Vol. 10 •Issue 4 • Page 77
Ludwig’s Angina:
A Compelling Reason to Check Your Patients’ Oral Hygiene
A 75-year-old woman presents to our clinic with complaints of left facial and jaw swelling that began 24 hours ago. Her family dentist had prescribed cephalexin (Keflex) 500 mg orally q.i.d. for a possible tooth abscess. Today she noticed increased swelling and redness of her left lower jaw that had spread to include a small area to the right of the midline of her throat. She has noticed more difficulty with swallowing and an increase in pain when swallowing. She can manage her own saliva, however.
The patient’s past medical history is significant for dyslipidemias, which is being treated with atorvastatin (Lipitor). She has type 2 diabetes, which is controlled with diet. Her only allergy is to penicillin. The examination reveals left mandibular swelling with left upper cervical lymphadenopathy, along with edema of the tissues surrounding the #20 left lower molar. The mouth and oropharynx show evidence of poor dental hygiene with numerous dental caries. No obvious abscess is visible. The tongue remains midline.
There is no apparent sublingual edema. Erythema and edema exist from the left jaw line to the third rib, crossing the midline. The area is firm and tender to the touch. Her lungs are clear and there is no evidence of respiratory difficulty. Lateral neck films are negative. The white blood count is within normal limits, but the sedimentation rate is 46.
We admit the patient to the hospital for intravenous antibiotic treatment with clindamycin (Cleocin) and an ENT consult. The diagnosis is Ludwig’s angina. Over the course of the next few days, her condition improves and she is discharged and instructed to continue oral clindamycin 300 mg q.i.d. and to follow up with her primary care provider in 3 to 4 days. Her sedimentation rate upon discharge is 26.
Background
Ludwig’s angina is a rapidly spreading cellulitis of the submandibular space that affects the submaxillary and sublingual spaces. The sublingual space contains the submental area, which lies between the anterior bellies of the digastric muscles. The submaxillary space lies below the mylohoid muscle, and the sublingual space is above it, but below the tongue. Both spaces communicate with each other via the space between the mylohoid and geniohyoid muscles.1-3
The spread of infection is contained anteriorly by the mandible and inferiorly by the mylohoid. Because of this, infection spreads in a superior and posterior fashion, which elevates the loose soft tissues of the floor of the mouth and roof of the tongue. The hyoid also restricts the spread of infection inferiorly, which allows spreading to the anterior neck soft tissues, distorting the skin anterior to the larynx.4,5 Orodental disease, particularly of the second and third lower molars (whose roots extend inferior to the attachment of the mylohoid muscle to the body of the mandible) frequently precedes Ludwig’s angina (see illustration).1-3
Clinical Presentation
The symptoms of Ludwig’s angina are related to the site of the infection. If the infection is above the firm, unyielding mylohoid muscles, the edema displaces the tongue upward and posteriorly. The floor of the mouth is tender and edematous with a board-like induration. Trismus may be marked. Involvement of the submandibular spaces produces a tense, brawny supra-hyoid swelling of the neck and submental areas. The infection may travel to the lateral pharyngeal and retropharyngeal spaces downward to the mediastinum.1-3
Progression of soft tissue swelling results in restricted neck motion, trismus, dysphonia, odynophagia, dysphagia, drooling and displacement of the tongue posteriorly and cephalad. Generally there is no palpable fluctuance. Stridor with respiratory compromise progressing to acute airway obstruction and asphyxia can occur. The infection may dissect along head and neck fascial planes, resulting in mediastinitis. Other complications include aspiration, thrombophlebitis of the jugular vein, carotid artery rupture, metastatic abscesses and tongue necrosis.3
Microbiology
By the time the average American reaches adulthood, he has lost the integrity of 10 to 17 permanent teeth to decay or fillings. About half of all adults have gingivitis and 80% have some degree of periodonitis, leading to destruction of the bone supporting teeth. Alcohol, tobacco, poor diet and some medications, as well as co-existing medical illnesses such as diabetes and HIV, can increase the risk of dental infection.6 In 86% of patients with dental infection, the assault originates from a dental cause.3,7 The remaining cases are caused by sources such as trauma, tooth extraction, mandibular fracture or salivary calculi (sialoadenitis).3,7 Streptococci and mouth flora are the most common etiologic agents, but H. influenzae, Staphylococci and gram-negative bacilli have been implicated and thus initial broad-spectrum antibiotics are needed.3,7 A 10% mortality rate is associated with undiagnosed and untreated Ludwig’s angina infection.
Management
Attempts at direct visualization of the laryngeal structures may result in laryngospasm, so radiographs or CT scans are the diagnostic modalities of choice. An image of the lateral soft tissue of the neck in an affected patient may demonstrate airway narrowing, soft tissue swelling or air in the soft tissues.3
Treatment of Ludwig’s angina requires admission to the hospital for administration of analgesics and broad-spectrum intravenous antibiotics. The airway must be protected, since obstruction can progress within hours. Possible surgical drainage to relieve pressure on surrounding structures is sometimes necessary. High-dose penicillin is the drug of choice when there is no allergy. Clindamycin is the alternative, and aminoglycosides (gentamicin, torbramycin) can be added to treat suspected resistant organisms.3
Prevention
All patients should visit a dental care provider on a regular basis. Daily oral hygiene that includes brushing the teeth with fluoride-containing toothpaste and flossing is essential to good overall dental health.6 Reduced exposure of the teeth to certain dietary carbohydrates, especially refined sugars and carbohydrates that adhere to the teeth, may lower the risk of developing caries.6
When examining the oral cavity, be alert for obvious signs of untreated tooth decay or mottling, inflamed or cyanotic gingiva, loose teeth and severe halitosis.6 Appropriate referral and follow-up for any potential suspicious findings can prevent the life-threatening complications of Ludwig’s angina. Include regular counseling about oral hygiene in each patient encounter.
References
1. Hirschmann J. Localized infections and abscesses. In Harrison’s Principles of Internal Medicine. 12th Ed. New York: McGraw-Hill;1991:515-516.
2. Ballenger J, Snow J. Otorhinolaryngology: Head and Neck Surgery. 15th Ed. Philadelphia, Pa.: Williams and Wilkins; 1996: 223-224.
3. Peacock WF. Otolaryngologic emergencies. In: Emergency Medicine. 4th Ed. New York: McGraw-Hill; 1996: 1079-1080.
4. Tierney L. Current Medical Diagnosis and Treatment. 38th Ed. Stamford, Conn.: Appleton and Lange; 1999: 243.
5. Kurien M, Mathew J. Ludwig’s angina. Clinical Otolaryngology. 1997;22(3):263-265.
6. U.S. Preventive Services Task Force. Clinical Preventive Services. 2nd Ed. Baltimore, Md.: Williams and Wilkins; 1996: 711-718.
7. Simon H. Bacterial infections of the upper respiratory tract. Scientific American. 2000:XIX(8):7.
Diane Smith is a master’s-prepared nurse practitioner at the Community Outreach Health Clinic in Menomonee Falls, Wis. She is also a member of the clinical faculty at the University of Wisconsin in Milwaukee.
