Journal of Otology & RhinologyISSN: 2324-8785

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Case Report, J Otol Rhinol Vol: 3 Issue: 1

Lytic Lesion of the Clivus Following Intranasal Narcotic Abuse: First Case Report and Review of the Literature

Habib Rizk1*, Christine Emery2 and Neil Hockstein1
1Otolaryngology-Head and Neck Surgery, Christiana Care Health Systems, Delaware, USA
2Department of Radiology, Christiana Care Health Systems, Delaware, USA
Corresponding author : Habib Rizk
Otolaryngology – Head and Neck Surgery, Christiana Care Health Systems, Delaware, USA
Tel: 2154590435
E-mail: [email protected]
Received: October 28, 2013 Accepted: December 07, 2013 Published: December 15, 2013
Citation: Rizk H, Emery C, Hockstein N (2013) Lytic Lesion of the Clivus Following Intranasal Narcotic Abuse: First Case Report and Review of the Literature. J Otol Rhinol 3:1. doi:10.4172/2324-8785.1000139


Lytic Lesion of the Clivus Following Intranasal Narcotic Abuse: First Case Report and Review of the Literature

Intranasal narcotic delivery is increasingly frequent due to avoidance of intravenous injection from fear of HIV and because of availability of prescription drugs to treat chronic pain syndromes. Extensive destruction of the midfacial structures has been reported for over a decade.This is the first reported case of clival erosion related to intranasal narcotic abuse. Radiologists and clinicians should be aware of this potential complication because delayed detection and ongoing abuse can result in progressive damage and diminished success of attempted surgical repair.

Keywords: Intranasal Narcotic; Lytic Lesion; Clivus


Intranasal Narcotic; Lytic Lesion; Clivus


Intranasal drug abuse, most commonly cocaine and to a lesser extent heroin and methamphetamine, has been increasing in recent years [1]. A new practice involving snorting crushed prescription narcotics including oxycodone and hydrocodone has been recognized for about a decade. Medical complications include destruction of mid facial structures [1,2]. We present the case of a young adult with a history of intranasal abuse of Percocet and Vicodin with resultant near-total nasal septal necrosis, soft palate perforation, and the first report of destruction of the bony clivus secondary to opioid abuse.

Clinical Vignette

The patient is a 34-year old Caucasian woman who presented to our clinic complaining of nasal obstruction and nasal regurgitation of food and liquids for the past 4 years. External facial examination was normal. Intranasal examination demonstrated a large septal perforation. Nasal obstruction by white chalky debris precluded visualization of the posterior extent of the perforation. Intraoral examination demonstrated a 1cm perforation of the midline soft palate with similar chalky debris herniating through the perforation.
A CT scan demonstrated a large nasal septal perforation, straddled by moderate frothy and dense material within the bilateral nasal cavities, without mass-like appearance. There was a defect in the midline soft palate anterior to the uvula. A sharply circumscribed lobulated lytic clival lesion demonstrated a thin sclerotic rim, anterior extraosseous extension, low attenuation (HU 24), and lack of internal calcification or chondroid matrix (Figure 1).
Figure 1: A) Midline sagittal bone window CT image demonstrates the frothy nasal material, a defect in the posterior soft palate (red arrow), and the osseous defect of the inferior clivus (blue arrow); B) and C) Coronal and axial soft tissue window CT show the large nasal septal perforation and high density frothy material in the nasal cavity; D) Axial CT bone window image demonstrates a large nasal septal perforation straddled by frothy material in the bilateral nasal cavities; E) Bone window axial CT demonstrates a sharply circumscribed expansile lesion with anterior and posterior cortical dehiscence and sclerotic rim in the inferior clival midline (blue arrow); F) Soft tissue window CT image at the same level shows low attenuation of the clival lesion HU 24( bluearrow).
MRI revealed low signal on T1 and fat-suppressed T2 weighted series and lack of enhancement of the nasal cavity process. The clival lesion was low in signal on T1 weighted images and bright on T2 weighted images, and did not enhance. On the basis of the imaging appearance, the nasal process was thought to represent packing material and associated blood products. The differential diagnosis for the clival lesion included chordoma, chondrosarcoma (less likely in the midline), ecchordosisphysaliphora and, less likely given the young age of the patient, metastatic disease or multiple myeloma (Figure 2).
Figure 2: A) Axial T2 fat saturated MR image shows low intensity of nasal cavity material, which was hypointense and nonenhancing on T1 weighted sequences (not shown); B) Coronal T2 fat saturated MR image showing the lobulated hyperintense clival lesion (arrow); C) Axial T2 fat suppressed image shows extraosseous extension of the low signal clival lesion (arrow); D) Enhanced T1 weighted axial image demonstrates low signal and lack of enhancement of clival lesion (arrow).
Nasal endoscopy demonstrated impacted necrotic chalk-white debris completely filling the nasal cavity. The patient initially denied use of intranasal drug abuse. However, after reviewing the imaging results, the patient finally admitted a history of narcotic addiction and stated that she had been snorting crushed Acetaminophen-Oxycodone and Acetaminophen-Hydrocodone tablets when this problem started. She denied abuse of any other substance. She indicated that she had discontinued these practices.
The patient was taken to the operating room and nasal endoscopy was performed to evacuate the debris from the nose. Following thorough debridement, examination of the nasal mucosa revealed necrosis of most of the inferior and middle turbinates affecting mucosa and cartilage and near-total necrosis of the septum with absent cartilaginous septum and destruction of a portion of the osseous septum (vomer). The nasopharyngeal mucosa was inflamed and ulcerated but not completely necrotic. The nasopharyngeal mucosa was incised and dissection to the clivus was performed. Necrotic clival material was sampled and sent to pathology. There was isolated necrosis of the soft palate with an intact hard palate (Figures 3 and 4).
Figure 3: Peroperative view of the nose. A) Nasopharynx with mass of debris resting on the clivus; B) Near-total nasal septal erosion.
Figure 4: A) Chalky debris corresponding to the crushed narcotic pills; B) Oronasal fistula due to soft palate necrosis.
Intraoperative cultures revealed only scant yeast, felt to represent colonization. Histopathologic examination of the intranasal necrotic debris demonstrated fragments of keratin with associated inflammatory changes consisting predominantly of neutrophils and multiple fragments of foreign material. The nasopharyngeal and clival samples demonstrated squamous epithelium with mucosal erosion and inflammatory changes suggestive of chronic inflammation.


According to the US department of Health and Human Services, in 2007 an estimated 5.2 million persons used prescription pain relievers non-medically within the past month. As of 2010, it was predicted that two million new users will abuse prescription narcotics each year, most commonly hydrocodone [3]. The most commonly prescribed form is hydrocodone-acetaminophen (HA). Many individuals crush the tablets and snort the product to take advantage of the rapid transmucosal delivery of narcotics [3].
Intranasal opioid abuse causes both acute and chronic changes in the nasal mucosa that can extend to the nasopharynx and the oropharynx. Few case reports describe these sequelae. One larger case series was recently published describing these sequelae in 35 patients [3]. have been described with cocaine and can be regrouped under the name of Cocaine-induced midline destructive lesions (CIMDL).
Cocaine-induced septal perforation is well described but palatal necrosis is much more infrequent. A recent review in 2010 found 36 palatal perforations secondary to cocaine abuse with 77.7% affecting only the hard palate (28 cases), 16.6% both soft and hard palate (6 cases), and 5.5% only the soft palate (2 cases) [2,5,6]. The mechanism of action of cocaine-induced midline destructive lesion is felt to be a combination of several pathogenic mechanisms [5-9]. Primary mechanism is intense local vasoconstrictive effect from cocaine itself with repeated exposure leading to localized ischemia and reperfusion inflammatory rhinitis. Chemical irritation from the additives used with the cocaine leading to a severe inflammatory reaction is also incriminated and dependent on the specific substance admixed with the cocaine and the percentage of contribution of this substance in the cocaine composition. Mechanical trauma is due to crystalline form of cocaine that has microscopically sharp barbed edges that can injure the nasal mucosa when snorted at high velocity, as well as the paraphernalia used by the abusers. The anesthetic effect of cocaine on the nasal mucosa, due to blockage of sodium and potassium channels, contributes to the mechanical trauma without the warning signs of pain [6]. Infection of the initial lesion is also often implicated [5,6]. Indeed, decreased oxygen tension, chronic inflammation, and open lesions are a nidus for anaerobic infections. This is further compounded by evidence of local immunosuppressive effects as well as reduced mucociliary clearance induced by cocaine. It is noteworthy that some authors think that chronic bacterial infiltration leads to ANCA formation in cocaine-induced midline destructive lesions, (CIMD) especially human neutrophil elastase (HNE-ANCA). It is believed that ANCA is a pathogenic agent here rather than a marker [6]. CIMD seems to be the result of a necrotizing inflammatory tissue triggered by cocaine abuse in a subset of patients predisposed to produce ANCA, particularly those reacting to HNE. The presence of HNE-ANCA seems to promote or define the disease phenotype.
This is similar to antiphospholipid antibodies associated with microthromobtic cutaneous vasculopathies [7,10,11]. Immunosuppressive treatment is usually ineffective in CIMDL. Cocaine cessation and treatment of infection is the mainstay of treatment and would predict the outcome of any attempted reconstruction surgery [5-12].
Several hypotheses are advanced to explain extensive destruction caused by intranasal opioid abuse. Some authors suggest a direct mechanical, irritative effect that results in chronic inflammation [2]. This is theorized to be similar to the effect of the additives with which cocaine is diluted (such as mannitol and talc) in that it adds a foreign body inflammatory reaction to the ischemia [13].
Other authors suggest a possible localized immunosuppression due to the inhaled narcotics [1]. Yewell et. al. report a series of 5 patients, two of whom developed chronic Aspergillus fungal rhinosinusitis although they were otherwise immunocompetent. In contrast, our patient’s cultures showed only a few colonies of fungus, probably saprophytic to the nasal mucosa. Lymphocytes and macrophages are known to possess opioid receptors, and morphine has been shown to cause some degree of immunosuppression [1].
Alexander et al. [3] showed that a link between the narcotic abuse and invasive fungal rhinosinusitis probably exists but to a lesser extent than suggested by Yewell et al. [1]. They also postulated that a high concentration of narcotics in the nose along with hyperosmotic effects can cause the necrosis of the nasal structures. Acetaminophen which has been shown to be toxic to olfactory mucosa at hepatotoxic doses, might contribute to the pathophysiology as well as some excipient that constitutes the tablet or pill [3]. Intranasal opioid abuse appears to demonstrate greater propensity to extend to the nasopharynx and the posterior pharyngeal wall [3,6]. However, there are at least six cases in the literature of chronic cocaine abuse causing extensive osteocartilaginous destruction extending even to the sphenoid sinus [14-19].
Alexander et al. [3] suggest that the frequency of involvement of structures deep to the mucosa seems to be higher than with cocaine with resultant higher rates of perforation [3,6,9]. A review of their patients presenting with sinonasal symptoms such as congestion or orofacial pain, and that were eventually diagnosed as secondary to chronic opioid abuse, showed 51% had septal perforation and 26% palatal perforation. In contrast, several longitudinal studies of cocaine users followed for a significant duration of time found a low incidence of septal perforation and osteocartilaginous destruction [3,9,11,20,21]. The most widely cited is the Messinger study that followed 2185 cocaine abusers and reported only 4.8% of study subjects developing septal perforation. There is to date no longitudinal study that follows chronic opioid users to determine an incidence or prevalence of midline destructive lesions or even septal perforation incidence. Even if we cannot do a comparison between the Alexander et al study and the ones cited in the literature at this point the difference in numbers is noteworthy. Given that most authors agree that cocaine abusers have a tendency to self treat and to avoid medical attention, could the discrepancy in the numbers be related to a more severe presentation among intranasal opioid users that precludes self-treatment? There is limited data at this point to answer this question.
No erosive lesion of the clivus has ever been reported with the chronic opioid abuse. There are at least two reports of clival lesions related to cocaine abuse. One of these patients presented with rhombencephalitis and cranial nerve palsies [22,23]. The differential diagnosis for a destructive clival lesion includes chordoma, chondrosarcoma, metastatic disease, multiple myeloma, lymphoma, and benign lesions including ecchordosis, neurenteric cyst and uncommonly fibrous dysplasia. Chordoma and chondrosarcoma demonstrate similar signal characterisitics to our patient including T1 hypointensity and T2 hyperintensity, but would demonstrate enhancement. While chordomas are typically midline, chondrosarcomas are off midline, characteristically centered at the petroclivalsynchondrosis. Chordomas may demonstrate internal osseous debris. Chondrosarcomas may show chondroid calcification. Ecchordosis is typically an unenhancing intradural retroclival lesion which may show clival T2 signal abnormality especially if a calcified stalk is seen on CT. Neurenteric cysts are rare in the clivus and may demonstrate similar signal characteristics and lack of enhancement, but may be T1 hyperintense if proteinaceous. Metastatic lesions, myeloma and lymphoma would typically enhance. Fibrous dysplasia typically enhances and is variable in signal [22-30].


Intranasal narcotic abuse has become increasingly frequent due to avoidance of injection route from fear of HIV [4], and because of availability of prescription drugs in patients treated for neoplastic or non-neoplastic chronic pain syndromes. Extensive destruction of the mid facial structures, including the nasal septum, the turbinates, and the soft palate, has been reported for over a decade. This is the first reported case of clival erosion related to intranasal narcotic abuse. Radiologists and clinicians should be aware of this potential complication to appropriately include it in the differential diagnosis of erosive lesions of the skull base and to detect these patients early because ongoing abuse can result in progression of damage and might interfere with the success of any attempt to repair the defects.


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