Dentistry

Diagnosis and management of Ludwig’s angina: An evidence-based review

a b s t r a c t

Background: Ludwig’s angina is a potentially deadly condition that must not be missed in the emergency depart- ment (ED).

Objective: The purpose of this narrative review article is to provide a summary of the epidemiology, pathophys- iology, diagnosis, and management of Ludwig’s angina with a focus on emergency clinicians.

Discussion: Ludwig’s angina is a rapidly spreading infection that involves the floor of the mouth. It occurs more commonly in those with poor dentition or immunosuppression. Patients may have a woody or indurated floor of the mouth with submandibular swelling. Trismus is a late finding. Computed tomography of the neck soft tis- sue with contrast is preferred if the patient is able to safely leave the ED and can tolerate lying supine. Point-of- care ultrasound can be a useful adjunct, particularly in those who cannot tolerate lying supine. Due to the threat of rapid airway compromise, emergent consultation to anesthesia and otolaryngology, if available, may be helpful if a definitive airway is required. The first line approach for airway intervention in the ED is flexible intubating endoscopy with preparation for a Surgical airway. broad spectrum antibiotics and surgical source control are keys in treating the infection. These patients should then be admitted to the intensive care unit for close airway observation.

Conclusion: Ludwig’s angina is a life-threatening condition that all emergency clinicians need to consider. It is im- portant for clinicians to be aware of the current evidence regarding the diagnosis, management, and disposition of these patients.

Published by Elsevier Inc.

  1. Introduction
    1. Epidemiology

Ludwig’s angina (LA) is a rapidly spreading infection involving the floor of the mouth. It was named after Karl Friedrich Wilhelm von Ludwig in 1836, who first described the fatal and rapidly progressive in- fection [1]. Airway compromise is the leading cause of death in these pa- tients [2].

There are numerous etiologies and risk factors associated with LA (Table 1). Odontogenic infection accounts for 70% of LA cases [3]. In adults, Periapical abscesses between the mandibular molars (teeth # 19 and #30) are the most common etiology, while upper respiratory in- fections account for most cases of LA in children [3]. Of note, patients with IgG hypogammaglobulinemia are at particularly high risk for se- vere complications, as hypogammaglobulinemia has been associated

* Corresponding author at: 3841 Roger Brooke Dr, Fort Sam Houston, TX 78234, United States of America.

E-mail address: [email protected] (B. Long).

with severity of illness in sepsis, especially in patients without other ob- vious comorbidities. However, of all IgG immunodeficiencies, only IgG1 levels are independently associated with mortality, with one case reporting severe LA with a prolonged course in a patient with IgG1 de- ficiency [4-6]. Mortality is most often from airway compromise and is as high as 50% in untreated LA patients, although it is closer to 8% among those who receive adequate treatment [1,7,8]. Therefore, it is important for emergency clinicians to be aware of this condition.

  1. Methods

Authors searched PubMed and Google Scholar for articles using the keywords “Ludwig’s angina” and “deep space neck infection”. The liter- ature search was restricted to studies published in English. Authors evaluated case reports and series, retrospective and prospective studies, systematic reviews and meta-analyses, and other narrative reviews. Au- thors also reviewed guidelines and supporting citations of included ar- ticles. The literature search focused on emergency medicine and Critical care literature. Authors decided which studies to include for the review by consensus. When available, systematic reviews and

https://doi.org/10.1016/j.ajem.2020.12.030 0735-6757/Published by Elsevier Inc.

Table 1

Risk factors for Ludwig’s Angina [3,9-13]

Medical Recent dental infection Oral piercings Immunosuppression Malnutrition

Diabetes mellitus Oral or dental trauma

Lifestyle Injection drug use

Chronic alcohol use Recent tongue piercing

meta-analyses were preferentially selected. Three authors selected a total of 61 articles for inclusion from 467 resources found on literature search, with majority voting to resolve any disagreement.

  1. Discussion
    1. Pathophysiology and microbiology

It is important to review the anatomy of the oropharynx in order to understand the Rapid progression and eventual airway occlusion that can occur from LA [14]. The mylohyoid muscle subdivides the subman- dibular space into the sublingual space and the submylohyoid space. The roots of the mandibular teeth are located below the mylohyoid mandibular attachments, allowing infection to enter the submylohyoid space. The infection then spreads posteriorly and superiorly, tracking to the sublingual and submandibular spaces [1,14]. Involvement of these spaces may result in tongue enlargement by a factor of 2-3 and eleva- tion against the hypopharynx, eventually leading to airway occlusion if no intervention is performed. The infection may also result in edema involving the epiglottitis, true and false vocal cords, and aryepiglottic folds [14]. Edema of the airway structures may progress rapidly, occur- ring within 30-45 min of initial presentation [14]. The infection can also spread via the styloglossus muscle into the parapharyngeal space, retropharyngeal space, and finally into the superior mediastinum [14,15].

The infection is typically polymicrobial, primarily including oral cav- ity flora. Viridans group streptococci are found in over 40% of cases, followed by Staphylococcus aureus (27%) and Staphylococcus epidermidis (23%) [16,17]. Other commonly involved bacteria include Enterococcus species, E. coli, Fusobacterium, Streptococcus species, S. aureus, Klebsiella pneumonia, and Actinomyces species [18-20]. Klebsiella may be present in over half of cases involving diabetics [14]. Streptococcus anginosus is a virulent strain of viridans group streptococci that may result in a more rapidly progressive disease compared to other bacteria [4]. Dis- ease originating from dental abscesses often includes oral anaerobes such as Actinomyces, Peptostreptococcus, Fusobacterium, and Bacteroides [4,19-21]. Immunocompromised patients are at high risk of Gram- negative aerobic infection as well as methicillin-resistant Staphylococcus aureus (MRSA) [21-23]. Risk factors for MRSA include diabetes, injection drug use, hemodialysis, hospitalization in the preceding year, or resi- dent of a long-term care facility [24].

    1. History and physical examination

While LA initially begins as an oral infection, patients often present with fever, malaise, chills, and generalized weakness. More advanced symptoms, such as trismus, meningismus, drooling, dysphagia, and tri- pod positioning suggest airway involvement, which may occur later in the clinical course as severe obstruction worsens and there is risk of impending airway loss. As symptoms worsen, patients may lean for- ward in the tripoding position in order to maximize their airway diam- eter [25]. Respiratory distress and failure are marked by difficulty breathing, stridor, cyanosis, and Mental status changes. Trismus

suggests extension to the parapharyngeal space, while meningismus suggests involvement of the retropharyngeal space.

Examination may reveal a tender, symmetric, tense, woody, and in- durated submandibular area [26]. Lingual swelling may keep the mouth held open, while the floor of the mouth can be erythematous, tender, and elevated. The outer neck may appear erythematous and edematous. Sublingual, submental, and cervical lymphadenopathy may also be present, although their absence should not exclude the diagnosis [25].

    1. Laboratory testing

Laboratory testing has limited utility in these patients. Culture of the involved area, either through Needle aspiration or swab is not recom- mended as the diagnostic yield is low, it has a high rate of contaminants, and it can trigger worsening airway obstruction. Blood cultures should be obtained.

    1. Imaging

While the diagnosis of LA is clinical, further imaging can be helpful to better diagnose or exclude this condition in early or unclear cases. Com- puted tomography (CT) of the neck with intravenous (IV) contrast is the imaging modality of choice, as it can assist in determining the location and extent of infection [27]. Findings on CT can include soft tissue thick- ening, increased attenuation of the subcutaneous fat, loss of fat planes in the submandibular space, soft tissue gas, focal fluid collections, and muscle edema (Fig. 1) [26].

CT demonstrates a sensitivity of 95% and a specificity of 53% for LA [28]. However, one study found that when the CT was combined with clinical examination, the specificity increased to 80% while the sensitiv- ity remained at 95% [28]. Magnetic resonance imaging can also be used for diagnosis, but due to the time required to obtain the test, it is not typically feasible in the ED setting. If imaging is pursued, the provider must first ensure the patient is appropriate to leave the ED for testing. As the patient will be laying supine during imaging, the provider must

Image of Fig. 1

Fig. 1. Sagittal slice of a CT neck with contrast demonstrating sublingual, submental, and submandibular enhancing regions with fluid collection (arrow) characteristic of LA. Case courtesy of Dr. Yair Glick, Radiopaedia.org, rID: 51942.

also ensure the patient can lay supine in an area with resuscitation equipment prior to imaging. Point-of-care ultrasound can also be used to detect LA by evaluating for hypoechoic lesions within the face and neck by utilizing a curvilinear or linear array transducer in a submandib- ular view [29-31]. Ultrasound can also reliably assess for airway involve- ment and estimate the subglottic airway diameter, especially in those who cannot tolerate a supine position [29,32-37].

    1. Treatment

Management focuses on serial assessments of the patient’s airway and hemodynamic status. Many cases may be initially managed with antibiotics and close observation in an intensive care setting, but pa- tients with significant airway swelling, dyspnea, stridor, cyanosis, or worsening airway symptoms require airway intervention [27,38,39]. Emergent consultation with otolaryngology and anesthesia is recom- mended if available, as these patients are best managed in the operating room if they can be safely transported there [27,38,40-42]. Patients should be started on supplemental oxygen if hypoxic. Mask ventilation will likely be difficult due to neck swelling, so it is important to pre-oxygenate these patients using whichever approach works best. Blind oral or Nasotracheal intubation in which an endotracheal tube is passed without a laryngoscope or visualization of the larynx can result in airway trauma leading to worsening edema and even severe laryngospasm; therefore, this approach is not recommended [26]. supraglottic airway devices should also be avoided because they can be displaced as the swelling progresses [14]. If possible, patients should be nasotracheally intubated in the seated position with a flexible intubating endoscope using an awake intubation technique with prepa- ration for a surgical airway (i.e., cricothyrotomy) [42]. Awake intubation should incorporate lidocaine (atomized, topical, and viscous) with con- sideration of a Sedative agent (Table 2) [38]. While clinicians should prepare for a surgical airway, cricothyrotomy may be particularly chal- lenging in these patients due to the distortion of the anterior neck in cases of extensive infection [38,39]. Awake tracheotomy may be neces- sary in patients with LA who have severe edema [14,27].

broad-spectrum antibiotics covering anaerobic, aerobic, and oral

flora are recommended. Table 3 depicts antibiotic regimens for LA. Of

Table 2

Awake intubation procedure

Steps for awake intubation Preparation 1. Sit patient upright

      1. If time is available, glycopyrrolate 0.2-0.4 mg IV can assisting with drying mucous membranes, though this may require 15 min for onset of action
        • If using nasal route, utilize oxymetazoline
      2. Administer topical lidocaine:
        • Atomized lidocaine 2-4% to the posterior pharynx, soft palate, and glottic inlet
        • 4-5% lidocaine ointment to tongue and posterior pharynx; apply to nasopharynx if the nasal route will be used
      3. Can consider sedatives such as ketamine in small doses

Intubation 5. Utilize flexible intubating endoscope

        • If using oral route, use an intubating oral airway through the mouth to pass the endoscope
        • If using nasal route, insert a lubricated and warmed endotra- cheal tube through the nasal passage
        • Spray additional lidocaine while advancing the endotracheal tube past the vocal cords
        • Pass the endotracheal tube over the endoscope through the vocal cords

6. Provide post intubation sedation (e.g., propofol, ketamine) with

consideration to maintain a mean arterial pressure greater than 65 mmHg.

IV, intravenous.

note, clindamycin alone is not recommended, as resistance rates ap- proach over 30% for Streptococcal species and MRSA.

Other adjunctive treatments include steroids and nebulized epi- nephrine. Steroids may reduce facial swelling and airway edema, as well as improve antibiotic penetration [1,27,44-46]. The most common steroid utilized is dexamethasone (10 mg IV). nebulized epinephrine (1 mL of 1:1000 diluted to 5 mL in 0.9% normal saline) may also reduce airway obstruction, but the evidence is limited [47].

While the evidence is controversial, early surgical intervention may improve airway status [27,48-55]. Therefore, otolaryngology should be consulted, as well as oromaxillofacial surgery, depending upon the insti- tution and resources available [39]. One study of 55 patients found that those undergoing surgical intervention had lower rates of airway com- promise (2.9%) compared with those undergoing medical therapy alone (26.3%) [56]. Surgical intervention typically includes debriding necrotic tissue and draining all pathologic fluid collections. Indications for sur- gery include patients who fail to improve with antibiotics, if fluctuance is detected on examination, or if there are visible abscesses on imaging [27]. If otolaryngology and/or anesthesia consultation is not available, the emergency clinician should focus on early airway management if there is concern for airway compromise, appropriate antibiotic adminis- tration, and rapid transfer to a higher level of care with consultants who can acquire operative source control.

    1. Complications

Although the mortality rate has decreased, ranging from 10% if expe- diently treated to 50% in those not receiving appropriate management, several complications can occur, with descending mediastinitis com- prising one of the most severe complications [57,58]. Others include necrotizing fasciitis of the neck and chest, pericarditis, carotid artery rupture, jugular vein thrombosis, pleural empyema, pneumonia, and acute respiratory distress syndrome [59,60]. Complications may occur in over one quarter of patients [61].

    1. Disposition

Due to the risk of airway compromise and severe complications, pa- tients with LA should be admitted to the intensive care setting. Close ob- servation of the patient’s airway is necessary. Patients with the highest risk for mortality and complication include those with age greater than 65 years, diabetes, alcohol use, and immunocompromise.

Table 3

antibiotic recommendations for LA [43]

Patient population Recommended medication Immunocompetent Ampicillin-sulbactam 3 g IV every 6 h

or

Ceftriaxone 2 g IV every 12 h plus metronidazole 500 mg IV every 8 h

or

Clindamycin 600 mg IV every 6-8 h plus levofloxacin 750 mg IV every 24 h

Immunocompromised Cefepime 2 g IV every 8 h plus metronidazole 500 mg IV every 8 h

or

Imipenem 1 g IV every 6-8 h or

Meropenem 2 g IV every 8 h or

Piperacillin-tazobactam 4.5 g IV every 6 h MRSA Coverage To the above coverage, add:

Vancomycin 20 mg/kg IV or

Linezolid 600 mg IV every 12 h

IV, intravenous.

  1. Conclusion

LA is a rapidly progressing infection of the floor of the mouth, which can quickly compromise the patient’s airway. It occurs more commonly in those with poor dentition or immunosuppression. Patients may have a woody or indurated mouth floor with submandibular swelling. Tris- mus is a late and serious finding. CT of the neck soft tissue with intrave- nous contrast is an accurate imaging modality for diagnosis if the patient is able to safely leave the ED. Point-of-care ultrasound can be a useful adjunct, particularly in those who cannot tolerate lying supine. Due to the threat of rapid airway compromise, emergent consultation to anesthesia and otolaryngology is vital, especially if a definitive airway is required. The first line approach for airway intervention in the ED is flexible intubating endoscopy with preparation for a surgical airway. Broad spectrum antibiotics, such as ampicillin-sulbactam, and surgical source control are key in controlling infection. Emergency clinicians should be aware of this emergent diagnosis, requiring rapid recognition and airway protection.

Declaration of Competing Interest

None.

Acknowledgements

BL, RB, AK, and MG conceived the idea for this manuscript and con- tributed substantially to the writing and editing of the review. This man- uscript did not utilize any grants, and it has not been presented in abstract form. This clinical review has not been published, it is not under consideration for publication elsewhere, its publication is approved by all authors and tacitly or explicitly by the responsible authorities where the work was carried out, and that, if accepted, it will not be published elsewhere in the same form, in English or in any other language, includ- ing electronically without the written consent of the copyright-holder. This review does not reflect the views or opinions of the U.S. govern- ment, Department of Defense, U.S. Army, U.S. Air Force, or SAUSHEC EM Residency Program.

References

  1. Saifeldeen K, Evans R. Ludwig’s angina. Emerg Med J. 2004;21(2):242-3. https://doi. org/10.1136/emj.2003.012336.
  2. Pak S, Cha D, Meyer C, Dee C, Fershko A. Ludwig’s angina case presentation. Cureus. 2017;9(8):8-11. https://doi.org/10.7759/cureus.1588.
  3. Lin HW, O’Neill A, Cunningham MJ. Ludwig’s angina in the pediatric population. Clin Pediatr (Phila). 2009;48(6):583-7. https://doi.org/10.1177/0009922809333095.
  4. Baez-Pravia OV, Diaz-Camara M, De La Sen O, et al. Should we consider IgG hypogammaglobulinemia a risk factor for severe complications of Ludwig angina? A case report and review of the literature. Med (United States). 2017;96(47): e8708. https://doi.org/10.1097/MD.0000000000008708.
  5. Venet F, Gebeile R, Bancel J, et al. Assessment of plasmatic immunoglobulin G, A and M levels in septic shock patients. Int Immunopharmacol. 2011;11(12):2086-90. https://doi.org/10.1016/j.intimp.2011.08.024.
  6. Bermejo-Martin JF, Rodriguez-Fernandez A, Herran-Monge R, et al. Immunoglobu- lins IgG1, IgM and IgA: a synergistic team influencing survival in sepsis. J Intern Med. 2014;276(4):404-12. https://doi.org/10.1111/joim.12265.
  7. Nanda N, Zalzal HG, Borah GL. Negative-pressure wound therapy for Ludwig’s an- gina: a case series. Plast Reconstr Surg - Glob Open. 2017;5(11). https://doi.org/10. 1097/GOX.0000000000001561.
  8. Moreland LW. Ludwig’s angina. Report of a case and review of the literature. Arch Intern Med. 1988;148(2):461-6. https://doi.org/10.1001/archinte.148.2.461.
  9. Owens B, Schumann N. Ludwig’s angina: historical perspective. J Tenn Dent Assoc. 1993;73(1):19-21.
  10. Owens BM, Schuman NJ. Ludwig’s angina. Gen Dent. 1994;42(1):84-7.
  11. LeJeune H, Amedee R. A review of odontogenic infections. J La State Med Soc. 1994; 146(6):239-41.
  12. Finch RG, Snider GE, Sprinkle PM. Ludwig’s Angina. JAMA J Am Med Assoc. 1980;243

(11):1171-3. https://doi.org/10.1001/jama.1980.03300370045027.

  1. Candamourty R, Venkatachalam S, Ramesh Babu M. Kumar Gs. Ludwig’s angina - an emergency: a case report with literature review. J Nat Sci Biol Med. 2012;3(2):206. https://doi.org/10.4103/0976-9668.101932.
  2. Dowdy RAE, Emam HA, Cornelius BW. Ludwig’s angina: anesthetic management. Anesth Prog. 2019;66(2):103-10. https://doi.org/10.2344/anpr-66-01-13.
  3. Pandey M, Kaur M, Sanwal M, Jain A, Sinha S. Ludwig’s angina in children anesthe- siologist’s nightmare: case series and review of literature. J Anaesthesiol Clin Pharmacol. 2017;33(3):406. https://doi.org/10.4103/0970-9185.214318.
  4. Har-El G, Aroesty JH, Shaha A, Lucente FE. Changing trends in deep neck abscess. Oral Surg Oral Med Oral Pathol. 1994;77(5):446-50. https://doi.org/10.1016/0030- 4220(94)90221-6.
  5. Kurien M, Mathew J, Job A, Zachariah N. Ludwig’s angina. Clin Otolaryngol Allied Sci. 1997;22(3):263-365. https://doi.org/10.1046/j.1365-2273.1997.00014.x.
  6. Botha A, Jacobs F, Postma C. Retrospective analysis of etiology and comorbid diseases associated with Ludwig’s angina. Ann Maxillofac Surg. 2015;5(2):168. https://doi. org/10.4103/2231-0746.175758.
  7. Brook I. Microbiology and management of deep facial infections and Lemierre syn- drome. ORL. 2003;65(2):117-20. https://doi.org/10.1159/000070776.
  8. Brook I. Microbiology of abscesses of the head and neck in children. Ann Otol Rhinol Laryngol. 1987;96(4):429-33. https://doi.org/10.1177/000348948709600416.
  9. Dixon EE, Steele RW. Ludwig angina caused by MRSA: a new syndrome. Clin Pediatr (Phila). 2016;55(4):316-9. https://doi.org/10.1177/0009922815609400.
  10. Boscolo-Rizzo P, Da Mosto MC. Submandibular space infection: a potentially lethal infection. Int J Infect Dis. 2009;13(3):327-33. https://doi.org/10.1016/j.ijid.2008.07. 007.
  11. Patel M, Chettiar TP, Wadee AA. Isolation of Staphylococcus aureus and black- pigmented bacteroides indicate a high risk for the development of Ludwig’s angina. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2009;108(5):667-72. https://doi. org/10.1016/j.tripleo.2009.06.033.
  12. Siddiqui AH, Koirala J. Methicillin resistant Staphylococcus aureus (MRSA). StatPearls

Publishing; 2020.

  1. Reynolds SC, Chow AW. Life-threatening infections of the Peripharyngeal and deep Fascial spaces of the head and neck. Infect Dis Clin N Am. 2007;21(2):557-76. https://doi.org/10.1016/j.idc.2007.03.002.
  2. Costain N, Marrie TJ. Ludwig’s angina. Am J Med. 2011;124(2):115-7. https://doi. org/10.1016/j.amjmed.2010.08.004.
  3. Parhiscar A, Har-El GH. Deep neck abscess: a retrospective review of 210 cases. Ann Otol Rhinol Laryngol. 2001;110(11):1051-4. https://doi.org/10.1177/ 000348940111001111.
  4. Miller WD, Furst IM, Sandor GKB, Keller MA. A prospective, blinded comparison of clinical examination and computed tomography in deep neck infections. Laryngo- scope. 1999;109(11):1873-9. https://doi.org/10.1097/00005537-199911000-

00029.

  1. Gaspari RJ. Bedside ultrasound of the soft tissue of the face: a case of early Ludwig’s angina. J Emerg Med. 2006;31(3):287-91. https://doi.org/10.1016/j.jemermed.2005. 11.044.
  2. Shih CC, Wang JC, Chen SJ, Hsu YP. Focused ultrasound assists in diagnosis and man- agement of difficult airway in Ludwig’s angina. J Med Ultrasound. 2019;27(2):61-2. https://doi.org/10.4103/JMU.JMU_95_18.
  3. Narendra PL, Vishal NS, Jenkins B. Ludwig’s angina: need for including airways and larynx in ultrasound evaluation. BMJ Case Rep. 2014;2014. https://doi.org/10. 1136/bcr-2014-206506.
  4. Kristensen MS, Teoh WH, Graumann O, Laursen CB. Ultrasonography for clinical decision-making and intervention in airway management: from the mouth to the lungs and pleurae. Insights Imaging. 2014;5(2):253-79. https://doi.org/10.1007/ s13244-014-0309-5.
  5. Lakhal K, Delplace X, Cottier JP, et al. The feasibility of ultrasound to assess subglottic diameter. Anesth Analg. 2007;104(3):611-4. https://doi.org/10.1213/01.ane. 0000260136.53694.fe.
  6. Shibasaki M, Nakajima Y, Ishii S, Shimizu F, Shime N, Sessler DI. Prediction of pedi- atric endotracheal tube size by ultrasonography. Anesthesiology. 2010;113(4): 819-24. https://doi.org/10.1097/ALN.0b013e3181ef6757.
  7. Adhikari S, Zeger W, Schmier C, et al. Pilot study to determine the utility of point-of- care ultrasound in the assessment of difficult laryngoscopy. Acad Emerg Med. 2011; 18(7):754-8. https://doi.org/10.1111/j.1553-2712.2011.01099.x.
  8. Sustic A. Role of ultrasound in the airway management of critically ill patients. Crit Care Med. 2007;35(5 SUPPL). https://doi.org/10.1097/01.CCM.0000260628.88402. 8A.
  9. Gottlieb M, Holladay D, Burns KM, Nakitende D, Bailitz J. Ultrasound for airway man- agement: an evidence-based review for the emergency clinician. Am J Emerg Med. 2020;38(5):1007-13. https://doi.org/10.1016/j.ajem.2019.12.019.
  10. Neff SPW, Merry AF, Anderson B. Airway management in Ludwig’s angina. Anaesth Intensive Care. 1999;27(6):659-61. https://doi.org/10.1177/0310057×9902700323.
  11. Marple BF. Ludwig angina: a review of current airway management. Arch Otolaryngol Head Neck Surg. 1999;125(5):596-600. https://doi.org/10.1001/ archotol.125.5.596.
  12. Parker E, Mortimore G. Ludwig’s angina: a multidisciplinary concern. Br J Nurs. 2019;28(9):547-51. https://doi.org/10.12968/bjon.2019.28.9.547.
  13. Kremer M, Blair T. Ludwig angina: forewarned is forearmed. AANA J. 2006;74(6): 445-51.
  14. Ovassapian A, Tuncbilek M, Weitzel EK, Joshi CW. Airway management in adult pa- tients with deep neck infections: a case series and review of the literature. Anesth Analg. 2005;100(2):585-9. https://doi.org/10.1213/01.ANE.0000141526.32741.CF.
  15. Bansal A, Miskoff J, Lis RJ. Otolaryngologic critical care. Crit Care Clin. 2003;19(1): 55-72. https://doi.org/10.1016/S0749-0704(02)00062-3.
  16. Spitalnic SJ, Sucov A. Ludwig’s angina: case report and review. J Emerg Med. 1995;13

(4):499-503. https://doi.org/10.1016/0736-4679(95)80007-7.

  1. Busch RF, Shah D. Ludwig’s angina: improved treatment. Otolaryngol Head Neck Surg. 1997;117(6). https://doi.org/10.1016/S0194-59989770093-7.
  2. Freund B, Timon C. Ludwig’s angina: a place for Steroid therapy in its management? Oral Health. 1992;82(5):23-5.
  3. Macdonnell SPJ, Timmins AC, Watson JD. Adrenaline administered via a nebulizer in adult patients with upper airway obstruction. Anaesthesia. 1995;50(1):35-6. https://doi.org/10.1111/j.1365-2044.1995.tb04510.x.
  4. Rowe DP, Ollapallil J. Does Surgical decompression in Ludwig’s angina decrease hos- pital length of stay? ANZ J Surg. 2011;81(3):168-71. https://doi.org/10.1111/j. 1445-2197.2010.05496.x.
  5. Potter JK, Herford AS, Ellis E. Tracheotomy versus endotracheal intubation for airway management in Deep neck space infections. J Oral Maxillofac Surg. 2002;60(4): 349-54. https://doi.org/10.1053/joms.2002.31218.
  6. Wolfe MM, Davis JW, Parks SN. Is surgical airway necessary for airway management in deep neck infections and Ludwig angina? J Crit Care. 2011;26(1):11-4. https:// doi.org/10.1016/j.jcrc.2010.02.016.
  7. Schuman N, Owens B. Ludwig’s angina following dental treatment of a five-year-old male patient: report of a case - PubMed. J Clin Pedatr Dent. 1992;16(4):263.
  8. Flynn TR, Shanti RM, Hayes C. Severe odontogenic infections, part 2: prospective outcomes study. J Oral Maxillofac Surg. 2006;64(7):1104-13. https://doi.org/10. 1016/j.joms.2006.03.031.
  9. Swift JQ, Gulden WS. Antibiotic therapy-managing odontogenic infections. Dent Clin N Am. 2002;46(4). https://doi.org/10.1016/S0011-8532(02)00031-9.
  10. Iwu CO. Ludwig’s angina: report of seven cases and review of current concepts in management. Br J Oral Maxillofac Surg. 1990;28(3):189-93. https://doi.org/10. 1016/0266-4356(90)90087-2.
  11. Candamourty R, Venkatachalam S, Babu MRR, Kumar GS. Ludwig’s angina - an emer- gency: a case report with literature review. J Nat Sci Biol Med. 2012;3(2):206-8. https://doi.org/10.4103/0976-9668.101932.
  12. Edetanlen BE, Saheeb BD. Comparison of outcomes in conservative versus surgical treatments for Ludwig’s angina. Med Princ Pract. 2018;27(4):362-6. https://doi. org/10.1159/000490740.
  13. Furst I, Ersil P, Caminiti M. A rare complication of tooth abscess-Ludwig’s angina and mediastinitis. J Can Dent Assoc. 2001;67(7):324-7.
  14. Estrera A, Landay M, Grisham J, Sinn P, Platt M. Descending necrotizing mediastinitis. Surg Gynecol Obstet. 1983;157(6):545-52.
  15. Manasia A, Madisi NY, Bassily-Marcus A, Oropello J, Kohli-Seth R. Ludwig’s angina complicated by fatal cervicofascial and mediastinal necrotizing fasciitis. IDCases. 2016;4:32-3. https://doi.org/10.1016/j.idcr.2016.03.001.
  16. Blanchard A, Garcia LG, Palacios E, Bordlee B, Neitzschman H. Ludwig angina progressing to fatal necrotizing fasciitis. Ear Nose Throat J. 2013;92(3):102-4. https://doi.org/10.1177/014556131309200306.
  17. Bross-Soriano D, Arrieta-Gomez JR, Prado-Calleros H, Schimelmitz-Idi J, Jorba-Basave

S. Management of Ludwig’s angina with small neck incisions: 18 years experience. Otolaryngol Head Neck Surg. 2004;130(6):712-7. https://doi.org/10.1016/j.otohns. 2003.09.036.