A 25 year old female presented with rapidly progressive respiratory distress after chlorine inhalation exposure. She subsequently developed stridor with nasopharyngoscopic evidence of vocal cord dysfunction. This case substantiates and emphasizes the importance of identifying irritant-associated vocal cord dysfunction.
The patient was a 25 year old female who presented with headaches, shortness of breath, chest pain on deep inspiration, burning in throat, nausea, cough and wheezing five minutes after an outdoor exposure to chlorine from a chemical spill near her work place. Her significant physical examination included erythematous mucosa of the oral pharynx, stridor and bilateral diffuse wheezing of lungs. Significant laboratory data on admission revealed an ABG with pH of 7.5. pCO2 23 mm Hg, pO2 98 mm Hg, oxygen saturation of 100 % on room air. Chest x- ray showed mild hyperinflation without pulmonary edema, effusion or infiltrate. She was subsequently admitted to the intensive care unit for acute upper and lower airway injury secondary to chlorine inhalation exposure and was treated with racemic epinephrine nebulizer, intravenous steroids and intravenous antibiotics. Pulse oximetry was normal. She was discharged six days later on home racemic epinephrine nebuliser and tapering dose of prednisone. She was unable to perform spirometry. Direct laryngoscopy showed true vocal cord dysfunction with paradoxic vocal cord movement. Upon discharge she also underwent speech therapy evaluation with short-term voice therapy to retrain the voluntary muscles that cause laryngeal dysfunction.
Vocal cord dysfunction has been well documented in the literature in patients presenting with respiratory symptoms occuring after irritant exposure. Eleven cases have been reported in association with occupational or enviromental exposure have been described in the past. Clinical criteria for vocal cord dysfunction includes documented absence of prior vocal cord dysfuncion, onset of symptoms after irritant exposure, symptoms of wheezing, stridor, dyspnea, cough, or throat tightness and abnormal direct nasolaryngoscopy. Direct laryngoscopic evidence of adduction of the anterior two thirds of the vocal cords with a posterior chink during inspiration is the current gold standard for making the diagnosis of vocal cord dysfunction. Early recognition of vocal cord dysfunction is important as treatment differs from that of asthma or reactive airway disorder. Patients with vocal cord dysfunction will benefit from short term speech training to retrain their laryngeal muscles.
This report emphasizes the importance of distinguishing vocal cord dysfunction from reactive airways dysfunction syndrome or irritant induced asthma since it can mimic other forms of asthma.
P.V. Reddy, None.