The patient is scheduled for urgent surgery for a proximal humeral fracture and may have some significant internal bleeding. Significant COPD, history of multiple fainting episodes in the past, and chronic hypertension are the presenting problems.

It is important to know if the patient’s fall was precipitated by a fainting episode or if the patient simply tripped or lost footing. The patient should be questioned whether any additional
trauma occurred at the time of the fall: Has the patient’s history of fainting been evaluated in the past? Does the patient have any known cardiac disease? Does he have any history of stroke or carotid disease?

The patient’s use of atenolol may exacerbate COPD, especially if there is a reversible component of airway disease. It would be useful to determine whether the atenolol is being taken for the treatment of hypertension or syncope. Although uncontrolled and small controlled clinical trials have shown some benefit from the use of β-blockers, larger, long-term controlled trials have not supported their use for the treatment of reflex syncope. There is some evidence that β-blockers may be protective with regard to development of severe bradycardia or sudden asystole during surgical procedures performed in the “beach chair” or head-up position.

Immobilization of the arm following humeral fracture is important to avoid injury to the brachial plexus or its terminal branches.

The radial nerve is at particular risk, especially with midshaft humeral fracture. Following proximal humeral fracture, the shoulder can be dislocated, and malpositioning can cause stretching or pressure on components of the brachial plexus. To this extent, it is important to document any preexisting neurologic findings on examination, especially if brachial plexus block is being considered.

Syncope is defined by a complete loss of consciousness that is of rapid onset and short duration, accompanied by loss of postural tone and a complete and spontaneous recovery. The major categories of syncope include reflex or neurally mediated syncope (vasovagal, situational, carotid sinus), orthostatic syncope (autonomic failure, drug-induced, hypovolemia), and cardiac syncope (arrhythmia, drug-induced, structural disease). Syncope is fairly common, affecting approximately 11% of the population. Vasovagal syncope is the most common cause, accounting for 21% of cases. Most affected patients experience a first episode between the ages of 10 and 30 years; only 5% of patients experience their first episode after age 40 years. The incidence of syncope increases with age, peaking after the age of 65 years.

The workup of syncope should include a detailed history and physical examination, including a measurement of orthostatic blood pressure and an electrocardiogram. An echocardiogram is indicated if the history or physical exam is suggestive of cardiac disease. Tilt-table testing or a neurologic workup may also be appropriate depending on the history and physical exam.

This patient had a prior evaluation that documented an abnormal response to head-up tilt-table testing during isoproterenol infusion and received a diagnosis of reflex (vasovagal) syncope. He has managed this conservatively with physical maneuvers (sitting, leg crossing) upon feeling faint and has not experienced a complete loss of consciousness for over 20 years.

No single premedication regimen has been shown to be consistently more effective than others. This patient has already received a recent significant intravenous dose of hydromorphone in the emergency room. If careful history rules out any significant problems or other drug intake, intravenous midazolam can be carefully titrated in the operating room while the patient is monitored with pulse oximetry in the presence of the anesthesia practitioner. Opiates should be avoided because the patient has already received intravenous hydromorphone.

Although benzodiazepines almost certainly cause a dose-related, centrally mediated respiratory depression, overall respiratory depression is not nearly as profound as with the administration of intravenous opiates. Use of carefully titrated smaller therapeutic doses of midazolam is usually well tolerated, without significant respiratory depression. Use of benzodiazepines has been shown to elevate the seizure threshold during local anesthetic administration.

Both interscalene and supraclavicular brachial plexus blocks provide excellent operating conditions and allow for postoperative analgesia. Concomitant intravenous sedation and oxygen via nasal cannula may be appropriate, or laryngeal mask airway or endotracheal intubation may be preferred depending on the surgical positioning and access to the airway.

The brachial plexus supplies the nerves to the upper limb. It is formed by the ventral primary divisions of the fifth to the eighth cervical and the first thoracic nerves, with possible contributions from the fourth cervical and second nerve thoracic roots. The roots join to form the superior, middle, and inferior trunks, which divide into anterior and posterior divisions (Fig. 46.1). The three posterior divisions form the posterior cord, whose major branches are the radial and the axillary nerves. The upper two anterior divisions form the lateral cord, whose major branches are the musculocutaneous nerve and the lateral root of the median nerve. The lowest anterior division forms the medial cord, which gives the medial root to the median nerve and terminates as the ulnar nerve. The sympathetic contributions to the brachial plexus are derived from the middle cervical ganglion and the stellate ganglion.

The brachial plexus begins at the level of the nerve roots, usually at C5-T1. It is at this level that the interscalene brachial plexus block, first described by Winnie, is performed. Injections at this level result in a block with central characteristics, much like a one-sided neuraxial block. Resulting sensory block at this level is characterized by a dermatomal pattern. If the block is incomplete, the typical cause is inadequate spread of local anesthetic to certain nerve roots. For example, the C8-T1 nerve roots are often spared during interscalene block anesthesia because local anesthetic distribution fails to include the lower, most caudal, nerve roots of the brachial plexus. As the brachial plexus courses more peripherally from the neck to the axilla, the nerve roots transform to trunks, divisions, and cords and finally form fully differentiated peripheral nerves. At the level of the axilla, where axillary block is performed, the plexus is composed of terminal nerves that include the median, radial, ulnar, and musculocutaneous nerves. At this level, an incomplete block typically spares sensory or motor blockade in the distribution of a given peripheral nerve, for example, the lateral antebrachial cutaneous nerve (the terminal sensory branch of the musculocutaneous nerve), which exits the surrounding fascia high in the brachial plexus. At this level, the nerves are spread out anatomically around the axillary artery, and depending upon the location of the needle tip during injection and the volume of local anesthetic, any of the four nerves could be spared. This has resulted in the description of multiple injection techniques for axillary block to ensure complete brachial plexus anesthesia.

At the level of the nerve roots or trunks, the brachial plexus is simply a neural plexus, being devoid of major consistently identifiable blood vessels. At this level, brachial plexus identification (i.e., needle tip location) relies on a neural response (paresthesia or motor response to electrical nerve stimulation) or direct imaging (e.g., using ultrasonographic guidance) of the neural tissue itself. At the level of the clavicle and first rib, the plexus picks up the subclavian artery, later to become the axillary artery. At this level or below, one can take advantage of the blood vessels (by palpation, Doppler flow guidance, or ultrasonographic guidance) to assist in the performance of brachial plexus block, and true perivascular techniques of brachial plexus block are the commonly preferred techniques.

The brachial plexus in the neck has multiple significant anatomic relationships that include the phrenic nerve, subarachnoid space, epidural space, spinal cord, proximal nerve roots, vertebral artery, jugular veins, and the apex of the lung. Errant needle passes can hit any one of these, and in fact, there are published case reports of complications from needle injury or local anesthetic injection for each of these anatomic structures.

Below the neck, the major relevant structures are the blood vessels in the neurovascular plexus, which include the subclavian artery and vein, which more distally become the axillary artery and vein, as well as the parietal pleural, visceral pleural, and lung.

Interscalene block gives the most complete block for shoulder surgery and facilitates the placement of a catheter that can be used to extend the operative anesthesia or to administer prolonged postoperative analgesia if this is desired. The supraclavicular block has not historically been used for shoulder surgery due to the concern that it may not block the supraclavicular nerve
(C3-C4) and thus not provide anesthesia over the cape of the shoulder. Recent experience suggests that at higher volumes of local anesthetic (50 mL), supraclavicular block provides equivalent anesthetic conditions to interscalene block. The supraclavicular block may also have a decreased incidence of phrenic nerve blockade when compared to the interscalene block when lower volumes of local anesthetic (20 mL) are used, although this is not guaranteed. If coverage of the shoulder cape is a concern with the use of lower volumes of local anesthetic, the supraclavicular nerve can anesthetized separately with a superficial cervical plexus block.