Ludwig Angina: Definition and Etiology

Ludwig angina is a rare, life-threatening cellulitis of the floor of the mouth and neck, involving three compartments (sublingual, submental, and submandibular), named after Wilhelm Friedrich von Ludwig who described it in 1836. This condition is characterized by a rapid progression of symptoms, including pain, swelling, and difficulty swallowing. If left untreated, Ludwig angina can lead to airway obstruction, sepsis, and even death. Prompt medical attention is crucial to prevent serious complications and improve outcomes.

Etiology

• Mainly originates from dental infections in the mandibular molars, particularly the second and third molars (90% of cases).
• Periapical abscesses in the second or third mandibular molars are primarily responsible for the condition.
• Other less common etiologies include oral piercing or laceration, mandibular fracture, traumatic intubation, osteomyelitis, peritonsillar or parapharyngeal abscess, submandibular sialadenitis, otitis media, and infected thyroglossal cysts.

Pathophysiology

• Knowledge of regional anatomy is essential for understanding the spread of the infection.
• Ludwig angina typically initiates at the floor of the mouth and rapidly extends to the submandibular space.
• 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, which allows the spread of odontogenic infections into the submandibular space.
• The infection may also result in edema of the airway structures (epiglottitis, vocal cords, and aryepiglottic folds), which can occur after half an hour of initial presentation.

Clinical Presentation

• Patients may report a history of recent dental pain.
• Common symptoms include fever, fatigue, chills, and weakness.
• Trismus is a typical complaint, indicating a more advanced stage of the disease.
• Signs of respiratory involvement include tripod positioning, drooling, and dysphagia.
• Other signs or symptoms include mouth pain, hoarse voice, drooling, tongue swelling, and stiff neck.

Diagnosis and Evaluation

• Ludwig angina is primarily diagnosed based on clinical evaluation.
• Imaging studies do not play a direct role in the immediate assessment of the patient.
• A neck CT with intravenous contrast is the most appropriate imaging modality to evaluate the severity of the infection and assess for abscess.
• Blood cultures should be obtained to determine if the infection has a hematogenous spread.

Treatment and Management

• The primary objective in treating Ludwig angina is to secure the airway.
• Next steps include controlling the infection with intravenous broad-spectrum antibiotics and surgical drainage in some cases.
• Intravenous steroids and nebulized adrenaline can be adjuvant treatments to improve facial and airway edema and antibiotic penetration.

Complications

• Ludwig angina can cause airway obstruction requiring immediate intervention.
• The presence of airway symptoms or the inability to manage oral secretions are clear indications for elective intubation.
• 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, and sepsis resulting in multiple organ failure.

Ludwig Angina: Definition and Etiology

• Ludwig angina is a rare, life-threatening, diffuse cellulitis of the soft tissue of the floor of the mouth and neck.
• Named after Wilhelm Friedrich von Ludwig, who described it in 1836.
• The term "angina" comes from the Latin "angere," meaning to choke.
• Involves 3 compartments of the floor of the mouth: sublingual, submental, and submandibular.

Etiology

• Mainly originates from dental infections in the mandibular molars, particularly the second and third molars (90% of cases).
• Periapical abscesses in the second or third mandibular molars are primarily responsible for the condition.
• Other less common etiologies include oral piercing or laceration, mandibular fracture, traumatic intubation, osteomyelitis, peritonsillar or parapharyngeal abscess, submandibular sialadenitis, otitis media, and infected thyroglossal cysts.

Pathophysiology

• Knowledge of regional anatomy is essential for understanding the spread of the infection.
• Ludwig angina typically initiates at the floor of the mouth and rapidly extends to the submandibular space.
• 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, which allows the spread of odontogenic infections into the submandibular space.
• The infection may also result in edema of the airway structures (epiglottitis, vocal cords, and aryepiglottic folds), which can occur after half an hour of initial presentation.

Clinical Presentation

• Patients may report a history of recent dental pain.
• Common symptoms include fever, fatigue, chills, and weakness.
• Trismus is a typical complaint, indicating a more advanced stage of the disease.
• Signs of respiratory involvement include tripod positioning, drooling, and dysphagia.
• Other signs or symptoms include mouth pain, hoarse voice, drooling, tongue swelling, and stiff neck.

Diagnosis and Evaluation

• Ludwig angina is primarily diagnosed based on clinical evaluation.
• Imaging studies do not play a direct role in the immediate assessment of the patient.
• A neck CT with intravenous contrast is the most appropriate imaging modality to evaluate the severity of the infection and assess for abscess.
• Blood cultures should be obtained to determine if the infection has a hematogenous spread.

Treatment and Management

• The primary objective in treating Ludwig angina is to secure the airway.
• Next steps include controlling the infection with intravenous broad-spectrum antibiotics and surgical drainage in some cases.
• Intravenous steroids and nebulized adrenaline can be adjuvant treatments to improve facial and airway edema and antibiotic penetration.

Complications

• Ludwig angina can cause airway obstruction requiring immediate intervention.
• The presence of airway symptoms or the inability to manage oral secretions are clear indications for elective intubation.
• 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, and sepsis resulting in multiple organ failure.