Introduction

Interventions for making a diagnosis in the patient with chronic pain can present certain therapeutic challenges. The etiology and type of pain is not always clear and diagnostic or therapeutic blocks can be of value with injectable agents. Injectables given are steroids, local anesthetics, hyaluronacid, and neurolytic agents.

A) Steroids

1. Indications

Injection of corticosteroids can have a positive effect on inflammatory pain conditions. The role of corticosteroids in pain treatment has impressively expanded from degenerative to inflammatory conditions of the peripheral joint, extra-articular tissues, and the neuraxial structures and spaces.

Corticosteroids have been proven effective in painful radiculopathy: disc herniation, spondylolysis, spinal stenosis, annular tears, and degenerative conditions of the spine, but also osteoarthritis of the spine and peripheral joints, rheumatoid arthritis, and extra-articular disorders, dermatosis, tendinitis, bursitis, ligament sprain, tenosynovitis, and other pain syndromes.

1. Complications

Glucocorticoids are potent antiinflammatory and immunosuppressive hormones with a rapid mechanism of action. Systemic potential risks include metabolic and endocrine disturbances, weight gain, skin reactions, hypertension, osteoporosis, infections, psychiatric disorders, and hypothalamic-pituitary-adrenal (HPA) axis suppression. Very serious neurologic complications are rare but can be major and described after cervical transforaminal epidural injections.

Corticosteroids cause bone demineralization even in small doses in oral or intermittent administration, which appears from the fact that the number of fractures double [1]. A retrospective study of 3000 patients showed that each epidural steroid injection increased the fracture risk by 31% [2].

The HPA axis can be suppressed by intermittent administration of corticoids. In a study of 30 patients with two dosing strategies triamcinolone acetate 20 mg or 40 mg given in the epidural space were analyzed and the T40 mg group had longer HPA suppression than the T20 mg group and there was no difference in pain reduction [3].

Minor complications are described in Table 9.1 and are without permanent damage.

Serious neurologic complications are seen with injections using corticoids. Serious adverse events included death, spinal cord infarction, paraplegia, quadriplegia, cortical blindness, stroke, seizures, nerve injury, and brain edema. Many cases were temporally associated with corticosteroid injections, with adverse events occurring within minutes to 48 h following injection. The FDA Adverse Event Reporting System (FAERS) database exposed 131 cases (41 cases of arachnoiditis and 90 serious nervous system disorders) until 2014 and some of these cases were published. Diagnosis of the neurologic adverse events were established through magnetic resonance imaging (MRI) or computed tomography (CT) scan. Many patients did not recover from these reported adverse events. With the estimation that around 9 million epidural injections are performed each year in the United States, major complications are rare but can be very serious.

As an example, the following figures are shown from a published case of a 50-year old woman with radiating pain from the left cervical area to the scapula in one arm and a pain score of 7/8. MRI revealed central canal stenosis at C3–4, C4–5, C5–6, and C6–7, and neural foraminal stenosis at C3–4, C4–5, C5–6, and C6–7. First, a fluoroscopy-guided cervical interlaminar epidural steroid injection was done at the level of C7–T1 and then repeated. Despite the fact that the patient’s NRS score reduced to 3 from 4 points, the patient still complained, and it was decided to perform a left C6 cervical intra-foraminal injection to deliver the drug to the anterior part of the epidural space and nerve root. After a nice technique of needle position and contrast spreading, a mixture of 1% mepivacaine, dexamethasone 5 mg, 1500 IU hyaluronidase was given in the foramen of C6 (Figure 9.1). The patient reported a shock-like pain in her left arm with the injection. After 10 minutes post-procedure, the patient noted weakness in the left arm and bilateral lower limbs, and temporarily lost consciousness. An emergent cervical MRI was an intramedullary high-signal intensity seen at the left-sided spinal cord from C4 to T4 with an ill-defined edema (Figure 9.2). The patient was treated with high-dose methylprednisolone and the motor function improved and, after six months, the patient had mild pain and some motor deficits were reported in her left hand. On MRI after six months, the edema decreased intramedullary [5] (Figure 9.3).

B) Local anesthetics

Local anesthetics (LA) are safe, and complications due to use of local anesthetics are rare and depend on the skills of the practitioner performing any block, the correct indication and patient selection, anatomy, and pharmacology knowledge, as well as the technique and equipment used [6].

The low volume required for intrathecal dosing is rarely a problem. However, the higher volume required for epidural anesthesia and peripheral nerve and/or field blocks increases the risk of local anesthetic systemic toxicity (LAST). The incidence of LAST associated with peripheral nerve blocks (PNB) varies between the databases but, in general, hardly exceeds 1/1000 blocks [7]. Some of the complications involve particular LAs, such as allergic reactions to aminoesthers or methemoglobinemia caused by prilocaine. The effect of action of LAs is based on blocking voltage-gated sodium channels, what prevents sodium influx, subsequent depolarization, and action potential generation. Toxicity of LAs occurs when they affect thalamocortical neurons in the brain [8] or cardiac sodium channels [9]. If local anesthetics are injected intravascularly or in higher dosage than recommended, they can cause systemic toxicity, involving neurologic and cardiovascular symptoms. Toxic reaction evolves shortly after the injection of local anesthetics with minor neurologic symptoms such as metallic taste, perioral tingling or tinnitus, followed by major neurologic symptoms, with loss of consciousness and seizures, and leading to cardiovascular symptoms, like bradycardia, ventricular arrhythmias, eventually leading to cardiac arrest.

Risk factors for LAST include patient-dependent and patient-independent risk factors [10]. Patient-dependent risk factors include age, co-morbidities, cachexia, hypoalbuminemia, impaired cardiac, hepatic, and renal function. Pre-existing cardiac conditions may predispose patients to the arrhythmogenic and myocardial depressant effects of LAs. Caution is advised in people with decompensated heart failure. Hepatic or renal dysfunction can result in decreased metabolism and clearance and a higher amount of circulating LA. In addition, liver and/or kidney failure, malnutrition, or any other disease process resulting in decreased serum albumin can indirectly increase the free fraction of the LA. Extreme age patients are more susceptible to toxicity. Elderly people are more likely to have organ dysfunction, which will contribute to toxicity. Further, both elderly and pediatric patients have a relatively reduced muscle mass and therefore are more likely to have a higher concentration of LAs for their weight [10].

Patient-independent risk factors include the LA type, dosage and volume, injection site and absorption. Cardiac toxicity corresponds with the anesthetic potency for neural blockade, therefore more potent bupivacaine is more cardiotoxic than lidocaine. The use of ropivacaine and levobupivacaine may help reduce cardiotoxicity and cause fewer CNS symptoms than bupivacaine, but does not eliminate the risk for LAST, particularly at higher doses. LAs lipophilicity is associated with toxicity. More lipophilic LA such as bupivacaine has an increased risk of toxicity compared to the less lipophilic LA such as mepivacaine and lidocaine. The injection site also adds to the risk of LAST, with the highest rate following penile blocks and local tissue infiltration [11].

LAs may have specific cardiac effects: lidocaine and mepivacaine primarily affect contractility, while bupivacaine and ropivacaine tend to be more arrhythmogenic [12].

Ester local anesthetics, such as chlorprocaine are metabolized by plasma cholinesterases. Therefore, plasma half-life of chloroprocaine may be prolonged in patients with pseudocholinesterase deficiency. Patients who take anticholinesterase medication, such as pyridostigmine for treatment of myasthenia gravis are also probably at risk for LAST events.

Hypersensitivity to LAs is difficult to diagnose because it is based on different mechanisms and a variety of reactions are possible. Allergic reactions involve immune system with IgE-dependent and IgE-independent (T-cell mediated allergic reactions) response. The other cases are diagnosed as nonallergic-type hypersensitivity [13

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