emDOCs Podcast: Episode 33 – Ludwig’s Angina

Today on the emDOCs cast with Brit Long, MD (@long_brit) and Rachel Bridwell, MD (@rebridwell), we cover the challenge of Ludwig’s Angina

Epidemiology:

• • Risk Factors: Poor dental hygiene, recent dental infection, immunosuppression, IVDU, DM, chronic EtOH abuse, recent tongue piercing.
  • Odontogenic infection accounts for 70% of Ludwig’s Angina.¹
    • Most commonly periapical abscesses of mandibular molars (esp. 2^ndand 3^rd) in adults.
    • URI more commonly causes Ludwig’s Angina in children.¹
  • IgG hypogammaglobulinemia possible risk factor for severe complication.²
  • Named for Karl Friedrich Wilhelm von Ludwig in 1836, who first described the fatal and rapidly progressive infection of the mouth floor.

Anatomy and Pathophysiology:

• • Mylohyoid subdivides submandibular space:
    • Sublingual space
    • Submaxillary (submylohyoid) space
  • Infection extends posteriorly and superiorly, elevating tongue against hypopharynx.
  • Untreated, extension inferiorly to retropharyngeal space and into superior mediastinum.³
  • Polymicrobial oral flora, but most common bacterial culprits:⁴
    • Enterococcus
    • E. coli
    • Fusobacterium
    • Streptococcus spp.
    • S. aureus
    • Klebsiella pneumonia
    • Actinomyces spp.

Clinical Presentation:

• • Initially oral infection, progressing to trismus, tongue protrusion, inability to handle secretions, odynophagia, tripoding, respiratory distress. Patients may demonstrate signs of systemic toxicity with fever, tachycardia, and hypotension.

Evaluation:

• • Assess ABCs and begin resuscitation.
  • Patient may be leaning forward to optimize diameter of the airway.
  • Perform a complete physical examination.
    • ENT: Decreased intercisal mouth opening distance, indurated mouth floor, brawny neck with submandibular and submental edema, sublingual and submental lymphadenopathy, superior displacement of tongue.
    • Integumentary: Erythema with inferior tracking denotes spreading infection.
  •  Laboratory evaluation:
    • CBC, BMP, VBG with lactate.
  •  Imaging: Consider CT head/neck to assess anatomic reaches of infection if clinical situation permits. Highly accurate, but ensure the patient can tolerate lying flat prior to going to CT.

Treatment:

• • ABCs—Sit upright.
  • Early airway management is paramount.
    • Intubation often unsuccessful, with a majority of cases requiring surgical airways.^4-5
  • Source control of infection—Typically to OR for needle aspiration versus surgical decompression.
  • Early antibiotics—Coverage for beta-lactamase producing aerobic or anaerobic GPC, GNR +/- MRSA
    • PCN G + metronidazole, clindamycin, or unasyn.⁶
  • Steroids
    • 10 mg dexamethasoneà4 mg q6hrs x 48 hrs
      • Thought to chemically decompress for airway protection and increase antibiotic penetration.⁶
  • Nebulized epinephrine
  • Resuscitation and pain control

Disposition:

• • Consult ENT, OMFS, and anesthesia for airway assistance .and surgical decompression of infection, extraction of infected teeth.
    • Awake fiberoptic vs surgical airway
  • Admit to ICU.
  • May progress to cervical necrotizing fasciitis or descending necrotizing mediastinitis through carotid sheath or retropharyngeal space.²
  • Consider negative pressure wound therapy.⁷

Pearls:

• • Mortality in treated Ludwig’s Angina is approximately 8%.⁷
  • Airway compromise is the leading cause of death.⁸