Ludwig Angina

Article Author:
Jason An
Article Author (Archived):
Jennifer Madeo
Article Editor:
Mayank Singhal
Updated:
7/3/2019 6:27:05 PM
PubMed Link:
Ludwig Angina

Introduction

Ludwig's angina is a life-threatening 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 lymphatic system nor it forms abscess. Infection of the lower molars is the most common cause of Ludwig’s angina.[1]  The infection is rapidly progressive leading to aspiration pneumonia and airway obstruction.

Etiology

The most common cause is dental disease in the lower molars mainly second and third which accounts for over 90% of cases.[2]  Any recent infection or injury to the area may predispose the patient to develop Ludwig's angina. Some 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

Prior to the development of antibiotics, mortality exceeded 50%.[3]  With antibiotic therapy, along with advanced imaging and surgical procedures, mortality is approximately 8%.[4]

Pathophysiology

Ludwig's angina usually starts as a cellulitis of the submandibular space.[1]  The infection usually starts as a dental infection of the second or third mandibular molar teeth.[1]  Other sources of infection include local spread from a peritonsillar abscess or suppurative parotitis. The infection spreads medially rather than laterally because the medial side of the periodontal bones is thin. The infection initially spreads to the sublingual space and progresses to the submandibular space. Since the infection does not spread via the lymphatic system, the infection is bilateral. The infection is usually polymicrobial involving the oral flora. 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 fever and chills with neck swelling, neck pain, odynophagia and dysphagia. People often describe the appearance as a "bull neck." Less common symptoms include mouth pain, hoarse voice, drooling, tongue swelling, stiff neck and sore throat.[4]  Stridor may indicate impending airway obstruction. Patients will not have trismus unless the infection has spread into the parapharyngeal space. On physical exam, patients will have a fever with bilateral induration due to submandibular swelling and tenderness, swelling to the floor of the mouth, tenderness to the involved teeth, stiff neck, edema in the upper part of the neck, and crepitus.[3]  The patient will not typically have lymphadenopathy.

Evaluation

A clinical diagnosis should be made based on presentation. Laboratory testing, although common in clinical practice, may be of little value as this is a clinical diagnosis. Blood cultures should be obtained to determine if there is the hematogenous spread of the infection. CT scan of the soft tissue neck with intravenous (IV) contrast is used to evaluate the severity of the infection and airway obstruction. CT is also useful to determine which patients will require surgical intervention for the formation of an abscess.[6]  Ultrasound may also be useful to identify the formation of an abscess. However, Ludwig’s angina usually does not result in an abscess formation. Therefore, it is often difficult to obtain cultures to determine what bacteria is causing the infection.

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 clinician's favored method of intubation.[7]  The provider with the most experience should manage the airway as it will often be very challenging. Video laryngoscopy may be an option although there are no studies to date on this issue. Standard direct laryngoscope may be very challenging because of the swelling of the upper airway. 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. Cricothyrotomy is very challenging because of the edema in the neck which can obscure the anatomy.[8]

Early broad-spectrum IV antibiotics have been shown to be helpful.[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 for pseudomonas. Some options include cefepime, meropenem, or piperacillin-tazobactam. MRSA coverage should be considered for patients who are immunocompromised, increased risk of methicillin-resistant Staphylococcus aureus (MRSA) or prior MRSA infection. IV steroids are controversial. Several case reports have shown the decrease in the need for airway management with the use of steroids.[9]  However, more studies are needed before it becomes standard of care. Duration of the antibiotics are usually two to three weeks. WBC count and Fever needs to be monitored closely.

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.[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. Typically, it does not result in abscess formation and it does not involve the lymphatic system. 

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 a rapidly progressive cellulitis which can cause airway obstruction requiring immediate intervention. Close monitoring is required to prevent extension of the cellulitis to the adjacent areas. It can cause mediastinitis or necrotizing 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 a 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 an interprofessional approach involve the nurse, provider, and if needed a consultant such as an anesthesiologist. This will provide the best outcome and highest patient safety. [Level V]


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]