Ludwig's Angina
Named after Karl Friedrich Willhelm von Ludwig, Ludwig's angina is characterized as a rapidly progressive gangrenous cellulitis of the soft tissues of the neck and floor of the mouth.[52] With progressive swelling of the soft tissues and elevation and posterior displacement of the tongue, the most life-threatening complication of Ludwig's angina is airway obstruction. Prior to the development of antibiotics, mortality for Ludwig's angina exceeded 50%.[3] As a result of antibiotic therapy, along with improved imaging modalities and surgical techniques, mortality currently averages approximately 8%.[3,53]
In Ludwig's angina, the submandibular space is the primary site of infection.[54] This space is subdivided by the mylohyoid muscle into the sublingual space superiorly and the submaxillary space inferiorly. The majority of cases of Ludwig's angina are odontogenic in etiology, primarily resulting from infections of the second and third molars. The roots of these teeth penetrate the mylohyoid ridge such that any abscess, or dental infection, has direct access to the submaxillary space. Once infection develops, it spreads contiguously to the sublingual space. Infection can also spread contiguously to involve the pharyngomaxillary and retropharyngeal spaces, thereby encircling the airway.
Odontogenic infections account for over 90% of cases.[55] Additional etiologies include mandible fracture, neck trauma, tongue piercing, sialdenitis, neoplasm, and other parapharyngeal infections.[3,52,54] Polymicrobial infection occurs in over 50% of cases.[54] The most commonly cultured organisms include Staphylococcus, Streptococcus, and Bacteroides species.[3] Patients with immunocompromising conditions, such as HIV, diabetes, transplant recipients, and alcoholics, are at risk for infection from a variety of atypical organisms. Atypical organisms isolated in these patients include Pseudomonas, Escherichia coli, Klebsiella, Enterococcus faecalis, Candida, and Clostridium.[54]
The majority of cases of Ludwig's angina occur in healthy patients with no comorbid diseases.[3] Nevertheless, there are several conditions that have been shown to predispose patients to Ludwig's angina. These conditions include diabetes mellitus, alcoholism, acute glomerulonephritis, systemic lupus erythematosus, aplastic anemia, neutropenia, and dermatomyositis.[3,54]
Ludwig's angina is a clinical diagnosis. The majority of patients report dental pain, or a history of recent dental procedures, and neck swelling. Less common complaints include neck pain, dysphonia, dysphagia, and dysarthria. Less than one third of adults will present in respiratory distress with dyspnea, tachypnea, or stridor.[53] On physical examination, over 95% of patients have bilateral submandibular swelling and an elevated or protruding tongue.[3,53] The submandibular swelling is often characterized as brawny and tense, with overlying erythema.
Airway management is the foundation of treatment for patients with Ludwig's angina. Unfortunately, the decision to secure the airway continues to rely on clinical judgment and experience. At present, there are no established guidelines for airway control in patients with Ludwig's angina. Current recommendations are primarily based on individual experience and institution-specific resources.[56] Clearly, any patient presenting in respiratory distress or impending airway obstruction requires immediate intubation. Recommended techniques include routine orotracheal intubation and fiber-optic nasotracheal intubation. Blind nasotracheal intubation should not be attempted in patients with Ludwig's angina given the potential for bleeding and abscess rupture.[54,56,57] In nonintubated patients with Ludwig's angina, airway equipment, including tracheostomy and cricothyroidotomy instruments, must be at the bedside.
Antibiotics should be initiated as soon as possible. Antibiotics should initially be broad-spectrum and cover gram-positive, gram-negative, and anaerobic organisms. Combinations of penicillin, clindamycin, and metronidazole are typically used.[3] Recent case reports have advocated the use of intravenous steroids.[52,54,58] In these reports, corticosteroid administration potentially avoided the need for airway management. To date, there are no randomized controlled trials that demonstrate the efficacy of corticosteroids in patients with Ludwig's angina.
Up to 65% of patients with Ludwig's angina develop suppurative complications that require surgical drainage.[3,53,59] Physical examination alone is insufficient in determining which patients require a surgical procedure. In a recent study of deep neck space infections, the clinical exam underestimated the true extent of infection in 70% of patients.[60] As a result, imaging is indicated in patients with Ludwig's angina once antibiotics have been administered and decisions in regard to airway management have been made. Although plain films can demonstrate submandibular soft-tissue swelling, they are inadequate in detecting patients who require surgical drainage. As a result, a CT scan with intravenous contrast is recommended to detect patients who have developed suppurative complications.[60]
American Academy of Emergency Medicine © 2007 American Academy of Emergency Medicine
Cite this: Evidence-Based Diagnosis and Management of ENT Emergencies - Medscape - Feb 16, 2007.
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