INTRODUCTION: Vocal cord dysfunction or paradoxical vocal cord movement (PVCM) is a laryngeal disorder characterized by paradoxical adduction of the vocal cords during inspiration and/or expiration. PVCM presents with shortness of breath, stridor, wheezing, and in severe cases can lead to acute respiratory failure. The etiology of PVCM includes central nervous system injury, inhaled irritants, laryngeal dystonias, conversion disorders, and psychological stresses. PVCM can also occur following cardiac surgery and is described in association with asthma. Diagnosis is made by laryngoscopic visualization of the vocal cords during inspiration showing discordant movement of the anterior and posterior segments. Botulinum toxin type A (BT-A) is used to treat a variety of conditions caused by muscular spasticity or rigidity. It provokes a chemical denervation of the neuro-muscular junction via inhibition of exocytosis of acetylcholine. Its use has been reported for the treatment of mild PVCM. We present a case of severe PVCM following cardiac surgery that was successfully treated with bronchoscopic vocal cords injection of BT-A.
CASE PRESENTATION: A 65 year-old male underwent coronary artery bypass surgery for the treatment of coronary artery disease. Post-operatively he suffered an acute ischemic stroke which led to a prolonged intubation and failed extubation. Bronchoscopy revealed PVCM and the patient underwent tracheostomy placement. Over a period of six months, the patient repeatedly removed his tracheostomy tube and required multiple surgical revisions and replacements. As a solution to the patient’s non-compliance, permanent tracheostomy was being considered. We proposed utilization of BT-A as a less invasive alternative to permanent tracheostomy. Using therapeutic bronchoscope, 0.2 cc of 12.5 U/ml of botulinum toxin A was injected into each vocal cord using a 25 gauge needle. Following a second session of BT-A injection one week later, the patient was successfully decannulated. He remained asymptomatic for a six-week follow up period.
DISCUSSIONS: To our knowledge, this is the first case to report the efficacy of BT-A injection in the treatment of post cardiac surgery PVCM s. We describe the successful use of BT-A in chronic PVCM after prolonged tracheostomy (6 months). Most reported cases of the use of BT-A in the treatment of PVCM have been in the acute setting, whereas most long-term therapeutic modalities consist of a combination of speech therapy, patient education, and psychotherapy. The mechanisms responsible for post cardiac surgery PVCM are not well understood. Proposed mechanisms include endotracheal intubation (traumatic or non-traumatic), traumatic injury from central line insertion, direct surgical trauma, and cold injury. Besides tracheostomy, treatment options for refractory and persistent post cardiac surgery PVCM include arytenoidectomy, or vocal cords injection with Teflon or autogenous fat. In normal subjects, the posterior cricoarytenoid (PCA) muscles are responsible for abduction of the vocal cords and the lateral cricoarytenoid (LCA) muscles produce adduction of the vocal cords. In our patients, the PCA muscles were likely permanently injured during the cardiac surgery or in the post operative period secondary to multiple and prolonged intubations, or his perioperative cerebro-vascular accident. This explains the inability of the vocal cords to normally abduct during inspiration; leading to unopposed adduction of the vocal cords by LCA muscles during the respiratory cycle. The injection of BT-A into the LCA muscles prohibited the tonic adduction of vocal cords during respiration and improved the subject’s symptoms.
CONCLUSION: In summary in post cardiac surgery PVCM, when symptoms are severe, persistent, and refractory to non-invasive therapeutic measures such as psychotherapy, speech therapy and axiolytics, a trial of BT-A injection into the LCA muscles might save the patient multiple intubations and permanent tracheostomy.