EM@3AM: Ludwig’s Angina

Author: Rachel Bridwell, MD (EM Resident Physician, SAUSHEC / San Antonio, TX) // Edited by: Brit Long, MD (@long_brit, EM Attending Physician, San Antonio, TX)  and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 28-year-old male presents for dysphagia and inability to handle secretions. He states that his mouth hurts and noticed his neck looked larger than usual. He has been unable to eat for the past 12 hours due to pain with swallowing, drooling, and difficulty opening his mouth. Review of systems is remarkable for a recent dental infection of his right bottom molar.

Triage vital signs (VS): BP 105/50, HR 130, T 100.2 temporal, RR 24, SpO2 95% on room air.

Pertinent physical examination findings include a reduced intercisal mouth opening distance, tongue protrusion, “woody” mouth floor, and prominent submandibular and submental swelling bilaterally, with corresponding lymphadenopathy. There is erythema overlying the right mandible, tracking inferiorly and terminating at sternal notch.

What’s the diagnosis, and what’s your next step in your evaluation and treatment?

Answer: 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. 2ndand 3rd) 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.
  •  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

A 62-year-old man presents with progressive swelling, pain and erythema of the anterior neck. He has difficulty opening his mouth and is drooling. He has a temperature of 38.4ºC, heart rate 110 beats per minute and blood pressure 104/67 mm Hg. There is firm erythema of the submandibular region with elevation of the tongue. What is the most likely organism responsible for his infection?

A) Corynebacterium diphtheriae

B) Peptostreptococcus species

C) Staphylococcus aureus

D) Viridans streptococci



Answer: D

Ludwig’s angina is a rapidly progressive cellulitis involving the floor of the mouth and submandibular space that can lead to death via asphyxiation in a matter of hours. A preceding dental infection, most often involving the second or third mandibular molars, is the most common cause. Other causes include mandibular fracture, oral lacerations, submandibular sialadenitis, and peritonsillar abscess. While viridans streptococci are the most commonly implicated organisms due to their abundance in the mouth, the infection is often polymicrobial with a mixture of streptococcal and staphylococcal flora. Anaerobic species such as Bacteroides are also frequently seen. Gram negative organisms may be present in immunocompromised patients. Patients present with anterior neck pain and swelling, dysphagia, odynophagia, and fever. On examination, there may be trismus and drooling. Elevation of the floor of the mouth with “woody” edema may cause protrusion or posterior displacement of the tongue. The anterior neck is tender, erythematous and edematous. Diagnosis is made clinically. Definitive airway management should be considered early as these patients can rapidly decompensate. Emergent ENT consultation and intravenous antibiotics are also necessary. For immunocompetent patients, a regimen of ampicillin-sulbactam or clindamycin would be appropriate. Those patients at risk for methicillin-resistant Staph. aureus should also receive vancomycin. Broader spectrum antibiotics, such as piperacillin-tazobactam or cefepime with metronidazole, would be indicated in immunocompromised individuals.

Corynebacterium diphtheriae (A) is responsible for diphtheria, a respiratory infection that presents with sore throat, malaise, fever and cervical lymphadenopathy. On examination, there will be an adherent pseudomembrane on the posterior pharyngeal wall that can extend to any portion of the respiratory tract. Treatment includes airway management as needed, diphtheria antitoxin and antibiotics (e.g. erythromycin or penicillin G). Peptostreptococcus sp. (B) and Staphylococcus aureus (C) can also play a role in the development of Ludwig’s angina, but they are not the most common species seen.

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  1. Lin HW, O’Neil A, Cunningham MJ. Ludwig’s Angina in the Pediatric Population. Clin Pediatr (Phila) 2009;48:583-7.
  2. Baez-Pravia, Orville V. et al. “Should We Consider IgG Hypogammaglobulinemia a Risk Factor for Severe Complications of Ludwig Angina?: A Case Report and Review of the Literature.” Medicine. 2017;96(47):e8708.
  3. Pandey M, Kaur M, Sanwal M, Jain A, Sinha SK. Ludwig’s Angina in children anesthesiologist’s nightmare: Case series and review of literature. J Anaesthesiol Clin Pharmacol. 2017 Jul-Sep;33(3):406-409.
  4. Botha A, Jacobs F, Postma C. Retrospective analysis of etiology and comorbid diseases associated with Ludwig’s Angina Ann Maxillofac Surg. 2015 Jul-Dec;5(2):168-73.
  5. Parhiscar A, Har-El G. Deep neck abscess: a retrospective review of 210 cases. Ann Otol Rhinol Laryngol 110: 1051, 2001.
  6. Saifeldeen K, R Evans. Ludwig’s Angina. Emerg Med J 2004; 21: 242-243
  7. Nanda N, Zalzal HG, Borah Gl. Negative-Pressure Wound Therapy for Ludwig’s Angina: A Case Series.Plast Reconstr Surg Glob Open2017 Nov 7;5(11):e1561.
  8. Pak S, Cha D, Meyer C, Dee C, Fershko A.Ludwig’s Angina. Cureus. 2017 Aug 21;9(8):e1588.


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