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Table of Contents    
COMMENTARY
Year : 2016  |  Volume : 64  |  Issue : 4  |  Page : 692-693

“Vices of my blood” — Risk factors of subarachnoid hemorrhage


Department of Neurosurgery, Sher-i-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India

Date of Web Publication5-Jul-2016

Correspondence Address:
Abrar Ahad Wani
Department of Neurosurgery, Sher-i-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.185403

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How to cite this article:
Wani AA. “Vices of my blood” — Risk factors of subarachnoid hemorrhage. Neurol India 2016;64:692-3

How to cite this URL:
Wani AA. “Vices of my blood” — Risk factors of subarachnoid hemorrhage. Neurol India [serial online] 2016 [cited 2019 Jul 21];64:692-3. Available from: http://www.neurologyindia.com/text.asp?2016/64/4/692/185403


Subarachnoid hemorrhage (SAH) has haunted mankind since times immemorial, with its estimated incidence being between 10 and 28 cases per 100,000 individuals. In the prebiblical era, Hippocrates described that “when persons in good health are suddenly seized with pains in the head, and straightway are laid down speechless, and breathe with stertor, they die in seven days, unless fever comes on.” It was only in the early part of the tenth century that Symonds coined the term “spontaneous subarachnoid hemorrhage.”[1],[2] Surprisingly, the surgical morbidity and mortality too, did not change much since the landmark study by Sundt in 1978, in which he reported the combined morbidity and mortality rates of 1.6% in the good-grade patients and 35% in the poor-grade group.[3] The risk factors for SAH include age, female gender, hypertension, smoking, alcohol, drugs, oral contraceptives, stimulant drugs, aneurysm characteristics, polycystic kidney disease, coarctation of the aorta, collagen vascular diseases, connective tissue diseases such as Marfan syndrome and Ehler–Danlos disease, and familial history. Numerous studies were done on the aforementioned risk factors for SAH and the predictors of outcome, but the conclusions showed conflicting results.[4],[5] In the study in focus, the authors have tried to assess the relationship between SAH and hypertension, multiplicity of aneurysms, and anterior communicating artery (ACom) aneurysms.

The association of hypertension with aneurysm rupture and formation has been studied in numerous studies, with results varying between the two extremes.[4],[5]

In the Rochester study, 28% of the 98 patients with SAH had systolic blood pressures >160 mmHg, and only 30% had diastolic blood pressures >95 mmHg; in the Cooperative study, 41% of patients with unruptured aneurysms had hypertension; in Walnut Creek Contraceptive Drug Study, the patients with SAH had twice the incidence of HT compared with controls; and in two prospective cohort studies, the Framingham Study and the Honolulu Heart Study, hypertension was a significant risk factor for hemorrhagic strokes. Although the Honolulu study did not consider patients with SAH separately, the Framingham study did.[5] However, some studies like the Mayo study and some experimental studies failed to show any association. Despite many shortcomings, the finger points toward HT being a risk factor for bleeding in aneurysms. As the authors have pointed out, this finding is significant as HT is the only modifiable factor in the rupture of aneurysms.

The patients presenting with SAH have multiple aneurysms (MAs) to the tune of 15–35%. Apparently, it appears that patients with MAs should have bad prognosis, but studies could not prove that with certainty.[6],[7] The volume of blood in the cisterns is not more in these patients than in patients harbouring a single aneurysm. This is a logical conclusion as only one aneurysm has ruptured even in a patient having multiple aneurysms, and so a higher Fisher grade is not expected. The authors of the study in focus, however, have shown the association between MAs and higher Fisher grades, but to prove it, studies with a larger number of patients may be needed to increase the statistical power of the analysis.

Long-term survivors of SAH have a higher mortality as compared with the general population. One of the factors in this group is the presence of multiple aneurysms. The dictum that patients with multiple aneurysms should be meticulously followed up, is justified.[7] The guidelines for the management of these unruptured aneurysms have been described in many multicentric studies.[4]

In patients with MAs, the ACom aneurysm is more often the site of rupture than other aneurysms. The reason for this high rate of rupture is the very high incidence of associated vascular variations in the circle of Willis in these patients, leading to a greater hemodynamic stress on the vessel wall, which is one of the etiological factors in the genesis and also in the rupture of aneurysms.[6],[7]

The authors have used the modified Fisher scale for evaluating the association, and this modification might be needed because the original grading did not keep intraventricular hemorrhage (IVH) and intracerebral hemorrhage (ICH) as separate factors in predicting the incidence of vasospasm, as presence of blood in the subarachnoid cisterns and an associated IVH have an additive effect in causing vasospasm. In more than half of the patients with SAH, delayed vasospasm develops between 3 and 14 days after SAH; this has been considered as the single and the most important cause of delayed cerebral ischemia and a poor outcome.[8],[9] The culprit is the blood in cisterns, and the more it is, the worse it is for the patients. As Shakespeare mentioned in his famous play Othello: “I do confess the vices of my blood.”

 
  References Top

1.
McHenry LC Jr. Garrison's History of Neurology: Revised and Enlarged with a Bibliography of Classical, Original and Standard Works in Neurology. Springfield, Illinois: Charles C Thomas; 1969. p. 11.  Back to cited text no. 1
    
2.
Symonds CP. Spontaneous subarachnoid haemorrhage. Q J Med 1924;18:93-123.  Back to cited text no. 2
    
3.
Sundt TM Jr, Whisnant JP. Subarachnoid hemorrhage from intracranial aneurysms. Surgical management and natural history of disease. N Engl J Med 1978; 299:116-22.  Back to cited text no. 3
[PUBMED]    
4.
Steiner T, Juvela S, Unterberg A, Jung C, Forsting M, Rinkel G; European Stroke Organization. European Stroke Organization guidelines for the management of intracranial aneurysms and subarachnoid haemorrhage. Cerebrovasc Dis 2013;35:93-112.  Back to cited text no. 4
    
5.
Longstreth WT, Thomas DK, Mark SY, Gerald VB. Risk factors for subarachnoid hemorrhage. Stroke 1985;16:377-85.  Back to cited text no. 5
    
6.
Kaminogo M, Yonekura M, Shibata S. Incidence and outcome of multiple intracranial aneurysms in a defined population. Stroke 2003;34:16-21.  Back to cited text no. 6
    
7.
Huhtakangas J, Lehto H, Seppä K, Kivisaari R, Niemelä M, Hernesniemi J, et al. Long-term excess mortality after aneurysmal subarachnoid hemorrhage: Patients with multiple aneurysms at risk. Stroke 2015;46:1813-8.  Back to cited text no. 7
    
8.
Frontera JA, Claassen J, Schmidt JM, Wartenberg KE, Temes R, Connolly ES Jr, et al. Prediction of symptomatic vasospasm after subarachnoid hemorrhage: The modified fisher scale. Neurosurgery 2006;59:21-7.  Back to cited text no. 8
    
9.
Krishna H, Wani AA, Behari S, Banerji D, Chhabra DK, Jain VK. Intracranial aneurysms in patients 18 years of age or under: Are they different from aneurysms in the adult population? Acta Neurochir (Wien) 2005;147:469-76.  Back to cited text no. 9
    




 

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