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.