Case Report: Diagnosis of hypogeusia after oral exposure to commercial cleaning agent and considerations for clinical taste testing

Introduction

Disordered taste, referred to as dysgeusia, can lead to dramatic changes in weight and reduce quality of life. Causes for dysgeusia are variable and include primary medical disorders¹, medication side effects², chemicals and toxins³, local disorders of the mouth⁴, insufficient production of saliva⁵, and gastroesophageal reflux disease. Here we describe a case of hypogeusia following oral contact with a commercial cleaning agent, and discuss diagnostic considerations in determining the nature and extent of taste dysfunction.

Patient information

A 54-year-old Caucasian man presented with complaints of a dull sensation of the tongue, describing that his “taste seems off,” associated with numbness and occasional dry mouth. The patient reported that the taste disturbance began 1.5 years prior to presentation, immediately after accidental oral exposure to a cleaning agent, which he gargled with and immediately expectorated. At the time of injury he noted tongue numbness and throat irritation, and subsequently reported to the emergency department. There, examination of the oral cavity revealed no findings indicative of serious mucosal injury such as significant swelling, deep ulceration, or chemical burn. At an urgent dental visit one day following the incident, the patient reported tongue burning and tingling sensations, with increased tooth and gum sensitivity, and the dentist’s examination noted superficial irritation on the tongue and cheeks along with pharyngeal erythema. The patient was seen by an otolaryngologist approximately 3 weeks following the incident for complaints of burning and soreness of the tongue and loss of taste. His physical exam was notable for an area of mild erythema of the right lateral tongue, tender to palpation but without ulceration, and he was prescribed a supersaturated calcium phosphate rinse for oral mucositis and topical benzocaine for symptomatic relief. Approximately 6 weeks following the incident, the patient was seen in follow-up by the otolaryngologist for tongue soreness. At that time, examination revealed erythema and shallow erosion/ulceration of the dorsal tongue just anterior to the foramen cecum, and light erythema of the lateral tongue. The patient was diagnosed with candidiasis and prescribed nystatin. A follow-up appointment approximately 9 weeks after the incident showed resolution of physical exam findings, however, he continued to have symptoms.

The patient presented to our department 1.5 years after the injury, for evaluation of persistent subtotal loss of tongue sensation, both taste and somatosensation. During this visit, a complete head and neck examination was performed and was essentially normal, specifically with normal ear examination and intact cranial nerve exam. Intraoral examination demonstrated normal mucosa with no evidence of erythema or ulceration (Figures 1C, 1E, 1F). A shallow fissure was noted along the medial surface of the tongue (Figures 1A, 1D). An atrophic patch was noted on the posterior right tongue (Figure 1B), possibly consistent with geographic tongue. The patient’s medical history was significant for hypertension and his surgical history was unremarkable. His body mass index was 25.8. Medications at the time of our evaluation included aspirin 81mg, lisinopril, naproxen, and various vitamins and supplements including zinc.

Figure 1. Images of patient’s tongue taken 1.5 years following oral exposure to toxic cleaning agent.

The oral mucosa appears normal, though there is some evidence of possible geographic tongue. Panels 1A and 1D show a slight fissure (arrow). Panel 1B demonstrates an atrophic patch (arrow) consistent with possible geographic tongue. The circumvallate papillae are intact as demonstrated in 1C (arrows). The lateral lingual mucosa appears normal (1E, 1F).

A series of tests was assembled and administered to determine the nature and extent of the patient’s dysgeusia, including: two-cup forced choice test, two-point tactile discrimination, trigeminal nerve testing, three-drop taste threshold testing, and swish and spit whole mouth taste testing (Table 1).

Diagnostic assessment

Discussion

Taste buds in the anterior tongue are superficial receptor end organs, making them susceptible to direct chemical injury; however, reports of toxin-induced dysgeusia in the literature are rare even in surveys of specialty clinics. Smith et al.³ described a patient with severe hypogeusia after oral contact with ammonia that resulted in a chemical burn. Workers exposed to hydrocarbons have reported subjective disturbances in taste¹⁴, and taste thresholds are elevated in workers exposed to dichromate, chromic acid, and zinc chromate¹⁵. In our patient, a bathroom cleaner containing a proprietary organic salt made contact with the oral mucosa; based on comparison to similar cleaning materials, the presumed compound was likely urea sulfate, a mildly corrosive salt that rapidly breaks down into urea and sulfuric acid.

There are multiple potential reasons for the paucity of reported cases of chemical-induced taste dysfunction cases. First, clinical assessment of taste is not as standardized a practice as testing other senses like hearing and smell is; therefore, patients may not be objectively evaluated to determine the degree of taste dysfunction until several months or years have passed since the initial exposure. This obscures identification of a particular chemical or toxin as the causative agent. Further, taste cells are continually renewed¹⁶, so a superficial mucosal injury will likely resolve over time as damaged cells are replaced. Finally, several factors known to be associated with dysgeusia may confound determination of cause and effect, including various medications⁵, comorbid conditions like oral candidiasis⁴, diabetes⁵, hypothyroidism⁵, Sjogren’s syndrome¹⁷, and age¹⁸.

The constellation of symptoms and signs reported by the patient in this case may also be consistent with some features associated with burning mouth syndrome (BMS). BMS affects the oral mucosa, lips and/or tongue and is characterized by the sensation of burning, tingling, or numbness in the absence of visible inflammation or lesions¹⁹. BMS has been associated with two factors detailed in this report: angiotensin converting enzyme (ACE) inhibitors¹⁹ and oral candidiasis¹⁹. ACE inhibitors inhibit zinc action in the salivary glands and taste receptor cells thereby reducing saliva production and affecting taste²⁰. Brown et al.²¹ described two cases of BMS associated with ACE inhibitors that subsequently improved after changes in drug therapy. Oral candidiasis caused by Candida albicans is a common fungal infection and estimates indicate that anywhere from 36–60%^22,23 of the population are carriers without clinical symptoms. Sakashita et al.²⁴, reported that 70% of Candida carriers in their 50’s demonstrated dysgeusia. The patient presented herein was treated for suspected (although unconfirmed) oral candidiasis approximately 6 weeks following reported onset of taste loss, suggesting that he may be a carrier for Candida albicans.

Thoroughly investigating the cause of a patient’s dysgeusia allows the clinician to offer potential treatment options, but it is equally important to document and determine the extent of the taste disturbance in order to track a patient’s recovery over time. Quantitative taste testing is relatively easy to perform in the clinic and should be used to assess taste function of patients complaining of both acute and chronic alterations in taste. Subjective patient reports may exaggerate or minimize the nature and extent of dysgeusia, and testing can determine whether the degree of dysfunction is normal relative to age. This information can be used for patient counseling, and may also be helpful to evaluate longitudinal improvement in an objective fashion. It is also possible to detect malingering by administration of simple, forced-choice tests.

Given the chronic nature of the patient’s hypogeusia, we expect that it is unlikely that he will experience spontaneous resolution at this time point. If his taste dysfunction was truly a direct result of chemical injury to the oral cavity mucosa, the gustatory system exhibits a robust regeneraitve capacity, with taste cell renewal every 10–14 days (see Barlow, 2015¹⁶ for a review). This suggests that function should have recovered within months of the incident. Medical treatment options that could be attempted include discontinuing lisinopril and trialing a different (nonsulfhydryl) ACE inhibitor²⁰, or dietary supplementation with selenium methionine²⁵.

We employed multiple tests targeting somatosensory function, trigeminal nerve response, taste thresholds for sweet, sour, bitter, and salty, and odor detection. There are additional tests reported in the literature that can also be used for measuring dysgeusia, some of which are commercially available. These include electrogustometry²⁶ (e.g., TR-06 Rion Electrogustometer, Sensonics, Inc.), Taste Strips (Burghart), filter paper discs²⁷, taste tablets²⁸, and subjective health-related quality-of-life questionnaires. For a standardized taste intensity testing protocol, clinicians may opt to follow the technical manual and scoring and interpretation guidelines included in the National Institutes of Health (NIH) Toolbox, as established by the National Health and Nutrition Examination Survey (NHANES)²⁹. As a very basic measure, it is also possible to create testing solutions from store-bought sugar (low concentration=3 tsp; high concentration=24 tsp) and salt (low concentration=2 tsp; high concentration=14 tsp) dissolved in 8 oz (237 ml) distilled water to perform both tongue tip and whole mouth testing.

Conclusion

This case report adds to the limited literature on toxin-induced hypogeusia following oral exposure. We promote the concept that taste testing is relatively easy to perform and should be completed as soon as possible following an incident in order to determine the extent of injury and track improvement in function over time.

Consent

Written informed consent for publication of their clinical details and clinical images was obtained from the patient.