642
Pneumoparotitis Associated With the Use of an Air-Powder Prophylaxis Unit Frederic H. Brown,
*
Robert C.
Ogletree, * and Glen D. Houston*
the parotid gland secondarily to the use of an airis unit presented. Air pressure associated with these units usually powder prophylaxis exceeds that for air/driven turbines or air/water dental syringes, yet the reported incidence of iatrogenic trauma is very low. Improper angulation in the use of these instruments may result in serious sequellae. Differential diagnosis and physical examination following trauma to the parotid is discussed. J Periodontol 1992; 63:642-644.
A
case reporting barotrauma to
Key Words: Parotid gland/injuries; barotrauma/etiology; dental instruments/adverse effects.
Air-powder prophylaxis units have been widely used since 1980 and are reported to be an effective method for removal of exogenous stains from teeth as well as for plaque removal.1,2 These units utilize
a mixture of water and an abrasive powder driven by compressed air. Different units vary in air pressure and consumption of powder per minute, with one of the more widely used units utilizing about 55 to 60 psi of pressure.2,3 The air pressure in these units is usually greater than that needed to drive air turbine handpieces or dental air water syringes, yet the reports of serious sequellae from air powder units remains very low.4 The incidence of subcutaneous and mediastinal emphysema associated with dental procedures, however, is ever increasing.520 Reports of barotrauma associated with dental procedures date back to 1900.21 The purpose of this report is to present a case of barotrauma to the parotid gland secondarily to the use of an air-powder prophylaxis unit.
CASE REPORT A 30-year old Caucasian male was referred to the Department of Periodontics with a chief complaint of "a shooting pain when my teeth were being cleaned." The patient noticed a unilateral swelling of the left side of his face shortly after undergoing a routine dental prophylaxis appointment, and returned to the dental clinic for evaluation. Physical examination revealed a well circumscribed swelling of the left parotid space (Fig. 1), which was painful to palpation, and the overlying skin was erythematous and warm. Crepitus was absent, and the patient was not experiencing any breathing difficulty. Intraoral examination was unremark*AFSC Regional Hospital Eglin, Eglin Air Force Base, FL. +Wilford Hall U.S. Air Force Medical Center, Lackland Air Force Base, TX. The views expressed herein are those of the authors, and do not necessarily reflect those of the United States Air Force nor the Department of Defense.
1. Left barotrauma.
Figure
parotoid
area.
Well-circumscribed
swelling following
able except for an ulcération in the area of the left carúncula of the parotid duct (Stensen's duct) (Fig. 2). Systems review as well as the patient's past medical history were unremarkable. The patient gave no history of recurrent parotitis, nor did he report any present medications nor drug allergies. The patient also exhibited a normal periodontium, with no evident attachment loss nor mucogingival defects. Tissue damage to the gingiva following the use of the airpowder prophylaxis unit was minimal. Further physical examination failed to reveal barotrauma beyond the parotid area, and a diagnosis of pneumoparotitis of the left parotid gland was established. A complete blood count taken shortly
Volume 63 Number 7
Figure 2. Enlarged parotoid carúncula
BROWN, OGLETREE, HOUSTON
with minor ulcération,
left area.
after the incident was unremarkable. Treatment consisted of non-steroidal, anti-inflammatory analgesics, 6 mg of dexamethasone intramuscularly to reduce further edema, and antibiotic prophylaxis with amoxicillin/clavulanate potassium, 250 mg tablets, every 8 hours. Antibiotic coverage was initiated due to the possible contamination of the powder, which had been forced into the duct and gland. The patient was seen 48 hours post-trauma; he reported decreased pain, and additionally reported "a very dry mouth." Intraoral examination revealed a slight dessication of the oral tissues, with no salivary flow produced on manual manipulation of the left parotid area. The area of the left parotid gland was still painful to palpation, but no exúdate was noted at the orifice of the duct. The patient was placed on lemon drops to stimulate salivation, and continued on the present medications. Complete blood count was repeated, and the same was within normal limits. Followup at 5 days post-injury revealed a normal salivary flow, resolution of pain and swelling, and final hematology studies were essentially unchanged from baseline. DISCUSSION
Pneumoparotitis is described as a non-neoplastic enlargement of the salivary glands, associated with barotrauma.22,23 This entity is also referred to as "trumpet parotitis," as a descriptive term for barotrauma associated with blowing into wind instruments, which can result in this condition. Recently, a case of pneumoparotitis as a facticial injury was reported by Mandel et al.24 This entity has also been reported in association with hay fever25 as well as with psychosocial problems in adolescents.26'27 In the absence of the history of trauma and rapid onset of the condition described in this case, the differential diagnosis
643
for parotid gland swellings can be a challenge for the clinician. Banks23 has summarized a variety of neoplastic and non-neoplastic conditions in his classification of parotid gland swellings. The following classifications were proposed:23 neoplastic, inflammatory, hypersensitive and drug reactions, metabolic, and miscellaneous. Neoplasms of salivary gland origin constitute a heterogeneous group of lesions of great morphologic variation and may be benign or malignant. Such neoplasms would include the following: pleomorphic adenoma, Warthin's tumor, adenoid cystic carcinoma, acinic cell carcinoma, and mucoepidermoid carcinoma.22 The acute, rapid onset of the parotid gland swelling in this case for the most part ruled out such a neoplastic process. Inflammatory swellings of the parotid gland should include the following: subacute and acute parotitis, viral infections, and chronic inflammatory diseases (i.e., tuberculosis, actinomycosis, sarcoidosis).23 The patient presented in this case had no evidence of systemic disease in other areas. The clinical history and physical findings did not support an inflammatory process as described above. Hypersensitivity and drug reactions such as allergic parotitis and drug idiosyncrasy may also yield parotid gland swelling. According to Banks,23 in allergic parotitis coexistent involvement of the submandibular gland and, in some cases, all the salivary glands is observed as an important diagnostic point. Additionally, profuse lacrimation, sneezing, and even bronchospasm may be present. Among the drugs implicated in parotid swelling we find Phenylbutazone, iso-
prenaline, iodine, thiouracil, thiocyanate, guanethidine, bretylium tosylate, and thioridazine.23 In this case, the patient was taking no medications at the time of onset nor did he convey a history of drug allergies. Metabolic causes of parotid gland swelling include such disorders as malnutrition, alcoholic cirrhosis of the liver, latent diabetes, and
obesity.23 A systems review and physical examination of the patient in this case were accomplished and were unremarkable for any metabolic source of parotid gland swell-
ing. The miscellaneous group includes such conditions as mechanical obstruction secondary to calculi, congenital atresia of the parotid duct, functional hypersécrétions, and pneumoparotitis.23 The first three conditions could not be supported based on the clinical observation and history. Pneumoparotitis (surgical emphysema) of the parotid gland due to air pressure from the air-powder prophylaxis unit appeared to be the cause of the parotid swelling in this case. Physical examination of the patient should include a thorough examination of the parotid gland and ductal system as well as the fasciai spaces of the face and neck. The parotid gland is composed of two distinct lobes. The superficial lobe overlies the ramus of the mandible from the zygomatic arch superiorly to the angle of the mandible inferiorly, and lies superficial to the masseter muscle. The deep lobe wraps posteriorly around the ramus of the mandible and lies between the ramus and the mastoid process of the temporal bone. An accessory portion of the gland lies more anteriorly above the duct. The duct of the parotid
644
(Stensen's duct) courses anteriorly from the superficial lobe, and enters the oral cavity opposite the maxillary molar region. It is of interest to note that while a normal parotid gland is not palpable, the duct in health can be felt against a
J Periodontol July 1992
PNEUMOPAROTITIS ASSOCIATION WITH THE USE OF AN AIR-POWDER PROPHYLAXIS UNIT
flexed masseter.
Pneumoparotitis literally inflates the parotid gland allowing it to be easily palpated. Enlargements of the deep lobe can visually displace the pinna of the ear outwards. Along with distention of the gland and duct, prominence of the papilla can be seen and palpated intraorally (Fig. 2). Bubbling can occasionally be elicited from the duct orifice while pressing the gland. Pneumoparotitis contained within the gland can present as firm edema of the structure without crepitus, but if the air embolism violates the continuity of the acini, crepitus is usually felt. The capsule of the gland arises from a separation of the deep cervical fascia, a twolayered investing sheath which communicates from the zygomatic arch and occipital bone superiorly to the acromion, clavicle, and sternum inferiorly. Air escaping from the acini thereby has access to potential spaces from the base of the skull to the chest cavity, including the retropharyngeal space. If extracapsular extravasation of the air embolism is suspected, soft tissue radiographs of the neck, in two planes, should be ordered to assess the fasciai spaces. Computerized tomography or magnetic resonance imaging would be alternative studies. Injury to the gingival tissues, usually of a minor extent, have been reported by Weaks et al. clinically1 and by Snyder et al.28 histologically. While the potential for serious sequellae still remains uncommon in the literature in association with air-powder abrasive units, precautions such as avoiding deep periodontal pockets or vulnerable anatomic structures should be cautioned.
REFERENCES 1. Weaks LM, Lescher NB, Barnes CM, Holroyd SV. Clinical evaluation of the Prophy-Jet (R) as an instrument for routine removal of tooth stain and plaque. / Periodontol 1984;55:486-488. 2. Horning G. Clinical use of an air-powder abrasive. Compend Contin
6. Hunt RB, Sahler OD. Mediastinal emphysema produced by air turbine dental drills. JAMA 1968;205:101-102. 7. Argon JB, Dolwick MF, Buckley S. Pneumomediastinum and subcutaneous cervical emphysema during third molar extraction under general anesthesia. J Oral Maxillofac Surg 1986;44:141-144. 8. Hylton RP, Laskin JL. Subcutaneous emphysema with Pneumomediastinum following tooth extraction. Gen Dent 1985;33:350-351. 9. Habal MB, Beart R, Murray JE. Mediastinal emphysema secondary to fracture of the orbital floor. Am J Surg 1972;123:606-608. 10. Toofield JJ. Pneumomediastinum following fixation of the maxillary antrum. Br J Plast Surg 1977;30:179-181. 11. Wilson GA, Golle S, Green C. Subcutaneous emphysema after extraction of maxillary teeth: Report of a case. J Am Dent Assoc
1983;106:836-837. VA, Mooney JW, Stratigos GT. Iatrogenic dental-air emphysema: Report of a case. J Am Dent Assoc 1972;85:144-147. Snyder MD, Rosenberg ES. Subcutaneous emphysema during periodontal surgery: Report of a case. J Periodontol 1977;48:790-791. Woehrlen AE. Subcutaneous emphysema. Anes Prog 1985;32:161-
12. Cardo 13. 14.
163. 15. 16. 17. 18.
Hayduk S, Benett AC, Monheim LM. Subcutaneous emphysema after operative dentistry: Report of a case. J Am Dent Assoc; 1970;80:1362. Barber JW Burns JB. Subcutaneous emphysema of the face and neck after dental restoration. J Am Dent Assoc 1967;75:167-168. Falomo OO. Surgical emphysema following root canal therapy: Report of a case. Oral Surg Oral Med Oral Pathol 1984;58:101-102. Feinstone T. Infected subcutaneous emphysema: Report of a case. J
Am Dent Assoc 1971;83:1309-1311. 19. Reznick JB, Ardary WC. Cervicofacial subcutaneous air emphysema after dental extraction. J Am Dent Assoc 1990;120:417-419. 20. Buckley MJ et al. Orbital emphysema causing vision loss after dental extraction. J Am Dent Assoc 1990;120:42T424. 21. Turnbull AA. A remarkable coincidence in dental surgery. Br Med J
190O;l:1131. 22. Shafer WG, Hine MK, Levy BM. In: A Textbook of Oral Pathology, 4th ed., Philadelphia: W.B. Saunders Co. 1983;732-741. 23. Banks P. Nonneoplastic parotid swellings: A review. Oral Surg
1968;25:732-744. L, Kaynar A, Surg 1991;72:22-24.
24. Mandel
Pneumoparotid:
A
case
report. Oral
25. Garber MW. Pneumoparotitis: An unusual manifestation of hay fever. Am J Emerg Med 1987;5:40-41. 26. Telfer MR, Irvine GH. Pneumoparotitis. BrJSurg 1989;76:978. 27. Markowitz-Spence L. et al. Self-induced pneumoparotitis in an adolescent. Report of a case and review of the literature. Int J Pediatr
Otorhinolaryngol 1987;14:113-121. Snyder JA, McVay J, Brown FH et al. Systemic effects of air abrasive polishing. J Periodontol 1990;61:81-86.
1987;8:652-662. 3. Cooley RL, Brown FH, Lubow RM. Evaluation of air-powder abrasive prophylaxis units. Gen Dent 1990;38:24-27. 4. Finlayson RS, Stevens FD. Subcutaneous facial emphysema secondary to use of the Cavi-Jet. / Periodontol 1988;59:315-317.
28.
5. Noble WH. Mediastinal emphysema resulting from extraction of an impacted mandibular third molar. J Am Dent Assoc 1972;84:36-38.
ville,
Educ Dent
Wazen J.
Send reprint requests to: Dr. Frederic Brown, 317 Curacao Cove, NiceFL 32578. Accepted for publication January 28, 1992.
Pneumoparotitis Associated With the Use of an Air-Powder Prophylaxis Unit Frederic H. Brown,
*
Robert C.
Ogletree, * and Glen D. Houston*
the parotid gland secondarily to the use of an airis unit presented. Air pressure associated with these units usually powder prophylaxis exceeds that for air/driven turbines or air/water dental syringes, yet the reported incidence of iatrogenic trauma is very low. Improper angulation in the use of these instruments may result in serious sequellae. Differential diagnosis and physical examination following trauma to the parotid is discussed. J Periodontol 1992; 63:642-644.
A
case reporting barotrauma to
Key Words: Parotid gland/injuries; barotrauma/etiology; dental instruments/adverse effects.
Air-powder prophylaxis units have been widely used since 1980 and are reported to be an effective method for removal of exogenous stains from teeth as well as for plaque removal.1,2 These units utilize
a mixture of water and an abrasive powder driven by compressed air. Different units vary in air pressure and consumption of powder per minute, with one of the more widely used units utilizing about 55 to 60 psi of pressure.2,3 The air pressure in these units is usually greater than that needed to drive air turbine handpieces or dental air water syringes, yet the reports of serious sequellae from air powder units remains very low.4 The incidence of subcutaneous and mediastinal emphysema associated with dental procedures, however, is ever increasing.520 Reports of barotrauma associated with dental procedures date back to 1900.21 The purpose of this report is to present a case of barotrauma to the parotid gland secondarily to the use of an air-powder prophylaxis unit.
CASE REPORT A 30-year old Caucasian male was referred to the Department of Periodontics with a chief complaint of "a shooting pain when my teeth were being cleaned." The patient noticed a unilateral swelling of the left side of his face shortly after undergoing a routine dental prophylaxis appointment, and returned to the dental clinic for evaluation. Physical examination revealed a well circumscribed swelling of the left parotid space (Fig. 1), which was painful to palpation, and the overlying skin was erythematous and warm. Crepitus was absent, and the patient was not experiencing any breathing difficulty. Intraoral examination was unremark*AFSC Regional Hospital Eglin, Eglin Air Force Base, FL. +Wilford Hall U.S. Air Force Medical Center, Lackland Air Force Base, TX. The views expressed herein are those of the authors, and do not necessarily reflect those of the United States Air Force nor the Department of Defense.
1. Left barotrauma.
Figure
parotoid
area.
Well-circumscribed
swelling following
able except for an ulcération in the area of the left carúncula of the parotid duct (Stensen's duct) (Fig. 2). Systems review as well as the patient's past medical history were unremarkable. The patient gave no history of recurrent parotitis, nor did he report any present medications nor drug allergies. The patient also exhibited a normal periodontium, with no evident attachment loss nor mucogingival defects. Tissue damage to the gingiva following the use of the airpowder prophylaxis unit was minimal. Further physical examination failed to reveal barotrauma beyond the parotid area, and a diagnosis of pneumoparotitis of the left parotid gland was established. A complete blood count taken shortly
Volume 63 Number 7
Figure 2. Enlarged parotoid carúncula
BROWN, OGLETREE, HOUSTON
with minor ulcération,
left area.
after the incident was unremarkable. Treatment consisted of non-steroidal, anti-inflammatory analgesics, 6 mg of dexamethasone intramuscularly to reduce further edema, and antibiotic prophylaxis with amoxicillin/clavulanate potassium, 250 mg tablets, every 8 hours. Antibiotic coverage was initiated due to the possible contamination of the powder, which had been forced into the duct and gland. The patient was seen 48 hours post-trauma; he reported decreased pain, and additionally reported "a very dry mouth." Intraoral examination revealed a slight dessication of the oral tissues, with no salivary flow produced on manual manipulation of the left parotid area. The area of the left parotid gland was still painful to palpation, but no exúdate was noted at the orifice of the duct. The patient was placed on lemon drops to stimulate salivation, and continued on the present medications. Complete blood count was repeated, and the same was within normal limits. Followup at 5 days post-injury revealed a normal salivary flow, resolution of pain and swelling, and final hematology studies were essentially unchanged from baseline. DISCUSSION
Pneumoparotitis is described as a non-neoplastic enlargement of the salivary glands, associated with barotrauma.22,23 This entity is also referred to as "trumpet parotitis," as a descriptive term for barotrauma associated with blowing into wind instruments, which can result in this condition. Recently, a case of pneumoparotitis as a facticial injury was reported by Mandel et al.24 This entity has also been reported in association with hay fever25 as well as with psychosocial problems in adolescents.26'27 In the absence of the history of trauma and rapid onset of the condition described in this case, the differential diagnosis
643
for parotid gland swellings can be a challenge for the clinician. Banks23 has summarized a variety of neoplastic and non-neoplastic conditions in his classification of parotid gland swellings. The following classifications were proposed:23 neoplastic, inflammatory, hypersensitive and drug reactions, metabolic, and miscellaneous. Neoplasms of salivary gland origin constitute a heterogeneous group of lesions of great morphologic variation and may be benign or malignant. Such neoplasms would include the following: pleomorphic adenoma, Warthin's tumor, adenoid cystic carcinoma, acinic cell carcinoma, and mucoepidermoid carcinoma.22 The acute, rapid onset of the parotid gland swelling in this case for the most part ruled out such a neoplastic process. Inflammatory swellings of the parotid gland should include the following: subacute and acute parotitis, viral infections, and chronic inflammatory diseases (i.e., tuberculosis, actinomycosis, sarcoidosis).23 The patient presented in this case had no evidence of systemic disease in other areas. The clinical history and physical findings did not support an inflammatory process as described above. Hypersensitivity and drug reactions such as allergic parotitis and drug idiosyncrasy may also yield parotid gland swelling. According to Banks,23 in allergic parotitis coexistent involvement of the submandibular gland and, in some cases, all the salivary glands is observed as an important diagnostic point. Additionally, profuse lacrimation, sneezing, and even bronchospasm may be present. Among the drugs implicated in parotid swelling we find Phenylbutazone, iso-
prenaline, iodine, thiouracil, thiocyanate, guanethidine, bretylium tosylate, and thioridazine.23 In this case, the patient was taking no medications at the time of onset nor did he convey a history of drug allergies. Metabolic causes of parotid gland swelling include such disorders as malnutrition, alcoholic cirrhosis of the liver, latent diabetes, and
obesity.23 A systems review and physical examination of the patient in this case were accomplished and were unremarkable for any metabolic source of parotid gland swell-
ing. The miscellaneous group includes such conditions as mechanical obstruction secondary to calculi, congenital atresia of the parotid duct, functional hypersécrétions, and pneumoparotitis.23 The first three conditions could not be supported based on the clinical observation and history. Pneumoparotitis (surgical emphysema) of the parotid gland due to air pressure from the air-powder prophylaxis unit appeared to be the cause of the parotid swelling in this case. Physical examination of the patient should include a thorough examination of the parotid gland and ductal system as well as the fasciai spaces of the face and neck. The parotid gland is composed of two distinct lobes. The superficial lobe overlies the ramus of the mandible from the zygomatic arch superiorly to the angle of the mandible inferiorly, and lies superficial to the masseter muscle. The deep lobe wraps posteriorly around the ramus of the mandible and lies between the ramus and the mastoid process of the temporal bone. An accessory portion of the gland lies more anteriorly above the duct. The duct of the parotid
644
(Stensen's duct) courses anteriorly from the superficial lobe, and enters the oral cavity opposite the maxillary molar region. It is of interest to note that while a normal parotid gland is not palpable, the duct in health can be felt against a
J Periodontol July 1992
PNEUMOPAROTITIS ASSOCIATION WITH THE USE OF AN AIR-POWDER PROPHYLAXIS UNIT
flexed masseter.
Pneumoparotitis literally inflates the parotid gland allowing it to be easily palpated. Enlargements of the deep lobe can visually displace the pinna of the ear outwards. Along with distention of the gland and duct, prominence of the papilla can be seen and palpated intraorally (Fig. 2). Bubbling can occasionally be elicited from the duct orifice while pressing the gland. Pneumoparotitis contained within the gland can present as firm edema of the structure without crepitus, but if the air embolism violates the continuity of the acini, crepitus is usually felt. The capsule of the gland arises from a separation of the deep cervical fascia, a twolayered investing sheath which communicates from the zygomatic arch and occipital bone superiorly to the acromion, clavicle, and sternum inferiorly. Air escaping from the acini thereby has access to potential spaces from the base of the skull to the chest cavity, including the retropharyngeal space. If extracapsular extravasation of the air embolism is suspected, soft tissue radiographs of the neck, in two planes, should be ordered to assess the fasciai spaces. Computerized tomography or magnetic resonance imaging would be alternative studies. Injury to the gingival tissues, usually of a minor extent, have been reported by Weaks et al. clinically1 and by Snyder et al.28 histologically. While the potential for serious sequellae still remains uncommon in the literature in association with air-powder abrasive units, precautions such as avoiding deep periodontal pockets or vulnerable anatomic structures should be cautioned.
REFERENCES 1. Weaks LM, Lescher NB, Barnes CM, Holroyd SV. Clinical evaluation of the Prophy-Jet (R) as an instrument for routine removal of tooth stain and plaque. / Periodontol 1984;55:486-488. 2. Horning G. Clinical use of an air-powder abrasive. Compend Contin
6. Hunt RB, Sahler OD. Mediastinal emphysema produced by air turbine dental drills. JAMA 1968;205:101-102. 7. Argon JB, Dolwick MF, Buckley S. Pneumomediastinum and subcutaneous cervical emphysema during third molar extraction under general anesthesia. J Oral Maxillofac Surg 1986;44:141-144. 8. Hylton RP, Laskin JL. Subcutaneous emphysema with Pneumomediastinum following tooth extraction. Gen Dent 1985;33:350-351. 9. Habal MB, Beart R, Murray JE. Mediastinal emphysema secondary to fracture of the orbital floor. Am J Surg 1972;123:606-608. 10. Toofield JJ. Pneumomediastinum following fixation of the maxillary antrum. Br J Plast Surg 1977;30:179-181. 11. Wilson GA, Golle S, Green C. Subcutaneous emphysema after extraction of maxillary teeth: Report of a case. J Am Dent Assoc
1983;106:836-837. VA, Mooney JW, Stratigos GT. Iatrogenic dental-air emphysema: Report of a case. J Am Dent Assoc 1972;85:144-147. Snyder MD, Rosenberg ES. Subcutaneous emphysema during periodontal surgery: Report of a case. J Periodontol 1977;48:790-791. Woehrlen AE. Subcutaneous emphysema. Anes Prog 1985;32:161-
12. Cardo 13. 14.
163. 15. 16. 17. 18.
Hayduk S, Benett AC, Monheim LM. Subcutaneous emphysema after operative dentistry: Report of a case. J Am Dent Assoc; 1970;80:1362. Barber JW Burns JB. Subcutaneous emphysema of the face and neck after dental restoration. J Am Dent Assoc 1967;75:167-168. Falomo OO. Surgical emphysema following root canal therapy: Report of a case. Oral Surg Oral Med Oral Pathol 1984;58:101-102. Feinstone T. Infected subcutaneous emphysema: Report of a case. J
Am Dent Assoc 1971;83:1309-1311. 19. Reznick JB, Ardary WC. Cervicofacial subcutaneous air emphysema after dental extraction. J Am Dent Assoc 1990;120:417-419. 20. Buckley MJ et al. Orbital emphysema causing vision loss after dental extraction. J Am Dent Assoc 1990;120:42T424. 21. Turnbull AA. A remarkable coincidence in dental surgery. Br Med J
190O;l:1131. 22. Shafer WG, Hine MK, Levy BM. In: A Textbook of Oral Pathology, 4th ed., Philadelphia: W.B. Saunders Co. 1983;732-741. 23. Banks P. Nonneoplastic parotid swellings: A review. Oral Surg
1968;25:732-744. L, Kaynar A, Surg 1991;72:22-24.
24. Mandel
Pneumoparotid:
A
case
report. Oral
25. Garber MW. Pneumoparotitis: An unusual manifestation of hay fever. Am J Emerg Med 1987;5:40-41. 26. Telfer MR, Irvine GH. Pneumoparotitis. BrJSurg 1989;76:978. 27. Markowitz-Spence L. et al. Self-induced pneumoparotitis in an adolescent. Report of a case and review of the literature. Int J Pediatr
Otorhinolaryngol 1987;14:113-121. Snyder JA, McVay J, Brown FH et al. Systemic effects of air abrasive polishing. J Periodontol 1990;61:81-86.
1987;8:652-662. 3. Cooley RL, Brown FH, Lubow RM. Evaluation of air-powder abrasive prophylaxis units. Gen Dent 1990;38:24-27. 4. Finlayson RS, Stevens FD. Subcutaneous facial emphysema secondary to use of the Cavi-Jet. / Periodontol 1988;59:315-317.
28.
5. Noble WH. Mediastinal emphysema resulting from extraction of an impacted mandibular third molar. J Am Dent Assoc 1972;84:36-38.
ville,
Educ Dent
Wazen J.
Send reprint requests to: Dr. Frederic Brown, 317 Curacao Cove, NiceFL 32578. Accepted for publication January 28, 1992.
