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Diagnosis of cerebral vasospasm and risk of delayed cerebral ischemia related to aneurysmal subarachnoid haemorrhage: an overview of available tools

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Abstract

In the first weeks following aneurysmal subarachnoid haemorrhage, cerebrovascular alterations may impact the outcome significantly. Diagnosis of cerebral vasospasm and detection of alterations at risk of delayed cerebral ischemia are key targets to be monitored in the post-acute phase. Available tools include clinical monitoring, as well as studies that can detect possible arterial narrowing, alterations of perfusion, metabolism and neurophysiology. Each technique is able to investigate possible vascular impairment and has different advantages and limits. All available techniques have been described. Among these, the most practical have been selected and compared for their peculiar characteristics. Based on this analysis, a flowchart to monitor these patients is finally proposed.

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Abbreviations

99 mTc-HMPAO:

Technetium 99 m coupled to hexamethylpropyleneamine oxime

ACA:

Anterior cerebral artery

AJDO2 :

Arterio-venous difference of O2

BA:

Basilar artery

BOLD MRI:

Blood oxygen level-dependent magnetic resonance imaging

CBF:

Cerebral blood flow

CBV:

Cerebral blood volume

CMRO2 :

Cerebral metabolic rate of oxygen

CT:

Computed tomography

CTA:

Computed tomographic angiography

CTP:

Computed tomographic perfusion

CV:

Cerebral vasospasm

CVR:

Cerebral vascular reserve

DCI:

Delayed cerebral ischemia

DSA:

Digital subtraction angiography

DWI:

Diffusion weighted image

EEG:

Electroencephalography

GADPH:

Glyceraldehyde-3-phosphate dehydrogenase

GCS:

Glasgow Coma Score

HSP7C:

Heat-Shock Cognate 7

ICA:

Internal carotid artery

LI:

Lindegaard index

MCA:

Middle cerebral artery

MFV:

Mean flow velocity

MRA:

Magnetic resonance angiography

MRI:

Magnetic resonance imaging

MTT:

Mean transit time

NIH-SS:

National Institute of Health Stroke scale

NIRS:

Near infrared spectography

OEF:

Oxygen extraction fraction

PCA:

Posterior cerebral artery

PCO2 :

Partial CO2 pressure

PET:

Positron emission tomography

PI:

Pulsatility index

PO2 :

Partial oxygen pressure

PWI:

Perfusion-weighted magnetic resonance imaging

RI:

Resistance index

ROI:

Region of interest

SAH:

Subarachnoidal haemorrhage

SJO2 :

Jugular venous oxygen saturation

SPECT:

Single photon emission computed tomography

TCD:

Transcranial Doppler

TOF:

Time of flight

VA:

Vertebral artery

WFNS:

World Federation of Neurological Surgeons grading scale

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Acknowledgments

This work is in part supported by the Umberto Veronesi Foundation, (Young Investigator Program, Postdoctoral Fellowship Award 2013-2014 to S.B.).

The authors would like to acknowledge the generous contribution of Dr. Lucio Castellan and of Prof. Antonio Uccelli of the Departments of Neuroradiology and Neurology of the University Hospital of Genova and of Dr. M. Federica Ferrio of the Department of Neuroradiology of the University Hospital of Torino for the helpful discussions and critical manuscript revision.

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Correspondence to Susanna Bacigaluppi.

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Jose Alberto Landeiro, Rafael Leal, Rio de Janeiro, Brazil

Subarachnoid haemorrhage, due to aneurysm rupture, is a significant cause of morbidity and mortality in relatively young patients. Its pathophysiology even today is not completely understood; hence, the development of proper strategies to prevent delayed neurological deficit is a great challenge.

Every paper that focuses on the management of this complex disease should be welcomed. This paper discusses about SAH and delayed cerebral ischemia in a concise and yet very enlightening manner. Its major strength is undoubtedly the multidisciplinary approach. Health-care providers with different backgrounds see problems with different perspectives; hence, complex diseases are much better managed. They not only described the methods involved in the detection of ischemia with their pros and cons, but most importantly, they also proposed a simple algorithm that helps the medical staff identify and treat high-risk patients.

The classic view that cerebral vasospasm is only responsible for brain ischemia has given place to a more contemporary understanding of this disease. This paper points out that delayed cerebral ischemia may be caused not only by vasospasm but also by several other factors such as inflammation and electrical disturbances (cortical spreading depression).

Inflammation, for instance, may lead to microcirculation impairment which leads to autoregulation disturbances. This makes patients more vulnerable to arterial blood pressure fluctuations that may ultimately lead to ischemia.

The knowledge on cerebral metabolism and its relationship with autoregulation, vasospasm, hydrocephalus and endothelial damage, among others, are critical when one intends to manage severe SAH and prevent brain damage. This paper certainly helped us further improve our knowledge.

References

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Giuseppe Lanzino, Ondra Petr, Rochester, USA

In this manuscript, the authors present a structured overview of available tools for the diagnosis, monitoring and measurements of the effects of vasospasm after aneurysmal SAH. An incredible number of publications have been devoted to the diagnosis and treatment of vasospasm, and yet, there are no strict evidence-based guidelines as to its proper management. After trying various and increasingly sophisticated tools, we now prefer a ‘minimalistic approach’, and we have come to the conclusion that ‘less is more’ in the diagnosis and treatment of vasospasm and we have seen excellent results (1,2).

In our unit, the most important and reliable method to monitor vasospasm is the ‘simple’ neurological examination. Patients at risk (with thick collection of blood in the subarachnoid cisterns) are closely monitored in the intensive care unit especially during the ‘high-risk’ period (i.e. between days 5–10 after the bleed). In these patients, we try to maximize cerebral perfusion by preventing hypovolemia and by aggressively draining cerebrospinal fluid (with the goal of decreasing the transmural pressure across the vessel wall). We pay close attention to warning signs of impending severe vasospasm such as a progressive, spontaneous increase of systemic blood pressure, fever, worsening headache and/or neck stiffness and pain and increasing velocity on TCDs. We avoid, as much as possible, the use of narcotics, which may mask early signs and symptoms of vasospasm. In addition, in patients with an already edematous brain, narcotics can induce further retention of pCO2 and increase the likelihood of further neurological deterioration.

When we suspect severe vasospasm, we perform a CT angiogram with perfusion studies. If this CT suggests severe spasm or, worse, parenchyma at risk, then we proceed with a catheter angiography. During angiography, the decision to proceed with either pharmacological (verapamil in our institution) or mechanical angioplasty is based on multiple factors like clinical condition of the patient and time elapsed from the bleeding. We tend to be more aggressive in patients who develop severe vasospasm early in their clinical course, i.e. within the first 6 days, as compared to those that manifest symptomatic vasospasm in the later stages after SAH. With the abovementioned management protocol, the incidence of severe vasospasm requiring pharmacological or mechanical angioplasty is very low.

The few patients who present poor clinical condition and do not improve after medical and neurological resuscitation represent a major challenge. As these patients remain in poor condition, there is no meaningful neurological exam to follow and their clinical management becomes very difficult. Despite all available technologies and diagnostic tools, the risk of missing the time point between reversible and irreversible ischemia remains high in these patients.

References

1. Burrows AM, Korumilli R, Lanzino G: How we do it: acute management of subarachnoid hemorrhage. Neurol Res 35:111-116;2013.

2. Pegoli M, et al.: Predictors of excellent outcomes after aneurysmal SAH. J Neurosurg (In Press)

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Bacigaluppi, S., Zona, G., Secci, F. et al. Diagnosis of cerebral vasospasm and risk of delayed cerebral ischemia related to aneurysmal subarachnoid haemorrhage: an overview of available tools. Neurosurg Rev 38, 603–618 (2015). https://doi.org/10.1007/s10143-015-0617-3

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