Ludwig's Angina

The hallmark of Ludwig's angina is the sudden and abrupt appearance of symptoms. Bilateral symmetric neck swelling and pain, fever and dysphagia are seen in initial stages [11]. Toothache, odynophagia, trismus and palpable crepitus may be encountered as well [1] [7]. Airway compromise is manifested by stridor, cyanosis, inability to swallow saliva, laryngeal edema and physical examination can reveal an elevated tongue that prevents air passage [13]. Brawny, bilateral tender induration of the submandibular space is observed during palpation, with absence of lymphadenopathy [6].

The diagnosis can be made by characteristic clinical findings that are highly suggestive of Ludwig's angina. Cyanotic patients with a superiorly and posteriorly displaced tongue and severe neck swelling observed on physical examination are hallmarks of this infection. The diagnostic criteria include bilateral involvement of submandibular and sublingual spaces, rapidly spreading cellulitis without involvement of lymph nodes or abscess formation and onset of the infection in the floor of the mouth [6]. All of these findings can be confirmed by imaging studies such as CT [13]. Additionally, the attempts to determine the causative agent should be made through microscopic evaluation of aspirated samples.

To ensure good patient outcomes, it is imperative to establish proper airway passage, as hypoxia and asphyxiation can rapidly develop. Oral, endotracheal or nasal fiberoptic intubation are often necessary, while severe airway compromise may necessitate tracheotomy or cricothyrotomy [3]. Drainage of the floor of the mouth through small incisions has shown positive results in treating patients, which is why it is often considered in practice [14]. In addition to airway management, prompt administration of intravenous antibiotics is equally important. Penicillin G in combination with metronidazole is considered as first-line therapy, while piperacillin-tazobactam or clindamycin (in penicillin-allergic patients) are also recommended in treating Ludwig's angina [5]. Vancomycin is a drugs that can be added to the regimen if gram-positive microogranisms are found on microscopy [5]. The role of corticosteroids has shown to be beneficial in some studies and dexamethasone given for 48h has shown to reduce edema [7].

Before antibiotics were used, mortality rates from Ludwig's angina were more than 50%, but the introduction of antimicrobial therapy has substantially reduced death rates and are now between 0-8% [10]. Due to the abrupt onset and marked progression of airway obstruction, this infection can still be fatal if not recognized on time and complications such as mediastinitis, pericarditis, pleural empyema and endocranial spread may further increase the risk for fatal outcome [11]. For these reasons, an early diagnosis and aggressive management are life-saving steps for the majority of patients [12].

Spread of an odontogenic infection (most commonly of 2nd and 3rd mandibular molars) to the submandibular space is the most common cause of Ludwig's angina and between 50-90% of cases are thought to originate by this pathway [6]. Recent tooth extraction has also been listed as one of the causes [1], while peritonsilar and parapharyngeal abscesses, oral lacerations, submandibular siadenitis and mandibular fractures can also serve as a source [7]. Numerous pathogens have been identified, including β-hemolytic streptococci, Staphylococcus aureus, Staphylococcus epidermidis, Peptostreptococcus, Bacteroides sp., but also Eikenella corrodens, Clostridium sp. and Prevotella [3] [8]. In up to 50% of cases, the infection involves more than one microbial agent [2].

The introduction of antibiotics into medical practice has substantially reduced the appearance of Ludwig's angina, but several risk factors have been identified. Dental caries, recent dental procedures such as tooth extraction, malnutrition, alcohol abuse, systemic illnesses such as diabetes mellitus and immunosuppression due to human immunodeficiency virus (HIV) infection and organ transplantation have all been described as conditions that predispose individuals to Ludwig's angina [3].

The pathogenesis of Ludwig's angina starts with spread of the infection from other sites, most commonly the mandibular teeth. Firstly, the infection is spread to the submandibular, sublingual and submental spaces and the entire floor of the mouth becomes infiltrated. An intense inflammatory reaction leads to rapidly progressive development of bilateral gangrenous cellulitis of the floor of the mouth [9], causing abrupt and severe induration of the neck. More importantly, it displaces the tongue superiorly and posteriorly, thus contributing to airway compromise [4], whereas spread to the retropharyngeal and pharyngomaxillary spaces can fully constrict the trachea and disable air passage [3]. Neither abscess formation nor lymphatic involvement is seen in Ludwig's angina, which are some of the features that may distinguish it from other types of infection [6].

Since poor dental hygiene, dental carries and immunosuppression are shown to be the most significant risk factors for Ludwig's angina, major steps in prevention can be made by maintaining proper dental care and regular check-ups. Management of underlying disease that cause immunosuppression is also important.

Ludwig's angina is a potentially fatal infection of the submandibular and sublingual space that was initially described almost 200 years ago [1]. It is a form of rapidly developing gangrenous cellulitis that involves the soft tissues of the floor of the mouth [2]. It is shown that Ludwig's angina stems from preceding dental infection or tooth extraction, most commonly involving the lower teeth (second and third molars) and the gums [1], and a number of pathogens have been described as causative agents. β-hemolytic streptococci (including Streptococcus viridans), Peptostreptococcus, Bacteroides sp., Staphylococcus aureus, Staphylococcus epidermidis and several other have been mentioned in literature [3], but up to 50% of cases of Ludwig's angina are polymicrobial infections. The pathogenesis starts with local spread of the bacteria from the oral cavity to the sublingual, submandibular and submental spaces, where an intense inflammatory reaction occurs and produces a rapid onset of symptoms [4]. The spaces are infiltrated bilaterally, without the classical formation of an abscess and involvement of lymph nodes and most common symptoms include neck swelling, fever, pain and dysphagia. The most significant and most serious complication of this infection is airway compromise (angina meaning strangling) due to superior and posterior displacement of the tongue as a result of intense swelling of the floor of the mouth. Signs of airway obstruction include cyanosis, stridor and inability to swallow saliva and may call for immediate therapeutic measures [1]. The diagnosis can be made based on clinical criteria, but to confirm Ludwig's angina, computed tomography (CT) is an efficient method. Treatment primarily focuses on ensuring proper ventilation and air passage, which may sometimes require endotracheal intubation or tracheostomy. Intravenous antibiotic should be administered immediately and drugs such as clindamycin, penicillin and metronidazole are recommended [5]. Prior to the introduction of antibiotic therapy, mortality rates of this infection were up to 50%, but numerous advances in both antimicrobial therapy and intensive care management have substantially improved patient outcomes. Although in rare cases complications may ensue, including mediastinal, pleural, pericardial and endocranial spread, which presents as a significant risk for the patient, whereas asphyxiation due to sudden airway compromise may develop if the diagnosis is not made early on.

Ludwig's angina is a rare, but potentially life-threatening bacterial infection of the floor of the mouth. In most cases, an infection of the tooth or adjacent tissues that spreads to this space is the cause, but several other types of infections in the head and neck region may trigger this condition. Streptococci and Staphylococci are bacterial species that are most commonly identified as culprits, but various other species have been identified and in 50% of patients, more than one bacteria is present. Certain risk factors have been established, such as recent dental procedures, poor oral hygiene, diabetes mellitus and immunosuppression due to human immunodeficiency virus (HIV) infection or organ transplantation. As the infection spreads to the spaces below the tongue, an intense inflammatory reaction occurs, which leads to extensive swelling and the appearance of a bulged neck together with symptoms such as fever, neck pain and swallowing difficulties. One of the most feared complications of Ludwig's angina is breathing compromise that can develop because of displacement of the tongue by swelling and spread of the infection to spaces that surround the trachea. It is manifested by voice changes, inability to swallow saliva and blue discoloration of the face and skin (cyanosis). These symptoms appear abruptly and death may ensue rapidly if treatment is not initiated promptly, which is why an early diagnosis can save the patient's life. In addition to findings during physical examination, computed tomography of the neck (CT scan) and identification of bacteria from patient samples are performed to confirm Ludwig's angina and determine the causative agent, respectively. Immediate intravenous administration of antibiotics and ensuring adequate airway passage that may often require intubation are the mainstay of therapy. Before antibiotics were discovered, almost 50% of patients suffering from Ludwig's angina did not survive, but despite the introduction of antibiotic and advanced intensive care management, fatal outcomes are still encountered in up to 8% of cases. For these reasons, an early diagnosis is detrimental.

1. Kulkarni AH, Pai SD, Bhattarai B, Rao ST, Ambareesha M. Ludwig’s angina and airway considerations: a case report. Cases Journal. 2008;1:19.
2. Osunde O, Bassey G, Ver-or N. Management of Ludwig’s Angina in Pregnancy: A Review of 10 Cases. Ann Med Health Sci Res. 2014;4(3):361-364.
3. Candamourty R, Venkatachalam S, Babu MRR, Kumar GS. Ludwig’s Angina – An emergency: A case report with literature review. J Nat Sci Biol Med. 2012;3(2):206-208.
4. Kassam K, Messiha A, Heliotis M. Ludwig’s Angina: The Original Angina. Case Rep Surg. 2013;2013:974269.
5. Gilbert DN, Chambers HF, Eliopoulos GN, Saag MS. The Sanford Guide to Antimicrobial Therapy 2015. 45th ed. Antimicrobial Therapy, Inc, Sperryville, VA; 2015.
6. Mandell GL, Bennett JE, Dolin R. Mandel, Douglas and Bennett's Principles and Practice of Infectious Diseases. 8th ed. Philadelphia, Pennsylvania: Churchill Livingstone; 2015.
7. Srirompotong S, Art-Smart T. Ludwig's angina: a clinical review. Eur Arch Otorhinolaryngol. 2003;260(7):401-403.
8. Duprey K, Rose J, Fromm C. Ludwig’s angina. Int J Emerg Med. 2010;3(3):201-202.
9. Boscolo-Rizzo P, Da Mosto MC. Submandibular space infection: a potentially lethal infection. Int J Infect Dis. 2009;13(3):327-333.
10. Sujatha M, Madhusudhana R, Amrutha K, Nupoor N. Anaesthetic management of Ludwig’s angina with comorbidities. Indian J Anaesth. 2015;59(10):679-681.
11. De Bast Y, Appoloni O, Firket C, Capello M, Rocmans P, Vincent JL. Ludwig's angina [Article in French]. Rev Med Brux. 200;21(3):137-141.
12. Marcus BJ, Kaplan J, Collins KA. A case of Ludwig angina: a case report and review of the literature. Am J Forensic Med Pathol. 2008;29(3):255-259.
13. Porter RS, Kaplan JL. Merck Manual of Diagnosis and Therapy. 19th Edition. Merck Sharp & Dohme Corp. Whitehouse Station, N.J; 2011.
14. Bross-Soriano D, Arrieta-Gómez 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):712-717.