Ludwig Angina

Etiology

Ludwig angina most commonly originates from dental infections involving the mandibular molars, particularly the second and third molars, which account for 90% of cases.[5] Periapical abscesses of these teeth are the most common specific source of infection.[6] Less common etiologies include oral piercings or lacerations, mandibular fractures, traumatic intubation, osteomyelitis, peritonsillar or parapharyngeal abscess, submandibular sialadenitis, and infected thyroglossal duct cysts.[7][8]

Predisposing dental factors for Ludwig angina include poor oral hygiene, dental caries, and recent dental treatment.[6] Although the condition often develops in otherwise healthy individuals, several systemic risk factors have been identified. These include diabetes mellitus, alcohol use disorder, malnutrition, and immunosuppression, such as in patients with acquired immunodeficiency syndrome or those who have undergone an organ transplant.[3][9]

Epidemiology

Ludwig angina does not demonstrate a significant sex predilection. Airway compromise remains the leading cause of mortality.[10] Before the advent of antibiotics, the mortality rate exceeded 50%.[8] Advances in airway management, antibiotic therapy, imaging, and surgical intervention have decreased mortality to approximately 8% in the modern era.[11]

Pathophysiology

Ludwig angina typically begins in the floor of the mouth and rapidly extends to the submandibular space.[12] The floor of the mouth is divided by the mylohyoid muscle into the sublingual space (above the muscle) and the submandibular space (below the muscle). The roots of the mandibular molars are located inferior to the attachment of the mylohyoid muscle, facilitating the direct spread of odontogenic infections into the submandibular space.[6] Involvement of both the sublingual and submandibular spaces can lead to tongue elevation and airway obstruction if not promptly addressed.[6] Additionally, the infection may cause edema of critical airway structures, such as epiglottitis, vocal cords, and aryepiglottic folds, which can occur within 30 minutes after symptom onset.[6]

The infection may further extend to the parapharyngeal space, retropharyngeal space, and superior mediastinum via the styloglossus muscle (see Image. The Upper Respiratory System).[12] Spread occurs through direct extension along fascial planes rather than via the lymphatic system.[12] Clinically, the progression of infection into the neck is often characterized by a "bull neck" appearance, resulting from the swelling and induration.[12]

Microbiology

Ludwig angina is usually polymicrobial, involving both aerobic and anaerobic oral flora. The most commonly isolated organisms include Staphylococcus, Streptococcus, Peptostreptococcus, Fusobacterium, Bacteroides, and Actinomyces.[13] Infection with Streptococcus anginosus is associated with a more rapid disease progression than other bacteria.[14] In patients with diabetes, Klebsiella pneumoniae is isolated in cultures from over half of Ludwig angina cases.[12] Additionally, individuals with diabetes, those on hemodialysis, or with recent hospitalization (within 1 year) have an increased risk of infection with methicillin-resistant Staphylococcus aureus.[6]

History and Physical

Patients often report recent dental pain, particularly involving the lower molars. Common systemic symptoms include fever, fatigue, chills, and generalized weakness. As the infection progresses, trismus (limited jaw opening) may develop, indicating involvement of the parapharyngeal space and more severe disease. Signs of respiratory distress, such as tripod positioning (leaning forward with hands on knees to optimize breathing), drooling (due to inability to manage oral secretions), and dysphagia, may also appear. These symptoms collectively signal impending airway obstruction, necessitating urgent intervention.[5][15]

Other signs and symptoms include mouth pain, changes in voice, drooling, tongue swelling, elevation of the floor of the mouth, and a stiff neck.[11] These features reflect the extent of soft tissue involvement and can help differentiate Ludwig angina from other deep neck infections. The physical appearance of Ludwig angina is often described as a "bull neck," characterized by pronounced submental fullness and loss of mandibular angle definition (see Image. Submandibular Swelling).[16] On examination, patients typically present with fever, submental and submandibular swelling, and tenderness. Intraoral findings include swelling of the floor of the mouth, trismus, tongue elevation, and tenderness of the affected teeth. Common extraoral findings include induration of the submental neck and edema in the upper neck. Notably, palpable lymphadenopathy is typically absent.[8]

Evaluation

Ludwig angina is primarily diagnosed through clinical evaluation, as imaging does not play a direct role in the initial assessment. The most critical clinical decision is airway management, given the potential for rapid deterioration. Once the airway is secured, contrast-enhanced neck computed tomography (CT) is the imaging modality of choice for assessing the extent of infection and evaluating for the presence of abscess formation.[17] CT findings suggest Ludwig angina include soft tissue stranding, muscle edema, subcutaneous fat attenuation, loss of fat planes in the submylohyoid space, and soft tissue thickening.[6] Ultrasound, including point-of-care ultrasound, may also be helpful in early detection and airway evaluation.[6]

Although commonly performed in clinical practice, laboratory testing has limited immediate value in diagnosing Ludwig angina, which is primarily a clinical diagnosis. Blood cultures should be obtained to assess for possible hematogenous spread. While cultures from the affected area, obtained via swab or needle aspiration, have limited diagnostic value in the early stages of Ludwig angina, they may be helpful if an abscess is subsequently drained and can be sent for microbiological analysis.[6]

Treatment / Management

The primary objective in treating Ludwig angina is to secure the airway, as asphyxiation from airway obstruction is the leading cause of mortality. Once the airway is stabilized, management focuses on infection control through the use of intravenous broad-spectrum antibiotics and surgical drainage, if an abscess is present, often necessitating the extraction of the involved teeth. Intravenous corticosteroids and nebulized adrenaline can be adjuvant treatments to reduce facial and airway edema.[6][18]

Airway Management

Patients who are hypoxic should receive supplemental oxygen.[6] Neck swelling and trismus can complicate mask ventilation, making pre-oxygenation essential before any airway intervention.[6] Tongue elevation and trismus complicate the placement of an oropharyngeal airway. Additionally, patients often poorly tolerate airway distress, reducing their ability to cooperate with airway manipulation. Awake, flexible fiberoptic nasotracheal intubation is the preferred method of securing the airway; however, preparations for a surgical airway, such as cricothyrotomy, must be in place before attempting any procedure.[19][20] Flexible nasotracheal intubation requires an experienced clinician. If intubation is not possible, emergency cricothyrotomy or tracheostomy may be necessary, especially in the advanced stages of the infection.[21] Early airway management is critical, as stridor and cyanosis are late and ominous signs of impending airway failure.(B2)

Blind nasotracheal intubation, which involves placing an endotracheal tube without direct visualization of the larynx, should be avoided in patients with Ludwig angina. This procedure can provoke bleeding, rupture abscesses, exacerbate edema, and trigger laryngospasm.[6][21] Supraglottic airway devices may be difficult or impossible to insert due to trismus and can be rendered ineffective or displaced as swelling progresses.[6](B3)

Intravenous Antibiotics

Once the airway is secured, broad-spectrum intravenous antibiotics are the first-line treatment.[8] Antibiotic therapy should provide coverage against both aerobic and anaerobic microflora, as well as oral microflora.[6] Commonly prescribed agents include ampicillin-sulbactam or clindamycin. For individuals who are immunocompromised, broader coverage is necessary to include gram-negative rods and beta-lactamase-producing aerobes and anaerobes. Suitable options in these cases include cefepime, meropenem, or piperacillin-tazobactam.[22] Additionally, clinicians should consider methicillin-resistant Staphylococcus aureus (MRSA) coverage in immunocompromised individuals, those with increased risk factors for MRSA, or individuals with a prior history of MRSA infection. MRSA coverage includes the addition of vancomycin or linezolid to the existing antibiotic regimen (see Image. Antibiotic Coverage for Ludwig Angina).[6][8](B3)

Intravenous Corticosteroids

Intravenous steroids and nebulized adrenaline (epinephrine) can be used as adjuvant treatment to reduce edema and cellulitis, facilitate intubation, and enhance antibiotic penetration into the fascial spaces.[18] Several case reports have noted a reduced need for airway intervention with the use of steroids.[7] Dexamethasone (10 mg intravenous) is the most commonly administered corticosteroid in these cases.[6] However, due to limited evidence, steroid use has not yet become a standard of care and remains at the discretion of the treating physician. Similarly, while data are limited, nebulized epinephrine may also help reduce airway obstruction.[6](B3)

Surgical Drainage 

Although the evidence remains controversial, early surgical decompression of the submandibular space may improve airway patency in patients with Ludwig angina.[6][23] Surgical intervention aims to relieve pressure and reopen the oropharyngeal airway by allowing the tongue to shift into a more anteroinferior position.[24] Incisions are typically made parallel and approximately 2 fingerbreadths inferior to the mandibular angle; in some cases, multiple incisions are required.[25] (B2)

Subsequent steps include displacing the submandibular gland and dividing the mylohyoid muscles to decompress the affected fascial compartments.[9] Although surgical decompression of the floor of the mouth may reduce the need for prolonged intubation and shorten the hospital stay, performing this procedure without a discrete abscess is not considered the standard of care.[24] Surgical decompression is indicated in Ludwig angina when imaging reveals a visible abscess, fluctuance is present on physical examination, or there is no clinical improvement with antibiotic therapy alone.[26][27] Prompt surgical intervention under these circumstances can prevent further airway compromise and reduce the risk of systemic complications.(B2)

Differential Diagnosis

While Ludwig angina is primarily diagnosed through clinical evaluation, distinguishing it from other conditions can be challenging in the early stages. In such cases, imaging can be helpful to rule out alternative diagnoses. However, imaging should only be performed after securing the airway or in stable individuals who can breathe comfortably and manage their secretions while in a supine position.

Prognosis

Before the advent of antibiotics, the mortality rate of Ludwig angina exceeded 50%, primarily due to life-threatening airway obstruction.[8] Advances in antibiotic therapy, imaging modalities, and surgical techniques have significantly reduced the mortality rate to approximately 8%.[11]

Complications

Ludwig angina is a rapidly progressive cellulitis that can lead to airway obstruction, often requiring immediate intervention. The presence of airway symptoms or an inability to manage oral secretions is a clear indication for elective intubation to prevent life-threatening complications. Furthermore, close monitoring is essential to prevent the spread of cellulitis to adjacent areas, which can lead to complications such as mediastinitis or neck cellulitis. Additionally, Ludwig angina can progress to aspiration pneumonia. Descending necrotizing mediastinitis, which predominantly occurs through the retropharyngeal space (71%) or the carotid sheath (21%), is a severe complication that requires immediate recognition and management.[7] Sepsis resulting in multiple organ failure is common, particularly in those who are immunocompromised.[2]