of choice is amoxycillin with clavulanic acid.
Metronidazole must also be administered. Clindamycin can be administered in
resistant cases.

Role of surgical drainage: Wide decompression of the supra hyoid region may be
considered. The approach is through a median horizontal incision three to four
finger breadths below the mandibular margin. The mylohoid muscle is split in the
midline, and drainage is established both medially and laterally. Pus is very rarely
encountered during this procedure, but starts to drain several days after the
procedure.

Complications:

1. Airway compromise

2. Extension to mediastinum causing mediastinitis. This can be suspected if there

is persistent swelling in the neck with pain, spiking fever and persistent
leukocytosis.

3. Extension into the carotid sheath and retropharyngeal space.


CT scan of a patient with Ludwig's angina
CT scan of a patient with Ludwig's angina
CT scan of a patient with Ludwig's angina