More Than A Sore Throat: Ludwig's Angina

What is Ludwig’s Angina?

Figure 1.  Ludwig’s Angina typically originates from dental infections of 2nd mandibular molar  [ADAPTED FROM]

Figure 1. Ludwig’s Angina typically originates from dental infections of 2nd mandibular molar


Ludwig’s angina is a diffuse, rapidly expanding infection of the submandibular space [1]. The submandibular space is subdivided by the mylohyoid muscle into the sublingual space superiorly and the submaxillary space inferiorly. These areas communicate freely without the aid of lymphatics, therefore once an infection is present, it can disseminate quickly [2,3]. To complicate things further, the spaces of the neck also communicate freely with one another making it easy for infection to spread over a wide area. This gives the potential for submandibular infections to involve the pharyngomaxillary and retropharyngeal spaces with minimal resistance [2,3].

Most cases of Ludwig’s angina are due to dental infections, with the second mandibular molar being the most common site (Figure 1) [3]. Other causes include: sialadenitis, injury to the floor of the mouth (ex: frenulum or tongue piercings), peritonsillar abscess, lymphadenitis, infected mandibular fractures, infected abscess of the chin, and oral lacerations [2,3].

Presentation and Work-up

Presentation: Ludwig’s angina presents in males more often than females at a 2:1 ratio. The table below shows the initial symptoms of Ludwig’s angina as well as red flag symptoms that could indicate imminent airway compromise (Table 1).

Table 1. Common symptoms and red flags of Ludwig’s Angina [1,4,5,6]

Physical exam: Patients will classically present with a “board-like” or “brawny” swelling of the submandibular or sublingual spaces which are tender to palpation (Figure 2). If severe swelling is present, you may see elevation of the floor of the mouth with the tongue displaced superiorly and the mouth forced open [1].

Imaging: The diagnosis of Ludwig’s angina is typically made clinically, however obtaining CT or MRI scans of the neck can help determine the location and extent of the infection. Furthermore, imaging can assist in determining if the patient can be managed with antibiotics versus requiring surgical management.


The mainstay treatment for Ludwig’s angina is airway control, antibiotics, and surgical intervention.

Fig. 2  “Brawny” swelling involving submandibular space typical of Ludwig’s Angina.  [Image from]

Fig. 2 “Brawny” swelling involving submandibular space typical of Ludwig’s Angina.

[Image from]

Airway control: Oral intubation is often difficult due to displacement of the tongue and swelling of the posterior pharynx. If airway compromise is imminent, the patient can be intubated via fiberoptic nasotracheal intubation. If unsuccessful, the patient will require a cricothyroidotomy or surgical tracheostomy depending on the severity of the situation, however this may be challenging given the location and extent of the swelling.

Antibiotics: Patients should be treated with broad spectrum antibiotics to cover anaerobic, aerobic, and oral flora. Ampicillin/sulbactam, penicillin G and metronidazole, or clindamycin are appropriate first-line choices. If there is concern for MRSA infection or the patient is immunocompromised, consider using vancomycin (15-20mg/kg IV every 8 to 12 hours without exceeding 2 grams) or linezolid (600mg every 12 hours via oral or intravenous route) [7]. Although there are few studies on the use of steroids given the rarity of the disease, prior studies have shown decrease in facial swelling and airway edema for both adult and pediatric populations with both IV and oral formulations [8,9]. They has also been studies demonstrating that steroids may assist in treating Ludwig’s Angina by increasing antibiotic penetrance while also reducing airway inflammation.

Surgical intervention: While there is a debate about the necessity of operative intervention, studies have shown a higher incidence of airway compromise in groups who received antibiotic therapy only vs early surgical intervention [6]. Severity of the infection may warrant consulting a variety of surgical services including oral and maxillofacial surgery for infections without imminent airway compromise to otolaryngology if a surgical airway is necessary.


Since the advent of penicillin, the mortality rate for Ludwig’s angina has decreased from >50% to about 8% [3]. Those at highest risk for morbidity and mortality include patients older than 65, diabetics, alcohol abusers, and immunocompromised patients [2]. Due to the open communication of the spaces in the mouth and neck, infection can spread down the fascial planes of the neck and carotid sheath towards the mediastinum. Prior to the discovery of penicillin, this infection would commonly evolve into a descending mediastinitis, hence the name “Ludwig’s angina.” Though this rarely occurs now, other complications include necrotizing fasciitis of the neck and chest, carotid artery rupture, pericarditis, jugular vein thrombosis, pneumonia, pleural empyema, and ARDS. The biggest predictor for these complications is anterior visceral space involvement as this area extends from the hyoid to the superior mediastinum and involves the larynx, thyroid gland, trachea, and cervical esophagus [2].

Author: Shawn Hassani, MD

Peer Editor: Shan Modi, MD

Faculty Editor: Edmond Hooker, MD