Acute Respiratory Insufficiency During Interscalene Plexus Block

Abstract

Shoulder operations are often performed on outpatients by using interscalene blockade (ISB) of the brachial plexus and IV sedation (1). Interscalene local anesthetic injection may produce ipsilateral vagus, phrenic, cervical sympathetic, and recurrent laryngeal nerve blockade as acceptable and typically inconsequential components of an appropriately placed injection (2–4). Although the reported symptoms of ISB may include mild and self-limiting dyspnea and/or hoarseness, we encountered a patient who developed acute respiratory insufficiency associated with an obstructive inspiratory stridor, requiring endotracheal intubation. Case Report Our 78-yr-old, ASA physical status II patient weighed 72 kg, was 172 cm tall, and presented for arthroscopy and acromioplasty for right shoulder impingement. His preoperative evaluation disclosed a history of benign prostate hypertrophy, which was previously treated with transurethral resection and daily oral doxazosin. He had undergone bilateral cataract extraction and was taking amitriptyline 25 mg at night and ibuprofen as needed for his chronic pain. All other systems reviewed were reported as “without complaint.” All laboratory evaluations were within normal limits, including electrocardiogram and chest roentgenogram. After sedation with IV midazolam 2 mg and fentanyl 100 μg, ISB was performed on the right side in the preoperative holding area by using 40 mL 0.5% ropivacaine with epinephrine added to provide a concentration of 1:200,000. After 30 min of slow onset, the patient was taken to the operating room, exhibiting motor and surgical sensory block of the shoulder and arm, and placed in a “beach chair”/sitting position for surgery. He was further sedated with fentanyl 50 μg and a propofol infusion containing ketamine 1 mg/mL at 25 to 75 μg·kg-1·min-1. Seventy-six minutes after block placement and 14 min into the procedure, significant stridor became apparent, and the propofol/ketamine was discontinued. Although the oxygen saturation remained in the 98%–100% range, the alert patient had difficulty speaking and increasing inspiratory stridor, despite assistance, including a nasal trumpet and positive pressure ventilation via mask. Recognizing that apneic oxygenation in an oxygen enriched environment can maintain arterial oxygenation within and above the normal range, and despite extreme limitations in ventilation, including apnea itself, the decision to control the patient’s airway was made on clinical grounds (5). General anesthesia was induced by using a 200-mg propofol bolus to allow application of a size 4 laryngeal mask airway and assisted ventilation, without satisfactory improvement. Endotracheal intubation followed, successfully facilitated by using 100 mg of succinylcholine and with direct visualization of the vocal cords. Surgery then proceeded uneventfully. At the end of surgery, laryngoscopy was performed under anesthesia while the patient was tracheally intubated, disclosing a normal appearance of the airway down to the vocal cords. Before the patient had emerged from anesthesia, an endotracheal tube exchanger was placed via the endotracheal tube, and the tube was removed. The patient was able to dislodge the exchanger, however, and immediately the respiratory distress with stridor resumed. An attempt at intubation without relaxant was unsuccessful. On a second attempt, reintubation was accomplished by using 100 mg of succinylcholine. The patient was taken to the recovery room tracheally intubated. At this time, the attending anesthesiologist met with the patient’s wife regarding the current difficulty. At this point, she indicated for the first time that the patient had suffered an idiopathic paralysis of the left vocal cord 5 yr earlier. With this new information, bilateral cord paresis causing complete laryngeal obstruction was diagnosed, secondary to right vocal cord paresis from the right ISB combined with a preexisting left vocal cord palsy. The patient remained sedated with propofol and intubated overnight. The next morning, he was allowed to awaken from the propofol sedation and extubated without incident. Discussion The patient developed bilateral paresis of the recurrent laryngeal nerves with the ISB. Because the recurrent nerve innervates all intrinsic laryngeal muscles except the cricothyroid muscle, which is a vocal cord tensor, bilateral lesions of the recurrent nerves can lead to obstructive positioning of the vocal cords (6,7). The preoperative history and physical documentation of the family physician specifically listed “ENT: no problems,” and the patient was not noted to be overtly hoarse during the preoperative interview. Because of the idiopathic and temporally distant nature of the paresis, there was no surgical history or scar (i.e., thyroid) to raise suspicions. Indeed, the matter of vocal cord problems was apparently forgotten by the patient and his wife (who was also present during the preoperative interview). His voice was now regarded as “normal,” and thus, hoarseness was never mentioned to his primary physician or any perioperative consultants. Seltzer (8) suggested, in an earlier discussion of unilateral recurrent nerve block from ISB, that “block of the recurrent nerve in a heavily sedated patient with contralateral cord paresis might produce some impairment to ventilation.” However, the degree of distress in our patient was severe and life-threatening, greatly exceeding this expectation. The role of the sedation itself in contributing to the distress is questionable, particularly as bilateral recurrent nerve paresis, as described in thyroid surgical lesions, has also proved incapacitating and requiring tracheostomy. Further, our patient developed progressive respiratory distress despite cessation of the sedative infusion. In conclusion, severe respiratory distress can occur in the event of bilateral recurrent nerve paresis resulting from ISB and preexisting contralateral recurrent nerve paresis, which quite probably occurred here (7). Although respiratory reserve is typically evaluated before ISB, vocal cord function per se is not. This case report suggests that eliciting routine and specific vocal cord histories may help avoid this rare complication.