Cocaine-induced oronasal fistulas with external nasal erosion but without palate involvement. (Original Article).

Abstract

The effects of chronic cocaine abuse have been widely described in the literature. Common complications include nasal septal perforation, saddle-nose deformity, and palatal perforation. Erosion of the external structures of the face has not been as extensively described, nor have oronasal fistulas that involve structures other than the hard or soft palate. In this article, we present the first reported case of cocaine-induced external nasal erosion that included multiple oronasal fistulas in the anterior gingival sulcus but did not involve the hard or soft palate. We stress the importance of a thorough history in such patients and consideration of all possible diagnoses, including drug abuse.

Introduction

The mechanism by which chronic cocaine abuse causes local necrosis of external structures is thought to involve many different factors, including ischemia from vasospasm, caustic erosion by adulterants, and local superinfection. (1,2) Several case reports of cocaine-induced local destruction of structures in the nasal cavity--including the cartilaginous nasal septum and turbinates--have been published in the literature, but only a few have described destruction of external structures of the face. (3-5) To our knowledge, the only type of oronasal fistula in cocaine abusers that has been reported to date has been perforation of the hard palate. (4,5) In this article, we describe a case of multiple oronasal fistulas involving the anterior gingival sulcus without palatal involvement.

Case report

A 43-year-old woman was referred to us by the Immunologic Diseases Section of the National Institute of Allergy and Infectious Diseases (National Institutes of Health) with a chief complaint of intractable nasal crusting. She had had no history of nasal problems until approximately 2 years earlier, when a sublabial abscess was discovered during a routine dental procedure. Over the next 6 months, she experienced a progressive destruction of both the internal and external portions of her nose, which was accompanied by epistaxis and a worsening of the nasal crusting.

The results of a preliminary laboratory work-up--including measurements of the erythrocyte sedimentation rate, antineurrophil cytoplasmic antibody level, fluorescent treponemal antibody level, and rheumatoid factor level--were all negative, and her rapid plasma reagin test was nonreactive. She underwent two intranasal biopsies, which revealed the presence of acute and chronic inflammation without granulomas or vasculitis. The patient experienced no clinical improvement despite several courses of empiric broad-spectrum antibiotic treatment.

Her medical history included T12 paraplegia as a result of a motor vehicle accident 24 years earlier. She had undergone multiple subsequent spinal surgeries, but she had no history of facial trauma. Her social history was notable for tobacco use, but she adamantly denied recreational drug use of any kind.

The physical examination revealed that the patient was well developed, well nourished, and in no acute distress. The nasal alae were intact bilaterally, but erosion of the columellar skin was evident (figure 1). Most of the cartilaginous nasal septum was absent, but she did not demonstrate a saddle-nose deformity. Two oronasal fistulas were present just above the upper incisors on either side of the superior labial frenulum (figure 2). The hard and soft palates were intact. The remainder of the head and neck examination was significant for severe acneiform facial lesions with pitting scars.

Basic laboratory values, including a serum creatinine level, were within normal limits. The results of her routine urinalysis were normal, but a urine drug screen was positive for cocaine on two occasions (maximum concentration: 1,510 ng/ml of benzoylecgonine). When questioned about cocaine use, the patient continued to adamantly deny it.

A chest x-ray was notable for an absence of nodules or granulomatous changes. Computed tomography (CT) demonstrated extensive bony and soft-tissue erosions intranasally (figure 3). The patient expressed an interest in facial reconstructive surgery, but she was subsequently lost to follow-up. We concluded that the fistulas and erosion had been caused by intranasal cocaine use.

Discussion

In 1912, Owens reported the first case of nasal septal perforation as a result of intranasal cocaine use. (2) It is now widely known that chronic cocaine use can result in many other local complications, including nasal collapse with saddle-nose deformity, palatal retraction and/or perforation, pharyngeal wall ulceration, sinusitis, and turbinate necrosis. Very few cases have been reported in the literature that were characterized by destruction of external facial structures. In 1995, Sevinsky et al described a case of total nasal septal destruction and a necrotic ulcer on the philtrum that mimicked a midline granuloma. (6) In 1999, Tierney and Stadelmann reported a case of extensive necrosis of the nose and upper lip following intranasal impaction of crack cocaine. (1) In both reports, as in our case, destruction involved the nasal septum, as well as the columella.

Reports of oronasal fistulas caused by cocaine abuse are infrequent in the literature. Those that have been published all describe fistulas that occurred as a result of necrosis of the hard plate. (4-6) To our knowledge, our case is the first to involve the presence of oronasal fistulas without palatal involvement.

Many patients with drug abuse problems are in denial, which makes their history less reliable. It is important that intranasal cocaine abuse always be considered in the differential diagnosis of midline nasal destruction. Cocaine abuse should also be included in the differential diagnosis of sublabial abscess and oronasal fistula. Urine toxicology testing is strongly recommended prior to embarking on reconstructive nasal surgery in these patients. Rehabilitation of the patient should be a priority, because abstinence from further abuse must occur in order to halt further tissue destruction.

References

(1.) Tierney BP, Stadelmann WK. Necrotizing infection of the face secondary to intranasal impaction of "crack" cocaine. Ann Plast Surg 1999;43:640-3.

(2.) Owens WD. Signs and symptoms presented by those addicted to cocaine. JAMA l912;58:329-30.

(3.) Talbott JF, Gorti GK, Koch RJ. Midfacial osteomyelitis in a chronic cocaine abuser: A case report. Ear Nose Throat J 2001;80:738, 740, 742-3.

(4.) 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;81:172-4, 176-7.

(5.) Lancaster J, Belloso A, Wilson CA, McCormick M. Rare case of nasooral fistula with extensive osteocartilaginous necrosis secondary to cocaine abuse: Review of otorhinolaryngological presentations in cocaine addicts. J Laryngol Otol 2000;114:630-3.

(6.) Sevinsky LD, Woscoff A, Jaimovich L, Terzian A. Nasal cocaine abuse mimicking midline granuloma. J Am Acad Dermatol 1995;32:286-7.

From the National Institute of Deafness and Other Communication Disorders (Mr. Vilela, Ms. McCullagh, and Dr. Kass) and the National Institute of Allergy and Infectious Diseases (Dr. Langford), National Institutes of Health, Bethesda, Md.

Reprint requests: Erik S. Kass, MD, National Institutes of Health, Bldg. 10, Room 5C400, 10 Center Dr., MSC 1750, Bethesda, MD 20892-1750. Phone: [phone]; fax: [phone]; e-mail: [e-mail]