Neurol India Home 

Year : 2016  |  Volume : 64  |  Issue : 6  |  Page : 1388--1389

Volume of hemorrhage in aneurysmal subarachnoid hemorrhage

Aaron Mohanty 
 Department of Surgery, University of Texas Medical Branch at Galveston, Galveston, Texas - 77555-0517, USA

Correspondence Address:
Aaron Mohanty
Department of Surgery, University of Texas Medical Branch at Galveston, Galveston, Texas - 77555-0517

How to cite this article:
Mohanty A. Volume of hemorrhage in aneurysmal subarachnoid hemorrhage.Neurol India 2016;64:1388-1389

How to cite this URL:
Mohanty A. Volume of hemorrhage in aneurysmal subarachnoid hemorrhage. Neurol India [serial online] 2016 [cited 2019 Aug 24 ];64:1388-1389
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Full Text


Rupture of intracranial aneurysm results in blood release under high pressure into the basal subarachnoid spaces and often into the adjacent cerebral parenchyma and ventricular system. The presence of blood triggers a series of complex molecular events, which result in vasospasm. Although radiological vasospasm can be demonstrated in two-thirds of patients with subarachnoid hemorrhage, clinical vasospasm occurs in approximately 30% of subarachnoid hemorrhage patients. Approximately 10% of patients will have permanent disability as a result of vasospasm.

Several factors have been described in literature that help in predicting the occurrence and severity of vasospasm. These have been conventionally classified into non-modifiable variables and modifiable variables. The non-modifiable variables include age, race, site of aneurysm, preexisting hypertension, nicotine usage, cocaine usage, neurological grade, and amount of hemorrhage visible on the computed tomography (CT) scans. The potentially modifiable variables include the treatment administered, velocity of blood flow measured with transcranial Doppler (TCD) angiography, serum markers (hyperglycemia, leukocytosis, low platelets, antiphospholipid antibodies, the complement system), and cerebrospinal fluid (CSF) markers (lipid peroxides).

Of the above, the amount and location of blood in the initial CT scan has been shown to be a powerful predictor for the development of vasospasm and subsequent occurrence of delayed cerebral ischemia. The “initial hemorrhage burden,” as evidenced in the preadmission CT scan, has been shown to affect the overall outcome independent of other prognostic factors such as age and clinical grade. Although traditionally, the amount of blood is not estimated and grading scales have been used to assess the degree of bleeding, usage of computerized quantitative measurement of the initial clot burden has been suggested to reduce interobserver variability that is commonly observed with routinely used grading scales. Lagares et al., estimated 20 ml to be a critical volume of blood, and found that at 20 ml (which included a sum total of intraventricular, subarachnoid and intraparenchymal blood), the proportion of patients with poor outcome more than doubled.[1] The rate of clearance of clot from the subarachnoid space also has been considered to influence the outcome. In a study among 75 patients, Reilly et al., reported that the initial clot volume and the percentage of clot cleared per day were significant predictors of development of vasospasm.[2] However, other studies have not shown an association between clot clearance and delayed cerebral ischemia, thus indicating that clot clearance is not an independent predictor for a poor outcome.[3]

There have been several grading systems to grade the degree of bleed, as evidenced in the initial CT scan. The most commonly used grading system is the Fisher scale. Though the scale is simple and easy to use, lack of linear correlation between the grade and the degree of vasospasm led researchers to modify the scale. The modified Fischer scale has been more intuitive and demonstrates a linear relationship between the grade and the occurrence of vasospasm. The other reported scales include Claassen scale, which is almost similar to the Modified Fischer scale, and the Subarachnoid sum score (Hijdra scale), which is more comprehensive but cumbersome to use in clinical practice.[4] In a comparative study of the Fisher, Modified Fisher, and Classen scales, Kramer et al., suggested that the modified Fisher scale correlated best with the overall outcome because each unit increase was associated with an incremental risk for worsened outcome.

In the present article, the authors have tried to enumerate the risk factors associated with the volume of hemorrhage in patients with aneurysmal subarachnoid hemorrhage.[5] One of the significant prognostic factors was pre-diastolic blood pressure, and the authors were able to correlate a preadmission high diastolic blood pressure with a greater hemorrhage volume. The authors also reported that anterior communicating artery aneurysms and multiple intracranial aneurysms were associated with greater hemorrhage volume. This study, which is a retrospective analysis of 155 patients admitted between September 2013 and February 2015, would have been more useful if it had correlated the predisposing factors and hemorrhage volume with the overall outcome.

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1Lagares A, Jiménez-Roldán L, Gomez PA, Munarriz PM, Castaño-León AM, Cepeda S, et al. Prognostic value of the amount of bleeding after aneurysmal subarachnoid hemorrhage: A quantitative volumetric study. Neurosurgery. 2015;77:898-907.
2Reilly C, Amidei C, Tolentino J, Jahromi BS, Macdonald RL. Clot volume and clearance rate as independent predictors of vasospasm after aneurysmal subarachnoid hemorrhage. J Neurosurg 2004;101:255-61.
3Ko SB, Choi HA, Helbok R, Schmidt JM, Badjatia N, Claassen J, et al. Quantitative analysis of hemorrhage clearance and delayed cerebral ischemia after subarachnoid hemorrhage. J Neurointerv Surg 2016;8:923-6.
4Kramer AH, Hehir M, Nathan B, Gress D, Dumont AS, Kassell NF, et al. A comparison of 3 radiographic scales for the prediction of delayed ischemia and prognosis following subarachnoid hemorrhage. J Neurosurg 2008;109:199-207.
5Liu J, Zhao D, Li H, Lu Y, Wu G, Hou K, et al. Risk factors of the volume of hemorrhage in aneurysmal subarachnoid hemorrhage. Neurol India 2016;64:686-91.