Management of vasospasm seems to be a favourite topic among CICM exmainers. It has come up several times in the past papers and vivas. The following is a list of representative SAQs:
A chapter of Oh's Manual (Ch. 51, pp 568) is the canonic resource for these topics. The gospel of subarachnoid management seems to be this 2012 Guidelines Statement from the AHA. Another good resource is available from Expert Reviews - it is an article from 2015 which lists and discusses all the successfull and unsuccessful trials in this area. The Dabus-Noguiera article quoted in LITFL also offers some opinions about the weirder therapies for AH, such as fasudil, colforsin, IABP, partial aortic occlusion, and so forth.
As far as non-journal study resources go, the LITFL review of vasospasm and DCI is a treatment with satisfying levels of detail; with its authors' interest in neurocritical care being well known, its value is significant as a distillate of his expertise.
For the purpose of this short summary, all these sources have been combined and remixed.
These are a selection of the Class I recommendations made by the AHA.
No difference in risk between clipping and coiling.
This is a much-spoken-of complication of subarachnoid blood. Generally speaking, 70% of patients will develop this complication.
Firstly, the definitions. They seem to overlap somewhat. And there are thousands of them; just see this table from Nature (2011). Some of the definitions quoted below are derived from proposals made by a multidisciplinary research group, published in Stroke in 2010; others were made by researchers who pined for a clinically relevant definition.
Delayed Cerebral Ischaemia (DCI):
Clinical deterioration caused by DCI
In brief, you know it's vasospasm when...
Or, alternatively, there are no symptoms, and your patient is having a silent vasospasm. Therein lies the disadvantage of clinical examination.
There are several techniques of imaging which can be used to recognise vasospasm:
Conventional 4 vessel DSA (Digital Subtraction Angiography):
On DSA assessment, the vasospasm may be graded:
Transcranial Doppler (TCD):
The classical risk factors are as follows:
A recent analysis of 370 patients has added several more risk factors:
That's important to know.
One could (and perhaps one day will) devote a massive excess of attention to this fascinating area.
For now, I will limit myself to quoting LITFL's article by Oliver Flower, which mentions the following:
The reference for this is likely an article by Kolias and Belli from 2008 (Journal of Neuroscience Research).
The BRANT trial from England has demonstrated a massively decreased risk of SAH-induced stroke in patients receiving nimpodipine - they were 34% less likely to develop stroke. One ought to continue nimodipine for 21 days to get the optimal effect. The usue of nimodipine undergoes a more thorough dissection in the following chapter (Evidence for the use of nimodipine in SAH)
This -drug the other calcium channel blocker for vasospasm - also appears to have some sort of cerebral vessel selectivity. Trials from the 1990s support its use as a means of preventing vasospasm; however there was no heroic stroke reduction, and both the treatment and placebo groups had the same outcomes at 3 months. In more recent research focus has shifted to using it intrathecally, or intrarterially, or as a slow-release implant. A 2013 meta-analysis of RCTs (5 of them) has finally found some outcome benefit, but only after combining all the intravenius intrathecal and intraarterial data, which seems like a strange strategy.
Since its debut in 1990, "Triple H" therapy for subarachnoid haemorrhage has been used in ICUs worldwide as a means of protecting the SAH patients from vasospasm-induced stroke.
Hypertension, hypervolaemia, hemodilution. In order to prevent hypoperfusion injury, the prevailing theory was that the blood pressure should be high, the blood volume should be hyperexpanded, and the hematocric should be low (to decrease blood viscosity). This theory seems to have arisen from the simple relationships of fluid dynamics, where pressure gradients and fluid viscosity are the governing determinants of flow rate.
Myburgh has offered this strategy a nice overview in CCR(2005) and couldn’t recommend it on the balance of evidence. Cerebral autoregulation thresholds are too variable among patients, he says, and probably vary regionally among different parts of the cerebral circulation.
Do the experts agree? No of course they do not. Myburg’s opinion is contradicted by Dhar et al, whose prospective physiological study found that Triple H therapy (all three independently) improve cerebral oxygen delivery to vulnerable regions. The debate about this is ongoing. Thus far, the 2009 iteration of the Stroke guidelines for management of SAH has concluded that induced hypertension as part of Triple H therapy is a “reasonable approach”, even though the enthusiastic evidence for its use is far from satisfactory.
The most recent spoonfulls of evidence added into this cauldron have been generally unsupportive of "Triple H" therapy. In 2010, a review of the literature found no evidence to support the use of the full package, or any of its components individually. In 2014, the Japanese have confirmed a lack of improvement in clinical outcdomes in a prospective multicentre study. With such a heterogeneously lumpy porridge of evidence, it is little wonder that a 2014 survey of management protocols has found "striking variability in the practice patterns of European physicians", with 44% of responders using "Triple-H" therapy in spite of the patchiness of the evidence in support of it.
Spilled blood causes vasospasm(it is thought), so one might think that causing a premature breakdown of this blood is beneficial in the prevention of vasospasm. The injection of urokinase followed by some unusual head movements was viewed as a good idea by some Japanese investigators, and had yielded a 50% decrease in vasospasm and associated complications. It is still viewed as an "experimental" therapy.
There was some interest in the idea that statin therapy might somehow decrease the morbidity from subarachnoid haemrorrhage . The STASH trial has compared placebo to an 80mg dose of simvastatin, and was forced to conclude that the findings "do not support a beneficial effect of simvastatin in patients with SAH "
Given the smooth-muscle-relaxing effects of magnesium cations, its application to cerebral vasospasm seems no great logical leap. The MASH-2 trial from 2012 was a multi-center investigation of 64mmol of MgSO4 per day, randomised among 606 patients, which somberly concluded that "intravenous magnesium sulphate does not improve clinical outcome after aneurysmal subarachnoid haemorrhage".
Clazosentan (a relative of bosentan) is an endothelin-1 receptor antagonist, and it has been investigated in the aptly named Clazosentan to Overcome Neurological iSChemia and Infarct OccUrring after Subarachnoid hemorrhage (CONSCIOUS-1) trial. The complications of clazosentan therapy (such as anaemia and hypotension) were "manageable". Its use, at least in in severe and moderate vasospasm, demonstrated "a trend toward improvement", as opposed to actual improvement. In short, these drugs only merit the most lukewarm of recommendations.
Nicardipine (as above) has been used intra-arterially to selectively dilate the spasming vessels. Similarly, papaverine ( phosphodiesterase inhibitor) and verapimil (another calcium channel blocker) have been used with some effect, and remain in routine use today. The most recent Critical Care Guidelines on the Endovascular Management of Cerebral Vasospasm have found papaverine to be the most extensively studied agent, and the one with the greatest amount of support behind it; less data exists in support of verapimil and nicardipine. Milrinone has also showed some promise, both as an intrarterial agent and as an inthrathecal irrigation; there may be an additive effect with nimdipine in the setting of refractory vasospasm.
If one does not wish to expose the patient to intraarterial vasodilators, one may instead address the spasm in a very direct and brutally mechanical way, but dilating the spasmed vessel with a balloon. The abovementioned guidelines statement had identified 27 studies. There seems to be some disagreement as to which is better (intraarterial papaverine vs. balloonoplasty studies have a substantial degree of heterogeneity in their reported outcomes). There is no disagreement, however, about the risks - balloons have a known association with arterial rupture and fatal haemorrhage.