CC BY-NC-ND 4.0 · J Neuroanaesth Crit Care 2018; 05(03): 131-132
DOI: 10.1055/s-0038-1675439
Indian Society of Neuroanaesthesiology and Critical Care

Current Status of Stellate Ganglion Block for the Management of Cerebral Vasospasm

Girija Prasad Rath
1   Department of Neuroanaesthesiology and Critical Care, All India Institute of Medical Sciences (AIIMS), New Delhi, India
Ritesh Lamsal
1   Department of Neuroanaesthesiology and Critical Care, All India Institute of Medical Sciences (AIIMS), New Delhi, India
› Author Affiliations
Further Information

Publication History

Publication Date:
30 October 2018 (online)

Delayed cerebral ischemia (DCI) is an important cause of mortality and long-term morbidity in patients with aneurysmal subarachnoid hemorrhage (aSAH). Historically, cerebral vasospasm was considered as the only major underlying pathology leading to cerebral ischemia and infarct in these patients. Several attempts to mitigate the effect of vascular spasm have been made in the form of oral,[1] intravenous,[2] and intra-arterial nimodipine,[3] intra-arterial papaverine,[4] intrathecal drugs,[5] hemodynamic augmentation,[6] pharmacologic sympatholysis,[7] and various intra-arterial catheter-based techniques.[8] However, we now understand that the pathophysiology of DCI is complex, and vasospasm is only one of many contributing pathologies.

The cerebral vessels are innervated by noradrenergic sympathetic nerves that constrict these vessels on stimulation, forming the basis of pharmacologic sympatholysis to reverse the effects of vasospasm. The stellate ganglion block (SGB) is the most popular technique to achieve pharmacologic sympatholysis in established vasospasm. The technique of SGB has evolved over the years from being a landmark-based, blind procedure to fluoroscopic-guided, and more recently, ultrasound-guided. The use of the ultrasound has become ubiquitous in the intensive care units (ICUs), and intensivists are becoming increasingly adept at ultrasound techniques for several clinical applications. The appearance of Horner's syndrome is described as an indicator of successful cervical sympathetic block. However, even in experienced hands, it is not possible to reliably block the stellate ganglion in every patient using blind percutaneous techniques. Use of ultrasound technique facilitates accurate deposition of local anesthetic at the desired site, reduces the required volume of the anesthetic, and prevents procedure-related complications, such as inadvertent vascular, neural, pleural, and other soft tissue injury. Moreover, anatomic variations exist in the formation of the stellate ganglion from one person to another. Hence, it is difficult to justify the use of the blind technique for SGB in modern ICUs.

Since Tregiarri et al[7] first reported improved outcome with cervical ganglion block using bupivacaine and clonidine in patients with angiographically confirmed vasospasm, several similar attempts have been made and reported. Gupta et al[9] reported a significant increase in estimated cerebral perfusion pressure and decrease in zero-flow pressure (a surrogate of vascular tone), without any deleterious effect on cerebral autoregulation with SGB, using 2% lidocaine in patients with complex regional pain syndromes of upper limbs. There are several case reports documenting the utility of SGB in reducing vasospasm related to both anterior and posterior circulation aneurysms.[10] [11] Jain et al[12] found improvement in Glasgow coma score, significant reduction in ipsilateral middle cerebral artery flow velocity, and reduction in neurologic deficits after SGB in patients who had established vasospasm following surgical clipping of aneurysm. However, all these studies have reported their findings based on a small number of patients. None of these underpowered studies have enrolled more than 20 patients raising serious questions about the statistical implications of the study results.

The sympathetic nervous system is a potent modulator of vascular tone in peripheral vessels, but the effect of sympathetic stimulation on cerebral vasculature remains a matter of debate in both human and animal-based models, with many studies reporting contradictory results. Magnetic resonance angiography in healthy volunteers after SGB has shown variable effects on extra- and intracranial blood vessels.[13] Some studies have shown a significant increase in the caliber of intracranial major vessels, while others have failed to demonstrate meaningful reduction in cerebral blood flow velocity after SGB.[14] [15] [16]

From the viewpoint of pharmacodynamics, it seems prudent to assume that any maneuver that causes cerebral vasodilatation should reverse the detrimental effect of vasospasm, at least to some degree. However, other than inducing hypertension and administration of nimodipine, no other pharmacologic measure has conclusively proven to ameliorate the long-term neurologic outcome in patients with established vasospasm. Even nimodipine is believed to exert its beneficial effect possibly by neuroprotective mechanisms and not due to its vasodilatory properties.[17] This highlights the pathophysiologic complexities of managing DCI, and that an interaction of incompletely understood distal cellular events, such as inflammation and leucocyte infiltration, microthrombosis, free-radical injury, cortical spreading depolarization, endothelial proliferation, and cellular apoptosis, have a pivotal role in determining the overall neurologic outcome. Studies in animal models suggest that in addition to cerebral vasodilatation, SGB can exert its beneficial effects by altering the expression of several proteins in the brain and promoting antiapoptotic signaling.[18]

Delayed cerebral ischemia is a dreaded complication of aSAH, which can leave the patient with crippling complications and poses a huge burden on the health care delivery system. There are several ongoing studies using protein kinases, sildenafil citrate, newer nitric oxide progenitors, and intracisternal instillation of various drugs, but as of now, lack of high-quality evidence has left the physician with very few tools for successfully managing DCI. SGB emerged as a promising bed-side intervention for managing refractory vasospasm nearly two decades back but has seemingly fallen out of favor in the recent past. The recent combined guidelines from the American Heart Association and the American Stroke Association for the management of aSAH provided no recommendation on the use of SGB for vasospasm.[17] There may be some justification in the recent loss of popularity of SGB but the lack of an adequately powered randomized study on its utility in treating DCI is glaring. SGB continues to be practiced in some centers around the world. Anecdotal mention of SGB in some recent literature encourages the debate on its role as an adjunct to standard therapy for cerebral vasospasm, albeit, with a strong need for further evaluation.

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