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Stellate Ganglion Blockade for Ventricular Arrythmias: An Effective Tool for an Ineffective Rhythm

Oct 30, 2019, 13:13 PM by Akshat Gargya, MBBS; Nam Ly, MD; Ran Abdallah, MD, PhD, MBA

Sympathectomy has been studied and used for centuries in the treatment of pain and currently has varied applications in pain management.[1] Sympathetic signals from the stellate ganglion (SG) contribute to the pathophysiology of multiple conditions, including complex regional pain syndrome (CRPS) of the upper extremities, postherpetic neuralgia, and arrythmias. During the early part of 20th century, scientific theories emerged to explain the role of stellate ganglion blockade (SGB), including blocking adrenergic-induced hypersensitivity, and reducing central hyperexcitability by interrupting the coupling of sympathetic noradrenergic neurons with primary afferent neurons.[1],[2] During World War I, researchers investigated the SG’s structure and function because soldiers with limb injuries manifested CRPS symptoms. By the end of World War II, SGB was commonly used to treat CRPS of the head, neck, and upper extremities.[3] As its use grew, the scope of treatment expanded to other pain syndromes, including intractable angina, phantom limb pain, postherpetic neuralgia, cancer pain, ischemic pain, hot flashes, and intractable cardiac arrythmias.

The sympathetic system arises from the thoracolumbar division of the spinal cord, where the sympathetic chain ganglia are positioned at the dorsal and ventral roots. Sympathetic nerve fibers exit the spinal cord through the ventral root and enter the sympathetic chain from the white rami. While in the sympathetic ganglia, some nerves may travel up or down spinal cord levels prior to synapsing, exiting through the grey rami before making their way to end organs. Cervical sympathetic chain ganglia are formed when nerves (preganglionic) from the thoracic spinal cord (predominantly T1–T6) communicate and synapse before innervating (postganglionic) portions of the head, neck, and upper extremities.[3],[4] The cervical ganglion’s three paravertebral ganglia (superior, middle, and inferior cervical) provide sympathetic innervation to the blood vessels, structures (eyes, larynx, pharynx, and trachea), and glands (lacrimal, salivary, and thyroid) in the head, neck, and upper extremities.[4] The cervical sympathetic chain also sends signals to the heart through the cardiac plexus.[4] In 80% of the population, the inferior cervical and the first thoracic ganglia fuse to form the cervicothoracic ganglion, which is named SG for its appearance.[4]

SGB can be a diagnostic, therapeutic, or even preventive tool. Sympathetic innervation to the head and neck and upper extremities comes from T1–T3 and T2–T6, respectively. Hence, SGB will abolish most sympathetic input to the head, neck, and ipsilateral upper extremities, in addition to blocking the cardiac accelerator fibers (T1–T4).[5] Cardiac sympathovagal imbalance via accelerated discharge from cardiac accelerator fibers can contribute to various arrythmias, including electrical storm (ie, multiple ventricular arrhythmias in a short period of time). Management strategies for ventricular tachycardia include drug therapy, implantable cardioverter defibrillators (ICDs), and cardiac radiofrequency catheter ablation. Refractory cases are highly challenging, especially when patients are deemed too sick for conventional ablation treatments.[6-8]


SGB can be a diagnostic, therapeutic, or even preventive tool.... SGB will abolish the majority of sympathetic input to the head, neck, and ipsilateral upper extremities, in addition to blocking the cardiac accelerator fibers.


Sympathetic supply plays a significant role in the initiation of ventricular arrhythmias, and sympathectomy has also been reported as a helpful tool. A meta-analysis of 22 unique case series since the 1970s, which included patients whose arrhythmias were not controlled by drug or mechanical support, showed reduction in arrhythmia burden and need for defibrillation after SGB.[9] Another study also supported the effectiveness of sympathetic blockade in electrical storm patients with recent myocardial ischemia when compared with standard arrhythmic therapy.[10] In cases of myocardial injury, the rationale for the use of SGB stems from animal studies, which have shown maladaptive remodeling of the autonomic nervous system and spinal cord neuronal pathways after myocardial insult.[11]

Sympathetic denervation has also shown its potential usefulness in the treatment of patients with long QT syndrome.[12] In the past year, we have successfully performed five SGBs in patients with uncontrolled ventricular arrhythmias and succeeded in decreasing their frequency. In one case, we achieved a silencing of ventricular arrhythmia for 6 weeks. We plan to publish our case series in the near future.

Figure 1: Cross sectional anatomy of stellate ganglion.

ASM, anterior scalene muscle; IJV, internal jugular vein; SG, stellate ganglion; Th, thyroid; VA, vertebral artery. Image courtesy of NYSORA.

SG is surrounded by multiple structures, increasing the likelihood of iatrogenic complications during SGB. Hence, a good understanding of the anatomy is paramount prior to the block. SG lies at the C7 level in between the C7 transverse process and the neck of the first rib.[4] Anterior to the ganglion is the carotid sheath (carotid artery, internal jugular vein, vagus nerve) and apex of the lung (see Figure 1). The vertebral artery also crosses anteriorly to the SG before diving deep into the transverse foremen of C6 as it ascends superiorly. Posterior to SG lies the C7 transverse process, phrenic nerve, and brachial plexus.[4] Medial to SG are the C7 vertebral body, longus colli muscle, esophagus, and trachea, and laterally are the scalene muscles.[2] Inferiorly lies the subclavian artery and the apex of the lung.

In a 2017 study, the most common complication noted was hoarseness and dysphagia, seen in 54% of patients.[13] Other less common complications included pneumothorax and contralateral Horner syndrome, both of which manifested in 3% of patients who underwent SGB.[13] Retropharyngeal hematoma, although rare with an incidence of 1 in 100,000 SGB, may require urgent intubation for airway protection.[14] A need to reduce complications has driven the standard of care away from the initial non–image-guided techniques toward approaches that employ various imaging modalities for localization.

For first SGBs, described during the early 20th century, physicians achieved localization with surface landmarks and palpation. SGB’s target is the C6 tubercle (Chassaignac’s tubercle), which is a level above the position of SG at C7. This allows for local spread to the ganglion and decreases the chances of accidental vertebral artery injury. Currently, ultrasound is the preferred imaging modality because it decreases the chance of intrathecal or intravascular injection and minimizes the possibility of injuries, including recurrent laryngeal nerve paralysis or esophageal perforation, to surrounding structures.[3] Other imaging modalities that can be used include fluoroscopy (C-arm) and computed tomography scan.

When performing SGB under ultrasound guidance, the patient is initially placed in the supine position with the neck in slight extension. The ultrasound probe is positioned at the level of the thyroid cartilage, which usually correlates to the C6 level. Local anesthetics can be used for patient comfort. Following a lateral, in-plane approach, a 22 G needle is directed to the prevertebral fascia between the carotid artery and the tip of C6 anterior tubercle (see Figure 2). Local anesthetic (8–10 mL) is injected in the prevertebral fascia plane. The patient should then be monitored for signs of a successful block, which include ipsilateral development of Horner’s syndrome (ptosis, miosis, and anhidrosis), nasal congestion, facial flushing, or increase in temperature of the upper extremity.

Figure 2: Patient positioning and ultrasound image of stellate ganglion block. ASM, anterior scalene muscle; CA, carotid artery; IJV, internal jugular vein; L, lateral; M, medial; N, needle; SCM, sternocleidomastoid muscle; SG, stellate ganglion; VB, vertebral body.

 

Double-blinded, randomized trials and long-term patient follow-up to prove the efficacy of sympathectomy in patients with intractable ventricular arrhythmia are still lacking. Further research is required to investigate conventional or pulsed radiofrequency ablation of the SG as a potential tool for prevention of ventricular arrthymias. Current indications for SGB include chronic head and neck pain and CRPS, and some case reports have shown encouraging results for patients with ventricular arrthymias.[15] SGB can be a blessing in the debilitated cardiac patient population, many of whom suffer regularly from ventricular arrhythmias and associated distress of repeat ICD firing. Currently, SBG may be a valuable tool for pain physicians and cardiologists when treating patients with refractory ventricular arrhythmias who have failed conventional therapeutic and electrophysiological stimulation.

References

  1. Gunduz O, Kenis-Coskun O. Ganglion blocks as a treatment of pain: current perspectives. J Pain Res. 2017;10:2815–2826. https://doi.org/10.2147/JPR.S134775
  2. Jänig W, Baron R. Complex regional pain syndrome: mystery explained? Lancet Neurol. 2003;2:687–697.
  3. Sekhadia M, Chekka KK, Benzon HT. Stellate banglion blockade. In: Deer TR, Leong MS, Buvanendran A, Kim PS, Panchal SJ, eds. Treatment of Chronic Pain by Interventional Approaches. New York, NY: Springer;2015:139–147.
  4. Arslan O. Neuroanatomical Basis of Clinical Neurology. 2nd ed. Boca Raton, FL: CRC Press;2014:200–207.
  5. Rajesh M, Deepa KV, Ramdas EK. Stellate ganglion block as rescue therapy in refractory ventricular tachycardia. Anesth Essays Res. 2017;11:266–267. https://dx.doi.org/10.4103%2F0259-1162.194566
  6. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med. 2005;352:225–237. https://doi.org/10.1056/NEJMoa043399
  7. Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. New Engl J Med. 2002;346:877–883. https://doi.org/10.1056/NEJMoa013474
  8. Baher A, Valderrabano M. Management of ventricular tachycardia in heart failure. Methodist Debakey Cardiovasc J. 2013;9:20–25. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3600880
  9. Fudim M, Boortz-Marx R, Ganesh A, et al. Stellate ganglion blockade for the treatment of refractory ventricular arrhythmias: a systematic review and meta-analysis. J Cardiovasc Electrophysiol. 2017;28:1460–1467. https://doi.org/10.1111/jce.13324
  10. Nademanee K, Taylor R, Bailey WE, Rieders DE, Kosar EM. Treating electrical storm: sympathetic blockade versus advanced cardiac life support-guided therapy. Circulation. 2000;102:742–747. https://doi.org/10.1161/01.cir.102.7.742
  11. Ajijola O, Yagishita D, Reddy NK, et al. Remodeling of stellate ganglion neurons after spatially targeted myocardial infarction: neuropeptide and morphologic changes. Heart Rhythm. 2015;12:1027–1035. https://doi.org/10.1016/j.hrthm.2015.01.045
  12. Schwartz PJ , Snebold NG, Brown AM. Effects of unilateral cardiac sympathetic denervation on the ventricular fibrillation threshold. Am J Cardiol. 1976;37:1034–1040. https://doi.org/10.1016/0002-9149(76)90420-3
  13. Datta R, Agrawal J, Sharma A, Rathore VS, Datta S. A study of the efficacy of stellate ganglion blocks in complex regional pain syndromes of the upper body. J Anaesthesiol Clin Pharmacol. 2017;33:534–540. https://doi.org/10.4103/joacp.JOACP_326_16
  14. Higa K, Hirata K, Hirota K, Nitahara K, Shono S. Retropharyngeal hematoma after stellate ganglion block: analysis of 27 patients reported in the literature. Anesthesiology. 2006;105:1238–1245. https://doi.org/10.1097/00000542-200612000-00024
  15. Hayase J, Vampola S, Ahadian F, Narayan SM, Krummen DE. Comparative efficacy of stellate ganglion block with bupivacaine vs pulsed radiofrequency in a patient with refractory ventricular arrhythmias. J Clin Anesth. 2016;31:162–165. https://doi.org/10.1016/j.jclinane.2016.01.026

 

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