Unique Treatment of Ventricular Tachycardia Storm in a Patient With Cervical Spine and Chest Wall Injuries

Ventricular tachycardia storm (VTS/ES) is defined as the occurrence of three or more episodes of sustained ventricular tachycardia within a twenty-four-hour period, with or without a defibrillator. It has not been reported de novo in trauma patients. The literature indicates blunt cardiac injury as a potential etiology of ventricular dysrhythmia. We present a patient with a history of atrial fibrillation and a cardiac resynchronization device with a defibrillator who presented neurologically intact with cervical vertebral, internal, and bony thoracic injuries following a ground level fall. Within 24 hours, the patient developed VTS/ES that was ultimately resolved with a stellate ganglion block. This is the first report of a trauma patient with suspected blunt cardiac injury undergoing a stellate ganglion block following the onset of VTS/ES. Blunt cardiac injury is worth consideration as an etiology in post-trauma patients with ventricular tachycardia storm, particularly when no other source is identified. Stellate ganglion block, which can be performed at bedside with appropriate specialist availability, can be considered among treatment options in trauma patients.

Ventricular tachycardia (VT) has an estimated incidence of 15 per 100 000 people. ¹ The incidence of ventricular tachycardia increases with age and is more likely in persons with pre-existing cardiac disease. However, ventricular tachycardia can also occur in people with no symptoms or prior history and has a strong association with sudden cardiac death, thereby requiring early recognition and treatment. Ventricular tachycardia storm (VTS/ES), also known as electrical storm, is defined as the occurrence of multiple episodes of sustained VT within a twenty-four-hour period, with or without a defibrillator. ² Blunt cardiac injury (BCI) has been identified as an etiology of cardiac dysrhythmias in general. These most commonly develop 24-48 hours after the initial BCI. ³ We report a unique case of a patient who developed VTS/ES following a ground level fall with multiple injuries and suspected BCI and discuss a therapeutic intervention not previously reported in the trauma population. IRB approval and informed consent for publication were obtained.

The patient is a 76-year-old female who suffered a presyncopal fall onto a hard surface. She had a history of chronic atrial fibrillation treated with amiodarone, digoxin, and warfarin, as well as a cardiac resynchronization device with a defibrillator (CRT-D) due to a strong family history of sudden cardiac death in first-degree relatives. Her original CRT-D was explanted prior to her trauma in order to receive chest wall radiation therapy for breast cancer. A new CRT-D was reimplanted 12 weeks prior to her injury presentation. She reported never experiencing shocks from either CRT-D prior to admission. Interrogation of the device substantiated the patient’s report of no defibrillation events on the device before or within the initial hours of this admission. Her injuries were a subarachnoid hemorrhage, C6-C7 vertebral fractures with no neurological deficits, a left clavicle fracture, a left pleural effusion, and mediastinal hemorrhage surrounding the esophagus inferior to the aortic arch, measuring 4 × 2.7 centimeters. The thoracic aorta appeared intact on CT scan. The patient was admitted to the intensive care unit for monitoring and preoperative optimization. Her initial EKG showed atrial fibrillation with a controlled rate. In the first 24 hours, she began exhibiting recurrent, sustained episodes of ventricular tachycardia with marginal mean arterial pressures. Her high-sensitivity troponin T was elevated at 38 ng/L; however, CPK-MB was within normal limits. Cardiology consultants evaluating her clinical picture determined it was not consistent with significant myocardial ischemia or infarction. Digoxin toxicity was investigated as a cause of her symptoms but was ruled out after obtaining a “stat” digoxin level. The patient stated she was compliant with home oral amiodarone dosage. Cardiology recommended an amiodarone bolus and infusion. Her CRT-D was interrogated by the cardiac electrophysiologist and was found to have fired over 100 times since her admission, but none before. To investigate underlying structural and functional causes, she underwent a 2D echocardiogram, showing an ejection fraction of 47.7% and mild left ventricular enlargement with no additional significant findings. The cardiology team recommended an esmolol infusion.

Neurosurgery consultants delayed a planned stabilization procedure of her cervical spine fracture until the patient was deemed sufficiently stable from her cardiac dysrhythmia. The patient went to the operating room on hospital day three and underwent a successful posterior cervical fusion and fixation from the fourth cervical vertebra to the third thoracic vertebra. Postoperatively, the patient was transitioned to oral amiodarone but continued to have multiple episodes of ventricular tachycardia and CRT-D shocks. The cardiology team, in consultation with the neurosurgeon, did not wish to utilize external cardioversion or ablation techniques due to the presence of an internal defibrillator and potential associated risks with cervical injury. Both cardizem and lidocaine infusions added postoperatively failed to control the VTS/ES. The patient underwent a left heart catheterization on hospital day five that demonstrated no major coronary artery occlusions. On hospital day six, the lidocaine drip was discontinued and guideline-directed medical therapy (GDMT: renin-angiotensin system inhibitors, beta-blocker, mineralocorticoid receptor antagonists, and sodium-glucose cotransporter-2 inhibitors) was initiated. Despite numerous pharmacological interventions, the patient continued to have sustained episodes of VTS/ES. On hospital day six, a stellate ganglion block was recommended as an option. This intervention took place under ultrasound guidance at bedside in the ICU, was performed by an anesthesiologist, and resolved the ventricular tachycardia. The patient continued to recover, experiencing no further episodes of ventricular tachycardia, and was discharged home on hospital day thirteen with a regimen of GDMT as described above.

The differential for VTS/ES is broad and includes inherited, structural and functional heart diseases, and immune and infectious etiologies. In consultation with the cardiology team, including interventional and electrophysiology specialists, our patient did not meet criteria for these diagnoses. Ultimately, the cardiologists classified the etiology as “occult.” Despite trauma being omitted from cardiology literature as a cause of VTS/ES, we postulate based on the patient’s injury patterns, clinical history, timing of onset, lab results, and imaging findings, blunt cardiac injury was the most likely etiology or, at minimum, a significant catalyst to her dysrhythmia. Due to its indistinct clinical presentation and heterogeneous definition, BCI is not always evident during the initial survey of trauma. This patient’s clinical picture of elevated troponin in the absence of laboratory and EKG findings suggestive of cardiac ischemia, a mediastinal hemorrhage surrounding the esophagus just inferior to the aortic arch measuring 4 × 2.7 centimeters, left-sided pleural effusion, clavicular fracture, and ultimately direct evidence of coronary patency suggest significant potential for BCI as the etiology. The time frame of VTS/ES <24 hours after injury is typical of dysrhythmias resulting from BCI. ³ Information from the patient and interrogation of the patient’s CRT-D detecting VTS/ES only after admission and prior to her cervical spine fixation procedure essentially rules out VTS/ES as a pre-existing condition.

Management of VTS/ ES is challenging with limited available medical evidence. In general, a multidisciplinary approach including medical therapies such as antiarrhythmic drugs, sedation, external and internal defibrillation, as well as interventional approaches such as catheter ablation and stellate ganglion block, may be required. Accurate patient risk assessment is pivotal and should take into account hemodynamic tolerability as well as comorbidities like low LVEF, advanced New York Heart Association class, and chronic pulmonary disease. In high-risk patients, prophylactic mechanical circulatory support with left ventricular assistance devices or extracorporeal membrane oxygenation should be considered as a bridge to ablation accomplished by either radiofrequency, trans-coronary ethanol, and/or surgical cryotherapy methods as a conduit to recovery. In both high- and low-risk patients, every effort should be made to suppress VTS/ES and avoid further ICD shocks which lead to heart and multiple organ failure. ⁴

It is well established that the sympathetic nervous system plays an integral role in initiating and driving electrical storm. ⁵ Additional animal studies have shown that denervation of the stellate ganglion increased the threshold of ventricular fibrillation and it is likely this is the mechanism by which stellate ganglion block can halt electrical storm. ⁶ Pharmacological approaches to sympathetic blockade in hospitalized patients using β-blockers, though sometimes effective, have several shortcomings. The sympathetic nervous system involves multiple noradrenergic pathways and neuromodulators which are unaffected by these medications. Additionally, the β2 receptor which is untouched by the conventionally cardio-selective β-blockers appears to play an integral proarrhythmic role as well. Treatment failures can be overcome by approaches where the cardiac sympathetic supply in its entirety is decentralized with a number of interventions targeting multiple sites along the sympathetic chain. These include thoracic epidural/general anesthesia, stellate ganglion blockade, renal artery denervation, and surgical stellate ganglion resection. Cardiac sympathetic denervation is undeniably beneficial in certain conditions; however, consensus about where it fits into regular cardiology practice remains to be established. ⁷ Previous utilization of stellate ganglion block for VTS/ES in a hospitalized trauma patient has not been reported.

Fortunately, we were able to terminate the cascade of options for VTS/ES treatment at stellate ganglion block with the reported patient. We do not currently have long-term follow-up for recurrence. This is, to our knowledge, the first reported case of a trauma patient undergoing a stellate ganglion block following onset of VTS/ES with a suspected BCI mechanism. Stellate ganglion block can be performed as a bedside procedure and may be desirable for patients who failed medical management, whose injuries might be exacerbated by other treatment options, or in whom transport away from an ICU setting presents a risk factor in itself.