The term “athlete,” derived from the Greek word athlon meaning “prize” or “contest,” conjures images of a healthy, fit person. Although athletes possess physical speed, strength, and/or particular talents, they also have a repertoire of medical problems. Additionally, because athletes often experience sports-related injuries, trips to the operating suite are not uncommon. This chapter discusses common medical problems in the context of surgical and anesthetic implications. Perioperative athletic concerns are also discussed, including preparation of the sports medicine patient for surgery, anesthetic choice, pain management, and common postoperative complications and concerns.
Preoperative Care and Concerns: Common Medical Issues Found in Athletes
A common pulmonary disorder in athletes, asthma is marked by restriction of airflow in the lungs, narrowing of the airways, and inflammation of the bronchi. Bronchoconstriction and inflammation induce shortness of breath, wheezing, coughing, and chest tightness. Asthma can occur as early as infancy and is a disease that can either be treated adequately or lead to long-term disability. The prevalence of exercise-induced asthma is 8% to 12% in the general population but may be as high as 50% in elite athletes and those competing in cold-weather sports. Several high-profile athletes with asthma, including Billy Jean King, Dennis Rodman, Jackie Joyner-Kersee, Bob Dola, and Amy Van Dyke, have performed at the highest level with adequate treatment.
Triggers include smoking, dust mites, molds, viral colds, pollen, strong odors, and exercise. Exercise-induced asthma may occur after mild to strenuous exercise and is most common in sports involving running and exercise in cold weather. During exercise, minute ventilation can increase exponentially, increasing the work of breathing, friction, airway cooling, and airway drying. Additionally, hyperventilation and breathing through the mouth lead to hypoventilation, which results in bronchoconstriction. Collectively, all these factors produce the bronchoconstriction and inflammation noted in persons with asthma.
The specifics of diagnosis and therapy for persons with asthma are detailed in a separate chapter in this book. Briefly, asthma can be diagnosed with a combination of a thorough history and physical examination and various provocative tests. Although multiple options are available to treat asthma, an important tenet is prevention by avoidance of triggering agents. However, this approach may not be a suitable option for a person with exercise-induced asthma who participates regularly in vigorous activity. Common strategies for maintenance and treatment of exacerbations include β 2 agonists (with albuterol being the most commonly used), inhaled corticosteroids, systemic corticosteroids, anticholinergic drugs, leukotriene-receptor antagonists, and methylxanthine agents. Drugs may be administered by nebulizer, metered-dose inhaler, orally, or intravenously in emergency situations. Before a patient undergoes elective surgery, it is important that asthma be optimally controlled. Despite the bronchodilating properties of most anesthetics, asthmatics are more prone to bronchospasm after airway manipulation under anesthesia. Avoidance of general anesthesia and endotracheal intubation may be beneficial.
Obstructive Sleep Apnea
Obstructive sleep apnea (OSA) is defined by periods of hypoventilation or apnea caused by airway obstruction during sleep. The severity of disease can be determined by the number of obstructive episodes, degree of associated oxygen desaturation, number of microarousal episodes, and number of arrhythmias per unit of time. It is estimated that OSA occurs in up to a quarter of the population, yet the majority of cases remain undiagnosed. OSA may be more common in athletes than originally thought. A study of eight randomly selected NFL teams and 302 players demonstrated a 14% incidence of sleep apnea with a 34% incidence in linemen. Dr. Archie Roberts, a retired heart surgeon who has teamed with the Mayo Clinic to screen retired NFL players, has noted an alarming incidence of OSA. The incidence of sleep-disordered breathing was present in 52.3% of the former football players. Furthermore, a study of sumo wrestlers in Tokyo found that 11 of 23 wrestlers had significant sleep-disordered breathing. Clearly, OSA is a problem that entails clinical vigilance, even in athletes who are presumed to be healthy. Several famous athletes have been diagnosed with OSA. Reggie White of the Green Bay Packers died unexpectedly during sleep in 2004 due in part to complications from untreated OSA. Shaquille O’Neal of basketball fame has spoken out about his diagnosis of OSA in an effort to increase public awareness.
Obstruction of the upper airway occurs as persons relax and drift into sleep, at which time a decrease in oropharyngeal and laryngopharyngeal tone leads to partial or complete airway obstruction. An increase in airway resistance, hypoxia, and hypercarbia ensue, resulting in an increase in sympathetic tone and subsequent patient arousal. This cycle can occur repeatedly throughout the night and results in poor sleep quality. OSA poses both short- and long-term risks to patients. Complications of OSA include chronic hypoxia, hypoxemia, and hypercarbia leading to pulmonary hypertension, right heart failure, and sudden death. Less obvious associations between OSA and long-term sequelae include depression, hypertension, coronary artery disease, and stroke.
OSA is a significant problem in the postoperative period. Sedatives, narcotic drugs, hypnotic agents, and muscle relaxants can exacerbate symptoms. Because of pain and the inherent stress of surgery, patients experience disturbances in rapid eye movement sleep patterns for several days after the immediate postoperative period, and thus accurate screening and management are imperative. The increased risk of obstruction and other complications should be considered when planning intraoperative and postoperative care. Limiting narcotics, benzodiazepines, and general anesthesia (GA) in addition to educating patients about the risks of OSA may be helpful.
A thorough clinical history and appropriate screening may suggest a diagnosis of OSA. Symptoms of OSA include daytime sleepiness, snoring, witnessed apnea, poor concentration, morning headaches, moodiness, and irritability. Males who have hypertension, are overweight, smoke, and have a larger neck circumference are more likely to have OSA. Because many risk factors for OSA are well known, a screening tool to help identify patients with OSA has been validated and is used extensively. In a recent study, 746 patients undergoing inpatient surgery were first screened with the STOP-BANG questionnaire ( Fig. 34-1 ), after which they undertook polysomnography to determine if they had OSA. The predictive probability for moderate or severe OSA increased from 0.36 to 0.60 when the STOP-BANG score increased from 3 to 7. Diagnosis of OSA can be made with polysomnography and a multiple sleep latency test. Polysomnography uses an electroencephalogram, an electromyelogram, and an electrooculogram to help categorize sleep behaviors. The multiple sleep latency test quantifies sleepiness from microarousal episodes in five, 20-minute nap attempts. Sleep latency is another surrogate for severity of OSA, because shorter mean sleep latency correlates with the severity of OSA.
The mainstay of treatment is the use of a CPAP machine, which opens the upper airway and prevents obstruction. Oral or nasal masks are custom-fit for ease of use and comfort. CPAP can enhance sleep quality, increase energy, and improve well-being. Unfortunately it can be obtrusive for some patients, leading to noncompliance. Other treatments for OSA include weight loss, uvulopalatopharyngoplasty, tonsillectomy and/or adenoidectomy, craniofacial advancement techniques, somnoplasties, and nasal surgeries. It is imperative to educate patients about the importance of compliance with treatment. OSA has been implicated in both inpatient and outpatient deaths and is exacerbated by many factors that occur in the perioperative period.
Cardiac issues in athletes are discussed in detail elsewhere in this book, but two entities, the athletic heart syndrome (AHS) and hypertrophic cardiomyopathy (HCM), are discussed here.
Athletic Heart Syndrome
AHS is an adaptive physiologic condition manifested by enlargement of the heart in response to vigorous and frequent exercise, enhanced efficiency, and bradycardia (as low as 30 to 40 beats per minute). First described in 1899 by the Swedish physician Henschen, AHS was discovered by percussing hearts and comparing the heart sizes of cross-country skiers and sedentary patients. The heart increases in size in response to recurrent systemic oxygen deficits, resulting in increased muscle mass and increased ventricular chamber size, which facilitates cardiac output during exercise. Data suggest that over time, the heart returns to normal size after the cessation of exercise. AHS is benign yet vital to recognize, because bradycardia and cardiac hypertrophy can be a concern for clinicians. AHS can be diagnosed by an electrocardiogram, a chest radiograph, or a transthoracic echocardiogram. Findings include bradycardia and increased ventricular size and should be distinguished from life-threatening HCM. Lastly, although AHS is not a health concern, a low resting heart rate may predispose athletes to vasovagal reactions manifested by diaphoresis, nausea, and syncope.
Also known as hypertrophic obstructive cardiomyopathy, HCM is a disease process that must be expeditiously diagnosed and treated to prevent significant morbidity and mortality. HCM is the most common cause of sudden cardiac death and has led to the untimely death of many well-known athletes. Notable athletes who succumbed to HCM include Gaines Adams of the Chicago Bears, who died at age 26 years; Ryan Shay, a 28-year-old marathoner, who died 5.5 miles into a race; and Marc-Vivin Foe, the brilliant Cameroon midfielder, who died at age 28 years during a semifinal soccer match. None of these athletes was diagnosed with HCM prior to their deaths.
HCM is a genetic disorder that leads to asymmetric thickening of the heart muscle that can induce life-threatening arrhythmias. Whereas most forms of HCM are inherited, others are caused by sporadic mutations. The prevalence is thought to be as high as 1 in 500 people in the 23- to 35-year age group. Although myocardial hypertrophy usually occurs in the ventricular septum, hypertrophy can occur in various locations, which can lead to outflow obstruction, particularly during vigorous exercise or during states of hypotension or dehydration.
For persons with HCM, it is imperative that medical clearance for participation in athletics be withheld pending consultation with a cardiologist. Obtaining a thorough personal and family history is critical because symptoms and signs typically do not present until teenage years. Common symptoms and signs include chest pain (which may present in the postexercise period), shortness of breath, arrhythmias or palpitations, syncope, dizziness, and sudden death. Unfortunately, 1% of patients with HCM present with sudden death. In a study of 158 sudden deaths in athletes between the ages of 12 and 40 years in a 10-year period, it was found that 90% of all sudden deaths occurred during or immediately after competition. Postmortem examinations and toxicologic data suggested that 134 of these deaths were related to cardiac pathology, of which 36% were the result of HCM. Physical examination in asymptomatic athletes who have occult HCM may be normal or may reveal a fourth heart sound and/or a left ventricular lift (nonspecific). In persons with a significant obstruction, a harsh crescendo-decrescendo systolic murmur may be heard that begins shortly after S1, is typically best auscultated at the apex and lower left sternal border, and may radiate to the axilla and base, yet not usually into the neck. As a result of increased obstruction, the murmur may increase with an assumption of an upright posture from a supine, sitting, or squatting position or after the Valsalva maneuver.
It is beyond the scope of this chapter to detail various diagnostic and therapeutic tools or to discuss the controversies of screening athletes for HCM. Preparticipation screening for HCM is an ardently debated subject, with conflicting recommendations from varying organizations. The American Heart Association has indicated that a thorough preparticipation history and physical examination may be adequate to detect underlying pathology in many cases and that more detailed testing (to improve sensitivity), including an electrocardiogram and transthoracic echocardiogram, be reserved for cases with features that raise concern on clinical examination. Conversely, in Italy, preparticipation screening for athletes includes a detailed patient and family history, physical examination, and electrocardiogram (with additional cardiac testing as needed). After institution of the mandated nationwide systematic screening program, the incidence of sudden cardiovascular death in young competitive athletes between 1979 and 2004 significantly decreased in the Veneto region of Italy. Therapeutic interventions included medications (β- or calcium channel blockers and antiarrhythmic agents), pacemakers and/or defibrillators, and/or invasive, surgical management (i.e., a myomectomy or ablation of the cardiac septum).
Diabetes mellitus (DM) is prevalent in athletes. Although athletes of different ages may have either type 1 or type 2 DM, type 1 DM occurs commonly in athletes and is briefly discussed in this section. It is estimated that about 215,000 people in the United States who are younger than 20 years have some form of diabetes. Long-term complications of diabetes include cardiovascular disease, cerebrovascular disease, peripheral neuropathy, retinopathy, and nephropathy. Common symptoms of type 1 DM include increased thirst, increased urination, weight loss, increased appetite, visual changes, and fatigue. Diagnostic tests include fasting plasma glucose level, oral glucose tolerance, or random plasma glucose level tests. Fasting glucose levels should be less than 100 mg/dL; levels between 100 and 125 mg/dL reflect impaired glucose tolerance, and levels greater than 200 mg/dL raise concern for diabetes.
Treatment of diabetes consists of maintaining normal or near-normal glucose levels and preventing hypoglycemia. Although hypoglycemia rarely occurs in persons with type 2 DM, it can lead to significant morbidity and mortality in persons with type 1 DM. Common symptoms of low blood sugar include irritability, dizziness, headache, diaphoresis, tachycardia, and tremor. Severe hypoglycemia can lead to seizures and brain damage because the brain relies heavily on glucose for normal metabolic activity. Treatment of hypoglycemia includes immediate administration of glucose in the form of carbohydrates, glucose tablets, or IV dextrose. Maintenance therapy for DM is discussed elsewhere in this book. However, clinicians caring for athletes who are undergoing surgery should be aware that symptoms of hypoglycemia may be masked in diabetics who are sedated or undergoing GA. Furthermore, in the perioperative period, hyperglycemia may lead to an increased number of wound infections and poor wound healing.
Intraoperative Care and Considerations of the Sports Medicine Patient
The term regional anesthesia implies analgesia and immobility of a region of the body. Regional anesthesia techniques may be further subdivided into those that target segmental spinal levels (i.e., central or neuraxial blocks such as spinal or epidural blocks), peripheral nerves (e.g., peripheral nerve blocks [PNBs] and plexus blocks), or extremities via IV regional block (i.e., Bier block). Central nerve blocks and PNBs are achieved with the use of local anesthetic agents, narcotics, and other adjuvant medications to induce the level of desired anesthesia. Field blocks typically describe the more superficial injection of local anesthetics. Both neuraxial nerve blocks and PNBs can be modified by the insertion of a catheter to continuously infuse medication during surgery, as well as for postoperative analgesia. Peripheral nerve catheters can be used in an inpatient or outpatient setting with proper patient selection and education. PNBs and neuraxial anesthetic agents may be used as the primary anesthetic or as an adjuvant to GA.
Orthopaedic Surgeries and Pain
A study of ambulatory surgeries showed that orthopaedic patients have the highest incidence of postoperative pain. Inadequately treated pain can significantly affect recovery time, rehabilitation, and patient satisfaction and may increase readmission rates. When choosing the anesthetic, various factors should be considered, including the precise location of surgical intervention, extent of bone manipulation, instrumentation, osteotomies, ligamentous involvement, expected or planned nerve manipulation, use of bone or tendon autografts, size of incisions, the use of intraoperative tourniquets, and the requirements for postoperative physical therapy and range-of-motion exercises. These perioperative factors will help the anesthesiologist predict the level of postoperative pain, determine if a regional technique is indicated, and determine the needed duration of effect. The details of the proposed surgical procedure will further dictate whether a regional approach in itself will be sufficient.
A PNB may provide excellent analgesia postoperatively but may not be sufficient to cover the entire surgical field or for intraoperative retraction and manipulation. The necessary positioning for surgery can induce nonoperative discomfort. Lying flat and immobile for lengthy periods can be difficult for some patients because of either preexisting back or lower extremity pain or claustrophobia. Often this problem can be overcome with conscious sedation alone, but occasionally very deep sedation or GA is necessary. Pain induced by use of a tourniquet can be a source of substantial discomfort for a patient who is awake. Occlusion times in excess of 45 to 60 minutes may be intolerable despite the use of a PNB. Finally, certain surgical procedures put the patient at high risk for nerve injury or compartment syndrome; the surgeon may wish to identify this risk early in the postoperative course. In this setting, a regional technique may confound the postoperative examination for the first 24 hours.
Several clinical features, including the aforementioned medical comorbidities, play an important role in shaping the anesthetic plan. In the younger, athletic population, cardiovascular risk factors are fortunately rare. GA is known to increase the risk of significant cardiac events in persons with certain cardiac risk factors. For persons with OSA, the use of nonnarcotic means of analgesia and avoidance of GA is recommended to reduce the risk of perioperative complications. If a patient has a history of difficult intubation or ventilation or if airway examination is a concern, GA should be avoided to prevent potential airway complications. Patients with increased risk of aspiration as a result of preexisting esophageal or gastric pathology, or more commonly as a result of gastroesophageal reflux disease, may also benefit from the avoidance of GA. Patient psychological factors may play a prominent role in the anesthetic choice. Promising young athletes may fear a protracted nerve injury after undergoing a regional technique. The decision to place an ambulatory peripheral nerve catheter for use at home will depend on the patient’s maturity, reliability, and support system.
Contraindications to Regional Anesthesia
Absolute and relative contraindications to regional anesthesia typically vary by the type of planned intervention, and young and healthy athletes may present an additional challenge. Patient refusal, the inability to lie still during administration of a block, infection at the site of injection, recent use of thrombolytic agents, and operator inexperience for the proposed regional technique are perhaps the only shared absolute contraindications. Increased intracranial pressure may lead to brainstem herniation, which precludes use of neuraxial procedures. Other relative contraindications include evidence of systemic infection, preexisting neurologic disease, coagulopathy attributable to intrinsic disease or medication, or aberrant anatomy. All risks and benefits should be weighed thoroughly before proceeding with regional anesthesia.
Complications of Regional Anesthesia
The incidence of infection associated with neuraxial techniques is approximately 1 in 40,000. The risk of PNB infection has yet to be clearly defined but appears to be greater with the use of continuous, indwelling catheters in the axillary or femoral areas for more than 48 hours. Skin contaminants either by colonization or local infection, systemic infection via seeding of catheter sites, or immune suppression enhance risk. Spinal hematomas may form after induction of spinal or epidural anesthesia in patients with underlying coagulopathy. Detailed recommendations for management are well described in the American Society of Regional Anesthesia 2010 Practice Advisory. Although the data are less instructive for PNBs, the literature includes rare case reports of a hematoma causing nerve injury, which seems to be more prevalent with use of deeper techniques such as lumbar plexus block. Nerve injuries are a major concern for both the orthopaedic surgeon and anesthesiologist, yet the overall risk of permanent nerve injury is fortunately small. A metaanalysis in 2007 showed rates of permanent nerve injury between 0 and 7.6 per 10,000 for neuraxial procedures and approximately 1 in 15,000 for PNBs. The incidence of short-term paresthesias or dysesthesias is thought to be between 1% and 3%, with the highest incidence following interscalene brachial plexus blocks. The diagnosis and management of nerve injury associated with PNB is discussed in further detail later in this chapter.
Benefits of Regional Anesthesia in the Sports Medicine Patient
The benefits of regional anesthesia are abundant. Compared with narcotic analgesic agents, postoperative pain control is notably improved with peripheral nerve and neuraxial blocks. As expected, these studies also demonstrate less nausea, vomiting, ileus, pruritus, and sedation because of the opiate-sparing effects. It is also well established that the use of regional anesthesia improves functional recovery. Peripheral nerve catheters resulted in earlier ambulation, shorter hospital stays, and shorter rehabilitation periods after discharge, as well as improved range of motion and mobilization after knee surgery. Epidural catheters also offer similar analgesic and postoperative mobilization benefits when compared with peripheral nerve catheters, although hypotension and nausea are more common. In the ambulatory setting, orthopaedic procedures can account for a significant percentage of unplanned readmissions for pain control. Use of outpatient perineural catheters resulted in fewer unplanned admissions after discharge in patients undergoing anterior cruciate ligament (ACL) surgery.
Regional anesthesia may also benefit patients in measures that transcend pain control and its associated secondary gains. Operative blood loss may be decreased through decreased arterial and venous pressure and blockade of sympathetic tone in the affected extremity. The incidence of deep venous thrombosis (DVT) and pulmonary embolism (PE) may be lower with neuraxial anesthesia because of increased blood flow, decreased viscosity, and modification of inflammatory mediators. Neuraxial anesthesia may also reduce the risk of infections at surgical sites, possibly through modulation of inflammation and immune responses. Furthermore, the avoidance of GA in high-risk patient populations is an immeasurable benefit.
A precious commodity during orthopaedic procedures, tourniquets provide a bloodless field for surgery. However, complications associated with tourniquet placement are not uncommon. Pain with resulting hypertension and tachycardia, “sickling” in sickle cell disease, nerve injury, and tissue damage may result. Nerve injury can result from ischemia, pressure, or shearing at the edges of the tourniquet. The pain is typically dull and begins with inflation. Progressive symptoms may include tingling, numbness, paresthesia, and a change in quality of pain. Pain typically begins at 20 minutes and can become severe at approximately 40 minutes. No duration of tourniquet use is guaranteed to be safe, yet most experts consider 2 hours to be the “maximum ischemic time.” At the conclusion of procedures, release of the tourniquet can lead to hypotension and metabolic acidosis as metabolites from an ischemic limb are released into the circulation. In patients with congestive heart failure, a sudden increase in circulating volume can lead to volume overload and acute heart failure. Occluding venous blood flow distal to the tourniquet predisposes a patient to thrombi formation. Systemic release of the thrombi after tourniquet deflation may lead to stroke and PE.
Although many orthopaedic surgeries may be performed in a supine intraoperative position, some operations require more complicated positions and padding. Proper positioning and padding is thus of the essence to minimize complications.
Beach Chair Position
The beach chair position has become the chosen intraoperative position for many orthopaedic surgeons who perform procedures on the shoulder. This position is favored for many reasons, including better exposure of the shoulder joint, avoidance of the lateral position, decreased risk for brachial plexus injuries and hypotension, and reduced bleeding in the joint. Nonetheless, the beach chair position has multiple physiologic consequences, including a decrease in mean arterial blood pressure, central venous pressure, stroke volume, cardiac output, and arterial oxygen content. Additional concerns include venous pooling, increased risk for air embolus, and poor access to the airway. Reports of fluid extravasation from the shoulder joint into soft tissue have led to airway compromise.
An important concern is the discrepancy that can exist between cerebral perfusion and the site of blood pressure measurement. This issue is especially vital in the hypertensive patient who may have a rightward shift of the cerebral autoregulatory curve and needs higher mean arterial blood pressure to maintain adequate perfusion. Blood pressure should be measured in the arm at the brachial artery, and the distance between the heart and external auditory meatus should be calculated. The hydrostatic gradient can be determined using the conversion of 0.77 mm Hg decrease for every centimeter height difference between the brain and the site of blood pressure measurement. Additionally, placing a blood pressure cuff on the ankle (which could be as much as 150 cm below the brain) has been implicated in providing the anesthesiologist and surgeon with a false sense of increased cerebral perfusion pressures. Serious neurologic injury, presumably due to inadequate cerebral perfusion during beach chair positioning, has been documented in four patients.
Specific Regional Anesthesia Techniques
Epidural, caudal, and spinal blocks are collectively referred to as neuraxial anesthetics. Spinal block also may be referred to as an intrathecal or subarachnoid block. Neuraxial techniques can be used for surgical anesthesia for any lower extremity, hip, or pelvic procedure. Most commonly, a mix of a local anesthetic and a narcotic is used, but other adjuncts exist to enhance block quality and duration. Placement of a catheter, which is most commonly used with epidural blockade, facilitates the ability to augment or lengthen the duration of the block intraoperatively or provide ongoing postoperative analgesia. The chief difference between epidural and spinal blockade is the location of drug administration. Whereas a spinal block requires puncture of the dura mater and injection of the drug into the cerebrospinal fluid, thus bathing the spinal cord and nerve roots, an epidural block requires injection of medicine past the ligamentum flavum, outside the dura mater. Because of varying anatomy within the epidural space and the presence of vasculature, fat, and potential septations, an epidural block can occasionally result in a patchy or unilateral block quality when compared with a spinal block.
The most common adverse effects encountered with neuraxial blocks are hypotension, pruritus, nausea, sedation, and urinary retention. Hemodynamic effects, including hypotension and bradycardia, are more noticeable with a spinal block, which is due to rapid onset of sympathectomy, as well as blockade of cardioaccelerator fibers in the upper thoracic spinal levels. Pruritus and nausea are more pronounced with use of a narcotic in the neuraxial mixture. Postdural puncture headache is another complication of neuraxial anesthesia. Believed to occur from an alteration in cerebrospinal fluid dynamics due to dural puncture, the incidence is fortunately low (0%-2%) with spinal anesthesia when performed by an experienced provider with a small gauge, noncutting needle. Typically an epidural block should not interrupt the dura mater, yet an accidental puncture can occur. A “wet tap” or cerebrospinal fluid return during epidural placement with a large 17-gauge Tuohy needle can induce a headache in more than 50% of affected persons. In such cases, definitive treatment with an epidural blood patch is highly effective. A transient backache is also infrequently reported after a spinal block. The use of certain local anesthetic agents and traumatic needle placement may increase this risk. Major complications such as “high spinal,” local anesthetic toxicity, infection, neurologically significant bleeding, and permanent nerve damage are extremely rare.
Practically, for outpatient sports medicine procedures, neuraxial blocks can be used to limit risks and costs associated with GA and subsequent recovery. In the setting of outpatient procedures such as knee arthroscopy, comparisons between GA and epidural, spinal, or PNBs have yielded conflicting results regarding speed, cost, and complications. Although discharge readiness may be expedited for neuraxial anesthetics when considering pain control, mental status, and nausea, other factors, such as urinary retention, may ultimately delay discharge.
Peripheral Nerve Blocks
Surgical anesthesia, immobility, and analgesia can be achieved with the precise deposition of local anesthetics and adjuvants near peripheral nerves. This can be accomplished by using surface landmarks, nerve stimulation, and ultrasound-guided techniques. The duration of the block may be manipulated by altering the type of local anesthetic or adjuvant or by placement of a perineural catheter. Localization of the nerves to be blocked may involve several techniques. Incorporating knowledge of the surface anatomy along with palpation of vessels and bony structures can help identify the location for blockade. PNBs were initially performed by provoking paresthesias in the desired nerve distribution with needle advancement. For nerve stimulation, an insulated needle is used to apply a low level current at the tip, which can elicit a twitch in a corresponding muscle group supplied by a target nerve. Alternatively, “real-time” ultrasonography may be used to visualize the peripheral nerves and needle, which enables anesthesiologists to administer medications with great anatomic specificity. Thus far, no one technique has been shown to decrease neurologic complications or local anesthetic toxicity. Nonetheless, ultrasound-guided blocks have numerous advantages, including a faster onset of action, improved quality, decreased volume of local anesthetic used, and a decrease in accidental vascular puncture rates.
Upper Extremity Innervation and the Brachial Plexus
The brachial plexus forms from the ventral rami of spinal nerves C5 to T1, with occasional contribution from C4 and T2. The plexus exits between the anterior and middle scalene muscles of the neck, courses over the first rib and under the clavicle, surrounds the axillary artery, and divides into peripheral nerves that supply motor and sensory innervation to the upper extremity. A fascial sheath surrounds the plexus from the intervertebral foramina to the upper arm and can serve both to compartmentalize injected block medicine and provide a safe barrier to this approach. Several techniques can be used to block the brachial plexus, each of which differs in coverage of the plexus and adverse effect profiles. Figure 34-2 demonstrates the different approaches used to block the brachial plexus.