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Transforaminal Cervical Epidural Injections
Letters to the Editor
Transforaminal Cervical Epidural Injections To the Editor: After reading the letter to the editor by Provenzano and Fanciullo,1 and the responses by Beckman et al.2 and Hoeft and Rathmell,3 I believe that the case report published by Beckman et al.4 still requires further comments, as it perfectly illustrates a condition that is seemingly not well recognized by pain specialists. In their report, Beckman et al.4 described a patient who underwent a transforaminal epidural steroid injection (TESI) with methylprednisolone and lidocaine at the right C7-T1 level with a 25-gauge, 2.5-inch short-bevel needle with no evidence of intravascular injection. The patient complained of neck pain and nonspecific headache during the injection, which prompted the practitioner to stop the injection. In the postprocedure room, the patient complained of migraine headache and vomited upon sitting up, symptoms that he had experienced prior to the procedure. The patient received symptomatic treatment and eventually was discharged without signs or symptoms of cerebellar/brainstem dysfunction. However, later that night, he developed neurologic changes that led to his admission to an emergency department. A computed tomography scan showed hydrocephalus, effacement of the fourth ventricle, and right cerebellar areas of attenuation and mass effect. He then underwent an emergency ventriculostomy followed by emergency cerebellar debridement that was life-saving. The patient eventually recovered and is able to work and function independently. There are 2 critical points in this case that are noteworthy. First, the patient did not have symptoms immediately after the steroid/local anesthetic injection. In fact, symptoms developed several hours after the procedure, suggesting that steroid embolism was not responsible for the complication. Indeed, the case description accurately depicts the clinical course of vertebral artery dissection: thrombosis of the artery leads to brainstem and cerebellar ischemic infarctions and swelling that blocks the outflow of the cerebrospinal fluid from the fourth ventricle resulting in acute hydrocephalus and acute increase in intracranial pressure. Early emergency ventriculostomy, as performed in this case, may be life saving. However, if the affected artery is the dominant vertebral artery and consequently, most of the blood flow to the brainstem and the cerebellum is dependent on the integrity of this artery, the dissection and thrombosis that follow usually result in death. Under these circumstances, the massive ischemic infarct affecting both the brainstem and the cerebellum progresses to a hemorrhagic infarct when both the capillary and the blood brain barrier are disrupted due to the ischemia and brain death follows due to the acute, severe increase in intracranial pressure. In fact,
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the case reported in reference 75 quoted by Beckman et al.4 illustrates this situation. The other point that deserves discussion is the mechanism of vertebral artery injury by a 25-gauge, 2.5 inch, short-bevel needle that results in a dissection. It is difficult for me to understand how this can happen in the face of normal anatomy of the artery. The postmortem description of a case of vertebral dissection and death after a TESI5 points out that “there was minute, barely visible hemorrhage over the vertebral artery and along the cervical spinal cord,” suggesting that the needle indeed did not produce major trauma to the artery. I submit that the patients described in these 2 manuscripts4,5 already had a small dissection of the vertebral artery and that there was an unintentional artery puncture during the procedure that resulted in a small hemorrhage between the intima and the wall of the artery that led to further dissection and thrombosis with the resultant clinical picture already described. In fact, the literature suggests that this condition is prevalent in patients with: (1) history of chiropractic or osteopathic neck manipulations, particularly when performed with the head in the neutral or extended position;5-8 (2) migraine headaches;9 and (3) automobile accidents, even when the neck is exposed to mild acceleration/deceleration forces.10 It is also noteworthy that there is a 3:1 ratio between females and males affected by this condition.10 The patient in Beckman’s report4 had a history of migraine headaches and was a pilot. It would be interesting to know if he was exposed to acceleration/decelerations during his tenure as a pilot (e.g, fighter pilot). Re-evaluation of the magnetic resonance image of the cervical spine that was performed prior to the TESI could reveal if he indeed had a preprocedure dissection. Considering the chain of events that trigger an infarction of the cerebellum/brainstem culminating in massive cerebral edema and cerebellar tonsillar herniation, I suggest that it is critical for pain specialists to recognize: (1) the concept of dominant vertebral artery in humans;11 (2) the high prevalence of vertebral artery dissection at the low cervical levels in young patients with a history of neck manipulations, motor vehicle accidents and/or acceleration and deceleration injuries to the neck, and migraine headaches; (3) the role of magnetic resonance imaging of the neck in identifying these patients prior to a TESI;11 (4) that this potentially lethal complication may occur after puncture of a vertebral artery with an ongoing dissection at the lower cervical levels in patients with dominant flow; and (5) the potential role of emergency ventriculostomy and cerebellar debridement as a lifesaving procedure. This information brings further arguments against performing TESI in the cervical spine, particularly at the low cervical levels where the course of the artery is unpre-
Regional Anesthesia and Pain Medicine, Vol 33, No 2 (March–April), 2008: pp 190 –193
Letters to the Editor dictable and the risk for dissection is high in patients that are likely to present with chronic neck pain. Oscar A. de Leon-Casasola, M.D. Department of Anesthesiology State University of New York at Buffalo Pain Medicine and Oncology Roswell Park Cancer Institute Buffalo, NY References 1. Provenzano DA, Fanciullo G. Cervical transforaminal epidural steroid injections: Should we be performing them? Reg Anesth Pain Med 2007;32:168. 2. Beckman WA, Mendez RJ, Paine GF, Mazzilli MA. In reply. Reg Anesth Pain Med 2007;32:169-170. 3. Hoeft MA, Rathmell JP. In reply. Reg Anesth Pain Med 2007; 32:169. 4. Beckman WA, Mendez RJ, Paine GF, Mazzilli MA. Cerebella herniation after cervical transforaminal epidural injection. Reg Anesth Pain Med 2006;31:282-285. 5. Rozin L, Rozin R, Koehler SA, Shakir A, Ladham S, Barmada M, Dominick J, Wecht CH. Death during transforaminal epidural steroid nerve root block (C7) due to perforation of the left vertebral artery. Am J Forensic Med Pathol 2003;24: 351-355. 6. Barinagarrementeria F, Amaya LE, Cantu C. Causes and mechanisms of cerebellar infarction in young patients. Stroke 1997;28:2400-2404. 7. Nakamura CT, Lau JM, Polk N, Popper JS. Vertebral artery dissection caused by chiropractic manipulation. J Vasc Surg 1991;14:122-124. 8. Haldeman S, Kohlbeck FJ, McGregor M. Stroke, cerebral artery dissection, and cervical spine manipulation therapy. J Neurol 2002;249:1098-1104. 9. Smith WS, Johnston SC, Skalabrin EJ, Weaver M, Azari P, Albers GW, Gress DR. Spinal manipulative therapy is an independent risk factor for vertebral artery dissection. Neurology 2003;60:1424-1428. 10. Rubinstein SM, Peerdeman SM, van Tulder MW. A systematic review of the risk factors for cervical artery dissection. Stroke 2005;36:1575-1580. 11. Yoshimoto Y, Wakai S. Unruptured intracranial vertebral artery dissection. Clinical course and serial radiographic imagings. Stroke 1997;28:370-374.
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which they administered 8 to 10 mL of 1 percent procaine at the C7 level. And, in the monograph3 as well as our article of over 2,000 SGBs,4 10 mL of local anesthetic was injected also at the C7 level. In the majority of described applications, SGB is used to provide temporary sympathetic denervation of the upper extremity.3,4 Whether 5 or 10 mL is administered probably makes little or no difference, unless all the sympathetic fibers to the upper extremity are to be blocked. In 1947, Kirgis and Kuntz5 showed that complete sympathetic denervation of the upper extremity requires block of the second and third thoracic ganglion in a relatively high percentage of cases. This is necessary because rami from the second and third thoracic ganglia bypass the stellate ganglion (Fig 1). These nerves have been termed the “nerves of Kuntz.” The study by Feigl et al.1 confirms our findings in corpses as well as in subsequent clinical studies3,4 that if all the sympathetic nerves to the upper extremity are to be blocked, performing SGB with less that 10 mL of injectate is unlikely to do so. Indeed, with the use of 5 mL, they found that contrast distribution ended at level T2 in 17 of 28 cases (61%). In contrast, with 10 mL, the peak of caudal extension most often ended at the level of T2 to T3. Furthermore, the present study1 was con-
Accepted for publication May 7, 2007. doi:10.1016/j.rapm.2007.05.007
Therapeutic Stellate Ganglion Block: 5 Versus 10 mL of a Local Anesthetic To the Editor: The anatomical and radiologic study of bilateral stellate ganglion block (SGB) at C6 in 42 cadavers by Feigl et al.1 proposed a reduction of local anesthetic, ideally to as low as 5 mL. This study and their recommendation regarding reduced injectate volumes would benefit from a historical review. To support administering 5 mL, the authors state: “Volumes lower than 10 mL [for SGB] are cited by Smith and Moore.”1 However, they have misinterpreted our original data. Neither of us used significantly less than 10 mL or injected at the level of C6. Smith2 described 1,500 injections on 400 patients in
Fig 1. Variations in the sympathetic nerve distribution to the brachial plexus showing the intrathoracic rami from second and third thoracic nerves bypassing the stellate ganglion on their way to the upper extremity. Model after Kirgis and Kuntz.5 Reprinted from Moore.3
Transforaminal Cervical Epidural Injections To the Editor: After reading the letter to the editor by Provenzano and Fanciullo,1 and the responses by Beckman et al.2 and Hoeft and Rathmell,3 I believe that the case report published by Beckman et al.4 still requires further comments, as it perfectly illustrates a condition that is seemingly not well recognized by pain specialists. In their report, Beckman et al.4 described a patient who underwent a transforaminal epidural steroid injection (TESI) with methylprednisolone and lidocaine at the right C7-T1 level with a 25-gauge, 2.5-inch short-bevel needle with no evidence of intravascular injection. The patient complained of neck pain and nonspecific headache during the injection, which prompted the practitioner to stop the injection. In the postprocedure room, the patient complained of migraine headache and vomited upon sitting up, symptoms that he had experienced prior to the procedure. The patient received symptomatic treatment and eventually was discharged without signs or symptoms of cerebellar/brainstem dysfunction. However, later that night, he developed neurologic changes that led to his admission to an emergency department. A computed tomography scan showed hydrocephalus, effacement of the fourth ventricle, and right cerebellar areas of attenuation and mass effect. He then underwent an emergency ventriculostomy followed by emergency cerebellar debridement that was life-saving. The patient eventually recovered and is able to work and function independently. There are 2 critical points in this case that are noteworthy. First, the patient did not have symptoms immediately after the steroid/local anesthetic injection. In fact, symptoms developed several hours after the procedure, suggesting that steroid embolism was not responsible for the complication. Indeed, the case description accurately depicts the clinical course of vertebral artery dissection: thrombosis of the artery leads to brainstem and cerebellar ischemic infarctions and swelling that blocks the outflow of the cerebrospinal fluid from the fourth ventricle resulting in acute hydrocephalus and acute increase in intracranial pressure. Early emergency ventriculostomy, as performed in this case, may be life saving. However, if the affected artery is the dominant vertebral artery and consequently, most of the blood flow to the brainstem and the cerebellum is dependent on the integrity of this artery, the dissection and thrombosis that follow usually result in death. Under these circumstances, the massive ischemic infarct affecting both the brainstem and the cerebellum progresses to a hemorrhagic infarct when both the capillary and the blood brain barrier are disrupted due to the ischemia and brain death follows due to the acute, severe increase in intracranial pressure. In fact,
190
the case reported in reference 75 quoted by Beckman et al.4 illustrates this situation. The other point that deserves discussion is the mechanism of vertebral artery injury by a 25-gauge, 2.5 inch, short-bevel needle that results in a dissection. It is difficult for me to understand how this can happen in the face of normal anatomy of the artery. The postmortem description of a case of vertebral dissection and death after a TESI5 points out that “there was minute, barely visible hemorrhage over the vertebral artery and along the cervical spinal cord,” suggesting that the needle indeed did not produce major trauma to the artery. I submit that the patients described in these 2 manuscripts4,5 already had a small dissection of the vertebral artery and that there was an unintentional artery puncture during the procedure that resulted in a small hemorrhage between the intima and the wall of the artery that led to further dissection and thrombosis with the resultant clinical picture already described. In fact, the literature suggests that this condition is prevalent in patients with: (1) history of chiropractic or osteopathic neck manipulations, particularly when performed with the head in the neutral or extended position;5-8 (2) migraine headaches;9 and (3) automobile accidents, even when the neck is exposed to mild acceleration/deceleration forces.10 It is also noteworthy that there is a 3:1 ratio between females and males affected by this condition.10 The patient in Beckman’s report4 had a history of migraine headaches and was a pilot. It would be interesting to know if he was exposed to acceleration/decelerations during his tenure as a pilot (e.g, fighter pilot). Re-evaluation of the magnetic resonance image of the cervical spine that was performed prior to the TESI could reveal if he indeed had a preprocedure dissection. Considering the chain of events that trigger an infarction of the cerebellum/brainstem culminating in massive cerebral edema and cerebellar tonsillar herniation, I suggest that it is critical for pain specialists to recognize: (1) the concept of dominant vertebral artery in humans;11 (2) the high prevalence of vertebral artery dissection at the low cervical levels in young patients with a history of neck manipulations, motor vehicle accidents and/or acceleration and deceleration injuries to the neck, and migraine headaches; (3) the role of magnetic resonance imaging of the neck in identifying these patients prior to a TESI;11 (4) that this potentially lethal complication may occur after puncture of a vertebral artery with an ongoing dissection at the lower cervical levels in patients with dominant flow; and (5) the potential role of emergency ventriculostomy and cerebellar debridement as a lifesaving procedure. This information brings further arguments against performing TESI in the cervical spine, particularly at the low cervical levels where the course of the artery is unpre-
Regional Anesthesia and Pain Medicine, Vol 33, No 2 (March–April), 2008: pp 190 –193
Letters to the Editor dictable and the risk for dissection is high in patients that are likely to present with chronic neck pain. Oscar A. de Leon-Casasola, M.D. Department of Anesthesiology State University of New York at Buffalo Pain Medicine and Oncology Roswell Park Cancer Institute Buffalo, NY References 1. Provenzano DA, Fanciullo G. Cervical transforaminal epidural steroid injections: Should we be performing them? Reg Anesth Pain Med 2007;32:168. 2. Beckman WA, Mendez RJ, Paine GF, Mazzilli MA. In reply. Reg Anesth Pain Med 2007;32:169-170. 3. Hoeft MA, Rathmell JP. In reply. Reg Anesth Pain Med 2007; 32:169. 4. Beckman WA, Mendez RJ, Paine GF, Mazzilli MA. Cerebella herniation after cervical transforaminal epidural injection. Reg Anesth Pain Med 2006;31:282-285. 5. Rozin L, Rozin R, Koehler SA, Shakir A, Ladham S, Barmada M, Dominick J, Wecht CH. Death during transforaminal epidural steroid nerve root block (C7) due to perforation of the left vertebral artery. Am J Forensic Med Pathol 2003;24: 351-355. 6. Barinagarrementeria F, Amaya LE, Cantu C. Causes and mechanisms of cerebellar infarction in young patients. Stroke 1997;28:2400-2404. 7. Nakamura CT, Lau JM, Polk N, Popper JS. Vertebral artery dissection caused by chiropractic manipulation. J Vasc Surg 1991;14:122-124. 8. Haldeman S, Kohlbeck FJ, McGregor M. Stroke, cerebral artery dissection, and cervical spine manipulation therapy. J Neurol 2002;249:1098-1104. 9. Smith WS, Johnston SC, Skalabrin EJ, Weaver M, Azari P, Albers GW, Gress DR. Spinal manipulative therapy is an independent risk factor for vertebral artery dissection. Neurology 2003;60:1424-1428. 10. Rubinstein SM, Peerdeman SM, van Tulder MW. A systematic review of the risk factors for cervical artery dissection. Stroke 2005;36:1575-1580. 11. Yoshimoto Y, Wakai S. Unruptured intracranial vertebral artery dissection. Clinical course and serial radiographic imagings. Stroke 1997;28:370-374.
191
which they administered 8 to 10 mL of 1 percent procaine at the C7 level. And, in the monograph3 as well as our article of over 2,000 SGBs,4 10 mL of local anesthetic was injected also at the C7 level. In the majority of described applications, SGB is used to provide temporary sympathetic denervation of the upper extremity.3,4 Whether 5 or 10 mL is administered probably makes little or no difference, unless all the sympathetic fibers to the upper extremity are to be blocked. In 1947, Kirgis and Kuntz5 showed that complete sympathetic denervation of the upper extremity requires block of the second and third thoracic ganglion in a relatively high percentage of cases. This is necessary because rami from the second and third thoracic ganglia bypass the stellate ganglion (Fig 1). These nerves have been termed the “nerves of Kuntz.” The study by Feigl et al.1 confirms our findings in corpses as well as in subsequent clinical studies3,4 that if all the sympathetic nerves to the upper extremity are to be blocked, performing SGB with less that 10 mL of injectate is unlikely to do so. Indeed, with the use of 5 mL, they found that contrast distribution ended at level T2 in 17 of 28 cases (61%). In contrast, with 10 mL, the peak of caudal extension most often ended at the level of T2 to T3. Furthermore, the present study1 was con-
Accepted for publication May 7, 2007. doi:10.1016/j.rapm.2007.05.007
Therapeutic Stellate Ganglion Block: 5 Versus 10 mL of a Local Anesthetic To the Editor: The anatomical and radiologic study of bilateral stellate ganglion block (SGB) at C6 in 42 cadavers by Feigl et al.1 proposed a reduction of local anesthetic, ideally to as low as 5 mL. This study and their recommendation regarding reduced injectate volumes would benefit from a historical review. To support administering 5 mL, the authors state: “Volumes lower than 10 mL [for SGB] are cited by Smith and Moore.”1 However, they have misinterpreted our original data. Neither of us used significantly less than 10 mL or injected at the level of C6. Smith2 described 1,500 injections on 400 patients in
Fig 1. Variations in the sympathetic nerve distribution to the brachial plexus showing the intrathoracic rami from second and third thoracic nerves bypassing the stellate ganglion on their way to the upper extremity. Model after Kirgis and Kuntz.5 Reprinted from Moore.3