Anesthetics

Local anesthetics are used in diagnostic and therapeutic spinal injections. The volume of the anesthetic is variable depending on the type of procedure performed. A typical interlaminar lumbar epidural injection may consist of 3–10 mL of anesthetic while a transforaminal epidural injection may consist of 1–3 mL.

Allergic reactions to local anesthetic, although rare, may occur either from the local anesthetic agent, or if present, the methylparaben used as a preservative. There is a higher likelihood of reaction to procaine than amide-based local anesthetics. In a prospective review of 10 440 patients who received lidocaine for spinal anesthesia, the incidence of adverse reactions was reported to be about 3% for positional headaches, hypotension, and backache, 2% from shivering, and less than 1% each for peripheral nerve symptoms, nausea, respiratory inadequacy, and diploplia. Many of these observations may be related to injection techniques, with or without a contribution from the local anesthetic used.²

Inadvertent puncture of the thecal sac while injecting local anesthetic for an epidural can result in prolonged paresthesia, pains in the legs, and even transient paralysis.³ Bupivacaine can cause degeneration of muscle fibers after a single injection into a skeletal muscle.⁴ There have been reports of anesthetic injections outside of the neurofascicle which can lead to alterations in the blood–nerve barrier and consequent edema and swelling of the nerve.⁵ This can lead to a progressive decrease in nerve blood flow as the concentration increases.⁶ If a local anesthetic is injected intrafascicularly there can be devastating consequences from cytotoxicity and edema.^7,8 These possible complications can be avoided using appropriate techniques, and utilizing contrast media prior to introduction of anesthetic near a nerve.

Attention must be given to the amount of anesthetic administered in order to avoid the possibility of central nervous system toxicity. The total dosage of lidocaine should remain below 400–500 mg or 40 mL of 1% lidocaine. Bupivacaine is about 4 times more toxic than 1% lidocaine with a toxic bolus of 175 mg (or 17.5 cc) in a 70 kg patient.⁹ The signs of central nervous toxicity are disorientation, light-headedness, nystagmus, tinnitus, and muscle twitching in the face or distal extremities. Peak plasma concentrations occur 10–20 minutes after injection. Therefore, ongoing monitoring of the patient for the postoperative period for over 30 minutes is suggested strongly to avoid any possible potential nervous system toxicity from anesthetics.

Other complications which can arise from local anesthetics for epidural analgesia include motor block, hypotension, urinary retention, and pressure necrosis.¹⁰ Higher doses of local anesthetics appear to increase the risk of motor block and hypotension.^11,12

Cardiovascular complications

If high systemic levels of local anesthetics are injected intravascularly and/or intrathecally during a spinal interventional procedure cardiovascular complications can arise. Usually, such reactions are preceded by central nervous system toxicity prior to cardiovascular complications arising. The cardiovascular toxicity is a direct result of anesthetics acting upon the myocardium and peripheral vasculature. In vitro studies using isolated myocardial tissue have shown anesthetics to have a dose-dependent negative inotropic action.^13,14 The effects of local anesthetics on the cardiovascular system when at low levels can slightly increase blood pressure due to an increase in cardiac output and heart rate, which can enhance sympathetic activity and cause direct vasoconstrictor action. At higher concentrations, which produce CNS toxicity, they can cause a marked increase in heart rate, cardiac output, peripheral resistance, and blood pressure. With further increase in dosage there can be severe hypotension and cardiovascular collapse due to decreased cardiac output and peripheral vascular dilation. Prevention of such complications certainly depends on avoiding intravascular injection. Thus, appropriate needle localization with fluoroscopy and contrast media is essential.

Once CNS toxicity symptoms are present, the interventionist needs to prepare for possible cardiovascular complications. Institution of appropriate cardiopulmonary resuscitation is imperative for the management of such complications. Management of the patient using advanced cardiac life support (ACLS) would be implemented any time there is such a need. Appropriate management through emergency cardiac care algorithms is recommended and the reader is referred to more detailed sources for further information with regard to these algorithms and management.^15–17

Corticosteroids

Several injectable corticosteroid preparations have been utilized in interventional spinal procedures. These include, most commonly, triamcinolone, methylprednisolone, and betamethasone. Each of these corticosteroids has a different chemical composition. There have been several reports in the literature that have stated arachnoiditis may be related to the use of intrathecal steroids.^18–22 A study by Latham²³ has been done to assess intrathecally injected betamethasone in sheep, which did not reveal any evidence of arachnoiditis until high doses were utilized, and thus the study concluded intrathecal injection of betamethasone in low doses, such as those given in humans, is unlikely to cause arachnoiditis.²³ Several studies have examined the effects of epidural and subarachnoid-deposited injections into the meninges and spinal cord.

Cicala et al.²⁴ looked for evidence of acute neurotoxicity (within 30 days) after injection of epidural corticosteroids. They examined the effects of a mixture of 1% lidocaine and methylprednisolone on the meningeal membranes and nerve roots 4 or 10 days after epidural injection. Microscopic examination revealed a complete lack of inflammatory changes in neural tissue and meningeal thickening.

Abram et al.²⁵ examined histological sections of spinal cords of rats that received 4 subarachnoid injections of triamcinolone at 5-day intervals and compared them with sections from animals that received subarachnoid saline solution during the same time periods. They found a few large, common dark-stained neurons in several preparations, but these were invariably in areas adjacent to spinal catheters, where mechanical compression of the cord was evident. There was no difference in the incidence of such occurrences between steroid-treated and saline-treated animals.

A study by Delaney and colleagues²⁶ evaluated possible long-term histological effects of a mixture of 2% lidocaine and triamcinolone following epidural injection and catheterizations. They found that the nerve root and the root entry zone in the meninges when examined by light microscopy 30 and 100 days after injection showed only a minor inflammatory response at the 30 day period. The reaction was completely resolved at 100 days.

It has been proposed that polyethylene glycol (PEG), a preservative agent in methylprednisolone, has been implicated in cases of sterile meningitis and arachnoiditis when injected intrathecally.²⁰ A study performed on the toxicity of PEG was performed by Benzon et al.²⁷ They showed a concentration of 20% PEG or greater resulted in a swelling and a reduction in compound muscle potential in isolated nerve preparations. However, this concentration is clearly higher than that found in commercial corticosteroids preparations, which is 3–9%. These preparations are subsequently diluted with saline and local anesthetics, which would indicate an even lower predisposition for any neurotoxicity.

Epidural administration of corticosteroids has several known side effects. These include fluid retention, which can lead to congestive heart failure.^28–30 Case reports of steroid myopathy have been reported.¹³ There have also been reports of irregular menses.³¹ Epidural lipomatosis has been associated with prolonged corticosteroid therapy.^32–34 Minor digestive disturbances and occasional minor changes in serum glucose have been documented.³⁵ Less-common side effects are elevated temperature, euphoria, depression, mood swings, local fat atrophy, deep pigmentation of the skin, and pain flare. Other rare but reported side effects include weight gain,²⁸ deep vein thrombosis,³⁶ and hypertension,³⁷ and allergic reactions to triamcinolone.¹

An uncommon but serious complication is development of Cushing’s syndrome from excess glucocorticoid administration.³⁸ This syndrome usually occurs when exceptionally high dosages of corticosteroid are given over a short period of time. One such case occurred when a patient received two 80 mg injections of methylprednisolone 1 week apart.³⁹ Serum cortisol levels have been shown to be depressed for 1–2 weeks after epidural injections but may return to normal after 3 weeks.^40,41 The recommended dose to avoid systemic side effects from epidural steroids has been stated by Knight and Burrell⁴² to be no more than 3 mL/kg of methylprednisolone. Despite adhering to this, there have been reports of cumulative effects from long durations of steroid preparations. Kay⁴³ and coworkers have shown both acute and chronic suppression of the hypothalamic–pituitary–adrenal axis in a clinically relevant study of 14 patients who received a total of three epidural steroid injections once weekly with 80 mg of triamcinolone in 7 mL of 1% lidocaine. Within 15 minutes of injection, there was evidence of the suppression of endogenous corticosteroids, manifested by a significant decrease in both ACTH and cortisol. The median duration of such effect was 1 month, but 5 of 14 patients showed suppression for up to 3 months. Adrenal function returned to a normal status after 3 months.

In a study by Manchikanti⁴⁴ it was concluded that low-dose administration of neuroaxial steroids are not deleterious and did not result in any significant deterioration in bone mineral density, causing neither osteopenia or osteoporosis.

Contrast media

Because fluoroscopic procedures are combined with introduction of radiographic contrast media, it is important to know the potential adverse effects of contrast media. The largest study to compare the effects of intrathecal nonionic (iopmanidol) to ionic (metrizamide) contrast found substantially fewer adverse reactions in the nonionic group.⁴⁵

The contrast currently used in myelography and fluoroscopic injections is nonionic, either iso-osmolar or of a low osmolality. The risk of anaphylactic reaction using iso-osmolar contrast is extremely low (0.04%)

In 337 647 cases in which iso-osmolar contrast was used, only 1 death occurred.⁴⁶ Patients with a known sensitivity to iodine, prior reaction to contrast media, food allergies, asthma, and hay fever have a higher incidence of anaphylactic or cardiovascular reactions. Premedication with histamine H₁ and histamine H₂ blockers and corticosteroids may reduce the incidence and severity of life-threatening reactions in patients with a known allergy. Controlled studies on nonionic contrast agents used intrathecally in myelography have shown adverse reactions including headache (18%), nausea (7.3%), muscular pain (3.7%), and hypotension (1.1%).⁴⁷ These studies were performed using 10–15 mL of contrast injectate, which is a larger dose than the 1–3 mL used during fluoroscopic injections.

The fluoroscopic technique in combination with extradural myelography can avoid intrathecal injections. Intravascular injection can occur in 9.2% of cases despite a negative aspiration for blood in lumbar epidural injections, without fluoroscopic guidance.⁴⁸ When utilizing fluoroscopy and contrast media, Sullivan et al.⁴⁹ found a similar overall incidence of 8.5% intravascular uptake in lumbar spinal injections. The caudal and transforaminal routes were intravascular 10.9% (Fig. 20.2) and 10.8% of the time, respectively, sacroiliac joint injections 6.3% (Fig. 20.3), zygapophyseal joint injections 6.1%, and interlaminar injections 1.9%. The intravascular pattern in lumbar transforaminal epidural injections was also described by Furman to be 11.2%⁵⁰ and in cervical transforaminal injections, and intravascular uptake is 19.4%.⁵¹ These studies unequivocally demonstrate the importance of introducing contrast media prior to the infusion of anesthetics or corticosteroids in spinal interventional injections. Prophylaxis may be utilized in patients with known allergy to contrast media (Fig. 20.4). An alternative in patients allergic to iodinated contrast is to utilize gadolinium contrast.⁵²

Fig. 20.2 AP/PA fluoroscopic image showing intravascular contrast during a caudal injection.

Fig. 20.3 Fluoroscopic image of sacroiliac joint showing intervascular contrast pattern.

Fig. 20.4 Pro-phylaxis for patients with known allergy to contrast media.

Epidural abscess

These have been reported after epidural injections in the cervical, thoracic, and lumbar spine. There have been cases of epidural abscess following thoracic epidural injections of steroids and bupivacaine to treat postherpetic neuralgia.^57,60 A thoracic epidural abscess has also been reported after four epidural injections in a patient with metastatic disease.⁵³ Five other cases of abscesses were reported, three after lumbar, one after cervical, and one after caudal epidural injections.^{54,55,61–63} The bacteria identified in these cases was Staphylococcus aureus. Of these patients, three patients had diabetes mellitus, one had a surgical infection with S. aureus 2 weeks prior to the epidural injection, and one had carcinoma with spinal metastasis. All of these patients presented with fever, spinal pain, radicular pain, and/or progressive neurologic deficit 3 days to 3 weeks following their injections. It is presumed that the most common bacterial etiology for spinal infection from a spinal injection is S. aureus. The likely mechanism of infection is introduction by the needle, carrying an inoculum from the skin to deeper structures.

In order to diagnose an epidural abscess resulting from a spinal procedure, there must be careful and close clinical observation. There should be a high suspicion for this potential complication in any patient with a history of an immunocompromised condition or diabetes mellitus.

Clinically, the patient with epidural abscess presents with pain in the local area, neck or back stiffness, soreness, fever, and/or malaise. Prompt diagnosis of infection is necessary in order for a patient to recover with intact neurologic function.

Laboratory evaluation with erythrocyte sedimentation rate (ESR), C-reactive protein, and complete blood count (CBC) needs to be obtained. Magnetic resonance imaging (MRI) with contrast is the radiological procedure of choice for the diagnosis of epidural abscess.^55,64 Once diagnosed, appropriate antibiotic therapy can be administered and surgical debridement performed if necessary.

Meningitis

This is a rare phenomenon, which can occur following spinal injections. It can occur when the dura is accidentally punctured during epidural procedures or other spinal interventional procedures. There are two types of meningitis that have been reported following spinal injections: bacterial and aseptic. Several cases of bacterial meningitis have been reported following lumbar epidural injections.⁵⁷ Of the two cases reported by Dougherty, one patient had a documented dural puncture and the other patient had an inadvertent unrecognized dural puncture.

Cases of aseptic meningitis have been reported by Nelson et al.¹⁹ following subarachnoid injection with methylprednisolone. The manifestations included headache, fever, nausea, leg pain, and convulsions. Cerebrospinal fluid (CSF) analysis revealed elevated protein, leukocytes, and red blood cells, while CSF culture was negative. Spontaneous recovery ensued over a 3-week period. Several other cases of aseptic meningitis have been reported after a subarachnoid injection.^25,64,65 In each instance the symptoms resolved within several days. A case report by Morris⁶⁶ of aseptic meningitis began 48 hours after an epidural injection of methylprednisolone without any anesthetic. The symptoms included fever, headaches, lethargy, and meningismus. CSF evaluation in this case revealed pleocytosis, elevated protein values, and diminished glucose levels. CSF culture was negative.

Thus, in a patient with presumptive meningitis, appropriate evaluation of CSF fluid is needed in order to appropriately treat this potential complication. A history needs to be obtained from the patient regarding headache, lethargy, and photophobia, followed by evaluation for signs of meningeal irritation.

Prevention of meningitis can be enhanced by utilizing a strict sterile technique, but even the best precautions do not entirely mitigate this possible complication.

Osteomylitis/discitis

Cases of osteomyelitis and discitis have been reported following cervical, thoracic, and lumbar discography. This is a potential life-threatening complication if it develops in the cervical or thoracic spine. As previously mentioned, these infectious complications can be minimized by adhering to sterile technique along with the use of intravenous and intradiscal antibiotics. The use of antibiotics are further discussed in the section on discography. Patients who have undergone a discographic procedure should be observed clinically for symptoms of osteomyelitis or discitis. The typical signs of infection include fever, malaise, lethargy, pain, and/or neurological symptoms. These typically present 1–4 weeks after injection although neurological symptoms are uncommon. Laboratory studies can reveal leukocytosis, elevated sedimentation rate, and/or an increase in C-reactive protein. MRI with contrast has been shown to be superior to bone scan for the early diagnosis of discitis and osteomyelitis.⁶⁷

In summary, early detection of infectious complications from injection procedures is necessary in order to avoid morbidity and mortality. In patients who have a history of prior infection, consideration should be given to prophylactic antibiotic treatment in these patients, prior to their procedure. An algorithmic approach to managing these infectious complications is seen in Figure 20.5.

Fig. 20.5 Possible spinal abscess, meningitis, or osteomyelitis/discitis.

Epidural hematoma

Epidural hematomas can develop spontaneously and in patients with no evidence of any bleeding tendency, anticoagulation, or traumatic needle insertion.^83,84 In a review of epidural steroid injections in 65 published series with a total of 69 047 patients receiving one or more epidural injections, there was only one case of an epidural hematoma.⁸⁵ Hematomas can be localized in the cervical, thoracic, or lumbosacral spine. Symptoms will vary depending on the location and size f the hematoma. The presentation can be immediate or delayed up to several days.^86,87 In order to diagnose patients with such a complication, prompt spinal imaging is recommended. MRI is the most sensitive modality in order to diagnose a hematoma, define the extent of its spread, and distinguish it from other space-occupying lesions.^88–90 Once identified, treatment of the hematoma can involve high-dose corticosteroid therapy and/or emergency decompressive surgery in order to prevent further compromise of neurologic function. If an epidural catheter is present with a hematoma, infusion should be stopped and the catheter removed in order to avoid increasing compression.⁸⁴ In order to minimize the risks to the patient when performing spinal interventional procedures, the interventionist can do several things that can minimize the potential possibility of causing an epidural hematoma. These include minimizing the passes of the needle (needle trauma) utilizing fluoroscopic guidance, use of smaller-caliber needles,⁹¹ and aspiration can be performed in order to determine if the needle is intravascular. See Figure 20.6 for an algorithmic approach to the evaluation of a patient with a presumptive epidural hematoma.

Fig. 20.6 Evaluation of patient with suspected epidural hematoma.

Management of anticoagulant medications in interventional spinal procedures

Clinically apparent epidural hematomas are rare, with an incidence between 1:40 000 and 1:150 000.^84,85,92,93 Aspirin and nonsteroidal antiinflammatory drugs may effect platelet function and subsequently increase the risk of an epidural hematoma. These medications have been reported to increase the occurrence of epidural hematoma from both spinal anesthesia and epidural injection.^94–97 It should be noted, however, that there are other studies, which report no increased incidence of epidural hematomas in patients who are receiving aspirin and nonsteroidal antiinflammatory medications.^98–101

Patients using thienopyridine derivatives and glycoprotein receptor antagonists have developed hematomas from interventional spinal injections.^86,102 Since the risk associated with these medications is unknown, the American Society of Regional Anesthesia recommends withholding ticlopidine 14 days, clopidogrel 7 days, and Gp antagonists for 4 weeks prior to procedure.⁸⁷ Oral anticoagulation with warfarin is a contraindication to spinal anesthesia.⁸⁷ The American Association of Regional Anesthesia suggests that warfarin should ideally be stopped 4–5 days prior to spinal injection. The prothrombin time (PT) and international normalized ratio (INR) should be checked prior to a spinal injection. There is no consensus regarding the delineation of a safe PT/INR prior to performing a spinal injection. There is some literature that supports an INR of 1.5 as safe for major surgical procedures including spinal injections while an INR greater than 1.5 is unsafe.^103,104 It should be noted that identification of risk factors for bleeding disorders does not eliminate the risk of a spinal hematoma. This has been shown in the study by Vandermeulen⁹⁴ in which 87% of patients who had spinal hematomas had a hemostatic abnormality but, 13% had no identifiable risks. See Figure 20.7 for an algorithmic approach to the management of patients on warfarin, aspirin, or NSAIDs.

Fig. 20.7 Anticoagulated patterns,

Dural puncture and post-dural puncture headache

The potential complication of entering the subarachnoid space due to penetration of the dura exists with any spinal injection. This can occur in any region of the spine (cervical, thoracic, or lumbosacral). The incidence of an inadvertent dural puncture in lumbar epidural injections has been reported to be as low as 0.5% and as high as 5%.^109,123 Incidence of dural puncture in the cervical spine can be as high as 20%.¹⁰⁸ The incidence of headache following dural puncture in the lumbar spine has been reported to be 7.5–75% depending on technique, experience, and size of needle used.^124,125 These headaches may emanate from an unrecognized dural puncture causing a leakage of cerebrospinal fluid (CSF) or they may result from inadvertent injection of air into the subarachnoid space.^126,127

When small-gauge needles are used in spinal anesthesia there is a lower incidence of postdural puncture headache. The incidence is approximately 40% with a 22-gauge (ga) needle, 25% with a 25-ga needle,^128,129 2–12% with a 26-ga Quincke needle,¹³⁰ and less than 2% with a 29-ga needle.¹³¹

If a postdural puncture headache occurs, the headache will usually occur within 3 days of the procedure. Up to 66% start within the first 48 hours.^132,133 The headache can also present immediately following a dural puncture.¹³⁴

The pain associated with the headache is described as being a shearing and severe spreading pain. Distribution of the pain appears to be in the frontal and occipital areas, which can radiate into the neck and shoulders. There tends to be stiffness in the neck and the pain is exacerbated with head movements and relieved by lying down.^134,135 Symptoms that can also appear in dural puncture headaches include nausea, vomiting, hearing loss, tinnitus, vertigo, dizziness, paresthesias of the scalp, and upper/lower limb pains. There have also been reports of visual disturbances such as diplopia or cortical blindness.^3,136,137 There are also reports of intracranial subdural hematomas, cerebral herniation, and death.¹³⁸

A review of the literature has revealed that the spontaneous rate of recovery from postdural puncture headache is typical with 85% recovering within 6 weeks.^3,139,140 Even though this side effect can spontaneously resolve, there are frequent circumstances during which the severity of the headaches necessitates treatment. A variety of strategies can be undertaken including rehydration, acetaminophen, nonsteroidal antiinflammatory drugs, opioids, and antiemetics.¹⁴¹ Caffeine has been utilized in the treatment of postdural headache at a dose of 300–500 mg of oral or i.v. caffeine once or twice daily.^142,143

The most definitive method of treatment, however, is an epidural blood patch.^144–146 The first report of epidural blood patch for treatment of postdural puncture headache was described by Gormley in 1960.¹⁴⁷ This technique has a success rate of 70–98%.¹⁴⁸