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Ludwigs 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.

 

 

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.


 

Figure 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.

 

 

Figure showing the relationship of the 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 ludwigs 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.

 

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