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| Figure 1: From the upper right to the lower left, there is a low attenuation collection tracking from submandibular into sublingual, parapharyngeal and pharyngeal spaces on the right side, anterior to carotid space. No definitive dental abnormality in the right side of the mandible is visualized. Note the edema of the pharyngeal soft tissues. |
Diagnosis: Ludwig’s angina
Discussion: Ludwig’s
angina is a cellulitis of the fascial spaces of the floor of the
mouth and upper neck, initiated most frequently by dental infection,
which has a fatal outcome in as many as 10% of cases because of
compromise of the upper airway, spread to the anterior mediastinum,
or both [1].
More than 70% of Ludwig’s angina cases have
dental etiology. The causative odontogenic infections classically located in
the second and third lower molar
teeth, since their apices are located just below mylohyoid ridges and are therefore
in close anatomic proximity to the submandibular space [2].
Less common primary infections include quinsy,
sialadenitis, epiglottitis, and
infection of thyroglossal cyst. In addition, Ludwig’s angina can follow
infections after compound fractures of the mandible and penetrating injuries
of the mouth, or even trauma from endotracheal intubation or bronchoscopy [2].
Although majority of patients are otherwise healthy, conditions that predispose
to severe periodontal infection, such as immunodeficiency, diabetes mellitus,
neutropenia, aplastic anemia, glomerulonephritis, are suggested to put an individual
at a higher risk of having Ludwig’s angina [2].
Patients present with tooth pain, a history of
recent dental extraction or poor dental hygiene, dysphagia, odynophagia, upper
neck pain and swelling, and dysphonia
and/or dysarthria. On physical examination there is usually an aggressive gangrenous
cellulitis, fever, tachycardia, brawny induration, swelling and tenderness of
submandibular space, and an elevated tongue [2].
The majority of the patients have mixed polymicrobial
infections. Recent papers reported the most commonly isolated organism was Streptococcus
viridans in up
to 39%, followed by anaerobes in about 35% [3].
The complications of the Ludwig’s angina
include airway compromise, mediastinitis, subphrenic abscess formation, pericardial
and/or pleural effusion, empyema, osteomyelitis
of the mandible, infection of the carotid sheath and possible rupture of the
carotid artery, and suppurative thrombophlebitis of the internal jugular vein
[2].
Plain radiographs of the neck and chest may demonstrate
the extent of soft tissue swelling, as well as reveal gas in the tissues, particularly
in the setting of
anaerobic infection. Plain chest radiography can also be used to look for intrathoracic
extension of the infective process. Ultrasonography may highlight collections
of puss, as well as reveal metastatic abscess formation. CT and MR may be used
to confirm the presence of the airway edema and to identify and localize the
fluid collection [2].
Since supraglottic airways are usually edematous
the airway maintenance becomes extremely important. Since endotracheal intubation
is frequently difficult and
edema may persist for along time, tracheotomy is frequently favored. Intravenous
antibiotic therapy is a cornerstone. A combination of clindamycin, penicillin
and metronidazole is commonly recommended until a specific pathogen is identified.
Early surgical drainage is recommended in the setting of suppurative infection
with dual goal: to evacuate the puss and to decompress closed fascial spaces
in the neck. Infected teeth need to be extracted [2].
References:
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