It is estimated that 43% of cases of vocal cord paralysis result from medical procedures, 25% are induced by malignant processes developing within the head, neck and chest, and the aetiology of 18% is difficult to establish . The throat, larynx and respiratory tract are the field of everyday intense activity for anaesthetists. It is therefore no surprise, that in cases of peri-operative vocal fold paralysis that it is the anaesthetists who are the most interested in the diagnosis of the causative mechanisms.
A case is presented of transient vocal cord paralysis which occurred soon after completion of a laparoscopic repair of an oesophageal hiatus hernia.
The patient, aged 45 years (body weight 90 kg, height 180 cm) was admitted to hospital with a burning sensation in the oesophagus and a sensation of gastric contents reflux into the oesophagus, which had persisted for many years and which was particularly troublesome in the lying position. An oesophagogastroduodenoscopy revealed a large oesophageal hiatus hernia. The diagnosis was confirmed using a 24-h oesophageal pH monitor and a manometric examination. An intense reflux of acid gastric contents into the oesophagus, which occurred both in the standing and the lying positions was found. Oesophageal peristalsis was maintained but its effectiveness was significantly reduced, particularly in the lying position. On this basis the patient qualified for laparoscopic fundoplication.
The patient was in a good general condition (ASA II). Medical examination of the respiratory and circulatory systems failed to reveal any significant abnormalities. The alveolar air sounds over the lungs were normal, arterial blood pressure was 120/70 mmHg and heart rate was 72 bpm. Both in the ECG record, the chest X-ray and in the results of laboratory tests no abnormalities were found.
On the eve of the surgery and 2 h before its beginning, the patient was given midazolam 15 mg orally. During induction of general anaesthesia, propofol 100 mg and suxamethonium 150 mg were administered intravenously (i.v.), and then without any difficulty the trachea was intubated with a 9-mm diameter tube, the sealing cuff of this was inflated with 2 mL of air. On the other hand, significantly, greater than usual, difficulties were met during the introduction of the 16F tube into the stomach.
General anaesthesia was maintained with propofol which was administered i.v. in a continuous infusion at a rate of 7 mg kg−1min−1. Additionally, fentanyl and atracurium were administered, the total doses of these during surgery were 0.75 mg and 90 mg, respectively. During surgery, artificial lung ventilation was maintained with an oxygen-air mixture (FIO2=0.3) with positive end-expiratory +10 cm H2O pressure. ETCO2 (end-tidal CO2) was maintained within a 4.8-5.4 KPa range. Arterial blood saturation with oxygen, being 98% before surgery, ranged from 99 to 100%. Arterial pressure being 135/71 mmHg before surgery was maintained within a 120/80-145/85 mmHg range for the greater part of the procedure, and heart rate was 95-105 bpm. During surgery, the patient received i.v. 2000 mL Ringer acetate and was given an antibiotic (Unasyn 1500 mg).
The peritoneal cavity was filled with carbon dioxide, the pressure of which was automatically maintained at the 1.6 KPa level. After insertion of trocars and a laparoscope into the abdominal cavity, visual inspection was carried out. The presence of a large oesophageal hiatus hernia was confirmed, while no abnormalities of other organs were identified. During surgery, the oesophagus and diaphragmatic crura were exposed. The crura were then sutured and the gastric fundus was sewed onto the anterior side of the abdominal part of the oesophagus (anterior 180° fundoplication). A drain was introduced into the abdominal cavity, the tip being placed in the region of the sutured oesophagus. After completion of surgery, which lasted 2 h and 50 min, the gastric tube and tracheal intubation were removed.
Soon after tracheal extubation, verbal contact was established with the patient. He answered the questions asked by the anaesthetist with a hoarse but strong voice. However, with passing time his voice became much softer and after more than 10 min he could only whisper. Because the above signs failed to regress after 24 h, a laryngological consultation was sought and it was reported that he had a hoarse voice but without pain in the throat. The laryngeal mucosa was pale and smooth. The left vocal ligament was immobile while the right remained mobile. No disturbances in swallowing were observed. The following treatment was given: triamcinolone, vitamins B1, B2, B12, cocarboxylase and laryngeal physiotherapy (neofaradic stimulation). During successive days, gradual improvement in voice strength was observed. Every day during the morning hours the voice was strong and resonant but with the passing of time it became ever more hoarse and soft. The patient was discharged home on the eighth day following surgery in good general condition. Further treatment was conducted in a phoniatric counselling unit. After 3 months, the strength of the voice returned to the pre-operative level.
If after surgery vocal fold paralysis occurs, it is usually connected with tracheal intubation [2,3]. Tracheal intubation should not be a brutal procedure and tissue damage in the oral cavity, throat and larynx due to the pressure of laryngoscope blade can occur in cases in which visualization of the glottic rima is difficult due to anatomical anomalies. Usually, laryngological complications are the consequence of obvious technical errors, such as tracheal intubation when the vocal cords are not sufficiently relaxed, use of intubation tubes with too large a diameter, excessive inflation of the sealing cuff or the cuff is placed between the cords . It is estimated that in 42% of patients mechanical damage of the larynx occurs during intubation. In most cases vocal fold oedema develops and causes hoarseness, pain in the throat and phonation disturbances which regress spontaneously after 2-3 days. However, sometimes, after intubation tube removal stridor and dyspnoea, or long-lasting phonation disturbances occur. Damage of recurrent laryngeal nerves or shifting of arytenoid cartilages can then be suspected. The causative mechanism for these complications is similar. Strong, direct pressure exerted by a laryngoscope blade on the larynx in the region of the arytenoid cartilages or pressure exerted by the bent part of the intubation tube on the posterior wall of the glottis leads to subluxation of the arytenoid cartilages [5,6] or to compression of the anterior ramus of the recurrent laryngeal nerve (which provides motor innervation to the lateral crico-arytenoid muscle) between the arytenoid cartilage and the lamina of the thyroid cartilage . The diagnosis depends on direct laryngoscopy, while CT of the larynx makes possible the differentiation between arytenoid shift and nerve damage. In such cases electromyography and strobovideo-laryngoscopy may also be useful . The latter method also makes possible identification of those patients in whom the risk for tissue damage during intubation is particularly high .
It is not likely that, in the case described here, tracheal intubation was the cause of vocal cord paralysis because the trachea was intubated without any difficulty. Although the tube used was of relatively large diameter, 9 mm, this size was appropriate for this male patient.
On the other hand, it seems likely that vocal cord paralysis in this patient developed due to damage of the recurrent laryngeal nerve during the introduction of the oesophagogastric tube. During laparoscopic fundoplication, the gastric tube is introduced in order to facilitate the procedures completion. In this case the oesophageal tube was placed correctly only after several failed attempts and it is very probable that nerve damage occurred at that time. This case is not an isolated case of its type, because vocal cord paralysis as the consequence of a gastric tube [9, 10] or an oesophageal stethoscope  introduction has been described already. Certainly, the risk of such a complication increases when the tube introduction creates difficulties. If the tube is in the midline, beyond the arytenoid cartilages, it may cause local inflammatory reaction damaging the posterior ramus of the recurrent laryngeal nerve, which provides motor innervation to the posterior cricoarytenoid muscle and interarytenoid muscles. It should be also kept in mind that the recurrent laryngeal nerves run towards the larynx close to the oesophagus or even on its surface, and damage to them due to pressure on the side of the oesophagus cannot be excluded.
Certainly, a condition favouring damage to the recurrent laryngeal nerves is chronic inflammatory disease of the tissues surrounding them, caused by gastroesophageal reflux disease (GERD). The cause of GERD is decreased tonus of the lower oesophageal sphincter which promotes the reflux of gastric contents into the oesophagus. The prolonged duration of acid gastric contact with oesophageal mucosa causes ulceration, which leads to narrowing of the oesophageal lumen . The anatomical proximity of the larynx, laryngeal part of the throat and proximal part of the oesophagus ensures that acid gastric contents easily reach the lower part of the throat, larynx and lungs [12-14]. In studies involving a group of over 100 000 patients, it has been demonstrated that there is an evident relation between GERD and sinusitis, pharyngitis, aphonia, laryngeal stenosis, chronic bronchitis, asthma, chronic obstructive lung disease, lung fibrosis, bronchiectases, pneumothorax and pneumonia . Acid laryngitis developed significantly more frequently in this group of patients and led to dysphonia (hoarseness induced by damage to the speech organ) and inflammatory changes in the crico-arytenoid joints [14, 16]. The manifestations of laryngitis in GERD may be so intense that tracheal intubation becomes impossible .
On the other hand, it should be also remembered that there are many diseases associated with vocal fold paralysis. Such diseases include: progressive supranuclear palsy  and malignant metastases  in the medulla oblongata (in which the motor nuclei of the vagus nerves are located). In cases of multisystem atrophy (MSA), vocal fold palsy appears abruptly  and is sometimes the first manifestation of the disease [21,22]. External factors also may damage the laryngeal nerves and can, in consequence, cause vocal fold paralysis. They include: Epstein-Barr  and Herpes simplex viruses , intoxication by insecticides [25,26], radiotherapy to the head and neck in cases of a tumour in these regions [27,28].
On the basis of the case described it seems that close attention should be paid to patients in whom oesophageal hiatus hernia is diagnosed. In such cases 'acid laryngitis' can create conditions under which a relatively minor tissue trauma during intubation or introduction of gastric tube can cause vocal cord paralysis. Therefore, laryngological examination should be performed in order to assess vocal cord mobility both before and after surgery.
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