International Journal of Pediatric Otorhinolaryngology 52 (2000) 79 87 www.elsevier.

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Case report

Ludwigs angina in the pediatric population: report of a case and review of the literature
John C. Britt a, Gary D. Josephson b,*, Charles W. Gross a
a

Department of Otolaryngology-Head and Neck Surgery, Uni6ersity of Virginia Health Sciences Center, P.O. Box 10008, Charlottes6ille, VA 22906 -0008, USA b Department of Otolaryngology-Head and Neck Surgery, Di6ision of Pediatric Otolaryngology, Uni6ersity of Miami, P.O. Box 016960 (D-48), Miami, FL 33101, USA Received 18 April 1999; received in revised form 11 June 1999; accepted 11 October 1999

Abstract Ludwigs angina is a rapidly progressing cellulitis involving the submandibular neck space. It is characterized by brawny induration of the submental region and oor of mouth, bearing the potential for rapid airway obstruction. Airway management, antibiotics, and judicious surgical intervention are the mainstays of successful therapy. We present a case of Ludwigs angina in a 5-year-old child and offer a meta-analysis of pediatric cases of Ludwigs angina described in the literature over the past 30 years. The presentation, etiology, management, and potential complications of this disorder in the pediatric population are discussed. 2000 Elsevier Science Ireland Ltd. All rights reserved.
Keywords: Ludwigs angina; Odontogenic infection; Child; Adolescence

1. Introduction Ludwigs angina is a rapidly progressive cellulitis of the oor of mouth characterized by rm induration and elevation of the tongue with the potential for airway obstruction. This was described by Wilhelm Frederick von Ludwig in 1836, who presented clinical observations and necropsy ndings of patients suffering from a condi* Corresponding author. Tel.: +1-305-585-7130; fax: + 1305-326-7610.

tion that despite the most skilful therapy is almost always fatal [1]. He described a rm connective tissue tumefaction that extends uniformly about the periphery of the neck, at rst under the jaw to the chin and beyondto involve the tissues which cover the small muscles between the larynx and the oor of mouth. A similar process was documented by Hippocrates in the 4th century BC, describing an edematous tongue which changes from broad and becomes round, its natural color turns to livid, from a soft consistence it grows hard, instead of being ex-

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ible, it becomes inexible, so that the patient would soon be suffocated unless speedily relieved [2]. Not surprisingly, the word angina derives from the Latin term angere, meaning to strangle. Understanding the pathophysiology of Ludwigs angina requires a knowledge of the anatomy of the submandibular space. This space is bounded superiorly by the oor of mouth mucosa and inferiorly by the supercial layer of the deep cervical fascia as it extends from the hyoid bone to the mandible. This space is sub-divided by the mylohyoid muscle into two spaces: the submaxillary space below the mylohyoid and the sublingual space above. These two spaces are effectively in continuity with one another as infection can spread around the free posterior edge of the mylohyoid. Furthermore, extension posteriorly along the intrinsic tongue musculature can lead to involvement of the parapharyngeal space and retropharyngeal space, with the potential for descent into the superior mediastinum [3,4]. Ludwigs angina is odontogenic in origin in up to 90% of cases [5,6], although oral lacerations [7,8], mandible fractures [9,10], and infection of an oral malignancy [11] have also been implicated. Recent infections or extractions of the second or third mandibular molars are the most common etiologies, as the roots of these teeth extend inferiorly below the mylohyoid line of the mandible, providing a route of extension to the submaxillary space [12]. As edema progresses, extension is limited inferiorly by the supercial layer of the deep cervical fascia which extends between the hyoid bone and the mandible. Cellulitis typically spreads superiorly from the submaxillary space to the sublingual space producing rm induration of the oor of mouth, elevation and posterior displacement of the tongue, and insidious airway compromise. Criteria for the accurate diagnosis of Ludwigs angina have been described in Ludwigs original paper and later by Grodinsky [3]. They typify Ludwigs angina as a cellulitic infection of the submandibular space, usually involving more than one neck space, producing oor of mouth induration with elevation and posterior displacement of the tongue. It spreads by continuity along fascial

planes, rather than by lymphatics and rarely involves the glandular structures. Mortality rates for Ludwigs angina exceeded 50% in the preantibiotic era [13]; however, recent series quote mortalities of 010% [5,6,14,15]. Because this infection is often rapidly progressive and potentially fatal, prompt recognition and treatment are essential. While the occurrence of Ludwigs angina in adults is infrequent, its presentation in the pediatric population is even more uncommon. We report a case of Ludwigs angina in a 5-year-old and review the presentation and management of this disease in the pediatric population.

2. Methods For this review, MEDLINE was used to identify English language articles over the past 30 years regarding Ludwigs angina. Additional cases referenced in these articles were also studied to identify patients 18 years of age or younger. Twenty-eight cases were identied (in addition to the case presented below), with sufcient clinical data for analysis of treatment and outcome.

3. Case history A 5-year-old male presented with a 10- to 12-h history of neck and submandibular swelling, dysphagia, and drooling. There was no history of cough, dyspnea, or stridor. There was no prior history of toothache or trauma and the child was otherwise healthy. On exam, the patient had a temperature of 38.2C, pulse of 120, and respiratory rate of 32. He was sitting comfortably without dyspnea or stridor, unable to manage his secretions as evidenced by frequent drooling. There was rm, brawny induration of the submental region extending to the angles of the mandible bilaterally, accompanied by erythema extending to each ear and below the clavicles inferiorly. The oral cavity revealed healthy dentition and non-inamed tonsils. There was oor of mouth induration with mild protrusion of the tongue (Fig. 1). Labora-

Table 1 Pediatric cases of Ludwigs angina Age (years) Outcome Length of stay (days) 5 7 12 15 5 8 25 18 18 3 6 6 8 Source Isolates Surgical drainage Tooth extracted None None None None I&D I&D None I&D None None I&D Tooth extracted I&D Articial airway Medical therapy Ref.

12 14 2 2 6 10 12 days 5 18 9 weeks 5 9 17 14

Survived Survived Survived Survived Survived Survived Survived Survived Survived Survived Survived Survived Survived Survived

1st molar 1st molar Unknown Unknown

None None None None None None Intubation None None Intubation Intubation None None Tracheostomy

FOM laceration No growth 1st molar Streptococcus Oral laceration Staphylococcus aureus 2nd molar Streptococcus mixed ora Mandible frac- Streptococcus ture 6iridans Unknown Unknown No growth Bacteroides mixed ora Unknown Anaerobes Streptococcus, Hemophilus inuenzae FOM laceration No growth Pseudomonas aeruginosa Pseudomonas aeruginosa Candida albicans 2nd molar 2nd molar

Penicillin Penicillin Oxacillin, chloramphenicol Nafcillin, penicillin Penicillin Penicillin Methicillin, cephalothin Penicillin Cephaloridine Penicillin Oxacillin, chloramphenicol Penicillin Penicillin Penicillin

[15] [15] [15] [15] [7] [7] [32] [33] [9] [16] [34] [15] [15] [15] J.C. Britt et al. / Int. J. Pediatr. Otorhinolaryngol. 52 (2000) 7987

14 19 months

Survived Death (pneumonia/sepsis) Death (obstruction) Death (pneumonia/empyema)

I&D None

None Intubation

7 10

None None

Obstructed None

4 18

Survived Survived

4 5

Unknown 1st molar

None Tooth extracted

None None

Cloxacillin, gentamicin Gentamicin, carbenicillin, ampicillin Gentamicin, carbenicillin Gentamicin, chloramphenicol, tetracycline, amphotericin Ampicillin, nafcillin Penicillin

[8] [17]

[17] [17]

[17] [35] 81

82

Table 1 (Continued) Age (years) Outcome Length of stay (days) 17 Source Isolates Surgical drainage Articial airway Medical therapy Ref. J.C. Britt et al. / Int. J. Pediatr. Otorhinolaryngol. 52 (2000) 7987

18

Survived

3rd molar

10 14

Survived Death (mediastinitis/sepsis) Survived

1st molar Mandible fracture 1st molar

Anaerobes gram None neg rods Streptococcus 6iridans, Branhamella mixed ora I&D, tooth extracted Streptococcus, I&D bacteroides I&D

None

Cloxacillin, ampi- [36] cillin

Intubation Intubation

14

Tracheostomy

17 15 9 10 5

Survived Survived Death (obstruction) Survived Survived

77 7

Hx of toothache Dental caries 1st molar 1st molar Unknown

Streptococcus No growth

I&D None None I&D I&D

Intubation None Obstructed Intubation

Penicillin, streptomycin Penicillin, metronidazole, gentamicin Penicillin, metronidazole, gentamicin, chloramphenicol, steroids Ampicillin, steroids Penicillin

[37] [10]

[18]

[38] [39] [40] [28] Case report

3 3

Streptococcus

Amp/sulbactam, dexamethasone Clindamycin, dexamethasone

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83

tory data included a white blood cell count of 20 500 with a moderate left shift. The patient had received intravenous (i.v.) antibiotics at the referring hospital and again received i.v. penicillin and dexamethasone at our institution; however, the erythema and oor of mouth induration progressed. Due to the chronicity of the childs illness, he was taken to the operating room where an endotracheal tube was placed without difculty. Direct laryngoscopy at that time revealed no epiglottic or laryngeal edema. A submental incision was made and carried down through the mylohyoid muscle, yielding no purulence. A passive drain was placed and the patient was taken to the intensive care unit intubated, where he continued to receive i.v. steroids and clindamycin. Cultures of the deep wound were obtained and eventually grew b-hemolytic group A streptococcus. The inammation rapidly resolved and on the rst post-operative day, the patient was extubated without difculty. He continued to receive i.v. antibiotics and was discharged on the third post-operative day.

4. Results

4.1. Epidemiology
Twenty-nine cases of Ludwigs angina in patients age 18 or less were analyzed (Table 1). Ages ranged from 12 days to 18 years with a mean of 9.7 years and a median of 10 years. There were 18 males and 11 females.

4.2. Pathogenesis
Information regarding possible etiologic factors was given for 26 cases (Table 2). In 14 cases, there was evidence of dental pathology, the molar teeth specically in 12 cases. Three cases were from traumatic lacerations of the oral mucosa and two cases were secondary to mandible fractures. Seven patients demonstrated no etiologic factors. Of these, all but one were under the age of 6. Five patients had underlying conditions predisposing them to severe infection, including: hereditary immune deciency, immunosuppressant therapy following bone marrow transplantation, neutropenia, diabetes mellitus, and sepsis.

4.3. Clinical e6aluation

Swelling of the neck and submandibular area, along with elevation or protrusion of the tongue were present in almost all patients. Dysphagia, trismus, and pain were common complaints as well. Only ve patients were mentioned as demonstrating respiratory compromise at the initial presentation. Fever and leukocytosis were not always commented upon; however, 23 of 24 had temperatures above 38C and 10 of 14 patients exhibited white blood cell counts above 11 800. White blood counts in two patients were normal and two patients were neutropenic.

Fig. 1. Five year old patient with Ludwigs angina. Note oor of mouth induration causing elevation of the tongue. Table 2 Aetiology of Ludwigs angina (26 patients) Source Dental caries or recent extraction Oral cavity laceration Mandible fracture Unknown c of cases 14 3 2 7

4.4. Bacteriology
Wound cultures demonstrated a predominance of streptococcus species in addition to gram negative rods, anaerobes, and mixed ora (Table 3). Blood cultures were positive in seven patients, four of which grew gram negative rods.

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Table 3 Organisms isolated from wound cultures Organism Streptococcus species Staphylococcus aureus Anaerobes Bacteroides Gram negative rods Pseudomonas aeruginosa Hemophilus inuenzae Branhamella Candida albicans Mixed No growth c of isolates 8 1 4 2 5 2 1 1 1 3 4

4.5. Management
An articial airway was used in 10 of 28 cases (airway management was not commented upon in one case); eight endotracheal intubations and two tracheotomies. Of the eight endotracheal intubations, four were required for patients undergoing general anesthesia for incision and drainage procedures and two were required for the management of respiratory distress at initial presentation. A 9-week-old was intubated initially for septic shock and soon thereafter developed Ludwigs angina of unknown etiology [16]. Intubation was employed in another young child who eventually succumbed to the complications of pneumonia and sepsis [17]. Of the two tracheotomies performed, one was used to secure a compromised airway prior to surgical decompression of the submental compartment [15]. An emergent tracheostomy was successfully accomplished in a case from the Solomon Islands, a 14-year-old suffering from airway distress on the second day of hospitalization [18]. There were two deaths from acute airway obstruction. In 16 patients the airway was managed with observation alone (Table 4). Intravenous antibiotics were used in all cases, most commonly penicillin G. Other penicillins, aminoglycosides, and chloramphenicol were also used in multiple patients. Eight cases were successfully managed with antibiotics alone, without surgery or use of an articial airway. The duration of hospitalization was noted in 22 of the successfully treated cases, ranging from 3 to 77 days with a mean of 9 days (excluding a single admission of 77 days) and a median of 7 days. Incision and drainage procedures were used in 12 cases of which eight yielded purulence. Tooth extractions were performed in four cases and on 13 occasions no surgery was performed (Table 5).

Table 4 Airway intervention for Ludwigs angina (28 patients) Intervention required Intubation For acute airway distress At the time of incision and drainage Other Tracheostomy No intervention required Death from airway obstruction c of patients 8 2 4 2 2 16 2

Table 5 Surgical intervention for Ludwigs angina (27 patients) Intervention required Incision and drainage Tooth extraction No surgery required Tracheostomy c of patients 12 4 13 2

Table 6 Complications of Ludwigs angina in children Complication Death Empyema Mediastinitis Pneumonia Sepsis Cardiac arrest Airway obstruction c of patients 5 3 2 2 2 1 2

4.6. Complications
Of the 29 cases, there were ve deaths. Reported causes of death included: airway obstruction, mediastinitis, empyema, pneumonia, and sepsis (Table 6). There was one non-fatal cardiac arrest in a patient who eventually succumbed to supparative mediastinitis.

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5. Discussion This review of Ludwigs angina in the pediatric population demonstrates a predominance of male patients as seen in other large series [14,15]. The prevalence of an odontogenic source for Ludwigs angina was noted in 54% (14/26) cases as compared to 70 90% as found in other predominantly adult series [5,6,14,15]. When a dental etiology was found, the mandibular molars were the primary offenders. The etiology was unknown in 27% (7/26) of children, compared to 9% as reported by Moreland et al. [5]. Interestingly, of the nine patients less than 9 years old, only one was identied as having an odontogenic source. This dissociation of dental caries and Ludwigs angina in children has also been noted by Kurien et al., who treated 10 patients under the age of 15 years, none of which had predisposing dental pathology [19]. The documentation of two cases of Ludwigs angina in children less than 10 weeks old, indicates the possibility of Ludwigs angina in the edentulous patient. The predominant organisms isolated from wound cultures were streptococcus species in 40% (8/20) of patients. Gram negative rods were cultured from 25% (5/20) of patients and anaerobes in four cases. Three cultures produced mixed ora and there was a single isolate of staphylococcus. In the literature, streptococcus species have been implicated in 42 91% of cases, followed by staphylococcus in up to 38% [5,13,14,20]. Less commonly noted have been anaerobes in 27% of cases and gram negative rods in 20% [5]. This prole is similar to that seen with other deep neck space infections [21]. The role of anaerobes may be under-estimated due to difculties in culturing these organisms. Of note, blood cultures were positive in seven pediatric patients, growing gram negative rods in four cases. Moreland et al. reviewed 36 cases in which blood cultures had been obtained, 12 of which were positive [5]. Airway maintenance should be the primary concern in Ludwigs angina, although controversy exists regarding the method of airway protection. Presenting two series of patients in the

1940s, Williams advocated prophylactic exposure of the trachea, leaving the neck packed open to facilitate cannulation in the event of acute obstruction [13,20]. Morelands review showed that tracheotomy was performed in 42% of 120 patients [5]. In a series of 15 patients presented by Har-El et al., 11 required tracheostomy, four as an emergent intervention [21]. These authors proposed that tracheotomy was indicated for all cases of Ludwigs angina. Other authors recommend close observation and airway intervention only for cases of threatening obstruction or for patients requiring incision and drainage under anesthesia. Patterson et al. [15] and Holland [22] have advocated tracheotomy under local anesthesia for such instances. Conversely, Allen et al. [23] and Schwartz et al. [24] have advocated intubation. Our analysis of pediatric patients reects the trend toward airway observation and use of intubation rather than tracheostomy. Sixteen of 28 patients were managed with no articial airway and only two tracheotomies were performed. The cornerstone of medical management is antibiotic agents active against streptococcus, staphylococcus, and anaerobic species. Penicillin has been commonly used; however, various combinations of penicillins, aminoglycosides, chloramphenicol, and metronidizole have been employed. Steroid therapy has been suggested as an adjunct to halt the progression of edema and prevent the need for an articial airway [19,25]. Steroids were used in only four of the reviewed cases, three of which received an articial airway at some point in their care. In two cases, patients were subsequently intubated prior to general anesthesia for surgical decompression, and in another case steroids were employed to reduce edema following tracheotomy. While there may be merit in the use of steroids for Ludwigs angina, there is limited experience reported in the literature. Incision and drainage procedures were once recommended in all cases of Ludwigs angina [13,20]. Many authors now agree that with prompt initiation of antibiotics, surgical intervention can be reserved for infections that persist or progress despite optimal medical therapy

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or cases presenting with evidence of localized abscess [15,22]. Morelands review of 138 patients found a 65% incidence of drainage procedures [5]. Patterson et al. used surgical drainage in 45% of their 20 cases [15]. Similarly, the pediatric patients in our review show a slightly more conservative approach with 44% (12/27) of patients undergoing surgical decompression. In this series of pediatric patients, the mean hospital stay was 16.9 days (9.4 days, excluding a single 77 day admission) for those undergoing incision and drainage. This compares with a mean stay of 8.6 days as seen in patients not undergoing surgery. The benets of surgical intervention in the absence of abscess formation have not been demonstrated conclusively. Ludwigs angina has long been considered a process without purulence. In the pre-antibiotic period, surgical decompression was often performed as initial therapy, although this rarely produced purulent drainage [3,5,13]. Ludwigs angina will often resolve with antibiotic therapy alone; however, some cases prove to be resistant as cellulitis organizes into abscess, necessitating surgery. Patterson et al. performed incision and drainage in three patients at initial presentation, none of which yielded pus [15]. In six patients that failed to respond to antibiotics (at least 36 h of therapy), drainage was performed, nding pus in four patients. The incidence of purulence seen in our review of pediatric patients, eight of 11 cases, is most likely the result of selective surgical intervention in cases demonstrating uctuance at presentation or developing an abscess after the initiation of antibiotics. Computed tomography can evaluate for the presence of an abscess if not clinically obvious, although this was seldom mentioned in the reviewed literature. Surgical techniques for surgical decompression include intraoral and external approaches to the submandibular space and have been elaborated upon in other publications [26,27]. The overall mortality rate for the cases reviewed was 17% (5/29 patients). Of the ve pediatric deaths reported, three were in immunocompromised patients. One of these patients, a 7-year-old following bone marrow transplant, succumbed to acute airway obstruction.

The other fatal airway event occurred in a 9-yearold that presented to the emergency department in extremis after 4 days of progressive submental edema [28]. The other deaths resulted from infectious complications of Ludwigs angina. Overall, signicant predisposing illnesses existed in ve patients, the three immunocompromised patients mentioned above, one poorly controlled diabetic, and a 9-week-old infant who was intubated because of sepsis and 24 h later developed Ludwigs angina. Complications of Ludwigs angina cited in the literature include: sepsis, pneumonia, asphyxia, empyema [29], pericarditis [29], mediastinitis [30], and pneumothorax [31].

6. Conclusion Ludwigs angina can present in the pediatric age group, carrying the potential for lethal complications, especially in the immunocompromised patient. However, with attention to airway maintenance, appropriate antibiotic therapy, and judicious surgical intervention, favorable outcomes can be expected. While an odontogenic etiology is often seen in older children, the etiology of Ludwigs angina in the very young is often obscure. In caring for the patient with Ludwigs angina, airway management is the principal concern. The airway is best managed by intubation in the operating room with preparation for possible surgical airway intervention. However, in the absence of respiratory compromise, patients can and have been managed successfully without an articial airway providing they can be observed in an intensive care setting. Penicillin remains the drug of choice although broader spectrum drugs may be indicated based on culture results and clinical progression of disease. Although incision and drainage procedures were once recommended in all cases, Ludwigs angina in the pediatric population can often be managed with medical therapy. Surgical intervention is reserved for infections forming a localized abscess collection and those unresponsive to optimal medical therapy.

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References
[1] J. Burke, Angina Ludovici: a translation, together with a biography of Wilhelm F.V. Ludwig, Bull. Hist. Med. 7 (1939) 1115 1126. [2] H.S. Muckleston, Angina Ludovici and kindred infections: a historical and clinical study, Ann. Otol. Rhinol. Laryngol. 37 (1928) 711 735. [3] M. Grodinsky, Ludwigs angina: an anatomical and clinical study with review of the literature, Surgery 5 (1939) 678696. [4] H.H. Linder, The anatomy of the fasciae of the face and neck with particular reference to the spread and treatment of intraoral infections (Ludwigs) that have progressed into adjacent fascial spaces, Ann. Surg. 204 (6) (1986) 705714. [5] L.W. Moreland, J. Corey, R. McKenzie, Ludwigs angina report of a case and review of the literature, Arch. Intern. Med. 148 (1988) 461466. [6] D.S. Sethi, R.E. Stanley, Deep neck abscesses changing trends, J. Laryngol. Otol. 108 (1994) 138143. [7] S.J. Gross, P.I. Nieburg, Ludwig angina in childhood, Am. J. Dis. Child. 131 (1977) 291292. [8] C.O. Iwu, Ludwigs angina: report of seven cases and review of current concepts in management, Br. J. Oral Maxillofac. Surg. 28 (1990) 189 193. [9] E.A. Rosen, R.H. Shulman, A.S. Shaw, Ludwigs angina: a complication of a bilateral mandibular fracture: report of a case, J. Oral Surg. 30 (1972) 196200. [10] A.F. Dreyer, S.E. de Kock, J.L.A. Rantloane, Ludwigs angina: a case report and review, J. Dent. Assoc. S. Afr. 45 (1990) 397 400. [11] G.E. Fischmann, B.S. Graham, Ludwigs angina resulting from the infection of an oral malignancy, J. Oral Maxillofac. Surg. 43 (10) (1985) 795796. [12] K. Tschiassny, Ludwigs angina; an anatomic study of the lower molar teeth in its pathogenesis, Arch. Otolaryngol. 38 (1943) 485 496. [13] A.C. Williams, Ludwigs angina, Surg. Obstet. Gynecol. 70 (1940) 140 149. [14] R.T. Hought, B.E. Fitzgerald, J.E. Latta, R.D. Zallen, Ludwigs angina: report of two cases and review of the literature from 1945 to January 1979, J. Oral Surg. 38 (1980) 849 855. [15] H.C. Patterson, J.H. Kelly, M. Strome, Ludwigs angina: an update, Laryngoscope 92 (1982) 370377. [16] P. Patamasucon, J.D. Siegel, G.H. McCracken, Streptococcal submandibular cellulitis in young infants, Pediatrics 67 (3) (1981) 378 380. [17] R.G. Barkin, S.L. Bonis, R.M. Elghammer, J.K. Todd, Ludwigs angina in children, J. Pediatr. 87 (1975) 563565. [18] C.J. Sparks, Ludwigs angina causing respiratory arrest in the Solomon Islands, Anaesth. Intensive Care 21 (4) (1993) 460 462. [19] M. Kurien, J. Mathew, A. Job, N. Zachariah, Ludwigs Angina, Clin. Otolaryngol. 22 (1997) 263265. [20] A.C. Williams, W.C. Guralnick, The diagnosis and treatment of Ludwigs angina, N. Engl. J. Med. 228 (1943) 443 450.

[21] G. Har-El, J.H. Aroesty, A. Shaha, F.E. Lucente, Changing trends in deep neck abscess, Oral Surg. Oral Med. Oral Pathol. 77 (1994) 446 450. [22] C.S. Holland, The management of Ludwigs angina, J. Oral Surg. 13 (1975) 153 159. [23] D. Allen, T.E. Loughnan, R.A. Ord, A re-evaluation of the role of tracheostomy in Ludwigs angina, J. Oral Maxillofac. Surg. 43 (6) (1985) 436 439. [24] H.C. Schwartz, R.A. Bauer, N.J. Davis, Ludwigs angina: use of beroptic laryngoscopy to avoid tracheostomy, J. Oral Surg. 32 (8) (1974) 608 611. [25] I.L. Hutchinson, D.R. James, New treatment for Ludwigs angina [letter], Br. J. Maxillofac. Surg. 27 (1) (1989) 83 84. [26] H.H. Weisengreen, Ludwigs angina: historical review and reections, Ear Nose Throat J. 65 (1986) 457 461. [27] G.W. Lewitt, Cervical fascia and deep neck infections, Otolaryngol. Clin. North Am. 9 (1976) 703 716. [28] R.F. Busch, D. Shah, Ludwigs angina: Improved treatment, Otolaryngol. Head Neck Surg. 117 (1997) S172 S175. [29] H.R. Strauss, D.M. Tilghman, J. Hankins, Ludwigs angina, empyema, pulmonary inltration, and pericarditis secondary to extraction of a tooth, J. Oral Surg. 38 (1980) 223 229. [30] L. Cordero, W. Torre, D. Freire, Descending necrotizing mediastinitis and respiratory distress syndrome treated by aggressive surgical treatment, J. Cardiovasc. Surg. 37 (1996) 87 88. [31] J.G. Barsamian, R.B. Scheffer, Spontaneous pneumothorax: an unusual occurrence in a patient with Ludwigs angina, J. Oral Maxillofac. Surg. 45 (2) (1987) 161 168. [32] P.F. Steinhauer, Ludwigs angina: report of a case in a 12 day old boy, J. Oral Surg. 25 (1967) 251 254. [33] N.J. Schuman, B.M. Owens, Ludwigs angina following dental treatment of a ve-year-old male patient: report of a case, J. Clin. Pediatr. Dent. 16 (4) (1992) 263 265. [34] K.N. Shaw, G.S. Marshall, L.W.C. Tom, S.J. Kovacs, Ludwigs angina caused by Haemophilus inuenza type b, Pediatr. Infect. Dis. J. 7 (3) (1988) 203 205. [35] L. Nelson, J. Elfman, A. Cohen, Management of Ludwigs angina in a patient with severe hemophilia A with factor VIII inhibitors: report of a case, ASDC J. Dent. Child. 52 (4) (1985) 306 311. [36] B.D. Whitley, Ludwigs angina: a rare case of dental origin, N. Z. Dent. J. 82 (368) (1986) 48 50. [37] K.G. Ghorpade, Ludwigs angina a case report, J. Indian Dent. Assoc. 51 (1979) 57 58. [38] X. van der Brempt, G. Derue, F. Severin, L. Colin, J.P. Gilbeau, F. Heller, Ludwigs angina and mediastinitis due to Streptococcus milleri: usefulness of computed tomography, Eur. Respir. J. 3 (6) (1990) 728 731. [39] P.C. Briggs, Submandibular duct stenosis as a complication of Ludwigs angina, Oral Surg. Oral Med. Oral Pathol. 47 (1) (1979) 14 15. [40] M.H. Goldberg, R.G. Topazian, Odontogenic infections and deep fascial space infections of dental origin, in: R.G. Topazian, M.H. Goldberg (Eds.), Oral and Maxillofacial Infections, 3rd edn, Saunders, Philadelphia, PA, 1994, pp. 198 250.