Acute Laryngeal Trauma from Vitamin C Ingestion

Significance Statement

An 88-year-old female presented to the Emergency Department with acute-onset dysphonia after choking on an ascorbic acid tablet. Flexible laryngoscopy showed laryngeal injury with significant exudative, ulcerated mucosa. Treatment consisted of proton pump inhibitor and H₂ blocker therapy and humidification. She presented to the clinic 4 weeks after ED discharge, where systemic corticosteroids were added to the treatment plan. A month later, the patient’s hoarseness significantly improved, despite minimal mucosal changes of the vocal folds.

Case

An 88-year-old nonsmoker with allergic rhinitis, hypertension, syndrome of inappropriate antidiuretic hormone secretion, and hypothyroidism postthyroidectomy was admitted to the hospital for acute shortness of breath after choking on an ascorbic acid tablet a few hours prior to arrival to the Emergency Department. At initial admission, she was febrile (101.6°F) with leukocytosis (White blood cell 15 × 10⁹/L) and was breathing comfortably at rest without distress. Flexible endoscopic evaluation of swallow performed by speech therapy showed mild pharyngeal dysphagia and gray-white discoloration of the laryngeal mucosa, prompting otolaryngology consultation. Flexible laryngoscopy demonstrated a gray discoloration in bilateral piriform sinuses and the laryngeal surface of the epiglottis, extending to the medial surfaces of the aryepiglottic folds, arytenoids, false vocal folds, and true vocal folds (Figure 1). A proton pump inhibitor (PPI) and H2-blocker were initiated, and she was discharged the following day after symptomatic and laryngeal exam improvement. She returned to the otolaryngology clinic 4 weeks later with improvement, reporting a less gravelly voice but persistent hoarseness and limited vocal range. Videostroboscopy revealed decreased right true vocal fold wave motion and right greater than left vocal fold edema and, while the mucosal discoloration had improved, there were persistent exudative mucosal changes on bilateral true folds and the laryngeal surface of the epiglottis (Figure 2). Exam findings were most consistent with focal chemical injury to the larynx. She was counseled to continue her PPI and H2 blocker, and she was started on a methylprednisolone taper for the vocal fold edema. A month later at the follow-up, the patient reported significant improvement in hoarseness. Despite this, the objective findings on videostroboscopy remained similar to those seen at the previous visit (Figure 3).

Figure 1.

Laryngoscopic findings of acute caustic injury. Flexible laryngoscopy demonstrates bilateral true vocal fold edema with exudative irregularity and mucosal changes extending onto the laryngeal surface of the epiglottis.

Figure 2.

Flexible videostroboscopy findings 4 weeks postinjury. Videostroboscopy revealed decreased right true vocal fold motion with both adduction (right) and abduction (left). The wave motion is out of phase, and there is exudative appearing, irregular tissue on bilateral true vocal folds and laryngeal surface of epiglottis.

Figure 3.

Flexible videostroboscopy findings 2 months postinjury. There is persistent evidence of mucosal changes and decreased right vocal fold motion on videostroboscopy. Other findings include infraglottic edema and granulation tissue on the laryngeal surface of the epiglottis.

A differential diagnosis including reflux laryngitis, benign laryngeal lesions, neoplasm, or neuromuscular dysfunction were less likely, given the acute temporal link to acid exposure, focal mucosal abnormalities, and stroboscopic findings consistent with chemical trauma. ¹ Caustic injuries differ by agent: acids like ascorbic acid cause localized coagulative necrosis and are less extensively studied, whereas alkaline exposures produce liquefactive necrosis with higher risk of airway compromise due to deeper tissue injury. ² Injury is also impacted by concentration, contact time, and form (solid vs liquid). Caustic liquid ingestion is more dangerous as much greater surface area is exposed. ³ Further, due to the risk of vomiting and re-injury, liquid ingestion discourages the use of intubation. ² Evaluation and management following caustic ingestion requires early airway assessment, acid suppression (PPI or H2-blocker), and avoidance of neutralizing agents, as an exothermic reaction may worsen tissue injury. ³ Zhang et al ⁴ documented a case of ascorbic acid-induced esophagitis in an adult who ingested vitamin C tablets with minimal water and in the supine position. The ulcer healed with initiation of PPI therapy, supporting outpatient management with acid suppression in less severe settings. In contrast, Boonekamp et al ² described a case a solid sodium hypochlorite tablet aspiration causing supraglottic necrosis and severe edema requiring steroids, intubation, and tracheotomy. This underscores the full spectrum of airway involvement and the need for readiness to secure the airway if necessary.

Currently, there is no universally accepted protocol for laryngeal caustic injury, but consensus from gastroesophageal caustic management endorses endoscopic evaluation within 24 hours if stable, ICU-level observation, acid suppression, and avoidance of neutralizing agents. ⁵ Randomized control trials on administration of corticosteroids to adults with caustic airway injuries are limited; however, a recent intensive care narrative review emphasizes early airway protection and suggests considering a short course of corticosteroids in airway obstruction. ⁶ Further, pediatric-controlled trials of corticosteroids in esophageal caustic injury reduced stricture formation. ⁷ Our decision to administer a short methylprednisolone course to reduce edema and improve vocal fold mobility in the airway was guided by esophageal caustic injury treatment. Preventive recommendations align with both Zhang’s esophagitis case and general pill-safety guidelines: instruct swallowing with adequate water, maintain upright posture postingestion, and properly label/store medications. Continued surveillance is warranted for late sequelae such as granulation tissue, stenosis, or chronic dysphonia.

Prior reports have described ascorbic acid-induced esophagitis, ⁴ and laryngeal necrosis from other tablet with caustic potential, like sodium hypochlorite. ² Based on the current available literature, to our knowledge, this is the first reported case of laryngeal caustic injury following aspiration of an ascorbic acid tablet. This underscores the importance of considering even commonly used supplements as potential agents of airway injury when aspirated. Further, the use of corticosteroids, PPIs, and H2-blockers for this patient, with success at the 1-month follow-up, highlights a potential guideline for the treatment of caustic laryngeal injuries.