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.

Anterior Paratracheal Technique

Longstanding use of SGB has allowed description and experience with a variety of nonfluoroscopically guided techniques. The most common technique in present use is the anterior paratracheal approach popularized by Moore and Bridenbaugh 50 years ago,34 now augmented by use of fluoroscopy for identification of anatomic landmarks instead of the traditional palpation of the transverse process of C6, as performed by earlier generations of anesthesiologists and neurosurgeons. For the anterior paratracheal technique, the patient is placed in a supine position on a radiolucent operating table with a small (10 cm) folded towel roll placed between the dorsal scapulae with the head midline and cervical spine slightly extended. The arms are placed at the patient’s sides after appropriate physiologic monitors are applied. A small degree of head-up table tilt is often incorporated to reduce the distention of venous vasculature. The anterolateral cervical region is prepared with a suitable disinfectant agent, draped as the operator may prefer, and aseptic technique is employed throughout the injection procedure.

Using midline anteroposterior (AP) fluoroscopic imaging, the cervical vertebrae are enumerated, the superior edge of the C6 vertebral body is squared off in planar fashion by adjustment of cephalocaudad beam angle and the transverse process of C6 is identified. The presence of cervical ribs may mislead the operator regarding the correct spinal level to be treated and careful enumeration is required. The carotid artery is palpated at the C6 level and the middle and index fingers of the operator’s gloved nondominant hand are inserted, angling dorsally to grasp the carotid sheath and its contents at the medial sheath border and to displace these laterally by rotation of the hand on the wrist as the trachea and underlying esophagus are simultaneously displaced medially by the operator’s thumb. A 25-gauge, 2.5-inch, short-bevel tip needle is held in the dominant hand and visualized on intermittent fluoroscopy to overlie the proximal aspect of the ipsilateral C6 transverse process, which should appear in the space between the operator’s thumb and index finger. A skin wheal of local anesthetic can be raised and the needle is then inserted and advanced directly posterior to contact the anterior aspect of the C6 transverse process near its junction with the vertebral body. Maintaining continuous contact of the needle tip against the bone to prevent needle dislodgement, the needle should be connected to the prepared Luer-Lok extension tubing, stopcock, and syringe assembly. After verification that the stopcock is turned open to the contrast agent and not to the local anesthetic, the needle is withdrawn 2 to 4 mm from the bony surface and held firmly with the hand while the contrast syringe, opened through the stopcock to the needle, is gently aspirated for blood or CSF. Withdrawal of the needle assures that the needle tip is not entirely invested in periosteum where flow cannot occur. Although withdrawing the needle tip as little as 2 mm may leave the needle tip within the longus colli muscle, the multi-pennate nature of this muscle will allow for flow of injectate within the musculofascial plane to reach the stellate ganglion.

At the operator’s discretion, the operation of the stopcock and syringes may be delegated to an assistant. Negative aspiration does not exclude entirely the possibility of intravascular injection and must be followed by live fluoroscopic observation of the resultant spread of 2 to 5 mL of radiographic contrast to confirm appropriate anatomic spread into a nonvascular paravertebral area with extraspinal pooling of injected contrast. Should blood or CSF be aspirated or should inappropriate vascular contrast distribution be observed or should contrast outline the radicular or vertebral canals, no further injection should be made. The needle is disconnected from the syringe, stylet is inserted, and redirected prior to aspiration and contrast injection. After adequate distribution of radiocontrast is noted and documented in at least one, but preferably two radiographic planes, the stopcock is rotated open to the local anesthetic syringe and the local anesthetic is injected in aliquots of 2 to 5 mL with negative intermittent aspiration to a maximum volume of 5 to 10 mL. The needle is removed and gentle digital pressure is applied to obtain hemostasis. An adhesive bandage may be applied. The postprocedure monitoring protocol is described subsequently.

The principal hazards of the fluoroscopically guided anterior paratracheal technique are the lack of stabilization of the needle placement by passage through connective tissue or muscle and the routine direct exposure of the operator’s hands within the field of the x-ray fluoroscopic beam. Collimation of the beam is insufficient to manage radiation exposure to the operator. Although the operator can don leaded gloves in an attempt to mitigate direct fluoroscopic beam exposure, the presence of lead attenuating the average beam energy at the image intensifier will cause many fluoroscopy units to automatically increase the beam energy delivered, ultimately increasing radiation exposure to the patient and substantially increasing the backscatter radiation exposure to the operator.

Small-gauge needles are available that have a side orifice placed several mm proximal to the distal tip. The principle advantage of such a needle is that no withdrawal of the needle from the periosteal surface is necessary and the needle position remains stabilized throughout the procedure by continued bony contact rather than by the operator’s steadiness of hand. These needles typically have a blunted or pencil tip, requiring use of an introducer needle or use of a 20-gauge needle or scalpel blade to “pre-stick” the skin entry site to allow entry of the needle with a noncutting bevel.

Lateral Approach Technique

A more optimal technique for skilled interventionalists is the lateral approach.35,36 This can be performed with the patient in the supine position with interscapular roll as described for the anterior paratracheal technique or with the patient placed in a semilateral “park bench” position on a radiolucent table. The initial approach is somewhat similar to that used for a C7 selective nerve root injection with anteroinferior adjustment of needle path to target the stellate ganglion.

One advantage of the park bench position is that the needle axis is near-vertical allowing easy and familiar control of the needle trajectory by the physician. Excellent fluoroscopic visualization of the neural foramina is obtainable in this position. Optimal visualization typically requires displacement of the dependent (“down”) shoulder inferiorly so that the contralateral humeral and clavicular shadow do not overlay or impede radiologic visualization of the ipsilateral C6-7 neural foramen. This is accomplished by manual downward pressure on the shoulder with only modest traction on the extremity. Park bench position will require additional time for positioning, padding, and securing the patient on the operating table and may require gentle manual traction on the nondependent extremity by an assistant.

The sterile stopcock, extension set, and filled syringes are assembled and labeled as described earlier. Following antiseptic skin preparation and application of sterile drape, the C-arm fluoroscope is oriented initially to obtain a true AP image of the cervical spine. Subsequent cephalocaudad adjustment of the fluoroscope is used to level the C6-7 disc space, providing a crisp superior edge of the C7 vertebral body, which allows identification of the uncinate process at the cephalad aspect of the C7 body. The C-arm axis is then rotated ipsilaterally and obliquely about 30 to 50 degrees to bring the ipsilateral C6-7 neural foramen into direct en face view. In this view, the anteroinferior border of neural foramen formed by the anterior tubercle will be directly adjacent to or will minimally overlap the uncinate process of C7. The target is the midpoint of the linear junction of the ipsilateral uncinate process of C7 with the C7 vertebral body. The longus colli muscle fills the angular groove between the anterior tubercle and the vertebral body.

After raising a skin wheal with local anesthetic, a 25-gauge, short bevel 2.5-inch needle is placed though the skin and advanced in small increments using intermittent fluoroscopy with rotation as needed to steer the needle to contact the target. A 5-degree bend away from the direction of the bevel in the distal 5 mm of the needle tip facilitates needle steering, but larger angulations or longer distal bent segments are best avoided because they produce larger and less predictable arcs of needle travel. The needle trajectory should be approximately parallel to the longitudinal axis of the intervertebral foramen, with direct entry into the neural foramen actively avoided to prevent inadvertent injection of the rare vertebral artery at C7 or the more frequently encountered radicular or medullary arteries. Avoiding entry into the foramen also prevents inadvertent nerve root or subdural injection as well as direct needle trauma to the spinal cord. Similarly, the needle should not stray cephalad into the disc space or anteroinferiorly to avoid pleural trespass and subsequent pneumothorax. Straying too medial onto the anterior aspect of the vertebral body risks esophageal or tracheal entry. After the needle contacts the target point at the junction of the C7 body and the uncinate process, the needle is then withdrawn 1 mm and contrast agent is injected following negative aspiration as described earlier using the Luer-Lok tubing, stopcock, and syringe apparatus prepared previously.

Local distribution of injected contrast without vascular runoff should be observed on live fluoroscopy and confirmed in the fluoroscopic AP view. 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. If there is no evidence of erroneous placement, the stopcock is then rotated and the local anesthetic is injected in aliquots as described earlier for the anterior paratracheal approach and the needle is removed. Postinjection care and monitoring protocols are described subsequently. The lateral technique provides superior stabilization of the needle by the sternocleidomastoid and the longus colli muscles. It allows improved avoidance of the carotid and vertebral arteries and does not require direct fluoroscopic exposure of the operator’s extremities.

Postinjection Monitoring Protocol

The patient is closely observed for ECG changes or seizure activity in the first few minutes after injection. Blood pressure and SaO2 are monitored in a standard postanesthesia protocol for at least 30 minutes postprocedure. Evaluation should be made for complications including pneumothorax, hematoma, hypotension or bradycardia, inadvertent intraarticular or intraspinal injection.

Assessment of airway patency and signs or symptoms of sympathetic neural blockade are made prior to discharge. Hoarseness or dysphagia is not uncommon due to recurrent laryngeal nerve anesthesia. Oral fluids should not be administered until the hoarseness or dysphagia resolves.

Assessment of Adequacy of SGB

The monitoring of skin temperature differentials between upper extremities is often performed, but has not been established to be either a necessary or completely reliable finding of the onset of satisfactory sympathetic blockade. The development of a Horner syndrome [ptosis due to loss of sympathetic supply to the superior tarsal muscle, miosis (pupillary constriction), conjunctival injection, ipsilateral facial warmth, anhidrosis, ipsilateral vasodilation] is commonly taken to indicate a technically adequate SGB. Nasal stuffiness may be present, but does not reliably indicate adequacy of sympathetic blockade.

As noted earlier, competent SGB may not produce complete sympatholysis because of an anatomic inability to interrupt sympathetic fibers traveling outside the main sympathetic trunk. This may be more common in extremity pain syndromes and does not unequivocally constitute operator failure. If satisfactory sympathetic blockade of the head and face occur, but the extremity is spared, consideration may be given to a single repetition of SGB, but repeated failure would suggest that other techniques, such as neural blockade of the sympathetic chain at T2, may be merited.

Sphenopalatine Ganglion Block

Current indications for sphenopalatine ganglion block include the management of acute migraine, acute and chronic cluster headache, and a variety of facial neuralgias, the classic example being vidian neuralgia. Permanent destruction of the sphenopalatine ganglion may be accomplished by creating a radiofrequency lesion in the ganglion37 or by use of the Gamma Knife.

Anatomy

The sphenopalatine (pterygopalatine) ganglion resides in the pterygopalatine fossa, located posterior to the middle nasal concha and anterior to the pterygoid canal. It is adjacent to and inferior to the maxillary nerve, a branch of the trigeminal nerve, and connects with it via the pterygopalatine nerves. Only parasympathetic fibers arising in the facial nerve synapse in the ganglion via fibers of the nerve of the pterygoid canal and the greater petrosal nerve. Postganglionic fibers continue to the lacrimal, palatine, and nasal glands via orbital branches of the maxillary, lacrimal, and zygomatic nerves. Postganglionic sympathetic fibers originating in the internal carotid plexus pass through the ganglion (without synapsing) via the nerve of the pterygoid canal and the deep petrosal nerve. Sensory fibers connect the maxillary nerve to the ganglion by way of branches of the ganglion (primarily maxillary nerve fibers) that extend from the nasopharynx, nasal cavity, palate, and orbit. Five branches are usually described: The pharyngeal branch supplies the sphenoid sinus and the mucosa of the roof of the pharynx, the greater palatine nerve provides posterior inferior nasal branches that supply the palate via the greater palatine foramen (with components of the maxillary and facial nerves). The tonsil and soft palate are supplied via the lesser palatine nerve as it arises from the lesser palatine foramen. The nasopalatine nerve emerges through the sphenopalatine foramen, passes along the nasal septum, and emerges through the median incisive foramen to reach the hard palate. Posterior ethmoid and sphenoid sinuses below the periosteum of the orbit are supplied via orbital branches. The nasal cavity is supplied via the posterior superior nasal branches.

In addition to sensory fibers, the nasopalatine, palatine, and nasal nerves contain vasomotor fibers and secretory fibers to the palatine and nasal glands. Also, fibers related to taste can be found in the palatine nerves that pass via the greater petrosal nerve to reach the facial nerve.38

Technique (Fig. 42-2)

The patient is placed supine. A cotton-tipped applicator soaked with viscous lidocaine 4% is advanced through the nares, along the middle turbinate posteriorly until it comes in contact with the posterior wall of the nasopharynx. The zygomatic arch may be used as a landmark because it corresponds to the level of the middle turbinate. A second applicator is then generally placed somewhat posterior and superior to the initial one. A response is seen in 5 to 10 minutes, although it may be left in position for 30 minutes for an adequate evaluation of the block’s effectiveness. Common side effects are tearing or lacrimation, bleeding, lightheadedness, generalized discomfort, and complaints of numbness of the posterior oropharynx.39,40

image

Figure 42-2 Sphenopalatine ganglion block. A, Anteroposterior (AP) view. B, Lateral View: Needle target on lateral view is occasionally referred to as an ‘Inverted flower vase’.

(Images courtesy of Ted Kline, MD.)

Pterygopalatine fossa anesthetic block typically is done under fluoroscopy with the patient in the supine position. A true lateral view is obtained with the head rotated to produce superimposition of the right and left rami of the mandible, zygoma, and lateral pterygoid plates. The pterygopalatine fossa is most clearly visualized in this view as an “upside down vase.” A 22-gauge, B-bevel needle is inserted anterior to the mandible in the condylar notch between the condylar and coronoid processes and under the zygoma and directed in a medial and slightly posterior direction with continuous visualization under fluoroscopy as it is advanced into the pterygopalatine fossa until it comes in contact with the pterygoid plate. Paresthesias may be elicited if the needle impinges on the nasopalatine, greater or lesser palatine, or maxillary nerves. The C-arm is rotated in the anteroposterior view so that the tip of the needle is seen just under the lateral nasal mucosa. Approximately 1 mL of contrast agent may then be injected to check for venous runoff, because this is a highly vascular area. Needle position may be additionally confirmed by passing a small amount of electrical current through an insulated needle using a frequency of 50 Hz (sensory) and 2 Hz (motor) and low voltage (<1 volt). Stimulation may provoke some palatal or facial paresthesia but should not cause muscular twitching or paresthesia in other areas. Following successful stimulation 1 mL of 2% lidocaine or 0.25% bupicacaine is injected. Elimination of pain confirms the diagnosis.

Dual sphenopalatine ganglion blocks can be used for diagnosis prior to use of stereotactic Gamma Knife lesioning technique.41,42 This avoids risks of repetitive instrumentation of this highly vascular area. Excellent landmarks for the sphenopalatine ganglion are obtained with coronal plane CT scan.

Radiofrequency Lesioning Technique

A 100 mm, 22-gauge probe with a 2-mm active electrode tip is placed in the same way as described for pterygopalatine fossa anesthetic block. After needle contact with the pterygoid plate in the pterygopalatine fossa, sensory electrical stimulation is performed up to 1 volt at 50 Hz. Correct stimulation is obtained when the patient reports the sensation to be within or just posterior to the nose. If stimulation is achieved in the soft palate, the needle should be advanced slightly medially. To confirm that the probe is placed in an extravascular position, a 1-mL of contrast is injected. After confirmation of the extravascular position 1 mL of 2% lidocaine is injected. Following successful relief of symptoms, radiofrequency lesioning may be carried out for 60 seconds while maintaining the probe temperature above 65° C. The probe is then advanced 1 mm medially and the process is repeated.

Generally the patient should be kept for observation after the procedure for approximately 2 hours, because 10% to 20% of patients experience epistaxis. Discomfort for 10 days to 2 weeks is expected. Loss of sensation on the soft palate also may occur. Additional complications are rare.37

Celiac Plexus and Splanchnic Nerve Block

Indications for celiac plexus block include use as a diagnostic tool to determine whether flank, retroperitoneal, or upper abdominal pain is mediated via the celiac plexus, to palliate pain secondary to acute pancreatitis and intraabdominal malignancies, and to reduce the pain of abdominal “angina” associated with visceral arterial insufficiency.43–47

Strictly speaking, the celiac plexus is a mixed sympathetic and parasympathetic plexus with most of the sympathetic component provided by the greater and lesser splanchnic nerves. Neurolysis of the celiac plexus with alcohol or phenol is indicated to treat pain secondary to malignancies of the retroperitoneum and upper abdomen, but is usually avoided in chronic benign abdominal pain syndromes, such as chronic pancreatitis, because the durability of relief is several months only. Although it is technically more challenging, advantages to splanchnic nerve block include an exclusively retroperitoneal approach, which reduces pneumothorax risk; ability to guide RF lesioning with stimulation mapping; and the absence of painful neuritis caused by unwanted neurolytic agent spreading to the somatic nerve roots.

All usual contraindications to major neuraxial blockade apply to these procedures with the addition of bowel obstruction because increased motility and diarrhea can result from establishment of adequate neural blockade. Use of alcohol as a neurolytic agent should be avoided in patients on disulfiram therapy for alcohol abuse.

Anatomy

Sympathetic innervation of the abdominal viscera originates in the anterolateral horn of the spinal cord, but fibers do not synapse until reaching the celiac plexus. Preganglionic fibers from T5-12 exit the spinal cord in conjunction with the ventral roots to form white communicating rami and the greater, lesser, and least splanchnic nerves which provide principal preganglionic (sympathetic) contributions to the celiac plexus. The greater splanchnic nerve has its origin from the T5-10 spinal roots, travels along the thoracic paravertebral border, through the crus of the diaphragm and into the abdominal cavity, terminating on the ipsilateral celiac ganglion. The lesser splanchnic nerve arises from the T10-11 roots and passes with the greater splanchnic nerve to the celiac ganglion. The least splanchnic nerve arises from the T11-12 spinal roots and passes through the diaphragm to the celiac ganglion. Greater, lesser, and least splanchnic nerves are preganglionic structures that synapse at the celiac ganglia.46 Blockade of these nerves is properly termed splanchnic nerve block.

Celiac Ganglia

The three splanchnic nerves synapse at the celiac ganglia, which lie anterior and anterolateral to the aorta. The number of ganglia in the celiac plexus ranges from one to five and from 0.5 to 4.5 cm in diameter.48 Left-sided ganglia are typically more inferior than their right-sided counterparts by as much as a vertebral level, but both groups of ganglia are inferior to the level of the celiac artery. In most instances, the ganglia lie approximately at the level of the first lumbar vertebra. Postganglionic fibers form a diffuse perivascular plexus along blood vessels that supply abdominal viscera and are derived from the embryonic foregut.49 This includes distal esophagus, stomach, duodenum, small intestine, ascending and proximal transverse colon, the adrenal glands, pancreas, spleen, liver, and biliary system.

Celiac Plexus

The celiac plexus arises from the preganglionic splanchnic nerves, vagal preganglionic parasympathetic fibers, sensory fibers from the phrenic nerve, and postganglionic sympathetic fibers.50 The celiac plexus is anterior to the diaphragmatic crura.51 It extends in front of and around the aorta, with the greatest concentration of fibers anterior to the aorta. Blockade of these neural structures, which include the afferent fibers carrying nociceptive information, is properly termed celiac plexus block. Note that the phrenic nerve also transmits nociceptive information from the upper abdominal viscera that may be perceived as poorly localized pain referred to the supraclavicular region.50

The normal configuration of these structures may be altered due to organomegaly or tumor. The aorta lies anterior and slightly to the left of the anterior margin of the vertebral body. The inferior vena cava lies to the right of the midline, and the kidneys are posterolateral to the great vessels. The pancreas lies anterior to the celiac plexus. All of these structures lie within the retroperitoneal space.

Celiac Plexus Block

The patient is placed in the prone position with a pillow beneath the abdomen to reverse the thoracolumbar lordosis, which increases the distance between the costal margins and the iliac crests as well as between the transverse processes of adjacent vertebral bodies. The patient’s spine is surveyed under fluoroscopic visualization. The lumbosacral junction and thoracolumbar junction, and lumbar vertebrae are enumerated. T12 ribs are identified. Anatomic anomalies are noted so that appropriate adjustments may be made. Beginning with a true AP fluoroscopic image, the C-arm is rotated to a posterolateral projection, stopping as the ipsilateral tip of L1 aligns with the lateral border of the of the L1 vertebral body. This angle will be between 30 and 45 degrees from the sagittal plane. If the ipsilateral T12 rib is superimposed on the L1 vertebral body, the C-arm should be rotated in a caudad to cephalad manner to just resolve this superimposition. Skin entry is made with a 6-inch, 22- or 25-gauge needle with 10-degree distal curve to facilitate steering just lateral to the junction of the L1 transverse process with the body after local anesthetic is infiltrated in the skin using the lateral L1 vertebral body as a target. After the needle tip contacts bone, the C-arm is rotated back to an AP projection to demonstrate a needle tip at the ipsilateral longitudinal interpedicular line. Cross table lateral fluoroscopy should show the needle tip at the anterior vertebral body. At this point, the needle is rotated and aspirated in all four quadrants and 4 to 6 mL of nonionic contrast agent is injected. The contrast should remain immediately anterior to the anterior vertebral line on cross table lateral view, superimposed on the ipsilateral interpedicular line on sagittal view, and without vascular uptake. If the contrast column extends in an inferolateral projection on sagittal view, the needle tip remains too lateral and should be cautiously advanced 1 cm medially, taking care not to penetrate a major vessel. A bend on the end of the needle as described will aid appropriate placement of the needle in this situation. If the contrast column is whisked away in a longitudinal fashion, the needle tip is in a major vessel and should be withdrawn slightly and contrast should be reinjected. If this does not correct the migration of the contrast column, needle placement should be reexamined and probably repeated. If the contrast column runs off in a serpentine fashion, the needle tip lies within Batson plexus and should be repositioned. If the needle tip cannot be repositioned to allow for appropriate contrast column as described, the procedure should be repeated.

After the needle is appropriately placed as demonstrated by both contrast injection and radiographic evaluation, 10 mL of 1% lidocaine or 0.25% bupivacaine is administered in divided aliquots. Local anesthetics should be administered in incremental doses.52 For treatment of the pain of acute or chronic pancreatitis, the historical practice of adding a depot steroid to the local anesthetic used for celiac plexus or sympathetic block is not presently supported by data.

Splanchnic Nerve Block

Splanchnic nerve block may provide relief of pain in a subset of patients who fail to obtain relief from celiac plexus block.49,54 The splanchnic nerves transmit the majority of nociceptive information from the viscera54 and are contained in a narrow compartment made up of the vertebral body and the pleura laterally, the posterior mediastinum ventrally, and the pleural attachment to the vertebra dorsally. This compartment is bounded caudally by the crura of the diaphragm. The volume of this compartment is approximately 10 mL on each side.54

The technique for splanchnic nerve block differs little from the approach to the celiac plexus, except that the needle is placed more cephalad to ultimately rest at the anterolateral margin of the T12 vertebral body. Needle placement medially against the vertebral body reduces the incidence of pneumothorax.

An alternate approach to splanchnic nerve block uses 31⁄2- or 6-inch, 22-gauge spinal needles.55 The needles are placed 3 to 4 cm lateral to the midline just below the 12th ribs. Their trajectory is slightly mesiad so that their tips come to rest at the anterolateral margin of the T12 body.

Complications of these techniques include hypotension, altered (increased) gastrointestinal motility, paresthesias or deficits of the lumbar somatic nerve, intravascular injection (venous or arterial), subarachnoid or epidural injection, diarrhea, renal and other visceral injury, paraplegia, pneumothorax, chylothorax, pleural effusion, vascular thrombosis or embolism, vascular trauma, perforation of cysts or tumors, injection of the psoas muscle, intradiscal injection, abscess, peritonitis, retroperitoneal hematoma, urinary abnormalities, ejaculatory failure, postprocedure pain, and failure to relieve pain.

Lumbar Sympathetic Block

Anatomy

Preganglionic sympathetic outflow to the lower extremity originates in the nerves of the lower thoracic and first two lumbar segments. Within the ventral rami of the nerve roots, small myelinated fibers form the white rami communicans; these preganglionic fibers synapse with small unmyelinated fibers in the ganglia of the lumbar sympathetic chain ganglia.56–58 The lumbar sympathetic ganglia lie along the anterolateral surface of the lumbar vertebrae just anterior to the prevertebral fascia of the psoas muscle. The number of lumbar sympathetic chain ganglia varies considerably from one individual to another.56,57 Postganglionic fibers exit the ganglia as gray rami communicantes and supply one or more lumbar nerve roots. Deposition of local anesthetic along the sympathetic chain of the L2 or L3 levels will provide sympathetic denervation of the lower extremity.60 Bilateral blockade is not recommended due to the potential for significant hypotension.

Technique (Fig. 42-3)

The patient’s lower thoracic and upper lumbar region is prepped in a sterile fashion. The patient is positioned prone. The fluoroscopic beam is rotated until the tip of the ipsilateral L2 transverse process is completely superimposed on the lateral border of the L2 vertebral body forming the target entry point. The needle is advanced until the needle tip gently contacts the inferior anterolateral L2 vertebral body.2,59,60 A cross table lateral view is taken, and the needle tip should be at the anterior vertebral line at the inferior L2 or superior L3 vertebrae. A sagittal view is obtained and the needle tip should be within the ipsilateral longitudinal interpedicular line. At this point 4 to 6 mL of nonionic contrast is injected, and the contrast column should extend up and down the ipsilateral thoracolumbar spine. On lateral view, the column remains immediately anterior to the anterior longitudinal line. A contrast column that extends in a caudal and lateral direction is outlining the psoas muscle, which generally will provide a suboptimal sympathetic block and often will also block the anterior rami of the upper lumbar region. As a result, when a psoas shadow is seen, the needle should be advanced slightly and contrast should be reinjected. A vascular pattern should not be seen. If a suboptimal contrast column or a vascular pattern occurs and the needle cannot be manipulated to obtain correct placement, the procedure should be aborted.61

image

Figure 42-3 A through C, lumbar sympathetic nerve block at left L1, L2 and L3 levels. A single injection can be performed, most commonly at L1 or L2 using a 10 mL injectate volume.

(Images courtesy of Way Yin, MD.)

After both radiographic and contrast injection have confirmed correct needle placement, 10 to 15 mL of 0.25% bupivacaine is slowly injected.2,5 Successful sympathetic blockade is indicated by a rise in lower extremity temperature of at least 3° C.59

Complications

Potential complications of LSB include intravascular injection, intradural injection with spinal anesthesia, postural headache, hypotension, lumbar plexus block, renal puncture, or genitofemoral neuralgia.2,58,59

Postprocedural Care

After successful SGB or LSB has been performed, it is important to carefully examine the involved extremity for resolution of pain or pain-producing stimuli. Significant reduction of pain (>50% to 75%) or painful stimuli in the absence of somatic blockade suggests the presence of SMP. Serial diagnostic blocks may be required to rule out a placebo response.

Patients whose pain returns following a pain-free interval with SGB or LSB may be candidates for treatment with serial blocks. Additionally, arranging for the patient to participate in physical therapy for limb mobilization immediately following a successful block may greatly enhance the long-term treatment benefits of sympathetic blockade. Unfortunately, little controlled data exist to indicate the optimal frequency or ultimate number of serial blocks that are indicated in the management of SMP.

Superior Hypogastric Plexus Block

Indications for this procedure include the diagnosis and treatment of pelvic pain originating from malignancy, endometriosis, pelvic inflammatory disease, adhesions, and other pathologic processes. The block was introduced in 1990, and several studies show good relief of intractable pelvic pain.62–64 However, as is the case for most of these procedures, the evidence for efficacy is low grade, suggesting that superior hypogastric plexus block should be recommended as alternative and not as primary therapy.65 Contraindications are similar to those listed for the aforementioned procedures and include infection, sepsis, and coagulopathy.

Anatomy

The superior hypogastric plexus is a retroperitoneal structure located bilaterally at the level of the lower third of the fifth lumbar vertebral body and upper third of the first sacral vertebral body at the sacral promontory and in proximity to the bifurcation of the common iliac vessels.66 This plexus (sometimes referred to as the presacral nerve) is formed by the confluence of the lumbar sympathetic chains and branches of the aortic plexus that contains fibers that have traversed the celiac and inferior mesenteric plexuses. In addition, it usually contains parasympathetic fibers that originate in the ventral roots of S2-4 and travel as the slender nervi erigentes (pelvic splanchnic nerves) through the inferior hypogastric plexus to the superior hypogastric plexus.

The superior hypogastric plexus divides into the right and left hypogastric nerves that descend lateral to the sigmoid colon and rectosigmoid junction to reach the two inferior hypogastric plexuses. The superior plexus gives off branches to the ureteric and testicular (or ovarian) plexuses, the sigmoid colon, and the plexus that surrounds the common and internal iliac arteries. The inferior hypogastric plexus is a bilateral structure situated on either side of the rectum, lower part of the bladder, and (in the male) prostate and seminal vesicles or (in the female) uterine cervix and vaginal fornices. In contrast to the superior hypogastric plexus, which is situated in a predominantly longitudinal plane, the configuration of the inferior hypogastric plexus is oriented more transversely, extending posteroanteriorly and parallel to the pelvic floor. Because of its location and configuration, the inferior hypogastric plexus does not lend itself to surgical or chemical extirpation.

Technique

The patient is placed in the prone position with a pillow under the pelvis to reduce lumbar lordosis. The lumbosacral region is cleansed aseptically. The lumbar region is surveyed under fluoroscopy. The fluoroscopy tube is rotated approximately 45 degrees for a posterolateral view of the L5 vertebral body. At this point, an image of the iliac crest will most likely be superimposed on the L5 vertebral body. The fluoroscopy tube is then rotated in a cephalad-caudad direction (the appropriate view is posterolateral and cephalad to caudad) so that the image of the iliac crest is no longer superimposed on the L5 vertebral body. At this point a 31⁄2- or 6-inch, 22- or 25-gauge spinal needle is inserted using an en pointe method down to the anterolateral L5 vertebral body. The fluoroscopic image is rotated in a sagittal plane and cross table manner. In the sagittal plane, the needle tip should lie in the ipsilateral longitudinal interpedicular line, and in the cross table lateral view the needle tip should rest at the anterior longitudinal line. If the needle repeatedly encounters the L4 or L5 transverse processes, a slightly more axial trajectory requiring repeated biplanar fluoroscopic views to properly place the needle may be necessary. If this method fails, a 30-degree bend should be placed in the needle 1 to 2 cm from the end of the needle with the convexity on the bevel side of the needle. By alternately rotating the needle while the needle is advanced, the needle tip may be steered around anatomic impediments. After fluoroscopic visualization confirms needle placement, 2 to 4 mL of nonionic contrast agent should be injected. The contrast column should remain along the midline or paramedian region in the sagittal view and the prevertebral space in the cross table lateral view. For diagnostic blocks, 8 mL of 0.25% bupivacaine or 1% lidocaine is injected.

Complications

Vascular puncture with risks of subsequent hemorrhage and hematoma formation is possible because of the proximity of the bifurcation of the common iliac vessels. Intramuscular or intraperitoneal injection may result from an improper estimate of needle depth. These and less likely complications (e.g., subarachnoid and epidural injection, somatic nerve injury, renal or ureteral puncture) can be avoided by diligent technique and frequent fluoroscopic views during needle placement.

Ganglion Impar Block

Anatomy

The ganglion impar, also known as the ganglion of Walther, is the uniquely unpaired caudad terminus of the bilateral sympathetic chains and provides sympathetic innervation to the perineum.67,68 The ganglion is typically about 0.5 cm in length and is located in the midline, anterior to the first and second coccygeal vertebra and dorsal to the rectum.

Indications

Ganglion impar block (GIB) is used to treat chronic, recalcitrant perineal or pericoccygeal pain when it is considered that there is a sympathetic or neuropathic component to the pain. Thus, local symptoms might include burning pain and signs include cutaneous allodynia and hyperalgesia. Specific conditions for which it is used include SMP or CRPS I/II of perineum, coccygodynia, and perineal hyperhidrosis.

Contraindications

Pregnancy, although contraindicating exposure to ionizing radiation and fluoroscopy, may not prevent performance of GIB with ultrasound guidance; however, details of the ultrasound technique and potential obstetric issues are beyond the scope of this chapter.

Technique

There are two general techniques described for GIB: trans-discal or trans-anococcygeal ligament approach. In the trans-discal approach, a 22- or 25-gauge 1 to 1.5” single or double needle is inserted in the midline just through the sacrococcygeal, first intercoccygeal or second intercoccygeal joint. In the trans-anococcygeal ligament approach a single curved needle is inserted through the midline ano-coccygeal ligament and advanced against the anterior midline concavity of the inferior sacrum and coccyx to contact the ventral coccyx. The disadvantage of the former technique may include difficulty placing the needle into or through a calcified joint space. The disadvantage of the trans-anococcygeal ligament techniques is the risk of infection posed by adjacency to the rectum and the risk of rectal perforation and bleeding owing to the longer needle course. Commonly used anesthetic agents include bupivacaine in 0.25% concentrations. A volume of 2 to 4 mL of contrast is typically sufficient to document satisfactory injection technique.

If RF lesioning is contemplated, a pair of 20-gauge curved RF needles are used with 10 mm active tips placed parallel to and straddling the midline, just anterior to the coccyx about 5 to 6 mm apart. A bipolar strip lesion can be created at temperatures of 70 to 80° C for 90 seconds. Assessment of pain and function should be documented postoperatively including the proportion and ultimate duration of improvement that follows each GIB.

Complications

Potential adverse effects include infection of subcutaneous or deep tissues, including discs/joints at sacrococcygeal or intercoccygeal junctions, rectal perforation, and bleeding.

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