Ludwig’s Angina. St Emlyn’s

There’s two reasons why Ludwig’s angina sends a shiver down my spine but probably only one of them will apply to you.

Back in 2003 when I was a third year medical student my consultant was quizzing my fellow students and me on eponymous sydromes.

‘What are the signs and symptoms of Ludwig’s angina?’ he asked me.

After a long, painful, drawn out awkward silence, I blurted out in a hopeful voice,

‘Chest pain?’

He shook his head disappointedly and moved onto one of my brighter colleagues and I could hear the words of another famous doctor (Dr. Ross Geller in The One with Ross and Monica’s cousin) in my head,

‘Yeah you really shouldn’t have said anything’.

The second is more relevant and that’s because it’s a really scary disease and potential airway risk. Helpfully a new evidence-based review by Bridwell et al has just been published which we’ll look at now. [1]

Introduction

Ludwig’s angina is a cellulitis of the floor of the mouth and soft tissues of the neck. If left untreated it can rapidly lead to an airway obstruction and death with an untreated mortality as high as 50% and mortality 8% for treated disease. The condition is named after the German physician Karl Freidrich Wilhelm von Ludwig who first described the disease in 1836.[1] The angina part of the name comes from the latin word angere which means ‘to strangle’ which is appropriate as the airway swelling would certainly feel like strangulation.

Etiology

The most common cause of Ludwig’s angina is a dental infection of the mandibular molars especially the second and third (90% of cases) [2] as they are at the junction of numerous fascial spaces. The roots of these teeth are below the level of the attachment of the mylohyoid muscle to the mandible and so infection can spread to the submylohyoid space and then into the submandibular and sublingual space leading to tongue enlargement and airway obstruction. Infection can also spread to the epiglottitis, true and false vocal cords and aryepiglottic folds leading to rapid airway oedema within 30-45 minutes of arrival to the ED. Spread of infection through the styloglossal muscle can reach the retro and parapharyngeal space and then eventually the superior mediastinum. [1]

Relationship of mylohyoid muscle and the submandibular and sublingual space. [3]

Submandibular space highlighted in green[3]

Risk factors include

• Recent dental infection or trauma e.g. mandibular fractures
• Oral piercings
• Poor nutrition states
• Peritonsillar abscess
• Diabetes
• Sialadenitis
• Intravenous drug use
• Chronic alcohol abuse [1]

Organisms

Ludwig’s angina is typically polymicrobial with organisms mostly from the oral cavity flora. They include,

• Viridans Streptococci (40%)
• Staphylococcus aureus (27%)
• Staphylococcus epidermidis (23%)
• Also Enterococcus, E. coli, Fusobacterium, Klebsiella pneumonia and Actinomyces species.
• Streptococcus anginosus may cause a rapidly progressing course of Ludwig’s angina.
• MRSA particularly in the immunocompromised. [1]

There is a nice description in the video below from the great blog at EM in 5 and the excellent @AnnaEMin5. It’s worth checking the EM in 5 site out as it’s got some great stuff on there.

Presentation

In the early course of the infection symptoms may be those of dental infection with pain, fever and generalised tiredness being common.

More advanced symptoms, such as trismus, meningismus, drooling, dysphagia and tripod positioning suggest airway involvement and the need to act quickly.

The hallmark signs of Ludwig’s angina are a tender, firm, woody and indurated submandibular area. The tongue can be markedly enlarged and neck swelling and erythema may be profound. [1]

Erythema and swelling spreading down the anterior neck[4].

Below is a nice video from Larry Mellick showing a typical presentation in the ED.

Imaging

Whilst the diagnosis is generally clinical CT with contrast has a sensitivity of 95% and is the modality of choice in early or borderline cases.

MRI scanning can be used but it may not be practical to lie patients flat for a prolonged period of time with a potential airway compromise.

We’re big fans of POCUS at St. Emlyns so I’m pleased to say there is evidence that ultrasound can help in diagnosing Ludwig’s angina. Certainly in the cases I’ve seen of Ludwig’s angina I’ve seen I’d always be cautious about moving patients to a scanner so POCUS has real advantages. As we’ll discuss, definitive airway management in this cohort of patients is problematic so it’s helpful that we can also use ultrasound in identifying distorted neck anatomy to aid in a potentially very difficult tracheostomy. [5-6]

Management

Airway management is the main priority and biggest challenge in patients with Ludwig’s angina. If there are no immediate airway concerns patients can be managed with antibiotics and close monitoring of the airway in a critical care environment.

Antibiotic choice should be governed by your own hospital’s antibiotic policy but should use broad spectrum antibiotics and include anaerobic cover. Typically ampicillin, ceftriaxone, clindamycin can be used in non-immunosupressed patients and meropenem or tazocin in immunocompromised patients. If suspected MRSA then add vancomycin or linezolid. [1]

IV dexamethasone has been used to reduce oedema and can improve antibiotic penetration. [7]

Nebulised adrenaline (1ml 1:1000 with 4ml 0.9% saline) can also be used to reduce airway swelling but has limited evidence. [8]

For patients who need a definitive airway blind oral or nasal intubations without a laryngoscope are clearly not recommended as this can cause further trauma, bleeding or oedema. Supraglottic airways are also not recommended as on-going oedema can displace them. Awake nasal intubation in a sitting position with preparation for a surgical airway is the recommended approach. This is explained much better than I could do here [9] and here [10].

There is debate over the role of surgery in Ludwig’s angina but some evidence suggests it may be beneficial for airway protection. A retrospective cohort study of 55 patients in Nigeria found higher rates of airway compromise (26.3% vs 2.9%) in patients treated conservatively compared to patients who had a surgical intervention. [11] Surgical intervention is indicated if antibiotics aren’t improving the situation or if abscesses are demonstrated on imaging.

There’s a nice case study on the twitter link below.

Thanks for reading and I hope you’ve found this useful.

Stay safe.

Pete Hulme

@Dr_Pete_EmMed

See also

References

1. Bridwell, R., Gottlieb, M., Koyfman, A. and Long, B., 2020. Diagnosis and management of Ludwig’s angina: An evidence-based review. The American Journal of Emergency Medicine.
2. An, J., Madeo, J. and Singhal, M., 2019. Ludwig angina. In StatPearls [Internet]. StatPearls Publishing.
3. https://en.wikipedia.org/wiki/Submandibular_space accessed 4/1/21
4. https://litfl.com/the-true-angina/ accessed 8/1/21.
5. Shih, C.C., Wang, J.C., Chen, S.J. and Hsu, Y.P., 2019. Focused ultrasound assists in diagnosis and management of difficult airway in Ludwig’s angina. Journal of Medical Ultrasound, 27(2), p.101.
6. Narendra, P.L., Vishal, N.S. and Jenkins, B., 2014. Ludwig’s angina: need for including airways and larynx in ultrasound evaluation. Case Reports, 2014, p.bcr2014206506.
7. Freund, B. and Timon, C., 1992. Ludwig’s angina: a place for steroid therapy in its management?. Oral Health, 82(5), p.23.
8. MacDonnell, S.P.J., Timmins, A.C. and Watson, J.D., 1995. Adrenaline administered via a nebulizer in adult patients with upper airway obstruction. Anaesthesia, 50(1), pp.35-36.
9. https://first10em.com/difficult-airway-society-guidelines-on-awake-intubation/?subscribe=success#498 accessed 4/1/21
10. https://litfl.com/awake-intubation/ accessed 4/1/21
11. Edetanlen, B.E. and Saheeb, B.D., 2018. Comparison of outcomes in conservative versus surgical treatments for Ludwig’s angina. Medical Principles and Practice, 27(4), pp.362-366