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Ludwig's angina
By
Dr. T. Balasubramanian M.S.
D.L.O.
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.

Fig
showing the 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.

Fig
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.

Fig
showing the relationship of 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.

Fig showing a
patient with ludwig's angina
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.
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