Commonly Used Medications in Procedures

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Last modified 06/06/2015

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2 Commonly Used Medications in Procedures

Local anesthetics, corticosteroids, contrast agents, neurolytic agents, and viscosupplementation are used commonly in pain management procedures. At times, medications to treat adverse reactions are required. As emphasized throughout this text, every interventional physician must be knowledgeable of the pharmacology, pharmacokinetics, and potential adverse reactions of the drugs he or she administers. Furthermore, the physician needs to be familiar with medications used to treat potential procedure complications. This chapter examines medications commonly employed during pain management procedures.

Local Anesthetics

Local anesthetics are widely used and are generally safe when administered properly. Local anesthetics are therapeutically employed in most injections to provide local anesthesia or analgesia of a painful structure. The ability of local anesthetics to relieve pain can also be used diagnostically to help confirm a pain generator. Common applications include skin and soft tissue anesthesia for other procedures; intraarticular injections; injection for bursitis, tenosynovitis, entrapment neuropathies, painful ganglia; spinal injections; and nerve blocks.

Local anesthetics are subdivided into esters and amides, referring to the bond that links the hydrophilic and lipophilic rings. The amide class is less allergenic and more commonly employed in local, intraarticular, and spinal injections. The most widely used agents in pain management practice are lidocaine (Xylocaine) and bupivacaine (Marcaine), both amide local anesthetics.

Amide local anesthetics are hydrolyzed by the liver microsomal enzymes to inactive products. Thus, patients with hepatic failure or reduced hepatic flow are more sensitive to those agents. For this reason, patients taking beta blockers or who have congestive heart failure, have a lower maximum dosage because of their reduced hepatic flow and decreased elimination rates of the amide local anesthetics.

In contrast, the ester anesthetics are rapidly hydrolyzed by plasma cholinesterase into para-aminobenzoic acid (PABA) and other metabolites that are excreted unchanged in the urine. Para-aminobenzoic acid is a known allergen in certain individuals. However, the rapid metabolism of ester local anesthetics lowers their potential for toxicity. Procaine is an amino ester commonly, but not exclusively, employed in differential spinal blocks. 2-Cholorprocaine can be used for infiltration, epidural or peripheral nerve block, and is also an ester.

Mechanism of Action

Local anesthetics exert their effect by reversibly inhibiting neural impulse transmission. The local anesthetic molecules diffuse across neural membranes to block sodium channels and inhibit the influx of sodium ions; therefore, proximity of the local anesthetic to the nerve to be blocked is required. Only a short segment of the nerve (5 to 10 mm) needs to be affected to cease neural firing. Epidural analgesia from local anesthetic is believed by some to occur because of uptake across the dura, a back door approach to spinal block.

The ability of a local anesthetic to diffuse through tissues and then block sodium channels relies on the ability of these molecules to dissociate at physiologic pH of 7.4. The pKas for local anesthetics are greater than the pH found in tissue. As a result, local anesthetics in vivo exist primarily as cations, the form of the molecule that blocks the sodium channel. The base form of the local anesthetic allows it to penetrate the hydrophobic tissues and arrive at the axoplasm.

In addition to host factors, neural blockade by local anesthetics is affected by the volume and concentration of local anesthetic injected, the absence or presence of vasoconstrictor additives, the site of injection, the addition of bicarbonate, and temperature of the local anesthetic.1 Increasing the total milligrams of a local anesthetic dose shortens the onset and increases the duration of the local anesthetic. Epinephrine, norepinephrine, and phenylephrine are sometimes added to local anesthetics to reverse the intrinsic vasodilation effects of many of the local anesthetics and thereby reduce their systemic absorption. This increases the amount of local anesthetic available to block the nerve. More anesthetic means a quicker onset and longer duration. Application of the local anesthetic close to the nerve improves its ability to diffuse across the axon and block sodium channels. Highly vascular sites such as the intercostal nerve and caudal epidural space tend to result in slightly shorter duration of action. The addition of bicarbonate or CO2 (700 mm Hg) to local anesthetics hasten their onset. Bicarbonate raises the pH and the amount of uncharged local anesthetic for diffusion through the nerve membrane. CO2 will diffuse across the axonal membrane and lower the intracellular pH making more of the charged form of the local anesthetic available intracellularly to block the sodium channels. Temperature elevations decrease the pKa of the local anesthetic and hasten the onset of action.

Individual Agents

Local anesthetics are administered in the intradermal, subcutaneous, intraarticular, intramuscular, perineural, and epidural spaces during pain management procedures. Injections into vascular regions such as the oral mucosa and epidural space may result in rapid absorption and higher systemic concentrations. Local anesthetics administered into or near the epidural space should be preservative free. Methylparaben is a common preservative in multidose vials and is also a common allergen.2


Action of local anesthetics is affected by numerous factors reviewed above. Location of injection plays a primary role in determining the onset, duration, and toxic dose of these agents (Table 2-1). Vasoconstrictors such as epinephrine reduce local bleeding and thereby prolong the onset and duration, but are generally not employed in a pain management practice.

Excess amounts of local anesthetics may cause CNS effects including confusion, convulsions, respiratory arrest, seizures, and even death. The risk for complications increases if the local anesthetics are given intravascularly. Other potential adverse reactions to local anesthetics include cardiodepression, anaphylaxis, and malignant hyperthermia. Patients with decreased renal function, hepatic function or plasma esterases eliminate local anesthetics more slowly and, therefore, have an increased risk of toxicity. Toxic blood levels of lidocaine are approximately 5 to 10 μg/mL, but adverse effects can be seen at lower blood levels.

Patients should be monitored for signs of toxicity including restlessness, anxiety, incoherent speech, lightheadedness, numbness, and tingling of the mouth and lips, blurred vision, tremors, twitching, depression or drowsiness. Injections into the head and neck area require the utmost care.3 Even small doses of local anesthetic may produce adverse reactions similar to systemic toxicity seen with unintentional intravascular injections of larger doses. Deaths have been reported.4

Resuscitative equipment and drugs should be immediately available when local anesthetics are used. Management of local anesthetic overdose begins with prevention by monitoring total dose administered, frequently aspirating for vascular uptake, and use of contrast to avoid vascular uptake when appropriate. Recognition of symptoms of toxicity and support of oxygenation with supplemental oxygen are keys to the initial management. Airway must be maintained and respiratory support should be provided as needed. Hypotension is the most common circulatory effect and should be treated with intravenous fluids and a vasopressor such as ephedrine in appropriate candidates. Convulsions persisting despite respiratory support are often treated with a benzodiazepine such as diazepam. If cardiac arrest occurs, standard cardiopulmonary resuscitative measures should be instituted.


Corticosteroids are administered in a pain practice for their potent antiinflammatory properties. These injections to relieve pain and inflammation work well temporarily, but questions remain regarding their role in the management of many chronic musculoskeletal conditions. Corticosteroids may result in significant side effects. The potential for these adverse effects, ranging from a relatively innocuous facial flushing effect to joint destroying avascular necrosis, must be weighed against potential benefits. Some locally injected corticosteroids are absorbed systemically and can produce transient systemic effects.

Corticosteroids can be helpful in a variety of conditions including rheumatoid arthritis, bursitis, tenosynovitis, entrapment neuropathies, crystal-induced arthropathies in patients who cannot tolerate systemic treatment well, radiculopathies, and at times, osteoarthritis (OA). Corticosteroids should never be injected directly into a tendon or nerve, subcutaneous fat, or an infected joint, bursa, or tendon (Table 2-2).

Mechanism of Action

All corticosteroids have both glucocorticoid, antiinflammatory, and mineralocorticoid activity. Agents with significant glucocorticoid and minimal mineralocorticoid activity include betamethasone (Celestone), dexamethasone (Decadron), methylprednisolone acetate (Depo-Medrol) and triamcinolone hexacetonide (Aristospan). Corticosteroids can be mixed in the same syringe with local anesthetics.

Corticosteroids produce both antiinflammatory and immunosuppressive effects in humans. The primary mechanism of action may be their ability to inhibit the release of cytokines by immune cells.5 The effects of corticosteroids are species specific.6 Lymphocytes in humans are much less sensitive to the effects of corticosteroids than lymphocytes in common laboratory animals including the mouse, rat, and rabbit. In humans, corticosteroids reduce the accumulation of lymphocytes at inflammatory sites by a migratory effect.7 In contrast to this lymphopenia, is the neutrophilia seen by demargination of neutrocytes from the endothelium and an accelerated rate of release from the bone marrow.8 A temporary rise in white blood cell count is commonly observed for this reason after a corticosteroid dose and in isolation does not mark a post injection infection.

The antiinflammatory effects of corticosteroid also occur at the microvascular level. They block the passage of immune complexes across the basement membrane, suppress superoxide radicals, and reduce capillary permeability and blood flow.9 Corticosteroids inhibit prostaglandin synthesis,10 decrease collagenase formation, and inhibit granulation tissue formation.

The immunosuppressant effects of corticosteroids are generally via effects on T cells. These effects are not the desired effect of corticosteroid used in pain management procedures and are not observed following epidural injections.11 A review of these immunosuppressant effects can be found in other texts.1114

Individual Agents

Commonly used corticosteroid preparations include betamethasone, methylprednisolone, triamcinolone, dexamethasone, prednisolone, and hydrocortisone. Of these, betamethasone and dexamethasone have the strongest glucocorticoid or antiinflammatory effects. Corticosteroid effects can be highly variable between individuals and it is not possible to definitively state a safe dosage of corticosteroid. The following should serve only as a guide and must be tailored to each individual.


An equal mixture of two betamethasone salts, Celestone Soluspan, allows for both immediate and delayed corticosteroid responses. Betamethasone sodium phosphate acts within hours, whereas betamethasone acetate is a suspension that is slowly absorbed over approximately 2 weeks. Betamethasone (Celestone Soluspan) is approved for intraarticular or soft tissue injection to provide short-term adjuvant therapy in osteoarthritis, tenosynovitis, gouty arthritis, bursitis, epicondylitis, and rheumatoid arthritis.15 It is also commonly employed in epidural injections. Typical intraarticular doses vary with the size of the joint and range from 0.25 to 2 mL (1.5 mg to 12 mg). Typically epidural injections range from 1 to 3 mL (6 to 18 mg). Betamethasone should not be mixed with local anesthetics that contain preservatives such as methylparaben as these may cause flocculation of the steroid.


Methylprednisolone acetate (Depo-Medrol) has 1/5 to 1/6 the glucocorticoid potency of betamethasone but similar antiinflammatory effects to prednisolone. It has an intermediate duration of action. It, like the other corticosteroids, is approved for intraarticular and soft tissue injections for short-term adjuvant therapy of osteoarthritis, bursitis, tenosynovitis, gouty arthritis, epicondylitis, and rheumatoid arthritis.15 Depo-Medrol has been used for epidural administration also. Preparations of methylprednisolone acetate include polyethylene glycol as a suspending agent. Concerns developed as to whether the polyethylene glycol can cause arachnoiditis with (inadvertent) intrathecal injections.16 Animal studies have not demonstrated any adverse effects on neural tissues from the application of glucocorticoid.17 Methylprednisolone is now available without polyethylene glycol, PEG free. Typical doses range from 4 to 80 mg. Small joints are typically injected with 4 to 10 mg, medium joints 10 to 40mg, large joints 20 to 80 mg, bursae and peritendon 4 to 30 mg.15

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