A Rare Presentation of Severe Hypothyroidism: Supraglottic Myxedema Causing Impending Airway Collapse in the Setting of Cervical DISH

Background

Laryngeal myxedema is a rare life-threatening manifestation of severe hypothyroidism caused by mucopolysaccharide deposition in laryngeal tissues. While myxedema coma is a recognized endocrine emergency, laryngeal myxedema presenting with critical airway obstruction is exceptionally rare. When concurrent with structural airway disease, management becomes particularly challenging.

Case Presentation

A 78-year-old male with a 40 pack-year smoking history presented with one week of progressive hoarseness and slurred speech, followed by two days of inspiratory stridor. He had long-standing hypothyroidism managed with levothyroxine 200 mcg daily, though with improper administration technique.

On examination, vital signs revealed sinus bradycardia (56 beats/minute) and tachypnea with audible stridor. Bedside videolaryngoscopy demonstrated marked supraglottic edema with limited vocal cord visualization. The patient rapidly deteriorated with respiratory distress and oxygen desaturation, requiring awake intubation for airway protection.

Laboratory evaluation revealed profound hypothyroidism with TSH 92 mIU/L and free T4 below 0.10 ng/dL. Additional abnormalities included hyponatremia and elevated proBNP. Cervical spine imaging revealed severe diffuse idiopathic skeletal hyperostosis (DISH) with large anterior osteophytes displacing the pharynx anteriorly and contributing to airway narrowing at multiple levels with central canal stenosis.

Discussion

The clinical presentation of progressive supraglottic edema, symptomatic bradycardia, hyponatremia, and severe biochemical hypothyroidism established the diagnosis of laryngeal myxedema causing critical upper airway compromise. Severe cervical DISH represented a major predisposing factor by chronically narrowing the upper airway and lowering the threshold for acute decompensation. Additional contributing factors included improper levothyroxine administration and tobacco exposure.

A multidisciplinary team initiated treatment using a myxedema coma protocol with intravenous levothyroxine, liothyronine, and corticosteroids with mechanical ventilation for airway protection. Serial thyroid function testing demonstrated progressive biochemical improvement with declining TSH and rising free T4 levels. Successful extubation occurred four days after intubation with complete resolution of inspiratory stridor.

Post-extubation, formal swallowing evaluation confirmed significant oropharyngeal dysphagia with aspiration risk, attributed to extrinsic pharyngeal compression from DISH. Despite resolution of laryngeal edema and optimization of hypothyroidism, unsafe swallowing mechanics persisted, necessitating surgical management.

Conclusion

This case highlights laryngeal myxedema as a rare but critical presentation of severe hypothyroidism. Recognition of concurrent predisposing factors, is essential for comprehensive management. Multidisciplinary collaboration and individualized treatment approaches using a myxedema coma protocol may be effective when established guidelines are unavailable.