Osteocartilaginous necrosis of the sinonasal tract following cocaine abuse

Kuriloff, Daniel B.; Kimmelman, Charles P.

doi:10.1288/00005537-198909000-00005

Cited by 57 publications

(22 citation statements)

References 27 publications

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“…Vascular ischemia from excessive cocaine use is widely considered to be a major element in the development of CIMDL. [3][4][5][6][7][8] However, given the widespread abuse of nasal cocaine insufflation on the one hand and the relative rarity of CIMDL on the other, differentiating host factors must hold the key to the undoubtedly multifactorial pathogenesis of CIMDL. 20 The ischemic and direct traumatic effects of cocaine crystals should affect all users similarly.…”

Section: Discussionmentioning

confidence: 99%

“…The minimum time interval free of cocaine use remains controversial, and there is no consensus or large body of experience to provide guidance. Some authors insist on the need to confirm the cessation of cocaine abuse with toxicological tests, ensuring full rehabilitation for 6 or even 12 months prior to surgery, [7][8][9][10] to avoid treatment failure. The surgical procedures most often requested by patients are septal and palate perforation closure.…”

Section: Discussionmentioning

confidence: 99%

“…The surgical procedures most often requested by patients are septal and palate perforation closure. [2][3][4][5][6][7][8][9] However, some patients ask for aesthetic procedures such as rhinoplasty and closure of nasocutaneous fistulas. 6,12,26 In the literature currently available, involvement of the craniovertebral junction or the spine in general in CIMDL has never been reported.…”

Section: Discussionmentioning

confidence: 99%

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Craniovertebral junction instability as an extension of cocaine-induced midline destructive lesions: case report

Brembilla¹,

Lanterna²,

Risso³

et al. 2015

SPI

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With the increasingly widespread illicit use of cocaine, a broad spectrum of clinical pathologies related to this form of drug abuse is emerging. The most frequently used method of administration of powdered cocaine is intranasal inhalation, or “snorting.” Consequently, adverse effects of cocaine on the nasal tract are common. Habitual nasal insufflations of cocaine can cause mucosal lesions. If cocaine use becomes chronic and compulsive, progressive damage of the mucosa and perichondrium leads to ischemic necrosis of the septal cartilage and perforation of the nasal septum. Occasionally, cocaine-induced lesions cause extensive destruction of the osteocartilaginous structures of the nose, sinuses, and palate and can mimic other diseases such as tumors, infections, and immunological diseases. In the literature currently available, involvement of the craniovertebral junction in the cocaine-induced midline destructive lesions (CIMDLs) has never been reported. The present case concerns a 44-year-old man who presented with long-standing symptoms including nasal obstruction, epistaxis, dysphagia, nasal reflux, and severe neck pain. A diagnosis of CIMDL was made in light of the patient’s history and the findings on physical and endoscopic examinations, imaging studies, and laboratory testing. Involvement of the craniovertebral junction in the destructive process was evident. For neurosurgical treatment, the authors considered the high grade of atlantoaxial instability, the poorly understood cocaine-induced lesions of the spine and their potential evolution overtime, as well as cocaine abusers’ poor compliance. The patient underwent posterior craniovertebral fixation. Understanding, classifying, and treating cocaine-induced lesions involving the craniovertebral junction are a challenge.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Craniovertebral junction instability as an extension of cocaine-induced midline destructive lesions: case report

Brembilla¹,

Lanterna²,

Risso³

et al. 2015

SPI

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“…It is characterized as an ulcerative process involving the nose, septum, palate and pharynx and presents clinically similar to a malignant disease. Three cases have been reported to date, all in the United States of America [4,5]. In order to bring greater attention to this clinical complex of cocaine abuse, we here report the first such case in Europe.…”

Section: Introductionmentioning

confidence: 92%

Nasal cocaine abuse presenting as a central facial destructive granuloma

Sittel

Eckel

1998

European Archives of Oto-Rhino-Laryngology

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We describe a 36-year-old patient with an aggressive, midline intranasal and naso- and oropharyngeal destructive process. For months the patient denied heavy abuse of nasal cocaine, but finally admitted it. Necrosis and atrophy of the inferior and middle nasal turbinates bilaterally, prominent naso and oropharyngeal ulcers, nasal septal as well as hard palate perforation were observed clinically. Repeated biopsies revealed focal areas of chronic inflammation and necrosis, but there was no evidence of vasculitis or granuloma formation. Since serum was slightly positive for antineutrophil cytoplasmic antibody, the initial diagnosis was Wegener's granulomatosis. In the United States there have been a few reports on a new cocaine-associated syndrome presenting as an aggressive, midline, intranasal and intrapharyngeal destructive process mimicking limited Wegener's granulomatosis and midline reticulosis. We report the first such case in Europe and offer guidelines for the diagnostic work-up of such cases.

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“…To date, only a few cases of palatal perforation from cocaine inhalation 3,9,14,16,21,22 have been reported in the literature, and an efficient management protocol is far from being established. Several reconstructive techniques of the palate and different surgical options have been reported.…”

mentioning

confidence: 99%