Discussion

Cocaine is an alkaloid extracted from the Erythroxylum coca plant leaves. It was first introduced for ophthalmic use in medicine, given its anaesthetic and vasoconstrictive actions, in 1884 by Carl Koller.^{Reference Goerig, Bacon and van Zundert5} Cocaine is also commonly used as a topical preparation in nasal surgery, in combination with adrenaline, sodium bicarbonate and sodium chloride.^{Reference Lutfallah, Brown, Spillers, Tandon, Kelkar and Ahmadzadeh6} Known as Moffett's solution, this is an effective mucosal decongestant via vasoconstriction, as well as a topical anaesthetic.

Recreationally, its use is attributed mainly to the stimulating action on the central nervous system.^{Reference Businco, Lauriello, Marsico, Corbisiero, Cipriani and Tirelli7} It is usually self-administered by intravenous injection, smoking, topical administration (orally via the gums), or most commonly, nasally via inhalation (‘snorting’).^{Reference Sittel and Eckel8}

Given that the most common administration method for recreational cocaine use is via nasal inhalation, the pathophysiology of osseocartilaginous destruction associated with chronic cocaine use is thought to be multifactorial. Primarily, repeated vasoconstriction and trauma to the nasal mucosa by cocaine occurs, which can induce ischaemia and necrosis. There is also an irritant effect from chemical adulterants, as well as bacterial infections of disturbed mucosa and activation of the autoimmune system.^{Reference Trimarchi, Gregorini, Facchetti, Morassi, Manfredini and Maroldi2,Reference Subesinghe, van Leuven, Yalakki, Sangle and D'Cruz9,Reference Trimarchi, Bussi, Sinico, Meroni and Specks10} These may subsequently lead to damage of the cartilaginous structures of the nose, most frequently the cartilaginous part of the nasal septum, as well as the surrounding bony structures such as the hard palate, anterior skull base and maxilla.^{Reference Colletti, Autelitano, Chiapasco, Biglioli, Giovanditto and Mandala11,Reference Lancaster, Belloso, Wilson and McCormick12} This can cause deformities to the external nose and middle third of the face, due to loss of the facial midline support structures.^{Reference Colletti, Autelitano, Chiapasco, Biglioli, Giovanditto and Mandala11,Reference Millard and Mejia13,Reference Molteni, Saibene, Luciano and Maccari14}

This report focuses on a case of unilateral Eustachian tube stenosis associated with nasal cocaine use, something not previously reported in the published literature. A literature search was conducted on 18 September 2023, using the Web of Science, Medline, Cochrane Library and Clinicaltrials.gov databases, for Eustachian tube abnormalities associated with cocaine. Only one paper was found that directly associated a lesion of the Eustachian tube with cocaine use.^{Reference Bacciu, Ghirelli, Ingegnoli and Bozzetti15} This was a 2018 case report showing multiple areas of cocaine-associated lytic destruction in the sinonasal complex, including ‘erosion and widening of the cartilaginous and bony portions of the left Eustachian tube’; however, no stenosis was reported. This occurred in a patient presenting with oronasal reflux, rhinolalia, anosmia and bilateral otitis media.^{Reference Bacciu, Ghirelli, Ingegnoli and Bozzetti15}

A 2022 systematic review of the distribution of cocaine-induced midline destructive lesions found that 99 per cent of reported cocaine-induced midline destructive lesion patients had a septal perforation.^{Reference Nitro, Pipolo, Fadda, Allevi, Borgione and Cavallo16} The prevalence of damage to the inferior third of the sinonasal complex was lower, at 59 per cent in the nasal floor and 30 per cent in the inferolateral nasal wall. The middle third was damaged in 23 per cent (middle turbinate and ethmoid disease), and the lowest prevalence was expectedly seen in the skull base and lamina papyracea at 8 per cent. There were no direct reports of pathology to the Eustachian tubes in this review.^{Reference Nitro, Pipolo, Fadda, Allevi, Borgione and Cavallo16}

At a microscopic level, cocaine-associated damage shows a vasculitis-like granulomatous pattern, with progressive loss of tissue through ischaemic and thrombotic events.^{Reference Trimarchi, Gregorini, Facchetti, Morassi, Manfredini and Maroldi2} This can be histologically indistinguishable from diseases such as granulomatosis with polyangiitis, sarcoidosis, or non-Hodgkin's lymphoma.^{Reference Kuriloff and Kimmelman17–Reference Westreich and Lawson19} Therefore, whilst a full investigation is required to rule out other aetiologies for nasal tissue loss, the clinical identification of a cocaine-induced midline destructive lesion is generally reported when a structural lesion of the sinonasal complex is seen in the context of confirmed chronic cocaine snorting.^{Reference Trimarchi, Gregorini, Facchetti, Morassi, Manfredini and Maroldi2} Other diagnostic criteria have also been suggested.^{Reference Seyer, Grist and Muller20}

Consideration of managing conductive hearing loss in a case such as this is key, as it was the leading symptom in the patient's presentation. It is well recognised that Eustachian tube dysfunction has implications in the development of chronic otitis media with middle-ear effusion.^{Reference Bluestone and Doyle21} In this case, following the EUA, it became clear that the complete stenosis evident at the left Eustachian tube orifice was the principal cause of the middle-ear effusion and subsequent conductive hearing loss. Surgical aeration of the middle ear, in cases not responding to conservative or medical therapies, is often the treatment of choice, via myringotomy and ventilation tube insertion.^{Reference Sade and Ar22} This may have improved this patient's conductive hearing loss; however, otorrhoea and persistent tympanic membrane perforation are known complications, even in routine cases.^{Reference Silverstein, Light, Jackson, Rosenberg and Thompson23} Given that our patient no longer had a drainage pathway from the left middle ear into the nasal cavity, the risk of otological complications, primarily persistent tympanic membrane perforation with chronic discharge, were greatly increased. This creates a treatment dilemma of two options: ventilation tube insertion to improve hearing loss with the risk of chronic otorrhoea, or conservative treatment to avoid further otological complications but with hearing loss remaining. It is therefore suggested that patients with similar presentations are well-counselled on such risks, and that conservative treatment with hearing devices be considered in the first instance.

This case highlights the rare finding of Eustachian tube stenosis associated with cocaine use. We demonstrate the importance of thorough investigation when a cocaine-induced midline destructive lesion is suspected, including otological and post-nasal space examinations and audiometry, to screen for and diagnose Eustachian tube pathology. We also highlight the complexities associated with managing such cases, particularly when concurrent otological symptoms are present. Surgical decision-making is difficult and revision surgery is often necessary. Whilst this patient's hearing loss was treated medically, decisions must be made on a case-by-case basis, with other options including Eustachian tuboplasty or myringotomy and ventilation tubes.