SECTION B: Injections and Neurolytic Therapies for Pain

OVERVIEW

Spinal injections have been performed for many years, most often for the management of axial, paraspinal, and radicular pain. They have evolved over the years with increasing popularity, with the number of epidural steroid injection procedures doubling from 2000 to 2008,¹ and have become essential therapies for the pain management clinician. Spinal injections can be used therapeutically, for treatment, or diagnostically, for the localization and identification of potential painful targets. As a result of their increasing use in pain management and their economic impact, they have been studied extensively, and their efficacies have been challenged. Despite controversy and contradicting results of numerous outcome studies, spinal interventional therapies will likely continue to play a significant role in interdisciplinary pain care.

The purpose of this chapter is to discuss commonly performed spinal interventions, especially epidural steroid injections and facet injections, with an emphasis on information that is clinically relevant to pain management specialists.

HISTORY OF SPINAL INJECTIONS

Spinal injections of substances for the treatment of low back and lower extremity pain^2,3 and for inoperable cancer of the rectum⁴ were described in 1901,⁵ with the use of medications, including cocaine and procaine, via multiple routes of administration, including epidurally, intrathecally, and via the sacral hiatus. In 1909, reports were published on the use of epidural anesthesia for the treatment of sciatica⁶ followed in the 1920s and 1930s by emerging treatments for sciatica with varying degrees of benefit and duration.^7,8

With the discovery of Compound E (cortisone) in 1936^9-11 and by 1950 its improvement of conditions, including rheumatoid arthritis,¹² and with the beneficial intraarticular effects of a longer acting steroid, Compound F (hydrocortisone),¹³ including the histologically confirmed reduction of synovial membrane inflammation, the stage was set for numerous anti-inflammatory pain management procedures along with continuing investigations of its efficacy and mechanisms of actions.^14-20 By the 1950s, many pain management clinics were in operation,^21,22 and today, many interdisciplinary pain treatment facilities are in existence.

CLASSIFICATION OF SPINAL INJECTIONS

Spinal injections for pain management have been performed for many years, both for diagnostic and therapeutic purposes. They can be functionally categorized both by location (i.e., cervical, thoracic, lumbar, or sacral) and by purpose: (i.e., diagnostic or therapeutic). A significant proportion of procedures performed at modern pain clinics include epidural steroid injections and facet joint injections. Other common interventions include sympathetic blocks, provocative discography, and medial branch radiofrequency neurotomy. Epidural steroid injections can be subcategorized by the route of administration of medication, usually via transforaminal, interlaminar, or caudal approaches, with or without the use of a catheter.

Zygapophyseal or facet injections that are therapeutic in nature tend to be intraarticular, and although they can be therapeutic and diagnostic, medial branch blocks are usually performed to provide diagnostic information and to predict the potential benefit of facet denervation via radiofrequency neuroablation.

LOW BACK PAIN

EPIDURAL STEROID INJECTIONS

Epidural injections of glucocorticoids may be helpful in some patients for the treatment of axial lumbar, thoracic, and cervical pain, and radicular lower and upper extremity and thoracic radicular pain. Historically, injection of steroids into the epidural space followed the observation of the beneficial effects of intraarticular injection of steroids into osteoarthritic joints,²³ with the first use of hydrocortisone in 1952 periradicularly²⁴ and in 1953 caudally.²⁵

The emergence of interventional pain management as a specialty has led to a significant increase in the use of interventional techniques, prompting continuous review and the establishment of evidence-based practice guidelines for the management of spinal pain.²⁶ With hospital-based and dedicated pain treatment facilities performing these and other types of injections²⁷ and with a 100% increase in the frequency of epidural injections between 1998 and 2003²⁸ and between 2000 and 2008, epidural steroid injections are the most commonly performed intervention used in the United States to manage chronic and subacute low back pain (LBP).²⁹

Various causes of sciatic pain have been proposed, including pressure on the spinal nerve by disc fragment or bone spur;³⁰ however, nerve root compression does not always produce pain, and patients without a history of sciatic pain have had disc protrusion or herniation found on postmortem examination.³¹ Additionally, myelographic and magnetic resonance imaging (MRI) abnormalities have been found in asymptomatic individuals,^32,33 and surgical decompression does not relieve symptoms in every case. Confusing the picture even more, many patients with sciatic pain have no imaging-based evidence of nerve root compression. This may suggest that radicular pain is multifactorial.

Although mechanical nerve root compression can cause sensory and motor dysfunction, inflammation may also be a source of neural pain.³⁴ Structures in the vicinity of the nerve root, including injured disc tissue,³⁵ injured vertebral endplates leading to disc degeneration,³⁶ degenerated lumbar intervertebral discs per se,³⁷ facet joints, and epidural tissues, may each modulate neural activity, leading to increased sensitivity and pain-generating discharges and heightened sensitivity to pressure.³⁸ Current imaging modalities may be unable to demonstrate anatomic abnormalities responsible for spinal or radicular pain, especially if the abnormalities are not macroscopic.

In 1950, inflammation and edema was noted in nerve root biopsy samples from patients undergoing laminectomy,³⁹ and it was observed that swollen nerve roots shrank as sciatic symptoms improved.⁴⁰ Similar observations were found in patients treated with intramuscular dexamethasone.⁴¹ Increased concentrations of inflammatory and neurochemical mediators found in intervertebral discs, including phospholipase A₂,⁴² and pain-related neuropeptides in nerve endings in the discs and epidural structures^43,44 may contribute to axial or radicular symptoms. Cells from degenerated disc fragments produce numerous inflammatory mediators, including tumor necrosis factor (TNF) and inflammatory cytokines,⁴⁵ and the released inflammatory mediators and TNF may penetrate within intraneural capillaries, causing axonal ischemia, which is responsible for nerve root pain.⁴⁶

Glucocorticoids inhibit the synthesis or release of many inflammatory substances⁴⁷ and may prevent cell-mediated inflammation that can stimulate nociceptive nerve endings.⁴⁸ In radicular pain, glucocorticoids may mitigate early effects of inflammation, including edema, fibrin deposition, capillary dilation, leukocyte aggregation, and phagocytosis, and late effects such as capillary and fibroblast proliferation, collagen deposition, and scar formation.²⁷ LBP per se may respond to the effects of glucocorticoid through its reduction of inflammation specifically in the posterior longitudinal ligament and the outer annulus of the intervertebral disc.²⁷ Injecting glucocorticoid near the sites of inflammation achieves a higher concentration than that obtained by systematic administration.

Many studies have investigated the efficacy of epidural steroid injections in the cervical, thoracic, and lumbar regions, reporting conflicting results, likely because of the difficulty in studying pain treatment modalities. Significant variations exist with regard to the numerous mechanisms of pain generation and the natural course of acute and chronic back and upper and lower extremity pain. Factors that must be considered in these investigations include injection variability, the route of administration (transforaminal vs. interlaminar), the use of fluoroscopic guidance and contrast, operator experience, spinal anatomy, degenerative change, surgical hardware or granulation tissue affecting the spread of medication, timing and frequency of administration, and prior surgical procedures.

Results from one systematic review of lumbar interlaminar epidural steroid injections show a significant reduction of pain scores in patients with lumbar radiculitis compared with no therapy and compared with conservative management without injection therapy.⁴⁹ In the cervical region, a study regarding immediate pain score after a single image-guided cervical transforaminal epidural steroid injection does not predict the long-term effectiveness of the procedure.⁵⁰ The literature supporting or refuting the use of epidural steroid injections for the treatment of chronic mid and upper back pain caused by disc herniation, radiculitis, and other causes is scant.⁵¹

There will likely continue to be emerging and sometimes conflicting evidence on the cost effectiveness⁵² and efficacy^53-58 of epidural steroid injections or the choice of medications, routes of administration, and the timing of injections.

ZYGAPOPHYSEAL JOINT INJECTIONS

Sources of axial spinal pain (cervical, thoracic, and lumbar) are numerous. These include intervertebral discs, nerve root dura, facet joints, ligaments, muscles, and fascia; in the lumbar region, the sacroiliac joints; and in the cervical region, the atlanto-axial and atlanto-occipital joints. The lumbar facet joint was suspected as a source of LBP, spinal instability, and leg pain in 1911,⁵⁹ and by 1933, the lumbar facet joint was recognized by Ghormley as part of a distinct LBP syndrome “facet syndrome.”⁶⁰ Provocative intraarticular facet joint injections of hypertonic saline were used and described in 1976⁶¹ to investigate lumbar facet–mediated pain patterns. Medical literature has identified the lumbar, thoracic, and cervical facet joints as independent pain generators.

Inflammation within the joint capsule can decrease thresholds of nerve endings in the facet capsules with resulting elevated baseline discharge rates, and stretch or excessive stretch may damage axons or the joint capsule, with activation of nociceptors leading to prolonged neural discharges.⁶² In the lumbar region, facet-mediated pain may present with axial spinal, paraspinal, buttock, or leg distribution patterns;⁶³ similarly, cervical facet–mediated pain may present as axial and paraspinal pain with radiation to the upper extremities or as headache.⁶⁴ In the thoracic region, based on experience with cervical and lumbar facet joints, thoracic facet–mediated pain can be axial or paraspinal, with radiation to the upper back and chest wall.⁶⁵ Because facet-mediated pain may coexist with other sources of axial pain or radicular pain, in clinical practice, it may be helpful to consider each component individually.

The diagnostic and therapeutic utility of cervical, thoracic, and lumbar facet injections has been investigated in numerous studies. Medial branch blocks, named for targeting the sensory innervations of facet joints, are frequently performed for diagnostic purposes to determine the role of the facet joint as a mediator of pain in lumbar, thoracic, and cervical regions. Localizing the facet joints to target may be difficult with two facet joints at each vertebral level (left and right), and the potential variations in symptoms, historical, imaging and physical examination information may be helpful.

To establish a consensus among interventional pain management specialists in the diagnosis and management of spinal pain, particularly specifics of treatment techniques (treatment modality, medication, frequency of administration), an algorithmic approach for the clinical management of chronic spinal pain based on evidence-based guidelines has been suggested.⁶⁵

In facetogenic pain, diagnostic blocks targeting suspected painful joints can identify sources of lumbar, thoracic, and cervical pain. Medial branch blocks can also aid in the selection of patients who might respond to facet radiofrequency denervation. For LBP, a systematic review⁶⁶ of 122 studies, leading to the inclusion of 11 randomized trials and observational studies concluded that the evidence is good for radiofrequency neurotomy and fair to good for lumbar facet joint nerve blocks for short- and long-term improvement. Evidence for intraarticular injections and pulsed radiofrequency neurotomy is limited.

In the cervical region, a systematic review⁶⁷ including four randomized trials and six observational studies concluded that evidence for cervical radiofrequency neurotomy and medial branch blocks is fair, and evidence for cervical intraarticular injections with local anesthetic and steroid is limited. However, the study noted a paucity of published literature for cervical facet joint injections. In the thoracic region, there is evidence that the facet joints are responsible pain generators for thoracic pain⁶⁸ and that the diagnostic accuracy of controlled facet joint blocks is strong for cervical and lumbar facet joints and moderate for thoracic facet joints.⁶⁹

STEROID MEDICATIONS

OVERVIEW

Corticosteroids are steroid hormones produced in the adrenal cortex, and this class consists of glucocorticoids and mineralocorticoids. Mineralocorticoids, such as aldosterone, are responsible for regulation of electrolyte and fluid balance.⁷⁰ Glucocorticoids (named for their modulation of the metabolism of carbohydrates) exert their action via the glucocorticoid receptor (GR).⁷¹

With respect to their use in pain management, corticosteroids can be compared pharmacologically with focus on each medication's mineralocorticoid and glucocorticoid potency, duration of action, and particulate size.

Glucocorticoids have been useful in the treatment of inflammatory diseases for more than 50 years, but their usefulness has been limited by complications and side effects. These include, but are not limited to, suppression of the hypothalamic–pituitary–adrenal (HPA) axis and the immune system, exacerbation of diabetes, hypertension, and osteoporosis.^72-78 Pharmacologic research has focused on modifying the chemical structure of glucocorticoids in hopes of increasing their potency while decreasing the likelihood of side effects. The separation of anti-inflammatory activity from the systemic side effects of glucocorticoids has been difficult. The anti-inflammatory potency of steroids is related to the GR binding affinity.⁷⁹ While steroid preparations are typically injected in proximity to regions of inflammation, they cross into the systemic circulation and affect every major organ system in the body.⁸⁰

STEROID MECHANISM OF ACTION

The mechanism of action of the glucocorticoids is complex but in part involves the inhibition of phospholipase A2 activity with a resulting reduction in the release of arachidonic acid from membrane phospholipids.⁸¹ Arachidonic acid is the precursor for the synthesis of eicosanoids (including prostaglandins, thromboxanes, leukotrienes, and lipoxins), which mediate a wide range of inflammatory responses. Additionally, methylprednisolone has been shown in the rat to suppress transmission in thin unmyelinated C-fibers but not in myelinated A-β fibers, suggesting a direct membrane effect of the steroid per se.⁸² Thus, inhibiting phospholipase A2 reduces the presence of inflammatory mediators, some of which cause hyperalgesia,⁸³ edema, and decreased blood flow.

STEROID PREPARATIONS USED FOR INJECTIONS

Although adverse events relating to neuraxially administered steroid medications are rare, their severity, especially with regard to brain and spinal cord infarction with regard to transforaminal administration, has prompted numerous reviews.⁸⁴ Studies have investigated particulate size, route of administration, and the use of sedation because embolic phenomena have resulted in spinal cord injuries, stroke, and deaths.^85-89 Etiologies for the sequelae have been postulated to include embolic infarction secondary to particulate injection into an arterial vessel; direct vascular injury causing spasm, trauma, or compression; or neurotoxicity from medications injected or the vehicle or additives to the preparation.⁹⁰

Corticosteroids used for injection that are commercially available in the United States can be categorized as soluble, insoluble, or a combination of both. Insoluble corticosteroid preparations (methylprednisolone, triamcinolone) are typically corticosteroid esters and offer theoretical advantages in their longer duration of action because they require hydrolysis by cellular esterases for the active steroid moiety to be released.⁹¹ Additionally, preparations of insoluble crystalline powder in aqueous suspensions are less likely to be absorbed soon after injection in comparison with soluble preparations.⁹² Soluble steroid preparations (dexamethasone, betamethasone) are taken up rapidly by cells and have a quicker onset but reduced duration of action.⁹³ Betamethasone is unique in its availability as a water-soluble ester, betamethasone sodium phosphate, or as the practically water-insoluble salt, betamethasone phosphate. One formulation containing both betamethasone ester and salt (Celestone Soluspan; Schering, Kenilworth, NJ) may offer both a rapid onset and longer duration of action.

There are substantial variations in the size of the crystals found in insoluble corticosteroid preparations, and this has been demonstrated in numerous in vitro studies.^94-98 Ester corticosteroid preparations tend to contain larger particulate sizes, and because of variations in crystal concentrations and physical characteristics and with mixture with other injected medications or with plasma,⁹⁹ crystals may aggregate into larger particles. This phenomenon is of extreme importance given the potential for these particles, injected intravascularly, to cause distal embolization and tissue injury.

STEROID PARTICULATE SIZE AND MECHANISMS FOR SERIOUS ADVERSE EVENTS

Infarction of central nervous system (CNS) tissue has been postulated to be secondary to embolic occlusion by particulate steroid.^100-102 Particulate size may influence the degree of arterial occlusion and size and variability of particles in the injectate have been investigated,^103-106 as well as their dilution or mixture with other medications.¹⁰⁷ In comparison to the red blood cell, particles larger than the lumen of an arteriole may occlude arterioles, however collateral blood supply may decrease the likelihood of tissue damage.^108,109

Particles smaller than an arteriole but greater than the size of a red blood cell may occlude terminal arterial vessels and cause infarction. The diameter of an arteriole ranges from 100 to 500 µm, and that of vertebral arteries ranges from 600 to 2600 µm. The size of corticosteroid ester particles can exceed 500 µm, and particles can aggregate or precipitate in the vascular space or in blood to form larger particles.

Use of nonparticulate steroid preparations (pure betamethasone, dexamethasone) may decrease the risk of embolic phenomena and may strengthen the postulate that embolic occlusion is the source of CNS damage. Ongoing investigations are looking at the incidence and clinical presentations of major complications associated with cervical transforaminal epidural steroid injections to make evidence-based recommendations.¹¹⁰ Based on animal studies of the serious CNS sequelae after injection of insoluble methylprednisolone acetate versus no noticeable deficits after the injection of soluble dexamethasone phosphate,¹¹¹ MacMahon et al. suggest no longer performing transforaminal epidural steroid injections in the cervical, thoracic, or lumbar regions with insoluble corticosteroid preparations and believe that this reduces, if not removes, the risk of CNS embolization during the procedure.¹¹²

Additionally, two case reports describe significant CNS injury (bilateral lower extremity paralysis with neurogenic bowel and bladder) after a fluoroscopically guided (left L3–L4) lumbar transforaminal epidural steroid injection with betamethasone and a computed tomography–guided (right L3–L4) transforaminal injection of methylprednisolone, with MR images consistent with spinal cord infarction without evidence of intraspinal mass or hematoma.¹¹³ In each of these cases, the use of particulate corticosteroid with embolization in a radicular artery is asserted as a likely mechanism of injury, and statements discuss reducing or eliminating this risk by the utilization of particulate-free steroids and testing for intraarterial injection with digital subtraction angiography and a preliminary injection of local anesthetic.

An alternative mechanism of injury suggests retrograde flow into a common arterial trunk with subsequent antegrade flow into vulnerable arteries and should be considered as a possible mechanism by which spinal cord or brain injury may occur.¹¹⁴ Spinal cord infarction has also been reported after a (right L2–L3) transforaminal epidural steroid injection with spinal angiography demonstrating occlusion of the right L2 segmental artery with reconstitution of the radicular branch from collaterals. The artery of Adamkiewicz was presumably occluded by steroid injection.¹¹⁵

Numerous case reports and reviews describe and attempt to quantify both minor and devastating neurologic complications of epidural steroid injections and their mechanisms. Although embolic phenomena may be responsible for tissue infarction, direct injury to the vessel may also be problematic. Perineural hematoma after lumbar transforaminal steroid injection was described in a case report and demonstrated by MRI after the observation of progressive motor and sensory loss.¹¹⁶ Although digital subtraction angiography (DSA) has been suggested as an adjunct to aid in the identification of vascular compromise during interventional neuraxial procedures, irreversible paraplegia was reported after a lumbar transforaminal epidural steroid injection despite the administration of a local anesthetic test dose and the use of DSA.¹¹⁷

Suggestions made from this case report include the use of blunt or larger bevel needles in place of sharp, cutting needles and the consideration of eliminating the use of particular steroids for transforaminal epidural steroid injections. In contrast, however, despite the use of an atraumatic pencil-point needle, simultaneous epidural and radicular artery spread were observed fluoroscopically during a cervical transforaminal corticosteroid injection using a 25-gauge Whitacre spinal needle,¹¹⁸ although no complications were associated with the procedure.

An additional study comparing the use of sharp versus blunt tip needles in transforaminal epidural steroid injections¹¹⁹ showed a statistically significantly higher incidence of vascular penetration with the sharp tip but no statistical difference with respect to the occurrence of paresthesias, dural puncture, and headache. The authors concluded that blunt needles seem to be more advantageous.

An additional case report describes the subdural spread of local anesthetic in a selective transforaminal cervical nerve root block, after which transient flaccid paralysis developed.¹²⁰ This underscores the risk of serious complication and the need for emergency airway management, ventilation, and cardiovascular support.

Although many serious reported adverse outcomes involve the transforaminal injections of local anesthetics and corticosteroids, a case report describes paraplegia after a low lumbar epidural steroid injection via the interlaminar route.¹²¹ Although the mechanism was unclear, theories suggested ischemia caused by accidental interruption of the medullary blood supply by direct damage to a medullary artery, arterial spasm, or corticosteroid-induced occlusion caused by undetected intraarterial injection.

A prospective evaluation¹²² of more than 10,000 fluoroscopically guided epidural procedures of the cervical, thoracic, and lumbar spine via interlaminar, transforaminal, and caudal approaches and including percutaneous adhesiolysis procedures reported overall event rates of intravascular penetration of 4.3%; dural puncture of 0.5%, with postdural puncture headache of 0.05%; and transient nerve root irritation and transient spinal cord irritation of 0.08%. The infection and abscess rates were both 0.0%, and there were no major complications.

ROUTE OF ADMINISTRATION

Because there are different routes to administer steroid medications, studies have attempted to evaluate and compare outcomes based on variables. These include the medications and their dosages; their timing in relation to the onset of symptoms; their frequencies; the routes and methods of administration (transforaminal, interlaminar, caudal) and condition treated (LBP, radicular pain), and cause (disc herniation, spinal stenosis). Evidence of the efficacy of lumbar epidural steroid injections is difficult to summarize.¹²³

Of the available approaches to access the lumbar epidural space, the interlaminar approach is the most commonly used versus the transforaminal and caudal approach,^124-126 and blind or nonimage-guided interlaminar approaches do not represent contemporary interventional pain management practice.¹²⁷ The transforaminal approach offers an advantage of selectivity and can provide valuable diagnostic information in the treatment of radiculopathy to identify symptomatic nerve roots.¹²⁸ Numerous studies summarized in a recent, comprehensive evidence-based review of epidural steroid injections¹²⁹ support the general consensus by pain management practitioners that the transforaminal approach is superior to the interlaminar or caudal approaches. Previous surgical interventions, the presence of surgical hardware, or particular spinal anatomy may preclude one approach or favor another.

Caudal epidural steroid injections may offer alternative anatomic approaches to treating LBP and sciatica and may be less technically demanding to perform.¹³⁰

INFECTION

Although generally considered safe and performed under strict aseptic conditions, the potential for infection after spinal injections exists and can lead to devastating consequences. Infections resulting from spinal injections have been considered rare. Overall infection rates have been reported to occur in 1% to 2% of spinal injections, and severe infections have been reported with an incidence of 0.01% to 0.1% of all spinal injections.¹³¹ Causes may be bacterial, including the most common organism being Staphylococcus aureus, introduced via the skin through needle puncture, usually because of poor sterile technique.¹³² Gram-negative infections may occur theoretically secondary to needle penetration into the intestine or the pelvic cavity,¹³³ which may occur most easily anatomically via S1 to S2 transforaminal injections.¹³⁴

Pyogenic arthritis of the spinal facet joint, although rare, has been reported after intraarticular steroid injections¹³⁵ and can lead to epidural and paraspinal abscess formation.¹³⁶ Vertebral osteomyelitis has been reported in an immunocompromised diabetic male patient after lumbar epidural steroid injections.¹³⁷

Fungal infections have also been reported and have been brought to light after recent outbreaks. In 2002, two occurrences of Exophiala meningitis, one leading to death, after epidural injections of methylprednisolone acetate prepared by a compounding pharmacy after the medication became difficult to obtain from the manufacturer; unopened vials from this pharmacy were analyzed by the Centers for Disease Control and Prevention.¹³⁸ Similarly, in 2012, an investigation of fungal infections associated with the injection of preservative-free methylprednisolone purchased from a compounding pharmacy in Massachusetts led to the discovery of fungal contamination from unopened vials. In April 2013, a Subcommittee on Oversight and Investigations reported a total of 733 cases of fungal meningitis and 53 deaths as a result of this contamination.

The potential effects of epidural glucocorticoid injections in modulating the immune system are not well described,¹³⁹ and data show that prolonged high-dose systemic glucocorticoid therapy for immunosuppression is a risk factor for invasive aspergillosis.¹⁴⁰

STEROID-RELATED SIDE EFFECTS

Despite the therapeutic anti-inflammatory effects of corticosteroid therapy, their use can lead to obesity, diabetes, osteoporosis, insulin resistance, hyperglycemia, hyperlipidemia,¹⁴¹ dermatologic conditions, peptic ulcer formation, and Cushing's syndrome.¹⁴² The mechanisms underlying the side effects of short- or long-term use of steroid medications are complex; certain side effects are mediated via transactivation (e.g., diabetes, glaucoma), transrepression (e.g., suppression of the HPA axis), or both (e.g., osteoporosis).¹⁴³

Side effects from intraarticular and epidural steroid injections may be underrecognized, and symptoms arising from the systemic absorption of steroids, such as a hormonal profile suggestive of hypopituitarism or Cushing's syndrome, may divert historical investigation of the iatrogenic cause, leading to expensive investigation, false diagnoses, and unnecessary treatment.¹⁴⁴

Some side effects from chronic steroid therapy have direct implications in the differentiation of symptoms of LBP, radiculopathy, or paraparesis, as described in a case report of chronic steroid therapy–induced spinal epidural lipomatosis with MRI findings of accumulations of fatty deposits in the spinal canal not resolving with surgical intervention.¹⁴⁵ Neuropsychiatric effects of glucocorticoids range in scope, including the most severe psychotic symptoms designated as steroid psychosis,¹⁴⁶ can occur rapidly after exposure even to low doses from oral, epidural, or intraarticular administration.¹⁴⁷ Identifying patients at risk for steroid psychosis can be difficult because the neuropsychiatric effects of glucocorticoids are unpredictable.

Factors to consider in the evaluation of changes in mental status in the pain management setting include the current or recent use of steroids for pain or non–pain-related conditions, the dosage (including the timing and frequency and cumulative quantity of steroid), the presence of preexisting neuropsychiatric conditions, and a history of previous adverse reactions to steroid administrations.

Other studies have investigated the role of administrations of corticosteroid on glucose metabolism. Studies have shown that glucose metabolism can be disturbed in nondiabetic and diabetic patients after intraarticular injections of corticosteroids^148,149 secondary to the diffusion of medication into the systemic circulation. The degree of systemic absorption varies based on the degree of inflammation within the joint and the solubility and dosage of the injected steroid.¹⁵⁰

Single-session intraarticular injections of methylprednisolone have been shown to cause impaired adrenocorticortical reserve, with most patients recovering after 1 to 2 weeks.¹⁵¹ A recent study compared the effect of intraarticular versus epidural steroid injection in patients with diabetes and the diffusion of steroid in the two procedures.¹⁵² The glycemic profile remained unchanged after epidural administration versus an increase in blood glucose in the 2 days after intraarticular injections of 80 mg of methylprednisolone. The study suggests that methylprednisolone injected epidurally remains mostly local.

In contrast, a prospective cohort study showed that epidural steroid injections caused a significant increase in blood glucose levels in patients with diabetes without correlation between preinjection blood glucose control represented by Hgb A1C levels.¹⁵³ Documentation of previous responses of blood glucose levels after epidural steroid injections may help to adjust changes in blood glucose monitoring regimen in the immediate postinjection period.

ANTICOAGULATION AND NEURAXIAL INJECTIONS

Performing diagnostic and therapeutic neuraxial injections carries the risk of iatrogenic hemorrhagic complications, although the actual incidence of neurologic dysfunction from these complications is unknown.¹⁵⁴ The incidence of these complications is rare, Horlocker and Wedel report it as less than one per 150,000 in epidurals and one per 220,000 for spinal anesthetics,¹⁵⁵ the incidence may be increasing and may be as high as one per 12,000 in epidurals for chronic pain relief.¹⁵⁶ Given the potential consequences of compressive hematomas, a great deal of effort has been made to understand the incidence, and much information has been gathered from the historical analysis of spinal and epidural injections, including catheter insertions, for the initiation and maintenance of regional anesthesia^157-160 and more recently through the investigation of complications occurring as a result of pain management–related neuraxial injections.^161,162 The potential for bleeding and hematoma formation can result from damage to vessels by the injection needle, either at the time of or after the injection. Although the use of contrast during fluoroscopy can help to identify intravascular needle placement, situations in which a vessel had been pierced before the injection of contrast would not be visualized.

The likelihood of bleeding and hematoma formation increases with primary coagulopathy and conditions associated with coagulopathy, such as liver disease, and in patients taking medications with anticoagulant properties. Factors predictive of difficulty in the performance of neuraxial blocks, such as anatomic variations, morbid obesity, prior spinal surgery, the presence of spinal hardware, severe degenerative change, or previous unsuccessful attempts, may influence the decision to perform neuraxial blocks. The risks associated with performing neuraxial procedures in patients receiving medications that affect components of the clotting system must be considered on an individual basis; factors to be considered include the consequences of temporary discontinuation of anticoagulants. As new medications with anticoagulant properties emerge, it is imperative that a careful review of these medications is performed before each neuraxial procedure. In contrast to the performance of neuraxial anesthesia for patients undergoing nonelective surgical procedures, the pain management clinic must facilitate all aspects of periprocedural care to optimize chances for success and minimize risk. Guidelines for performing spinal procedures in patients taking anticoagulants have been established by the American Society of Regional Anesthesia,¹⁶³ and specific recommendations regarding the time after discontinuing specific medications before neuraxial procedures are available.¹⁶⁴

Just as important as optimizing coagulation status is recognizing signs of compressive hematoma. Neurologic changes that occur after neuraxial procedures must be investigated immediately. In the pain management setting, where neurologic deficits are common, documentation of baseline neurologic function is critical to compare postprocedure outcomes, and spinal imaging as soon as possible is vital in the differential diagnosis of neurologic changes. Neurosurgical consultation can help to assess the role of decompressive surgery as soon as possible.

Because neurologic outcome is linked to early diagnosis and intervention, it is critical to obtain radiographic imaging, preferably MRI, as soon as possible. Consultation with a neurosurgeon should also occur as soon as possible to determine the urgency of surgery.

REFERENCES

INTRODUCTION

Ideally, the comprehensive interdisciplinary pain center would combat the scourge of fragmented musculoskeletal care. Chronic musculoskeletal pain is prevalent in 50% of adults and is the leading cause of disability in the United States [1=Burden MSK dz].¹ Systemic corticosteroid treatment of musculoskeletal pain began soon after the discovery and synthesis of cortisone in the 1940s.² Intraarticular steroid injections followed shortly thereafter, and in 1951, Hollander published the results of a large series of patients treated with corticosteroid joint injections.³ Corticosteroid injections continue to play an important role in the diagnosis and management of acute and chronic musculoskeletal pain. Pain physicians who recognize joint pain versus spine pain and who are proficient in multimodal management of both are well suited to coordinate reasonable utilization of intraarticular injections.

The spectrum of treatment options for painful joints includes tincture of time, education and counseling, activity and physical treatments, orthoses, medications, imaging, injections, and surgery. This chapter covers indications, techniques and anatomic details, sensitivity, specificity, outcomes, and associated adverse events of the most common intraarticular injections, as well as information on less frequently performed injections. Spine joint (facet and sacroiliac) intraarticular and certain nonarticular musculoskeletal injections are included. This chapter does not cover ultrasound-guided injections, a topic unto itself; please refer to the ultrasound chapter for more detail.

GENERAL PRINCIPLES

INDICATIONS AND CONTRAINDICATIONS

General principles favored by the authors are highlighted in the rules of Table 82-1. Indications for joint injections include (1) treatment of the painful joint, (2) for diagnosis to assess response to blockade of the joint, (3) for diagnosis to obtain joint fluid, or (4) for treatment to drain excess joint fluid causing pain. Corticosteroid injections are used for osteoarthritis (OA), rheumatoid arthritis (RA), psoriatic arthritis, lupus, crystalline arthritis (gout and pseudogout), reactive arthritis (Reiter's syndrome), and more. Other conditions include bursitis, tendonitis, and enthesopathy. Contraindications may include (1) infection, localized or systemic, or other immunity issues; (2) allergy or adverse reaction potential to substances involved; and (3) pregnancy or breastfeeding because of safety profiles of medications and radiation exposure. Infection in a joint may itself be a reason to access the joint with a needle to obtain fluid, but placing steroid there would not be done. Surgical implants give pause; truly consider the risk-to-benefit ratio. Pain in a joint that has been replaced is not likely to be cured with an injection. Anticoagulation is not a contraindication (see later discussion).

IMAGING AND LANDMARKS

As technology for image guidance has become more routinely available, it has been increasingly applied to interventional pain procedures previously performed with surface landmarks, and the trend of studies suggests increased accuracy in medication placement when using image guidance. The sterility and other rigorous protocols of the procedure suite may also benefit patients. For example, studies of major joint injections (knee, hip, and shoulder) have shown significant rates of failure to localize the joint when fluoroscopy was not used.⁴ Blind injection of the osteoarthritic hip joint can be inaccurate even with careful technique, traditional methods are not reliable, and image guidance during the injection seems to be necessary.⁵

Preprocedure imaging (e.g., joint radiography or magnetic resonance imaging [MRI]) is not routinely required.

MEDICATIONS

The most commonly used injectable steroids include betamethasone sodium phosphate/acetate (Celestone Soluspan; Schering-Plough, Kenilworth, NJ), methylprednisolone (Depo-Medrol; Upjohn, Kalamazoo, MI), triamcinolone acetonide (Kenalog; Bristol-Meyers Squibb, Princeton, NJ), and triamcinolone hexacetonide (Aristospan; Sandoz, Princeton, NJ).⁶ Triamcinolone hexacetonide has the longest duration of action, approximately 3 to 6 weeks, and pharmacokinetic studies have shown it to be absorbed from the joint over a period of 2 to 3 weeks.⁷ The duration of clinical effect of corticosteroid is longer if it has lower aqueous solubility (Table 82-2).

Mechanisms for pain relief due to corticosteroids include anti-inflammatory action, analgesic effect, systemic effects after systemic uptake, and action on local neurons. Corticosteroids reduce synovial inflammation in patients with RA⁸ and may reduce osteophyte formation in those with OA.⁹ Injected corticosteroids suppress neural discharge in inflamed nerves and neuropathic pain states.¹⁰ In synovial joints, corticosteroids promote secretion of phospholipid that may contribute to improved joint mobility.¹¹

Local anesthetics frequently used for joint and soft tissue injections are bupivacaine (Hospira; Lake Forest, IL, and Sensorcaine; AstraZeneca, Wilmington, DE) and lidocaine (Xylocaine; AstraZeneca, Wilmington, DE). Methylparaben-free and preservative-free anesthetics reduce clumping or flocculation of particulates.

Viscosupplementation is the intraarticular injection of hyaluronic acid derivatives. The technique of injection is the same as with steroid injections. A decreased concentration of hyaluronic acid in the synovial fluid of osteoarthritic joints results in decreased viscosity, which reduces its protective function. Numerous varieties of viscosupplementation are now on the market, including hyaluronan (Sinovial, Yaral, Intragel), 1% sodium hyaluronate (Euflexxa), cross-linked hyaluronate (Gel-One), sodium hyaluronate (Hyalgan), high-molecular-weight hyaluronic acid (Orthovisc), sodium hyaluronate (Supartz), hylan G-F 20 (Synvisc), and hylan G-F 20 (Synvisc One). For example, Synvisc, extracted from chicken combs, is supplied in 2-mL prefilled syringes and is administered as a series of three intraarticular knee injections over 3 weeks. Utilization has drifted now to other joints, but the evidence basis for viscosupplementation is mixed, with enthusiastic results tempered by a meta-analysis of controlled trials suggesting that effect size may be clinically irrelevant and risks may be underappreciated.¹²

Other medications are sometimes used for intraarticular injections. Ketorolac 40-mg vials are often used for intraarticular injection. Intraarticular ketorolac and intraarticular opiates have been studied for perioperative analgesia in joint surgery.¹³ Intraarticular botulinum toxin has had surprisingly positive results for shoulder and knee pain.^14,15 Literature search will reveal studies on numerous substances injected intraarticularly, including radiopharmaceuticals, precious metals, laser-absorbing agents, and more, not in common use.

Contrast agents are typically the same as for other interventional techniques. The authors prefer Isovue 300M or Magnevist in case of allergy.

ANTICOAGULATION

Anticoagulation is not routinely discontinued before peripheral joint and soft tissue injections. A prospective study of 32 injections and aspirations performed in patients taking therapeutic warfarin resulted in no cases of joint or soft tissue hemorrhage.¹⁶ In a retrospective review of 640 injections in patients anticoagulated on warfarin, none had hemarthrosis, and only one had clinically significant bleeding postprocedure. A prospective cohort of 15 injections on anticoagulated patients resulted in one frank hemarthrosis, in a patient with an international normalized ratio of 5 and taking concurrent nonsteroidal anti-inflammatory drugs (NSAIDs). In a practice survey including more than 1000 rheumatologists, only 1% had observed bleeding events after shoulder injections in patients taking aspirin compared with 10% in patients taking vitamin K antagonists.¹⁷

COMPLICATIONS

Several large series have demonstrated the risk of infection to be one in 50,000 injections or less with joint injections.¹⁸ The authors use strict aseptic technique and copious prep and drape.

Systemic absorption occurs following corticosteroid joint injection. Refer to the chapter on steroids for more detail. Possible systemic side effects after injection include any effect of systemic steroid administration. Using the lowest effective dose and limiting the number of injections minimizes the risk. Patients with diabetes may see a temporary (about 2-week) rise in blood glucose level. Corticosteroid injection may transiently suppress the hypothalamic–pituitary–adrenal (HPA) axis. Fluid retention, weight gain, and facial flushing have been reported following corticosteroid injection.¹⁹ Common steroid injection side effects also include postinjection flare and skin and fat atrophy.²⁰ Tissue damage, such as tendon rupture, cartilage breakdown, skin depigmentation, and fat atrophy, is often attributed to steroid injections; however, as noted earlier, there is also some evidence of protective effect of steroid in OA. Achilles tendon rupture is strongly associated with steroid injection. See the chapter on steroids for more detail.

Chondrocyte toxicity is an emerging concern with intraarticular injections. An in vitro study on effects of single-dose local anesthetic showed decreased chondrocyte viability with 1% lidocaine but not 0.25% bupivacaine or 0.5% ropivacaine.²¹ An in vitro study on effects of local anesthetic in combination with typical single injection doses of steroid showed decreased chondrocyte viability with 1% lidocaine or 0.25% bupivacaine combined with betamethasone sodium phosphate or betamethasone acetate or 1% lidocaine combined with methylprednisolone acetate or triamcinolone acetonide.²² Bupivacaine and triamcinolone, alone or in combination, have demonstrated chondrotoxicity in vitro.²³ These studies may not reflect in vivo conditions.

JOINT REPLACEMENT INFECTION

Although it may not be true, the common belief persists that intraarticular steroid injections in the hip predispose to later infection in primary hip arthroplasty of that joint. A retrospective of 40 patients who had received such hip injections 2 to 23 months before hip replacement revealed no infections in the follow-up of 11 to 37 months.²⁴ A survey of 36 patients who had received hip injections 5 to 19 months before hip replacement revealed no infections in the follow-up of 7 to 10 years.²⁵ A retrospective of 175 patients who had received hip injections within 1 year before hip replacement compared with controls revealed no increased risk of infections associated with hip injection before hip replacement.²⁶ A retrospective of 90 patients who had received knee injections before knee replacement compared with control participants revealed no increased risk of infections associated with knee injection before knee replacement.²⁷ An analysis of 38 patients with and 352 patients without postoperative infection after knee arthroplasty revealed that steroid injection did not increase the incidence of infection.

JOINT FLUID ANALYSIS

Joint fluid may be sent to a laboratory for assessment. Note the macroscopic appearance of the fluid, including color, clarity, and viscosity. (1) Crystals, (2) cell count (white blood cell count and PMN), (3) Gram stain, (4) culture, and (5) glucose are typically requested. Monosodium urate crystals of gout have strong negative birefringence under polarized light. The crystals of calcium pyrophosphate disease have weak positive birefringence.²⁸ See Table 82-3 for description of the types of synovial fluid.

SPECIFIC INJECTIONS

UPPER LIMB

Shoulder

Technique

Approaches for the shoulder include the anterior and posterior glenohumeral and subacromial. The acromioclavicular joint is also sometimes injected. Shoulder injection with surface landmarks is performed with the patient sitting on the examination table at a height comfortable for the clinician. With fluoroscopy, the patient is recumbent on the procedure table, prone for a posterior approach and supine for an anterior approach.

For the posterior approach, the arm is slightly internally rotated, and the scapula spine is palpated to find indentation just lateral to its edge to mark the entry spot. Then the coracoid process is identified anterior, and the needle insertion is directed toward the tip of the coracoid process. For the subacromial approach, the needle is inserted in the space posterolateral to the acromion process, parallel to the examination table, at a depth of approximately 3 cm.²⁹ The techniques are similar when fluoroscopic guidance is used.

For the anterior approach, the shoulder is slightly externally rotated. The point of entry is marked just medial to the head of the humerus and just below (inferolateral) the coracoid process (Figs. 82-1 and 82-2). The technique is similar when fluoroscopic guidance is used.

Subacromial bursa injection can be performed using the above posterior approach or the lateral approach. Using the lateral approach, the needle entry site is marked on the lateral shoulder just inferior to the acromion. The needle is advanced toward the inferior border of the lateral acromion (see Fig. 82-1). After the needle contacts the acromion, it is “walked” inferiorly until it slips off the inferior edge of the acromion. Then it is advanced perhaps 0.5 to 1.0 cm to where medication is injected. The technique is similar when fluoroscopic guidance is used.

The acromioclavicular joint space entry site is identified as a groove or depression between the acromion and clavicle. This can be done with palpation or fluoroscopy.

Evidence

Steroid injections are well tolerated and result in short-term relief of tendonitis.³⁰ Imaging-guided subacromial steroid injection may have short-term benefit in clinically and MRI-proven subacromial impingement; 83% of 69 patients reported symptom relief at 6-month follow-up evaluation. With a shorter duration of symptoms and minor-grade MRI findings, there is improved outcome.³¹ A meta-analysis of steroid injection for painful shoulder found that subacromial injections are effective for rotator cuff tendonitis up to a 9-month period. A dose–response association has been reported for subacromial steroid injection for rotator cuff tendonitis.³² In contrast, a randomized controlled trial (RCT) investigating corticosteroid dose in subacromial injection found no difference.³² In an RCT of patients with rotator cuff tears, injection of triamcinolone improved night and activity pain compared with control participants. Two injections at a 21-day interval compared with a single dose offered no potentiating or prolonged effect.³³ Other studies have found that subacromial injection for rotator cuff pathology results in small benefit compared with placebo but no benefit compared with NSAIDs, but for adhesive capsulitis, there is possible benefit of injection over placebo but with less conclusive evidence.^34-38

In an RCT, subacromial injection improved pain and disability and decreased range of motion (ROM) from poststroke hemiplegic shoulders.³⁷ In a prospective study, fluoroscopic-guided intraarticular steroid injection reduces pain and increases ROM in frozen shoulder syndrome.³⁸

Other Adverse Events

One study reported no significant effect of shoulder corticosteroid injection on blood glucose levels in patients with diabetes.³⁹ There is one reported case of steroid-induced psychosis from shoulder and interventional spine injections.^40a There is one reported case of livedoid dermatitis after shoulder injection.^40b There is also one reported case of fatal necrotizing fasciitis after steroid injection of the shoulder.⁴¹

Other Upper Limb

Elbow Injection

The elbow joint is injected using a lateral approach. The radial humeral joint can easily be palpated laterally at the level of the skin crease of the elbow.

The lateral epicondyle of the humerus is the most identifiable landmark. Identify and palpate the groove between the epicondyle and the plateau of the radius. Mark this spot as the needle entry point (Figs. 82-3 and 82-4). The needle is advanced to contact the epicondyle. Then walk the needle distally until it slides off the epicondyle and into the joint space. Advance the needle about 0.5 cm and inject the medication. If an ulnar paresthesia is elicited during needle placement, the needle is too dorsal, and a more volar approach should be used.

Olecranon Bursa Injection

The olecranon bursa lies between the soft tissue and the olecranon process of the ulna. It is injected with the needle advanced in a direction perpendicular to the olecranon (see Fig. 82-3) until the olecranon surface is contacted. Then the needle is withdrawn approximately 1 to 2 mm to the site where medication is injected. To avoid a subcutaneous injection, do not withdraw the needle too far after contacting the olecranon.

Finger Joint Injections

The carpometacarpal (CMC), metacarpophalangeal (MCP), and interphalangeal (IP) joints commonly are affected by RA and OA flare-ups and are amenable to injection therapy. The specific joint to be injected can easily be palpated. For the IP joints, a lateral or medial approach is used. For the MCP or CMC joints, a dorsal approach is used. It is best to avoid the more richly innervated volar (palmar) surface of the hand because these injections are more painful. The needle only needs to enter the superficial joint, just through the capsule (Figs. 82-5 and 82-6). Inject a small amount, perhaps 0.5 mL of anesthetic and corticosteroid solution.

Wrist Injections

A dorsal approach to the radiocarpal and ulnocarpal joints is preferred. These joints can easily be palpated and the needle entry site marked (Figs. 82-5 and 82-7). Care should be taken to avoid the extensor tendons. The joint space can be “opened up” slightly by placing the wrist in 45 degrees of flexion. The needle is advanced into the joint superficially, and 1 to 2 mL of solution is injected.

LOWER LIMB

Hip (Femoroacetabular)

Technique

Hip pain from the femoroacetabular joint can be confounded with spine, sacroiliac, or soft tissue processes in the same area. Intraarticular injection can be both diagnostic and therapeutic.⁴¹ Blind injection with surface landmarks can be inaccurate and unreliable; image guidance during the injection is preferred.⁵

An anterior or anterolateral approach is the most frequently used method of intraarticular hip injection. The patient is supine on the fluoroscopy table with the hip internally rotated; the femoral pulse is palpated and marked. The suggested skin entry site is 8 to 10 cm under the inguinal ligament, with the needle angled toward the femur head. This minimizes risk of vessel or femoral nerve injury.⁴² A more lateral approach has been demonstrated as safer in regards to potential neurovascular injury compared with the anterior approach.⁴³ The needle target is the lateral aspect of the femoral bone at the head–neck junction (Figs. 82-8 and 82-9).

The authors favor a posterior approach with the patient in the usual prone position, with the buttocks uncovered. This region is sterilely prepped with confidence. This approach easily avoids neurovascular bundles and allows down-the-beam advancement of the needle. It also may be more specific diagnostically because it does not directly target the psoas bursa. The needle target is the midpoint of the width of the femoral neck junction with the femoral head.

Evidence

The duration of pain relief after intraarticular corticosteroid hip injection typically is 1 to 3 months in patients with symptomatic OA.⁴⁴ Pain relief after intraarticular hip injection correlates with radiographic severity of OA.⁴⁵ Intraarticular hip injection after total hip arthroscopy has been shown to decrease opioid use and pain and increase rehabilitation activities.⁴⁶ In one study, injection volumes ranging from 3 to 9 mL did not result in different outcomes.⁴⁷

Other Adverse Events

There is one documented case of systemic septicemia after hip injection.⁴⁸

OTHER HIP GIRDLE INJECTIONS

Greater Trochanter

Trochanter injection may be performed with the patient lying on the asymptomatic side so the painful lateral hip area is superior and exposed. The area of greatest pain should be marked. Injection is targeted at this site.²⁸ Except when there is successful fluid aspiration, radiographic guidance is needed to ensure accuracy during trochanteric bursa injection.⁴⁸ However, the use of fluoroscopy may not improve outcomes in patients with greater trochanteric pain syndrome who receive corticosteroid injections. Comparable success rates were found for intra- and extrabursal injections.⁴⁹ A prosthetic joint is considered a relative contraindication by some authors⁵⁰ however, use of image guidance facilitates avoiding a surgical implant.

Evidence

Patients show improvement in trochanteric pain at short-term follow-up after corticosteroid injection, although improvement does not persist for the long term.⁵¹ Corticosteroid injection improves pain at 1 month of follow-up, but this effect does not persist, as noted in a study comparing injection, shockwave therapy, and home exercise.⁵² Trochanteric pain improved with corticosteroid injection, with greater relief experienced with higher steroid doses.⁵³

Other Adverse Events

Necrotizing fasciitis has been reported as a complication of injection into the greater trochanteric bursa.⁵⁴

Iliopsoas Bursa Injection

The iliopsoas bursa is the largest bursa in the body and lies between the iliopsoas muscle and the anterior hip capsule (see Fig. 82-8). It is a common but often overlooked cause of groin pain.^55,56 There may be direct communication between the bursa and the joint.

The injection is performed with the patient supine. The needle entry site is just below the inguinal ligament and 1 to 2 cm lateral to the neurovascular bundle (femoral artery pulsation) to avoid needle trauma to the femoral nerve and vessels (see Fig. 82-8). The needle is advanced perpendicular to the skin and advanced until the anterior bone of the acetabulum is contacted. The needle is then withdrawn 3 to 5 mm, and after careful aspiration, medication is injected. If blood is aspirated, or a femoral nerve paresthesia occurs during needle placement, the needle is redirected laterally. Be sure to check the patient for femoral nerve anesthesia before allowing ambulation.

Knee

Technique

Knee injection can be performed by having the patient lie supine, with a rolled towel under the lower thigh to angle the knee. Medial and lateral approaches may be done. Knee bursae are also sometimes injected. For a medial approach, palpate along the medial aspect of the patella from superior to inferior. Identify an indentation at around the 3 o'clock position and mark it for needle entry. The needle is inserted here parallel to the undersurface of the patella. Backpressure should be provided to determine if joint fluid is present and to ensure a blood vessel is not contacted.²⁹

The lateral approach is quite similar, with skin entry at the analogous position laterally. Lateral midpatellar injection (an injection into the patellofemoral joint) was intraarticular 93% of the time and was more accurate than other methods in one study.⁵⁸ A benefit of lateral approach includes avoiding the medial neurovascular bundle.

The anterior approach, easily used with fluoroscopy, uses a needle entry medial and inferior to the patella, and the target is the medial femoral condyle of medial joint compartment.

The prepatellar bursa lies between the patella and the overlying soft tissue. The anserine bursa lies between the medial knee joint and the pes anserinus (tendons of the semitendinous, gracilis, and sartorius muscles) and is found by palpating the area of maximal tenderness over the medial tibial plateau. Prepatellar bursitis and anserine bursitis are common causes of knee pain and respond well to injection. Local injection is rather superficial in each case: the needle is advanced until it contacts bone (Fig. 82-10) and is then withdrawn slightly, and the medication is injected.

Evidence

Common indications for knee injection include OA, Baker's cyst, and pes anserine bursitis. Literature review supports the use of intraarticular corticosteroid injections for RA, OA, and juvenile idiopathic arthritis.⁵⁹ RCTs support the long-term safety of intraarticular steroid injections for patients with symptomatic knee arthritis. No deleterious effects of the long-term administration of steroids on the anatomic structure of the knee were noted in one trial.⁶⁰ Moreover, long-term treatment of knee arthritis with repeated steroid injections appears to be clinically effective for the relief of symptoms of the disease. Studies have demonstrated short-term pain relief and improved periarticular muscle strength in patients after intraarticular corticosteroid injection of a symptomatic rheumatoid joint.⁶¹ Injection can provide short-term relief (2–4 weeks) in patients with symptomatic OA, allowing time for participation in an appropriate rehabilitation program.⁶²

Other Adverse Events

The risk of septic arthritis from intraarticular injections is less than 0.03%.⁶³ Case reports have identified rare but severe adverse events include septic arthritis and osteonecrosis.^64,65

Other Lower Limb

Ankle Injection

The ankle joint may be entered from an anterior approach to the joint between the tibia and the talus. The patient is positioned supine with the leg–foot angle placed at 90 degrees. The point of entry is just medial to the anterior tibial and extensor hallucis longus tendons on a line drawn between the medial and lateral malleoli (Figs. 82-11 and 82-12). These tendons can be easily identified by having the patient dorsiflex the foot and great toe. The needle is advanced directly posteriorly until contacting bone. The needle is then walked inferiorly until it slips between the tibia and talus. A total of 1 to 2 mL of solution is injected. Joints between the tarsal bones are best injected by using fluoroscopic guided injection.⁶⁶

Forefoot Injections

The injection technique for metatarsal, phalangeal, and IP joints is exactly the same as the techniques described for the IP and MCP joints on the hand (see Fig. 82-11). Again, a lateral or dorsal approach is usually favored over the more painful plantar approach.

Spine Joint

The paravertebral spine joints include zygapophyseal or facet joints, sacroiliac joints, and costovertebral joints. The costosternal and sternoclavicular joints are included here for convenience, although they are not spine joints.

Atlantoaxial Joint Injection

The first cervical facet joint, the atlantoaxial or C1 to C2 joint is markedly different from the remaining five cervical facet joints and the cervical–thoracic facet joint. This joint is responsible for at least 50% of axial rotation in the normal cervical spine. Suboccipital pain with rotation of the head to the left or right often is indicative of C1 to C2 joint pathology.

The C1 to C2 joint may be injected using a lateral or posterior approach.^67-70 Because the vertebral artery courses along the lateral edge of the joint, the posterior approach is preferred. The patient is positioned prone on the fluoroscopy table, and the fluoroscopy beam is positioned in a posteroanterior (PA) projection (Fig. 82-13). Because the teeth and jaw frequently project over the upper cervical spine, it is usually necessary to have the patient open the mouth. Once a clear view of the joint is obtained by adjusting the fluoroscopy column, the entry point is marked, sterilized, and anesthetized. Then a 3½-in, 22- or 25-gauge needle is advanced directly toward the joint with the target being the junction of the lateral one third and the medial two thirds of the joint. The needle is advanced to contact the bony edge of the joint at C2. The needle is then walked off the bone into the joint and advanced no more than 1 to 2 mm. Intraarticular placement is confirmed by the injection of 0.25 to 0.5 mL of radiopaque contrast. An appropriate arthrogram should be identifiable (Fig. 82-14), and there should not be any intravascular uptake or neuraxial spread. This is followed by the injection of a mixture of 0.25 mL of anesthetic (1% lidocaine is recommended) and 0.25 mL of corticosteroid. The C2 nerve root runs across the posterior surface of the joint (Fig. 82-15). If a paresthesia is obtained during needle placement, it is advisable to choose a slightly different trajectory. It is usually best to make the initial needle puncture sight slightly more caudad. Potential complications include intravascular injection, spinal axis injection, needle trauma to the nerve root or spinal cord, and vascular injury. Since most injectable corticosteroids are particulate, cerebral embolism is a risk.

Cervical Facet Joint Injection

The C2 to C3 through C6 to C7 joints can be injected using a posterior approach or a lateral approach.^71,72 The posterior approach is safer but technically more difficult because of the marked cephalocaudal angulation of the joints. The lateral approach is technically easier but more risky because the advancing needle can pass through the joint and into the spinal canal. This can be prevented by frequent PA and lateral fluoroscopic views.

For the posterior approach, the patient is prone, and the neck is slightly flexed (see Fig. 82-13). The fluoroscopy column is adjusted to identify the target joint(s). The needle entry site should be marked one level below the target joint. This allows angulation of the needle at an angle that will facilitate entry into the cephalocaudal oriented cervical facet joints. A 3½-in, 22- or 25-gauge needle is advanced into the joint under fluoroscopic guidance. Intraarticular placement is confirmed with PA and lateral fluoroscopy by injecting 0.25 to 0.5 mL of contrast. After proper needle placement is confirmed and following negative aspiration, a mixture of 0.25 mL of anesthetic plus 0.25 to 0.50 mL of corticosteroid is injected.

For the lateral approach, the patient may be positioned prone, lateral, or even supine. Lateral positioning usually is preferred by the patient and is convenient for the physician (Fig. 82-16). The target joint is identified and marked using fluoroscopy. After sterile preparation and local anesthesia, a 1½- to 2½-in, 25-gauge needle is advanced to contact bone at the inferior edge of the joint. The needle is walked off the bone and advanced 2 to 3 mm into the joint (Fig. 82-17). Posteroanterior fluoroscopy is used to confirm that the needle is in the lateral one third of the joint. The needle is withdrawn slightly if the tip is beyond the lateral one third of the joint. Injection is performed as described for the posterior approach.

Complications and side effects from cervical facet blocks include intravascular injection, spinal axis injection, joint trauma, nerve root and spinal cord trauma, infection, and side effects from the injected corticosteroid.

Thoracic Facet Joint Injection

Thoracic facet joint pain is not a common clinical problem. The thoracic facet joints are not as prone to arthritic involvement as are the cervical and lumbar facet joints. The most common cause of thoracic facet pain is trauma. For example, thoracic facets may be a source of pain around a previous compression fracture.

Similar to the lower cervical facets, the thoracic facets have a marked cephalocaudal angulation. The average angle of incline from the horizontal plane is 60 degrees in the midthoracic region. Accordingly, the technique for thoracic facet injection is very similar to the posterior approach to the cervical facet joint.⁷³ The patient is placed prone, and the fluoroscopy tube is angled in order to get the best view of the target joint. The needle entry site is one to two segments below the target joint to allow angulation of the needle to facilitate joint entry (Fig. 82-18A and 82-18B). The remainder of the technique is as described for posterior cervical facet injection.

Costovertebral Joint Injections

The pain related to costovertebral and costotransverse joints usually is unilateral, beginning in a paravertebral location, and often radiates in a bandlike fashion around the thorax.^74,75 The pain is described as aching and burning and is usually worse in the morning. It is also worsened by deep inspiration, coughing, and twisting or rotation of the torso.

The injection is performed with fluoroscopy guidance to minimize the risk of pneumothorax. The patient is placed in the prone position, and the lateral tip of the transverse process of the level in question is identified. The skin is entered just cephalad and lateral to this point, with the needle directed medially. The needle is advanced until contact is made with the vertebral body, which indicates that the needle tip is in the intertransverse space. The needle tip placement is then adjusted cephalad or caudad until it lies within the joint or pierces the articular capsule. At this point, 0.5 to 1 mL of medication is injected.

Pneumothorax is the most feared complication of this block, although the incidence should be low with proper technique and fluoroscopic guidance.

Lumbar Facet Joint Injection

Because of the prevalence of low back pain, lumbar facet injection is one of the most commonly performed pain management procedures. Intraarticular facet injections can be performed for diagnostic or therapeutic purposes.^76–78 Because of the oblique orientation of the lumbar facet joints, especially the lower two levels, it often is helpful to position the patient in a slightly oblique position with the side to be injected rotated up 30 to 45 degrees (Fig. 82-19).

With the patient appropriately positioned, the target joint is identified with fluoroscopic guidance, and the skin is marked. It is best to identify the level by starting at the lumbosacral junction and then working up to the thoracolumbar junction. Lumbosacral anomalies and transitional levels are common. To make communication among practitioners clear, it is important to specify the presence of any abnormalities and how it influences the counting and reporting of the level or levels injected.

The needle is advanced under fluoroscopic guidance toward the target joint until it contacts the bony edge and is then walked off the bone to slip into the facet joint.

In patients with severe OA, the joint space may be narrowed to the point that needle entry is not possible. A periarticular injection can be performed in this situation for therapeutic purposes, but a periarticular injection may be of less diagnostic value. Intraarticular position is confirmed by injecting a tiny amount of contrast. A typical lumbar facet arthrogram is shown in Figure 82-20.

It is not unusual for the facet capsule to have small fenestrations. The injectate may spread to contiguous structures, including the epidural space or intervertebral foramen. It is important to identify such spread during the contrast injection. Figure 82-21 is an example of contrast spreading from the L5 to S1 facet joint to the adjacent S1 nerve root. Arthrography is followed by the diagnostic or therapeutic injection. Typically, 0.25 to 0.50 mL of anesthetic is mixed with 0.25 to 0.50 mL of corticosteroid for each joint.

Complications after facet joint injection are uncommon and include intravascular injection, spinal injection, infection, and needle trauma to the joint or adjacent nerve root.

Sacroiliac Joint Injection

Diagnostic sacroiliac injections are considered an important part of the diagnostic workup for mechanical low back pain because history and physical examination are notoriously unreliable.⁷⁹ Sacroiliac joint injection can be performed with or without the use of fluoroscopy; however, when fluoroscopy is not used, there is a significant rate of failure to enter the joint. Therefore, if the block is being performed for diagnostic reasons, fluoroscopy or computed tomography guidance should be used.

For this injection, the patient is placed in the prone position. The sacroiliac joint is most accessible to injection at the most caudal or inferior portion of the joint.^80,81 Attempts to enter the synovial cavity of the joint at the middle and cranial or superior portions of the joint have a higher failure rate. Using fluoroscopy, or by palpation, the posterior superior iliac spine (PSIS) is identified. The needle entry site is approximately 1 cm below the PSIS (Fig. 82-22A and 82-22B). The needle is simply advanced toward the joint, with needle angle typically 20 to 30 degrees lateral from the sagittal plane (if using AP view). Upon initial entry, the needle will traverse through the thick and tough posterior sacroiliac ligament (Fig. 82-23). The needle must be advanced through this ligament to reach the synovial joint cavity. This joint cavity may be obliterated or replaced by fibrous tissue in some patients. If fluoroscopy is used, 1 to 2 mL of radiopaque contrast can be injected to confirm an intraarticular dye pattern (Fig. 82-24). This is followed by an injection of medication.

Costosternal Joint Injection

Costosternal joint pain can be posttraumatic or inflammatory in nature. The costosternal joints are synovial joints; however, the joint space can be obliterated or replaced by fibrous tissue.

The patient is placed supine, and the affected joint (or joints) is identified by palpation. The joint space is usually identifiable by palpating a groove between the costal cartilage and the sternum. After it is identified, the affected joint is injected with 0.5 to 1.0 mL of local anesthetic or corticosteroid (or both) using a 25-gauge short (e.g., 1-in) needle (see Fig. 82-2).

Sternoclavicular Joint Injection

The patient is placed in the supine position, and the gap between the medial end of the clavicle and the sternum is palpated. The joint is entered with a 25-gauge, 1-in needle, and 1 mL of local anesthetic and/or depot steroid is injected (see Fig. 82-2). There should be little resistance to injection. If resistance is encountered, the needle tip is most likely in the meniscal cartilage and should be withdrawn slightly or repositioned until the injectate flows freely.

If posterior sternoclavicular pain is suspected, the posterior ligament of the sternoclavicular joint may be injected. There are two ways to approach this ligament. With the patient in the supine position, a slightly longer 25-gauge needle may be passed completely through the joint, until ligamentous resistance is felt, and then 1 mL of local anesthetic and/or depot steroid is injected around the ligament. The alternate approach is to enter the skin above the superior aspect of the clavicle and walk the needle off the posterior aspect of the clavicle in a slightly medial direction. Again, the injection is carried out as described earlier.

With both costosternal and sternoclavicular joint injections, care must be taken to have the needle enter the skin perpendicularly in order to diminish the possibility of pneumothorax. With sternoclavicular joint injections, there is also the possibility of puncture of the subclavian artery or vein with a misplaced needle. Careful attention to technique and use of short needles should minimize these complications.

REFERENCES

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INTRODUCTION

The autonomic nervous system (ANS) is a powerful system that has important homeostatic functions. Disorders of this system can lead to many disease states and may contribute to some pain disorders such as complex regional pain syndrome (CRPS). Having a good working knowledge of the anatomy and physiology of the ANS is of paramount importance when considering sympathetic blocks. The higher neural centers in the brainstem, the hypothalamus, and the prefrontal cortex have nerve cells that tightly control the function and the output of the ANS. The ANS is composed of the sympathetic and parasympathetic nervous systems. The parasympathetic outflow has cranial (several cranial nerves), vagal (mainly via the vagus nerve, which innervates many intrathoracic and intraabdominal structures), and sacral outflow that controls the urinary and reproductive organs. The sympathetic nervous system is formed by neurons in the intermediolateral cell column of the thoracolumbar spinal cord. These are in turn modulated by descending autonomic projections from the hypothalamus, the suprachiasmatic nucleus, and the supraparaventricular nucleus.¹ Axons from these neuron cells exit the spinal cord by the anterior spinal roots and white rami communicantes to the sympathetic chain ganglia located along the left and right anterolateral margins of the spinal column. Upon reaching these paravertebral ganglia, the preganglionic sympathetic axons may synapse, pass cephalad or caudad for variable distances within the sympathetic chain before synapsing, or continue uninterrupted to a more distant ganglion or plexus, such as the celiac or hypogastric plexus.

Nerves from the cervical and thoracic ganglia innervate the head and neck and control the blood supply to these structures. The nerves from the thoracic ganglia control the function of the heart and lungs. The nerves that bypass paravertebral sympathetic chain ganglia to more distant ganglia (celiac, hypogastric) are called splanchnic nerves. Splanchnic nerves are the primary sympathetic fibers that innervate visceral organs. Nerves from the lumbar ganglia innervate the legs and control the blood supply to the legs.

The A-δ and C fibers transmit pain and discomfort sensations from the visceral organs to the spinal cord dorsal horn lamina. These fibers develop from the dorsal root ganglion cells and travel along the blood vessels, ganglia, and mesenteric nerves. Hence, blockade of the sympathetic nerves not only causes sympatholysis but also sensory denervation of the abdominal organs.

Kappis originally used paravertebral sympathetic blocks² as treatment for severe pain and visceral pain syndromes. Mandl³ first introduced percutaneous interruption of the sympathetic chain in the early 20th century, and for many years thereafter it was a mainstay therapy for vascular insufficiency of the lower extremities. Sympathetic nervous system blocks may be performed to diagnose sympathetically mediated pain (SMP), to diagnose visceral abdominal pain (by blocking splanchnic afferents), and for short-term benefit in conditions of pathologic vasoconstriction (e.g., Raynaud's disease)⁴ or when sympathectomy can provide therapeutic benefit (e.g., digit reimplantation, limb ischemia). Stellate ganglion block has also been successfully used to treat recurrent ventricular tachycardia.⁵

PATIENT PREPARATION

The patient should not be overly sedated during the procedure because verbal contact with the patient is extremely valuable and is needed to assess the response to the block, especially when the diagnostic phase is to be followed by neurolysis such as celiac neurolysis. Monitoring and intravenous (IV) access should be used. For sympathetic blocks involving the limbs, skin temperature probes are placed bilaterally on the extremities undergoing sympathetic block (Fig. 83-1). The block is considered adequate if cutaneous temperature of the treated limb approaches core temperature.⁶ A careful evaluation of placebo effects, systemic uptake of drug, and blockade of somatic nerves must be performed in patients who have obtained relief after a sympathetic block. As with any invasive procedure, resuscitation equipment and drugs should be readily available. Major contraindications to sympathetic blocks include coagulopathy and patient refusal.

STELLATE GANGLION BLOCKS

ANATOMY

The cervical chain is composed of a superior, middle, and inferior cervical ganglion; the inferior ganglion is fused with the first thoracic ganglion, resulting in a “starlike” (stellate) appearance. It receives preganglionic sympathetic fibers via white rami communicantes from the intermediolateral cell column of T1 to T6 in the spinal cord. It is an oval-shaped structure approximately 2 cm long, 1 cm wide, and about 0.5 cm thick. The ganglion lies anterior to the transverse process of C7 and extends along the C7 to T1 interspace. It is bound inferiorly by the dome of the pleura, posteromedially by the longus colli muscle and laterally by the scalene muscles. It is also bound anteriorly in part by the subclavian artery and posteriorly by the transverse processes of C7 and T1 (Figs. 83-2 and 83-3). The prevertebral fascia, which originates posterior to the sympathetic chain in the cervical region, is pierced by the chain around C7 and becomes anterior to the stellate ganglion as the fascia forms a transition from the neck to the chest. Superior to the stellate ganglion is the transverse process of the sixth cervical vertebrae, or Chassaignac's tubercle, a prominence that is easily palpable along the paratracheal region of the neck (Figs. 83-4 and 83-5).

One must remember that although Chassaignac's tubercle is the major landmark for performing the anterior paratracheal block of the stellate ganglion, the location of the ganglion itself is inferior to the tubercle. Interestingly enough, ultrasonography and magnetic resonance imaging studies suggest that local anesthetic spread to the ganglion does not occur; rather, the spread occurs anterior to the ganglion.^7,8 Other radiographic and injection studies have supported this finding as well.^9-12 This anterior spread likely relates to prevertebral fascia being in the same plane as Chassaignac's tubercle at the C6 vertebra but then becomes more anterior at the stellate ganglion, thus preventing the spread of injectate onto the ganglion. The presence of this fascia also promotes mediastinal and even contralateral spread of injectate.⁸ Therefore, sympathetic neural blockade during stellate ganglion block may take place at sites other than the stellate ganglion.

INDICATIONS

The stellate ganglion block is used to diagnose facial and upper extremity SMP. It may be repeated as a therapeutic measure when prolonged pain relief response lasting several weeks is seen. This period may then be helpful to facilitate physiotherapy and desensitization. A positive response with pain relief in CRPS may also predict a favorable response to spinal cord stimulation.¹³ Other indications include circulatory insufficiency such as Raynaud's disease (short-term improvement), thromboembolic or vasospastic event, or conditions in which sympatholysis is highly desirable (e.g., digit reimplantation surgery).

TECHNIQUE

The block may be performed under fluoroscopic control or with ultrasound guidance with all sterile precautions.

With fluoroscopic assistance, the junction of the transverse process with the vertebral body (C6 or C7) is visualized. The patient is placed in supine position, and an IV line is started. Standard monitors are placed. A 3.5-in, 25-gauge needle is advanced to the junction of the transverse process with the vertebral body and then slightly withdrawn (Fig. 83-6). Under real-time fluoroscopy 1 to 5 mL of contrast agent is injected, and linear spread of the agent along the gutter confirms adequate placement. A total of 5 mL of local anesthetic without epinephrine is deposited there, and the needle is withdrawn. Because of the risk of particulate steroid embolization causing infarction, no adjuvant particulate steroid should be used. The amount of contrast agent and local anesthetic injected is determined by the spread.

Gofeld et al. describe ultrasound-guided stellate ganglion block based on cadaver studies.¹⁴ When using ultrasound guidance, Chassaignac's tubercle is identified by its characteristic shadow, and the transverse process at this level is clearly identified (Fig. 83-4). The transducer is translated inferiorly to assess if the C7 transverse process can be identified (Fig. 83-2). Injection at lower level will be in closer proximity to the stellate ganglion. When the transverse process is clearly identified, the longus colli muscle is seen overlying this and underlying the carotid artery. A 3.5-in, 25-gauge needle is advanced to this point in an in-plane approach. Thereafter, 5 to 6 mL of local anesthetic without additional epinephrine is injected, making sure it is underlying the prevertebral fascia. As with fluoroscopic guidance, because of the risk of particulate steroid embolization causing infarction, no adjuvant particulate steroid should be used.

Evaluation for the presence of sympathectomy must be performed. Although a Horner's sign (ipsilateral ptosis, miosis, anhydrosis, and conjunctival engorgement) is indicative of a sympathectomy of the head and face, it in no way suggests a sympathectomy of the arm and hand. Skin surface temperature probes placed bilaterally at the palmar thenar regions are simple yet effective. A 1.0° to 1.5°C increase in the blocked side or, perhaps more specifically, an increase in temperature toward core temperature that exceeds that of the contralateral side^15,16 is strongly suggestive of a successful sympathetic block of the arm. Somatic block of the arm must also be ruled out.

COMPLICATIONS

Minor complications are common. Because of the proximity of laryngeal nerves to the stellate ganglion, dysphagia and hoarseness are common with the anterior approach. Transient central nervous system events such as seizures, aphasia, blindness, loss of consciousness, and hemiparesis can occur after injected doses as low as 15 mg of lidocaine or 2.5 mg of bupivacaine.^17-21 Other complications include pneumothorax and seizure (vertebral artery injection). The incidence of complications can be reduced by using lower volumes, meticulous technique, aspiration before injection, and slow injection. Appropriate resuscitation equipment should be readily available and used as the clinical scenario dictates. Use of ultrasound guidance might further help reduce the complications because the needle and the target are well visualized.

CELIAC PLEXUS AND SPLANCHNIC NERVE BLOCKS

ANATOMY

The celiac plexus is a dense matrix of diffuse nerve fibers and ganglia located around the abdominal aorta and periaortic space at the level of the T12 and L1 vertebrae. The most distinct feature of the celiac plexus are the paired semilunar (“celiac”) ganglia that lie immediately superior to the pancreas in the midline and are flanked in close approximation by the adrenals. These “paired” ganglia can actually vary in number and size.²² The aorta is surrounded by the plexus, which makes this large vascular structure an important landmark in performing the block. In fact, transgression of the aorta has been used in identifying needle placement.²³ In addition to the celiac ganglia, the components of the celiac plexus include the greater, lesser, and least (also called lowest) splanchnic nerves; there are also contributions from the aorticorenal ganglia and aortic and superior hypogastric plexus. It is important to realize that the celiac plexus is not a distinct entity but a diffuse network that varies in size, network, and position. The most consistent landmark is the celiac artery because these elements intertwine around the base of this artery (Fig. 83-7).

There are sympathetic, parasympathetic, and visceral afferent contributions to the celiac plexus. The sympathetic fibers originate from the thoracic sympathetic chain via the greater and lesser splanchnic nerves, and the visceral afferents have cell bodies that originate from the dorsal root ganglion of the spinal cord and travel with the sympathetic nerves. The parasympathetics originate from the vagus nerve. The nerves of the celiac plexus innervate most of the abdominal viscera to include the pancreas, liver, kidneys, biliary tract, spleen, adrenals, intestines, and omentum.

INDICATIONS

The celiac plexus block is indicated for patients in pain from upper abdominal tumors such as pancreatic cancer. Pain relief rates vary from 70% to 100%, with an average of 85% of patients that experience at least temporary pain relief.^24,25 Pain from these tumors can be severe, and opioid therapy is often limited by the sedation and constipation that accompany the high doses required to manage the patient's discomfort. Neurolytic celiac plexus blocks in these patients can provide superior pain relief for up to 3 to 4 months. In most patients, relief will be immediate and effective. Furthermore, they can lessen the severity of opioid-induced side effects by decreasing requirements of these drugs. Gastrointestinal (GI) motility is also improved by the sympathectomy caused by the block. The predictive value of a neurolytic celiac plexus block can be determined by the degree of tumor invasion. Akhan et al.²⁶ found that the grade of tumor as measured by invasion of periaortic and paracaval fat planes was a good predictor for successful neurolytic celiac plexus block. More than 50% invasion of the fat planes correlated with little pain relief. Age and history of laparotomy, chemotherapy, or radiation therapy have not been shown to decrease the efficacy of neurolytic celiac plexus blocks.

Benign conditions such as acute and chronic pancreatitis may also respond to celiac plexus blocks. As with pancreatic cancer patients, acute pancreatitis is often resistant to opioid therapy; furthermore, the disease process may be improved by decreasing the ductal and sphincter spasm thought to be associated with acute pancreatitis. Addition of steroids to the local anesthetic injectate has been shown to decrease the severity of the attack,²⁷ but use of particulate steroids is no longer advisable given the embolic risk if intraarterial uptake occurs in this sensitive location. Continuous catheter techniques can be effective in chronic alcoholic patients diagnosed with acute pancreatitis who were previously unresponsive to epidural analgesia. Rykowski et al.²⁸ used 0.5% bupivacaine, 20 mL every 6 to 12 hours as intermittent injection, or 0.5% bupivacaine at 6 mL/hr with good results. Overall, celiac plexus blocks have shown to be an effective adjunct in managing chronic pancreatitis pain.²⁹ Using celiac plexus blocks, especially neurolytic celiac plexus blocks in chronic pancreatitis, is however controversial. Although 4 to 6 months of relief can be obtained from neurolytic celiac plexus blocks, a subset of alcoholic patients may view their pain-free state as an opportunity to resume the consumption of alcoholic beverages. Furthermore, because this block also interrupts the visceral afferents from abdominal organs, it may mask pain related to intraabdominal emergencies. Given the chronic recurrent nature of chronic pancreatitis and associated morbidities, including the psychological effects of pain, central sensitization, and the availability of other modalities (medications, epidural), celiac plexus block is now rarely used for acute pain control in chronic pancreatitis. Given the short-lasting benefit from neurolysis, this also is not an effective strategy for the management of pain in these patients.

TECHNIQUE

A variety of techniques can be used to approach the splanchnic nerves or celiac plexus. In general, they can be summarized as posterior or anterior approaches. The posterolateral approach has become the most practiced and proven technique by anesthesiologists, whereas the anterior techniques using computed tomography (CT) or ultrasound guidance are preferred by invasive radiologists. In recent years, endoscopic ultrasound guided celiac plexus neurolysis has become increasingly prevalent.³⁰ In all cases, noninvasive monitoring should be used, and an IV line should be established. IV vasoactive agents, volume expanders (crystalloid or colloids), and sedative and analgesics should be made available for use as needed. Procedure is performed with sterile precautions and resuscitation equipment available. The fragile condition of some of these patients should be taken into account.

Posterolateral Approaches

Posterolateral techniques allow access to both the splanchnic nerves and the celiac plexus. The posterolateral approach is one originally defined by Kappis and refined by Moore.³¹ Frequently used variations of the posterolateral approach include the transcrural approach, the transaortic approach, and the retrocrural or deep splanchnic approach.

The patient is placed in a prone position with a pillow placed at the midsection of the abdomen. This minimizes the lumbar lordosis and aids in patient comfort. Occasionally, the abdominal pain can be so severe that the prone position is not tolerated, and analgesics must be used or the patient must be positioned in the lateral decubitus position. The arms are underneath behind the head or allowed to hang off the table. An IV line is placed to provide light sedation if necessary, and a 200- to 500-mL crystalloid bolus may be administered depending on patient condition, to offset the sympathectomy-induced hypotension caused by the block. Anatomic landmarks are identified and marked in ink. Agents typically used for the celiac plexus block include 0.25% to 0.5% bupivacaine, 6% to 10% phenol, and 50% to 100% alcohol. Volumes are described for each technique (see the following sections).

The classic posterior approach is a two-needle technique; needle placement is similar for both sides. The needle is placed under radiologic control. The oblique fluoroscopic projection is used so that the tip of the L1 transverse overlies the vertebral body. The insertion points lie 6 to 9 cm from the midline and usually correspond to the junction of the paraspinal muscles and the 12th rib. After administering local anesthetic to create a skin wheal at this point, a 12- to 20-cm, 20- to 22-gauge subarachnoid needle is inserted percutaneously The needle is inserted in a coaxial approach. The needle may be “walked off” the lumbar body or placed directly sliding adjacent to the vertebral body. The final placement of the needle tip is 1.0 to 1.5 cm anterior to the vertebral margin. The needle pulsation occurs on the left side because the final position of the needle tip is often close to the aorta. The second needle is placed on the right side using the same technique as the first; depth is guided by the final needle depth used on the left side. Contrast agent is seen on fluoroscopy will indicate retrocrural, transcrural, transaortic, or intradiaphragmatic injection of agent (Figs. 83-8 and 83-9). If CT imaging is used, needle paths are traced from the skin to the celiac plexus to avoid injury to renal or vascular structures.

For the transcrural approach, advancing the needle tips an additional 1 to 2 cm will pierce the diaphragmatic crus and place the needle tip anterior to the diaphragm. A loss of resistance is usually felt as the crus is pierced. The anteroposterior (AP) and lateral radiographs with contrast will show a linear spread in the left lateral preaortic area. If contrast spread is predominately cephalad and appears to collect around the L1 vertebral body, the needle tip is likely to be retrocrural. Lateral radiographs can confirm that the contrast is posterior and superior to the diaphragm, also suggesting retrocrural spread. The procedure can then be performed as a deep splanchnic nerve block (see later section), or the needle is advanced to pierce the diaphragmatic crus (thus transcrural). If muscle striations are seen following contrast injection, the needle tip is likely contained within diaphragmatic muscle and should be advanced about 1 cm. On lateral fluoroscopy, contrast agent is typically seen to spread in a craniocaudal direction anterior to the vertebral body, but agent spread is limited to below the diaphragm (Fig. 83-8B). After negative aspiration of each needle, 10 mL of local anesthetic is injected through each needle. The patient is watched for more than 10 minutes for pain relief and to rule out somatic nerve block. If neurolysis is planned, then 10 to 25 mL of local anesthetic or neurolytic agent is injected through each needle in divided doses.

The transaortic approach is a single needle, left-sided technique that is also transcrural.²³ The intent of this approach is to pierce the aorta with the needle to ensure that the needle tip is anterior to the aorta. Placement of the injectate anterior to the aorta can minimize the risk of neurologic complications caused by unintended spread of neurolytic agents to the lumbar plexus. Needle placement is the same as for the transcrural approach, but the needle is advanced until aortic wall penetration occurs and free-flowing blood is aspirated. The needle is then advanced further through the anterior wall of the aorta until no blood is aspirated.

A 5-mL loss of resistance syringe filled with saline can be used to identify anterior aortic wall penetration. Once blood is aspirated through the block needle, the loss of resistance syringe is attached to the needle, and constant pressure is applied to the syringe plunger. A resistance to injection will be felt when the anterior aortic wall has been contacted followed by loss of resistance once the needle tip has entered the anterior periaortic space. After negative aspiration, contrast agent is injected and will appear anterior to the vertebral bodies (Figs. 83-8C and 83-9A). Local anesthetic, steroid, or neurolytic agent is then injected. A smaller total volume of agent (12–15 mL) is used for this technique.

Anterior Approach

With the anterior approach, a 12- to 15-cm, 22-gauge needle is passed through the midline epigastrium until the body of L1 is contacted. The needle is then withdrawn 1.0 to 1.5 cm, and placement is confirmed using fluoroscopy or CT imaging.^32,33 Patient comfort is a major advantage to this approach, especially when the patient is unable to lie prone. Only one needle is used with this technique, so there is less pain from posterior two-needle approaches. Furthermore, the risk of needle-related injury to motor nerves is significantly reduced compared with posterior approaches.

Splanchnic Nerve Blocks

An alternative technique to achieve abdominal sympathectomy and visceral nerve block is the splanchnic nerve block. The splanchnic nerve block specifically interrupts the sympathetic input to the celiac plexus without blocking the abdominal parasympathetics. The final position of the needle tip is superior to the diaphragm; the intention is to block the greater, lesser, and least splanchnic nerves before they traverse the diaphragm into the abdomen. The advantages of performing sympathectomy and visceral nerve block are multifold. GI motility is improved compared with the celiac plexus block because the parasympathetics (which join the splanchnics at the level of the celiac ganglia) are left unopposed. Also, because the lumbar sympathetics are not blocked by this technique, hypotension is decreased. Last, with the classic splanchnic nerve block, a smaller volume of local anesthetic or neurolytic agent can be used.

For the deep splanchnic approach^34,35 (also known as the retrocrural celiac plexus block), landmarks and needle approach are similar to the transcrural celiac plexus block. The needle is walked off the vertebral body and advanced until the needle pulsates (because of the proximity of the needle tip to the aorta) on visual inspection and tactile analysis. When the block is performed correctly, 3- to 5-mL injection of contrast will remain within the retrocrural space and migrate primarily cephalad (Figs. 83-8A and 83-9B). On fluoroscopic AP view, the contrast will be confined along the lateral border to the L1 vertebral body. On lateral view, layering of the contrast in a narrow line along the anterior vertebral column should be seen. The procedure is then repeated on the right side. Fifteen milliliters of local anesthetic or neurolytic agent is injected through each needle. Parasympathetics and the lumbar sympathetic chain are not blocked with this technique.

The classic splanchnic nerve block is performed in a manner similar to the deep splanchnic approach, but the needle is directed toward the anterolateral margin of T12 vertebral body. Radiographic contrast patterns are similar to the deep splanchnic nerve block. The disadvantages of this block relate to final position of the needle tips; compared with the transcrural and transaortic blocks, the needle tips lie posterior and cephalad to the diaphragm, which increases the risk of chylothorax and pneumothorax (Fig. 83-10).

COMPLICATIONS

The incidence of major complications with neurolytic celiac plexus blocks is 0.15% to 1.0%.^36,37 These complications typically occur from transgression of structures during needle placement or unintentional spread of neurolytic or local anesthetic solutions. Inadvertent injury to structures can result in pneumothorax, chylothorax (secondary to thoracic duct injury), genitourinary injury, somatic nerve injury, and retroperitoneal hematoma; complications secondary to inadvertent spread of agent include sexual dysfunction, groin neuralgia, paraplegia, retroperitoneal fibrosis after repeated neurolytic blocks,³⁸ and pleural effusion.³⁹ Complications are often self-limited. In a study of 136 cases after celiac plexus block, Brown et al. describe two cases of pneumothorax, neither requiring thoracostomy as therapy.²⁵ Renal perforation can occur, albeit typically without sequelae, especially if the block needles are placed more than 7.5 cm from the midline. When inserted lateral to this point, renal impalement can occur in 10% of cases.⁴⁰ Paraplegia has been described secondary to injury to the artery of Adamkiewicz during block placement⁴¹ and from arterial vasospasm causing anterior spinal artery syndrome.⁴² Paraplegia can also occur from incorrect needle placement and subsequent injection in the subarachnoid or epidural space or from intrapsoas muscle injection with blockade or neurolysis of the lumbar plexus. Radiographic imaging (biplanar fluoroscopy or CT) can minimize these risks.

Minor sequelae inherent to the celiac plexus block are relatively common. The most common side effects of the block include local pain (96%), hypotension (38%), and diarrhea (44%).³⁶ Systolic blood pressure decreases of 30 to 40 mm Hg are not uncommon and are usually seen when the patient assumes an upright or sitting position after celiac plexus block. The hypotension is caused by blood pooling in the splanchnic vessels after sympathectomy; this can be minimized by an IV fluid bolus at the time of block placement. Compensatory reflexes usually appear by 48 hours. Diarrhea is thought to be caused by unopposed parasympathetic activity; impairment of α-adrenergic stimulation to enterocytes that increase intestinal secretory activity as well as decrease absorptive processes may also play a role. Intractable diarrhea may respond to clonidine patches or to octreotide 0.1 mg subcutaneously twice a day.^43,44 The increase in GI activity can be used in a therapeutic manner. Weinstabl et al. used bupivacaine celiac plexus blocks to reduce the intestinal dysfunction (as measured by decreased gastric volumes) in several patients in a neurosurgical intensive care unit.⁴⁵ Nausea and vomiting can occur from the hypotension caused by the block or from alcohol intoxication when excessive amounts of neurolytic alcohol are absorbed at the block site. Chest pain can also occur after celiac alcohol block. It usually resolves within 1 hour.⁴⁶

SUPERIOR HYPOGASTRIC PLEXUS BLOCKS

ANATOMY

The superior hypogastric plexus is a retroperitoneal structure located bilaterally between the level of the lower third of the fifth lumbar vertebral body and the upper third of the sacral promontory; it is inferior to the bifurcation of the abdominal aorta and in proximity to the bifurcation of the common iliac vessels (Fig. 83-11). The superior hypogastric plexus along with the left and right inferior hypogastric plexus and the pelvic plexus comprise the hypogastric plexus; this network provides innervation to the pelvic viscera. The superior hypogastric plexus receives postganglionic sympathetic contributions from the inferior mesenteric ganglion and from the hypogastric nerves (lumbar splanchnics) that course along with the abdominal aorta.⁴⁷ Parasympathetic innervation arises from the second, third, and fourth sacral segments and contributes to the plexus via the pelvic nerve. Finally, visceral afferents from the pelvic organs course through the hypogastric plexus and enter the spinal cord via the L1 or L2 spinal nerve roots or via the sacral segments S2, S3, or S4. Pelvic organs innervated by the hypogastric plexus include the rectum, bladder, perineum, prostate, and uterus. Pain associated with these ganglia will often cause patients to complain of pain in the lower abdominal wall around the pubic region.

INDICATIONS

Pelvic pain secondary to neoplasm can be successfully managed by superior hypogastric plexus blocks. Lee et al. reported that surgical interruption of the hypogastric plexus (presacral neurectomy) can provide pain relief in various malignant and nonmalignant painful conditions.^48,49 Plancarte et al. then devised a reliable means to percutaneously block nerves in this region.⁵⁰ They showed that in patients with advanced pelvic neoplasms (to include cervical, prostate, and testicular cancers), pain scores are reduced up to 90% using superior hypogastric plexus blocks and nonopioid analgesics. As with other block techniques, the superior hypogastric plexus block is performed using local anesthetic to determine efficacy and then repeated as needed using a neurolytic agent.

TECHNIQUE

The patient is placed in the prone position with a pillow beneath the lower abdomen and hip to reduce the lumbosacral lordosis. This region is then prepared and draped in sterile fashion, and fluoroscopy is used to identify the L4 to L5 interspace. Oblique fluoroscopy with cranial tilt is used to visualize the anterolateral margin of vertebral body and this entry point is marked on the skin and a skin wheal raised. A 15- to 20-cm, 22-gauge needle is inserted through one of these skin wheals, and the needle advances in a caudad fashion medial to the iliac crest and inferior to the L5 transverse process and walked off the L5 vertebral body. Advancing the tip 1 cm past the vertebral body may result in a loss of resistance or “pop,” suggesting that the needle tip has traversed the anterior fascia of the psoas muscle. This typically occurs at a depth of 8 to 12 cm. A second block needle is inserted on the opposite side to the first, and the angles of entry and the depth of the first needle are then used as a guide. Needle tip placement is confirmed by using 3 to 5 mL of water-soluble contrast dye and fluoroscopy. On the lateral view, the dye is seen to spread in a smooth contour anterior to the L5 vertebral body and sacral promontory; on the AP view, the contrast medium should be confined to the midline (Fig. 83-12). Eight to ten milliliters of 0.25% bupivacaine or 1% lidocaine is injected through each needle. Six to eight milliliters of aqueous 10% phenol should be injected through each needle if neurolysis is desired.

Variations to the above technique include a single-needle approach, a transdiscal approach, and a transarterial approach. A single-needle approach follows the same technique as that described earlier; however, only one needle is placed, and a larger volume (20–30 mL) of local anesthetic is used. A transdiscal approach is another single-needle approach.⁵¹ Occasionally, the needle trajectory results in needle passage through part of the L5 to S1 disc; when this occurs, the final position of the needle tip is very close to the anterior border of the disc. Confirmation of needle placement with contrast agent is performed. A discogram is seen if the needle tip remains in the intervertebral disc. When the appropriate contrast pattern is achieved, a smaller volume of local anesthetic or neurolytic solution (10–15 mL) is then used. The transarterial approach is used when arterial blood is aspirated from the block needle. Aspirated blood suggests that the needle has inadvertently entered the iliac artery. The needle is then advanced until blood can no longer be aspirated. Because the iliac arteries are retroperitoneal and are in the same tissue plane as the superior hypogastric plexus, a loss of resistance technique (similar to the transaortic celiac plexus block) can then be used to confirm that the needle tip has traversed the anterior wall of the artery. Contrast dye followed by local anesthetic or neurolytic agent is then injected.

COMPLICATIONS

Complications are rarely serious and include hematoma from puncture of the iliac vessels, back pain and spasm from needle trauma, and intramuscular or intraperitoneal injection of local anesthetic or neurolytic solution. Other complications include inadvertent somatic block from subarachnoid or epidural injection, somatic nerve injury, and ureteral or renal puncture. According to Racz, if neurolytics are used, phenol at concentrations less than 6% should be used to minimize ureteral injury. He also notes that his experience in men is limited to unilateral blocks and recommends that bilateral neurolytic blocks in men should not be performed because of the possibility of sexual dysfunction.⁵² Proper technique with the use of fluoroscopy should negate these risks.

LUMBAR SYMPATHETIC BLOCKS

ANATOMY

The lumbar sympathetic chain is easily blocked with few complications compared with other levels of the sympathetic chain. This is primarily because of the consistent position of the chain next to the lumbar vertebrae as well as its relative separation from somatic nerves. When the sympathetic trunk extends into the abdomen, it assumes a prevertebral position compared with the paravertebral position occupied in the thorax. On the right side, it lies posterior to the inferior vena cava, and on the left side, it lies lateral and slightly behind the abdominal aorta. The lumbar sympathetic chain consists of several ganglia (average three per side) between the L1 and L5 vertebral bodies.⁵³ The ganglia are most frequently found at the level of the lower third of the second lumbar vertebra to the middle third of the third vertebra on both the right and left sides.^53,54 Most importantly, the psoas muscle always lies posterior to the sympathetic chain, thus separating the chain from the lumbar somatic roots. This separation of the sympathetic chain from the somatic lumbar plexus minimizes the spread of local anesthetic or neurolytic agent to these nerves during percutaneous lumbar sympathetic blocks. As a result, the untoward side effects are minimal and infrequent.

INDICATIONS

The common indications for lumbar sympathetic blocks are to diagnose SMP (CRPS) and vascular insufficiency. If the pain is relieved in a prolonged fashion, then this block may be repeated with the recurrence of pain. Pain relief with sympathectomy may also bode well for spinal cord stimulation therapy.¹³ In the past, means to achieve prolonged sympathetic blockade included the use of neurolytic agents⁵⁵ and radiofrequency lesioning,⁵⁶ but these practices have now fallen out of favor. It is important to ensure that sympathectomy therapy of the lower (and upper) extremity is complemented by aggressive physical therapy to optimize treatment success.

TECHNIQUE

The classic lumbar sympathetic block is performed by placing a needle at the anterolateral border of the L2, L3, and L4 vertebral bodies or higher volume deposited at one location, L2 or L3 (in case of foot) (Fig. 83-13). Patient positioning is similar to that used in the posterolateral approach to the celiac plexus block. The patient is placed prone with a pillow beneath the lower abdomen and hip. Oblique fluoroscopy is used to determine the entry point. The L2 or L3 transverse process tip is made to overlie the edge of the vertebral body. A local anesthetic skin wheal is raised at the entry point. A 15-cm, 22-gauge needle is advanced directly toward the anterolateral aspect of the vertebral body. Once the needle tip is positioned along the anterolateral aspect of the selected vertebral body, the needle is aspirated for cerebrospinal fluid or blood. Contrast agent (1–5 mL) is then injected and a characteristic longitudinal spread of contrast dye can be seen. Injected contrast will appear striated and spread in a diagonal pattern if the needle tip is in the psoas muscle; a “psoas stripe” can be seen. This is easily corrected by advancing the needle tip an additional 0.5 to 1.0 cm; injection of contrast is then repeated. The appropriate spread is in a craniocaudal direction and appears rather thin when seen in a lateral view with fluoroscopy. A 2-mL test dose of 1% lidocaine or 0.25% bupivacaine is injected, and the patient is evaluated for untoward side effects. About 5 mL of local anesthetic is then injected through the needle; the procedure is then repeated at the other two (L3 and L4) lumbar sites.

Alternatively, a single-injection technique can be performed using the same approach except that when the appropriate depth is obtained, a larger volume (10–20 mL) of local anesthetic is injected.⁵⁷ Because the ganglia are most often found at the lower portion of the second lumbar vertebral body to the middle of the third vertebral body, this area becomes the most favorable when using a single-needle technique. The advantage of a single-needle technique is decreased postprocedure pain and muscle spasm as a result of less needle trauma through the paraspinal and psoas muscles^53,54 A paradiscal, extraforaminal approach based on cadaveric study has also been described.⁵⁸

COMPLICATIONS

Serious complications are rare and are minimized with the use of radiographic imaging. The most common sequela is backache, typically related to needle trauma that usually responds to conservative therapy such as short-term oral opioids, nonsteroidal anti-inflammatory drugs, or ice and heat therapy. Somatic nerve block can occur from inadvertent injection of local anesthetic into the psoas muscle (psoas compartment block); it can also occur after posterior spread of local anesthetic along tendinous arches that bridge the concave sides of the lumbar vertebrae, thus blocking somatic nerves roots.⁵⁹ Hematuria occasionally occurs from needle puncture of the kidney or ureter. Although this finding usually resolves spontaneously after 2 to 3 days, the hematuria can be very distressing to the patient. Kidney puncture is avoided by limiting injections to below the L2 vertebral body.⁶⁰

Genitofemoral neuralgia occurs with an incidence of approximately 20% after fluoroscopically guided neurolytic lumbar sympathetic block.⁵⁰ This incidence is decreased by using smaller volumes of neurolytic agent (thus minimizing the spread of agent to the genitofemoral nerve) and injecting cranial to the L4 vertebral body.⁶¹ The symptoms consist of a burning dysesthesia in the anteromedial area of the upper thigh; the pain is frequently severe and can last 6 to 8 weeks but is usually controlled with neuropathic pain medications.⁶²

Because incidental genitofemoral nerve block is common, it is important to consider whether the pain syndrome in question unsuspectingly involves the genitofemoral nerve or the L1 nerve root. A “diagnostic” lumbar sympathetic block that unintentionally blocks the genitofemoral nerve may yield the false diagnosis that the pain syndrome was sympathetically maintained. Such a situation may exist when a somatic pain syndrome is present in the genitofemoral or anterior thigh area and the following sequence occurs: a lumbar sympathetic block is performed to diagnose SMP, an unintentional genitofemoral nerve block occurs that then alleviates the somatic pain, and the syndrome is incorrectly identified as involving sympathetic elements. Performing a sympathetic block at L2 may avoid this scenario by preferentially sparing the genitofemoral nerve.⁶¹

Other complications occur from inadvertent needle placement. Needle entry into the dural cuff of a somatic nerve can result in an epidural or subarachnoid block.⁶³ A case report of retroperitoneal hemorrhage has also been described with paravertebral blocks.⁶⁴

ALTERNATIVES FOR REGIONAL SYMPATHETIC BLOCKS

Certain conditions preclude pain specialists from using regional sympathetic blocks. These include coagulopathy, infection, and postsurgical changes in the region of interest (e.g., radical neck surgery or aortic graft placement). Alternatives to regional sympathetic blocks include peripheral nerve or plexus blocks and epidural administration of local anesthetic. Other options to nerve blocks include regional or systemic IV techniques, oral therapy, and surgical sympathectomy.

Even in the absence of contraindications, epidural block and peripheral nerve blocks (e.g., brachial plexus blocks) may be better options when prolonged sympathectomy is desired (e.g., digit reimplantation), and there is a lot more experience in using infusions in these locations.⁶⁵

Intravenous regional sympathetic blocks have been performed using guanethidine, bretylium, and reserpine. Complications of IV regional sympathectomy include transient syncopal episodes with apnea,⁶⁶ orthostatic hypotension, pain with administration, nausea, and vomiting.

Varying success rates have been reported with these agents; as a result, the use of IV regional sympathectomy is somewhat controversial.^67–72 In 1983, Bonelli et al. reported that in patients with reflex sympathetic dystrophy, IV regional guanethidine blocks provided comparable pain relief with a longer duration to stellate ganglion block therapy.⁷⁰ In a 10-year follow-up study of neuralgia in the hand, Wahren and colleagues noted that guanethidine therapy can provide 2 weeks to 6 months of prolonged pain relief.⁷¹

Hord et al. showed in a double-blind, randomized trial that IV regional bretylium also provided effective analgesia of reflex sympathetic dystrophy; however, a review of their data reveal that only a 30% improvement of pain relief was considered significant.⁷³ In contrast, randomized, double-blind studies evaluating the use of guanethidine^72,74 and reserpine⁷⁴ did not show any improvement in pain scores compared with IV regional therapy with placebo. A mechanism of tourniquet-induced analgesia may play a role.⁷⁴

Phentolamine infusion has gained some popularity as an alternative to diagnosing sympathetically maintained CRPS.^75,76 Incremental dosing of IV phentolamine to supine patients under a monitored setting can be safely performed⁷⁷; the total dose given over 30 to 60 minutes is 0.5 to 1.0 mg/kg. IV phentolamine can help determine responsiveness to the oral α-adrenergic blocking agents such as phenoxybenzamine. Pain relief of at least 50% or untoward effects such as hypotension, dizziness, or headache are the usual end points to this diagnostic test. Complications are rare and typically self-limited and include sinus tachycardia, premature ventricular beats, or wheezing.

Infusions to diagnose and treat SMP are now infrequently used and are more of historical significance.

NEUROLYTIC AGENTS

Neurolytic agents are used to provide long-term pain relief. Before injecting a neurolytic agent, a local anesthetic test block is useful to assess the feasibility of a “permanent” block. It should be noted, however, that a successful test block does not always predict the outcome of a neurolytic celiac plexus block.

Alcohol and phenol are the two neurolytic agents most commonly used. Alcohol is used in concentrations from 50% to 100%. The mechanism of neurolysis is via extraction of cholesterol and phospholipid from neural membranes. There is also precipitation of lipoproteins and mucoproteins. Alcohol probably provides more intense nerve destruction than phenol. Alcohol diffuses more rapidly through biological tissue, thereby increasing the degree of somatic nerve damage. Of note, although no controlled studies comparing the two agents exist, there may be an increased incidence of L1 neuralgia during lumbar sympathetic block when alcohol is used versus phenol.⁵⁵ Sedation, dysphoria, and nausea and vomiting can occur from excessive systemic absorption of injected alcohol. The plasma alcohol level can be measured, but levels are highly variable and depend on concentration, volume, and the metabolic rate of the patient. Phenol is usually used in concentrations of 6% to 10%. Phenol causes protein coagulation and necrosis of nerves. The higher concentrations of phenol must be made soluble in a glycerin base; as a result, the heavier viscosity makes it difficult to inject. The primary advantage of phenol is its inherent local anesthetic effect, which precludes pain on injection; in contrast, alcohol typically causes a severe, transient pain on injection. Phenol has a slower onset of action, is less efficacious, and is of shorter duration than alcohol.

REFERENCES

INTRODUCTION

The peripheral nervous system consists of numerous individual nerves, nerve trunks, nerve plexuses, and ganglia. This chapter discusses the blockade of somatic peripheral nerves. The sympathetic and visceral nerve blocks are discussed separately. The blockade of peripheral somatic nerves is the hallmark of regional anesthesia. This may be done for the facilitation of surgery as a sole technique or in combination with general anesthesia. Peripheral nerve blocks can be continued into the postoperative period via infusion through catheters for the purpose of continued postoperative pain relief. Excellent perioperative analgesia may help reduce the possibility of development of chronic pain.^1,2 Additionally, some evidence indicates that regional anesthesia may have a role in reducing the recurrence of disease in patients undergoing oncologic surgery.³

In the field of chronic pain management, peripheral nerve blocks are useful in the diagnosis of pain conditions. At times these may provide pain relief beyond the duration of the local anesthetic itself and hence serve a therapeutic purpose.⁴ Various adjuvants such as clonidine, steroids, and vasoconstrictors may be added to the local anesthetic to prolong the duration of the nerve block. In some select circumstances, once the pain generating nerve is identified, neurolysis of the nerve via chemical or thermal techniques can be done. Chemical neurolysis is often done with alcohol or phenol, and in general, use of these agents is reserved for patients with terminal illness because of the risk of recurrent pain that may be worse, as well as the risk of permanent neurologic sequelae. Thermal techniques such as medial branch thermal neurotomy and cryoablation of neuromas are useful in the management of chronic pain.⁵

Historically, peripheral nerve blocks were often performed as a blind technique using surface anatomy landmarks, as well as feel. The introduction of nerve stimulation techniques was instrumental in improving the success of peripheral nerve blockade. With this technology, the proximity of the needle tip to the neural tissue can be objectively verified. Recently, with the introduction of ultrasound, the nerve can be visually identified and a needle placed next to it in real time. The spread of the medication around the nerve can also be visualized in real time. The availability of portable ultrasound machines has led to exponential use of this modality in the performance of peripheral nerve blocks. There has been increased use of ultrasound guidance in the field of chronic pain management as well. Interventional pain management, however, has a strong reliance on fluoroscopy in the performance of peripheral nerve blocks near the spine because bony landmarks serve well to predict the location of the nerve, and ultrasound has limited utility.

The success of a nerve block depends on several factors. First, it is key that the purpose of performing the nerve block is clearly understood both by the patient and the physician. Second, in the case of diagnostic blocks, knowledge of the factors contributing to a false-positive result or a false-negative result is essential, along with attempts to minimize their influence. Third, the physician should have an excellent knowledge of the anatomy of the nerve and the anticipated effects of the block. Fourth, appropriate preparation is done to deal with any untoward effects of the block. Fifth, appropriate technology such as ultrasound, fluoroscopy, etc. is used when needed to improve the technical success of the procedure. Last, the results of the nerve block and inferences thereof should be clearly documented.

INDICATIONS FOR THE USE OF NERVE BLOCKS

Nerve blocks can be broadly divided into three categories, anesthetic blocks to facilitate surgery, diagnostic blocks for identifying the pain generator, and therapeutic blocks for prolonged benefit.

Diagnostic blocks are performed when the cause of a pain condition is suspected but not confirmed. Some examples of these include medial branch blocks to identify facet pain, lateral branch blocks to identify sacroiliac joint pain, ilioinguinal nerve blocks to differentiate ilioinguinal neuralgia from genitofemoral neuralgia, and transversus abdominis plane (TAP) blocks to differentiate abdominal wall somatic pain from visceral abdominal pain.

Blocks are considered therapeutic when prolonged meaningful relief of pain occurs beyond the duration of the nerve block itself or when permanent denervation is the intended outcome such as radiofrequency ablation of the medial branches.^4,5

NEUROPHYSIOLOGY AND PHARMACOLOGY

Neuronal membranes are characterized as semipermeable, double-thickness walls composed of lipid molecules with interspaced globular proteins. Small channels allow ions such as sodium and potassium to pass between the internal and external compartments of nerve membranes. Sensory stimulation causes a sudden influx of sodium ions, which results in depolarization of the nerve membrane. Local anesthetics such as lidocaine or bupivacaine produce temporary impairment of conduction of neural impulses by blocking sodium nerve channel conductance and maintaining the nerve in a polarized state.⁶ This effect on nerve membranes is temporary and reversible. The size of the nerve fiber affects its sensitivity to local anesthetics, with smaller, thinner, unmyelinated fibers being most susceptible. Peripheral nerves are composed of three types of nerve fibers:

• A fibers are the largest myelinated somatic nerve fibers. These are further subdivided into motor and sensory. The motor fibers are α, β, and γ fibers and innervate the muscle spindle. The sensory fibers are α (muscle sense, high conduction velocity), β (touch), and γ (pain and cold temperature) fibers.

• B fibers are myelinated preganglionic autonomic nerves. B fibers innervate vascular smooth muscle and are the most readily blocked nerve fiber. Successful blockade results in a sympathectomy, with increased warmth caused by increased blood flow and decreased sweating.

• C fibers, the thinnest nonmyelinated fibers, are the slowest conducting nerve fibers. They transmit postganglionic pain and temperature sensation.

• The two types of pain fibers, Aδ myelinated and nonmyelinated C fibers, have slightly different functions. Aδ fibers transmit sharp pain, while C fibers are responsible for the dull pain and burning sensations that accompany many chronic pain syndromes.

The choice of local anesthetic used will affect the density of the nerve block as well as the duration. Small nerve fibers (Aδ) and unmyelinated fibers (C fibers) can be interrupted with low concentrations of local anesthetic, with minimal effect on the larger myelinated efferent fibers. The subsequent nerve block would produce analgesia without any limb weakness. In contrast, a higher concentration of local anesthetic would produce a motor block, resulting in temporary limb weakness.

The duration of the analgesic effect depends on the choice of local anesthetic used. Lidocaine has a relatively short duration of action compared with bupivacaine, which typically lasts much longer. The addition of a vasoconstrictor such as epinephrine would prolong the duration of the nerve block by decreasing the absorption of the drug into the vascular system.

PRINCIPLES AND GUIDELINES FOR REGIONAL ANESTHESIA AND NERVE BLOCKS

PATIENT ASSESSMENT

Patients with chronic pain should always undergo a thorough evaluation before any interventional procedure. Patients may have numerous other medical problems that need to be addressed before deciding if a procedure is warranted. Examples of common medical problems include poorly controlled diabetes, asthma, and hypertension, to name a few. Elements of the patient workup and assessment should include:

• A history from the patient and any other records or diagnostic studies

• Psychological factors if any

• Details of type of pain, location, and duration, as well as exacerbating and relieving factors

• Medication and allergy review, including details of anticoagulant use with doses and indications (The performing physician should have a good knowledge of the anticoagulants used and the indications for the use. A risk-to-benefit ratio should be done on a case-by-case basis before stopping the anticoagulants and in concert with the primary care physician or the specialist).

• Measurement of pain

• Physical examination with clear documentation of neurologic findings

COMMUNICATION AND INFORMED CONSENT

Communication with the patient is equally important. The description of the procedure should be discussed, including why it is being performed, alternatives to it, expected outcome, and possible side effects. Sedation may be offered to minimize any discomfort, which should also be discussed. Oversedation and general anesthesia is not recommended as it is useful to maintain communication with the patient. Finally, the postprocedure recovery period should be discussed (e.g., return to work, physical activity).

LIMITATIONS AND CONTRAINDICATIONS OF NERVE BLOCKS

Nerve blocks can play an integral part in a comprehensive approach to pain management, but it is important that limitations are well understood. The placebo response can dramatically affect the positive predictive value.⁷ The spillover of the local anesthetic from the target structure, thus anesthetizing other structures, can also create false–positive results.⁸ Failure to appropriately anesthetize the nerve can give rise to false-negative results. Other causes of false-negative results include vascular uptake of the local anesthetic, improper technique, and inadequate amount of active agent to create nerve blockade. The results of the block need to be carefully interpreted. The mere absence of pain relief after successful blockade of the painful area does not necessarily imply psychogenic pain but may point toward a more central pain generator.⁹ Improper patient selection, psychological factors, compensation, and litigation issues can also create complexities in the interpretation of the results of a nerve blockade.

CONTRAINDICATIONS TO PERFORMING NERVE BLOCKS

Absolute contraindications are as follows:

• Infection at the proposed site of injection

• Local anesthetic allergy (Allergies to ester local anesthetics (procaine, tetracaine, and chloroprocaine) are known; however, these solutions are rarely used for regional nerve blocks. Amide local anesthetic allergy (lidocaine, bupivacaine, and ropivacaine) is rare. Some patients may report an allergic reaction after a dental procedure. Further investigation may be warranted to see if it was a true local anesthetic allergy or simply a reaction to epinephrine).

Relative contraindications are as follows:

• Blood clotting abnormalities secondary to intrinsic disease or extrinsic use; management is decided case by case

• Patients with systemic infection or hemodynamic instability

• Situations in which a single or continuous nerve block may mask other pathology, such as limb ischemia from a compartment syndrome that may develop after fractures or crush injuries

PERFORMANCE AND ASSESSMENT OF NERVE BLOCKS

The physician performing the procedure should possess the technical knowledge, experience, and expertise pertinent to the specific procedure. Knowledge of relevant anatomy, potential side effects, and complications of the procedure are essential in preventing adverse outcomes. The expertise to handle immediate serious complications related to the nerve block is also critical. Appropriate technology such as nerve stimulator, fluoroscopy, and ultrasonography should be available as needed to improve the technical success of the procedure.

Discomfort during the procedure may be minimized by using short-acting opioids such as fentanyl. Anxiolytics or short-acting agents such as midazolam are also useful intravenous (IV) medications for minimizing anxiety or discomfort during needle placement. Excess sedation may make accurate assessment of diagnostic or therapeutic blocks difficult.

Appropriate monitoring and resuscitation equipment should be available to manage the effects of the block or any untoward complications. Thus, an IV line should be in place when a large amount of local anesthetic is to be used. Additional intralipid and resuscitation equipment should be available.¹⁰ These preparations may not be needed when a low-volume block such as an occipital nerve block is being performed.

Before and after regional anesthesia, baseline pain measurements should be obtained. Various indicators or scales such as the visual analog scale can be used to help document baseline pain level and response to treatment.¹¹ For more specific nerve blocks, additional information may be helpful. For somatic nerve blocks, sensory and motor deficits should be consistent with the anticipated region or dermatome blocked.

The duration and onset of the physiologic effect of the block and its correlation with the duration of pain relief are important for several reasons. If the duration of pain relief is shorter than expected, it may indicate inaccurate needle placement, an incomplete or partial nerve block, or possibly an alternate pain source. If the duration is longer than expected or the onset much quicker than expected, a potential placebo effect should be considered.

SIDE EFFECTS AND COMPLICATIONS OF REGIONAL ANESTHESIA

Effects of the block may include physiological sequelae or side effects such as hypotension after sympathectomy or dizziness after occipital nerve block. Vagal stimulation can cause syncope; this is often seen in young patients. Other effects may relate to complications of the nerve block such as direct needle injury (pneumothorax after intercostal nerve block) or intravascular injection (seizure during a stellate ganglion block), and these remain specific to each block.

Large volume of local anesthetic can cause cardiac arrest, and intralipids should be available to manage this catastrophic complication when large volumes of local anesthetic are to be used.¹⁰ To safeguard against this, intermittent aspiration should be done to rule out intravascular placement. When using fluoroscopy, real-time contrast injection is useful in detecting this. When using ultrasound, the local anesthetic spread around the needle tip should be visualized in real time.

NEEDLE PLACEMENT AND POSITIONING

Utmost care should be taken when positioning the patients, and all pressure points should be checked. This is especially important in older individuals.

Needle advancement should be done slowly and incrementally in a goal-directed fashion. This is to reduce patient discomfort and to help minimize multiple redirections. This can take some practice. When approaching important structures, only small changes should be made. If the patient reports pain, determination as to local pain versus paresthesia is important. One necessitates more local anesthetic, whereas the other may require needle withdrawal or redirection. One important point is to refrain from injecting anything if the patient reports pain when the needle is in the vicinity of an important neural structure and to rather gently withdraw it. When using ultrasound the more perpendicular the needle is to the beam, the better it is visualized.^12,13

SPECIFIC NERVE BLOCKS

HEAD AND NECK

The skin of the face is supplied by the three divisions of the trigeminal nerve. The scalp is supplied by various divisions of the occipital nerve posteriorly and the auriculotemporal nerve in the temporal region. The branches from the dorsal rami of the cervical nerves supply the neck posteriorly, and the branches of the superficial cervical plexus supply the neck anteriorly. Various neuralgia can affect these nerves. In addition, different branches can be peripherally blocked for the provision of surgery such as dental surgery. Blockade of superficial pericranial nerves may also provide relief to patients with intractable headache.⁴

Trigeminal Nerve

Anatomy

The trigeminal nerve consists of three divisions: the ophthalmic nerve (V1), maxillary nerve (V2), and mandibular nerve (V3). These three branches supply sensation to most of the face. Trigeminal nerve blocks are used mainly to treat severe pain from trigeminal neuralgia and various malignancies affecting the face.

Gasserian Ganglion Block (Fig. 84-1)

Anatomy

The gasserian or trigeminal ganglion lies within the medial cranial fossa across the superior border of the petrous temporal bone. The posterior two-thirds is fully covered by dura mater. This posterior portion lies within a small recess called Meckel's cave. This invagination of the dura surrounding the posterior two-thirds of the ganglion allows direct continuity with the cerebrospinal fluid.

Indications