Orbit, 2013; 32(6): 405–408 ! Informa Healthcare USA, Inc. ISSN: 0167-6830 print / 1744-5108 online DOI: 10.3109/01676830.2013.815225
REVIEW ARTICLE
Dacryocystitis Secondary to Intranasal Cocaine Abuse: A Case Report and Literature Review Felicia D. Allard1, Eric U. Yee1, and Suzanne K. Freitag2 Department of Pathology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA and 2Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, USA
ABSTRACT Purpose: To report a case of dacryocystitis secondary to intranasal cocaine abuse and to review the literature on the effects of cocaine on sinus, nasal and lacrimal structures. Methods: Case report and literature review. Results: A 33-year-old male presented with unilateral epiphora and discharge, and clinical examination was consistent with dacryocystitis. He had a 2-year history of intranasal cocaine use. Computed tomography revealed extensive bilateral intranasal and sinus destruction, consistent with cocaine abuse. He was treated with antibiotics followed by dacryocystorhinostomy with silicone intubation. He had 2 recurrences of dacryocystitis and underwent one additional lacrimal surgery. Conclusions: Cocaine abuse and its accompanying intranasal and sinus destruction should be considered when determining the etiology of nasolacrimal obstruction and dacryocystitis. A medical and social history with specific questions about drug abuse may be useful. Computed tomography is helpful in delineating damage to the sinuses, nose and lacrimal system. Management with antibiotics and dacryocystorhinostomy surgery may result in resolution of symptoms. Keywords: Cocaine, dacrocystitis, drug, intranasal
INTRODUCTION
An additional cause of secondary acquired NLDO rarely mentioned in the literature is intranasal drug usage. We present a case of acquired NLDO and dacryocystitis in a patient with extensive intranasal and sinus destruction secondary to cocaine abuse.
Dacryocystitis is an infection of the lacrimal sac thought to occur secondary to obstruction of the nasolacrimal system. Acquired nasolacrimal obstruction may occur at any point along the lacrimal drainage pathway but is most commonly seen in the distal lacrimal sac and nasolacrimal duct.1 The most common presenting sign of nasolacrimal duct obstruction (NLDO) is epiphora. If the system becomes infected, patients may develop purulent discharge and a tender, enlarged lacrimal sac. Primary acquired NLDO is idiopathic and thought to be due to edema or fibrosis that occurs spontaneously.2 Secondary acquired NLDO is contributable to a constellation of etiologies including infection, inflammation, neoplasm, and trauma.3–5
CASE REPORT
20 13
Orbit Downloaded from informahealthcare.com by University of Laval on 07/16/14 For personal use only.
1
A 33-year-old male presented with a 2-year history of left-sided epiphora with worsening yellow discharge. One month prior to presentation he had undergone rib graft rhinoplasty to correct a saddle nose deformity secondary to nasal septum destruction caused by intranasal cocaine use. He reported nasal cocaine use for 2 years, with cessation 1 year prior to presentation. He denied any other significant past medical history.
Received 25 January 2013; Revised 26 March 2013; Accepted 10 June 2013; Published online 1 August 2013 Correspondence: Suzanne K. Freitag, M.D., Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston, Massachusetts 02114, USA. E-mail: [email protected]
405
Orbit Downloaded from informahealthcare.com by University of Laval on 07/16/14 For personal use only.
406 F. D. Allard et al. On examination, visual acuity was 20/20 in both eyes, pupils were normal, extraocular motility was intact and slit lamp biomicroscopy showed an elevated tear lake on the left. Puncta were normal in size and position, but purulent discharge was expressed from the left upper and lower puncta with pressure applied to the left lacrimal sac. There were no palpable masses, no erythema or edema overlying the lacrimal sac. Intranasal examination via speculum revealed absence of the inferior turbinates and nasal septum. Computed tomography (CT) revealed extensive destruction of sinus and nasal structures (Figure 1). There was absence of large portions of the nasal septum, bilateral middle and inferior turbinates, left uncinate process as well as bony defects in bilateral medial maxillary sinus walls with the left wall nearly absent. Concentric thickening of the left maxillary sinus mucosa and enlargement of the left lacrimal sac were observed. The patient was diagnosed with left dacryocystitis. He was empirically treated with oral azithromycin and topical gatifloxacin. Left dacryocystorhinostomy (DCR) with Crawford tube placement was performed after the infection had improved. A biopsy of the left lacrimal sac revealed a dense inflammatory infiltrate comprised of lymphocytes and plasma cells. One month later, he developed recurrent left dacryocystitis which was treated with a two-week course of oral augmentin. He remained asymptomatic and the Crawford tubes were removed 14 weeks after surgery. He returned 7 months later with complaints of pain in the left medial canthus and purulent discharge from the left puncta. He was diagnosed with recurrent left dacryocystitis; cultures of lacrimal discharge grew Streptococcus pneumoniae. The pain and discharge resolved following a course of oral augmentin and
he underwent repeat left DCR with Crawford tube placement. Left lacrimal sac biopsy revealed chronic inflammation of the mucosa, similar to earlier biopsy findings. His recovery was uneventful and Crawford tubes were removed 5 months later. He has had no further episodes of dacryocystitis.
DISCUSSION Cocaine is a naturally occurring crystalline alkaloid compound obtained from the leaves of the coca plant (Erythroxylon coca). The pharmacologic effects of cocaine, which include anesthesia and vasoconstriction, have made the compound a useful surgical anesthetic agent. Human consumption of cocaine dates back to at least 600 AD. The first reported use of cocaine as a local anesthetic occurred around 800 AD when cocaine-filled saliva was dribbled onto the skulls of patients prior to trephining operations. In 1855, the alkaloid compound of coca leaves was discovered by the German chemist Friedrich Gaedcke. It was isolated and named cocaine by Albert in 1860.6 Cocaine can be absorbed through any mucous membrane, smoked or injected. When insufflated intranasally, cocaine produces euphoria as well as a local anesthetic effect via a complex set of actions on the sympathetic peripheral nervous system and central nervous system. Intranasal insufflation also leads to local vasoconstriction via blockage of reuptake of catecholamines in synaptic clefts.7 It is this vasoconstriction that contributes to local tissue damage. The damaging effects of cocaine on mucosal tissues, bone, and cartilage of the nasal passage and oral cavity have been well documented.8–10 Direct effects of cocaine include constriction of the vasculature of the nasal passages that can lead to ischemia and tissue necrosis.11–14 Impurities and substances
FIGURE 1. Computed tomography revealed extensive tissue destruction. Axial (a) and coronal (b) images demonstrate absence of the nasal septum, bilateral middle and inferior turbinates, and bony defects in bilateral medial maxillary sinus walls (arrows). (c) The left lacrimal sac is enlarged (arrow). Orbit
Orbit Downloaded from informahealthcare.com by University of Laval on 07/16/14 For personal use only.
Dacryocystitis Secondary to Intranasal Cocaine Abuse 407 used to ‘‘cut’’ cocaine may produce an irritative effect on tissue.15 Mechanical trauma from picking or probing to remove intranasal crusts may cause further damage.12,16 Additionally, compromise of the nasal mucosa can impair the ability to combat potential pathogens, thereby leaving the nasal passage susceptible to infection.12 A combination of such insults may lead to damage or destruction of the mucosa and the underlying soft tissue, cartilage, and bone.10,12 The body’s normal response to irritation, foreign material and infection is inflammation. Depending on the severity and chronicity of tissue injury, a variety of responses can be seen: regeneration, metaplasia or fibrosis. Although the former 2 responses may be less concerning, fibrosis may be irreversible and may contribute to NLDO.8 Although NLDO is a clinical diagnosis, a variety of histologic findings can be seen from intranasal cocaine use. Affected portions of the mucosa often show an acute or chronic inflammatory response.8–10,17–19 The chronic inflammatory infiltrate can be dense, as in our case, and predominantly composed of lymphocytes and plasma cells8,9; associated Russell bodies have been reported.8 Polarizable foreign material has also been found.17 Alexandrakis et al. demonstrated a cross-section from the nasolacrimal sac and duct with a dense chronic inflammatory infiltrate in the mucosa, surrounding periductal fibrosis, and marked narrowing of the nasolacrimal duct lumen.8 Additionally, osteocartilagenous necrosis and acute osteomyelitis with bacterial overgrowth can be seen.10,20 Yewell et al. demonstrated fungal forms with Gomori’s methenamine silver staining.21 Ulceration, necrosis, granulomas and metaplasia can be seen in various tissue components biopsied from the nasal and oral cavity.9,12,17–19 Although none of these microscopic findings are pathognomonic for intranasal cocaine use, correlation of the histologic and radiologic findings with the physical examination and history aid in diagnosis. Although complications from chronic cocaine use such as perforation of the nasal septum and palate have been frequently reported,8,10,12 there are few descriptions of NLDO secondary to intranasal cocaine abuse. Alexandrakis et al. reported a series of 7 patients with a history of chronic nasal cocaine use that developed NLDO or orbital cellulitis.8 The average usage history in these patients was 11 years, with a range of 5 to 20 years. Histopathology was performed on lacrimal sacs in 2 cases with NLDO in this series and revealed chronic inflammation and fibrosis. Both of these patients had 12-year usage histories.8 Our patient reported a much shorter abuse history with a usage time of 2 years. This may explain the lack of fibrosis found on his histopathology. The nasolacrimal duct drains into the inferior nasal meatus, which lies below the inferior turbinate and !
2013 Informa Healthcare USA, Inc.
above the floor of the nasal cavity. The inferior turbinate may provide some protection by shielding the nasolacrimal duct from snorted cocaine. In the series by Alexandrakis et al., 4 of 7 patients had absent inferior nasal turbinates.8 Despite only 2 years of reported intranasal cocaine abuse, our patient developed extensive destruction of intranasal structures, demonstrated on CT imaging, predisposing him to NLDO and subsequent infections. This etiology should be included in the differential diagnosis of patients presenting with NLDO or dacryocystitis. A detailed social history and radiological correlation may aid in the diagnosis.
DECLARATION OF INTEREST The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
REFERENCES 1. DeAngelis D, Hurwitz J, Oestreicher J, Howarth D. The pathogenesis and treatment of lacrimal obstruction: The value of lacrimal sac and bone analysis. Orbit 2001 Sep; 20(3):163–172. 2. Linberg JV, McCormick SA. Primary acquired nasolacrimal duct obstruction. A clinicopathologic report and biopsy technique. Ophthalmology 1986 Aug;93(8):1055–1063. 3. Bartley GB. Acquired lacrimal drainage obstruction: an etiologic classification system, case reports, and a review of the literature. Part 3. Ophthal Plast Reconstr Surg 1993;9(1):11–26. 4. Bartley GB. Acquired lacrimal drainage obstruction: an etiologic classification system, case reports, and a review of the literature. Part 1. Ophthal Plast Reconstr Surg 1992; 8(4):237–242. 5. Bartley GB. Acquired lacrimal drainage obstruction: an etiologic classification system, case reports, and a review of the literature. Part 2. Ophthal Plast Reconstr Surg 1992;8(4):243–249. 6. Altman AJ, Albert DM, Fournier GA. Cocaine’s use in ophthalmology: our 100-year heritage. Surv Ophthalmol 1985 Jan–Feb;29(4):300–306. 7. Boghdadi MS, Henning RJ. Cocaine: pathophysiology and clinical toxicology. Heart Lung 1997 Nov–Dec;26(6):466–483; quiz 484–485. 8. Alexandrakis G, Tse DT, Rosa Jr RH, Johnson TE. Nasolacrimal duct obstruction and orbital cellulitis associated with chronic intranasal cocaine abuse. Arch Ophthalmol 1999 Dec;117(12):1617–1622. 9. Mari A, Arranz C, Gimeno X, et al. Nasal cocaine abuse and centrofacial destructive process: report of three cases including treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002 Apr;93(4):435–439. 10. Lancaster J, Belloso A, Wilson CA, McCormick M. Rare case of naso-oral fistula with extensive osteocartilaginous necrosis secondary to cocaine abuse: review of otorhinolaryngological presentations in cocaine addicts. J Laryngol Otol 2000 Aug;114(8):630–633. 11. Yanagisawa E, Latorre R. Endoscopic view of cocaine rhinitis. Ear Nose Throat J 1996 Mar;75(3):128–130.
408 F. D. Allard et al. 17. Seyer BA, Grist W, Muller S. Aggressive destructive midfacial lesion from cocaine abuse. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002 Oct;94(4):465–470. 18. Armstrong Jr M, Shikani AH. Nasal septal necrosis mimicking Wegener’s granulomatosis in a cocaine abuser. Ear Nose Throat J 1996 Sep;75(9):623–626. 19. Sittel C, Eckel HE. Nasal cocaine abuse presenting as a central facial destructive granuloma. Eur Arch Otorhinolaryngol 1998;255(9):446–447. 20. Talbott JF, Gorti GK, Koch RJ. Midfacial osteomyelitis in a chronic cocaine abuser: a case report. Ear Nose Throat J 2001 Oct;80(10):738–740, 42–43. 21. Yewell J, Haydon R, Archer S, Manaligod JM. Complications of intranasal prescription narcotic abuse. Ann Otol Rhinol Laryngol 2002 Feb;111(2):174–177.
Orbit Downloaded from informahealthcare.com by University of Laval on 07/16/14 For personal use only.
12. Smith JC, Kacker A, Anand VK. Midline nasal and hard palate destruction in cocaine abusers and cocaine’s role in rhinologic practice. Ear Nose Throat J 2002 Mar;81(3): 172–177. 13. Vilensky W. Illicit and licit drugs causing perforation of the nasal septum. J Forensic Sci 1982 Oct;27(4):958–962. 14. Chow JM, Robertson Jr AL, Stein RJ. Vascular changes in the nasal submucosa of chronic cocaine addicts. Am J Forensic Med Pathol 1990 Jun;11(2):136–143. 15. Schweitzer VG. Osteolytic sinusitis and pneumomediastinum: deceptive otolaryngologic complications of cocaine abuse. Laryngoscope 1986 Feb;96(2):206–210. 16. Sastry RC, Lee D, Har-El G. Palate perforation from cocaine abuse. Otolaryngol Head Neck Surg 1997 Apr; 116(4):565–566.
Orbit
REVIEW ARTICLE
Dacryocystitis Secondary to Intranasal Cocaine Abuse: A Case Report and Literature Review Felicia D. Allard1, Eric U. Yee1, and Suzanne K. Freitag2 Department of Pathology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA and 2Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, USA
ABSTRACT Purpose: To report a case of dacryocystitis secondary to intranasal cocaine abuse and to review the literature on the effects of cocaine on sinus, nasal and lacrimal structures. Methods: Case report and literature review. Results: A 33-year-old male presented with unilateral epiphora and discharge, and clinical examination was consistent with dacryocystitis. He had a 2-year history of intranasal cocaine use. Computed tomography revealed extensive bilateral intranasal and sinus destruction, consistent with cocaine abuse. He was treated with antibiotics followed by dacryocystorhinostomy with silicone intubation. He had 2 recurrences of dacryocystitis and underwent one additional lacrimal surgery. Conclusions: Cocaine abuse and its accompanying intranasal and sinus destruction should be considered when determining the etiology of nasolacrimal obstruction and dacryocystitis. A medical and social history with specific questions about drug abuse may be useful. Computed tomography is helpful in delineating damage to the sinuses, nose and lacrimal system. Management with antibiotics and dacryocystorhinostomy surgery may result in resolution of symptoms. Keywords: Cocaine, dacrocystitis, drug, intranasal
INTRODUCTION
An additional cause of secondary acquired NLDO rarely mentioned in the literature is intranasal drug usage. We present a case of acquired NLDO and dacryocystitis in a patient with extensive intranasal and sinus destruction secondary to cocaine abuse.
Dacryocystitis is an infection of the lacrimal sac thought to occur secondary to obstruction of the nasolacrimal system. Acquired nasolacrimal obstruction may occur at any point along the lacrimal drainage pathway but is most commonly seen in the distal lacrimal sac and nasolacrimal duct.1 The most common presenting sign of nasolacrimal duct obstruction (NLDO) is epiphora. If the system becomes infected, patients may develop purulent discharge and a tender, enlarged lacrimal sac. Primary acquired NLDO is idiopathic and thought to be due to edema or fibrosis that occurs spontaneously.2 Secondary acquired NLDO is contributable to a constellation of etiologies including infection, inflammation, neoplasm, and trauma.3–5
CASE REPORT
20 13
Orbit Downloaded from informahealthcare.com by University of Laval on 07/16/14 For personal use only.
1
A 33-year-old male presented with a 2-year history of left-sided epiphora with worsening yellow discharge. One month prior to presentation he had undergone rib graft rhinoplasty to correct a saddle nose deformity secondary to nasal septum destruction caused by intranasal cocaine use. He reported nasal cocaine use for 2 years, with cessation 1 year prior to presentation. He denied any other significant past medical history.
Received 25 January 2013; Revised 26 March 2013; Accepted 10 June 2013; Published online 1 August 2013 Correspondence: Suzanne K. Freitag, M.D., Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston, Massachusetts 02114, USA. E-mail: [email protected]
405
Orbit Downloaded from informahealthcare.com by University of Laval on 07/16/14 For personal use only.
406 F. D. Allard et al. On examination, visual acuity was 20/20 in both eyes, pupils were normal, extraocular motility was intact and slit lamp biomicroscopy showed an elevated tear lake on the left. Puncta were normal in size and position, but purulent discharge was expressed from the left upper and lower puncta with pressure applied to the left lacrimal sac. There were no palpable masses, no erythema or edema overlying the lacrimal sac. Intranasal examination via speculum revealed absence of the inferior turbinates and nasal septum. Computed tomography (CT) revealed extensive destruction of sinus and nasal structures (Figure 1). There was absence of large portions of the nasal septum, bilateral middle and inferior turbinates, left uncinate process as well as bony defects in bilateral medial maxillary sinus walls with the left wall nearly absent. Concentric thickening of the left maxillary sinus mucosa and enlargement of the left lacrimal sac were observed. The patient was diagnosed with left dacryocystitis. He was empirically treated with oral azithromycin and topical gatifloxacin. Left dacryocystorhinostomy (DCR) with Crawford tube placement was performed after the infection had improved. A biopsy of the left lacrimal sac revealed a dense inflammatory infiltrate comprised of lymphocytes and plasma cells. One month later, he developed recurrent left dacryocystitis which was treated with a two-week course of oral augmentin. He remained asymptomatic and the Crawford tubes were removed 14 weeks after surgery. He returned 7 months later with complaints of pain in the left medial canthus and purulent discharge from the left puncta. He was diagnosed with recurrent left dacryocystitis; cultures of lacrimal discharge grew Streptococcus pneumoniae. The pain and discharge resolved following a course of oral augmentin and
he underwent repeat left DCR with Crawford tube placement. Left lacrimal sac biopsy revealed chronic inflammation of the mucosa, similar to earlier biopsy findings. His recovery was uneventful and Crawford tubes were removed 5 months later. He has had no further episodes of dacryocystitis.
DISCUSSION Cocaine is a naturally occurring crystalline alkaloid compound obtained from the leaves of the coca plant (Erythroxylon coca). The pharmacologic effects of cocaine, which include anesthesia and vasoconstriction, have made the compound a useful surgical anesthetic agent. Human consumption of cocaine dates back to at least 600 AD. The first reported use of cocaine as a local anesthetic occurred around 800 AD when cocaine-filled saliva was dribbled onto the skulls of patients prior to trephining operations. In 1855, the alkaloid compound of coca leaves was discovered by the German chemist Friedrich Gaedcke. It was isolated and named cocaine by Albert in 1860.6 Cocaine can be absorbed through any mucous membrane, smoked or injected. When insufflated intranasally, cocaine produces euphoria as well as a local anesthetic effect via a complex set of actions on the sympathetic peripheral nervous system and central nervous system. Intranasal insufflation also leads to local vasoconstriction via blockage of reuptake of catecholamines in synaptic clefts.7 It is this vasoconstriction that contributes to local tissue damage. The damaging effects of cocaine on mucosal tissues, bone, and cartilage of the nasal passage and oral cavity have been well documented.8–10 Direct effects of cocaine include constriction of the vasculature of the nasal passages that can lead to ischemia and tissue necrosis.11–14 Impurities and substances
FIGURE 1. Computed tomography revealed extensive tissue destruction. Axial (a) and coronal (b) images demonstrate absence of the nasal septum, bilateral middle and inferior turbinates, and bony defects in bilateral medial maxillary sinus walls (arrows). (c) The left lacrimal sac is enlarged (arrow). Orbit
Orbit Downloaded from informahealthcare.com by University of Laval on 07/16/14 For personal use only.
Dacryocystitis Secondary to Intranasal Cocaine Abuse 407 used to ‘‘cut’’ cocaine may produce an irritative effect on tissue.15 Mechanical trauma from picking or probing to remove intranasal crusts may cause further damage.12,16 Additionally, compromise of the nasal mucosa can impair the ability to combat potential pathogens, thereby leaving the nasal passage susceptible to infection.12 A combination of such insults may lead to damage or destruction of the mucosa and the underlying soft tissue, cartilage, and bone.10,12 The body’s normal response to irritation, foreign material and infection is inflammation. Depending on the severity and chronicity of tissue injury, a variety of responses can be seen: regeneration, metaplasia or fibrosis. Although the former 2 responses may be less concerning, fibrosis may be irreversible and may contribute to NLDO.8 Although NLDO is a clinical diagnosis, a variety of histologic findings can be seen from intranasal cocaine use. Affected portions of the mucosa often show an acute or chronic inflammatory response.8–10,17–19 The chronic inflammatory infiltrate can be dense, as in our case, and predominantly composed of lymphocytes and plasma cells8,9; associated Russell bodies have been reported.8 Polarizable foreign material has also been found.17 Alexandrakis et al. demonstrated a cross-section from the nasolacrimal sac and duct with a dense chronic inflammatory infiltrate in the mucosa, surrounding periductal fibrosis, and marked narrowing of the nasolacrimal duct lumen.8 Additionally, osteocartilagenous necrosis and acute osteomyelitis with bacterial overgrowth can be seen.10,20 Yewell et al. demonstrated fungal forms with Gomori’s methenamine silver staining.21 Ulceration, necrosis, granulomas and metaplasia can be seen in various tissue components biopsied from the nasal and oral cavity.9,12,17–19 Although none of these microscopic findings are pathognomonic for intranasal cocaine use, correlation of the histologic and radiologic findings with the physical examination and history aid in diagnosis. Although complications from chronic cocaine use such as perforation of the nasal septum and palate have been frequently reported,8,10,12 there are few descriptions of NLDO secondary to intranasal cocaine abuse. Alexandrakis et al. reported a series of 7 patients with a history of chronic nasal cocaine use that developed NLDO or orbital cellulitis.8 The average usage history in these patients was 11 years, with a range of 5 to 20 years. Histopathology was performed on lacrimal sacs in 2 cases with NLDO in this series and revealed chronic inflammation and fibrosis. Both of these patients had 12-year usage histories.8 Our patient reported a much shorter abuse history with a usage time of 2 years. This may explain the lack of fibrosis found on his histopathology. The nasolacrimal duct drains into the inferior nasal meatus, which lies below the inferior turbinate and !
2013 Informa Healthcare USA, Inc.
above the floor of the nasal cavity. The inferior turbinate may provide some protection by shielding the nasolacrimal duct from snorted cocaine. In the series by Alexandrakis et al., 4 of 7 patients had absent inferior nasal turbinates.8 Despite only 2 years of reported intranasal cocaine abuse, our patient developed extensive destruction of intranasal structures, demonstrated on CT imaging, predisposing him to NLDO and subsequent infections. This etiology should be included in the differential diagnosis of patients presenting with NLDO or dacryocystitis. A detailed social history and radiological correlation may aid in the diagnosis.
DECLARATION OF INTEREST The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
REFERENCES 1. DeAngelis D, Hurwitz J, Oestreicher J, Howarth D. The pathogenesis and treatment of lacrimal obstruction: The value of lacrimal sac and bone analysis. Orbit 2001 Sep; 20(3):163–172. 2. Linberg JV, McCormick SA. Primary acquired nasolacrimal duct obstruction. A clinicopathologic report and biopsy technique. Ophthalmology 1986 Aug;93(8):1055–1063. 3. Bartley GB. Acquired lacrimal drainage obstruction: an etiologic classification system, case reports, and a review of the literature. Part 3. Ophthal Plast Reconstr Surg 1993;9(1):11–26. 4. Bartley GB. Acquired lacrimal drainage obstruction: an etiologic classification system, case reports, and a review of the literature. Part 1. Ophthal Plast Reconstr Surg 1992; 8(4):237–242. 5. Bartley GB. Acquired lacrimal drainage obstruction: an etiologic classification system, case reports, and a review of the literature. Part 2. Ophthal Plast Reconstr Surg 1992;8(4):243–249. 6. Altman AJ, Albert DM, Fournier GA. Cocaine’s use in ophthalmology: our 100-year heritage. Surv Ophthalmol 1985 Jan–Feb;29(4):300–306. 7. Boghdadi MS, Henning RJ. Cocaine: pathophysiology and clinical toxicology. Heart Lung 1997 Nov–Dec;26(6):466–483; quiz 484–485. 8. Alexandrakis G, Tse DT, Rosa Jr RH, Johnson TE. Nasolacrimal duct obstruction and orbital cellulitis associated with chronic intranasal cocaine abuse. Arch Ophthalmol 1999 Dec;117(12):1617–1622. 9. Mari A, Arranz C, Gimeno X, et al. Nasal cocaine abuse and centrofacial destructive process: report of three cases including treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002 Apr;93(4):435–439. 10. Lancaster J, Belloso A, Wilson CA, McCormick M. Rare case of naso-oral fistula with extensive osteocartilaginous necrosis secondary to cocaine abuse: review of otorhinolaryngological presentations in cocaine addicts. J Laryngol Otol 2000 Aug;114(8):630–633. 11. Yanagisawa E, Latorre R. Endoscopic view of cocaine rhinitis. Ear Nose Throat J 1996 Mar;75(3):128–130.
408 F. D. Allard et al. 17. Seyer BA, Grist W, Muller S. Aggressive destructive midfacial lesion from cocaine abuse. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002 Oct;94(4):465–470. 18. Armstrong Jr M, Shikani AH. Nasal septal necrosis mimicking Wegener’s granulomatosis in a cocaine abuser. Ear Nose Throat J 1996 Sep;75(9):623–626. 19. Sittel C, Eckel HE. Nasal cocaine abuse presenting as a central facial destructive granuloma. Eur Arch Otorhinolaryngol 1998;255(9):446–447. 20. Talbott JF, Gorti GK, Koch RJ. Midfacial osteomyelitis in a chronic cocaine abuser: a case report. Ear Nose Throat J 2001 Oct;80(10):738–740, 42–43. 21. Yewell J, Haydon R, Archer S, Manaligod JM. Complications of intranasal prescription narcotic abuse. Ann Otol Rhinol Laryngol 2002 Feb;111(2):174–177.
Orbit Downloaded from informahealthcare.com by University of Laval on 07/16/14 For personal use only.
12. Smith JC, Kacker A, Anand VK. Midline nasal and hard palate destruction in cocaine abusers and cocaine’s role in rhinologic practice. Ear Nose Throat J 2002 Mar;81(3): 172–177. 13. Vilensky W. Illicit and licit drugs causing perforation of the nasal septum. J Forensic Sci 1982 Oct;27(4):958–962. 14. Chow JM, Robertson Jr AL, Stein RJ. Vascular changes in the nasal submucosa of chronic cocaine addicts. Am J Forensic Med Pathol 1990 Jun;11(2):136–143. 15. Schweitzer VG. Osteolytic sinusitis and pneumomediastinum: deceptive otolaryngologic complications of cocaine abuse. Laryngoscope 1986 Feb;96(2):206–210. 16. Sastry RC, Lee D, Har-El G. Palate perforation from cocaine abuse. Otolaryngol Head Neck Surg 1997 Apr; 116(4):565–566.
Orbit
