DEMAS
AND
BRAUN
1239
5. Werber JL, Pincus RL: Oropharyngeal angioedema associated with the use of angiotensin-converting enzyme inhibitors. Otolaryngol Head Neck Surg 101:96. 1989 6. Slater EE, Merrill DD. Guess HA, et al: Clinical profile of angioedema associated with angiotensin-converting inhibition. JAMA 206:967, 1988 7. Deltino JJ. Sclaroff A. Giglio JA, et al: Management of a patient with hereditary angioneurotic edema. J Oral Surg 36:890, 1978 8. Fineman SM: Urticaria 14503. 1987
J Oral Maxlllofac
and angioedema.
Primary
Care
9. Mathews KP: Urticaria and angioedema. J Allergy Clin Immunol 72: 1, 1983 10. Singer RJ, MacGregor GA: Angioneurotic edema associated with two angiotensin-converting inhibitors. Br Med J 293: 1243. 1986 I I. Inman WH, Rawson NS: Angioedema and urticaria associated with enalapril. Br Med J 294:91. 1987 12. Nicholls MG, Maslowski AH, Hamid I, et al: Ulceration of the tongue: A complication of captopril therapy. Ann Intern Med 94:659. 1981 13. Jett GK: Captopril-induced angioedema. Ann Emerg Med 13:489. 1984
Surg
49 1239-1242.1991
Infection Associated With Orbital Subcutaneous Emphysema PETER N. DEMAS, DMD, MD,* AND THOMAS W. BRAUN, DMD, PHDt
Subcutaneous or surgical emphysema of the oral and maxillofacial region is a well documented but a relatively uncommon event. Although the sequelae are generally self-limiting and benign, serious local and systemic complications can result. Dramatic consequences attributed to the accumulated air displacing anatomic structures include loss of vision, ‘-’ pneumothorax, and pneumomediastinum.5-‘0 The risk of infection secondary to subcutaneous emphysema is often suggested, but rarely reported. ’ ’ Despite this rare incidence, infected subcutaneous emphysema of the maxillofacial region requires prompt attention. Also significant is awareness of the potential morbidity associated with emphysema confined to the periorbita. An air turbine high-speed drill with an exhaust directed toward the surgical field may force air into the subcutaneous and fascial planes of the head and neck. ‘.8.‘3.‘3 Other sources are the paranasal sinuses, which may cause emphysema secondary to
* Assistant Professor, Department of Oral and Maxillofacial Surgery, University of Pittsburgh, Pittsburgh, PA. t Chairman, Department of Oral and Maxillofacial Surgery. School of Dental Medicine, University of Pittsburgh, Pittsburgh, PA. Address correspondence and reprint requests to Dr Braun: Department of Oral and Maxillofacial Surgery, University of Pittsburgh, School of Dental Medicine. 3501 Terrace St. Pittsburgh. PA 15261.
Q 1991 American geons
Association
0278-2391/91/4911-0022$3.00/O
of Oral and Maxillofacial
Sur-
frontal, nasoethmoid, and maxillary facial trauma.‘*S,9.‘4-‘8 Fractures into the sinuses may involve the orbital walls. Reviews of these clinical and radiographic relationships are available.“-” After disruption of anatomic integrity, air can also be introduced into the tissues by nose blowing, sneezing, vomiting. and coughing.‘.’ Other reported events initiating emphysema include removal of endodontic erupted and impacted teeth, 1.8.17-.13.13.24 therapy,‘5.‘h orthognathic surgery,” positive pressure ventilation with endotrachael intubation, trachael-bronchial injury,6.9.‘3 and use of nasal cannuIas.’ Surgical emphysema causes soft-tissue swelling, often associated with crepitus. It may arise rapidly or have a delayed occurrence. Small accumulations of air are usually painless and benign. Extensive emphysema, however, may cause pain and a mass effect obstruction to respiration, cardiac function, and retinal perfusion.1-s*7.9 Radiographically, emphysema appears lucent and is described as free air or gas within the tissues.“.” Treatment is usually supportive, with the air being reabsorbed over a 2to 16day period. Surgical intervention is only necessary when respiratory or vascular compromise occurs.‘-4,7’9 Antibiotic prophylaxis is generally suggested due to possible bacterial contamination of the tissues. A differential diagnosis of rapid facial swelling includes hematoma, allergic reaction, edema, infection and surgical emphysema. Necrotizing fasciitis, in which bacterial gas production is possible. also should be considered.28,29
1240
INFECTION
WITH
ORBITAL
SUBCUTANEOUS
EMPHYSEMA
Report of a Case A 52-year-old man came to the emergency department following an altercation. He reported sustaining a single punch to his left eye. His main complaint was a 0.5 cm superficial laceration of his left lower eyelid near the infraorbital rim. Radiographic plain film findings were reported as negative. His only significant past medical history included borderline adult onset diabetes mellitis treated by diet modification. He was evaluated and treated by the emergency department physician. The laceration was repaired and he was discharged on cephalexin (Keflex, Eli Lilly, Indianapolis, IN) 250 mg every 6 hours and instructed to use iced compresses for the mild periorbital edema. The following morning he again reported to the emergency department complaining of rapidly increasing, painful swelling of his left eye which was swollen closed despite the use of iced compresses. He was evaluated by the opthalmology service, which reported the presence of left periorbital edema and erythema. mild chemosis, and subconjunctival hemorrhage. No proptosis was noted. The pupils were equally round and reactive and the extraocular muscles were intact. There was no hyphema, no lacrimal discharge, and funduscopic examination was negative. Vision was unchanged. The previously repaired lower lid laceration was intact and without drainage. The patient’s temperature was 38.O”C and his leukocyte count was elevated (13,800i~L). with 71% polymorphonuclear (PMN) leukocytes (PMN range, 54% to 62%) and 0% band neutrophils. The previous posterior-anterior, lateral, submental vertex and Water’s view facial films were again reviewed and reported as negative. There was no evidence of facial fractures or sinus opacification. The patient was admitted with a diagnosis of preseptal cellulitis and started on ampicillin-sulbactam (Unasyn, Pfizer, New York, NY) 3 g intravenously every 6 hours. Axial and coronal CT scans, along with infectious disease and oral and maxillofacial surgery consultations, were requested. The oral and maxillofacial findings concurred with those of ophthalmology. Further clinical evaluation was negative for any evidence of facial fractures. Noted during this examination, but not the prior examinations, were areas of crepitation on the left eyelids, upper cheek, and temporal region. Infraorbital sensation was normal. The patient was edentulous and there was no evidence of a source of infection or any adenopathy present. During general questioning regarding the previous events no additional information was volunteered. With specific questioning, however, the patient admitted to several episodes of left epistaxis and nose blowing after leaving the emergency department. He noted no immediate changes and continued the iced compresses as instructed. The increased swelling and erythema were present when he awakened the following day. He reported taking one dose of the prescribed antibiotic and used acetominophen for pain. Subsequently, axial and coronal CT scans showed extensive orbital emphysema and a localized area of left ethmoid opacification (Figs 1, 2). The patient’s cellulitis was attributed to posttraumatic infected emphysema of ethmoidal origin. The edema resolved slowly over the following 7 days with continued use of intravenous ampicillin-sulbactam (Unasyn) 3 g every 6 hours. At the time of discharge, the
FIGURE physema.
I.
Coronal CT scan with left facial subcutaneous
em-
erythema had resolved. Vision and extraocular muscle function were intact. The subconjunctival hemorrhage was resolving and the conjunctival chemosis had dissipated. The patient was afebrile and his leukocyte count had decreased to 9,700ipL. He was discharged on amoxicillin-potassium clavulanic acid (Augmentin) 500 mg three times per day for I week. Subsequent follow-up showed complete resolution. Discussion In this case the periorbital cellulitis was secondary to subcutaneous emphysema. The extensive emphysema resulted from a relatively minor traumatic incident. The isolated medial orbital wall fracture, without extraocular muscle entrapment, per-
FIGURE
2.
Axial CT scan with left ethmoid sinus opacification.
DEMAS
AND
1241
BRAUN
mitted air passage through the lamina papyracea of the ethmoid bone. The etiology of orbital cellulitis includes sinusitis. cutaneous infections, facial trauma, and odontogenic infections. The most common source remains sinusitis.30.3’ Orbital cellulitis is more often associated with children than adults.30.” The predominance of pediatric orbital infections is associated with sinus enlargement and maturation. The ethmoid sinuses begin as invaginations in the fetus.‘“.3’.3’ By the second year of life ethmoid pneumatization has advanced and reaches final form at about 14 years.” The sphenoid and maxillary sinuses are present at birth, while the frontal sinus begins at 5 to 7 years of age.3’.37-The classification of orbital infections as preseptal (periorbital) cellulitis, orbital cellulitis. subperiosteal abscess, orbital abscess, and cavernous sinus thrombosis has been detailed anatomically and radiographically.30.3’,“3 Although the normal sinuses are considered sterile,34-3h others have reported the presence of anermay be attributed to obes.” The disagreement study design? These reports concentrated on the maxillary rather than the ethmoid sinus. The bacteriology associated with orbital infections usually correlates with sinusitis. The most common bacteria isolated include Hemophilzrs infirenzae. Streptococcus pnrumoniae, Staphylococcus uureus, and S epidermis. and Bacteriodes species.30.31.~4.3X Occasionally E coli and Klebsiello are
reported.“’ Posttraumatic episodes are generally associated with streptococci or staphylococci, while acute respiratory causes include S pneumoniae and H in~uenzac,.3”.3’.34.38 The organisms associated with chronic sinusitis and odontogenic sources tend to be anerobic or mixed aerobic-aneroThe type of anerobic bacteria is asbit. 2V~3’~3h~3X~3y sociated with the duration of infection. This is a reflection of decreased oxygen concentration, increased carbon dioxide tension, and lower pH that occur with chronicity.” One chronic sinusitis study reported 44% of the Bacteriodes species were positive for B-lactamase. In pediatric patients H influenzae is the most common organism. This is attributed to a child’s immature immunologic development and inability to produce antibodies against the capsular antigen of H inJluenzae.‘n~3’.34 Also in children, Branhamella catarrhalis has been isolated and may be B-lactamase positive.3” lnitial antibiotic therapy for emphysema involves broad-spectrum and B-lactamase coverage for expected bacteria. Blood cultures and sinus aspirates are used as necessary. Eyelid aspirates correlate poorly with sinus or orbital abscess cultures.“’ A nasal decongestant may be helpful. If sinus origin is
suspected, possible antibiotic regimens include ampicillin-sulbactam (Unasynl/amoxicillin clavulanic acid (Augmentin. Beecham Laboratories, Bristol, TN), or cefoxitin (Mefoxin, Merck, Sharp, and Dohme. West Point, PA). Ampicillin or nafcillin combined with chloramphenicol is also suggested.‘“.33.38 If odontogenic sources are suspected, penicillin or clindamycin may be considered. Awareness of the expected bacterial pathogens is an important concern for initial therapy of subcutaneous emphysema. This becomes increasingly significant if cultures are inconclusive as a result of previously initiated antibiotic therapy inhibiting culture growth or the inability to identify fastidious organisms. The displacement effects of subcutaneous emphysema may have serious consequences in the maxillofacial region. Extensive retropharyngeal emphysema can cause respiratory obstruction.‘.‘.’ Loss of vision may result from orbital emphysema. External and internal orbital swelling can compress the eye and reduce arterial perfusion, or it may cause venous occlusion with subsequent retrograde obstruction of retinal blood flo~.‘-~.~” Visual loss may also occur secondary to inflammatory neuritis.“” Previous reports suggest the orbital septum must remain intact to sustain an increase in intraorbital pressure as air accumulates. An intact septum would not permit air escape and therefore contributes to retinal circulatory compromise.“.4 Our patient may have been spared visual injury because of air passage through his orbital septum. The superficial laceration repaired in the emergency department may actually have penetrated deeper than appreciated. This may account for emphysema extending to the upper cheek and temporal region from an ethmoidal origin. If visual acuity, pupillary reflexes. and ocular motion progressively deteriorate as a result of accumulated emphysema, surgical intervention is necessary. Orbital decompression is obtained by lateral canthotomy with cantholysis.3 Aspiration of orbital air also has been reported.’ These procedures reduce lid tension and back pressure on the eye. Of interest is the general soft-tissue response to extensive noninfected emphysema. Review of the literature found no indication of tissue scarring or functional limitation after uncomplicated reabsorption of subcutaneous emphysema. References I.
MJ. Turvey TA, Schumann SE’. et al: Orbital emphysema causing vibion loss after dental extraction. J Am Dent Assoc 120:431. 1990
Buckley
1242
2. Carter KD, Nerad JA: Fluctuating visual loss secondary to orbital emphysema. Am J Ophthalmol 104:664. 1987 3. Fleishman JA, Beck RW, Hoffman RO: Orbital emphysema as an opthalmic emergency. Ophthalmology 91: 1389, 1984 4. Linberg JV: Orbital emphysema complicated by acute central retinal artery occlusion. Case report and treatment. Ann Ophthalmol 14:747. 1982 5. Carmichael F, Ward-Booth RP. Banks JM: Pneumomediastinum after facial trauma. Oral Surg Oral Med Oral Path01 66540. 1988 6. Dripps RD. Eckenhoff JE, Vandam LD: Introduction to Anesthesia. Philadelphia, PA, Saunders, 1982 7. Larsen KD: Submucosal emphysema with airway obstruction from nasal oxygen cannula. Anesth Analg 67586, 1988 8. Horowitz I. Hirshberg A. Freedman A: Pneumomediastinum and subcutaneous emphysema following surgical extraction of mandibular third molars: Three case reports. Oral Surg Oral Med Oral Pathol 63:25. 1987 9. Henry CH, Hills EC: Traumatic emphysema of the head. neck, and mediastinum associated with maxillofacial trauma: Case report and review. J Oral Maxillofac Surg 471876, 1989 10. Hunt RB. Sahler OD: Mediastinal emphysema produced by air turbine dental drills. JAMA 205:24l, 1968 I 1. Feinstone T: Infected subcutaneous emphysema: Report of case. J Am Dent Assoc 83:1309, 1971 12. Reznick JB. Ardary WC: Cervicofacial subcutaneous air emphysema after dental extraction. J Am Dent Assoc 120:417. 1990 13. Wilson GA, Galle S, Greene C: Subcutaneous emphysema after extraction of maxillary teeth: Report of a case. J Am Dent Assoc 106:836. 1983 14. Rauch SD: Medial orbital blow-out fracture with entrapment. Arch Otolaryngol II 1:53, 1985 15. Visscher JG, van der Wal KG: Medial orbital wall fracture with enophthalmos. J Craniomaxillofac Surg 16:55, 1988 16. Holt GR. Holt JE: Nasoethmoid complex injuries. Otolaryngol Clin North Am 18:87. 1985 17. Habal MB, Beart R, Murray JE: Mediastinal emphysema secondary to fracture of orbital floor. Am J Surg 123:606. 1972 18. Martin PW, Williams AC: Frontal sinus fracture with supraorbital subcutaneous emphysema. J Oral Surg 30:901. 1972 19. Mattox DE, Delany RG: Anatomy of the ethmoid sinus. Otolaryngol Clin North Am 18:3, 1985 20. Chakeres DW: Computed tomography of the ethmoid sinuses. Otolaryngol Clin North Am l&29. 1985
INFECTION
WITH
ORBITAL
SUBCUTANEOUS
EMPHYSEMA
21. Dolan KD: The ethmoid sinus-Plain film and tomographic radiology. Otolaryngol Clin North Am 18:15. 1985 22. Hollinshead WH: Fascia and fascial spaces of the head and neck. in Anatomy for Surgeons. vol I. The Head and Neck ted 21. New York, NY, Harper & Row. 1968 23. Aragon S. Dolwick F. Buckley S: Pnuemomediastinum and subcutaneous cervical emphysema during third molar extraction under general anesthesia. J Oral Maxillofac Surg 44:141. 1986 24. Noble WH: Mediastinal emphysema resulting from extraction of an impacted mandibular third molar. J Am Dent Assoc 84:368, 1972 25. Reckles NH, Joslic BA: Death from air embolism during root canal therapy. J Am Dent Assoc 67:397. 1963 26. Falomo 00: Surgical emphysema following root canal therapy. Report of a case. Oral Surg Oral Med Oral Pathol 58: 101, 1984 27. Stringer DE, Dolwick MF. Steed DL: Subcutaneous emphysema after Le Fort I osteotomy: Report of two cases. J Oral Surg 37:115. 1979 28. Falender LG. Barbieri D. Leban SG: Gas producing necrotizing fasciitis following mandibular fracture. J Oral Maxillofac Surg 47:856, 1989 29. Topazian RG. Goldberg MH: Management of Infections of the Oral and Maxillofacial Region ted 2). Philadelphia, PA, Saunders, 1987 30. Schramm VL. Curtin HD, Kennerdell JS: Evaluation of orbital cellulitis and results of treatment. Laryngoscope 92~732, 1982 31. O’Ryan FO, Diloreto D. Barber HD. et al: Orbital infections: Clinical and radiographic diagnosis and surgical treatment. J Oral Maxillofac Surg 6:99l, 1988 32. Ritter FN: The Paranasal Sinuses, Anatomy and Surgical Technique fed 2). St Louis. MO. Mosby. 1978 33. Goodwin WJ: Orbital complications of ethmoiditis. Otolaryngol Clin North Am 18:139. 1985 34. Wald ER. Reilly JS. Casselbrandt M, et al: Treatment of acute maxillary sinusitis in childhood: A comparative study of amoxicillin and cefaclor. J Pediat 104:297. 1984 35. Shapiro ED, Wald ER, Doyle W. et al: Bacteriology of the maxillary sinus of Rhesus monkeys. Ann Otol Rhino1 Laryngol 91:159, 1982 36. Su WY, Liu C. Hung SY. et al: Bacteriological study in chronic maxillary sinusitis. Laryngoscope 93:93l, 1983 37. Brook I: Aerobic and anerobic bacterial flora of normal maxillary sinuses. Laryngoscope 91:372. 1981 38. Harris GJ: Subperiosteal inflammation of the orbit. A bacterial analysis of I7 cases. Arch Ophthalmol 106:947. 1988 39. Brook I: Bacteriology of chronic maxillary sinusitis in adults. Ann Otol Rhino1 Laryngol 98:426. 1989
AND
BRAUN
1239
5. Werber JL, Pincus RL: Oropharyngeal angioedema associated with the use of angiotensin-converting enzyme inhibitors. Otolaryngol Head Neck Surg 101:96. 1989 6. Slater EE, Merrill DD. Guess HA, et al: Clinical profile of angioedema associated with angiotensin-converting inhibition. JAMA 206:967, 1988 7. Deltino JJ. Sclaroff A. Giglio JA, et al: Management of a patient with hereditary angioneurotic edema. J Oral Surg 36:890, 1978 8. Fineman SM: Urticaria 14503. 1987
J Oral Maxlllofac
and angioedema.
Primary
Care
9. Mathews KP: Urticaria and angioedema. J Allergy Clin Immunol 72: 1, 1983 10. Singer RJ, MacGregor GA: Angioneurotic edema associated with two angiotensin-converting inhibitors. Br Med J 293: 1243. 1986 I I. Inman WH, Rawson NS: Angioedema and urticaria associated with enalapril. Br Med J 294:91. 1987 12. Nicholls MG, Maslowski AH, Hamid I, et al: Ulceration of the tongue: A complication of captopril therapy. Ann Intern Med 94:659. 1981 13. Jett GK: Captopril-induced angioedema. Ann Emerg Med 13:489. 1984
Surg
49 1239-1242.1991
Infection Associated With Orbital Subcutaneous Emphysema PETER N. DEMAS, DMD, MD,* AND THOMAS W. BRAUN, DMD, PHDt
Subcutaneous or surgical emphysema of the oral and maxillofacial region is a well documented but a relatively uncommon event. Although the sequelae are generally self-limiting and benign, serious local and systemic complications can result. Dramatic consequences attributed to the accumulated air displacing anatomic structures include loss of vision, ‘-’ pneumothorax, and pneumomediastinum.5-‘0 The risk of infection secondary to subcutaneous emphysema is often suggested, but rarely reported. ’ ’ Despite this rare incidence, infected subcutaneous emphysema of the maxillofacial region requires prompt attention. Also significant is awareness of the potential morbidity associated with emphysema confined to the periorbita. An air turbine high-speed drill with an exhaust directed toward the surgical field may force air into the subcutaneous and fascial planes of the head and neck. ‘.8.‘3.‘3 Other sources are the paranasal sinuses, which may cause emphysema secondary to
* Assistant Professor, Department of Oral and Maxillofacial Surgery, University of Pittsburgh, Pittsburgh, PA. t Chairman, Department of Oral and Maxillofacial Surgery. School of Dental Medicine, University of Pittsburgh, Pittsburgh, PA. Address correspondence and reprint requests to Dr Braun: Department of Oral and Maxillofacial Surgery, University of Pittsburgh, School of Dental Medicine. 3501 Terrace St. Pittsburgh. PA 15261.
Q 1991 American geons
Association
0278-2391/91/4911-0022$3.00/O
of Oral and Maxillofacial
Sur-
frontal, nasoethmoid, and maxillary facial trauma.‘*S,9.‘4-‘8 Fractures into the sinuses may involve the orbital walls. Reviews of these clinical and radiographic relationships are available.“-” After disruption of anatomic integrity, air can also be introduced into the tissues by nose blowing, sneezing, vomiting. and coughing.‘.’ Other reported events initiating emphysema include removal of endodontic erupted and impacted teeth, 1.8.17-.13.13.24 therapy,‘5.‘h orthognathic surgery,” positive pressure ventilation with endotrachael intubation, trachael-bronchial injury,6.9.‘3 and use of nasal cannuIas.’ Surgical emphysema causes soft-tissue swelling, often associated with crepitus. It may arise rapidly or have a delayed occurrence. Small accumulations of air are usually painless and benign. Extensive emphysema, however, may cause pain and a mass effect obstruction to respiration, cardiac function, and retinal perfusion.1-s*7.9 Radiographically, emphysema appears lucent and is described as free air or gas within the tissues.“.” Treatment is usually supportive, with the air being reabsorbed over a 2to 16day period. Surgical intervention is only necessary when respiratory or vascular compromise occurs.‘-4,7’9 Antibiotic prophylaxis is generally suggested due to possible bacterial contamination of the tissues. A differential diagnosis of rapid facial swelling includes hematoma, allergic reaction, edema, infection and surgical emphysema. Necrotizing fasciitis, in which bacterial gas production is possible. also should be considered.28,29
1240
INFECTION
WITH
ORBITAL
SUBCUTANEOUS
EMPHYSEMA
Report of a Case A 52-year-old man came to the emergency department following an altercation. He reported sustaining a single punch to his left eye. His main complaint was a 0.5 cm superficial laceration of his left lower eyelid near the infraorbital rim. Radiographic plain film findings were reported as negative. His only significant past medical history included borderline adult onset diabetes mellitis treated by diet modification. He was evaluated and treated by the emergency department physician. The laceration was repaired and he was discharged on cephalexin (Keflex, Eli Lilly, Indianapolis, IN) 250 mg every 6 hours and instructed to use iced compresses for the mild periorbital edema. The following morning he again reported to the emergency department complaining of rapidly increasing, painful swelling of his left eye which was swollen closed despite the use of iced compresses. He was evaluated by the opthalmology service, which reported the presence of left periorbital edema and erythema. mild chemosis, and subconjunctival hemorrhage. No proptosis was noted. The pupils were equally round and reactive and the extraocular muscles were intact. There was no hyphema, no lacrimal discharge, and funduscopic examination was negative. Vision was unchanged. The previously repaired lower lid laceration was intact and without drainage. The patient’s temperature was 38.O”C and his leukocyte count was elevated (13,800i~L). with 71% polymorphonuclear (PMN) leukocytes (PMN range, 54% to 62%) and 0% band neutrophils. The previous posterior-anterior, lateral, submental vertex and Water’s view facial films were again reviewed and reported as negative. There was no evidence of facial fractures or sinus opacification. The patient was admitted with a diagnosis of preseptal cellulitis and started on ampicillin-sulbactam (Unasyn, Pfizer, New York, NY) 3 g intravenously every 6 hours. Axial and coronal CT scans, along with infectious disease and oral and maxillofacial surgery consultations, were requested. The oral and maxillofacial findings concurred with those of ophthalmology. Further clinical evaluation was negative for any evidence of facial fractures. Noted during this examination, but not the prior examinations, were areas of crepitation on the left eyelids, upper cheek, and temporal region. Infraorbital sensation was normal. The patient was edentulous and there was no evidence of a source of infection or any adenopathy present. During general questioning regarding the previous events no additional information was volunteered. With specific questioning, however, the patient admitted to several episodes of left epistaxis and nose blowing after leaving the emergency department. He noted no immediate changes and continued the iced compresses as instructed. The increased swelling and erythema were present when he awakened the following day. He reported taking one dose of the prescribed antibiotic and used acetominophen for pain. Subsequently, axial and coronal CT scans showed extensive orbital emphysema and a localized area of left ethmoid opacification (Figs 1, 2). The patient’s cellulitis was attributed to posttraumatic infected emphysema of ethmoidal origin. The edema resolved slowly over the following 7 days with continued use of intravenous ampicillin-sulbactam (Unasyn) 3 g every 6 hours. At the time of discharge, the
FIGURE physema.
I.
Coronal CT scan with left facial subcutaneous
em-
erythema had resolved. Vision and extraocular muscle function were intact. The subconjunctival hemorrhage was resolving and the conjunctival chemosis had dissipated. The patient was afebrile and his leukocyte count had decreased to 9,700ipL. He was discharged on amoxicillin-potassium clavulanic acid (Augmentin) 500 mg three times per day for I week. Subsequent follow-up showed complete resolution. Discussion In this case the periorbital cellulitis was secondary to subcutaneous emphysema. The extensive emphysema resulted from a relatively minor traumatic incident. The isolated medial orbital wall fracture, without extraocular muscle entrapment, per-
FIGURE
2.
Axial CT scan with left ethmoid sinus opacification.
DEMAS
AND
1241
BRAUN
mitted air passage through the lamina papyracea of the ethmoid bone. The etiology of orbital cellulitis includes sinusitis. cutaneous infections, facial trauma, and odontogenic infections. The most common source remains sinusitis.30.3’ Orbital cellulitis is more often associated with children than adults.30.” The predominance of pediatric orbital infections is associated with sinus enlargement and maturation. The ethmoid sinuses begin as invaginations in the fetus.‘“.3’.3’ By the second year of life ethmoid pneumatization has advanced and reaches final form at about 14 years.” The sphenoid and maxillary sinuses are present at birth, while the frontal sinus begins at 5 to 7 years of age.3’.37-The classification of orbital infections as preseptal (periorbital) cellulitis, orbital cellulitis. subperiosteal abscess, orbital abscess, and cavernous sinus thrombosis has been detailed anatomically and radiographically.30.3’,“3 Although the normal sinuses are considered sterile,34-3h others have reported the presence of anermay be attributed to obes.” The disagreement study design? These reports concentrated on the maxillary rather than the ethmoid sinus. The bacteriology associated with orbital infections usually correlates with sinusitis. The most common bacteria isolated include Hemophilzrs infirenzae. Streptococcus pnrumoniae, Staphylococcus uureus, and S epidermis. and Bacteriodes species.30.31.~4.3X Occasionally E coli and Klebsiello are
reported.“’ Posttraumatic episodes are generally associated with streptococci or staphylococci, while acute respiratory causes include S pneumoniae and H in~uenzac,.3”.3’.34.38 The organisms associated with chronic sinusitis and odontogenic sources tend to be anerobic or mixed aerobic-aneroThe type of anerobic bacteria is asbit. 2V~3’~3h~3X~3y sociated with the duration of infection. This is a reflection of decreased oxygen concentration, increased carbon dioxide tension, and lower pH that occur with chronicity.” One chronic sinusitis study reported 44% of the Bacteriodes species were positive for B-lactamase. In pediatric patients H influenzae is the most common organism. This is attributed to a child’s immature immunologic development and inability to produce antibodies against the capsular antigen of H inJluenzae.‘n~3’.34 Also in children, Branhamella catarrhalis has been isolated and may be B-lactamase positive.3” lnitial antibiotic therapy for emphysema involves broad-spectrum and B-lactamase coverage for expected bacteria. Blood cultures and sinus aspirates are used as necessary. Eyelid aspirates correlate poorly with sinus or orbital abscess cultures.“’ A nasal decongestant may be helpful. If sinus origin is
suspected, possible antibiotic regimens include ampicillin-sulbactam (Unasynl/amoxicillin clavulanic acid (Augmentin. Beecham Laboratories, Bristol, TN), or cefoxitin (Mefoxin, Merck, Sharp, and Dohme. West Point, PA). Ampicillin or nafcillin combined with chloramphenicol is also suggested.‘“.33.38 If odontogenic sources are suspected, penicillin or clindamycin may be considered. Awareness of the expected bacterial pathogens is an important concern for initial therapy of subcutaneous emphysema. This becomes increasingly significant if cultures are inconclusive as a result of previously initiated antibiotic therapy inhibiting culture growth or the inability to identify fastidious organisms. The displacement effects of subcutaneous emphysema may have serious consequences in the maxillofacial region. Extensive retropharyngeal emphysema can cause respiratory obstruction.‘.‘.’ Loss of vision may result from orbital emphysema. External and internal orbital swelling can compress the eye and reduce arterial perfusion, or it may cause venous occlusion with subsequent retrograde obstruction of retinal blood flo~.‘-~.~” Visual loss may also occur secondary to inflammatory neuritis.“” Previous reports suggest the orbital septum must remain intact to sustain an increase in intraorbital pressure as air accumulates. An intact septum would not permit air escape and therefore contributes to retinal circulatory compromise.“.4 Our patient may have been spared visual injury because of air passage through his orbital septum. The superficial laceration repaired in the emergency department may actually have penetrated deeper than appreciated. This may account for emphysema extending to the upper cheek and temporal region from an ethmoidal origin. If visual acuity, pupillary reflexes. and ocular motion progressively deteriorate as a result of accumulated emphysema, surgical intervention is necessary. Orbital decompression is obtained by lateral canthotomy with cantholysis.3 Aspiration of orbital air also has been reported.’ These procedures reduce lid tension and back pressure on the eye. Of interest is the general soft-tissue response to extensive noninfected emphysema. Review of the literature found no indication of tissue scarring or functional limitation after uncomplicated reabsorption of subcutaneous emphysema. References I.
MJ. Turvey TA, Schumann SE’. et al: Orbital emphysema causing vibion loss after dental extraction. J Am Dent Assoc 120:431. 1990
Buckley
1242
2. Carter KD, Nerad JA: Fluctuating visual loss secondary to orbital emphysema. Am J Ophthalmol 104:664. 1987 3. Fleishman JA, Beck RW, Hoffman RO: Orbital emphysema as an opthalmic emergency. Ophthalmology 91: 1389, 1984 4. Linberg JV: Orbital emphysema complicated by acute central retinal artery occlusion. Case report and treatment. Ann Ophthalmol 14:747. 1982 5. Carmichael F, Ward-Booth RP. Banks JM: Pneumomediastinum after facial trauma. Oral Surg Oral Med Oral Path01 66540. 1988 6. Dripps RD. Eckenhoff JE, Vandam LD: Introduction to Anesthesia. Philadelphia, PA, Saunders, 1982 7. Larsen KD: Submucosal emphysema with airway obstruction from nasal oxygen cannula. Anesth Analg 67586, 1988 8. Horowitz I. Hirshberg A. Freedman A: Pneumomediastinum and subcutaneous emphysema following surgical extraction of mandibular third molars: Three case reports. Oral Surg Oral Med Oral Pathol 63:25. 1987 9. Henry CH, Hills EC: Traumatic emphysema of the head. neck, and mediastinum associated with maxillofacial trauma: Case report and review. J Oral Maxillofac Surg 471876, 1989 10. Hunt RB. Sahler OD: Mediastinal emphysema produced by air turbine dental drills. JAMA 205:24l, 1968 I 1. Feinstone T: Infected subcutaneous emphysema: Report of case. J Am Dent Assoc 83:1309, 1971 12. Reznick JB. Ardary WC: Cervicofacial subcutaneous air emphysema after dental extraction. J Am Dent Assoc 120:417. 1990 13. Wilson GA, Galle S, Greene C: Subcutaneous emphysema after extraction of maxillary teeth: Report of a case. J Am Dent Assoc 106:836. 1983 14. Rauch SD: Medial orbital blow-out fracture with entrapment. Arch Otolaryngol II 1:53, 1985 15. Visscher JG, van der Wal KG: Medial orbital wall fracture with enophthalmos. J Craniomaxillofac Surg 16:55, 1988 16. Holt GR. Holt JE: Nasoethmoid complex injuries. Otolaryngol Clin North Am 18:87. 1985 17. Habal MB, Beart R, Murray JE: Mediastinal emphysema secondary to fracture of orbital floor. Am J Surg 123:606. 1972 18. Martin PW, Williams AC: Frontal sinus fracture with supraorbital subcutaneous emphysema. J Oral Surg 30:901. 1972 19. Mattox DE, Delany RG: Anatomy of the ethmoid sinus. Otolaryngol Clin North Am 18:3, 1985 20. Chakeres DW: Computed tomography of the ethmoid sinuses. Otolaryngol Clin North Am l&29. 1985
INFECTION
WITH
ORBITAL
SUBCUTANEOUS
EMPHYSEMA
21. Dolan KD: The ethmoid sinus-Plain film and tomographic radiology. Otolaryngol Clin North Am 18:15. 1985 22. Hollinshead WH: Fascia and fascial spaces of the head and neck. in Anatomy for Surgeons. vol I. The Head and Neck ted 21. New York, NY, Harper & Row. 1968 23. Aragon S. Dolwick F. Buckley S: Pnuemomediastinum and subcutaneous cervical emphysema during third molar extraction under general anesthesia. J Oral Maxillofac Surg 44:141. 1986 24. Noble WH: Mediastinal emphysema resulting from extraction of an impacted mandibular third molar. J Am Dent Assoc 84:368, 1972 25. Reckles NH, Joslic BA: Death from air embolism during root canal therapy. J Am Dent Assoc 67:397. 1963 26. Falomo 00: Surgical emphysema following root canal therapy. Report of a case. Oral Surg Oral Med Oral Pathol 58: 101, 1984 27. Stringer DE, Dolwick MF. Steed DL: Subcutaneous emphysema after Le Fort I osteotomy: Report of two cases. J Oral Surg 37:115. 1979 28. Falender LG. Barbieri D. Leban SG: Gas producing necrotizing fasciitis following mandibular fracture. J Oral Maxillofac Surg 47:856, 1989 29. Topazian RG. Goldberg MH: Management of Infections of the Oral and Maxillofacial Region ted 2). Philadelphia, PA, Saunders, 1987 30. Schramm VL. Curtin HD, Kennerdell JS: Evaluation of orbital cellulitis and results of treatment. Laryngoscope 92~732, 1982 31. O’Ryan FO, Diloreto D. Barber HD. et al: Orbital infections: Clinical and radiographic diagnosis and surgical treatment. J Oral Maxillofac Surg 6:99l, 1988 32. Ritter FN: The Paranasal Sinuses, Anatomy and Surgical Technique fed 2). St Louis. MO. Mosby. 1978 33. Goodwin WJ: Orbital complications of ethmoiditis. Otolaryngol Clin North Am 18:139. 1985 34. Wald ER. Reilly JS. Casselbrandt M, et al: Treatment of acute maxillary sinusitis in childhood: A comparative study of amoxicillin and cefaclor. J Pediat 104:297. 1984 35. Shapiro ED, Wald ER, Doyle W. et al: Bacteriology of the maxillary sinus of Rhesus monkeys. Ann Otol Rhino1 Laryngol 91:159, 1982 36. Su WY, Liu C. Hung SY. et al: Bacteriological study in chronic maxillary sinusitis. Laryngoscope 93:93l, 1983 37. Brook I: Aerobic and anerobic bacterial flora of normal maxillary sinuses. Laryngoscope 91:372. 1981 38. Harris GJ: Subperiosteal inflammation of the orbit. A bacterial analysis of I7 cases. Arch Ophthalmol 106:947. 1988 39. Brook I: Bacteriology of chronic maxillary sinusitis in adults. Ann Otol Rhino1 Laryngol 98:426. 1989
