Ludwig Angina

Brandon Scott Hopkins and Allen M. Seiden

History

A 28-year-old woman arrives in the emergency department in mild distress. Her speech is garbled, she is drooling, and she complains of difficulty swallowing. On questioning, she notes that this has been worsening over the last 24 hours and points out that about 1 week ago she had an infection of her second left molar, which was treated with penicillin. She gives a history of diabetes, normally well-controlled with her insulin. She denies other medical problems and does not smoke.

On physical examination, the patient has a firm anterior neck and submental region, a firm floor of mouth, an elevated tongue, and mild trismus. She currently has no signs of respiratory distress, including no dyspnea, no retractions, no cyanosis, and an oxygen saturation of 95% on room air.

Within minutes the patient becomes more anxious, and her breathing becomes labored. The decision is made to take the patient to the operating room for an elective flexible fiber-optic intubation. After unsuccessful visualization of the larynx with the flexible scope, the patient’s airway is obtained via an awake tracheostomy.

Differential Diagnosis—Key Points

1. The rapid progression of this patient’s symptoms clearly suggests an inflamma-tory cause. Induration of the submental region and floor of mouth should raise concern for the possibility of Ludwig angina, as opposed to tonsillitis, epiglottitis, or other pharyngeal or deep neck space infection.

2. Ludwig angina is named after the German physician Wilhelm Frederick von Ludwig, who first described the condition in 1836. The word angina derives from the Greek word ankhon, which means “strangling,” and aptly emphasizes the feeling patients have and the potential for airway compromise in this condition.

3. The hallmarks of Ludwig angina are dysphagia, a change in speech, a rapidly expanding cellulitis associated with submandibular and submental neck swelling that is classically very hard and tense, and floor-of-mouth firmness. Pain, fever, fetid breath, and trismus are common. The sublingual edema pushes the tongue upward and backward, leading to airway compromise. This is often an insidious process but can abruptly lead to an airway emergency.

5. Ludwig angina is essentially a compartment syndrome of the sublingual and submandibular spaces, which are enclosed by the rigid superficial layer of the deep cervical fascia. It generally begins in the sublingual space, unilaterally, with the spread of infection limited anteriorly by the mandible and inferiorly by the mylohyoid muscle. Therefore the infection extends superiorly and posteriorly, elevating the tongue and floor of mouth. Infection may also spread more posteriorly to the parapharyngeal space or inferiorly to the anterior visceral compartment of the neck. Potentially inciting causes include pharyngitis, tonsillitis, sialadenitis, tongue piercing and oral trauma, but its most common source (75–90%) is an odontogenic infection involving the second or third molars. Their roots lie below the attachment of the mylohyoid to the mandible and thus cross the sublingual and submandibular spaces. Low socioeconomic status and poor oral hygiene are also associated with this infection. Comorbid conditions predisposing to Ludwig angina have included diabetes mellitus, malnutrition, alcoholism, neutropenia, lupus erythematosus, aplastic anemia, and glomerulonephritis.

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