Cauda Equina Syndrome After Epidural Steroid Injection: A Case Report

Case Report 

A 50-year-old woman with low back and right leg pain was scheduled for epidural steroid injection. Her medical history included no systemic diseases. She had a history of lower back and right leg pain for 2 years. The only medication she took was analgesic agents such as paracetamol. Her vital signs and laboratory findings were normal.

In the operating room, she was under monitored anesthesia care. To permit epidural injection, the patient was placed in the right lateral decubitus position, and the skin was cleansed with a solution containing iodine. Two milliliters of 2% lidocaine was injected subcutaneously at the L4-5 level. An 18-gauge Touhy needle was inserted, an air-filled 5-mL syringe attached, and the needle advanced until loss of resistance occurred. The needle was assumed to be in epidural space without difficulty in the second attempt. There was no spontaneous return of fluid through the needle. No pain, bleeding, or paresthesias were elicited during the needle placement. Correct placement was determined by administering contrast medium (2 mL) (Xenetic 350; Guerbet Ltd, Roissy CDG Cedex, France) through the needle. Spread within the epidural space was determined by radiographic imaging. After verifying the epidural space, 2 mL of 0.5% bupivacaine (Marcaine 0.5%; Astra Zeneca, Ltd, Istanbul, Turkey) and 60 mg of triamcinolone diacetate (Kenacort-A, Bristol Myers Squibb Co, Istanbul, Turkey) in 6-mL total volume was injected.

The patient did not complain of any symptoms for 3 hours, and there was a reduction in radicular symptoms. Three hours later, she complained of perineal numbness and lower extremity weakness. The neurologic evaluation revealed loss of sensation in the saddle area and medial aspect of her right leg. There was a decrease in the perception of pinprick test. Deep-tendon reflexes were decreased especially in the right leg. She was unable to urinate. The patient's symptoms improved slightly over the next several hours. She had a gradual return of motor function and ability to feel the Foley catheter. Her symptoms were completely resolved over the next 8 hours. We discharged the patient home once she had complete recovery. She gave a signed consent to have personal health information for publishing without divulging personal identifiers.

Discussion 

Neuroaxial steroid injections are generally considered to be safe; however, the incidence of epidural steroid–related complications is difficult to judge.2 Cauda equina syndrome is an acute neuropathy that, by affecting the smaller nerve fibers or autonomic fibers, leads to varying degrees of urinary and fecal incontinence, localized sensory loss in the perineal area, and varying degrees of leg weakness.4 This is a very rare complication of epidural injection. The potential etiologies of such symptoms are numerous and include trauma, ischemia, and neurotoxic reactions.

The potential of epidural local anesthetics to cause localized nerve damage is very low. The accidental subdural and subarachnoid injection of high doses of local anesthetics may be the cause of toxicity.4 Although the spinal roots are covered only by the pia mater in the subarachnoid space, they are covered by the pia and arachnoid maters in subdural space. In the epidural space, they are surrounded by these layers and by a thicker dura. Local anesthetics seem capable of inducing long-lasting structural and functional changes in neural tissue in large doses.5 Inadvertent subarachnoid injection of intended epidural doses of hexylcaine or chlorprocaine may result in persistent neurologic deficits, including cauda equina syndrome.3 In addition, high dose of lidocaine administered intrathechally may cause this syndrome.4 Schneider et al6 reported a syndrome of possible transient neurologic toxicity caused by the stretching of cauda equina by the lithotomy position stretched some of the nerve fibers within the cauda equina, rendering them vulnerable to toxic potentials of lidocaine. However, it is relatively infrequent with bupivacaine.7

In relevant concentration of epidurally administered triamcinolone, neurologic symptoms are uncommon. Abraham et al8 showed, in an animal study using chronic intrathecal administration of triamcinolone and methylpredisolone, no detection of histologic or behavioral signs of neurotoxicity. Benzyl alcohol was the preservative agent in triamcinolone that we used in our patient. It may be neurotoxic in sufficient doses applied to the subarachnoid space. A “wet tap” may occur during epidural needle placement for intended epidural steroid injection. As Hodgson et al9 discussed in their review, during this procedure, replacing the epidural needle at an adjoining interspace and injecting a standard dose epidurally (especially using the common diluted form of depot steroids and their preservatives in saline or local anesthetics solutions) would seem highly unlikely to endanger the patient.

In the present case, it is unlikely that cauda equina syndrome was caused by the inadvertent intrathecal injection of local anesthetic. Besides the radiographic images of the epidural space, our patient experienced neither hypotension nor significant motor block at any time. But it is postulated that local anesthetics injected in the epidural space are capable of diffusion in to the subarachnoid space.

The volume of the steroid and local anesthetic solution applied to the epidural space is important. Loculation of the injected fluid may cause transient neurologic symptoms.10 Mclain et al10 presented a case that had transient paralysis after epidural steroid injection. In their case, radiographic studies showed a focal, space-occupying lesion in the spinal canal at the level corresponding to the neurologic deficit, which spontaneously resolved over the next 2 to 3 hours. In our case, loculation of the steroid and local anesthetic solution may be the cause of the transient compressive lesion and neurologic symptoms. Because her symptoms did not advance and neurologic deficits began to resolve in a few hours, we preferred to observe the patient and wait for radiographic imaging. Eight hours after the procedure, all neurologic symptoms were resolved. The reversal of the symptoms in a short time may be a hint for the loculation that resolves.

Other factors might have been involved in predisposing the patient to this complication, such as arterial hypotension or compromise of blood supply to the cord by the position. In our case, hemodynamic parameters were in normal ranges through the time during the process. Because the needle was assumed to be in the epidural space in the second attempt, it was not a long time that the patient was positioned in the lateral decubitus position.

Conclusion 

In summary, epidural steroid therapy is a commonly used conservative therapy for lumbosacral radiculopathy. Transient neurologic symptoms may be caused by many factors, such as inadvertent intrathecal injections, neurotoxicity of the agents, compromise of blood supply to the cord, and loculation of the injected fluids. Although complications associated with this procedure are rare, it is important to be aware of them.

Practical Applications 

• Epidural steroid therapy is a commonly used conservative therapy for lumbosacral radiculopathy.

• Although complications associated with this procedure are rare, it is important to be aware of transient neurologic symptoms.

• Practitioners, such as doctors of chiropractic and other manual therapists, should be aware of this presentation because some patients may be undergoing concurrent therapies.