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A 70-year-old man was admitted to the hospital with sudden onset of left-sided facial erythema and edema. He denied antecedent trauma to the face. Three days before, he noted a small pustule on the internal aspect of his left naris, which drained a small amount of purulent fluid. On the day of admission, he awoke at approximately 3:30 am with a mildly swollen left face. Later that same day, the swelling progressed considerably and his speech became slurred, prompting him to seek medical attention. On admission, he reported having chills, jaw pain, and facial tenderness. He denied fevers, chest pain, shortness of breath, nausea, vomiting, diarrhea, light-headedness, headaches, ear pain, eye pain, changes in vision or hearing, and any sensation of swelling in his throat. Additionally, he denied a history of cough, sinus pressure, or purulent nasal drainage. He was able to swallow his oral secretions.
Review of the medical history revealed recent giant cell arteritis (GCA), diagnosed 2.5 weeks before admission via left temporal artery biopsy. Since that time, the patient had been taking 40 mg/d of prednisone. Notably, he had had a dental abscess of a right mandibular molar (#30) drained 3.5 weeks before admission. He did not have any other recent surgeries or infections of the head or neck.
On examination, the patient was afebrile, alert, oriented, and in no acute distress, with a blood pressure of 156/78 mm Hg and a pulse rate of 92 beats/min. He had substantial, poorly demarcated swelling of the entire left side of the face, extending to the midline. The area was erythematous, edematous, and tender to palpation. No blisters, bullae, vesicles, streaking, or regional lymphadenopathy were detected. The patient preferred to keep his left eye closed but was able to open it. Conjunctivae, extraoculomotor movements, and pupils were normal. A small (4-mm), nonpurulent, ulcerated lesion in the mucosa of the patient's left naris was noted. The incision from the left temporal artery biopsy was well healed and without signs of dehiscence or infection. The oropharynx was unremarkable. No oral lesions, ulcers, glossal edema, or oropharyngeal soft tissue swelling was evident. The neck was supple. Findings on cardiac, lung, and abdominal examinations were unremarkable. No stridor, wheezes, or rales were detected. Cranial nerves II through XII were grossly intact; however, the patient mumbled as a result of the facial swelling.
Initial laboratory testing yielded the following results (reference ranges provided parenthetically): leukocytes, 19.7 × 109/L (3.5-10.5 × 109/L); neutrophils, 18.2 × 109/L (1.7-7.0 × 109/L); hemoglobin, 15.2 g/dL (13.5-17.5 g/dL); platelets, 235 × 109/L (150-450 × 109/L); serum sodium, 137 mEq/L (135-145 mEq/L); potassium, 3.4 mmol/L (3.6-4.8 mmol/L); chloride, 98 mmol/L (100-108 mmol/L); bicarbonate, 31 mEq/L (22-29 mEq/L); blood urea nitrogen, 28 mg/dL (8-24 mg/dL); and creatinine, 1.0 mg/dL (0.9-1.4 mg/dL). Computed tomography of the head demonstrated inflammatory soft tissue stranding adjacent to the left mandible and extending to the level of the left zygoma. No evidence of orbital cellulitis was found.
Sudden, unilateral facial swelling has a relatively narrow differential diagnosis but includes a few potentially life-threatening conditions. These include cervicofacial actinomycosis, necrotizing fasciitis, and Ludwig angina.9 Any oral or facial trauma should be assessed, and attention should be focused on the patient's dental history. A thorough examination of the facial skin as well as the oral cavity and nasopharynx must be performed to identify any potential portals of entry for microorganisms. Computed tomography, Panorex radiography, and ultrasonography may be useful early diagnostic tools to help detect bony abnormalities or soft tissue masses.
Cellulitis was determined to be the cause of acute, unilateral, facial swelling in this patient, after more serious conditions were ruled out. Cellulitis is an inflammatory condition of the dermis and subcutaneous tissues resulting from an invasion of microorganisms through a breach in the skin's protective barrier. Cellulitis appears as a warm, red, swollen, tender, expanding lesion with poorly demarcated, nonpalpable borders (a distinguishing feature from erysipelas) that spreads rapidly through the entire layer of the skin. Untreated, cellulitis may also lead to infection of other surrounding tissues, including the blood vessels, lymphatics, or (rarely) the deep fascial lining, causing bacteremia, ascending lymphangitis, or necrotizing fasciitis, respectively.
Although most common on the legs,11 cellulitis can occur anywhere on the body, including the face. Risk factors for developing cellulitis include old age, intravenous drug use, lymphedema, immunosuppression, and any disruption in the skin surface. Most cellulitis infections are caused by bacteria, with the most common pathogens being S aureus and group A Streptococcus. Treatment regimens are generally targeted at these bacteria, even when cultures are unrevealing. Commonly used antibiotics are cephalexin, dicloxacillin, ceftriaxone, and clindamycin; however, because of the rising incidence of MRSA infections, vancomycin must be considered in the treatment of all hospital- and community-acquired cellulitis infections that do not respond to first-line therapeutic agents. Rarely, bacteria such as Pseudomonas species, Haemophilus species, Streptococcus pneumoniae, or an enterobacterium may be the etiologic agent of a cellulitis infection.11,12 These organisms should be considered in patients who do not respond to standard empirical therapy; in such cases, antibiotic coverage should be broadened to target these organisms.
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Correct answers: 1. d, 2. b, 3. c, 4. c, 5. c.