Rheumatoid Arthritis

RA is a chronic inflammatory disease that initially destroys joints and adjacent connective tissue and then progresses to a systemic disease affecting major organ systems ( Fig. 32.1 ). Implicated predisposing causes include genetic (over 100 gene loci have been identified), environmental, bacterial, viral, and hormonal factors. The role of T cells, autoimmunity, and inflammatory mediators are important in the progression of RA and may serve as sites for potential new treatments.

Systemic manifestations of rheumatoid arthritis.

Systemic manifestations of RA are widespread. They may include pulmonary involvement with interstitial fibrosis and cysts with honeycombing, gastritis, and ulcers from aspirin and other analgesics, neuropathy, muscle wasting, vasculitis, and anemia. Ultimately the anatomy of the airway is damaged and altered in patients with RA.

Airway and Cervical Spine Changes

The patient must be carefully evaluated for both complexity and risks of endotracheal intubation. For example, the airway may be difficult to visualize when attempting intubation. Furthermore, the performance of maneuvers to intubate the trachea may result in an increased risk of cervical spine injury. Many airway abnormalities may occur in patients with RA. Normal mouth opening may be decreased as a result of temporomandibular arthritis. This difficulty may be compounded by the presence of a hypoplastic mandible, which may fuse early in patients with juvenile RA. This results in the noticeable overbite in some patients with RA.

As with other joints, the cricoarytenoid joint may be affected. Cricoarytenoid arthritis may result in shortness of breath and snoring. Patients with RA have been misdiagnosed as having sleep apnea as a result of this condition. Patients with cricoarytenoid arthritis may present with stridor during inspiration, which may occur in the postanesthesia care unit (PACU) after surgery while recovering from anesthesia. Acute subluxation of the cricoarytenoid joint as a result of tracheal intubation can cause stridor as well, and it is not responsive to administration of racemic epinephrine.

The cervical spine is abnormal in as many as 80% of patients with RA. Subluxation and unrestricted motion of the cervical spine can lead to impingement of the spinal cord and its injury. Three anatomic areas of the cervical spine may become involved, resulting in atlantoaxial subluxation, subaxial subluxation, or superior migration of the odontoid ( Fig. 32.2 ).

Sites of potential involvement of rheumatoid arthritis in the cervical spine.

Atlantoaxial Subluxation

Atlantoaxial subluxation is the abnormal movement of the C1 cervical vertebra (the atlas) on C2 (the axis). Normally, the transverse axial ligament (TAL) holds the odontoid process, also referred to as the dens , which is the superior projection of the vertebra of C2, in place directly behind the anterior arch of C1 ( Fig. 32.3A ). With an intact TAL, as the cervical spine is flexed and extended, the odontoid moves with the cervical arch of C1 and the movement between the two is minimal. With destruction of the TAL by RA, movement of the dens is no longer restricted. As the neck is flexed and extended, the C1 vertebra can sublux on the C2 vertebra as the dens and C1 cervical spine no longer move together ( Fig. 32.3B ). This can result in impingement of the spinal cord, placing it at risk for damage. Subluxation of C1 on C2, referred to as atlantoaxial subluxation , can be quantified by a measurement made between the back of the anterior arch of C1 and the front of the dens or odontoid. This distance is referred to as the atlas-dens interval (ADI). Flexion and extension radiographs of the cervical spine are obtained in order to determine the distance between the atlas and dens and the degree of subluxation ( Fig. 32.4 ). If the ADI is 4 mm or more, atlantoaxial instability is present, the amount of subluxation is considered significant, and the patient is considered to be at risk for spinal cord injury. Because the ring of the cervical arch is an enclosed space, as the ADI increases, the safe area for the cord (SAC), that area left within the arch of C1, decreases and motion can lead to impingement of the cord. In a situation in which the TAL is disrupted, extension of the head minimizes the ADI and increases the SAC, whereas flexion increases the ADI ( Fig. 32.5 ) and decreases the SAC, making flexion a more frequent risk position. However, as RA affects more than just the TAL, all neck movements in patients with RA have to be evaluated carefully and extension of the neck can also lead to problems. Although uncommon, asymptomatic patients can have ADI measurements as high as 8 mm to 10 mm. These asymptomatic patients are able to compensate for their cervical spine instability with use of local musculature while awake, but this is not possible when anesthetized. Therefore, neck motion should be minimized after administration of sedation or general anesthesia in patients with atlantoaxial subluxation.

(A) Cross-sectional view demonstrating intact TAL (transverse axial ligament) holding odontoid in place against the anterior arch of C1 vertebra. (B) Rupture of TAL may result in spinal cord impingement.

Radiographs of cervical spine in flexion and extension. Note significant atlantoaxial instability with flexion in left panel where odontoid and arch of C1 are outlined. Note contrast in right panel where in extension odontoid and arch of C1 are in close proximity.

Flexion and extension views demonstrating how flexion increases the ADI (atlas-dens interval) and decreases the SAC (safe area for the spinal cord). In extension the ADI is decreased and the SAC is increased.

Superior Migration of the Odontoid

Inflammation and bone destruction can result in cervical spine collapse in patients with RA. Not all areas of the cervical spine are equally affected in any given patient. For example, if the odontoid is spared, cervical spine collapse may actually result in an intact odontoid process projecting up through the foramen magnum and into the skull. The odontoid can impinge on the brainstem and patients may suffer neurologic symptoms including quadriparesis or paralysis ( Fig. 32.6 ). This pathologic anatomic condition is referred to as superior migration of the odontoid . The odontoid needs to be removed in order to decompress the spinal cord and brainstem. A complicated operative procedure, a transoral odontoidectomy, may accomplish this and involves an incision in the posterior pharyngeal wall, followed by removal of the arch of C1 and then removal of the odontoid, or pannus, or both, which is causing the neurologic symptoms. With completion of the transoral portion of the procedure, the cervical spine is very unstable, necessitating a posterior spinal fusion.

Magnetic resonance image (MRI) and reconstruction demonstrating superior migration of the odontoid through the foramen magnum and impingement on medulla and pons. Also note subaxial subluxation.

MRI courtesy of Malcolm Dobrow, MD.

Ankylosing Spondylitis

Ankylosing spondylitis is an inflammatory rheumatologic disorder in which repetitive minute bone fractures followed by healing results in the characteristic bamboo spine, disease of the sacroiliac joint, fusion of the posterior elements of the spinal column, and fixed neck flexion that is characteristic in this patient population. There is an association between ankylosing spondylitis and HLA-B27, although most HLA-B27 positive patients are not affected with the disease. Patients also develop thoracic and costochondral involvement, which may result in a rapid shallow breathing pattern. The cervical spine becomes rigid, and direct laryngoscopy and airway manipulation should be performed only after careful assessment. A tracheal intubation assist device can help secure the airway. Return of the neck to the neutral position via cervical spine surgery involves removal of all the bony elements of the posterior portion of the spine followed by extension of the head back into a neutral position. This is a very complicated and dangerous procedure, especially at the time when the neck is extended back to the neutral position, which relies on spinal cord monitoring to assess neurologic function as the spine is manipulated.

Anesthetic Technique

The anesthetic technique is geared to provide anesthesia and analgesia for the procedure while avoiding drugs that may interfere with acquisition of the waveforms required for perioperative neurologic evaluation of the spine. Nitrous oxide/oxygen or air/oxygen are used in combination with opioids and an infusion of propofol or dexmedetomidine. If somatosensory evoked potentials (SSEPs) alone are being monitored, an inhaled anesthetic, equivalent to a small percentage (typically < 50%) of 1 MAC (minimum alveolar concentration), can be administered. Volatile anesthetics may interfere with signal acquisition in patients monitored with transcranial motor evoked potentials (TCMEPs) and may have to be discontinued, if used at all, if adequate signals cannot be obtained. Although neuromuscular blockade may be used to facilitate tracheal intubation, paralysis should not be maintained if TCMEPs are being continuously monitored. If the patient is having pedicle screws placed, then the neuromuscular blockade needs to be terminated before the electromyograms (EMGs) are obtained so that testing can be properly performed. A small dose of ketamine, either as a bolus or continuous infusion, can be given in the perioperative period as an additional pain relief modality to provide analgesia for major surgery including spine surgery (also see Chapter 8 ).

Awareness

Intraoperative awareness is a concern for patients and physicians (also see Chapter 47 ). Patients undergoing spine surgery may be at increased risk for intraoperative awareness as a result of the requirement that the anesthetic techniques administered to them be modified to allow for adequate intraoperative neurophysiologic monitoring waveforms to assess spinal cord function. Therefore, the use of brain function monitoring in these patients may help avoid intraoperative awareness. However, this is not a standard and, as noted in the Practice Advisory for Intraoperative Awareness and Brain Function Monitoring, a decision should be made on a case-by-case basis by the individual practitioner for selected patients (e.g., light anesthesia). There was a consensus in the advisory that brain function monitoring is not routinely indicated for patients undergoing general anesthesia as the “general applicability of these monitors in the prevention of intraoperative awareness had not been established.” In fact, Avidan and associates demonstrated that awareness is not decreased with use of brain function monitoring. The need for brain monitoring is still not clear.

Blood Conservation During Spine Surgery

Methods to decrease blood loss in spine surgery patients include predonation, hemodilution, wound infiltration with a dilute epinephrine solution, hypotensive anesthetic techniques, use of cell salvage devices, positioning to diminish venous pressure, careful surgical hemostasis, and administration of antifibrinolytics (also see Chapter 24 ). Medications that have been employed to decrease blood loss during spine surgery include the antifibrinolytics aprotinin, tranexamic acid, and ε-aminocaproic acid. Aprotinin, a serine protease inhibitor, effectively decreases blood loss in cardiac patients and has also been demonstrated to be efficacious in patients undergoing spine surgery. The synthetic lysine analogs tranexamic acid and ε-aminocaproic acid have also been employed in spine surgery as well as in patients undergoing orthopedic joint replacement surgery. Tranexamic acid can be administered by an initial bolus injection of 10 mg/kg over 30 minutes followed by a continuous infusion of 1 mg/kg/h, although other regimens may be used. Tranexamic acid may alternatively be given topically or intra-articularly in appropriate patients.

Although apparently ε-aminocaproic acid can be helpful, a meta-analysis of the use of antifibrinolytics in orthopedic patients demonstrated that although both aprotinin and tranexamic acid are effective in decreasing blood loss, the data were not sufficient to demonstrate efficacy with ε-aminocaproic acid. However, the negative side effects of aprotinin in cardiac patients include (1) increased risk of myocardial infarction (MI) or heart failure by approximately 55%, nearly double the risk of stroke; (2) increased long-term risk of mortality; and (3) a more frequent death rate in patients receiving aprotinin as demonstrated in a study over a 5-year period comparing aprotinin and lysine analogs in high-risk cardiac surgery. The study was terminated early and resulted in relabeling and ultimately withdrawing aprotinin from the market so that it is no longer available.

Positioning

Spine surgery is often performed with the patient in the prone position (also see Chapter 19 ). Careful positioning is crucial to avoid patient injury. Movement to the prone position should be performed in a carefully coordinated manner with the surgical team. The neck should not be hyperextended or hyperflexed but placed in the neutral position and the ETT is positioned so that it is not kinked. Contact areas are padded, and the face and eyes are protected. Prolonged prone positioning has resulted in pressure ulcers on the face, especially the chin and forehead, and other areas. When possible, periodic repositioning of the head during prolonged procedures may minimize the risk of such injuries. Direct pressure on the eye can result in visual loss. Pressure and stretch on nerves are avoided by proper padding and avoiding any extension over 90 degrees. The abdomen needs to be hanging free to avoid increased venous pressure and thereby increased venous bleeding. The prone position alters pulmonary dynamics, so pulmonary function must be reassessed in this position.

Intraoperative Spinal Cord Monitoring

Monitoring spinal cord function is an important component of major surgical procedures involving distraction and rotation of the spine such as occur with major anteroposterior spinal fusions and scoliosis surgery (also see Chapter 20 ). Spinal cord monitoring is employed in order to detect and hopefully reverse, in a timely manner, any adverse effects noted during the operative period. Spinal cord monitoring may include use of SSEPs, motor evoked potentials (MEPs) including TCMEPs, EMGs, or a wake-up test. The anesthetic technique must be adjusted appropriately when spinal cord monitoring is employed. Some anesthetics interfere with acquisition of the waveforms that are obtained intraoperatively and utilized to analyze spinal cord integrity.

SSEPs are sensory evoked potential waves generated in the cerebral cortex that result from sensory stimuli caused by repetitive peripheral nerve stimulation in the extremities that propagate up through the dorsum or sensory portion of the spinal cord and into the brain. These waveforms are then detected via electrodes placed over the scalp. Specific areas on the scalp coincide with the brain’s sensory areas for the upper and lower extremities and proper signal acquisition obtained over these sites indicates an intact sensory or dorsal portion of the spinal cord. The SSEP waveform generated from multiple repetitive stimulations is analyzed for its latency and amplitude ( Fig. 32.8 ). An increase in latency of more than 10% or a decrease in amplitude of 60% or more, as well as inability to obtain a proper waveform or signal, may be indicative of spinal cord dysfunction or disruption. Many factors can alter waveforms unrelated to surgery. They should be properly detected and eliminated. Surgically unrelated causes may include hypotension, hypothermia, high concentrations of volatile anesthetics, benzodiazepines, hyper- or hypocarbia, and anemia. Only a small concentration of volatile anesthetic (typically 1% to 2% desflurane) should be employed when SSEP monitoring is used. Midazolam and other benzodiazepines are avoided because they may interfere with obtaining a waveform. Some anesthesia providers avoid nitrous oxide and use a combination of air in oxygen.

Somatosensory evoked potentials (SSEPs) of tibial nerve demonstrating loss of SSEP waveform. Note how the newly acquired waveforms (purple) are flattened when compared to baseline tracings (red) as amplitude of tracings are decreased and latency increased. Tracings returned to normal after retraction of cauda equina was released.

Courtesy of Department of Neurophysiology, NYU Hospital for Joint Diseases.

Surgically related conditions resulting in loss of SSEPs include direct injury or trauma to the cord or impairment of blood supply. Distraction, rotation, excessive bleeding, and severing or clamping of arterial blood supply can result in ischemia to the cord and neurologic injury. Unlike direct injury, which is demonstrated immediately by changes in SSEPs, ischemia may take time, up to half an hour or longer, to manifest itself. Some areas of the spinal cord are more vulnerable and therefore more prone to ischemia as their blood supply is dependent on watershed blood flow. Surgical intervention as a result of either direct contact or stretching may impair blood supply and thus render the cord ischemic. Once a significant change in SSEPs or other monitor is noted, specific maneuvers should be used such as releasing the rotation and distraction of the spine if it has occurred. In addition, as a result of distraction there may be insufficient blood supply to the spine, and therefore, the mean arterial blood pressure should be increased in an effort to restore adequate blood flow. All variables such as hemoglobin, temperature, CO ₂ , and arterial blood pressure should be considered. Once these are all evaluated, a wake-up test (see following discussion) may be necessary if the waveforms do not improve.

Transcranial Motor Evoked Potentials

As SSEP monitoring only helps determine adequate status of the dorsal or sensory portion of the spinal cord, a method to monitor the motor or ventral aspect of the spinal cord became necessary. Initially this was provided via neurogenic MEPs, but these waveforms could be obtained only while the surgical incision was open and the spinous processes available for insertion of electrodes. Thus, some vulnerable operative time periods remained unmonitored. TCMEPs allow for monitoring the patient’s motor pathways throughout the entire procedure. Stimulation over the motor cortex of the brain generates a waveform, which is propagated down the motor pathways and detected distally in the arm or leg. This stimulation results in a characteristic waveform ( Fig. 32.9 ). Loss of the wave may be indicative of neurologic injury (see Fig. 32.9 ). As with SSEP waveforms, loss of the tracings requires the following steps: an evaluation to determine the cause, attention to physiologic variables, intervention to increase arterial blood pressure, and possibly a wake-up test as well.

Normal transcranial motor evoked potentials (left) and loss of waveform (right lower two panels) indicating possible neurologic issue with motor component of spinal cord.

Courtesy of Department of Neurophysiology, NYU Hospital for Joint Diseases.

In order to generate TCMEPs, the patient cannot have a residual neuromuscular blockade (also see Chapter 11 ). Importantly, it should be understood that the electric current causing the stimulus over the motor cortex also stimulates muscles directly in the area of the electrodes placed in the scalp—the masseter muscle and muscles of mastication. This muscle contraction may result in a strong bite, which can potentially injure the tongue, lip, and ETT. Instances of significant tongue lacerations and damage to ETTs can occur and potentially develop into emergency situations, especially with the patient in the prone position (also see Chapter 19 ). The tongue should not protrude through the teeth. Placing a bite block made of tongue depressors and gauze in the back of the mouth along the teeth line bilaterally will help prevent injury. In the prone (face-down) position, any motion may allow for the tongue to slip and fall between the teeth, rendering it vulnerable to laceration. Each stimulus is associated with a masseter muscle contraction so the patient is at risk as long as waveforms are being generated.

Vision Loss

Postoperative visual loss (POVL) is a rare but potentially devastating complication occurring in patients undergoing spine surgery (also see Chapters 19 and 31 ). Although its cause is unclear, patients having prolonged spine surgery (>6 hours) in the prone position who have large blood loss (>1 L) are particularly at risk. Yet, patients with small blood loss and short procedures also have had visual loss. Perioperative factors such as anemia, hypotension, prolonged surgery, blood loss, increased venous pressure from positioning in the prone position, edema, a compartment syndrome within the orbit, and resistance to blood flow such as direct pressure on the eye, as well as systemic diseases such as diabetes, hypertension, and vascular disease have all been considered possible etiologic factors.

Ischemic optic neuropathy (ION) is a major cause of POVL. Variations in blood supply to the optic nerve may play a role in the development of ION including reliance on a watershed blood supply to critical areas of the optic nerve. The head-down position allows edema to develop in the orbit and this increase in venous pressure may impact arterial blood flow. Ocular perfusion pressure (OPP), or the blood pressure supplying blood flow to the optic nerve, is a function of the mean arterial pressure (MAP) and intraocular pressure (IOP) such that OPP = MAP − IOP. Increases in IOP or decreases in MAP can have a negative impact on OPP. Increases in IOP can decrease OPP and lead to ischemia, and the prone position is associated with increases in IOP.

A visual loss registry has been established by the American Society of Anesthesiologists (ASA) to facilitate establishing the cause of POVL. An ASA Practice Advisory points to ION as the most likely cause of POVL ( Box 32.1 ). In a published report of 93 cases reported in the POVL registry, 83 resulted from ION, with the remainder attributed to central retinal artery occlusion (CRAO). CRAO may be embolic in nature or the result of direct pressure on the eyeball and tends to be unilateral. Most patients in the registry were healthy and placed in the prone position for spine surgery. Blood loss more than 1 L and procedures of 6 hours or longer were present in 96% of cases. Fifty-five of the POVL cases were bilateral, with 47 having total visual loss. The registry publication reveals that blood loss in patients with POVL varied widely with a mean of 2 L but ranged from 0.1 to 25 L. The advisory and registry publications promote a preoperative discussion with the patient and some suggest staged spine procedures for prolonged surgeries.

Box 32.1

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