Emergent Phenol Injection of Bilateral Stellate Ganglion for Management of Refractory Malignant Ventricular Arrhythmias

Background

The primary mechanism of death in the United State is sudden cardiac death, often due to malignant ventricular arrhythmias secondary to ischemic heart disease. Conventional management includes implantable cardiac defibrillator (ICD) therapy coupled with correction of all contributing features and management of cardiac disease. If ventricular tachycardia/fibrillation (VT/VF) episodes are frequent, then further therapy consists of antiarrhythmic drug and catheter ablation. Recurrent shocks from ICDs have been shown to increase morbidity and mortality in patients with refractory VT/VF [1,2]. “Electrical storm” is defined as 3 or more anti-tachycardia pacing or ICD shock therapy delivered within a 24-h period [3]. Recent publications discuss the use of cardiac sympathetic denervation to manage electrical storm, but management of ongoing electrical storm that is nearly incessant is not well defined [4–10]. This report describes 2 patient experiences utilizing emergent percutaneous stellate ganglion ablation (SGA) to achieve cardiac sympathetic denervation for acute management of recalcitrant electrical storm.

Case Reports

FIRST CASE REPORT:

The patient was a 51-year-old man with an ischemic cardiomyopathy, severe mitral regurgitation, atrial fibrillation, ICD, and a left ventricular ejection fraction of 25%. He presented with unstable angina and underwent elective coronary artery bypass graft surgery and mitral valve repair. His post-operative course was complicated by 7 episodes of VF occurring within 5 h and each successfully managed with a single ICD shock therapy. It is important to note that the VF episodes were not preceded by monomorphic VT nor triggered by a recurrent premature ventricular ectopic focus. His hemodynamic status deteriorated and he was placed on extracorporal mechanical oxygenation (ECMO) with systemic anticoagulation. The intended goal was to proceed with an empiric scar-based catheter ablation, but the ventricular arrhythmias could not be quieted. The patient continued with malignant ventricular arrhythmias (41 episodes treated with 24 ICD shocks and 17 pace-termination) despite intravenous amiodarone and lidocaine and correction of all electrolyte abnormalities. Left-heart catheterization showed patency of the bypass graft. With deteriorating hemodynamics, progressive ventricular arrhythmias, worsening heart failure, and all conventional therapies for malignant ventricular arrhythmias being unsuccessful, the patient underwent emergent percutaneous fluoroscopically-guided bilateral SGA. While supine, intubated, and with ECMO support, the left and then right stellate ganglion were identified guided by anatomic landmarks. Utilizing a 22-guage, 3.5-inch spinal needle, contrast dye was injected with appropriate outline of the stellate ganglion at the uncinate process of the C6 vertebra. Subsequently, a total of 8 ml of bupivacaine 0.5% was injected with aspiration every 2 ml, followed by 10 ml of phenol 6% (a total of 16 ml of bupivacaine and 20 ml of phenol was utilized bilaterally). Successful SGA was confirmed by intentional Horner’s syndrome with bilateral eye lag. The procedure was completed in 28 min, with a fluoroscopy time of 7.8 min. During the procedure, the patient received 2 ICD therapies.

The initial response to bupivacaine/phenol injection was an abrupt increase in ventricular ectopy and continued, albeit less frequent, ICD shock therapy (9 in 16 h); however, following this burst of VT/VF, there were no further ventricular arrhythmias for the subsequent 13 days. Intravenous antiarrhythmic medications and ECMO support were discontinued at about 72 h after SGA. The patient initially improved, but then subsequently died due to sepsis.

SECOND CASE REPORT:

The second patient was a 59-year-old man with an ischemic cardiomyopathy and left ventricular ejection fraction of 20%. Nine days after percutaneous endocardial ablation for recurrent ICD therapies for rapid VT (cycle length 250–280 ms), he presented with dyspnea, volume overload, and biventricular congestion. Within 12 h of admission, he experienced recurrent ventricular flutter with loss of consciousness, managed with 9 ICD shock therapies. He was intubated, oral antiarrhythmic medication was discontinued, and intravenous amiodarone was started. Left-heart catheterization demonstrated elevated left ventricular pressures and no stenosis amenable to intervention. Despite management of acute congestion, ventricular ectopy continued with long runs of rapid nonsustained VT, and then a subsequent day of rapid ventricular flutter and multiple ICD shocks (12 within 4 h) with subsequent cardiogenic shock. Emergently, the patient underwent bilateral SGA as described above in Case #1, but using a larger volume of 0.5% bupivacaine (10 ml), and 10 ml of 6% phenol on each side. The procedure was completed in 34 min with 9.2 min of fluoroscopy. Immediately following SGA, bilateral eyelid drooping consistent with Horner’s syndrome was noted. Following SGA, the patient did not undergo any further ICD therapies and eventually was managed with total heart replacement.

Discussion

CARDIAC SYMPATHETIC DENERVATION:

There are extensive bidirectional afferent and efferent signals and feedback continuously transmitted between the heart and brain [6]. In the presence of a cardiomyopathy, there is excess sympathetic output, with an associated increase in ventricular arrhythmias. Furthermore, particularly in ischemic cardiomyopathy, following initial myocardial and cardiac nerve injury, the response is axonal regeneration with nerve sprouting [12,13]. This neural remodeling results in regional heterogeneity of autonomic innervation which, coupled with increased sympathetic output, results in increased risk of malignant ventricular arrhythmias. Similar adverse changes have also been reported in stellate ganglion with hypertrophy, inflammation, and oxidative stress [17]. Cardiac sympathetic denervation interrupts, at the pre-ganglia level, the release of neurotransmitters and thus reduces cardiac adrenergic tone, which has been used to manage ventricular arrhythmias in the setting of inherited diseases (e.g., long QT syndrome) as well as structural heart disease.

PRIOR STUDIES:

Numerous publications have reported the benefit of cardiac sympathetic denervation using surgical techniques [4–7,10,14], but this approach is intended for patients not actively experiencing unstable ventricular arrhythmias. For patients who are unable to tolerate surgical denervation, prior studies have reported the use of percutaneous local anesthesia injection for temporary sympathetic blockade to stop the electrical storm [15,16,18,19]. Similar to the current case reports, bupivacaine was used for an immediate suppression of stellate ganglion function; however, unlike prior reports, the present case studies demonstrate that permanent SGA can be achieved with the use of phenol.

Conclusions

The case reports presented in this article suggest that in patients with refractory malignant ventricular arrhythmias, bilateral chemical SGA can be considered using bupivacaine with phenol. It is important be aware that SGA should be introduced only after exhausting routine interventions and after a thorough investigation for reversible causes of the ventricular arrhythmias, including catheter ablation, antiarrhythmic drug therapy, ECMO, optimization of medical therapy, exclusion/management of ischemia, and management of any acute heart failure. Certainly, SGA is aggressive considering the risk of complications (e.g., vascular uptake, high epidural blockade, pneumothorax, recurrent laryngeal nerve block, transmyelitis, and hematoma); however, for the rare patient in which there are no alternative therapies and the clinical course is dire, this readily implemented technique may halt the ventricular storm and provide a window for recovery.