Guided by rotational thromboelastometry, one unit of platelets and 2 grams of fibrinogen were administered, which resulted in reduced drain production (from 100 to 30 ml/hour). Anticoagulation therapy was withheld due to this continuous drain production. Chest X-ray showed a new shadowing in the left superior lobe of the lung (figure 1b). The cardiac surgeon was consulted for possible redo thoracotomy: in his opinion conservative treatment was indicated at this stage. Chest X-ray on the second postoperative day showed that the shadowing in the left superior lobe was progressive (figure 1c). CT of the thorax without contrast administration revealed an organised haematoma along the medial and dorsal aspects of the left upper lobe and along the major fissure of the left lung. The haemoglobin levels decreased again from 5.9 to 5.3 mmol/l. Two units of packed red blood cells were given. The platelet count was 146 x 109 /l which was considered sufficient. Blood gas analyses remained unremarkable. Again, in the opinion of the cardiothoracic surgeon, conservative treatment was the best option given the fragile tissues and sternum. The thorax drains were still in situ (but not located near the haematoma) and production was negligible.

On the third postoperative day, the patient developed severe progressive hoarseness within two hours. Her voice beforehand had been unremarkable. In combination with the localisation of the haematoma we suspected progressive development of the haematoma causing pressure on the left recurrent laryngeal nerve with palsy. The consulted ENT specialist confirmed our diagnosis and urgent decompression was warranted in his opinion. The decision was made to perform videoassisted thoracoscopic surgery to evacuate the haematoma. Approximately five hours after the start of her symptoms, she underwent video-assisted thoracoscopic surgery and 350 ml of blood clots localised in the proximal part of the left internal mammary artery was evacuated. No active bleeding sites were found on inspection. A few hours after surgery, she was extubated. Immediately it was noted that her hoarseness and weak voice had disappeared completely. Anticoagulation therapy (acetylsalicylic acid and acenocoumarin) was started and she was transferred to the cardiac unit the next day. Unfortunately, a follow-up by ENT was not performed. She was discharged one week later after DDD pacemaker implantation. Her voice remained normal, without stridor or aspiration.

Discussion

Vocal cord paralysis is a well-known complication after cardiac surgery. Reports vary from 1.1% clinically apparent vocal cord paralysis in all adult cardiac surgery,[2] to 5% clinically apparent after thoracic aortic and aortic arch surgery.[3] When all patients were examined by ENT specialists after cardiac surgery an incidence of 10.7% was found.[4] A review of the literature between 1980 and 2011 reported an incidence of 10.15% of vocal cord paralysis following cardiovascular surgery.[5] The left recurrent laryngeal nerve is more often affected (70%) than the right recurrent laryngeal nerve (30%). Symptoms are hoarseness (100%) associated with stridor (49%) and aspiration (15%).[5] The combination of left recurrent laryngeal nerve palsy with a cardiovascular disease or cardiovascular intervention surgery is called Ortner’s syndrome or cardiovocal syndrome. Norbert Ortner first described hoarseness of voice due to left recurrent laryngeal nerve palsy in three patients with mitral stenosis in 1897. He postulated that an enlarged left atrium was the culprit, pressing the left recurrent laryngeal nerve against the aortic arch. In that same light, Ortner’s syndrome can be the first symptom of diseases involving dilatation of the aortic arch to put traction on the left recurrent laryngeal nerve and produce hoarseness.[6]
Nowadays, various mechanisms are known to attribute to vocal cord paralysis after cardiac surgery. First of all, median sternotomy with sternal retraction can result in longitudinal strain on both subclavian arteries and hence to both laryngeal nerves. This is enhanced by unilateral or bilateral traction on the rib cage for harvesting of the internal mammary artery.[7] It has also been postulated that thermal injury by electrocautery during dissection of the internal mammary artery near its origin from the subclavian artery might contribute.[2] Also the use of cardioprotective ice slush might play a role.[2] In addition, direct trauma or neuropraxis to the left recurrent laryngeal nerve in the minimal aortic window (4 mm) where it curves around the aortic arch just above the pulmonary artery is a well-described mechanism. This can be the case in aortic aneurysms and their repair, left atrial enlargement, pathology of the ductus arteriosus or dysrhythmia ablation procedures.[6] Also direct (iatrogenic) trauma to the larynx or the arytenoid joints or vagus nerve in the carotid sheath has been described. This involves traumatic endotracheal tube placement which can cause dislocation of the cricothyroid or cricoarytenoid joints. Repeated unsuccessful attempts to insert a transoesophageal echocardiography probe can lead to laryngeal oedema or to laryngeal recurrent nerve palsy due to haematoma of the oesophageal wall in the tracheoesophageal groove.[7] Lastly, central venous catheterisation can cause laryngeal nerve injury, especially in the case of inadvertent arterial puncture because of close proximity of the vagal nerve in the carotid sheath. The prognosis of laryngeal recurrent nerve palsy depends on the cause. In general it is believed that the chance of recovery depends on the degree and duration of the injury. Ischaemic causes due to manipulation during cardiac surgery are not associated with a good outcome. Patients are assessed for aspiration, increased vocal effort, altered voice quality, dyspnoea on exertion and decreased quality of life. If the symptoms are well tolerated, only follow-up is warranted. Otherwise, medialisation of the affected vocal cord can be an option.[6]