Case Report

A.n atypical pathway of infection in an adolescentw th a deep neck space abscessRobyn R. Loewen, DDS Stephen F. Conley, MD, MS A. Charles Post, DDS

D eep neck space infections are a potential com-plication of odontogenic infection, but rarelyhave been reported in children. In a recent

study, 113 pediatric patients were hospitalized withmaxillofacial infections with 32 from dental sources;however, the extension of these infections into deepneck spaces was not documented.1 In a similar study of67 children with abscess of the head and neck, only 15cases were determined to have submandibular, lateralpharyngeal, or retropharyngeal space involvement, andonly nine were attributed to dental infection.2 Lateralpharyngeal space infections are more commonlyodontogenic in adults; in contrast, the likely predispos-ing factors in children are nasopharyngitis oradenoiditis.3 Eight pediatric patients with lateral pha-ryngeal space infections were identified by Broughton,4

but no etiological determinations were given.Early diagnosis and treatment of lateral pharyngeal

infections are essential because further progression ofinfection can be rapid. Severe trismus, limiting directexamination of the oropharyngeal region, often com-plicates clinical evaluation. In addition, the limited valueof conventional roentgenograms in locating the in-volved deep neck spaces makes definitive diagnosisdifficult. This case report describes a 14-year-old Afri-can-American female who developed a left peritonsillarand lateral pharyngeal abscess from an odontogenicsource. She was managed successfully with appropri-ate antibiotics and surgical intervention after diagno-sis using computerized tomography (CT).

Case report

A previously healthy 14-year-old African-Ameri-can female reported onset of dental pain in the leftmandibular quadrant in 1992. Two weeks later, thedental pain was accompanied by left cheek swelling,dysphagia, odynophagia, and decreased oral intake.Her pediatrician recommended dental treatment forthe offending tooth, but the family refused because ofthe patient’s fear of needles. The patient received intra-muscular penicillin and an oral aminopenicillin. Two

days later she came to Children’s Hospital of Wiscon-sin emergency department with a progression of symp-toms and painful left neck swelling.

Upon initial examination, the patient had a tem-perature of 38.7°C (101.6°F) without evidence of air-way distress. The oral cavity exam was limited by se-vere trismus, allowing only a 1-cm opening. Themandibular left permanent second molar had exten-sive decay with tenderness to percussion. No swellingor tenderness was present in either the floor of themouth or in the buccal vestibule. The left tonsil wasmedially displaced. Externally, a 3-cmodiameter areaof induration was present at the angle of the mandiblewith extension to the left jugulodigastric area. The whiteblood cell count was 18,200 with a leukocytosis. Alateral neck film indicated a good airway withoutretropharyngeal soft tissue swelling.

The patient was admitted to the otolaryngology ser-vice and intravenous clindamycin was initiated. A neckCT obtained I day after admission indicated soft tissueswelling of the left peritonsillar and lateral pharyngealspaces without evidence of abscess formation. A pan-oramic radiograph confirmed extensive decay of themandibular left permanent second molar withperiapical radiolucencies consistent with an acuteperiapical-alveolar abscess. The joint services deferredtooth extraction until the deep neck cellulitis andtrismus had resolved.

After 48 hr of parenteral antibiotic therapy, the physi-cal findings remained unchanged and a low-grade fe-ver of 38.4°C (101.1~F) persisted with nocturnal tem-perature spikes to 39.5 °C (103.1 °F). Induration becamemore localized at the left angle of the mandible and thesubmandibular area. Persistent unchanged trismus pre-cluded a detailed oral exam. Although the involvedtooth remained sensitive to manipulation, there wereno associated gingival changes. A repeat neck CT scanwas obtained to assess lack of clinical response. A largeleft lateral pharyngeal and peritonsillar abscess wasidentified with a tract originating from the posteriorand inferior left mandibular border (Figs I & 2).

220 American Academy of Pediatric Dentistry Pediatric Dentistry - 17:3,1995

Fig 1. CT demonstrating sinus tract (arrow)from posteroinferior mandibular margin tolateral pharyngeal space abscess.

Fig 2. CT illustrating abscess (arrow) oflateral pharyngeal and tonsillar spaceswith connection.

The patient had a quinsy tonsillectomy and extrac-tion of the mandibular left permanent second molarunder general anesthesia. No other treatment was per-formed. A bilobed abscess cavity involving theperitonsillar space with extension into the lateral pha-ryngeal space was confirmed intraoperatively. Culturesgrew Bacteroides melaninogenicus. Close inspection ofthe alveolar socket failed to identify a sinus tract. Ex-amination of the remaining dentition revealed minorcaries on both maxillary second permanent molars andthe mandibular right second permanent molar. Thepatient had an uneventful recovery, was discharged onthe third postoperative day of a 10-day course of oralclindamycin, and had no postoperative sequelae. Shewas referred to her private dentist for restoration of theother carious teeth.

DiscussionOdontogenic infections tend to spread to soft tis-

sues via planes of least resistance to adjacent potentialspaces and must perforate bone before spreading tothe deeper fascial spaces. The most common neck spacesinvolved in mandibular odontogenic infection includethe submandibular, masseteric, and sublingual.5 In theyoung child, the primary root apices are located super-ficially and anteriorly within the mandible and usuallydrain to the buccal aspect of the alveolus intraorally.The permanent first and second molar apices lie deeperand more posteriorly in the mandible and drainage ismore complex. Since the lingual bone of the posteriormandible is thinnest in relation to molar apices, infec-tions of the first and second permanent molars tend todrain lingually. The first molar has apices which arelocated superior to the mylohyoid muscle attachment,

and therefore drain to thesublingual space. The sec-ond and third molar api-ces are below the mylo-hyoid attachment andtypically drain to the sub-mandibular space without sublingual involve-ment. Therefore, thespread of infection to deepneck spaces through thesubmandibular spacemust be anticipated in theteenager.6 A lateral pha-ryngeal space infectioncan occur by extension ofthe infection from the in-ternal compartment of themasseteric space or,rarely, from the subman-dibular space.7

The lateral pharyngealspace (parapharyngealspace, pharyngomaxillary

space) is cone-shaped, with its base at the skull baseand its apex at the greater cornu of the hyoid. Thestyloid process and its muscles divide the lateral pha-ryngeal space into two compartments: 1) an anterior(prestyloid) space containing connective tissue,muscles, and lymph nodes, and 2) a posterior(retrostyloid) space containing the great vessels andnerves of the neck.7'9 An abscess of the anterior com-partment results in trismus from irritation of the inter-nal pterygoid muscle, medial deviation of the lateralpharyngeal wall, dysphagia, torticollis, swelling overthe parotid gland, and possible neck swelling with lossof the space behind the mandibular angle. An abscessof the posterior compartment has no trismus or tonsil-lar prolapse, but rather parotid swelling and medialdeviation of the posterior lateral pharyngeal wall.8 Res-piratory distress can ensue with significant lateral pha-ryngeal wall swelling.

The peritonsillar space is a potential space definedmedially by the fibrous capsule of the palatine tonsiland laterally by the superior constrictor muscle. Break-down of the tonsillar capsule during tonsillitis is theclassic source of infection of this space. Purulentmaterial in the midportion of the peritonsillar spaceappears to be prone to penetrate the superior constric-tor muscle and enter the lateral pharyngeal space.Trismus occurs from reflex irritation of the adjacentmuscles of mastication.10

Prompt and accurate diagnosis and treatment ofdeep neck space infections are crucial. The classic symp-toms of neck abscesses rarely are present today be-cause oral antibiotics can modify symptoms. Thus thedifferentiation of diffuse cellulitis from a distinct ab-scess cavity is complicated. In addition, the progres-

Pediatric Dentistry -17:3,1995 American Academy ofPediatric Dentistry 221

sion of infection may be difficult to ascertain clinicallydue to significant local edema and trismus. The atypi-cal aspect of this case was the direct involvement of theanterior compartment of the lateral pharyngeal spacevia a sinus tract in the mandible rather than the moretypical intervening masseteric space infection.

The limitations of conventional roentgenograms canhinder prompt diagnosis of head and neck-space infec-tions. CT has been used extensively to identify andmanage various maxillofacial pathoses.11-15 The diag-nostic value of CT for head and neck infection includeevaluating the degree of displacement of para-pharyngeal soft tissues, differentiating betweencellulitis and abscess formation, and locating an ab-scess anatomically25 An abscess on a CT scan can becharacterized by single or multiple loculations; lowdensity air and/or fluid at the center of the abscess;contrast enhancement of the abscess wall; and tissueedema surrounding the wall and anatomic boundariesthat correspond to known fascial planes22 In this case,the atypical direct path of infection to the lateral pha-ryngeal space could not have been detected with con-ventional roentgenograms. Incorporating a CT allowedprompt determination of abscess formation and delin-eated the abscess location to facilitate drainage.

Serious complications may develop from a lateralpharyngeal space infection. Contiguous spread to theretropharyngeal space is ominous, often seriously com-promising the airway and progressing to mediastinitisdue to its inferior communication with the posteriormediastinum. Along with septicemia, other complica-tions of deep neck space infection include jugularthrombosis, hemorrhage of the great vessels, laryngealedema, osteomyelitis of the mandible, pneumonia, va-gal nerve involvement, meningitis, parotid abscess, andaspiration of purulent material following spontaneousrupture of the abscess,g,16

Management of a lateral pharyngeal space infectionof odontogenic origin must be prompt and accurate,with removal of the odontogenic infection nidus andparenteral antibiotic therapy. In cases of diffuse cellulitiswithout localization, parenteral antibiotics alone oftenare curative27 Surgical intervention is advised if noimprovement is seen after 48-72 hr of parenteral anti-biotic therapy. Exploration and drainage of the abscessand removal of the offending tooth should then beaccomplished at the same time. In one recent study,more than 50% of children with deep neck infectionsdid not require surgical drainage.4 The eight nonsurgi-cal patients in this study became afebrile in a mean of3.8 days (range 1-7 days) after instituting antibiotictherapy. The author’s recommended therapy paradigmutilizes neck CT for differentiation of cellulitis fromabscess and the presence or absence of respiratory dis-tress to determine the need for early surgical incisionand drainage.

The microbiology of deep space neck infections con-tinues to evolve. In 1983, Streptococci (61%) and Staphy-

lococcus species (32%) comprised the majority of purecultures in maxillofacial infections28 More recently,Brook2 found that the most common isolates in pediat-ric head and neck infections are Staphylococcus aureus(aerobic) and Bacteroides species. In patients with den-tal infections as the predisposing factor, anaerobic iso-lates either as pure cultures or in a mixed flora pre-dominate. This is consistent with the observation thatanaerobic bacteria outnumber aerobic species in theoral cavity by 10 to one.19

Greater resistance of bacteria to antibiotics, especiallypenicillin, has been another trend. Recent findings couldpreclude penicillin as an automatic choice in head andneck infections. Beta-lactamase-producing organismscan survive penicillin therapy and may even protectpenicillin-susceptible organisms by enzymatic releasewithin the abscess. Brook2 found beta-lactamase activ-ity in 46% of head and neck infections in children. Halulaet al. 2° also described specific mechanisms for the trans-fer of clindamycin resistance in Bacteroides species.

Penicillin and clindamycin have been shown to pro-duce similarly good results in treating odontogenicinfections when the rate of penicillin resistance amongoral anaerobic bacteria is relatively low. Penicillin isfelt by some authors to still be the antibiotic of choicefor maxillofacial infections of odontogenic origin. 1, 21Clindamycin is indicated in cases of penicillin allergy,recent exposure to penicillin, failure of an infection torespond to penicillin therapy, or in cases where theknown pathogen is Bacteroides fragilis.21

Dr. Loewen is a pediatric dental resident, Department of PediatricDentistry, Children’s Hospital of Wisconsin, Milwaukee; Dr.Conley is assistant professor, departments of otolaryngology -human communication and pediatrics, Medical College of Wis-consin, Milwaukee; and Dr. Post is director, Department of Pedi-atric Dentistry, Children’s Hospital of Wisconsin, Milwaukee.

1. Dodson TB, Perrott DH, Kaban LB: Pediatric maxillofacialinfections: a retrospective study of 113 patients. J OralMaxillofac Surg 47:327-30, 1989.

2. Brook I: Microbiology of abscesses of the head and neck inchildren. Ann Otol Rhinol Laryngol 96:429-33, 1987.

3. Dzyak WR, Zide MF: Diagnosis and treatment of lateralpharyngeal space infections. J Oral Maxillofac Surg 42:243-9, 1984.

4. Broughton RA: Nonsurgical management of deep neck in-fections in children. Pediatr Infect Dis 11:14-8, 1992.

5. Chow AW, Roser SM, Brady FA: Orofacial odontogenicinfections. Ann Intern Med 88:392-402, 1978.

6. Megran DW, Scheifele DW, Chow AW: Odontogenic infec-tions. Pediatr Infect Dis 3:257-65, 1984.

7. Paonessa DF, Goldstein JC: Anatomy and physiology ofhead and neck infections (with emphasis on the fascia of theface and neck). Otolaryngol Clin North Am 9:561-80, 1976.

8. HoraJF: Deep neck infections. Arch Otolaryngo177:129-36,1963.

9. Rabuzzi DD, Johnson JT: Diagnosis and Management ofDeep Neck Infections. American Academy ofOtolaryngology, Washington, DC, 1978.

10. Brandow EC Jr: Immediate tonsillectomy for peritonsillarabscess. Trans Amer Acad Opthalmol Otolaryngol 77:412-16, 1973.

222 American Academy of Pediatric Dentistry Pediatric Dentistry - 17:3, 1995

11. Murphy JB, Ilacqua J, Bianchi M: Diagnosis of acute maxil-lofacial infections: the role of computerized tomography.Oral Surg Oral Med Oral Pathol 60:154-57, 1985.

12. Holt GR, McManus K, Newman RK, Potter JL, Tinsley PP:Computed tomography in the diagnosis of deep neck infec-tions. Arch Otolaryngol 108:693-96, 1982.

13. Hall MB, Arteaga DM, Mancuso A: Use of computedtomography in the localization of head-and-neck-space in-fections. J Oral Maxillofac Surg 43:978-80,1985.

14. Schwimmer AM, Roth SE, Morrison SN: The use of comput-erized tomography in the diagnosis and management oftemporal and infratemporal space abscesses. Oral Surg OralMed Oral Pathol 66:17-20,1988.

15. Endicott JN, Nelson RJ, Saraceno CA: Diagnosis and man-agement decisions in infections of the deep fascial spaces ofthe head and neck utilizing computerized tomography.Laryngoscope 92:630-33, 1982.

16. Beck AL: Deep neck infection. Ann Otol Rhinol Laryngol56:439, 722, 1947.

17. Beck AL: The influence of the chemotherapeutic and antibi-otic drugs on the incidence and course of deep neck infec-tion. Ann Otol Rhin & Laryngol 61:515-32, 1952.

18. Hunt DE, Meyer RA: Continued evolution of the microbiol-ogy of oral infections. J Am Dent Assoc 107:52-54,1983.

19. Socransky SS, Manganiello SD: The oral microbiota of manfrom birth to senility. J Periodontol 42:485-96, 1971.

20. Halula M, Macrina FL: Tn5030: a conjugative transposonconferring clindamycin resistance in Bacteroides species. RevInfect Dis 12(suppl. 2):S235-42,1990.

21. Gilmore WC, Jacobus NV, Gorbach SL, Doku HC, Tally FP:A prospective double-blind evaluation of penicillin versusclindamycin in the treatment of odontogenic infections. JOral Maxillofac Surg 46:1065-70, 1988.

M. MICHAEL. COHEN, SR., DMD, 19O5-1994

His legacy was pediatric stomatologyDr. M. Michael Cohen, Sr., an

internationally renowned clini-cian, researcher, and teacher inpediatric stomatology, was bornin Boston in 1905 and died inCambridge, Mass., on October17, 1994. He graduated fromTufts in 1928, practiced dentistryin Boston and Brookline, and wasaffiliated with Beth Israel Hospi-

M. Michael tal, Boston Floating Hospital,Cohen, Sr. New England Center Hospital,Children's Hospital Medical Center, Eunice KennedyShriver Center, and Lakeville Hospital.

Most of Dr. Cohen's academic career was at TuftsUniversity School of Dental Medicine. After his re-tirement from Tufts in 1971, he joined the faculty ofHarvard School of Dental Medicine, where in 1978the Michael Cohen, Sr. Teaching and Research Fundwas established to help support the departments ofpediatric dentistry and oral medicine and oral pathol-ogy. He was the 1982 recipient of the American Soci-ety of Dentistry for Children's Award of Excellence.

Dr. Cohen was the first dentist in the U.S. to holdprofessorial rank in a pediatrics department in a medi-cal school (Tufts University) and the first in the U.S.to be appointed stomatologist at a pediatric hospital(Boston Floating Hospital). Together with Dr. ManuelAlbum, he was instrumental in establishing the Acad-emy of Dentistry for the Handicapped (now the Acad-emy of Dentistry for Persons with Disabilities).

He was also instrumental in establishing the Mas-sachusetts Cerebral Palsy Association and was its firstPresident. He was a member of the MassachusettsCommittee on Childhood and Youth and a Consult-

ant in Dentistry for Children to the U.S. Public HealthService. He served as President of the Brookline Com-munity Council and presided over a wide range ofactivities during the 1950s. He was a member ofnumerous organizations, including the InternationalAssociation for Dental Research, Society for Researchfor Child Development, American Diabetic Associa-tion, New York Academy of Sciences, and the RoyalSociety of Health (UK). He was a Diplomate of theAmerican Board of Pedodontics and held Fellowshipin the American Public Health Association and Amer-ican Association for the Advancement of Science.

His first book, Pediatric Dentistry, went throughtwo editions in 1957 and 1961. The first edition wastranslated into Spanish. His second book, MinorTooth Movement in the Growing Child* appeared in1977 and was translated into Italian, Portuguese,and Japanese.

Dr. Cohen's academic legacy was pediatricstomatology. He was the first dentist to look at themouth as a window of pediatric disease and lecturedwidely on the subject. Early papers dealt with juve-nile diabetes, ectodermal dysplasia, the oral manifes-tations of erythroblastic anemia, dental developmentin pituitary dwarfism, dental age in the adreno-genital syndrome, the dentition in congenital syphilisand rubella syndrome, and various aspects of trisomy21 syndrome. For years, he taught oral manifesta-tions of systemic disease to pediatrics house staff anddental students.

Dr. M. Michael Cohen, Sr. was truly a man for allseasons who reached out to help others. His academiclegacy lives on in the endeavors of his students and thememories of the many people he influenced. He willbe greatly missed by all those whose lives he touched.

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