Laryngeal Manifestation of Intranasal Acetaminophen Abuse and Review of Literature

Introduction

Dysphonia is a common complaint to otolaryngologists and laryngologists. Intranasal drug abuse, specifically acetaminophen, is a rarely reported cause of dysphonia. In these patients, nasal complaints are common and therefore the head and neck examination is typically limited to the nasal cavities and nasopharynx, without further examination of the larynx. A complete evaluation of the upper airway, including the nose, nasopharynx, oropharynx, larynx, and potentially the subglottis, is warranted in patients with sinus complaints and a history of intranasal drug use.

Case Report

A 50-year-old female presented with dysphonia, which progressed to aphonia over the course of 6 months. Her voice was strained and effortful. She denied any precipitating factors. She had a history of chronic sinus disease, which was reported as nasal congestion, discolored nasal discharge, and nasal pain. Her past medical history was significant for lupus, asthma, and hypertension. She had recently decreased her smoking from 1 pack per day to 8 cigarettes per day. She had been smoking for 30 years. She denied intranasal substance abuse. She had had a rheumatologic workup given her background of Lupus. Investigations including nasal biopsies and blood work such as cytoplasmic antineutrophilic cytoplasmic antibodies (c-ANCA), perinuclear antineutrophilic cytoplasmic antibodies (p-ANCA), myeloperoxidase antibodies, and angiotensin-converting enzyme (ACE) had been negative. A computed tomography scan of her facial bones showed the absence of nasal septum and mucosal thickening of the maxillary sinuses. No destructive lesions were seen.

On endoscopic evaluation of her nose and larynx, she was found to have a large amount of fibrinous exudate along her upper airway with loss of nasal cartilage (Figure 1). She had cicatricial palatal scarring leading to nasopharyngeal stenosis (Figure 2). In addition, a significant amount of exudate was found on her bilateral true vocal folds extending to her subglottis and cervical trachea (Figure 3). There was normal bilateral vocal fold motion.

Figure 1.

Nasal endoscopy revealed a subtotal septal perforation with extensive necrosis and crusting throughout her nasal cavity distorting landmarks.

Figure 2.

The fibrinous material also lined the nasopharynx and the posterior pharyngeal wall. The soft palate was significantly scarred leading to nasopharyngeal stenosis.

Figure 3.

Laryngoscopy showed the same fibrinous material lining bilateral true vocal folds, subglottis, and the upper trachea.

The patient was taken to the operating room (OR) for laryngeal and nasal biopsies as well as debridement. After removing the exudate overlying the true vocal folds, subglottis, and cervical trachea, an anterior glottic web and extensive true vocal fold scarring were identified. Pathology report demonstrated abundant areas of acute inflammation and tissue necrosis intermixed with polarizable materials in both the larynx and the nasal cavities. Rare fungal organisms were identified within necrotic debris, but there was no evidence of fungal invasion into tissue. Differential diagnoses for this included intranasal substance use and packing material from the patient’s prior nasal debridement. On further inquiry, the patient admitted to intranasal acetaminophen abuse. The patient did not return for subsequent follow-up with either the laryngology or rhinology service.

Literature Review and Discussion

Sinus complications from intranasal abuse of opioids with and without acetaminophen have been reported in the literature. ^{1 -6} This is thought to be secondary to the induction of an intense inflammatory response from the drug itself or additives to the drug. ¹ In acetaminophen, the binding agent talc is the most likely agent causing localized inflammation. Talc is known to cause pulmonary talcosis, which is characterized by a foreign body giant cell reaction in the lungs surrounding polarizable birefringent crystals. ^7,8 These patients typically present with nasal pain and congestion and have various endoscopic findings such as septal perforation, palatal perforation, and severe nasal inflammation. ¹ Other than reports of dysphonia, no detailed description of laryngeal manifestations has been reported in the literature. In a case series of patients with intranasal abuse of opioids with and without acetaminophen, 29% of patients were dysphonic but no laryngeal findings were documented. ¹ Rheumotologic investigations including direct nasal biopsies were negative in the same series suggesting that intrinsic vasculitis or granulomatous processes did not contribute to the destructive process in the nose. Further, superficial fungal colonization of necrotic tissue and inert polarizable materials were found in all patients in this series.

Early and accurate diagnosis is imperative for patient management as most of these patients were initially diagnosed with bacterial or fungal sinus infections. ¹ In the absence of patient admission, however, only after debridement and appreciation of polarizable foreign materials in the upper airway fibrinous debris can aid the diagnosis. Therefore, it is still important to rule out granulomatous disease or malignancies that could lead to a similar presentation. Once the diagnosis has been confirmed, abstinence of intranasal acetaminophen abuse, frequent sinus irrigations and debridement, as well as possibly frequent laryngeal debridement are part of the armamentarium to manage these patients. Our patient was found incidentally to have an anterior glottic web once her vocal fold exudate had been debrided in the OR. Although we cannot make direct causal inferences regarding the development of laryngeal stenosis secondary to intranasal acetaminophen abuse, it is not surprising that upper airway stenosis can develop as a result of chronic inflammation, just as in patients with rheumatologic conditions. Once the acute inflammation has settled from substance abstinence, further laryngological procedures may be considered to address vocal fold scarring, voice rehabilitation, and possible upper airway stenosis.

Conclusion

Intranasal acetaminophen abuse should be part of the otolaryngologists’ differential diagnoses for chronic nasal complaints and dysphonia and when intense nasal and laryngeal inflammation are seen on endoscopic examination. Biopsy and debridement are important for diagnosis.