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Table of Contents    
COMMENTARY
Year : 2019  |  Volume : 67  |  Issue : 5  |  Page : 1240-1241

Early Detection of Delayed Cerebral Ischemia Following Aneurysmal Subarachnoid Hemorrhage – Is Computerized Tomography Perfusion Scan the Right Answer?


Neurosurgery, KMC, Manipal, Karnataka, India

Date of Web Publication19-Nov-2019

Correspondence Address:
Dr. Girish Menon
Neurosurgery, KMC, Manipal, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.271279

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How to cite this article:
Menon G. Early Detection of Delayed Cerebral Ischemia Following Aneurysmal Subarachnoid Hemorrhage – Is Computerized Tomography Perfusion Scan the Right Answer?. Neurol India 2019;67:1240-1

How to cite this URL:
Menon G. Early Detection of Delayed Cerebral Ischemia Following Aneurysmal Subarachnoid Hemorrhage – Is Computerized Tomography Perfusion Scan the Right Answer?. Neurol India [serial online] 2019 [cited 2019 Dec 10];67:1240-1. Available from: http://www.neurologyindia.com/text.asp?2019/67/5/1240/271279




Delayed cerebral ischemia (DCI) remains an unpredictable, devastating complication seen in 17%–40% of patients following aneurysmal subarachnoid hemorrhage (aSAH). DCI remains elusive to early detection, and recent advances in neuroimaging have failed to provide a safe and effective diagnostic tool to identify the subgroup of patients among aSAH who are prone to develop DCI. The authors have attempted to adress this issue by pooling the available data from the literature.[1]

Computerized tomography perfusion (CTP) scans performed following aSAH provide valuable indicators to predict the onset of DCI and appear to be the most effective diagnostic tool currently available in combating DCI.[2],[3],[4],[5] The authors performed a meta-analysis of all scientific publications which included patients with aSAH who underwent CT perfusion scan performed in the acute phase (<4 days after aSAH) for the prediction of DCI. CTP was measured quantitatively, semi-quantitatively (comparing quantitative perfusion in one hemisphere to contralateral side), or qualitatively (visual evaluation for side-to-side perfusion asymmetry on the different color maps). A meta-analysis of three major articles selected after a review of 22 relevant articles suggests that patients with a positive CTP test in the acute phase after aSAH were approximately 32 times as likely to develop DCI compared with those patients without. This meta-analysis thereby seeks to reinforce the existing conviction on the role of CTP in the identification of patients at risk for DCI during the acute phase (<4 days) after aSAH. These results notwithstanding, the battle against DCI is far from over.

DCI sets in about 4–14 days after aSAH, and at times late up to the third week. This definite undisputable fact apart, mystery shrouds the entire spectra of cerebral vasospasm and DCI which remains a nightmare for all cerebrovascular surgeons and interventionists. It was long believed that DCI resulting in devastating neurological deficits and occasionally even death is an irreversible end point of a dynamic process starting with asymptomatic vasospasm, followed by symptomatic vasospasm and transient delayed ischemic neurological deficist (DIND). Angiographic spasm is detected in 75% of the patients with aSAH, but DCI and morbid complications develop only in 17%–40% of cases. This discrepancy in the incidence of vasospasm and the occurrence of DCI along with the observation that reduction of relative cerebral blood flow (CBF) and relative cerebral blood volume (CBV) happen even in the absence of cerebral vasospasm suggests that vasospasm may not be the sole precursor or predictor of an imminent DCI.[6]

The clinical condition on admission, the amount of extravagated blood, age, fever, leukocytosis and hyponatremia are all important predictors for the development of DCI. As vasospasm was considered to be a precursor of DCI, earlier attempts have all been targeted at the detection of vasospasm. Digital subtraction angiography (DSA) remains the gold standard for confirming the diagnosis of cerebral vasospasm. DSA, however, is invasive and cannot be repeated frequently. Transcranial Doppler sonography (TCD) is an effective, user-friendly noninvasive bedside option suitable for daily monitoring. However, TCD interpretation is subjective and TCD does not allow the detection of peripheral vessel vasospasm. Because reduced perfusion in the acute stage after SAH is seen more often in patients who later develop DCI, the focus gradually shifted to perfusion measurement through CTP. A paradigm shift has thus evolved targeting detection and containment of cerebral ischemia through CTP rather than focus on vasospasm.

Few studies continuously monitoring cerebrovascular autoregulation have shown that patients developing DCI have lower tissue oxygenation levels following aSAH.[5] Similarly, studies have also shown that patients with initial CBF reductions or hemodynamic disturbances on admission were more vulnerable to develop DCI.[1],[2],[3],[4] CTP allows visualization of brain perfusion and monitoring the capacity of cerebrovascular autoregulation – two important determinants of DCI. Many authors have shown that baseline and periodically repeated CTP after aSAH conclusively predict the onset of DCI.[1],[3] CTP assessment of decreased CBF and prolonged mean transit time (MTT) and time to peak (TTP) reflects an impaired autoregulation and vasospasm. These are warning signals of an imminent DCI. CTP provides quantitative information on CBV, CBF, MTT, and TTP. Interpretation of these parameters gives adequate information on the functionality of autoregulation and the risk of DCI.

CTP, however, has significant limitations. The time point for the first CTP and the frequency and need for repetition are not clearly defined. The risk of radiation forbids multiple repetitions. The meta-analysis referred to conclusively proves the diagnostic value of an early CTP in the acute phase. Vasospasm and DCI are, however, known to occur later as well. Routine CTPs expose the patient to unnecessary radiation, whereas CTP at the moment of neurological decline might delay the initiation of appropriate treatment. Another disadvantage of this method is the limited brain volume included in the analyses of CTP [regions of interest (ROIs)]. Prediction of vascular territories in which hypoperfusion might occur is difficult and bilateral decreased perfusion can be missed. It is yet unclear as to is better suited to look for global, hemispheric, or regional perfusion. Preselection of ROIs carries the risk that areas of brain hypoperfusion remain undetected. Whole-brain CTP seems to mitigate and overcome this problem of focal perfusion measurement to some extent.

As admitted by the authors, CT perfusion maps are generated in different institutions by different CTP protocols and postprocessing softwares, and an uniform protocol is yet to be defined. Uniform definitions of an abnormal CTP test result are absent and different CTP parameters with various thresholds are used to evaluate the CTP test results. This lack of uniformity is a major challenge confronting universal acceptance of CTP.

CTP is an important tool in the early prediction of DCI following aSAH. The implementation of CTP in routine clinical practice needs further validation. The battle may have been won, but the war is far from over.



 
  References Top

1.
Sun H, Ma J, Liu Y, You C. CT perfusion for identification of patients at risk for delayed cerebral ischemia during the acute phase after aneurysmal subarachnoid hemorrhage: A metaanalysis. Neurol India 2019;67:1235-39.  Back to cited text no. 1
  [Full text]  
2.
Mir DIA, Gupta A, Dunning A, Puchi L, Robinson CL, Epstein HA, et al. CT perfusion for detection of delayed cerebral ischemia in aneurysmal subarachnoid hemorrhage: A systematic review and meta-analysis. AJNR Am J Neuroradiol 2014;35:866-71.  Back to cited text no. 2
    
3.
Malinova V, Dolatowski K, Schramm P, Moerer O, Rohde V, Mielke D. Early whole-brain CT perfusion for detection of patients at risk for delayed cerebral ischemia after subarachnoid hemorrhage. J Neurosurg 2016;125:128-36.  Back to cited text no. 3
    
4.
Sun H, Zhang H, Ma J, Liu Y, Wang K, You C. Accuracy of computed tomography perfusion in detecting delayed cerebral ischemia following aneurysmal subarachnoid hemorrhage: A meta-analysis. Neurol India 2013;61:507-12.  Back to cited text no. 4
  [Full text]  
5.
Gölitz P, Hoelter P, Rösch J, Roessler K, Knossalla F, Doerfler A. Ultra-early detection of microcirculatory injury as predictor of developing delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage. Clin Neuroradiol 2018;28:501-7.  Back to cited text no. 5
    
6.
Chai W, Sun X, Lv F, Wan B, Jiang L. Clinical study of changes of cerebral microcirculation in cerebral vasospasm after SAH. Acta Neurochir Suppl 2011;110:225-8.  Back to cited text no. 6
    




 

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