Paramandibular Abscess

July 1, 2007

A 22-year-old man complained of jaw pain, sore throat, and dysphagia to solids and liquids. A month earlier, he presented to another hospital with similar symptoms; an infection of the lower right third molar (tooth no. 32) was diagnosed, and oral penicillin and hydrocodone were prescribed. He finished the course of the antibiotic but failed to follow up with a dentist.

Figure 1 – A radiograph of the teeth shows an area of hypolucency suggestive of an abscess that surrounds the root of the right third molar of the mandible (tooth no. 32).

Figure 2 – A CT scan of soft tissues of the neck and mandible reveals a paramandibular abscess (black arrow) with osseous erosion of the mandible in the region of the right third molar (tooth no. 32). Other findings include a surrounding inflammatory change exerting mass effect on the oropharynx and a gas collection in the subcutaneous fat superficial to the necrotic tooth and anterior to the masseter muscle with a small gas-fluid level, which suggests a second abscess (white arrow). 

A 22-year-old man complained of jaw pain, sore throat, and dysphagia to solids and liquids. A month earlier, he presented to another hospital with similar symptoms; an infection of the lower right third molar (tooth no. 32) was diagnosed, and oral penicillin and hydrocodone were prescribed. He finished the course of the antibiotic but failed to follow up with a dentist.

The patient had no other significant medical history. He drank alcohol on occasion and smoked both marijuana and cigarettes. He denied any allergies to medications.

Temperature was 38.1°C (100.6°F); heart rate, 95 beats per minute; respiration rate, 20 breaths per minute; and blood pressure, 143/67 mm Hg. The patient reported the pain as 5 on a scale of 1 to 10. He was able to speak without hoarseness or drooling. He had halitosis. There was no facial or jaw swelling. Inspection of the pharynx, tonsils, molars, and soft palate was difficult because he could not fully open his mouth or protrude his tongue. The sublingual space was swollen. Tenderness and anterior cervical lymphadenopathy were noted on palpation of the neck. The remainder of the physical examination findings were normal.

The white blood cell count was 15,600/µL, with 85.5% neutrophils. Blood chemistry results were normal.

Intravenous clindamycin, fluids, and morphine sulfate were started. A radiograph of the teeth showed an area of hypolucency suggestive of an abscess that surrounded the root of the right third molar of the mandible (Figure 1).

A CT scan of soft tissues of the neck and mandible revealed a paramandibular abscess with osseous erosion of the mandible in the region of the right third molar (tooth no. 32), consistent with a right-sided pterygomandibular space infection (Figure 2).

The oral maxillofacial surgery service was consulted, and the patient underwent a 1-cm incision in the right pterygoid space followed by blunt dissection. The abscess was drained, and a 3-cm Penrose drain was inserted. The necrotic tooth was removed.

The patient did well after surgery. He was discharged 24 hours later; oral antibiotics and pain medications were prescribed for outpatient therapy. Follow-up with the oral maxillofacial surgery service was scheduled, and referral to a dentist was planned.

Figure 3 – The pathways by which dental infections may travel are the (A) postzygomatic (from the canine fossa in the cuspid and bicuspid region; the pterygomaxillary fossa communicates from the rear); (B) vestibular; (C) facial; (D) submandibular; (E) sublingual; (F) palatal; (G) antral; (H) pterygomandibular; (I) parapharyngeal; and (J) submandibular.(Rose LF et al.

Consultant.

1982.

6

)

ODONTOGENIC INFECTIONS AND COMPLICATIONS

Dental caries and periodontal disease are common. Plaque bacteria that colonize the tooth surfaces are the main cause of dental caries, which are a common cause of tooth loss in young adults. Ingestion of carbohydrates promotes the production of acids by these plaque bacteria. The result is demineralization of the enamel and tooth decay.1,2

 

Periodontal disease accounts for more tooth destruction and loss in older adults than in young adults.3 As the gingiva recedes, affected persons-particularly those who are elderly-become susceptible to tooth infection. Unlike dental caries, periodontal disease is not associated with diet.4

 

The microbes involved in dental caries and periodontal disease consist of both indigenous oral flora and those found in odontogenic infections.1,2,5Streptococcus, Peptostreptococcus, and obligate, as well as facultative, anaerobes are found in healthy oral cavities. Streptococcus mutans, Streptococcus sanguis, Streptococcus mitis, and Streptococcus salivarius are pathogenic bacteria that cause dental caries.5

 

Although the tooth pulp can become infected from hematogenous spread, infection more often results from a defect in the protective enamel and dentin layer of the tooth. The infection causes inflammation within the confined space of the tooth. The subsequent swelling prohibits blood flow to the pulp, and necrosis of the pulp tissue follows.

 

The inflammatory reaction can produce pus, which accumulates within the space of the tooth and later exits into the surrounding periodontal tissue. The result is an acute periapical periodontitis.1,2,5 The pus may also erode into the alveolar space and extend into the deep fascial spaces of the neck (Figure 3).6

 

As the infection and inflammation continue through the fascial planes, it can affect the masseter and pterygoid muscles of mastication and cause trismus-a clinical sign of a suppurative masticator space infection, usually of the third molar teeth. In patients who have trismus, the associated pain radiates to the mandible.7 The pain is caused by both inflammation and spasm of the muscles of mastication. In Ludwig angina-a periodontal infection that produces submandibular cellulitis with pain, trismus, and superior and posterior tongue displacement-the submandibular swelling can become a life-threatening condition when the airway is compressed from local swelling.7

 

TREATMENT

Definitive treatment consists of surgical drainage, removal of necrotic tissue, and extraction of the offending tooth. Antibiotic therapy is required to prevent further spread and hematogenous dissemination. Many of the indigenous organisms are sensitive to penicillin. Patients who have penicillin allergy or refractory infection can be treated with clindamycin, cefoxitin, or cefotetan.1,2,5 Antibiotics with activity against anaerobes and facultative Gram-negative bacilli may be considered, especially when the infection involves the deeper spaces of the head and neck.

References:

REFERENCES:


1.

Amsterdam JT. Oral medicine. In: Marx JA, Hockberger RS, Walls RN, eds.

Rosen’s Emergency Medicine Concepts and Clinical Practice

. 5th ed. St Louis: Mosby; 2002:892-898.

2.

Beaudreau R. Oral and dental emergencies. In: Tintinalli JE, Keler GD, Stapczynski JS, eds.

Emergency Medicine: A Comprehensive Study Guide

. 5th ed. New York: McGraw-Hill; 2000:1539-1543.

3.

Greenspan JS. Oral manifestations of disease. In: Braunwald E, Fauci AS, Kaspar DL, et al, eds.

Harrison’s Principles of Internal Medicine.

15th ed. New York: McGraw-Hill; 2001:194.

4.

Martin JH, Horan NM. Eye, ear, nose, and throat health. In: Meredith PV, Horan NM, eds.

Adult Primary Care

. Philadelphia: WB Saunders Co; 2000:258t.

5.

Kasper DL. Infections due to mixed anaerobic organisms. In: Braunwald E, Fauci AS, Kasper DL, et al, eds.

Harrison’s Principles of Internal Medicine

. 15th ed. New York: McGraw-Hill; 2001:1011.

6.

Rose LF, Hendler BH, Amsterdam JT. Temporomandibular disorders and odontic infections.

Consultant.

1982;22(Dec):110-136.

7.

Flynn TR. The swollen face. Severe odontogenic infections.

Emerg Med Clin North Am.

2000;18:481-519.