Sympathetic Neural Blockade

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42 Sympathetic Neural Blockade

Jeffrey D. Petersohn, MD

The sympathetic nervous system contains some of the afferent and efferent neural pathways necessary for generation, perpetuation, or treatment of certain clinical pain states. Sympathetic neural blockade may be useful in differentiating neuropathic pain processes that involve the sympathetic nervous system (sympathetically maintained/mediated pain—SMP) from those that do not (sympathetically independent pain—SIP). Most, but not all, SMP fulfills the clinical criteria for complex regional pain syndrome (CRPS) type 1 or type 2.1

The precise pathophysiology of SMP/CRPS is not fully understood, but loss of tonic sensory neuronal input associated with peripheral or other nerve injury produces chronically disordered information processing in the dorsolateral spinal cord with subsequently inappropriate responses to afferent sensory input and increased efferent sympathetic outflow.2–4 Typically, patients report severe burning discomfort or pain, or abnormal sensations, that may occur either spontaneously or secondary to even low-threshold stimuli. Physical findings, consistent with altered sympathetic tone, include erythema, edema, altered skin temperature, discoloration, and dystrophic changes of the skin, nails, and underlying bone and joints.2–5 Patients often exhibit guarding behaviors and physical findings consistent with disuse atrophy.

Other pain processes, such as visceral pain processes, may involve sympathetic afferents but may not produce a typical clinical composite of CRPS. Sympathetic nervous system involvement in visceral pain might be manifested as cutaneous hyperalgesia. Pain involving the sympathetic nervous system is accompanied by changes in central pain processing at spinal cord and higher levels. Functional magnetic resonance imaging (MRI) demonstrates changes in cerebral blood flow at thalamic and cortical levels in CRPS as well as in other chronic pain states,6,7 but the precise anatomic loci and molecular pharmacology of the sympathetic nervous system involvement remain ill-defined and generalized; changes are not limited to the painful side of the brain if the initial injury is unilateral.8

SMP is challenging to treat and it may be that earlier intervention increases the likelihood of successful treatment. The condition may be suspected when common limb disorders have been excluded and/or complaints of pain far exceed the nominal injury with or without signs or symptoms suggestive of altered sympathetic tone. SMP is a clinical diagnosis which may be supported by the presence of characteristic findings on physical examination, plain radiographs, triple-phase bone scan, thermogram, or significant pain relief with sympathetic blockade.2,4,5,9–11 MRI is often helpful in differentiating subacute or chronic nondisplaced fractures, pseudarthrosis, or neuroma, which are amenable to prompt surgical treatment, but manifest with a similar clinical constellation. Aggressive treatment protocols are required to obtain successful lasting pain relief and prevent chronic dystrophic changes. Local or regional sympathetic blockade is the cornerstone of treatment for SMP and is thought to help by interrupting and disorganizing the inappropriate sympathetic activity.3,4 Multimodal treatments appear to offer improved prospects for clinical success.12

Guanethidine, bretylium, or reserpine by intravenous or intravenous regional technique are not efficacious. Local anesthetics or analogs administered by oral, subcutaneous, intravenous, or intravenous regional techniques have also failed to demonstrate efficacy. These results may reflect the complexity of the underlying pathophysiology including, but not limited to, phenotypic shift of Aβ fibers to express substance P receptors, proliferation of ectopic α-adrenergic receptors, alterations in Na+ channel receptors or responsiveness to TNF-α which may accompany pathologic states. Changes noted in biologic markers, such as DRG calcitonin-gene-related peptide (CGRP) seen with neural blockade, do not correlate with treatment outcome. Specific effects of sympathetic neural blockade on receptors for glutamine, NMDA, TRK, other vanilloids, or substance P are not known. Although physical therapy may be beneficial for analgesic modalities, for reduction of edema, and for promotion of active mobilization and reconditioning of involved extremities, common psychological comorbid conditions include anxiety, depression, and emergence of clinical personality disorders, similar to those seen in other patients with chronic pain. Recalcitrant CRPS unresponsive to traditional techniques may respond to spinal cord stimulation.13 Surgical sympathectomy may be considered for refractory circumstances, but success is far from assured and the duration of improvement is variable.

Classic targets for sympatholysis are the stellate ganglion for facial and upper extremity pain, the celiac plexus for abdominal pain, the superior hypogastric plexus for pelvic pain, the lumbar sympathetic chain for lower extremity pain, and the ganglion impar for perineal pain. In addition, the thoracic sympathetic ganglia can be blocked for the treatment of hyperhidrosis or for pain of pleural or esophageal origin.

It is the purpose of this chapter to describe some of the most commonly employed techniques for sympathetic nerve block, including indications, techniques, complications, and where consensus exists, outcomes and recommendations for use.

In the past decade, the putative role of the sympathetic nervous system in clinical pain has become more subtle and more complex with emerging neuroanatomic evidence for dual sympathetic and somatic innervation of many structures including cervical and lumbar zygapophysial joint capsules. Curiously, however, painful zygapophysial spinal joints can be successfully treated with thermal radiofrequency neurolysis (of the medial branches) and the author is unaware of any proven case of zygapophysial joint pain resolved by sympathetic neural blockade. RF lesioning of the medial branch does not, when properly conducted, produce CRPS.14,15 The role of dual sympathetic and somatic innervation of the lumbar intervertebral disc has provided a putative basis for treatment of discogenic pain by sympathetic neural blockade or by RF lesioning of the gray rami communicantes by RF thermolysis.16

Sympathetic nerve block is often used in a diagnostic capacity for interruption of afferent or efferent neural pathways. Results of neural blockade generally, but do not always, correlate with outcomes from repetitive neural blockade, surgical sympathectomy, and percutaneous chemical, cryotherapeutic, or thermolytic (RF lesioning) procedures. Limb or visceral pain, and in particular CRPS, which responds only transiently to sympathetic block may be improved with spinal cord stimulation.17

Clinical series and trials provide statistical evidence supporting circumscribed use of sympathetic nerve blocks, but a Cochrane review recommends that these techniques require thoughtful consideration for incorporation into clinical practice as well as additional research. Much of the literature is confounded by issues of adequate epidemiologic case definition and, in many circumstances, the use of sympathetic nerve blocks to affirm an etiologic diagnosis may be a troublesome affirmation of the use of circular logic.

The specialty of interventional pain practice remains in active technologic transition with some practitioners continuing to perform sympathetic nerve block interventions without fluoroscopy, many routinely employing fluoroscopic or computed tomography (CT) guidance, and others adopting ultrasound-guided techniques. As in many areas of medicine, new knowledge and technology provide opportunities to verify and improve existing protocols for diagnosis and treatment of sympathetically mediated pain, as well as a responsibility to discard ineffective interventions. Unfortunately, economic pressures for rapid and highly successful treatments will inappropriately target procedures used for the diagnosis and treatment of obscure or ill-defined pain processes, including pain that may originate with or involve the sympathetic nervous system.

Research into SMP is challenging to interpret as physicians incorporate emerging knowledge, moving from the diagnosis of clinical syndromes of SMP by varied panoply of symptoms and findings to conditions with neuro-bioanatomically defined mechanisms. The practicing clinician is challenged when consulting experts or the literature because much of the literature on sympathetic nerve blocks is historically composed of case series. The limited number of patients with specific conditions who can be studied and the protean clinical presentations seen by individual practitioners or groups makes consistent evidence-based reviews or meta-analysis difficult and confounds efforts to delineate optimal treatment approaches. Literature often incorporates broad epidemiologic case definitions, which may not accurately reflect the underlying biologic basis for pain. Older studies use patients who might presently be excluded by imaging studies and diagnostic blocks, but whose conditions were diagnosed at the time of original literature publication with state-of-the-art care. Although truly efficacious procedures may exist for sympathetic pain, the limited effect size and number needed to treat analysis (NNT) often suggests clinical restraint and, frustratingly, further research.

In some situations, use of targets anatomically adjacent to sympathetic nerve structures, but without image guidance, may suggest clinical efficacy,18 but more highly directed treatments may not be supportive.19

Substantial literature is devoted to case reports of complications of interventional treatment for sympathetic pain, including inadvertent intravascular injection of local anesthetic, pneumothorax, inadvertent nerve root or plexus injection, subarachnoid injection, or neural injury—many of which may be reducible by use of intermittent multiplanar image-guided technique during needle placement. Inadvertent injection into adjacent neural or vascular structures can usually be detected by careful injection of radio-opaque contrast agents under continuous fluoroscopy with typical and suboptimal patterns of contrast for each procedure described in a number of textbooks and manuals. Expectable complications will continue to occur due to the physiologic effects of neural blockade, such as limb warmth, Horner syndrome, and hypotension. Practitioners must remain vigilant for such effects, especially when patients are taking an adrenergic antagonist medication, such as a beta blocker. Intravenous access and sufficient patient monitoring must be available within the facilities where such procedure are performed so that these problems can be safely managed. Unfortunately, complications resulting from pathologic or ill-described human anatomy or bleeding from needle passage through highly vascular tissue may be reduced by diligent technique, but not eliminated completely.

Sympathetic neural blockade should be performed with appropriate imaging guidance (fluoroscopy, ultrasound, CT, MRI) and practitioners should be generally knowledgeable regarding regional anatomy and potential complications. These procedures should only be conducted by physicians where adequate facilities are available for patient safety, including physiologic monitoring and imaging, and where resuscitative measures may be implemented expeditiously, if needed. Intravenous access should be established preoperatively when hypotension or bradycardia are reasonably likely so that expeditious management can ensue. Absolute or relative contraindications to procedural interventions must be respected or when reasonably possible, mitigated by medical means preoperatively, consistent with generally held standards for interventional pain practice, including, but not limited to the following:

• Pregnancy
• Local or systemic infection
• Coagulopathy, anticoagulant or antiplatelet agent use
• Coexisting medical or surgical disease including immunocompromised states
• Challenging anatomic circumstances (tumor, deformity, postsurgical changes including prosthetic vascular device placement)
• Morbid obesity, severe osteopenia, or deformity that limits imaging
• Moving, unwilling, or uncooperative patient

Patients should be counseled preoperatively regarding the anticipated procedure, likely outcomes, expectable complications, and risks. The practitioner should be aware of the relevant laws (state, province, or country) regarding the essence and nature of this required discussion and standards for documentation, including written consent. This chapter is not intended to be comprehensive in scope and is not intended as a substitute for formal training and supervised experience in the performance of the procedures discussed. This chapter will discuss the following techniques:

• Sphenopalatine (pterygopalatine) ganglion block
• Stellate ganglion block
• Celiac plexus block
• Celiac plexus and splanchnic nerve block
• Lumbar sympathetic nerve block
• Hypogastric plexus block
• Ganglion impar block

General Considerations for Sympathetic Neural Blockade

Preoperative evaluation with CT, MRI, or ultrasound imaging is not regularly required for sympathetic nerve blocks; however this may be considered when planning optimal approaches for patients with specific disease states, prior surgery, or deformity which may affect safe or efficient access to the planned anatomic target or where anatomic distortion of the target anatomy is anticipated.

Supplemental oxygen, intravenous access, and physiologic monitoring including ECG, oxygen saturation, and blood pressure is typically required. The patient should be maintained nothing by mouth (NPO) prior to all sympathetic blocks, consistent with usual standards for major regional nerve block, typically 4 hours minimum for clear liquids and 6 to 8 hours for solid foods. Apprehensive patients may benefit from oral or intravenous sedation, given solely at the discretion of the treating physician, if there are no other medical contraindications. All techniques require antiseptic skin preparation and most operators prefer use of sterile paper or cloth drapes. The operator customarily wears sterile gloves and follows aseptic technique.

Commonly used anesthetic agents include lidocaine 1%, or bupivacaine in 0.125%, or 0.25% concentrations. Choice of a specific local anesthetic agent or concentration is based on physician preference and experience because the literature analysis is confounded by wide variations in injectate volume, variable use of imaging guidance, and variable outcome criteria are used. Local anesthetics should be pyrogen and preservative free. No vasoconstrictor, such as epinephrine or phenylephrine, should be used. Second-generation, low osmolality radiologic contrast agents often used to verify anatomic distribution of injectate include iohexol or iopamidol in 240 to 300 mOsm concentration. A third-generation contrast agent or gadolinium, more commonly used for MRI imaging, may be considered in patients with documented allergy to second-generation agents. Compromised renal function is a contraindication to the use of gadolinium.

Although digital subtraction angiography (DSA) may be more sensitive than continuous fluoroscopy in demonstrating inadvertent arterial injection, DSA has not yet been widely adopted to represent a standard of care.

Local distribution of injected contrast, either outlining the targeted neural structure or filling of the surrounding anatomic osseo-musculo-fascial compartment without vascular runoff should be observed on live fluoroscopy and confirmed in at least two fluoroscopic planes. Biplanar fluoroscopic images should be retained for documentation of technical adequacy of the procedure. Evidence for vascular injection, seen as a “flash” of contrast on fluoroscopy or by visible pulsations of a rapidly running off of contrast agent, requires withdrawal of the needle and reassessment of the anatomy before further injection attempts are made.

Assessment of the visual analog scale (VAS) pain scores and function of the painful extremity or structure should be documented pre- and postoperatively. Documentation should also record any complications or side effects, as well as the ultimate duration of improvement that follows each procedure. Often optimal physical therapy can be undertaken immediately following recovery from sedation—during the period of most potent analgesia from the neural blockade. Careful coordination between interventionalists and physical therapy departments will optimize care.

Stellate Ganglion Block (SGB)

Anatomy

The stellate ganglion is formed by the fusion of the inferior cervical and superior thoracic sympathetic ganglia and provides most of the sympathetic innervation to the head, neck, upper extremity, and a portion of the upper thorax.

The ganglion is typically about 2.5 cm in length and is located at the root of the C7 transverse process; it lies anterolateral to the longus colli muscle. The ganglion is anterior to the transverse process in the sagittal plane and posterior to the apical pleura which rises above the level of the first rib, posing a hazard of pneumothorax for anterior approaches at the C7 level or below. The carotid artery is anterior to the ganglion and the vertebral artery is anterolateral inferiorly, subsequently crossing over the sympathetic chain as it ascends to enter the foramen transversarium at C6 or above in 95% of individuals.20,21 At C6, the inferior thyroid artery is also anterior to the ganglion. Sympathetic nerve branches from the stellate ganglion extend to the brachial plexus, subclavian and vertebral arteries as well as the brachiocephalic trunk.22 Cardiac sympathetic nerves arise from the ganglion as does the vertebral nerve, which provides sympathetic innervation of the fibrous capsules of the zygapophysial and intervertebral joints and meningeal structures.15

Merged inferior cervical and thoracic ganglia are present in approximately 85% of patients, but stellate ganglion block (SGB) may fail to fully interrupt the sympathetic neural innervation of the head, neck, upper extremity, and upper thorax for several reasons. Although limited spread of local anesthetic may potentially fail to deliver agent onto disunited sympathetic ganglia, the presence of these sympathetic ganglia within the same fascial plane makes this unlikely.23 The distribution of radiographic contrast agent or dye in cadaveric studies demonstrates that injected volumes of 5 to 10 mL are routinely adequate to envelop the ganglion and may extend as far caudad as the T2 vertebral level.24,25 The nerve(s) of Kuntz are ascending ramus communicans branches originating at T2, T3, or T4 in 66% to 80% of individuals.26 These nerves are located approximately 7 mm from the sympathetic chain and provide an alternate pathway for sympathetic nerve fibers to bypass the sympathetic chain and enter directly into the first intercostal nerve or into the T1 nerve root. These Kuntz nerve fibers are not routinely bathed in local anesthetic agent during SGB and increased volumes of local anesthetic do not increase efficacy, but may produce undesirable spinal nerve root or brachial plexus block as well as unpredictable contralateral spread.

Indications

Twentieth century medical literature records dozens of reported clinical series wherein SGB was performed for a variety of clinical indications, all incorporating diagnostic or therapeutic applications where putative interruption of sympathetic afferent or efferent function of the head, neck, upper extremity, or thorax was postulated as useful. Present indications for SGB include the following27:

• Complex regional pain syndromes of head, neck, upper extremities
• Carotidynia
• Sympathetically mediated headache
• Cranial, cervical, nasal, orofacial, and upper extremity pain syndromes including peripheral neuralgias
• Hyperhidrosis
• Postthoracotomy pain
• Phantom or postamputation pain of the upper extremities
• Electrical shock injuries to the head, face, and upper extremity
• Vasospastic or vasoconstrictive syndromes of the head, neck, and upper extremity including Raynaud phenomenon
• After vascular injury or as an adjunct to surgical or interventional procedures where vasospasm is anticipated or likely to be encountered
• Intractable angina
• Painful herpes zoster
• Intracranial vasospasm owing to cerebrovascular accident
• Treatment of postmenopausal “hot flashes” in women who have received chemotherapy28

Contraindications

Pregnancy, although contraindicating exposure to ionizing radiation and fluoroscopy, may not prevent performance of SGB with ultrasound guidance; however, details of the ultrasound technique and potential obstetric issues are beyond the scope of this chapter.29 Narrow angle glaucoma may be considered a contraindication owing to expectable miosis produced by the loss of sympathetic tone occurring with SGB.

Recent myocardial infarction was formerly considered to represent a relative contraindication to SGB owing to risk of dysrhythmia. Newer evidence, however, supports sympathetic nerve sprouting and spontaneous increased sympathetic activity, which may follow myocardial infarction as a mechanism for sudden cardiac death.30,31 A small experimental study of bilateral SGB in a rat coronary ischemia model demonstrated reduced ST segment elevations and substantially reduced incidence of ventricular tachycardia or fibrillation when compared to controls.32

Structural abnormalities such as a large goiter, skeletal deformity, lymphadenopathy or neoplasm may recommend preoperative imaging and specific alternative techniques to achieve SGB, including lateral or posterior approaches with which the operator may not be familiar.

Complications

Widespread experience with SGB has produced descriptions of multiple, but fortunately infrequent, complications resulting from nonfluoroscopically guided SGB. These complications are largely predictable on an anatomic basis and include direct injury to adjacent structures, including hematoma producing neural compromise; direct compression or deviation of the trachea; esophageal puncture; disc space entry; and pneumothorax. Inadvertent injection of local anesthetic into carotid or vertebral arteries is known to produce seizures. Venous or arterial injection of sufficiently large doses of local anesthetic can also result in cardiovascular collapse.

Local anesthetic blockade of adjacent neural structures can affect anesthesia of the recurrent laryngeal nerve, spinal nerve roots, brachial plexus, and epidural or intrathecal spaces producing anesthesia with consequences dependent on the particular neural structures anesthetized including bradycardia, hypotension, sensory or motor functional loss, and total spinal anesthesia. Other adverse consequences of anesthetic blockade may include:

• Hoarseness or dysphagia owing to anesthetization of the recurrent laryngeal nerve
• Hypertension with anesthetic injection of the carotid sinus nerve
• Interruption of sympathetic tone (theoretically) producing cardiac dysrhythmias, including bradycardia (see earlier)
• Infection including osteomyelitis of the vertebral body
• Discitis
• Horner syndrome

These should not be considered as complications but as expected side effects.

Technique (Fig. 42-1)

A 5 mL volume of local anesthetic is sufficient for adequate SGB performed under fluoroscopy, CT,33 MRI, or ultrasound imaging.29 Evidence from cadaveric and in vivo studies suggests that larger volumes (i.e., 20 mL) are neither necessary nor additionally efficacious because they often produce unwanted effects. Use of a 5 mL volume of bupivacaine 0.125%, bupivacaine 0.25%, or ropivacaine 0.2% minimizes risk of systemic local anesthetic toxicity.

image

Figure 42-1 Stellate ganglion block: lateral approach. A, Oblique fluoroscopic view—needle on target point at junction between uncinate process and C7 vertebral body. B, Oblique view with drawn outline of relevant anatomic structures. C, Oblique view with labeled structures. D, Oblique view with injected contrast, 3 mL. E, Anteroposterior (AP) view with contrast. F, AP view with drawn and labeled uncinate processes.

(Fluoroscopic images courtesy of Jeffrey D. Petersohn, MD.)

With any injection technique, a sterile 10 to 15 cm Luer-Lok small-bore extension tubing is attached to a three-way stopcock to which separate syringes of contrast agent and local anesthetic to be injected are attached. Syringes should be labeled or marked as to their contents. The assembly is primed with contrast agent and care should be taken to ensure that there is no remaining air in the tubing or syringes. The stopcock may be turned off to the extension tubing or open to the contrast agent, but in no case should this assembly be prepared with stopcock initially allowing the extension tubing to be filled with the local anesthetic. The syringe assembly should be constructed with aseptic technique and placed on a sterile table or Mayo stand for ready access by the operator or a gloved assistant during the procedure.

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