Ludwig Angina

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Ludwig's angina is life-threatening cellulitis of the soft tissue involving the floor of the mouth and neck. It involves three compartments of the floor of the mouth, the sublingual, submental, and submandibular. The infection is rapidly progressive, leading to potential airway obstruction. The most common etiology is a dental infection in the lower molars, mainly second and third, accounting for over 90% of cases. Any recent infection or injury to the area may predispose the patient to develop Ludwig's angina. Predisposing factors include diabetes, oral malignancy, dental caries, alcoholism, malnutrition, and immunocompromised status. This review addresses the management and acute treatment of this possibly lethal condition.


  • Summarize the recommended treatment of Ludwig's angina.
  • Outline the typical presentation of a patient with Ludwig's angina.
  • Review the pathophysiology of Ludwig's angina.
  • Explain the interprofessional team strategies for improving care coordination and communication regarding the management of patients with Ludwig's angina.


Ludwig's angina is life-threatening diffuse cellulitis of the soft tissue of the floor of the mouth and neck. The condition was named after a German physician, Wilhelm Friedrich von Ludwig, who first described it in 1836. It involves three compartments of the floor of the mouth, sublingual, submental, and submandibular. Infection of the lower molars is the hallmark cause of true Ludwig’s angina. However, this term is frequently applied to any floor of the mouth infection with sublingual or submandibular space involvement.[1] It rapidly progresses to the surrounding tissues, leading to various potentially lethal complications, such as airway obstruction, aspiration pneumonia, and carotid arterial rupture or sheath abscess.[2] Therefore, early recognition and treatment, including airway protection, antibiotic therapy, and surgical drainage in well-established infections, are crucial.


Ludwig's angina usually originates from dental infections in the mandibular molars, particularly the second and third molar, accounting for over 90% of cases.[3]

Other less common etiologies include injury or laceration to the floor of the mouth, mandible fracture, tongue injury, oral piercing, osteomyelitis, traumatic intubation, peritonsillar abscess, submandibular sialadenitis or sialolithiasis, otitis media, and infected thyroglossal cysts.[4][2]

In most cases, Ludwig's angina develops in previously healthy patients; however, some predisposing factors have been suggested, including diabetes mellitus, oral malignancy, alcoholism, malnutrition, and immunocompromised status.[1][5]


There is no significant gender predilection for Ludwig's angina. Approximately 1/3 of cases are associated with other systemic illnesses (i.e., HIV and diabetes mellitus), and poor dentition and dental hygiene are independent risk factors. Before the development of antibiotics, mortality exceeded 50%.[4] With rapid airway management and antibiotic therapy, along with advanced imaging and surgical procedures, mortality has decreased to around 8%.[6]


Ludwig's angina usually originates as a dental infection of the second or third mandibular molars, including partially erupted third molars.[1] The infection begins in the subgingival pocket and spreads to the musculature of the floor of the mouth. It progresses below the mylohyoid line, indicating that it has moved to the sublingual space. As the roots of the second and third mandibular molars lie below this line, infection of these teeth will predispose to Ludwig's angina. The infection spreads lingually rather than buccally because the lingual aspect of the tooth socket is thinner. It initially spreads to the sublingual space and progresses to the submandibular space.

The disease is usually polymicrobial, involving oral flora, both aerobes, and anaerobes. The most common organisms are Staphylococcus, StreptococcusPeptostreptococcus, Fusobacterium, Bacteroides, and Actinomyces.[7] Immunocompromised patients are at higher risk of Ludwig's angina.

History and Physical

Patients will commonly report a history of recent dental extraction or dental pain. The most frequent symptoms include neck swelling, neck pain, swallowing, and speaking difficulty. Trismus is another typical complaint, which is caused by the irritation of the muscles of the mastication.

The clinical aspect of the condition is often described as a "bull neck," with increased fullness of the submental area and a loss of the mandibular angle definition. Other common symptoms include mouth pain, hoarse voice, drooling, tongue swelling, stiff neck, and sore throat.[6]

Stridor indicates impending airway obstruction while speaking difficulty and increased tongue prominence signals sublingual space involvement.

On examination, patients will usually have a fever with submental and submandibular swelling and tenderness. Swelling of the floor of the mouth, the elevation of the tongue, and tenderness of the involved teeth are oral signs of the infection. The induration of the submental neck and edema in the upper part of the neck are common extraoral findings, although the patient will not typically have lymphadenopathy.[4] The presence of crepitus should raise suspicion for other pathologies, such as necrotizing fasciitis.


The most critical aspect of evaluation is the airway. If Ludwig's angina is diagnosed, the patient should be intubated immediately. Imaging has no role in the immediate assessment of the patient - the decision to intubate is made solely on clinical parameters, as sending a patient with an impending airway to the CT scanner will delay treatment and may be lethal. 

The safest manner to secure the airway is awake fiberoptic intubation, though preparations for an emergent awake tracheostomy must be in place before any airway intervention is attempted. 

Once the airway is secured, a CT scan of the neck with intravenous (IV) contrast can then be used to evaluate the severity of the infection and assess for any abscess.[8] In addition, CT scans and MRI can be used to identify mediastinal fluid cumulus and corroborate the airway edema. Neck and chest x-rays may demonstrate gas in the tissues in the case of infections caused by anaerobic microflora. Lastly, metastatic abscesses and pus may be seen with ultrasonography.[5]

Although common in clinical practice, laboratory testing is of little immediate value as this is a clinical diagnosis. Blood cultures should be obtained to determine if there is a hematogenous spread of the infection.

Treatment / Management

The treatment of Ludwig's angina is aimed principally at protecting the airways - the most common cause of death is asphyxiation from airway obstruction - controlling the infection with antibiotic therapy, and in some cases of well-established infections surgical draining.

Flexible fiberoptic nasal intubation is the favored method of intubation, though arrangements for emergency awake tracheostomy must be in place before any airway intervention is attempted.[9] Traditional direct laryngoscopy may be challenging because of trismus and tongue elevation. It is vital to manage the airway before stridor or cyanosis as these are late findings. If the patient cannot be intubated, the next step would be an emergency tracheotomy.[10]

Broad-spectrum intravenous antibiotics are the first-line treatment once an airway is secure and cultures have been obtained.[4] Antibiotics should cover gram-positive bacteria, gram-negative bacteria, and anaerobes.[1] Ampicillin-sulbactam or clindamycin are the most commonly prescribed antibiotics. In patients who are immunocompromised, the coverage should be broadened to involve pseudomonads. Some options include cefepime, meropenem, or piperacillin-tazobactam. Furthermore, clinicians should consider methicillin-resistant Staphylococcus aureus (MRSA) coverage for immunocompromised patients, those at increased MRSA risk or with prior history of MRSA infection.

The prescription of intravenous steroids is controversial. Several case reports have shown a decrease in the need for airway management with the use of steroids.[11] However, more studies are needed before it becomes a standard of care, and it is left to the judgment of the treating physician. The duration of the antibiotics is usually two weeks. White blood cell count and fever need to be monitored closely.

A dental extraction is recommended if the source of the infection is odontogenic. For patients who do not respond to initial antibiotics or develop a fluid collection on imaging, needle aspiration or surgical incision and drainage may be performed. 

Surgery is usually reserved for patients who fail medical therapy as early surgical decompression has not been shown to improve outcomes, except in patients requiring intubation from odontogenic infections where early tooth extraction and cultures are recommended.[4]

Surgical drainage is indicated in cases of suppurative infection: purulent needle aspirate, crepitus, fluctuance, and soft tissue air.[5] The surgical drainage is aimed at decompressing the fascial compartments of the neck and evacuating the pus. The incision is usually made parallel and at two fingerbreadths inferior to the mandibular angle, and, in some cases, many incisions are needed. The following steps include displacing the submandibular gland and dividing the mylohyoid muscles to decompress the affected fascial compartments.[5]

Differential Diagnosis

Although Ludwig's angina is a clinical diagnosis, it may be hard to differentiate from other diseases initially. Imaging may be helpful in this situation to rule out other causes of the patient's symptoms. Still, the clinician must only order an imaging test once the airway is secured or in the case of patients who can breathe comfortably and handle their secretions while supine.


Due to the life-threatening complication of airway obstruction from Ludwig's angina, mortality exceeded 50% before the development of antibiotics.[4] Thanks to antibiotic therapy, improved imaging modalities, and surgical techniques, mortality decreased to approximately 8%.[6]


As mentioned, Ludwig's angina is rapidly progressive cellulitis which can cause airway obstruction requiring immediate intervention. Any airway symptoms or the inability to handle oral secretions are indications for elective intubation to prevent mortality. In addition, close monitoring is needed to avoid the extension of the cellulitis to the adjacent areas, which may cause mediastinitis or cellulitis of the neck. It may also evolve to aspiration pneumonia.

Enhancing Healthcare Team Outcomes

Ludwig's angina is a rapidly progressive cellulitis that can quickly cause airway obstruction. It requires immediate intervention and close monitoring to prevent death from asphyxiation. It can also result in mediastinitis, necrotizing cellulitis of the neck, and aspiration pneumonia. The safest way to deal with these patients is a coordinated interprofessional approach involving the provider, nurse, and, if needed, a consultant such as an otolaryngologist or anesthesiologist. This will provide the best outcome and highest patient safety. [Level V]

(Click Image to Enlarge)
Swelling in the submandibular area in a patient with Ludwig's angina. This made it difficult for the assessment of neck extension.
Swelling in the submandibular area in a patient with Ludwig's angina. This made it difficult for the assessment of neck extension.
Contributed by Wikimedia Commons, Anand H Kulkarni, Et al., (CC by 2.0)

(Click Image to Enlarge)
Submandibular triangle
Submandibular triangle
Image courtesy S Bhimji MD
Article Details

Article Author

Jason An

Article Author

Jennifer Madeo

Article Editor:

Mayank Singhal


10/18/2021 12:01:58 PM

PubMed Link:

Ludwig Angina



Ludwig's angina: case report and review., Spitalnic SJ,Sucov A,, The Journal of emergency medicine, 1995 Jul-Aug     [PubMed PMID: 7594369]


Pak S,Cha D,Meyer C,Dee C,Fershko A, Ludwig's Angina. Cureus. 2017 Aug 21;     [PubMed PMID: 29062620]


Ludwig angina., Quinn FB Jr,, Archives of otolaryngology--head & neck surgery, 1999 May     [PubMed PMID: 10326824]


Otolaryngologic critical care., Bansal A,Miskoff J,Lis RJ,, Critical care clinics, 2003 Jan     [PubMed PMID: 12688577]


Barakate MS,Jensen MJ,Hemli JM,Graham AR, Ludwig's angina: report of a case and review of management issues. The Annals of otology, rhinology, and laryngology. 2001 May;     [PubMed PMID: 11372930]


Moreland LW,Corey J,McKenzie R, Ludwig's angina. Report of a case and review of the literature. Archives of internal medicine. 1988 Feb;     [PubMed PMID: 3277567]


Brook I, Microbiology and principles of antimicrobial therapy for head and neck infections. Infectious disease clinics of North America. 2007 Jun;     [PubMed PMID: 17561074]


Crespo AN,Chone CT,Fonseca AS,Montenegro MC,Pereira R,Milani JA, Clinical versus computed tomography evaluation in the diagnosis and management of deep neck infection. Sao Paulo medical journal = Revista paulista de medicina. 2004 Nov 4;     [PubMed PMID: 15692720]


Ludwig angina: a review of current airway management., Shockley WW,, Archives of otolaryngology--head & neck surgery, 1999 May     [PubMed PMID: 10326825]


Is surgical airway necessary for airway management in deep neck infections and Ludwig angina?, Wolfe MM,Davis JW,Parks SN,, Journal of critical care, 2011 Feb     [PubMed PMID: 20537506]


Saifeldeen K,Evans R, Ludwig's angina. Emergency medicine journal : EMJ. 2004 Mar;     [PubMed PMID: 14988363]