Ludwig Angina

Article Author:
Jason An
Article Author:
Jennifer Madeo
Article Editor:
Mayank Singhal
Updated:
6/22/2020 10:57:16 AM
For CME on this topic:
Ludwig Angina CME
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Ludwig Angina

Introduction

Ludwig's angina is life-threatening odontogenic cellulitis of the soft tissue involving the floor of the mouth and neck. It was named after a German physician, Wilhelm Friedrich von Ludwig, who first described the condition in 1836.  It involves two compartments on the floor of the mouth namely sublingual and submaxillary space. It usually does not involve the lymphatic system nor form an abscess. Infection of the lower molars is the hallmark cause of true Ludwig’s angina, though this term is frequently applied to any floor of mouth infection with sublingual and/or submaxillary space involvement.[1]  The infection is rapidly progressive leading to aspiration pneumonia and airway obstruction.

Etiology

The most common cause is dental disease in the mandibular molars, particularly the second and third, which accounts for over 90% of cases.[2]  The infection begins in the subgingival pocket and spreads via a direct extension to the musculature of the floor of the mouth. Progression below the myelohyoid line indicated the infection is in the sublingual space. As the roots of the second and thrid mandibular molars lie below this line, infection there will predispose to Ludwig's angina. 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, and infected thyroglossal cysts.[3]  Predisposing factors include diabetes, oral malignancy, dental caries, alcoholism, malnutrition, and immunocompromised status.[1]

Epidemiology

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

Pathophysiology

Ludwig's angina usually originates as a dental infection of the second or third mandibular molars, including partially erupted third molars.[1] The infection spreads lingually rather than buccally because the lingual aspect of the tooth socket is thinner. The infection initially spreads to the sublingual space and progresses to the submandibular space. The infection is usually polymicrobial involving oral flora, both aerobes and anaerobes. The most common organisms are Staphylococcus, StreptococcusPeptostreptococcus, Fusobacterium, Bacteroides, and Actinomyces.[5]  Immunocompromised patients are at higher risk of Ludwig's angina.

History and Physical

The most common presenting symptoms include neck swelling, neck pain, trismus, odynophagia, dysarthria, and dysphagia. Fever and chills are common. People often describe the appearance 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.[4]  Stridor indicates impending airway obstruction, while dysarthria and increased tongue prominence indicate sublingual space involvement. On physical exam, patients will have a fever with submental and submandibular swelling and tenderness, swelling to the floor of the mouth, elevation of the tongue, tenderness of the involved teeth, induration of the submental neck, edema in the upper part of the neck.[3]  The patient will not typically have lymphadenopathy. The presence of crepitus should raise suspicion for other pathologies, such as necrotizing fasciitis.

Evaluation

A clinical diagnosis should be made based on the presentation. Laboratory testing, although common in clinical practice, is of little immediate value as this is a clinical diagnosis. Blood cultures should be obtained to determine if there is hematogenous spread of the infection. The most important aspect of evaluation is the airway. If Ludwig's angina is diagnosed, the patient should be electively intubated immediately. Imaging has no role in the immediate, emergent, evaluation 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 can lead to death. The safest manner to secure the airway is via awake fiberoptic intubation, though preparations for an emergent awake tracheostomy must be in place before any airway intervention is attempted. CT scan of the soft tissue neck with intravenous (IV) contrast can then be used to evaluate the severity of the infection and assess for any abscess, once the airway is secured.[6] Once a secure airway has been established, a more formal oral exam can be performed, or imaging can be obtained, to identify the source of infection. As this is most often an odontogenic infection, treatment includes removal of the offending teeth, also allowing for cultures to be obtained. If there is an abscess present, it can be drained.

Treatment / Management

Early airway management is critical to the treatment of Ludwig’s angina, as the most common cause of death is sudden asphyxiation from airway obstruction. Flexible fiberoptic nasal intubation is the favored method of intubation, though arrangements for emergent awake tracheostomy must be in place before any airway intervention is attempted.[7]  The provider with the most experience should manage the airway, as it may be challenging. Traditional direct laryngoscopy may be very challenging because of the swelling of the oral cavity and trismus/tongue elevation. It is important to manage the airway before the presence of stridor or cyanosis as these are late findings. If the patient is not able to be intubated, the next step would be an emergency tracheotomy.[8]

Early broad-spectrum IV antibiotics are the first-line treatment once an airway is secure and cultures have been obtained.[3]  For patients who are immunocompetent, a reasonable first choice would be ampicillin-sulbactam or clindamycin. Antibiotics should cover gram-positive bacteria, gram-negative bacteria, and anaerobes.[1]  For patients who are immunocompromised, the coverage should be broadened to cover pseudomonads. Some options include cefepime, meropenem, or piperacillin-tazobactam. MRSA coverage should be considered for patients who are immunocompromised, at increased risk of methicillin-resistant Staphylococcus aureus (MRSA) or with prior history of MRSA infection. IV steroids are controversial. Several case reports have shown a decrease in the need for airway management with the use of steroids.[9]  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. WBC count and fever needs 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 is recommended.[3]

Differential Diagnosis

Differential diagnosis includes peritonsillar abscess, retropharyngeal abscess, submandibular abscess, epiglottitis, oral carcinoma, angioedema, submandibular hematoma, and diphtheria. Although Ludwig’s angina is a clinical diagnosis, it may be difficult to differentiate from other diseases initially. Imaging may be helpful in this situation for Ludwig’s angina and also to rule out other causes of the patient's symptoms, but must ONLY be ordered once the airway is secured, or in patients who are able to breathe comfortably and handle their own secretions while supine.

Prognosis

Due to the life-threatening complication of airway obstruction from Ludwig's angina, mortality exceeded 50% prior to the development of antibiotics.[3] With antibiotic therapy, along with improved imaging modalities and surgical techniques, mortality is approximately 8%.[4]

Complications

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. Close monitoring is required to prevent the extension of the cellulitis to the adjacent areas. It can cause mediastinitis or cellulitis of the neck. It can also cause aspiration pneumonia.

Consultations

Depending on the severity of the individual case, infectious disease, and ENT consultation can be sought for proper diagnosis, management and follow-up of the disease.

Enhancing Healthcare Team Outcomes

Ludwig's angina is rapidly progressive cellulitis which can quickly cause airway obstruction. It requires immediate intervention. Close monitoring is required to prevent sudden death. It can also result in mediastinitis, necrotizing cellulitis of the neck, and aspiration pneumonia. The safest approach to dealing with these patients is a coordinated interprofessional approach involve the nurse, provider, 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) https://creativecommons.org/licenses/by/2.0/

References

[1] Ludwig's angina: case report and review., Spitalnic SJ,Sucov A,, The Journal of emergency medicine, 1995 Jul-Aug     [PubMed PMID: 7594369]
[2] Ludwig angina., Quinn FB Jr,, Archives of otolaryngology--head & neck surgery, 1999 May     [PubMed PMID: 10326824]
[3] Otolaryngologic critical care., Bansal A,Miskoff J,Lis RJ,, Critical care clinics, 2003 Jan     [PubMed PMID: 12688577]
[4] 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]
[5] Brook I, Microbiology and principles of antimicrobial therapy for head and neck infections. Infectious disease clinics of North America. 2007 Jun;     [PubMed PMID: 17561074]
[6] 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]
[7] Ludwig angina: a review of current airway management., Shockley WW,, Archives of otolaryngology--head & neck surgery, 1999 May     [PubMed PMID: 10326825]
[8] 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]
[9] Saifeldeen K,Evans R, Ludwig's angina. Emergency medicine journal : EMJ. 2004 Mar;     [PubMed PMID: 14988363]