What is the pathophysiology, diagnosis, and treatment of Ludwig's angina?

Ludwig's Angina: Pathophysiology, Diagnosis, and Treatment

Ludwig's angina is a rapidly progressive, potentially life-threatening cellulitis of the submandibular, sublingual, and submental spaces that requires immediate intervention with airway management, antibiotics, and often surgical drainage to prevent fatal complications.

Pathophysiology

Ludwig's angina is characterized by:

• Rapidly spreading cellulitis and edema of the soft tissues of the neck and floor of the mouth 1
• Bilateral involvement of submandibular, sublingual, and submental spaces
• Spread along fascial planes that can extend to the anterior mediastinum 2
• Most commonly caused by odontogenic infections (dental origin) 3
• Involves both aerobic and anaerobic bacteria 4
• Can lead to airway obstruction due to elevation and posterior displacement of the tongue

The infection typically originates from:

• Dental infections (most common cause)
• Peritonsillar or parapharyngeal abscesses
• Mandibular fractures
• Oral lacerations
• Submandibular sialadenitis

Diagnosis

Clinical Presentation

• Visible anterior neck swelling (bilateral cervical swelling) 2, 5
• Dysphagia and odynophagia
• Drooling due to inability to swallow saliva
• Dysphonia (voice changes)
• Elevation and posterior distension of the tongue 4
• Trismus (limited mouth opening)
• Fever and chills
• Neck tenderness and restricted neck movement
• Progressive dyspnea and stridor (late signs indicating impending airway compromise) 4

Physical Examination Findings

• Firm, tender swelling of the floor of the mouth and submandibular region
• Elevated tongue position
• Sublingual edema with pooling of secretions 2
• Erythema and induration of the anterior neck
• Possible crepitus if gas-forming organisms are present
• "Woody" induration of the submandibular area

Diagnostic Studies

• CT scan with contrast: Shows involvement of submandibular spaces and potential spread to deeper neck spaces or mediastinum 2
• Ultrasound: Can identify abscesses and fluid collections 2, 5
• Laboratory studies: Elevated white blood cell count, C-reactive protein
• Blood cultures: To identify causative organisms
• In resource-limited settings, diagnosis must rely on thorough physical examination 5

Treatment

Immediate Management

1. Airway Management (Highest Priority)

   • Early recognition of potential airway compromise is crucial 3
   • Securing the airway may require:
     • Awake fiberoptic intubation (preferred method) 6
     • Marking external anatomical airway landmarks prior to manipulation 4
     • Emergency surgical airway (cricothyroidotomy or tracheostomy) if intubation fails
   • Patients with signs of impending airway obstruction should not be left unattended

2. Antimicrobial Therapy

   • Immediate empiric broad-spectrum antibiotics to cover both aerobic and anaerobic organisms
   • Typical regimens include:
     • High-dose penicillin plus metronidazole
     • Clindamycin (for penicillin-allergic patients)
     • Ampicillin-sulbactam or piperacillin-tazobactam
   • Adjust based on culture results when available

3. Surgical Intervention

   • Surgical drainage is often necessary 3
   • Indications include:
     • Presence of fluctuance
     • Evidence of abscess formation on imaging
     • Failure to improve with antibiotics alone
     • Worsening clinical status despite medical management
   • Extraction of causative teeth may be required 3

Supportive Care

• Intravenous fluid resuscitation
• Pain management
• Close monitoring in intensive care unit setting
• Nutritional support
• Corticosteroids may be considered to reduce edema (controversial)

Complications

• Airway obstruction (most feared and potentially fatal complication) 3, 4
• Spread to deep neck spaces
• Descending necrotizing mediastinitis
• Sepsis and septic shock
• Jugular vein thrombosis
• Aspiration pneumonia
• Rare cases of type 2 myocardial infarction due to supply-demand mismatch 2

Prognosis

With early recognition and appropriate management, mortality has decreased significantly from historical rates of 50% to current rates of 8-10% 6. Delay in diagnosis and treatment remains the most significant factor associated with poor outcomes.

Special Considerations

• In resource-limited settings, clinicians must rely heavily on physical examination findings 5
• Patients with comorbidities may have more complicated clinical courses 3
• Drug addiction may be a risk factor for more severe presentations 6
• Airway management remains the greatest challenge and should be addressed by experienced providers 4, 6